Knee replacement alternatives
One of the amputating surgeries in the field of medicine is a knee replacement. It involves removing the knee joint and replacing it with a modified prosthesis. However, several modifications of this surgery have been introduced into the high-powered world of surgery, including several alternatives for knee replacement. In this article, we are going to review the several modifications and knee replacement alternatives therein.
What is Knee Replacement?
Knee replacement, also known as knee arthroplasty, is a surgical procedure that involves the amputation or cutting out of a knee joint, the bones reams by a doctor, especially due to accidents or joint ailments such as arthritis. When the bone is removed, it is then replaced with a prosthetic device. Knee replacement can be partial, where selected or affected parts of the joints can be removed, such as the medial, lateral, and anterior compartments can also be removed and replaced with a modified prosthetic.
Why Should You Be looking for a Knee Replacement Alternatives?
Due to the dynamics of the human body, what works for the goose may not necessarily work for the gander. Certain post-symptoms of a knee replacement can be unbearable for most patients.
Pain After Knee Replacement.
Due to pain in the knee joint, a lot of patients embark on this old-time surgery to help reduce the pain they feel around their knee. But it is worthy of knowing that a substantial number of these patients still continue to feel pain after this audacious surgery. In a survey done by the government, 40% of patients that underwent knee replacement experienced miniature pain for over 3-4 years, while another 44% still felt some 3-5/10 degree of pain in 3-4 years. So, it is not worthy of looking in the direction of knee replacement alternatives in order to solve knee pain.
Knee Replacement Risks.
There is a risk in everything that we do, business, taking a walk, climbing a hill. Same way, certain risks exist in knee replacement which are:
- Patients become more susceptible to heart attack and stroke immediately after knee replacement surgery.
- Increased levels of metals in the blood.
- Allergic reactions to the prosthetic material.
- Possibility of infection.
- Reduced activity of the patient as they thrive to become accustomed to the new prosthesis.
Even though social media and digital marketers paint a vivid picture of beautiful seniors riding a bike, continuing in their daily activities and hobbies, but this may not be true for everyone; in a study conducted by the government, there was seldom activity by patients after knee replacement surgery. Another study showed that patients who weren’t running before a knee replacement surgery couldn’t run after the surgery. But there are always two ways to everything; some other patients also showed an increase in physical activity after their surgery.
What are Knee Replacement Alternatives?
Steroid Injections
Steroids are made up of corticosteroids and cortisone. These corticosteroids carry out an anti-inflammatory function to prevent swelling around the knee regions as well as help reduce pain. But they do have a side effect; they destroy cartilage and may not be efficient as they are thought to be. If you are considering this knee replacement alternative, you probably should bear in mind that they do not offer long term remedies. Steroid injections are viable for knee replacement needs caused by arthritis but may proffer short-termed solutions.
Viscosupplementation
Viscosupplementation is also another knee replacement alternative. They are in the form of gels for the knee, also knowns as hyaluronic acid varying across different brands in the market, likes of SynVisc, OrthoVisc, Supartz, and Euflexxa. They are administered to the patient, but a quick question one would ask is if really the shots help. The variations of results all over the web show support both sides of the notion. But one peculiarity of these results is that none says that they are hurtful or damaging as the steroid injections rather that they give a better solution to knee joint arthritis patients. In my own experience, these injections are efficient only when administered a few times, after which they begin to diminish in effects. The first dose may offer relief for some time, but a dose a far-reaching as the sixth dose may not offer any remedial effect at all.
Knee Nerve Ablation
Knee Nerve ablation is another breakthrough in the surgical world. Knee Nerve Ablation involves the use of technology to carry out a process where the specialist probes the nerves around the joint and passes electrical energy that is used to ablate (destroy) them. The work of these nerves is to relay signals from that region of the knee to the brain. So this technique deadens these nerves, and as such, you don’t feel any pain till those nerves grow back. The research on this type of knee replacement alternative is only a handful. Hence, they cannot conclude on the long term results since most of the studies on this new breakthrough are in their early stages.
Orthobiologics
Orthobiologics incorporation around the knee regions helps to enhance the healing of the knew joint or reduce the consequent degradation of orthopedic tissues. Orthobiologics are also knee replacement alternatives and can be gotten from the patient as autologous or a donor as allogeneic. The two primary derivations of orthobiologics are the PRP and the BMC short for Bone Marrow Concentrate. Another derivation that is commonly used is derived from natal tissues as in amniotic or umbilical cord. Just as the nerve ablation, the research on this type of knee replacement is at its early stages.
Platelet Rich Plasma (PRP)
We mentioned PRP earlier while discussing orthobiologics. PRP’s stand for Platelet-rich plasma that can be gotten from the patient. They contain healing factors that allow them to foster cartilage repair as well as reduce inflammation and balance the chemical dynamics of the knee. A lot of studies support the efficiency of PRP as knee replacement alternatives but may not offer much help when the arthritis is severe.
PKA (Percutaneous Knee Arthroplasty)
PKA (Percutaneous Knee Arthroplasty) comes in handy for severe cases of arthritic pain. This procedure involves the injection of rich bone marrow concentrates gotten from the patient or from a donor into the lax ligaments or other affected areas such as damaged meniscus tissues and tendons. This procedure is intricate and uses an ultrasound and fluoroscopy guides as compared to other quick knee shot techniques. Research proves that this method works pretty well, even in extreme cases of knee arthritis. This procedure also produces a lasting effect for about 2-7 years before the need for repetition.
Here you go!! Knee replacement alternatives. You sure would want to consider some of the alternatives; likes of PKA, PRP, and Bone Marrow concentrates that proffers a long-lasting solution.
- Published in Blog
ISSCA Offers New Online Cellular Therapy Course
With video lectures and additional tools from some of the most respected names in today’s stem cells field, the course arms practitioners with the necessary knowledge and resources to offer innovative regenerative medicine treatments in their existing practices
MIAMI LAKES, Florida— The International Society for Stem Cell Application (ISSCA) (www.issca.us) has announced it has launched a new online stem cells course, Cellular Therapy. The course adds to the group’s already existing robust offering of onsite and online courses designed to give physicians looking to incorporate regenerative medicine protocols into their practices the education and tools necessary to do so.
Regenerative medicine has been increasingly gaining attention in today’s fast-paced medical world. As more researchers and physicians become interested in studying the field and introducing treatment protocols into their practices, it can be difficult to know which products and practices yield the best results for patients seeking these treatments for relief from degenerative diseases, noted Benito Novas, ISSCA VP of Public Relations. Knowing which products work for which conditions and how to safely administer them to maximize results are key in leading a successful regenerative medicine practice.
