GAINESVILLE, Fla. and CAMBRIDGE, Mass., Aug. 01, 2022 (GLOBE NEWSWIRE) -- Applied Genetic Technologies Corporation (“AGTC” or the “Company”) (Nasdaq: AGTC), a clinical-stage biotechnology company focused on the development and potential commercialization of adeno-associated virus (AAV)-based gene therapies for the treatment of rare and debilitating diseases with an initial focus on inherited retinal diseases, today announced that management will be participating in the following investor conferences:

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SANTA MONICA, Calif., Aug. 01, 2022 (GLOBE NEWSWIRE) -- Opiant Pharmaceuticals, Inc. (“Opiant” or “Company”) (NASDAQ: OPNT), a specialty pharmaceutical company developing medicines to treat addictions and drug overdose, today announced it will report its financial results for the second quarter ended June 30, 2022, after the financial markets close on Thursday, August 11, 2022.

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Opiant Pharmaceuticals to Report Second Quarter 2022 Financial Results and Host Conference Call and Webcast on August 11, 2022

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SAN DIEGO, Aug. 01, 2022 (GLOBE NEWSWIRE) -- Belite Bio, Inc (NASDAQ: BLTE), a San Diego based clinical stage biopharmaceutical drug development company targeting untreatable eye diseases, will host a conference call on Thursday, August 11, 2022, at 4:30 p.m. Eastern time to discuss the Company’s financial results for the first half, ended June 30, 2022, and provide a corporate progress update. The financial results will be issued in a press release on Wednesday, August 10, 2022.

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CAMBRIDGE, Mass., Aug. 01, 2022 (GLOBE NEWSWIRE) -- Surface Oncology (Nasdaq: SURF), a clinical-stage immuno-oncology company developing next-generation immunotherapies that target the tumor microenvironment, today announced that Rob Ross, M.D., chief executive officer, will participate in a virtual panel discussion entitled, “IOs Wide Open - Opportunity and Challenges in Immuno-Oncology” at the 2022 Wedbush PacGrow Healthcare Conference. The panel discussion will take place on Tuesday, August 9, 2022, at 8:00 am ET.

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Montrouge, France, August 1, 2022

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DBV Technologies Reports Second Quarter 2022 Financial Results

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NEW YORK, Aug. 01, 2022 (GLOBE NEWSWIRE) -- Cellectis (the “Company”) (Euronext Growth: ALCLS - NASDAQ: CLLS), a clinical-stage biotechnology company using its pioneering gene-editing platform to develop life-saving cell and gene therapies, today announced that the U.S. Food and Drug Administration (FDA) has cleared Cellectis’ Investigational New Drug (IND) application to initiate a Phase 1/2a clinical trial of UCART20x22 for patients with relapsed or refractory Non-Hodgkin Lymphoma (r/r NHL). The Company plans to begin enrolling patients in the NatHaLi-01 study in the second half of the year.

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PITTSBURGH, Aug. 01, 2022 (GLOBE NEWSWIRE) -- Krystal Biotech, Inc. (the “Company”) (NASDAQ: KRYS), the leader in redosable gene therapy, today announced that the United States Food and Drug Administration (FDA) has accepted its Investigational New Drug (IND) application to evaluate KB407 in a clinical trial for cystic fibrosis (CF).

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TOKYO, Japan and CAMBRIDGE, United Kingdom, Aug. 02, 2022 (GLOBE NEWSWIRE) -- Sosei Group Corporation (“the Company”; TSE: 4565) and AbbVie (NYSE: ABBV), a research-based global biopharmaceutical company, announce they have entered a new drug discovery collaboration and option-to-license agreement to discover, develop and commercialize small molecules that modulate novel G protein-coupled receptor (GPCR) targets associated with neurological disease.

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Basel, 2 August 2022 - Roche (SIX: RO, ROG; OTCQX: RHHBY) today announced that the Phase III IMscin001 study evaluating a subcutaneous formulation of Tecentriq® (atezolizumab) met its co-primary endpoints. The study showed non-inferior levels of Tecentriq in the blood (pharmacokinetics), when injected subcutaneously, compared with intravenous (IV) infusion, in cancer immunotherapy-naïve patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) for whom prior platinum therapy has failed. The safety profile of the subcutaneous formulation was consistent with that of IV Tecentriq.

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SNIPR Biome Granted New US Patent Covering Lytic CRISPR Phage

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Type 1 diabetes (T1D) is a chronic immune-mediated disease characterized by the destruction of pancreatic -cells, resulting in absolute insulin deficiency and hyperglycemia. It is primarily a disease of youth, accounting for approximately 85% of cases in people under the age of 20 and 5% to 10% of all diagnosed cases of diabetes [1,2]. Although the exact mechanisms are unknown, T1D is thought to develop through immune system activation against -cell antigens and the initiation of proinflammatory cytokine responses. Environmental factors, obesity, viral infections, and nutritional factors were found to play a role in the pathophysiology as well [3]. T1D predisposes to a number of comorbidities, such as obesity, chronic kidney disease, metabolic syndrome, coronary artery disease, and hypertension. Such predispositions may account for higher mortality rates, affecting up to one in 10 adult patients within a year of diagnosis [4]. In fact, diabetic nephropathy (DN) is said to account for up to 40% of end-stage renal disease (ESRD) cases worldwide. Cardiovascular events account for up to 70% of T1D deaths and are 10 times more common in diabetics than in non-diabetics [5]. Therefore, it is critical to focus on novel therapies that aim to reduce the risks of acute complications such as hypoglycemia and diabetic ketoacidosis (DKA) while avoiding long-term complications such as DN, neuropathy, and retinopathy [5].

Exogenous insulin is currently the most prevalent treatment for T1D. Although exogenous insulin administration may be life-saving, it is not a cure for the disease. If patients are unable to maintain tight glycemic control by strictly adhering to their insulin regimen, they will invariably develop severe secondary complications that may shorten their life span [6]. Exogenous insulin is not a viable substitute for normal pancreatic islet function, mainly due to the absence of accurate temporal glucose control over time [7]. The administration of insulin can also result in hypoglycemic episodes [6]. A cross-sectional study conducted in Mexico revealed that patients' fear of hypoglycemic episodes prevented them from complying with their insulin treatment plan [8].

Replacement of the defective insulin-producing cells (IPC) is yet another potential therapy for T1D. This is possible through transplantation of the pancreas. Since the first pancreatic transplant took place in 1966, over 50,000 such transplants have been performed worldwide. Patients with T1D who receive a pancreatic transplant were found to have a reduced risk of subsequent complications and a longer life expectancy [9]. However, since transplantation is a major surgical procedure, patients must be fit for surgery [6]. Transplants necessitate permanent immunosuppression, which may put patients at risk for a variety of infections. In addition, they are associated with a number of postoperative complications, such as pancreatitis, due to low tolerance to cold ischemia, bleeding, thrombosis, and anastomotic leakage, which may require relaparotomy and graft pancreatectomy in recipients [9].

An alternative to pancreatic transplantation that is both safe and effective is islet cell transplantation. Scharp et al. published the first case of allogeneic intraportal islet transplantation for T1D in 1990, which led to short-term insulin independence and paved the way for clinical islet transplantation [10]. Despite the fact that the immunosuppressive regimen reported from Edmonton, Canada, also known as the Edmonton protocol (the Edmonton protocol introduced significant adjustments to the transplantation procedure, including the use of an immunosuppressive regimen free of steroids and the transplanting of an average islet mass of 11,000 islet equivalents per kilogram) has achieved unprecedented success in islet transplantation in terms of insulin independence, a number of factors continue to influence the outcome of this minimally invasive procedure [11]. Islet cell transplantation can induce a rapid inflammatory reaction in the circulation, leading to the loss of the vast majority of transplanted islets. The use of large doses of immunosuppressants during transplantation compromises the long-term viability and function of the graft, and the need for long-term immunosuppressive medications after the transplant poses a risk of organ damage, malignancies, new infections, and new-onset T1D in patients [12]. The high cost of islet transplantation and the paucity of human cadaveric islets highlight the urgent need for innovative pancreatic islet transplantation procedures [7]. This is where stem cells (SCs) pose an important role.

SCs are a highly promising novel treatment for T1D due to their ability to differentiate into several cell types and their regenerative potential. SCs can be categorized into four basic groups based on their origin as shown in Figure 1.

Mesenchymal stem cells (MSCs), also called mesenchymal stromal cells, are non-hematopoietic, multipotent SCs. They can be extracted from a variety of sources, including bone marrow, liver, kidney, adipose tissue, urine, umbilical cord blood, umbilical tissue, Wharton's jelly, placenta, and even endometrial tissue (menstrual blood-derived endometrial stem cells - MenSC). Several surface markers, including CD73, CD90, and CD105, can be utilized to identify MSCs. Due to their ability to differentiate into numerous cell types, they can be used to repopulate damaged tissues [13,14]. MSCs have gained enormous popularity in the treatment of T1D because of their ability to regulate fibrosis and tissue regeneration, as well as their ability to modulate immunological function. In addition, they produce a variety of secretory molecules, such as cytokines and exosomes, which play an essential role in the treatment of T1D [15]. Studies on animals treated with MSCs have shown a significant reduction in hyperglycemia, as evaluated by a decrease in serum glucose and an increase in insulin and C-peptide levels. In addition, they were able to restore normal levels of lipid fractions. Using MSCs lowered the serum levels of both liver and kidney function markers in diabetic rats, demonstrating their hepato-renal protective benefits in T1D [16].

