Posted in Reproductive Andrology, Embryology, Genomic Endocrinology, Preimplantation Genetic Diagnosis and Reproductive Genomics on December 26, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
causes, libido, main, what What Is Low Libido? Main Causes Of Low Libido In Men Its 100% a myth that men want sex 24/7… Men suffer from low libido, or if you want to call it Low sex drive just as much as women.
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See on Scoop.it – Cardiovascular Disease: PHARMACO-THERAPY
Posted in Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, mesenteric ischemia, MRI, Vascular Diseases on December 26, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
Watch VIdeo
https://www.youtube.com/v/Ms0PmQXxE-k?fs=1&hl=fr_FR
CONVENTIONAL,ultrasound.CT.MRI.PET,ISOTOPE,IMAGING
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Posted in FDA, FDA Regulatory Affairs, Regenerative Biology and Medicine on December 26, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
VIEW VIDEO
Posted in 3D Plotting Scaffolds, 3D Printing for Medical Application, Biopolymer Blend Open Porous, tagged 3D printing, Medical device, splint, tracheobronchomalcia on December 26, 2015| Leave a Comment »
Reporter: Irina Robu, PhD
Dr. Scott Hollister, a biomedical engineering professor at University of Michigan and Dr. Glenn Green, otolaryngologit at C.S. Mott Children’s Hospital invented a tracheal splint using 3D printing in 2012. The 3D printed trachea of a baby with tracheobronchomalacia (TBM),keeps the airway open until it can grow into a healty state and stay open on its own. The splint dissolves and is absorbed in the body and the process can take up to three years. Dr. Hollister and Dr. Green partnered with Materialise and Tissue Regeneration systems to commercialize the device, starting with clinical trial involving involving 30 patients at Mott Children’s Hospital sometime next year.
According to Dr. Green“This agreement is a critical step in our goal to make this treatment readily available for other children who suffer from this debilitating condition.We have continued to evolve and automate the design process for the splints, allowing us to achieve in two days what used to take us up to five days to accomplish. I feel incredibly privileged to be building products that surgeons can use to save lives.”
The bioresorbable splints will be manufactured by Plymouth, Michigan startup Tissue Regeneration Systems, which received its first commercial product clearance from the FDA in 2013 after several years of product development.
SOURCE
http://3dprint.com/109725/materialise-uom-trs-partners/
Posted in Bone Disease and Musculoskeletal Disease on December 24, 2015| Leave a Comment »
Scientists Create Injectable Foam To Repair Degenerating Bones
Reporter: Aviva Lev-Ari, PhD, RN
Researchers in France have developed a self-setting foam that can repair defects in bones and assist growth. Eventually, this advanced biomaterial could be used to quickly regenerate bone growth and treat degenerative diseases such as osteoporosis.
Sourced through Scoop.it from: gizmodo.com
Posted in Drug Delivery Platform Technology, Medical Imaging Technology, Image Processing/Computing, MRI, CT, Nuclear Medicine, Ultra Sound, Ultra Sound on December 24, 2015| Leave a Comment »
Reporter: Danut Dragoi, PhD
Using the property of sounds to proppagate in aqueous media, such that in human body, researcher from MIT and Massachusetts General Hospital (MGH) have found a way to enable ultra-rapid delivery of drugs to the gastrointestinal (GI) tract where this approach could make it easier to deliver drugs to patients suffering from GI disorders with inflammatory bowel disease, ulcerative colitis, and Crohn’s disease.
As we know from Physics the speed of sound in liquids, for example in water is 1,507 m/sec at 30 C degrees which is greater than that in air, 340m/sec, we can call them ultrasounds. Any sounds in human fluid or fluid composite carries on an accoustic energy that can excert a pressure or movement to any molecule of disolved drugg, that usually has a good solubility in water. If the molecules dissolved in GI truct that belongs to a specific drug are under a sonic field they can be moved accordingly, increasing the probability to get inside the targeted cells to be cured by that specific drug.