With the Cellular Therapy course and others offered by the ISSCA, physicians will learn these valuable protocols and more about product offerings and how to choose the most effective ones. The Cellular Therapy course will prepare physicians with the necessary theoretical and practical knowledge needed to effectively and safely secure better patient outcomes when using cellular therapies. With this training, physicians will gain knowledge from leading scientists in the field, learn valuable information on safety standards and quality control from top manufacturers, be positioned to perform these procedures and open a Stem Cell Center practice, join the ISSCA’s network, and enjoy the benefits of an exponentially growing industry worldwide.
Practitioners enrolling in the online course will gain access to online lectures from some of the leading names in the field of regenerative medicine spanning a number of topics critical to understanding the foundations of cellular therapy. In addition to online lectures, enrollees gain access to important supporting documents; The Condition Book, outlining stem cells treatment protocols for seven common conditions; and valuable case studies, all designed to deliver the knowledge needed to successfully implement stem cells treatments in a clinical setting.
And physicians looking to enroll in this course and other offerings by the ISSCA are in good hands. The group is widely considered as the global standard bearer when it comes to education and research in the regenerative medicine field. For years, the ISSCA has played a critical role in bridging the gap between the science behind stem cells and regenerative medicine and the practical application of that science in a clinical setting.
“We are pleased to add the online Cellular Therapy course to our growing number of course offerings designed to deliver the skills and education needed to practitioners eager to implement stem cells treatment protocols into their existing practices,” said Novas. “The course gives physicians the skills needed to utilize these highly effective treatments to help patients suffering from degenerative diseases while expanding on the ISSCA’s mission to continue to serve as the premier educational resource for physicians across the globe looking to introduce stem cells treatments into their practices.”
To learn more about the ISSCA, visit www.issca.us. To learn more about the group’s new online Cellular Therapy course or to register, visit https://www.cellulartherapycourse.com/
- Published in Press Releases
Conventional and novel stem cell based therapies for androgenic alopecia
Dodanim Talavera-Adame,1 Daniella Newman,2 Nathan Newman1
1American Advanced Medical Corp. (Private Practice), Beverly Hills, CA,
2Western University of Health Sciences, Pomona, CA, USA
Abstract
The prevalence of androgenic alopecia (AGA) increases with age and it affects both men and women. Patients diagnosed with AGA may experience decreased quality of life, depression, and feel self-conscious. There are a variety of therapeutic options ranging from prescription drugs to non-prescription medications. Currently, AGA involves an annual global market revenue of US$4 billion and a growth rate of 1.8%, indicating a growing consumer market. Although natural and synthetic ingredients can promote hair growth and, therefore, be useful to treat AGA, some of them have important adverse effects and unknown mechanisms of action that limit their use and benefits. Biologic factors that include signaling from stem cells, dermal papilla cells, and platelet-rich plasma are some of the current therapeutic agents being studied for hair restoration with milder side effects. However, most of the mechanisms exerted by these factors in hair restoration are still being researched. In this review, we analyze the therapeutic agents that have been used for AGA and emphasize the potential of new therapies based on advances in stem cell technologies and regenerative medicine.
Introduction
The prevalence of androgenic alopecia (AGA) increases with age, and is estimated to affect about 80% of Caucasian men.1 Female AGA, also known as female pattern hair loss, affects 32% of women in the ninth decade of life.2 The consumer market for products that promote hair growth has been increasing dramatically.3 These products promote hair regeneration based on the knowledge about the hair follicle (HF) cycle.4,5 However, in most cases, the mechanisms of action of these products are not well characterized and the results are variable or with undesirable side effects.6 At present, only two treatments for AGA have been approved by the US Food and Drug Administration (FDA): Minoxidil and Finasteride.7–10Although these medications have proved to be effective in some cases, their use is limited by their side effects.11,12 With the emergence of stem cells (SCs), many mechanisms that lead to tissue regeneration have been discovered.13 Hair regeneration has become one of the targets for SC technologies to restore the hair in AGA.14 Several SC factors such as peptides exert essential signals to promote hair regrowth.15,16 Some of these signals stimulate differentiation of SCs to keratinocytes which are important for HF growth.17 Other signals can stimulate dermal papilla cells (DPCs) that promote SC proliferation in the HF.18,19 In this review, we describe HF characteristics and discuss different therapies used currently for AGA and possible novel agents for hair regeneration. These therapies include FDA-approved medications, non-prescription physical or chemical agents, natural ingredients, small molecules, biologic factors, and signals derived from SCs.
HF and SC niche
The HF undergoes biologic changes from an actively growing stage (anagen) to a quiescent stage (telogen) with an intermediate remodeling stage (catagen).4 HFSCs are located in the bulge region of the follicle and they interact with mesenchymal SCs (MSCs) located in the dermal papilla (DP).18 These signal exchanges promote activation of some cellular pathways that are essential for DPC growth, function, and survival, such as the activation of Wnt signaling pathway.19–21 Other signals, such as those from endothelial cells (ECs) located at the DP, are also essential for HF maintenance.22 EC dysfunction that impairs adequate blood supply may limits or inhibits hair growth.22 For instance, Minoxidil, a synthetic agent, is able to promote hair growth by increasing blood flow and the production of prostaglandin E2 (PGE2).7 It has been shown that proteins that belong to the transforming growth factor (TGF) superfamily, such as bone morphogenetic proteins (BMPs), also exert signals to maintain the capacity of DPCs to induce HF growing in vivo and in vitro.23 These BMPs may be released by several cells that compose the follicle, including ECs.24–26 ECs may provide signals for BMP receptor activation in DPCs similar to those signals that promote survival of MSCs in human embryoid bodies composed of multipotent cells.24,25 DPCs have been derived from pluripotent SCs in an attempt to study their potential for hair regeneration in vitro and in vivo.27 Together, dermal blood vessels and DPCs orchestrate a suitable microenvironment for the growth and survival of HFSCs.28,29 Interestingly, the expression of Forkhead box C1 regulates the quiescence of HFSCs located in the bulge region (Figure 1).30 HFSCs are quiescent during mid-anagen and maintain this stage until the next hair cycle.29,30 However, during early anagen stage, these cells undergo a short proliferative phase in which they self-renew and produce new hair.30 Therefore, the bulge region constitutes a SC niche that makes multiple signals toward quiescence or proliferation stages.30–34 It is known that fibroblasts and adipocyte signals are able to inhibit the proliferation of HFSCs.34 Additionally, BMP6 and fibroblast growth factor 18 (FGF18) from bulge cells exert inhibitory effects on HFSC proliferation.34 Dihydrotestosterone (DHT) also inhibits HF growth.35 Agents that reduce DHT, such as Finasteride, promote hair regrowth by inhibiting Type II 5a-reductase.8,14,36 In contrast to these inhibitory effects, DPCs located at the base of the HF provide activation signals (Figure 1).18,34 The crosstalk between DPCs and HFSCs leads to inhibition of inhibitory effects with the resultant cell proliferation toward hair regeneration (anagen).30,31,37 With the self-renewal of HFSCs, the outer root sheath (ORS) forms, and signals from DPCs to the bulge cells diminish in a way that the bulge cells start again with their quiescent stage.4,34As mentioned earlier, Forkhead box C1 transcription factor has an important role in maintaining the threshold for HFSC activation.30 The knockdown of these factors in bulge cells reduces the cells’ threshold for proliferation, and the anagen cycle starts more frequently due to promotion of HFSC proliferation in shorter periods of time.30