Several mechanisms have been discovered to play a role in the management of T1D by MSCs (Figure 2).

MSCs, such as bone marrow stromal cells, promote angiogenesis through the secretion of cytokines such as basic fibroblast growth factor and vascular endothelial growth factor (VEGF) [17]. In addition, they play a crucial role in immunomodulation by moving to areas of inflammation and modifying the phenotype of dendritic cells (DC), T cells, B cells, and natural killer cells. They downregulate proinflammatory cytokines and escape CD8+ T cell-mediated apoptosis, inhibit maturation of DC, while reducing T-lymphocyte proliferation via transforming growth factor-beta 1 (TGF-1), hepatocyte growth factor, and nitric oxide. By stimulating the production of regulatory T cells, TGF-1 plays a significant role in the immunomodulation of MSCs. MSCs have also been found to improve the function, survival, and graft outcome of neonatal porcine islets by increasing the expression of genes involved in the formation of endocrine cells, insulin, and platelet-derived growth factor alpha (PDGFR-). PDGFR- suppresses Notch 1 signaling (Notch 1 downregulates transcription factors involved in the formation of endocrine cells and insulin), resulting in the maturation and development of islet cells [18]. Zhou et al. discovered that wild-type p53-induced phosphatase 1 (a serine/threonine phosphatase) regulates the immunomodulatory properties of MSCs via the expression of interferon-alpha and bone marrow stromal cell antigen 2, consequently playing an important role in the therapeutic effects of MSCs in T1D [19].

Even though studies have shown that MSCs are capable of reconfiguring the immune system, they must be rescued to some extent from immune-mediated destruction, indicating that immunomodulation will be necessary even if a viable MSCs therapy for T1D is produced [20]. When using -cells from an allogeneic stem cell source, an alloreactive response to donor antigens will be generated unless we obtain SCs from the patient's own cells. To circumvent this, researchers have investigated encapsulation strategies employing semipermeable immune barriers to provide immune shielding and prevent graft rejection [21]. Some studies have also demonstrated that the use of suicide genes together with stem cell transplants promotes functional immune reconstitution and thereby prevents graft-versus-host disease in patients [22].

It has been demonstrated that MSCs undergo apoptosis in the circulation of the host or in engrafted tissues following delivery to the patient's body, which plays a significant part in their therapeutic role in T1D. During the execution of apoptosis, apoptotic extracellular vesicles (apoEVs), formerly known as apoptotic bodies, have emerged as regulators of numerous biological processes, as opposed to being only debris. Specifically, apoEVs have been shown to regulate T cell and macrophage immunological function as well as stimulate tissue repair, including skin regeneration and vascular protection [23].

This game-changing discovery of MSCs in the treatment of T1D has propelled biological sciences to a new level of sophistication, allowing for the manipulation of cell fate and the cultivation of higher-order cellular structures. However, there is still a huge gap regarding its application in actual clinical practice.

We were only able to find 12 clinical trials on PubMed that evaluated the use of MSCs in the treatment of T1D. Ten of the 12 studies were undertaken in Asia, primarily in China and India. To date, the exact pathogenesis of T1D is not fully understood. Genetic factors have been found to play a role in the development of T1D, which may have affected the outcomes of previous clinical trials. Therefore, conducting multiple different studies worldwide would not only enable us to identify the effects of ethnicity and genetics on the response to MSC therapy in T1D patientsbut also help us to generalize the efficacy of MSCs to the entire population. In order to achieve the best outcomes while using medications to treat T1D, it is also crucial to perform additional research to more clearly identify the pathophysiology of T1D.

In the course of studying the patient selection criteria utilized in clinical trials, we made a fascinating discovery. We found that every clinical study had excluded patients with immunosuppression, viral illnesses such as hepatitis B and C, comorbidities including hematologic diseases, rheumatologic diseases, and kidney diseases, and pregnant patients, all of which could have influenced the results of the studies. Our present understanding of the action of apoEVs, as described by Fu et al., leads us to believe that in order for MSCs to undergo apoptosis, their recipients must be able to initiate apoptotic activity [23]. In order for this to occur, patients must have a particular number of cytotoxic T cells or natural killer cells; hence, patients who do not meet this criterion are unlikely to benefit from MSC delivery. To further elucidate the mechanisms of action of MSCs, it is essential to undertake additional studies with immunosuppressed patients in order to identify the optimal cohort of T1D patients for MSC therapy. In addition, further clinical research should be conducted to uncover the apoptotic signals that stimulate tissue regeneration and angiogenesis, as recognizing these signals would allow us to utilize a channel in parenchymal tissue to increase its regeneration capacity.

We also observed that the majority of trials exclusively enrolled patients with recent-onset T1D. A study conducted in Iran revealed that early transplantation of MSCs resulted in superior outcomes for T1D patients compared to late transplantation. This may be due to the honeymoon phase of diabetes, which may have obscured the effects of MSCs in these studies [24]. The honeymoon phase is the period during which a person with T1D appears to improve and may only require minimal amounts of insulin or experience normal or near-normal blood sugar levels without insulin. To extrapolate the results to a larger population and unmask the effects of the honeymoon period, it is necessary to conduct trials on patients with late-onset T1D.

To date, the exact mechanism by which MSCs contribute to the remission of T1D has not been identified; therefore, further research is required to get a better knowledge of mechanisms such as immunomodulation, homing, and paracrine signaling of MSCs. It is also vital to undertake studies to discover the appropriate number of MSCs, injection frequency, and optimal infusion route in order to maximize results. Cai et al. concluded that pancreatic arterial transfusion would assist in avoiding the first pass pulmonary effect of MSCs, hence lowering the sequestration of MSCs in the lungs and allowing for optimal results [25].

A few studies have used 3D microspheres to increase the proliferation capacity of MSCs with positive results. However, there is insufficient information available regarding the proliferation capacity, revascularization, efficiency of differentiation, and survival time of MSCs. Therefore, conducting studies to elucidate these aspects of MSC therapy is an urgent necessity. We would also be able to learn more about the graft's survival time and tumorigenic potential if we followed the patients for a longer period of time.

Patient-specific variables such as age, body mass index, lifestyle, socioeconomic status, level of activity, diet, autoimmune status, and drug interactions must be taken into consideration while conducting studies and analyzing data. In order to identify the ideal conditions necessary to create the desired quantities of MSCs to achieve remission of T1D, future research must also incorporate in-depth information regarding external factors that affect the viability of MSCs, such as storage conditions, plating density, and culture media.

In this article, we aim to discuss the role of MSCsderived from various tissues in the treatment of T1D, as well as their feasibility and limitations.

We present a summary of the extraction methods, advantages, limitations, and outcomes from several studies of MSCs derived from various types of tissues.

The majority of umbilical cord tissue-derived stem cells (UC-MSCs) are found in the subcortical endothelium of the umbilical cord, the perivascular area, and Wharton's jelly [26]. According to studies, roughly1 106UC-MSC can be extracted from a 20 cm human umbilical cord [27]. MSCs isolated from Wharton's jelly have been grown for over 80 population doublings without showing any signs of senescence, morphological alterations, an increase in growth rate, or a change in their ability to develop into neurons. Recent research has demonstrated that xenotransplantation of post-differentiated human UC-MSC without immunosuppressive therapy does not result in rejection [28]. This lack of immunogenicity may be attributable to the absence of major histocompatibility II and co-stimulatory molecules such as CD80 (B7-1), CD86 (B7-2), and CD40 [29]. Chao et al. successfully differentiated human UC-MSC into clusters of mature islet-like cells with insulin-producing capacity. In the islet cells, they detected an increase in insulin and other -cell-related genes, including Pdx1, Hlxb9, Nkx2.2, Nkx6.1, and Glut-2. Moreover, they discovered that hyperglycemia in diabetic rats was greatly under control after xenotransplantation of human pancreatic islet-like cell clusters [28]. Patients with newly diagnosed T1D who received repeated intravenous doses of allogeneic UC-MSC showed improved islet cell preservation and a significant rise in postprandial C-peptide levels. However, C-peptide levels did not alter significantly in patients with juvenile-onset T1D. The number of UC-MSC contributed more than other indicators to the prediction of clinical remission, bolstering the evidence of dose-dependent therapeutic efficacy. Therefore, appropriate doses and courses of MSC transplantation should be granted importance in future research [30].

UC-MSC can also be used to treat chronic complications of T1D, such as neuropathy, DN, and retinopathy [31]. Studies have shown that intraperitoneal injection of human UC-MSC can ameliorate renal injury in streptozotocin-induced diabetic mice.[32]. A mice study conducted in China demonstrated that the combination of human UC-MSC and resveratrol can better protect renal podocyte function and the resulting reduction in blood glucose levels and renal damage is superior to those obtained with insulin administration [33]. This suggests that the combination of resveratrol and human UC-MSC may be an innovative technique for treating T1D; however, additional research on humans is necessary to determine the effects of this combination treatment on the management of DN.Another investigation involving mice revealed that UC-MSC therapy restored erectile function by suppressing toll-like receptor 4, alleviating corpora cavernosa fibrosis, and boosting the production of VEGF and endothelial nitric oxide synthase [34]. Nonetheless, a significant advantage of UC-MSC is that they are a rich source of many SCs that can be easily manipulated [27]. They are collected at delivery by clamping and severing the umbilical cord. There are no ethical concerns regarding the use of UC-MSC because the collecting process is non-invasive and retains material that would otherwise be discarded as waste.