VIEW VIDEO
http://news.mit.edu/2015/ultrasound-drug-delivery-inflammatory-bowel-disease-1021
Currently, GI diseases are usually treated with drugs administered as an enema, which must be maintained in the colon for hours while the drug is absorbed. However, this can be difficult for patients who are suffering from diarrhea and incontinence. To overcome that, the researchers sought a way to stimulate more rapid drug absorption. The novelty of drugg delivery efficiently using ultrasounds is that of an enhanced delivery.
Ultrasound improves drug delivery by a mechanism known as transient cavitation. When a fluid is exposed to sound waves, the waves induce the formation of tiny bubbles that implode and create micro-jets that can penetrate and push medication into tissue. In the study shown here , the researchers first tested their new approach in the pig GI tract, where they found that applying ultrasound greatly increased absorption of both insulin, a large protein, and mesalamine, a smaller molecule often used to treat colitis. In order to demonstrate a better treatment the researchers next investigated whether ultrasound-enhanced drug delivery could effectively treat disease in animals.
In tests of mice, the researchers found that they could resolve colitis symptoms by delivering mesalamine followed by one second of ultrasound every day for two weeks. Giving this treatment every other day also helped, but delivering the drug without ultrasound had no effect.
They also showed that ultrasound-enhanced delivery of insulin effectively lowered blood sugar levels in pigs.
It is worth mentioning that a modeling of ultrasound -induced micro-bubble oscillations in a capillary blood vessel exists here
in which a study is focused on the transient blood–brain barrier disruption (BBBD) for drug delivery applications.
In other studies, the ultrasound mediated drug delivery for cancer treatment is shown as a review of therapeutic ultrasound used to thermally ablate solid tumors since the 90s. A variety of cancers are presently being treated clinically, taking advantage of ultrasound- or MR-imaging guidance. A review summary of in vivo ultrasound-based strategies shows the deliver drug payloads to tumor environments, to enhance permeability of vessel walls and cell membranes, and to activate drugs and genes in situ.
An important physical effect of ultrasounds is their action decrease with the square distance from the source. In order to avoid increasing power of ultrasounds with negative effects on human body, the study shown in here considers the mechanisms responsible for how ultrasound and biological materials interact and how ultrasound-induced bio-effect or risk studies focus on issues related to the effects of ultrasound on biological materials. Whenever ultrasonic energy is propagated into an attenuating material such as tissue, the amplitude of the wave decreases with distance. The wave attenuation is due to either
Absorption is a mechanism that represents that portion of ultrasonic wave that is converted into heat, and scattering can be thought of as that portion of the wave, which changes direction. Because the medium can absorb energy to produce heat, a temperature rise may occur as long as the rate of heat production is greater than the rate of heat removal. Current interest with thermally mediated ultrasound-induced bioeffects has focused on the thermal isoeffect concept. The non-thermal mechanism that has received the most attention is acoustically generated cavitation wherein ultrasonic energy by cavitation bubbles is concentrated. Acoustic cavitation, in a broad sense, refers to ultrasonically induced bubble activity occurring in a biological material that contains pre-existing gaseous inclusions. Cavitation-related mechanisms include radiation force, microstreaming, shock waves, free radicals, microjets and strain. It is more challenging to deduce the causes of mechanical effects in tissues that do not contain gas bodies.