Laser therapy
Light amplification by stimulated emission of radiation (LASER) generates electromagnetic radiation which is uniform in polarization, phase, and wavelength.45 Low-level laser therapy (LLLT), also called “cold laser” therapy, since it utilizes lower power densities than those needed to produce heating of tissue. Transdermal LLLT has been used for therapeutic purposes via photobiomodulation.46,47 Several clinical conditions, such as rheumatoid arthritis, mucositis, pain, and other inflammatory diseases, have been treated with these laser devices.48–50 LLLT promotes cell proliferation by stimulating cellular production of adenosine triphosphate and creating a shift in overall cell redox potential toward greater intracellular oxidation.51 The redox state of the cell regulates activation of signaling pathways that ultimately promotes high transcription factor activity and gene expression of factors associated with the cell cycle.52 Physical agents such as lasers have been also used to prevent hair loss in a wavelength range in the red and near infrared (600–1,070 nm).5,47,51,53 Laser therapy emits light that penetrates the scalp and promotes hair growth by increasing the blood flow.54 This increase gives rise to EC proliferation and migration due to upregulation of vascular endothelial growth factor (VEGF) and endothelial nitric oxide synthase.55,56 In addition, the laser energy itself stimulates metabolism in catagen or telogen follicles, resulting in the production of anagen hair.53,54A specific effect of LLLT has been demonstrated to promote proliferation of HFSCs, forcing the hair to start the anagen phase.57
Biologic agents that promote hair growth and their mechanisms of action
SC signaling
Recently, it has been found that SCs release factors that can promote hair growth.16 These factors and their mechanisms of action have been summarized in Table 3. These factors, known as “secretomes”, are able to promote skin regeneration, wound healing, and immunologic modulation, among other effects.58,59 Some of these factors, such as epidermal growth factor (EGF), basic fibroblast growth factor, hepatocyte growth factor (HGF) and HGF activator, VEGF, insulin-like growth factor (IGF), TGF-ß, and platelet-derived growth factor (PDGF), are able to provide signals that promote hair growth.15,60–64 As mentioned before, DPCs provide signals to HFSCs located in the bulge that proliferate and migrate either to the DP or to the epidermis to repopulate the basal layer (Figure 1).32,65 Enhancement in growth factor expression (except for EGF) has been reported when the adipose SCs are cultured in hypoxic conditions.15 Also, SCs increase their self-renewal capacity under these conditions.66–68 Low oxygen concentrations (1%–5%) increase the level of expression of SC factors that include VEGF, basic fibroblast growth factor, IGF binding protein 1 (IGFBP-1), IGF binding protein 2 (IGFBP-2), macrophage colony-stimulating factor (M-CSF), M-CSF receptor (M-CSFR), and PDGF receptor ß (PDGFR-ß).15,69,70 While these groups of factors promote HF growth in intact skin, another group of factors, such as M-CSF, M-CSFR, and interleukin-6, are involved in wound-induced hair neogenesis.71 HGF and HGF activator stimulate DPCs to promote proliferation of epithelial follicular cells.61 Epidermal growth factor promotes cellular migration via the activation of Wnt/ß-catenin signaling.60 VEGF promotes hair growth and increases the follicle size mainly by perifollicular angiogenesis.72 Blocking VEGF activity by neutralizing antibodies reduced the size and growth of the HF.72 PDGF and its receptor (PDGFR-a) are essential for follicular development by promoting upregulation of genes involved in HF differentiation and regulating the anagen phase in HFs.64,73 They are also expressed in neonatal skin cells that surround the HF.73 Monoclonal antibodies to PDGFR-a (APA5) produced failure in hair germ induction, supporting that PDGFR-a and its ligand have an essential role in hair differentiation and development.73 IGF-1 promotes proliferation, survival, and migration of HF cells.69,74 In addition, IGF binding proteins (IGFBPs) also promote hair growth and hair cell survival by regulating IGF-1 effects and its interaction with extracellular matrix proteins in the HF.70 Higher levels of IGF-1 and IGFBPs in beard DPCs suggest that IGF-1 levels are associated with androgens.74 Furthermore, DPCs from non-balding scalps showed significantly higher levels of IGF-1 and IGFBP-6, in contrast to DPCs from balding scalps.74
Table 3
Stem cell factors and small molecules that promote hair growth and their mechanisms of action
| Factor | Mechanism of action |
|---|---|
| HGF and HGF activator61 | Factor secreted by DPC that promotes proliferation of epithelial follicular cells |
| EGF60 | Promotes growth and migration of follicle ORS cells by activation of Wnt/ß-catenin signaling |
| bFGF62 | Promotes the development of hair follicle |
| IL-693 | Involved in WIHN through STAT3 activation |
| VEGF72 | Promotes perifollicular angiogenesis |
| TGF-ß63 | Stimulates the signaling pathways that regulate hair cycle |
| IGF-169 | Promotes proliferation, survival, and migration of hair follicle cells |
| IGFBP-1 to -670 | Regulates IGF-1 effects and its interaction with extracellular matrix proteins at the hair follicle level |
| BMP23 | Maintains DPC phenotype which is crucial for stimulation of hair follicle stem cell |
| BMPR1a23 | Maintains the proper identity of DPCs that is essential for specific DPC function |
| M-CSF71 | Involved in wound-induced hair regrowth |
| M-CSFR71 | Involved in wound-induced hair regrowth |
| PDGF and PDGFR-ß/-a64 | Upregulates the genes involved in hair follicle differentiation. Induction and regulation of anagen phase. PDGF and its receptors are essential for follicular development |
| Wnt3a97 | Involved in hair follicle development through ß-catenin signaling |
| PGE279,80 | Stimulates anagen phase in hair follicles |
| PGF2a and analogs79,80 | Promotes transition from telogen to anagen phase of the hair cycle |
| BIO98 | GSK-3 inhibitor |
| PGE2 or inhibition of PGD2 or PGD2 receptor D2/GPR4477 | Promotes follicle regeneration |
| Iron and l-lysine95 | Under investigation |
Abbreviations: bFGF, basic fibroblast growth factor; BIO, (2’Z,3’E)-6-bromoindirubin-3′-oxime; BMP, bone morphogenetic protein; DPCs, dermal papilla cells; EGF, epidermal growth factor; GSK-3, glycogen synthase kinase-3; HGF, hepatocyte growth factor; IGF-1, insulin-like growth factor 1; IGFBP-1, insulin-like growth factor-binding protein 1; IL-6, interleukin-6; M-CSF, microphage colony-stimulating factor; M-CSFR, microphage colony-stimulating factor receptor; ORS, outer root sheath; PDGF, platelet-derived growth factor; PDGFR-a, platelet-derived growth factor receptor alpha; PDGFR-ß, platelet-derived growth factor receptor beta; PGD2, prostaglandin D2; PGE2, prostaglandin E2; TGF-ß1, transforming growth factor ß1; VEGF, vascular endothelial growth factor; WIHN, wound-induced hair neogenesis; Wnt3a, wingless-type MMTV integration site family, member 3A.