Adipose tissue-derived mesenchymal stem cells (ADSCs) are a group of cells that arise from the mesoderm during embryonic development. Amongst several types, subcutaneous adipose tissue seems to be the most clinically relevant source, being available in abundance for harvest, and its isolation only slightly invasive [35,36].

While two major kinds of adipose tissue (white and brown) have been isolated and studied, we focus on white adipose, which produces ADSCs, as brown adipocytes have not yet demonstrated an association with insulin resistance. White adipose tissue expressing uncoupling protein 2 (an isoform of uncoupling protein 1in brown adipose) acts as a storage of excess energy in the form of triglycerides and is thus prone to causing obesity and abnormalities in metabolic pathways such as insulin resistance during hyperplasia [37].

The extracted cell group of interest consists of a putative stem cell population of fibroblast-like cells known as processed lipoaspirate (PLA), found within the stromal compartments of adipose tissue [38]. Obtaining the sample requires lipoaspiration, and although the technique does not negatively affect the function of ADSCs, the vacuum process involved can cause damage to mature adipocytes [37]. Studies have shown that successfully extracted PLA can then differentiate in vitro into multiple cell lineages (including adipogenic, myogenic, chondrogenic, and osteogenic cells), thus providing another source of SCs with multi-germ-line potential instead of the traditional bone marrow-derived MSCs [38-41]. The discovery of the ability of ADSCs to efficiently differentiate into IPC has shed new light on the approach to T1D management [41].

ADSCs utilization can help avoid ethical barriers and tumorigenic complications that are increasingly encountered during stem cell isolation from embryos and induced pluripotent SCs [36]. Yet another advantage of ADSCs for their therapeutic application happens to be the relatively painless procedure and high yields in harvested cell numbers compared to bone marrow procurement [40]. These cells are devoid of human leukocyte antigen-DR expression and therefore have been successfully transplanted via intravenous, intraperitoneal, and renal capsule administration in mice without the need for immunosuppression [36,42].

Insulin replacement therapy with the help of co-transplantation of insulin-secreting ADSCs has been studied as an alternative to lifelong insulin therapy. As with multiple studies, no adverse effects were observed with ADSCs infusion, and in fact, an impressive absence of DKA episodes in all participants was seen [43]. A prospective study conducted in 2015 on 20 patients with T1D found better diabetic control (hemoglobin A1c levels) and sustained improvements in fasting blood sugar, postprandial blood sugar, hemoglobin A1c, and C-peptide levels with the transplantation of autologous insulin-secreting ADSCs [44]. Dantas et al. concluded that combination therapy with ADSCs and Vitamin D (daily cholecalciferol for six months) without immunosuppression was safe, demonstrated immunomodulatory effects, and may play a role in -cell preservation in patients with newly diagnosed T1D [45]. The significant functional and morphological improvements in islet cells as early as two months after transplantation of IPC clusters derived from ADSCs point to the promising nature of this therapeutic approach for achieving target normoglycemia [46,47]. A recent study conducted in 2022 discovered that systemic administration of ADSCs protects male non-obese diabetic (NOD) mice against diabetes induced by programmed death-1 and programmed death-ligand 1 (PD-1/PD-L1) inhibition. Multiple injections of neutralizing antibodies against mouse PD-L1 induce a significant infiltration of immune cells in the islets and a decrease in the -cell area and insulin content of the pancreas. Despite this, systemic ADSCinjection partially protected the pancreas from -cell loss and preserved insulin content, indicating therapeutic potential in T1D [15].

Apart from the therapeutic uses in T1D, the ADSCtherapy has also been shown to reduce adverse effects brought about by complications such as DN and ESRD [48,49]. Inactivation of nuclear factor kappa B pathways and downregulation of VEGF-A, amongst others, are the major mechanisms involved in ameliorating the pathological manifestations of mice with DN [50].

The problem remaining, however, is the inability to become totally free of exogenous insulin. Research suggests that a much larger dose of IPC may be required for a sustained cure of T1D using ADSCs [51]. Therefore, the need of the hour is to conduct further research, placing emphasis on ways to either enhance the production of insulin in IPC derived from ADSCs or alter cell signaling pathways to obtain a greater number of IPC from ADSCs.

Bone marrow-derived mesenchymal stem cells (BM-MSCs) are a type of adult stem cell that is abundant in bone marrow and has low immunogenicity [52]. Bone marrow stem cells are broadly categorized into hematopoietic stem cells and MSCs. These cells are sourced from the same individual, potentially minimizing rejection problems and making it a form of therapy for T1D [53]. BM-MSCs can differentiate into functionally competent -cells in vivo, and NOD mouse studies have shown the formation of normal T cell and B cell function, implying that allogeneic bone marrow transplant could prevent islet destruction and restore self-tolerance [54,55]. Because of their well-documented hypoimmunogenic and immunomodulatory properties, BM-MSCs are an appealing therapeutic option for T1D [56].

One study looked at T1D patients with DKA and found BM-MSCs to preserve -cell function in T1D patients, reducing levels of fasting and post-prandial C-peptide levels, with one patient achieving insulin independence for a period of three months [57].

BM-MSCs have been demonstrated to mitigate the effects of metabolic and hepato-renal abnormalities, enhance lipid profiles, and improve carbohydrate and glycemic management. Following an eight-week period of injections with BM-MSCs in diabetic rats, an improvement was observed in their lipid profiles compared to diabetic rats that were not treated with BM-MSCs [16]. In addition, BM-MSCs therapy has been demonstrated to ameliorate diabetes-related liver damage by boosting endogenous hepatocyte regenerative mechanisms and enhancing liver function [58].

BM-MSCs have also been shown to effectively treat comorbidities of T1D, such as DN, poor wound healing, and erectile dysfunction (ED). Nagaishi et al. investigated a novel approach of mixing BM-MSCs with umbilical cord extracts in Wharton's Jelly to enhance the therapeutic effect of ameliorating renal injury in T1D patients with DN. The study demonstrated morphological and functional improvements of diabetes-derived BM-MSC in vitro and a therapeutic impact on DN in vivo, suggesting that this may be beneficial not only for patients with DN but also for patients with other diabetic complications [59]. One study looked to address the problem of impaired epithelial wound healing in T1D patients and found that BM-MSCs promote corneal epithelial wound healing via tumor necrosis factor-inducible gene 6-dependent stem cell activation [60]. Another promising phase I pilot clinical trial found that treating ED in T1D patients with two consecutive intracavernous injections of autologous BM-MSC was safe and effective [61].

Currently, several potential therapeutic approaches are being postulated to approach this issue of T1D from a new viewpoint. Suicide gene therapy is a strategy with potential. This method involves the introduction of suicide-inducing transgenes into the body via BM-MSC. As a result, several processes will be induced, including the suppression of gene expression, the production of intracellular antibodies that block the essential pathways of cells, and the transgenic expression of caspases and deoxyribonucleases. Current clinical trials are examining strategies to restore damaged organs with the use of stem cells as the delivery mechanism [62].

The idea of transplanting BM-MSCs provides patients with hope. Particularly significant are autologous BM-MSC (which are easy to obtain and avoid graft rejection after transplantation) in contrast to allogeneic BM-MSC transplantations, which may result in graft rejection and be accompanied by complications [52]. For stem cell therapy to be most beneficial, early delivery of stem cells following a diagnosis of T1D is necessary compared to intervention at later stages [63].

Table 1compares the properties of MSCs derived from the bone marrow, umbilical cord, and adipose tissue.

Recent research has demonstrated that menstrual blood-derived endometrial stem cells (MenSCs) have therapeutic promise for the treatment of T1D due to their exceptionally high rates of proliferation, noninvasive collection method, and significant immunomodulatory activity. In T1D model mice, MenSC and UC-MSC transplantation resulted in a significant decrease in blood glucose and insulin levels, as well as an improvement in the morphology and function of the liver, kidneys, and spleen [14]. A 2021 study found that MenSCs expressed pancreatic -cell genes such as INSULIN, GLUT-2, and NGN-3 and had a greater capacity to develop into pancreatic cells [64].

Dental pulp-derived mesenchymal stem cells (DP-MSCs) are one of the unique MSCs proposed for the treatment of T1D. DP-MSCs are derived from exfoliated human deciduous teeth and have the properties of being easy to obtain with minimal donor injury. In a study by Mo et al. DP-MSCs revealed the ability to differentiate into pancreatic -cells; nevertheless, before proceeding with larger-scale investigations to firmly establish this approach, it is necessary to devise procedures for optimal -cell differentiation in-vivo [65].

An in-vivo study revealed that conjunctiva-derived mesenchymal stem cells (C-MSCs) efficiently differentiated into pancreatic islet stem cells in 2D cultures and 3D scaffolds under optimal induction conditions. C-MSCs have a strong proliferative capacity, a spindle shape, a high potential for clonogenic differentiation, and are widely available. However, larger in vitro studies are necessary before C-MSCs can be deemed an established treatment for T1D [64].

Table 2 lists all clinical trials that have utilized MSCs in the treatment of T1D and complications related to T1D (Table 2).

Our article relies on a survey of free full-text research journals over the past decade; consequently, it is possible that we have omitted pertinent information from paid full-text as well as research articles published prior to 2010.In addition, the scope of this study is confined to studies in the English language, so we may have overlooked papers published in other languages.