SOURCE
[1] http://news.mit.edu/2015/ultrasound-drug-delivery-inflammatory-bowel-disease-1021
[2] https://www1.ethz.ch/ltnt/publications/Journal/pubimg/2012_Wiedemair1.pdf
Posted in BioPrinting in Regenerative Medicine, Cell Level, Stem Cells for Regenerative Medicine, Tissue Engineering on December 23, 2015| Leave a Comment »
Research on Scaffolds to support Stem Cells prior to ImplantationReporter: Aviva Lev-Ari, PhD, RN
Fibrous Scaffolds with Varied Fiber Chemistry and Growth Factor Delivery Promote Repair in a Porcine Cartilage Defect Model Iris L. Kim, Christian G. Pfeifer, Matthew B. Fisher, Vishal Saxena, Gregory R. Meloni, Mi Y. Kwon, Minwook Kim, David R. Steinberg, Robert L. Mauck, Jason A. Burdick Tissue Engineering Part A. November 2015: 2680-2690. Abstract | Full Text PDF or HTML | Supplementary Material | Reprints | Permissions |
| Hydrogel Microencapsulated Insulin-Secreting Cells Increase Keratinocyte Migration, Epidermal Thickness, Collagen Fiber Density, and Wound Closure in a Diabetic Mouse Model of Wound Healing
Ayesha Aijaz, Renea Faulknor, François Berthiaume, Ronke M. Olabisi Tissue Engineering Part A. November 2015: 2723-2732. Abstract | Full Text PDF or HTML | Reprints | Permissions |
| Bone Regeneration Using Hydroxyapatite Sponge Scaffolds with In Vivo Deposited Extracellular Matrix
Reiza Dolendo Ventura, Andrew Reyes Padalhin, Young-Ki Min, Byong-Taek Lee Tissue Engineering Part A. November 2015: 2649-2661. Abstract | Full Text PDF or HTML | Reprints | Permissions |
| In Vivo Evaluation of Adipose-Derived Stromal Cells Delivered with a Nanofiber Scaffold for Tendon-to-Bone Repair
Justin Lipner, Hua Shen, Leonardo Cavinatto, Wenying Liu, Necat Havlioglu, Younan Xia, Leesa M. Galatz,Stavros Thomopoulos Tissue Engineering Part A. November 2015: 2766-2774. Abstract | Full Text PDF or HTML | Supplementary Material | Reprints | Permissions |
| The Effects of Platelet-Rich Plasma on Cell Proliferation and Adipogenic Potential of Adipose-Derived Stem Cells
Han Tsung Liao, Isaac B. James, Kacey G. Marra, J. Peter Rubin Tissue Engineering Part A. November 2015: 2714-2722. Abstract | Full Text PDF or HTML | Reprints | Permissions |
| Ligament Tissue Engineering Using a Novel Porous Polycaprolactone Fumarate Scaffold and Adipose Tissue-Derived Mesenchymal Stem Cells Grown in Platelet Lysate
Eric R. Wagner, Dalibel Bravo, Mahrokh Dadsetan, Scott M. Riester, Steven Chase, Jennifer J. Westendorf,Allan B. Dietz, Andre J. van Wijnen, Michael J. Yaszemski, Sanjeev Kakar Tissue Engineering Part A. November 2015: 2703-2713. Abstract | Full Text PDF or HTML | Reprints | Permissions |
Posted in Diabetes Mellitus, Proteomics on December 20, 2015| Leave a Comment »
Reporter: Aviva Lev-Ari, PhD, RN
A recent publication in the journal Cell has shown that the SerpinB1 liver protein stimulates the growth of insulin producing pancreatic beta cells (also known as Islets of Langerhans). In mice and fish SerpinB1 stimulates the growth and even creation of Islets, boosting insulin production. In humans a lack of Serpin1B leads to insulin resistance, suggesting the same mechanism is active. These insights could lead to new and very effective therapies against Diabetes.
Using the Euretos Gene Expression Analysis application, all the main components of the mechanism described in the study, although never described before, were predicted to be likely associations including
This groundbreaking ability provides researchers with a unique capability to evaluate hypotheses before spending effort and resources on lab or clinical investigations.
In order to assess the scientific evidence of these predicted interactions, the researcher is provided with a very detailed analysis of the underlying biological mechanisms. In this case, hundreds of interactions were found such as gene-gene, RNA expression, protein-protein, chemical and pathway interactions. These indirect interactions would be very difficult and time consuming to find, one by one, using traditional search approaches and they provide excellent angles for further research into this promising mechanism.