Small molecules
Small molecules with low molecular weight (<900 Da) and the size of 10-9 m are organic compounds that are able to regulate some biologic processes.75 Some small molecules have been tested for their role in hair growth.76 Synthetic, non-peptidyl small molecules that act as agonists of the hedgehog pathway have the ability to promote follicular cycling in adult mouse skin.76 PGE2 and prostaglandin D2 (PGD2) have also been associated with the hair cycle (Table 3).77 PGD2 is elevated in the scalp of balding men and inhibits hair lengthening via GPR44 receptor.78 Also, it is known that PGE2 and PGF2a promote hair growth, while PGD2 inhibits this process.77,79 Prostaglandin analogs of PGF2a have been used originally to decrease ocular pressure in glaucoma with parallel effects in the growth of eyelashes, which suggests a specific effect in HF activation.80 PGD2 receptors are located in the upper and lower ORS region and in the DP, suggesting that these prostaglandins play an important role in hair cycle.81 Molecules such as quercetin are able to inhibit PGD2 and, in this way, promote hair growth.82–84 Antagonists of PGD2 receptor (formally named chemoattractant receptor-homologous expressed in Th2 cells) such as setipiprant have been used to treat allergic diseases such as asthma, but they also have beneficial effects in AGA.85–87 Another small molecule l-ascorbic acid 2-phosphate promotes proliferation of ORS keratinocytes through the secretion of IGF-1 from DPCs via phosphatidylinositol 3-kinase.88 Recently, it has been described that small-molecule inhibitors of Janus kinase–signal transducer and activator of transcription (JAK-STAT) pathway promote hair regrowth in humans.89 Janus kinase inhibitors are currently approved by the FDA for the treatment of some specific diseases such as psoriasis and other autoimmune-mediated diseases.90–94 Also, another group of small molecules such as iron and the amino acid l-Lysine are essential for hair growth (Table 3).95
Cellular therapy
The multipotent SCs in the bulge region of the HF receive signals from DPCs in order to proliferate and survive.27,28,65,84,96 It has been shown that Wnt/ß-catenin signaling is essential for the growth and maintenance of DPCs.19,97 These cells can be isolated and cultured in vitro with media supplemented with 10% fetal bovine serum and FGF-2.37,98 However, they lose versican expression that correlates with decrease in follicle-inducing activity in culture.98 Versican is the most abundant component of HF extracellular matrix.99 Inhibition of glycogen synthase kinase-3 by (2’Z,3’E)-6-bromoindirubin-3′-oxime (BIO) promotes hair growth in mouse vibrissa follicles in culture by activation of Wnt signaling.98 Therefore, the increase of Wnt signaling in DPCs apparently is one of the main factors that promote hair growth.19 DPCs have been also generated from human embryonic SCs that induced HF formation after murine transplantation.27
Platelet-rich plasma
Platelets are anucleate cells generated by fragmentation of megakaryocytes in the bone marrow.100 These cells are actively involved in the hemostatic process after releasing biologically active molecules (cytokines).100–102 Because of the platelets’ higher capacity to produce and release these factors, autologous platelet-rich plasma (PRP) has been used to treat chronic wounds.103 Therefore, PRP can be used as autologous therapy for regenerative purposes, for example, chondrogenic differentiation, wound healing, fat grafting, AGA, alopecia areata, facial scars, and dermal volume augmentation.101,104–108 PRP contains human platelets in a small volume that is five to seven times higher than in normal blood and it has been proven to be beneficial to treat AGA.10,105,109–111 The factors released by these platelets after their activation, such as PDGFs (PDGFaa, PDGFbb, PDGFab), TGF-ß1, TGF-ß2, EGF, VEGF, and FGF, promote proliferation of DPCs and, therefore, may be beneficial for AGA treatment.109,112–114 Clinical experiments indicate that patients with AGA treated with autologous PRP show improved hair count and thickness.109
In search of novel therapies
In this paper, we reviewed and discussed the use of therapeutic agents for hair regeneration and the knowledge to promote the development of new therapies for AGA based on the advances in regenerative medicine. The HF is a complex structure that grows when adequate signaling is provided to the HFSCs. These cells are located in the follicle bulge and receive signals from MSCs located in the dermis that are called DPCs. The secretory phenotype of DPCs is determined by local and circulatory signals or hormones. Recent discoveries have demonstrated that SCs in culture are able to activate DPCs and HFSCs and, in this way, promote hair growth. The study of these cellular signals can provide the necessary knowledge for developing more effective therapeutic agents for the treatment of AGA with minimal side effects. Therefore, advancements in the field of regenerative medicine may generate novel therapeutic alternatives. However, further research and clinical studies are needed to evaluate their efficacy.
Disclosure
The authors report no conflicts of interest in this work.
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- Published in Blog
Global Stem Cells Group Receives 2019 Best of Miami Lakes Award
Miami Lakes Award Program Honors the Achievement
MIAMI LAKES November 14, 2019 — Global Stem Cells Group has been selected for the 2019 Best of Miami Lakes Award in the Biotechnology Company category by the Miami Lakes Award Program.
Each year, the Miami Lakes Award Program identifies companies that we believe have achieved exceptional marketing success in their local community and business category. These are local companies that enhance the positive image of small business through service to their customers and our community. These exceptional companies help make the Miami Lakes area a great place to live, work and play.
Various sources of information were gathered and analyzed to choose the winners in each category. The 2019 Miami Lakes Award Program focuses on quality, not quantity. Winners are determined based on the information gathered both internally by the Miami Lakes Award Program and data provided by third parties.
About Miami Lakes Award Program
The Miami Lakes Award Program is an annual awards program honoring the achievements and accomplishments of local businesses throughout the Miami Lakes area. Recognition is given to those companies that have shown the ability to use their best practices and implemented programs to generate competitive advantages and long-term value.
The Miami Lakes Award Program was established to recognize the best of local businesses in our community. Our organization works exclusively with local business owners, trade groups, professional associations and other business advertising and marketing groups. Our mission is to recognize the small business community’s contributions to the U.S. economy.