MSCs are postulated to act in T1D and numerous other disorders through diverse mechanisms. Among these are homing and immunomodulation. Our review revealed that MSCs not only effectively reduce fasting blood sugar, C-peptide, and hemoglobin A1c levels but are also capable of treating microvascular complications associated with T1D. However, the specific pathophysiology of T1D diabetes is still unknown, making it difficult to develop novel treatments. To achieve remission of T1D, we must also consider the effects of additional factors on the efficacy of MSCs, including patient-specific variables such as age, body mass index, lifestyle, socioeconomic status, level of activity, diet, autoimmune status, and drug interactions, as well as external factors such as storage conditions, plating density, and culture media. Therefore, it is urgent to conduct larger-scale studies.

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The Role of Mesenchymal Stem Cells in the Treatment of Type 1 Diabetes - Cureus

Bone Marrow Stem Cells Comments Off on The Role of Mesenchymal Stem Cells in the Treatment of Type 1 Diabetes – Cureus | August 2nd, 2022

CASE SUMMARY

A 54-year-oldwoman presented with Revised International Staging System stage II multiple myeloma, based on evaluations that showed a hemoglobin level of 7.0 g/dL, 2-microglobulin of 6 mg/dl, albumin 3.2 g/dL, calcium 11.3 mg/dL, lactate dehydrogenase of 200 U/L, and creatinine clearance of 45 mL/min. Bone marrow showed 22% clonal plasma cells. Serum kappa free light chains were 24 mg/dL. She had no cytogenetic abnormalities and an ECOG performance score of 1. A PET/CT scan showed multiple bone lesions in the vertebrae. She had no extramedullary disease. She was diagnosed with IgG-kappa myeloma and was considered transplant eligible.

Daratumumab (Darzalex), bortezomib (Velcade), lenalidomide (Revlimid), and dexamethasone (Dara-VRd) induction therapy was initiated. She achieved a very good partial response (VGPR) post induction therapy. She underwent stem cell mobilization and 2 months later underwent autologous stem cell transplant (ASCT). Her post-ASCT response was a VGPR.

DISCUSSION QUESTIONS

CAITLIN COSTELLO, MD: This patient did get a quadruplet regimen with dara-VRd. She achieved a VGPR post-induction, had stem cells mobilized, underwent her transplant, and post-transplant her response is a VGPR. What would you do next?

THOMAS DEKKER, MD: Consolidation with CAR [chimeric antigen receptor] T-cell therapy.

COSTELLO: With CAR T cell, sure. Youre going for it; I like it. This patient is post-transplant, they have a VGPR. The GRIFFIN study [NCT02874742] would give these patients consolidation with dara-VRd.

PREETI CHAUDHARY, MD: I would not do CAR T-cell therapy.

COSTELLO: What would you do?

CHAUDHARY: In my opinion, in multiple myeloma, patients do a maximum of 11 months with CAR T-cell therapy. It has a good response, but I dont think thats sustainable.

COSTELLO: I appreciate throwing ideas out there. That is not something we have an option to do right now. Its an interesting option, and something we can talk about; but yes, I agree with you. I think for the meantime, short of trials that are looking at doing CAR T-cell therapyparticularly for those patients who have not had an adequate response to transplant or consolidation, or patients who relapse shortly after their transplantI think the standard of care as it stands now is doing consolidation or trying to find a maintenance regimen to get them to minimal residual disease [MRD] negativity.

With all that being said, what are we going to do now for these patients? Weve talked about what these transplant eligible patients are getting consolidation and maintenance; weve talked about maintenance approaches for these patients who get quadruplets, to put them on doublets. Seeing all those deep response rates, is anyone getting cold on transplants? If we are going to get 90% remission rates, does anyone reconsider the role of transplant here?

PAMELA MIEL, MD: I dont make that call, meaning I still send patients to the transplant doctors to see if theyre going to proceed with the transplant or not. But, if theyre transplant eligible, they get referred.

COSTELLO: As a transplanter, I thank you for that. We want to see these patients, make the decisions, have the discussion with the patients so we can look at their risk/benefit profile, and understand their responses to their current therapy. So, please still send them in their third cycle, if not earlier, so we can have those discussions and make plans.

There are a lot of maintenance regimens that are out there, and different things to choose from; a whole other conversation in and of itself. Lenalidomide is the mainstay where we have an overall survival benefit, where we dont have it in any other maintenance regimens.1 But it does allow for the option of continued doublets. I think we will soon see daratumumab and lenalidomide as a doublet get added on to that maintenance therapy once we have some of these randomized trials that are going on that show the continued benefit of patients to get daratumumab in the maintenance setting if they did not receive it in the up-front setting.

DISCUSSION QUESTION

How likely are you to change your practice with respect to management of transplant eligible newly diagnosed myeloma?

DEKKER: I already use quadruplet.

MILAN SHETH, MD: I feel that we still need a lot of long-term data to get a better sense of what it is that were achieving with the quadruplet therapy. Im still not convinced everybody needs quadruplet therapy. I think somebody else had already said that we know were going to get better responses because were using great drugs, but do we need to use everything up-front? I feel like theres still a lot of unanswered questions here.

MIEL: Ive been wanting to put patients on quadruplet treatment. I dont know if you know Nina Shah, MD, over at UC San Francisco, but Ive attended some of her talks, and shes pushing for the quadruplet treatment. The only thing that changed my mind was that when I spoke to the transplant doctor at UC San Diego, he said, If its not very high-risk disease, Id go with VRd [bortezomib, lenalidomide, and dexamethasone]. So, I put the patient on VRd. But I probably would want to put someone on dara-VRd, given the chance.

COSTELLO: Yes. I think that my takeaway from the data has been that we would, of course, love long-term data to come out, butwe have to wait a long time for it. While were waiting for some of these phase 3 studies to go on, which are happening now to look at real randomized data, to play out, I find that this is just too intriguing to not do quadruplets for everybody now.

Since [these data were presented at [the 2021 American Society of Hematology annual meeting], Ive transitioned just about everyone whos at least transplant eligible over to quadruplet regimens now.2 Any patients who are on the fence, where Im not sure if theyre going to be eligible for transplant, I still will try and give them the benefit of a quadruplet regimen, and very quickly drop the bortezomib if I get worried about them, and end up with dara-Vd [daratumumab, lenalidomide, dexamethasone]. But I think these MRD negativity rates are just too good, and if that is going to be the true surrogate end point that were all aiming for, dara-VRd has been my go-to for the last 6-plus months or so for these patients, until someone tells me otherwise.

References

1. Ho M, Zanwar S, Kapoor P, et al. The effect of duration of lenalidomide maintenance and outcomes of different salvage regimens in patients with multiple myeloma (MM).Blood Cancer J. 2021;11(9):158. doi:10.1038/s41408-021-00548-7

2. Laubach JP, Kaufman JL, Sborov DW, et al. Daratumumab (DARA) plus lenalidomide, bortezomib, and dexamethasone (RVd) in patients (pts) with transplant-eligible newly diagnosed multiple myeloma (NDMM): updated analysis of GRIFFIN after 24 months of maintenance. Blood. 2021;138(Suppl_1):79. doi:10.1182/blood-2021-149024

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Bone Marrow Stem Cells Comments Off on Treating Multiple Myeloma Following Quadruplet Induction Therapy and ASCT – Targeted Oncology | August 2nd, 2022

Researchers have revealed the cellular mysteries behind aging.

A new explanation for aging has been developed by researchers who have shown that genetic abnormalities that develop gradually over a lifetime cause substantial alterations in how blood is generated beyond the age of 70.

According to recent research, the drastic reduction in blood production beyond the age of 70 is likely caused by genetic alterations that steadily accumulate in blood stem cells throughout life.

Researchers from the Wellcome Sanger Institute, the Wellcome-MRC Cambridge Stem Cell Institute, and others have published a study that offers a new theory of aging in the journal Nature.

Somatic mutations, or alterations to the genetic code, occur in all human cells during the course of a lifetime. Aging is most likely caused by the accumulation of numerous sorts of damage to our cells over time, with one hypothesis proposing that the accumulation of somatic mutations causes cells to gradually lose functional reserve. However, it is still unknown how such slow-building molecular damage may result in the rapid decline in organ performance around the age of 70.

The Wellcome Sanger Institute, the Cambridge Stem Cell Institute, and collaborators examined the production of blood cells from the bone marrow in 10 people ranging in age from newborns to the elderly in order to better understand how the body ages.

3,579 blood stem cells had their whole genomes sequenced, allowing researchers to determine every somatic mutation present in each cell. Using this information, the team was able to create family trees of each persons blood stem cells, providing for the first time an impartial perspective of the connections between blood cells and how these ties develop over the course of a persons lifetime.

After the age of 70 years, the researchers discovered that these family trees underwent significant change. In adults under the age of 65, 20,000 to 200,000 stem cells contributed roughly equal amounts to the creation of blood cells. In contrast, blood production was exceedingly uneven in those above the age of 70.

In every elderly person investigated, a small number of enlarged stem cell clonesas few as 10 to 20contributed as much as half of the total blood output. Because of an uncommon class of somatic mutations known as driver mutations, these highly active stem cells have gradually increased in number during that persons life.

These findings led the team to propose a model in which age-associated changes in blood production come from somatic mutations causing selfish stem cells to dominate the bone marrow in the elderly. This model, with the steady introduction of driver mutations that cause the growth of functionally altered clones over decades, explains the dramatic and inevitable shift to reduced diversity of blood cell populations after the age of 70. Which clones become dominant varies from person to person, and so the model also explains the variation seen in disease risk and other characteristics in older adults. A second study, also published in Nature, explores how different individual driver mutations affect cell growth rates over time.

Dr. Emily Mitchell, Haematology Registrar at Addenbrookes Hospital, a Ph.D. student at the Wellcome Sanger Institute, and lead researcher on the study, said: Our findings show that the diversity of blood stem cells is lost in older age due to positive selection of faster-growing clones with driver mutations.

These clones outcompete the slower-growing ones. In many cases this increased fitness at the stem cell level likely comes at a cost their ability to produce functional mature blood cells is impaired, so explaining the observed age-related loss of function in the blood system.

Dr. Elisa Laurenti, Assistant Professor and Wellcome Royal Society Sir Henry Dale Fellow at the Wellcome-MRC Cambridge Stem Cell Institute at the University of Cambridge, and joint senior researcher on this study, said: Factors such as chronic inflammation, smoking, infection, and chemotherapy cause earlier growth of clones with cancer-driving mutations. We predict that these factors also bring forward the decline in blood stem cell diversity associated with aging. It is possible that there are factors that might slow this process down, too. We now have the exciting task of figuring out how these newly discovered mutations affect blood function in the elderly, so we can learn how to minimize disease risk and promote healthy aging.

Dr. Peter Campbell, Head of the Cancer, Ageing and Somatic Mutation Programme at the Wellcome Sanger Institute, and senior researcher on the study said: Weve shown, for the first time, how steadily accumulating mutations throughout life lead to a catastrophic and inevitable change in blood cell populations after the age of 70. What is super exciting about this model is that it may well apply to other organ systems too. We see these selfish clones with driver mutations expanding with age in many other tissues of the body we know this can increase cancer risk, but it could also be contributing to other functional changes associated with aging.

References: Clonal dynamics of haematopoiesis across the human lifespan by Emily Mitchell, Michael Spencer Chapman, Nicholas Williams, Kevin J. Dawson, Nicole Mende, Emily F. Calderbank, Hyunchul Jung, Thomas Mitchell, Tim H. H. Coorens, David H. Spencer, Heather Machado, Henry Lee-Six, Megan Davies, Daniel Hayler, Margarete A. Fabre, Krishnaa Mahbubani, Federico Abascal, Alex Cagan, George S. Vassiliou, Joanna Baxter, Inigo Martincorena, Michael R. Stratton, David G. Kent, Krishna Chatterjee, Kourosh Saeb Parsy, Anthony R. Green, Jyoti Nangalia, Elisa Laurenti, and Peter J. Campbell, 1 June 2022, Nature.DOI: 10.1038/s41586-022-04786-y

The longitudinal dynamics and natural history of clonal haematopoiesis by Margarete A. Fabre, Jos Guilherme de Almeida, Edoardo Fiorillo, Emily Mitchell, Aristi Damaskou, Justyna Rak, Valeria Orr, Michele Marongiu, Michael Spencer Chapman, M. S. Vijayabaskar, Joanna Baxter, Claire Hardy, Federico Abascal, Nicholas Williams, Jyoti Nangalia, Iigo Martincorena, Peter J. Campbell, Eoin F. McKinney, Francesco Cucca, Moritz Gerstung, and George S. Vassiliou, 1 June 2022, Nature.DOI: 10.1038/s41586-022-04785-z

The study was funded by Wellcome and the William B Harrison Foundation.

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Scientists Unlock the Secrets of Cellular Aging: What Happens After You Turn 70? - SciTechDaily

Bone Marrow Stem Cells Comments Off on Scientists Unlock the Secrets of Cellular Aging: What Happens After You Turn 70? – SciTechDaily | August 2nd, 2022

For those with cancer, the threat of serious illness from COVID-19 is often a major concern. Cancer treatments can weaken your bodys immune system, increasing your risk of a serious infection.

Immunotherapy is a type of cancer treatment that boosts and supports your immune system in responding against cancer. If you or a loved one is receiving immunotherapy treatment for cancer, you may have concerns about how the COVID vaccine may affect your immune system and your treatment.

This article will answer some common questions about immunotherapy cancer treatment and the COVID vaccines.

People with a weakened immune system due to cancer are at an increased risk for poor outcomes from COVID-19. No matter where you are in your treatment plan, vaccination can reduce your risk of developing severe COVID. Vaccination is important even for those with a robust immune system.

The National Comprehensive Cancer Network (NCCN) and the American Cancer Society recommend that people with cancer, including those receiving treatment, get vaccinated as soon as possible. NCCN notes a few exceptions regarding immediacy:

Since they weaken the immune system, some cancer treatments reduce but dont eliminate vaccine effectiveness. Even if youre getting one or more of these treatments, you will gain some protection from the vaccine. Treatments include:

Vaccination combined with protective measures, such as wearing a mask and avoiding large crowds, provides you with more protection from COVID than you would have without them. For that reason, experts strongly recommend vaccination for people with cancer or a history of cancer.

But check with your oncologist first about when you should get vaccinated. If you are currently receiving treatment for cancer, it may be best to wait until your immune system recovers from treatment. This will give you the best chance of mounting a strong immune response.

Both the Pfizer BioNTech and the Moderna mRNA vaccines are appropriate for use in people who take immunotherapy drugs. Neither vaccine is known to be better than the other for this population.

A 2021 study found that the Moderna vaccine was safe for people with solid tumors receiving chemotherapy, immunotherapy, or both. Their response to the vaccine was similar to those who did not have cancer. The groups also saw similar rates of side effects.

A separate 2021 study noted that people with solid tumors who had the Pfizer vaccine had similar antibody levels to those without cancer 6 months after vaccination. In the subgroup of people on immunotherapy, about 87% still had antibodies, compared to about 84% of the control group.

If you cannot get or do not want either of these vaccines, you can also get the Johnson & Johnson (Janssen) vaccine.

Having cancer or taking immunotherapy drugs does not increase the possibility of serious side effects, such as allergic reactions or myocarditis.

Swelling in the lymph nodes under the arm on the same side as the injection site is a potential side effect of vaccination. While temporary, this can be concerning for people with breast cancer and other cancers.

Tenderness and swollen lymph nodes caused by vaccination should subside within a few days to a few weeks. Let a healthcare professional know if the swelling increases or does not go away within this timeframe.

To date, researchers do not know definitively if immunotherapy drugs affect the effectiveness of COVID-19 vaccines, either positively or negatively.

Scientific articles from 2021 and 2022 suggest that checkpoint inhibitors could theoretically boost your immune response to the COVID-19 vaccine. But both articles also state that no study has demonstrated such an effect.

Some immunotherapy drugs, such as CAR T-cells, may weaken the immune system temporarily. This may make the vaccine less effective. Other types of immunotherapy drugs, such as monoclonal antibodies, should not have this effect.

People with compromised immune systems may find it difficult to generate a robust response to the vaccine, no matter what type of cancer treatment they receive. This may be particularly true for people with blood cancers. For that reason, dosing protocols for people who are immunocompromised and have cancer differ from those used for the general public.

To date, no data indicate that the COVID vaccine reduces the effectiveness of immunotherapy medication. But there may be a 17% to 48% risk of side effects due to an overstimulated immune response, according to research.

A case report published in May 2021 suggests the potential for cytokine release syndrome after COVID vaccination in patients taking certain immunotherapy drugs. The study authors state that more data is needed and still favor vaccination for people with cancer.

A 2021 study involving 134 people found no adverse effects from immunotherapy drugs after receiving the Pfizer vaccine. The studys authors also stressed the need for larger studies and more data, but supported vaccination for people receiving immunotherapy.

However, the impact of certain immunotherapy treatments on your immune system makes the timing of vaccination important. Talk with your oncologist about when you should schedule your vaccine.

People taking immunotherapy drugs should receive an additional primary dose of the vaccine if they have active cancer or are immunocompromised. You may fall into one of these categories if any of the following situations apply:

Yes. Getting COVID does not ensure you will not get it again. In fact, with ever-changing variants continually emerging, contracting the virus more than once has become commonplace.

If youre on cancer treatments that cause you to be immunocompromised, it is vital to get vaccinated, even if youve already had COVID. Talk with your oncologist about when you should get vaccinated after having COVID-19.

If you have cancer, you may be more likely to experience serious complications from COVID-19. Cancer treatments, including certain immunotherapy drugs, may affect your scheduling for vaccination. Talk with your oncologist about when you should schedule your vaccines and how many doses you should get.

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Immunotherapy and COVID Vaccine: Your Questions Answered - Healthline

Bone Marrow Stem Cells Comments Off on Immunotherapy and COVID Vaccine: Your Questions Answered – Healthline | August 2nd, 2022

Fibrosis is the thickening of various tissues caused by the deposition of fibrillar extracellular matrix (ECM) in tissues and organs as part of the bodys wound healing response to various forms of damage. When accompanied by chronic inflammation, fibrosis can go into overdrive and produce excess scar tissue that can no longer be degraded. This process causes many diseases in multiple organs, including lung fibrosis induced by smoking or asbestos, liver fibrosis induced by alcohol abuse, and heart fibrosis often following heart attacks. Fibrosis can also occur in the bone marrow, the spongy tissue inside some bones that houses blood-producing hematopoietic stem cells (HSCs) and can lead to scarring and the disruption of normal functions.