SOURCE: Miami Lakes Award Program
CONTACT:
Miami Lakes Award Program
Email: PublicRelations@2019localtop-selection.com
URL: http://www.2019localtop-selection.com
- Published in Press Releases
Q&A: What are exosomes, exactly?
by James R. Edgar
Abstract
Exosomes are extracellular vesicles first described as such 30 years ago and since implicated in cell–cell communication and the transmission of disease states, and explored as a means of drug discovery. Yet fundamental questions about their biology remain unanswered. Here I explore what exosomes are, highlight the difficulties in studying them and explain the current definition and some of the outstanding issues in exosome biology.
What is the current definition of an exosome?
That is a very good question. Since the original description of exosomes over 30 years ago, the term has been loosely used for various forms of extracellular vesicle, muddying the field and contributing to the scepticism with which the research has sometimes been met. Exosomes are best defined as extracellular vesicles that are released from cells upon fusion of an intermediate endocytic compartment, the multivesicular body (MVB), with the plasma membrane. This liberates intraluminal vesicles (ILVs) into the extracellular milieu and the vesicles thereby released are what we know as exosomes (Fig. 1).
Exosomes correspond to intraluminal vesicles of multivesicular bodies. A transmission electron micrograph of an Epstein–Barr virus-transformed B cell displaying newly expelled exosomes at the plasma membrane. Multivesicular bodies (MVB) can be seen which can deliver content to lysosomes for degradation or can fuse with the cell surface to release intraluminal vesicles as exosomes, indicated by the arrows at the top of the picture
There are other types of microvesicle, including apoptotic bodies and ectosomes, which are derived from cells undergoing apoptosis and plasma membrane shedding, respectively. Although apoptotic bodies, ectosomes and exosomes are all roughly the same size (typically 40–100 nm) and all also contain ‘gulps’ of cytosol, they are different species of vesicles and understanding differences between them is of paramount importance but has too often been overlooked.
How were exosomes first recognized as distinct entities?
The presence of membranous vesicles outside cells was first recognized 50 years ago, although these were originally assumed to be waste products released via shedding of the plasma membrane. The recognition of what we now call exosomes didn’t come until 1983, from studies on the loss of transferrin during the maturation of reticulocytes into erythrocytes [1]. These studies showed, by following transferrin-gold conjugates through the endocytic system, that ILVs generated in MVBs can be released to the extracellular space through fusion with the plasma membrane [2], although it was not until 1987 that the term ‘exosome’ was coined for them [3].
Even then, however, these extracellular vesicles were largely ignored, forgotten or, again, dismissed as a means of cellular waste disposal. It is only in the past decade that interest in exosomes has exploded, with a nearly tenfold increase in publications in as many years (115 in 2006, 1010 in 2015).
Why this explosion of interest?
For at least three reasons. First, they are thought to provide a means of intercellular communication and of transmission of macromolecules between cells. Second, in the past decade, exosomes have been attributed roles in the spread of proteins, lipids, mRNA, miRNA and DNA and as contributing factors in the development of several diseases. And third, they have been proposed to be useful vectors for drugs because they are composed of cell membranes, rather than synthetic polymers, and as such are better tolerated by the host. In fact, some of the earliest exosome research indicated that they can carry the MHC–peptide complexes that are recognized by T lymphocytes [4] and that secretion of such exosomes could promote antitumour immune responses in mice in vivo [5]. Exosome therapies are now being explored in anti-cancer clinical trials and recent reports claim taxol-filled exosomes can be used to treat cancers in mice at 50-fold lower doses than conventional treatments, with the additional benefit that exosomes do not invoke an immune response [6].
Yet despite 20 years of research, the very basics of exosome biology are in their infancy and we know little of the part they play in normal cellular physiology.
So do we know how they are generated?
Yes and no. We do know that they are made as ILVs; but first of all, not all ILVs finish up as exosomes, and second, the mechanism of their generation in endosomes is not fully understood. Most conventional membrane budding processes deform membrane from an organelle into the cytoplasm but in ILV formation the membrane buds away from the cytoplasm and into the endosome. This unconventional budding process is not limited to ILV generation but also takes place during enveloped virus budding from the cytosol and during cytokinesis [7], and it requires specialised machinery.
ILVs (and thus exosomes) can be generated at the endosomal limiting membrane by at least two mechanisms, one of which depends on the ESCRT machinery (ESCRT stands for endosomal sorting complexes required for transport) whereas the other is ESCRT-independent (Fig. 2).
ILVs are generated by invagination of the endosomal membrane and have three possible fates. Inset: intraluminal vesicles (ILV) are formed by invagination of the endosomal membrane by either ESCRT-dependent or ESCRT-independent mechanisms. Matured endosomes accumulate ILVs within their lumen and have three distinct fates. They may deliver content that contributes to the biogenesis of specialized lysosome-related organelles (for example, melanosomes, Weibel-Palade bodies, azurophilic granules), they may fuse with lysosomes or they may fuse with the plasma membrane where released ILVs are now termed ‘exosomes’
The ESCRT machinery consists of a set of cytosolic protein complexes that are recruited to endosomes by membrane proteins that have been tagged, usually with ubiquitin on their cytosolic domains. The ubiquitin tag is recognized by the first of the ESCRT complexes, ESCRT-0, which is thus recruited to the endosomal membrane and passes ubiquitinated cargos to ESCRT-I, one of whose components, Tsg101, also recognizes ubiquitin. The recruitment of the ESCRT machinery acts to both cluster the ubiquitinated cargo proteins on the endosome and induce curvature of the endosomal membrane to form ILVs.
But ILVs are still able to form in the absence of ESCRTs [8], so other means of generating ILVs must exist, although the mechanisms for their generation are less clear. Generation of these ESCRT-independent ILVs requires the tetraspanin CD63—a protein abundant on ILVs but with unclear function [9]—and may be facilitated by cone-shaped bending properties of lipids such as ceramide [10].
If not all ILVs become exosomes, what determines the fate of an ILV?
The destiny of ILVs is directed by the fate of the MVB they reside in. Confusingly, in addition to different types of ILVs, there are also different types of MVBs [11] and what regulates the fate of these endosomes is another interesting question. MVBs have several potential fates (Fig. 2) and can either fuse with lysosomes (where contents are degraded and recycled), fuse with the plasma membrane (where ILVs are released as exosomes), as I have already mentioned, or contribute to the generation of specialised organelles, such as melanosomes (in melanocytes), Weibel-Palade bodies (endothelial cells), azurophilic granules (in neutrophils) and secretory granules (in mast cells). The levels of cholesterol on MVBs appear to play a part in regulating their fate, cholesterol-rich MVBs being directed to the plasma membrane for exosome release, while cholesterol-poor MVBs are targeted to the lysosome [12].
But what regulates the balance between exosome release and alternative fates of ILVs remains engimatic.
What about differences between cells: do all cells release exosomes?