Chronic blood cancers known as myeloproliferative neoplasms (MPNs) are one example, in which patients can develop fibrotic bone marrow, or myelofibrosis, that disrupts the normal production of blood cells. Monocytes, a type of white blood cell belonging to the group of myeloid cells, are overproduced from HSCs in neoplasms and contribute to the inflammation in the bone marrow environment, or niche. However, how the fibrotic bone marrow niche itself impacts the function of monocytes and inflammation in the bone marrow was unknown.

Now, a collaborative team from Penn, Harvard, the Dana-Farber Cancer Institute (DFCI), and Brigham and Womens Hospital has created a programmable hydrogel-based in vitro model mimicking healthy and fibrotic human bone marrow. Combining this system with mouse in vivo models of myelofibrosis, the researchers demonstrated that monocytes decide whether to enter a pro-inflammatory state and go on to differentiate into inflammatory dendritic cells based on specific mechanical properties of the bone marrow niche with its densely packed ECM molecules. Importantly, the team found a drug that could tone down these pathological mechanical effects on monocytes, reducing their numbers as well as the numbers of inflammatory myeloid cells in mice with myelofibrosis. The findings are published in Nature Materials.

We found that stiff and more elastic slow-relaxing artificial ECMs induced immature monocytes to differentiate into monocytes with a pro-inflammatory program strongly resembling that of monocytes in myelofibrosis patients, and the monocytes to differentiate further into inflammatory dendritic cells, says co-first author Kyle Vining, who recently joined Penn. More viscous fast-relaxing artificial ECMs suppressed this myelofibrosis-like effect on monocytes. This opened up the possibility of a mechanical checkpoint that could be disrupted in myelofibrotic bone marrow and also may be at play in other fibrotic diseases. Vining will be appointed assistant professor of preventive and restorative sciences in the School of Dental Medicine and the Department of Materials Sciences in the School of Engineering and Applied Science, pending approval by Penn Dental Medicines personnel committees and the Provosts office.

Vining worked on the study as a postdoctoral fellow at Harvard in the lab of David Mooney. Our study shows that the differentiation state of monocytes, which are key players in the immune system, is highly regulated by mechanical changes in the ECM they encounter, says Mooney, who co-led the study with DFCI researcher Kai Wucherpfennig. Specifically, the ECMs viscoelasticity has been a historically under-appreciated aspect of its mechanical properties that we find correlates strongly between our in vitro and the in vivo models and human disease. It turns out that myelofibrosis is a mechano-related disease that could be treated by interfering with the mechanical signaling in bone marrow cells.

Mooney is also the Robert P. Pinkas Family Professor of Bioengineering at Harvard and leads the Wyss Institutes Immuno-Materials Platform. Wucherpfennig is director of DFCIs Center for Cancer Immunotherapy Research, professor of neurobiology at Brigham and Harvard Medical School, and an associate member of the Broad Institute of MIT and Harvard. Mooney, together with co-senior author F. Stephen Hodi, also heads the Immuno-engineering to Improve Immunotherapy (i3) Center, which aims to create new biomaterials-based approaches to enhance immune responses against tumors. The new study follows the Centers road map. Hodi is director of the Melanoma Center and The Center for Immuno-Oncology at DFCI and professor of medicine at Harvard Medical School.

Gleaning mechanical bone marrow failureThe mechanical properties of most biological materials are determined by their viscoelastic characteristics. Unlike purely elastic substances like a vibrating quartz, which store elastic energy when mechanically stressed and quickly recover to their original state once the stress is removed, slow-relaxing viscoelastic substances also have a viscous component. Like the viscosity of honey, this allows them to dissipate stress under mechanical strain by rapid stress relaxation. Viscous materials are thus fast-relaxing materials in contrast to slow-relaxing purely elastic materials.

The team developed an alginate-based hydrogel system that mimics the viscoelasticity of natural ECM and allowed them to tune the elasticity independent from other physical and biochemical properties. By tweaking the balance between elastic and viscous properties in these artificial ECMs, they could recapitulate the viscoelasticity of healthy and scarred fibrotic bone marrow, whose elasticity is increased by excess ECM fibers. Human monocytes placed into these artificial ECMs constantly push and pull at them and in turn respond to the materials mechanical characteristics.

Next, the team investigated how the mechanical characteristics of stiff and elastic hydrogels compared to those in actual bone marrow affected by myelofibrosis. They took advantage of a mouse model in which an activating mutation in a gene known as Jak2 causes MPN, pro-inflammatory signaling in the bone marrow, and development of myelofibrosis, similar to the disease process in human patients with MPN. When they investigated the mechanical properties of bone marrow in the animals femur bones, using a nanoindentation probe, the researchers measured a higher stiffness than in non-fibrotic bone marrow. Importantly, we found that the pathologic grading of myelofibrosis in the animal model was significantly correlated with changes in viscoelasticity, said co-first author Anna Marneth, who spearheaded the experiments in the mouse model as a postdoctoral fellow working with Ann Mullally, a principal investigator at Brigham and DFCI, and another senior author on the study.

Targeting dysregulated bone marrow mechanicsAn important question was whether monocytes response to the mechanical impact of the fibrotic bone marrow niche could be therapeutically targeted. The researchers focused on an isoform of the phosphoinositide 3-kinase (PI3K)-gamma protein, which is specifically expressed in monocytes and closely related immune cells. PI3K-gamma is known for regulating the assembly of a cell-stiffening filamentous cytoskeleton below the cell surface that expands in response to mechanical stress, which the team also observed in monocytes encountering a fibrotic ECM. When they added a drug that inhibits PI3K-gamma to stiff elastic artificial ECMs, it toned down their pro-inflammatory response and, when given as an oral treatment to myelofibrosis mice, significantly lowered the number of monocytes and dendritic cells in their bone marrow.

This research opens new avenues for modifying immune cell function in fibrotic diseases that are currently difficult to treat. The results are also highly relevant to human cancers with a highly fibrotic microenvironment, such as pancreatic cancer, says Wucherpfennig.

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University of Pennsylvania: Deconstructing the mechanics of bone marrow disease | India Education - India Education Diary

Bone Marrow Stem Cells Comments Off on University of Pennsylvania: Deconstructing the mechanics of bone marrow disease | India Education – India Education Diary | August 2nd, 2022

This week, the White House held a summit on the future of Covid-19 vaccines that brought together scientists and vaccine manufacturers to discuss new vaccine technologies. Officials said that new vaccines are an urgent priority as US Covid-19 cases and hospitalizations are rising once again, vaccination rates are hitting a plateau, Covid-19 funding is running low, and the virus itself is continuing to mutate.

But in recent months, scientists have also learned that the immune cells that provide lasting protection known as memory B cells and T cells can keep the worst effects of the most recent versions of the virus at bay, even if they were trained to corral older strains of SARS-CoV-2. Vaccine researchers are expanding their focus from antibodies to these memory immune cells as the new discoveries open a path toward universal coronavirus vaccines.

Universal vaccines, however, are still a long way off possibly years drawing on approaches never used before. Thats a scientific challenge, said Anthony Fauci, chief medical adviser to the president, during the summit.

The good news is that far fewer people are dying from the disease compared to the wave of cases this past winter spurred by the omicron variant of SARS-CoV-2, the virus that causes Covid-19. The first round of Covid-19 vaccines is still holding death rates down to around 360 per day, according to the Centers for Disease Control and Prevention. Still, health officials want to do better.

While the vaccines are terrific, hundreds of Americans, thousands of people around the world are still dying every day, Ashish Jha, the White House Covid-19 response coordinator, said Tuesday. Building a new generation of vaccines will make an enormous difference to bringing this pandemic to an end.

The National Institutes of Health is already funding several research teams developing Covid-19 vaccines that elicit protection against many different versions of the virus, shield against future changes to the virus before they arise, and protect against other coronaviruses.

From there, health officials are aiming not just to develop vaccines that provide more durable protection against a wider array of threats, but also rethinking the vaccination strategy overall. With a better understanding of long-term immunity, more robust vaccines, and a comprehensive public health approach, health officials say they have a better shot at restoring normalcy.

Much of the discussion around vaccines and immunity to Covid-19 centers on antibodies, proteins produced by the immune system that attach to the virus. And indeed, they are important.

Antibodies that prevent the virus from causing an infection in the first place are called neutralizing antibodies. A high concentration of antibodies in the body that blocks SARS-CoV-2 is a key indicator of good protection against reinfection. Antibodies can also serve as a way to mark intruders so that other immune system cells can dispose of them.

But making large quantities of antibodies takes a lot of resources from the body, so their production tapers off with time after an infection or a vaccination. Another concern is that antibodies are very particular about where they attach to the virus. If the virus has a mutation at that attachment site called an epitope antibodies have a harder time recognizing the pathogen. Thats why some antibody-based treatments for Covid-19 are a lot less effective at stopping the omicron subvariants.

Fortunately, the immune system has other tools in its chest. Inside bone marrow lie stem cells that differentiate to become B cells and T cells. Together, they form the core of the adaptive immune system, which creates a tailored response to threats. After a virus invades a cell, it hijacks its machinery to make copies of itself. White blood cells known as cytotoxic T cells, a.k.a. killer T cells, can identify the wayward cell and make it self-destruct. This mechanism doesnt prevent infections, but it stops them from growing out of control.

Another type of T cell, called a helper T cell, acts as an on switch for B cells, which are the cells that manufacture antibodies. After an infection is extinguished, some T cells and B cells turn into memory cells that stick around in parts of the body, ready to rev up if a virus dares to show up again.

So far, the adaptive immune system seems to hold up pretty well. The first round of Covid-19 vaccines was targeted against the earliest versions of the virus, so plenty of vaccinated people have had breakthrough infections, especially from the newer variants. But only a tiny fraction of those immunized have fallen severely ill or have died.

That likely means that their immune systems couldnt keep the virus out entirely, but their immune cells were able to spool up once an infection took root.

Someones neutralizing antibodies may not be up to the task, but if they have the T cell response, that may make all the difference with severe disease, said Stephen Jameson, a professor of microbiology and immunology at the University of Minnesota.

In just the past year, many studies have borne out the significance of memory B cells and T cells for long-term Covid-19 immunity and answered critical questions about whether they can respond to new variants.

Researchers have found that lower levels of memory B cells were associated with a greater risk of breakthrough infections from the delta variant. On the other hand, B cells induced by Covid-19 vaccines could reactivate months out from the initial vaccine doses to churn out antibodies.

Similarly, scientists found that T cells generated by vaccines were able to recognize SARS-CoV-2 variants like omicron months later. These data provide reasons for optimism, as most vaccine-elicited T cell responses remain capable of recognizing all known SARS-CoV-2 variants, scientists wrote in a March paper in the journal Cell.

Another study showed that Covid-19 vaccines generated strong T cell memory that protected against the virus even without neutralizing antibodies. I think the immunological memory which is induced by vaccines is pretty good and is actually sustained, said Marulasiddappa Suresh, a professor of immunology at the University of Wisconsin-Madison who co-authored the study, published in the Proceedings of the National Academy of Sciences in May.

Whether this protection will hold up over the course of years remains to be seen. Experiences with past coronaviruses like MERS showed that antibodies to the virus can last for four years. Covid-19, however, is spreading at much higher levels and mutating more than MERS did during its initial outbreak. Future protection against the disease hinges on the immune system as well as how much the virus itself will change, and scientists are closely watching both.

Most vaccines to date are designed to counter one or a handful of versions of a given virus. They present the immune system with a target that allows it to prepare its defenses should the actual virus ever invade.

In the case of Covid-19, most vaccines coach the immune system to target the spike protein of the SARS-CoV-2 virus, which it uses to start the infection process. This helps the immune system generate strong neutralizing antibodies. But the spike protein is one of the fastest mutating parts of the virus, making it a moving target.

The fact that B cells and T cells have managed to hold off newer variants hints that it may be possible to target the virus in other ways. Rather than just making neutralizing antibodies that attach to the spike, the adaptive immune system could also produce non-neutralizing antibodies that bind to other regions of the virus that mutate very little, if at all. While these antibodies may not block an infection from taking root, they may be able to provide more durable protection against severe illness that holds up against future SARS-CoV-2 variants.

Another approach is to present the immune system with a variety of different potential mutations of a virus, allowing white blood cells to prepare a response to a spectrum of threats and fill in the blanks.

Universal vaccines have not been deployed before, so researchers are in uncharted territory, and the shots likely wont be ready ahead of a potential fall spike in Covid-19 cases. But developing such a vaccine could eventually reduce the need for boosters and give health officials a head start on countering future outbreaks.

In the meantime, US health officials are planning to distribute vaccines reformulated to target newer Covid-19 variants by September, but its not clear yet what the optimal strategy will be to deploy them given the wide range of immune protection across the population. Between infections and vaccinations, the majority of people in the country have had some exposure to the virus, granting some degree of protection. And since the adaptive immune response to Covid-19 seems to be robust in most people, it may not be necessary for everyone to get an additional shot.

One option is to seek out those with weaker immune systems for boosters. Researchers have now developed a rapid test to measure T cell responses to Covid-19 that could identify people who are more vulnerable to reinfections or breakthrough infections.

Though vaccines are absorbing the most severe consequences from Covid-19, infections are still proving disruptive. Covid-19 outbreaks are contributing to staffing shortages at hospitals, schools, and airlines, leading to delays and cancellations. And the more the virus spreads, the more opportunities it has to mutate in dangerous ways. Stopping this threat requires limiting infections, which in turn still demands measures like social distancing and wearing face masks.

So as good as the next generation of vaccines may prove to be, they are only one element of a comprehensive public health strategy for containing a disease.

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How long-term Covid-19 immunity paves the way for universal Covid-19 vaccines - Vox.com

Bone Marrow Stem Cells Comments Off on How long-term Covid-19 immunity paves the way for universal Covid-19 vaccines – Vox.com | August 2nd, 2022

Abstract: Background Spinal cord injury (SCI) due to lack of restoration of damaged axons is associated with sensorimotor impairment. This study was focused on using the human Placental mesenchymal stem cells- exosome (hPMSCs- exosomes) in an animal model of severe SCI under a new myelogram protocol to confirm lumbar puncture (LP) injection accuracy and evaluate intrathecal space. Methods Mesenchymal stem cells (MSC) were extracted from human placenta tissue and were characterized. HPMSCs- exosomes were isolated by ultracentrifuge. After creating the severe SCI model, LP injection of exosomes was performed in the acute phase. Myelogram was also employed. The improved functional recovery of the animals in the treatment and control groups was followed by recording movement scores for 6 weeks. Hematoxylin-Eosin (H&E) staining was used to evaluate to detect pathological changes and glial scar size. The Immunohistochemistry (IHC) of GFAP and NF200 factors as well as the apoptosis tunnel test was investigated in the tissue samples from the injury site Results The results demonstrated that the use of the myelogram can be a feasible, appropriate and cost-effective method to confirm the accuracy of therapeutic agents LP injection and examine the subarachnoid space in the model of laboratory animals. Furthermore, intrathecal injection of hPMSCs-exosomes in the acute phase of SCI can improve motor function by attenuating apoptosis of neurons at the site of injury, decreased GFAP expression and increased NF200 in the treatment group, reducing glial scarring, and increasing axonal regeneration. Improving functional recovery by not creating bedsores in the treatment group and preventing hematuria were other effects of the exosome Conclusions In conclusion, the effects of hPMSCs-exosome can be considered to be not only in restoring function but also in preventing complications and managing symptoms. Thus, the neuroregenerative and anti-apoptotic potential of hPMSCs-exosome can be considered a therapeutic approach in SCI reconstructive medicine.

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Human placental mesenchymal stem cells derived exosomes improved functional recovery via attenuating apoptosis and increasing axonal regeneration...

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Glioblastoma multiforme (GBM) or simply glioblastoma, is a type of cancer characterized by the growth of an aggressive neoplasm (tumor) in the brain or spinal cord. This type of cancer often occurs in older adults, although the younger population may also be affected.

Read Also: Targeting Hox Gene Dysregulation a Promising Approach for the Treatment of Glioblastoma Multiforme

Glioblastoma

This cancer type is known to be difficult to treat because of its high tendency to reoccur in patients, even after the combination of the three known procedures to treat cancers: surgery, radiotherapy, and chemotherapy. Glioblastoma has been a thorn in the flesh in the world of medicine amongst all cancer types due to the low survival rate of patients affected by it (average survival of 18 months, with only 5% of patients living up to five years). The following factors make this possible: no specific signs or symptoms are noticed leading to late diagnosis and the ability of the cancer cells to resist treatment procedures (the major factor).

Studies have been ongoing to uncover the mechanism behind this major factor, and it has been revealed that Glioblastoma multiforme contains a functional subset of cells known as glioblastoma stem-like cells (GSCs) which are the brain behind its reoccurrence capacity. The identity of these cells remained hidden until a recent study done by a group of scientists finally uncovered it.

Read Also: Brain Cancer: A Promising New Treatment for Destroying Aggressive Glioblastoma Cell

The team found out that these functional subsets of cells can be identified through singular mitochondrial alternative metabolisms. After intensively studying the metabolic reactions of these cells, they developed a tumor model that possessed the features of the GBM cultured in the lab. This way, they discovered that GSCs use these two metabolic reactions alpha-ketoglutarate reductive carboxylation and pyruvate carboxylation within their cells. They also discovered that these reactions are catalyzed by the enzymes isocitrate dehydrogenase and pyruvate carboxylase respectively.

They were able to uncover that their high rate of survival which facilitated the recurrence of the tumor is linked to the pyruvate carboxylation reaction. This discovery is important as it means that doctors may now be able to tackle the reoccurring ability of the tumor effectively.

It has always been known that treating glioblastoma is difficult due to its high recurring ability. However, with the revelation from this study, it is now possible for physicians to come up with more effective treatment procedures that would result in a reduced recurrence of the tumors, and an increased survival rate of patients.

This study raises the hopes of both physicians and patients as it reveals a way to hinder the recurrence of glioblastoma tumors. More research is still ongoing to hasten the innovation of a more effective treatment technique.

Read Also: Brain Cancer: Researchers Reprogram Immune Cells to Improve the Effectiveness of Treatment

Pyruvate carboxylation identifies Glioblastoma Stem-like Cells opening new metabolic strategy to prevent tumor recurrence

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How the Regenerative Properties of Glioblastoma Can Be Terminated - Gilmore Health News

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LAS VEGAS, NV, Aug. 01, 2022 (GLOBE NEWSWIRE) -- via NewMediaWire Meso Numismatics, Inc. (Meso Numismatics or the Company) (MSSV), a technology company specializing in Biotech and Numismatics, is pleased to announce additional global expansion by opening stem cell therapy and regenerative medicine facilities in Indonesia. The new facilities emphasize Global Stem Cells Group's objective of introducing its therapies and technology to meet market demands in populous parts of the world.