Well, not all cells have an endomembrane system, so no. But most mammalian cells contain endomembranes and generate ILVs within MVBs, though remarkably little is known about exosome release in most cell types.
Some cells—for example, the B cells, dendritic cells and mast cells of the immune system—appear to release exosomes constitutively; in fact, most of the data we have on exosomes comes from immune cells. As well as releasing exosomes constitutively, these cells may also be stimulated to secrete exosomes by cellular interactions. For example, murine dendritic cells, which are specialized to activate T lymphocytes, secrete higher levels of exosomes upon interaction with antigen-specific CD4+ T lymphocytes [13]. In fact, lymphocyte interactions generally can be accompanied by exosome release; human T cells (including primary T cells from blood, T cell clones and Jurkat cell lines) release exosomes upon activation of their antigen receptors [14] and B cells release more exosomes upon engagement with antigen-specific CD4+ T cells [15].
Other cell types can be pushed to secrete exosomes by means of calcium ionophores or other stimuli[16, 17], but the extent of physiological exosome secretion in non-immune cells is largely unknown.
What happens when exosomes reach an acceptor cell?
We don’t know exactly. Exosomes that transfer membrane proteins or luminal content to the acceptor cell may be engulfed whole or the exosome membrane may fuse directly with the host plasma membrane (Fig. 3). Alternatively, exosomes may not need to be taken up by cells to elicit a physiological response: follicular dendritic cells, for example, carry on their cell surface exosomes that bear MHC–peptide complexes and other proteins that they do not express and are thereby enabled to activate immune cells with which they interact [18].
Exosome uptake by recipient cells. Fusion of MVBs with the cell surface releases ILVs as exosomes. In order for exosomes to elicit a response from recipient cells they might either fuse with plasma membrane (a) or be taken up whole via endocytosis (b), following which the exosome must be delivered to the cytosol, for example, via a back-fusion event (c). Alternatively, exosomes may attach to the surface of recipient cells to elicit a signalling response (d)
For intercellular transmission, various mechanisms of phagocytosis and endocytosis of extracellular vesicles have been described and which mechanism operates may depend upon vesicle size, which may in turn depend upon the cargo carried by the vesicle. In order for material to be released to an acceptor cell, exosomes must fuse with the host cell and this takes place via either direct fusion with the plasma membrane or a ‘back-fusion’ step from within a host endocytic organelle after the exosome has been engulfed. The process of back-fusion is not entirely clear, although it appears to require the unconventional lipid LBPA and protein Alix [19] (and is exploited by anthrax toxin lethal factor to escape from endosomes to the cytosol [20]).
Whether exosomes fuse with target cells or act via interactions with cell-surface proteins, or both, is another fundamental cell biology question that will need to be addressed if we are to understand the functions of exosomes.
So what are the consequences of all this information transfer? What biological functions have been established for exosomes?
There are many proposed functions for exosomes, the best-established being in immune responses. Exosomes isolated from B lymphocytes and bearing MHC class II molecules were shown in early experiments [4] to activate T lymphocytes in vitro, suggesting that they were communicating with the T lymphocytes in just the way that the parent B cells did. I have already mentioned later work by the same group, who showed that exosomes derived from dendritic cells, which are specialized to activate T cells in the initiation of immune responses, could promote antitumour immune responses in mice [5], exciting interest in the possibility of practical applications.
Or, as with follicular dendritic cells, exosome-associated MHC II can be found on the surface of cell types that neither express MHC II nor secrete exosomes, indicating that exosomes are delivered from one cell type to another [18].
However, exosomes may have roles other than in immune responses as several non-immune cells secrete exosomes. The only physiological role so far reported for non-immune cells is in keratinocyte-derived exosomes, which have been shown to modulate melanin synthesis by increasing the expression and activity of proteins within the melanosomes that modulate skin pigmentation [21].
How exactly would exosomes from one cell influence the expression and activity of proteins in an acceptor cell?
Exosomes transfer not only protein and lipids but mRNA and microRNA into acceptor cells and these RNAs have been shown in experiments in vitro to have functional effects in recipient cells. For example, exosomes from mice can be transferred to human cells and mRNA can be translated into mouse protein [22]. Similarly, microRNAs—double-stranded RNA fragments that can regulate specific sets of mRNA (and so protein levels)—can act functionally in acceptor cells. The mode of action of exosomes has been a focus of special interest in cancer biology. Exosomes from breast cancer cell lines, for example, have been shown to be enriched for miRNAs relative to nontumorigenic breast cell lines and exposure of normal cells to exosomes derived from breast cancer cell lines increased both cell survival and proliferation, accompanied by loss of expression of some tumour-suppressor proteins [23]. Exosome levels are elevated in the serum of some cancer patients versus controls. However, whether these vesicles are exosomes or other forms of extracellular vesicle, or a mix, is unclear—I have already mentioned this persistent problem in exosome research.
So exosomes can also contribute to disease?
Yes indeed. As exosomes provide a means of intercellular communication, they may also act as vehicles for ‘bad’ communication or spread. As well as miRNAs in the case of cancer, exosomes have been shown to contain numerous disease-associated cargos—for example, neurodegenerative-associated peptides, such as Aβ [24] (in Alzheimer’s disease), tau [25] (in numerous neurodegenerative diseases), prions [26] (in transmissible spongiform encephalopathies), alpha-synuclein [27] (in synucleinopathies, including Parkinson’s disease) and superoxide dismutase 1 [28] (in amyotrophic lateral sclerosis). Exosomes have thus been suggested to be propagators of neurodegenerative protein spread, although some cargos are easier to envisage than others.
Of the neurodegenerative-associated proteins, only some are integral membrane proteins, that is, proteins inserted into lipid bilayers, rather than cytosolic. Sorting of proteins into ILVs (and thus exosomes) is easier to envisage for membrane proteins, where tags such as ubiquitin regulate where they end up. So far, the presence of both Aβ [29] and PrPc [26] has in fact been shown in ILVs, though this has not been demonstrated for other membrane proteins, such as alpha-synuclein and tau.
The mechanism whereby cytosolic proteins may be sorted to ILVs/exosomes, however, is not clear. In order for cytosolic proteins to become concentrated in ILVs, they would require positive incorporation and sorting, possibly by membrane-associated components on endosomes. All we can say is that there is evidence that this does in fact happen; cytosolic factors such as miRNAs are enriched in exosomes relative to cytosol, indicating that sorting must occur whereby certain miRNAs are concentrated and others are not [30].
The means by which disease-associated factors spread between cells remains poorly understood and exosomes would provide a means for such transmission. The presence of exosomal proteins, such as Alix, in association with Alzheimer’s senile plaques strengthens the circumstantial case for exosomes as a mediator in such spread. The hope is that having a means to regulate exosome release and spread may be useful in combatting some of these diseases but much more basic biology needs to be established before then.