In partnership with the Dr. Yanti Aesthetic Clinics, which currently has 6 branches across Indonesia, this latest GSCG expansion will promote high standards of service in regenerative medicine across the country. As part of this effort, through GSCG the International Society for Stem Cells Applications (ISSCA) has granted Dr. Yanti Aesthetic Clinics membership and use of its brand, products, therapies, and training on how to apply stem cell therapies.

This new partnership seeks to expand the Global Stem Cells Group (GSCG) brand and create centers of excellence in cell therapy to meet the high demand within the vast Asian markets, said David Christensen, CEO of MSSV. GSCG is rapidly expanding its global operations as it seeks to become a significant player in the lucrative regenerative medicine industry. To achieve our expansion plans, our organization is partnering with healthcare providers specializing in regenerative medicine with at least five years of experience in the healthcare sector.

Video: https://youtu.be/T2CFjsps9qk

The vision behind the effort.

The Indonesia addition is the latest part of an expanding medical network of partners, and it will formalize and strengthen ties, establishing a global center of excellence to guarantee that we effectively use the underlying basic stem cell technology for medical conditions, where traditional therapeutic approaches seem to have failed. This is consistent with GSCG's overall strategy for developing regenerative medicine through data-driven studies, disease modeling, and cell-based therapeutics.

The Dr. Yanti Aesthetic Clinic is a key partnership because it provides the organizational and physical infrastructure needed to disseminate need-based stem cell locally. And Global Stem Cells Group's outstanding cell and stem cell biology and disease pathophysiology give an edge to patients for which they are prescribed.

The opening in Indonesia also presents the perfect opportunity to translate breakthrough therapies from basic discoveries to useful products by drawing upon the skills and local knowledge promoted within Dr. Yanti Aesthetic Clinics.

GSCG group managing director, Benito Novas, provided a clear description of the new strategic direction and objectives. "Our goal is to make regenerative medicine benefits a reality for both doctors and patients all around the world. We recently launched a very similar effort in Pakistan. Additional announcements are planned in the near future as we attempt to expand our presence." Meso Numismatics and Global Stem Cells Group Expand its Global Footprint

The current market outlook.

Stem cell therapy is striving to become an increasingly effective clinical solution to treat conditions that traditional or mainstream medicine offers only within palliative care and pain management. Patients all over the world are searching for a natural regenerative alternative without the potential risks and side effects sometimes associated with mainstream pharmaceuticals. With the opening of each new treatment center in populous regions such as Indonesia, GSCG is working to help stem cell therapy and regenerative medicine to eventually move from alternative and elective procedures to mainstream protocols.

This new clinic effort will play a significant role in the development of regenerative medicine in Indonesia and indeed the rest of the world by adding yet another opportunity for continuous improvement through research and development, Christensen continued. By adding busy clinics in population centers, we plan to consistently generate high volumes of reliable clinical data to assist us with the development and refinement of even more medicines and treatments.

About Dr. Yanti Aesthetic Clinics

Dr. Yanti Aesthetic Clinics is a premier cosmetic and aesthetics clinic based in Kelapa Gading, Jakarta Utara. Since its inception in 2004 in Surabaya by Dr. Khoe Yanti Khusmiran, the clinic has expanded to over 6 branches throughout Indonesia. Dr. Yanti clinics provide a range of skin and body enhancement treatments through minimally invasive and non-invasive procedures the expertise of which are a natural fit for the addition of a variety of stem cell therapies.

"Indonesians have a growing need for the latest medical technology that is reliable, potent, has reduced side effects, and leverages the bodys own healing biochemistry to resolve injury and aging, said Dr. Yanti. We are honored to be a part of GSCG, which has a proven 10-year track record in the market with a strong and growing international reputation. This new partnership is expected to create a wide variety of custom treatment options we can offer our patients and treat injury and illness in ways we could not before.

The newly formed partnership will deliver revolutionary medicines through Dr. Yanti clinics to assist patients in avoiding permanent harm and live a healthier life, while changing the paradigm from asymptomatic treatments to cures that may improve and restore quality of life.

More about Global Stem Cells Group

GSCG delivers leadership in regenerative medicine research, patient applications, and training through our strategic global networks. We endeavor to enable physicians to treat otherwise incurable diseases using stem cell therapy and to improve the quality of life and care across the world.

For this reason, GSCG works with innovative, next-generation therapy providers like Dr. Yanti Aesthetic Clinics to give access to one-of-a-kind holistic and safe treatment options.

More information regarding this transaction and the Global Stem Cells Group may be found at GSCG.

This press release should be read in conjunction with all other filings on http://www.sec.gov

For more information on Global Stem Cells Group please visit: http://www.stemcellsgroup.com

About Meso Numismatics: Meso Numismatics, Corp is an emerging Biotechnology and numismatic technology company. The Company has quickly become the central hub for rare, exquisite, and valuable inventory for not only the Meso region, but for exceptional items from around the world.

Meso has now added Biotechnology to its portfolio and will continue to grow the company in this new direction. With the Company's breadth of business experience and technology team, the Company will continue to help companies grow.

Forward-Looking Statements

Some information in this document constitutes forward-looking statements or statements which may be deemed or construed to be forward-looking statements, such as the closing of the share exchange agreement. The words plan, "forecast", "anticipates", "estimate", "project", "intend", "expect", "should", "believe", and similar expressions are intended to identify forward-looking statements. These forward-looking statements involve, and are subject to known and unknown risks, uncertainties and other factors which could cause the Company's actual results, performance (financial or operating) or achievements to differ from the future results, performance (financial or operating) or achievements expressed or implied by such forward-looking statements. The risks, uncertainties and other factors are more fully discussed in the Company's filings with the U.S. Securities and Exchange Commission. All forward-looking statements attributable to Meso Numismatics, Inc., herein are expressly qualified in their entirety by the above-mentioned cautionary statement. Meso Numismatics, Inc. disclaims any obligation to update forward-looking statements contained in this estimate, except as may be required by law.

For further information, please contact:investor.relations@mssvinc.com Telephone: (800) 956-3935

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Global Stem Cells Group Expands Its Stem Cell Therapy and Regenerative Medicine Centers to Indonesia - GlobeNewswire

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Cell Culture Media, Sera, and Reagents Market: Introduction

According to the report, the globalcell culture media, sera, and reagents marketwas valued at US$6.1 Bnin 2020 and is projected to expand at a CAGR of10.3%from 2021 to 2031. Cell culture media, also known as growth media, is an umbrella term that encompasses any gel or liquid created to support cellular growth in an artificial environment. It is a combination of compounds and nutrients designed to support cellular growth.

Cell culture reagents include cell culture media, media supplements, and sterile reagents. Common cell culture reagents are antibiotics and amino acid supplements. Serum is a key component for growing and maintaining cells in culture. It contains a mixture of proteins, hormones, minerals, and other growth factors. It is added to media as a growth supplement, and specialized forms can be used for different experimental conditions.

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Increase in Demand for Cost-effective and Highly Efficient Cell Culture Products to Drive Global Market

Cell culture technology is applied in various domains such as research, academics, bioprocessing & manufacturing, cell therapy, and regenerative medicines. Leading pharmaceutical companies are expanding their capabilities into biopharmaceutical manufacturing in order to leverage high market potential and due to increase in demand for these products.

Rise in demand for cost-effective and highly efficient cell culture products such as bioreactors, media, reagents, and sera for the production of high-yield cell lines has led to an increase in the number of new product launches. This factor is anticipated to provide lucrative opportunities in the global cell culture market during the forecast period.

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Contract Research & Manufacturing and Focus on Stem Cell Research to Propel Market

The cell culture media, sera, and reagents market is witnessing a shift toward contract manufacturing & research, primarily due to significant capital investment and specificity of each biomanufacturing process. For instance, cell cultures could be 2D, 3D, rotating, continuously stirred, batch-fed, and several other types. The expanding scope of cell culture into areas such as stem cell research is boosts the growth of the global market. Rise in importance of stem cell therapy is underlined by the fact that these therapies help treat the cause of the disease, while conventional treatment methods help in managing only the symptoms. This requires advanced capabilities in terms of capital, equipment, and resources; hence, contract manufacturing presents an economically beneficial solution.

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Major Players in Global Cell Culture Media, Sera, and Reagents Market

Key players operating in the global cell culture media, sera, and reagents market include Thermo Fisher Scientific, Inc., Merck KGaA, Cytiva (Danaher Corporation), Becton, Dickinson and Company, Corning Incorporated, HiMedia Laboratories, FUJIFILM Irvine Scientific, Inc., InvivoGen, SeraCare (LGC Clinical Diagnostics, Inc.), and Lonza. Each of these players has been profiled in the cell culture media, sera, and reagents market report based on parameters such as company overview, financial overview, business strategies, application portfolio, business segments, and recent developments.

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About Transparency Market Research

Transparency Market Research, a global market research company registered at Wilmington, Delaware, United States, provides custom research and consulting services The firm scrutinizes factors shaping the dynamics of demand in various markets.The insights and perspectives on the markets evaluate opportunities in various segments. The opportunities in the segments based on source, application, demographics, sales channel, and end-use are analysed, which will determine growth in the markets over the next decade.

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The Role of Cell Culture Media, Sera, and Reagents Market Industry Growth, Competitors Analysis, New Technology, Trends and Forecast 2021 2031 -...

Skin Stem Cells Comments Off on The Role of Cell Culture Media, Sera, and Reagents Market Industry Growth, Competitors Analysis, New Technology, Trends and Forecast 2021 2031 -… | August 2nd, 2022