Now I’m confused—what determines what exosomes contain?
Exosomes will contain whatever is sorted into them during their formation (as ILVs). For membrane proteins, this usually occurs through ubiquitination, which acts as a substrate for recruitment of the ESCRT machinery and subsequent generation of ESCRT-dependent ILVs.
The mechanisms that concentrate cytosolic factors are currently unknown. Although it seems clear that miRNAs, for example, are enriched relative to the amount in their parent cells, and are not randomly incorporated into exosomes, it is not clear how some are enriched more than others. There are currently a few hypotheses for miRNA sorting, including sorting via sumoylated heterogeneous nuclear ribonucleoproteins [31] or by a miRNA-induced silencing complex (miRISC) [32].
Because of the difficulties in separating exosomes from other extracellular vesicles, it is likely that some cargos reported to be enriched in ‘exosomes’ may in fact be contained in contaminant vesicles that are not exosomes. While many researchers are very stringent about applying the labels ‘exosomes’ and ‘extracellular vesicles’ correctly, others unfortunately are not. In addition, as I have said before, cytosolic proteins are likely to be found in exosome preparations because the exosome lumen is made of cytosol.
So how exactly can you be sure that a given extracellular vesicle is an exosome and not something else?
This is an interesting question that has a complex answer. Ideally, an intracellular compartment is identified by a specific biological marker, as, for example, in the case of the Golgi, nucleus or mitochondria, all of which carry proteins not found, or found at much lower levels, elsewhere.
One problem is that ILVs, and thus exosomes, represent an intermediate compartment of an intermediate. MVBs are not static organelles but rather undergo continuous maturation, in the course of which they gain and lose proteins. There will never be an exclusive marker for exosomes because any cargo on the ILV/exosome membrane must first be on the limiting membrane of the endosome and anything found inside must first come from the cytosol. A cargo may be concentrated on ILVs/exosomes but it will also be elsewhere. CD63 could be thought of as a pseudo-marker for exosomes. ILVs and exosomes are enriched in several such tetraspanins and my colleagues and I have show that CD63 is required for ESCRT-independent ILV formation [9]. Alix also appears to be concentrated in ILVs/exosomes [33], as does Tsg101, a component of ESCRT-I, which has been used as a marker of exosomes in numerous studies [33,34], although the presence of Tsg101 in ILVs or exosomes does not fit with conventional models of ILV formation. Although Tsg101 is involved in ESCRT-dependent ILV formation, as mentioned earlier, it, along with other ESCRT components, should disassociate from the endosomal membrane prior to an ILV pinching off the endosomal membrane to allow it to participate in further events [35]. Exactly when ESCRT-I components ‘fall off’ the membrane is unknown but it is conventionally thought to be prior to ILV formation, so Tsg101 should remain cytosolic and available for subsequent rounds of ILV formation. It is possible that some Tsg101 may be ‘swallowed’ into the forming ILV lumen, but levels should be negligible.
So are you saying there is no reliable marker for endosomes?
There may not be—not a single reliable one. Ultimately, perhaps the best method of defining exosomes biochemically may be through a combination of markers, including tetraspanins, Alix and others, with a concomitant exclusion of resident plasma membrane proteins. Although ILVs/exosomes will by their nature contain some plasma membrane proteins and the plasma membrane will contain some ILV/exosomal proteins, it should be possible to define relative levels and/or enrichment of proteins of exosomes that distinguish them from other microvesicles. Cargos such as MHC II from B cells and other cell type-specific antigens may also help to distinguish exosomes from other forms of extracellular vesicle. Common exosomal cargos include tetraspanins (CD63, CD81, CD9), antigen presentation molecules (MHC I and MHC II) and others (Alix, flotillin-1). An online database exists [36] where proteins, lipids and RNA are catalogued from published and unpublished exosomal studies.
If they are so hard to characterize reliably, how are exosomes isolated and studied?
Exosomes are rarely imaged by conventional methods as they are too small to be resolved by fluorescence microscopy and their release may be a rare event. A few studies have imaged exosome release occurring in cell cultures by various electron microscopic techniques but, more commonly, exosomes are pooled from cellular supernatant or animal fluids. Traditionally, they have been isolated by differential centrifugation from culture medium whereby larger contaminants are first excluded by pelleting out through increasing speeds of centrifugation before exosomes, small extracellular vesicles and even protein aggregates are pelleted at very high speeds (~100,000 × g) [37]. These preparations therefore represent an enrichment rather than a purification. Enriched preparations are commonly analysed by biochemistry, mass spectrometry or electron microscopy. Electron microscopy of isolated fractions as ‘whole mounts’ make it possible to immuno-label vesicles, with the limitation that isolated preparations do not provide the same internal controls as labelling sections of cells. Remarkably little attention has been paid to the characterization of exosomes, although efforts are being made to repair this omission with guidelines and criteria for defining groups of extracellular vesicles [38].
What would you say are the most important issues in exosome research?
Without doubt the single most important issue is actually understanding the biological significance of these structures. With so little known about their basic physiological functions, it may seem hard to understand how exosomes have been implicated in the pathogenesis of so many disparate disease states. Fundamental questions remain about exosome generation, fate and normal function but, ultimately, in order to understand exosomes, one must first understand ILVs, a fact that is too often overlooked. Meanwhile, it is important that publications on exosomes give a careful and explicit account of the criteria used for distinguishing them from other extracellular vesicles to avoid confusing the field and encouraging scepticism.
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Acknowledgements
The author wishes to thank Scottie Robinson, Paul Luzio and Paul Manna for critical reading of this article.
Competing interests
The author declares that he has no competing interests.
- Published in Blog
ISSCA Faculty Honored with Health Sciences Awards at Conference Held at the University of Miami
The awards recognize the physicians’ leadership in education and instruction in regenerative medicine
MIAMI LAKES, Florida—Three faculty members with the International Society for Stem Cell Application (ISSCA) were honored with awards at the organization’s recent regenerative medicine conference held at the University of Miami on October 24-27. The awards were sponsored by the Sociedad Internacional en Investigación, Salud, Desarrollo Empresarial y Tecnologías (SISSDET) and lauded the honorees for their commitment to leadership and education in the field of regenerative medicine.
The three recipients of the awards are Dr. Damian Ariel Siano, Dra. Maritza Novas, and Dra. Silvina Pastrana. All three have continued to partner with the ISSCA and have notable contributions to the field by offering courses in regenerative medicine, helping thousands of doctors around the world add stem cells therapies to their medical practices.
Dr. Damian Ariel Siano is an orthopedic physician from Argentina who has dedicated his professional life to treat sports injuries. He is one of the most renowned sports medicine specialists in South America. Dr. Siano currently works with one of the most famous soccer teams in Argentina, using cell therapies to help professional athletes avoid unnecessary surgery and recuperate quicker from injuries.
Dra. Maritza Novas currently serves as the Director of Research and Development for the Global Stem Cells Group. For the past 10 years, she has dedicated herself to educating doctors in the latest stem cells advancements and conducting stem cell research. Dra. Novas has visited all continents, sharing her knowledge as a stem cells practitioner and researcher.
Dra. Silvina Pastrana is one of the first doctors that helped form the ISSCA. She has become a visionary in the field and is noted for creating her own stem cells protocols and using complementary therapies to get better results in patient who utilize cell therapies. Dra. Pastrana combines both ozone and vitamin C therapies before employing stem cell protocols, obtaining excellent results in treating patients with arthritis.
“The ISSCA is committed to helping physicians who want to add regenerative medicine to their practices gain the education and tools to do that,” said Benito Novas, Vice President of Public Relations for ISSCA. “The three doctors recognized at our recent event at the University of Miami are prime examples of the high-quality instructors that physicians can anticipate working with when then attend one of our conferences. Congratulations to our faculty on receiving this prestigious award, and thank you to SISSDET for recognizing their accomplishments.”
ISSCA is a global leader in stem cells research, applications, and education, partnering with major global institutions and locations worldwide to host its independent medical congresses. To learn more about the ISSCA and its all of its past and upcoming events, visit http://www.issca.us
- Published in Press Releases
ISSCA Set to Host Upcoming Stem Cells Conferences, Reaching Physicians Across the Globe
The organization seeks to improve education and access to stem cells therapies for physicians and patients worldwideThe organization seeks to improve education and access to stem cells therapies for physicians and patients worldwide
MIAMI LAKES, Florida—Following two recent highly successful conferences, the International Society for Stem Cell Application (ISSCA) is set to offer six additional events on its training calendar to round out 2019. Recent events attracting physicians across the globe include a conference held at the University of Miami and the ISSCA’s 6th Annual Regenerative Medicine Symposium in Buenos Aires. With its upcoming slate of events, the group is hoping to receive the same positive response.
One of the ISSCA’s missions is to share the latest in stem cells protocols and clinical applications with physicians across the globe, so they can implement stem cells therapies into their practices. By adding these protocols to their practices, physicians can help alleviate suffering and improve recuperation times for patients diagnosed with a host of degenerative diseases and injuries.
To accomplish its mission, the ISSCA will host the following events in 2019:
- Uccle, Belgium – November 15-16
- Mexico City – November 22-23
- Cochabamba, Bolivia – November 22-23
- Miami, FL – November 29-30
- Buenos Aires, Argentina – December 6-7
- Bogota, Colombia – December 13-14
“We invite all physicians interested in adding stem cells therapies to their practices to join us at one of our upcoming conferences,” said Benito Novas, Vice President of Public Relations for ISSCA. “Attendees will learn from highly trained physicians and researchers in the field of regenerative medicine and take away the necessary education and tools to implement the latest stem cells therapies into their own practices.”
The ISSCA is a global leader in stem cells research, applications, and education, partnering with major global institutions and locations worldwide to host its independent medical congresses. To learn more about the ISSCA and its all of its past and upcoming events, visit http://www.issca.us
- Published in Press Releases
ISSCA Conference at University of Miami Attracts Regenerative Medicine Experts and Physicians from across the Globe
The regenerative medicine symposium was held on October 24-27 with nearly 200 attendees and over 20 expert speakers
MIAMI LAKES, Florida—The International Society for Stem Cell Application (ISSCA), in collaboration with SISDET, held a highly successful three-day medical conference on the University of Miami campus on October 24-26. The conference featured a host of international experts in regenerative medicine and introduced new standards in regenerative medicine protocols to those in attendance. The Miami conference is part of the ISSCA’s growing commitment to increasing the awareness and practice of regenerative medicine across the globe in an effort to help alleviate suffering for those diagnosed with degenerative diseases.
Around 200 physicians, scientists, and researchers interested in regenerative medicine traveled to the University of Miami campus for the event. The conference focused on providing attendees with information on today’s most successful stem cells treatment protocols and the latest advances in regenerative medicine. Attendees heard from more than 20 expert speakers within the stem cells field, with lecturers from Europe, the US, and Latin America on the conference agenda.
“This three-day event included recognized keynote speakers, as well as aspiring young physicians discussing the latest advances in stem cell biology in an informal and collaborative setting,” said Benito Novas, Vice President of Public Relations for ISSCA. “Our goal with all of our events is to strengthen the cooperative and dynamic spirit in this research area. We would also like to thank the University of Miami for hosting this event, as it was a great honor partnering with such a prestigious university.”
ISSCA is a global leader in stem cells research, applications, and education, partnering with major global institutions and locations worldwide to host its independent medical congresses. To learn more about the ISSCA and its all of its past and upcoming events, visit http://www.issca.us
- Published in Press Releases
ISSCA Hosting Two Upcoming Stem Cells Courses in Miami
The courses will target physicians based in the Americas, providing them with critical stem cells education and tools needed to implement protocols in their own practices
The International Society for Stem Cell Application (ISSCA), a multi-disciplinary community of scientists and physicians collaborating to treat diseases and lessen human suffering through science, technology, and regenerative medicine, is hosting two upcoming courses in Miami. The courses will inform physicians on a range of topics about the latest stem cells protocols and how they can be incorporated into physicians’ own practices.
In continuing its commitment to help alleviate human suffering through expanding physician access to today’s cutting-edge stem cells technologies, the ISSCA is bringing its globally renowned courses to Miami, offering physicians two opportunities to participate. The course offered on November 1-2 is sold out, but seats still remain for the November 29-30 session for physicians looking to incorporate stem cells treatment protocols into their practices.
Doctors attending the Miami courses will learn about the latest trends and breakthroughs in in-office stem cells protocols. The ISSCA has also added a new topic into the Miami sessions: previously, the course covered autologous cell therapy, but in this newest course iteration, speakers will discuss how to add heterologous cell therapy into medical practices. In this training, physicians will learn about treatment protocols utilizing stem cells derived from neonatal tissue, such as cord blood, exosomes, and amniotic liquid. Attendees will learn both how these products are obtained as well as their most common clinical applications.
For those interested in learning more about the ISSCA’s upcoming courses in Miami or to register, visit https://www.stemcelltraining.net/hands-on-course/
“The ISSCA is pleased to bring our highly lauded courses on stem cells protocols to physicians in the Miami area and beyond,” said Benito Novas, ISSCA VP of Public Relations. “Our goal is to help physicians better treat their patients suffering from degenerative diseases by giving them the tools and education they need to implement these highly effective protocols in their own practices. Like all of our educational sessions, our Miami courses have been met with a great response, proving the growing interest in and efficacy of stem cells treatments.”
To learn more about all of the ISSCA’s latest news and innovations, visit http://www.stemcellsgroup.com/
- Published in Press Releases