SOURCE
http://euretos.com/news/9-news/132-news151218
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While the etiopathogenesis of type 1 and type 2 diabetes is different (Boitard, 2012, Muoio and Newgard, 2008), a paucity of functional β cell mass is a central feature in both diseases (Butler et al., 2003, Henquin and Rahier, 2011, Lysy et al., 2013). Currently there is considerable interest in developing safe approaches to replenish bioactive insulin in patients with diabetes by deriving insulin-producing cells from pluripotent cells (D’Amour et al., 2006, Kroon et al., 2008, Pagliuca et al., 2014, Rezania et al., 2014) or promoting proliferation of pre-existing β cells (Dor et al., 2004, El Ouaamari et al., 2013, Yi et al., 2013). While the former approach continues to evolve, several groups have focused on identifying growth factors, hormones, and/or signaling proteins to promote β cell proliferation (cited in El Ouaamari et al., 2013 and Dirice et al., 2014). Compared to rodents, adult human β cells are contumacious to proliferation and have been suggested to turnover very slowly, with the β cell mass reaching a peak by early adulthood (Butler et al., 2003, Gregg et al., 2012, Kassem et al., 2000). Attempts to enhance human β cell proliferation have also been hampered by poor knowledge of the signaling pathways that promote cell-cycle progression (Bernal-Mizrachi et al., 2014, Kulkarni et al., 2012, Stewart et al., 2015). While two recent studies have reported the identification of a small molecule, harmine (Wang et al., 2015), and denosumab, a drug approved for the treatment of osteoporosis (Kondegowda et al., 2015) to increase human β cell proliferation, the identification of endogenous circulating factors that have the ability to replenish insulin-secreting cells is attractive for therapeutic purposes. We previously reported (Flier et al., 2001) that compensatory β cell growth in response to insulin resistance is mediated, in part, by liver-derived circulating factors in the liver-specific insulin receptor knockout (LIRKO) mouse, a model that exhibits significant hyperplasia of islets without compromising β cell secretory responses to metabolic or hormonal stimuli (El Ouaamari et al., 2013). Here we report the identification of serpinB1 as a liver-derived secretory protein that promotes proliferation of human, mouse, and zebrafish β cells.
Identification of molecules that have the ability to enhance proliferation of terminally differentiated cells is a desirable goal in regenerative medicine, particularly in diabetes where β cell numbers are reduced. Here, we identified serpinB1 as an endogenous liver-derived secretory protein that stimulates human, mouse, and zebrafish β cell proliferation.
One interesting aspect of serpinB1 viewed as a secretory molecule is its lack of the classical hydrophobic signal peptide. Our data indicate that inflammation stimulates unconventional secretion of serpinB1 in a caspase-1-dependent manner. It is important to note, however, that the levels of several circulating cytokines in the LIRKO model are comparable to those observed in age-matched controls (El Ouaamari et al., 2013) and hence excludes systemic inflammation as a physiological factor triggering serpinB1 release in vivo. It is possible that the absence of insulin signaling in the liver interferes with caspase-1 activation and thus serpinB1 release. This notion is compatible with a previous report suggesting the suppressive role of insulin/IGF-1 in caspase-1 processing (Jung et al., 1996) and is consistent with increased levels of active caspase-1 in LIRKO-derived hepatocytes that are blind to insulin.
Since inhibition of proteases is SerpinB1’s reported biochemical function to date (Cooley et al., 2001), we postulated that the enhancing effect of SerpinB1 on β cell proliferation involves the intermediacy of a protease. Indeed, recombinant SerpinB1 proteins lacking the ability to inhibit protease activity were unable to enhance β cell proliferation in vitro. This observation suggests that SerpinB1 neutralizes a protease that would otherwise interfere with proliferation. In fact, the small-molecule inhibitors of elastases, GW311616A and sivelestat, directly enhanced proliferation of mouse and human insulin-producing cells. The parallel findings for GW311616A, sivelestat, and SerpinB1 make elastases strong candidates. While SerpinB1 action could be explained by its ability to modulate phosphorylation of key molecules (e.g., MAPK3, GSK3β/α, and PKA) of the insulin/IGF-1 growth/survival pathways, it is unclear how SerpinB1 precisely regulates these pathways. One possibility is that these pathways are activated through SerpinB1-mediated protease inhibition, particularly inhibition of elastase molecules known to be expressed in pancreatic β cells (Kutlu et al., 2009). This idea is consistent with previous reports suggesting the role for neutrophil elastase in modulating proteins in the insulin/IGF-1 signaling pathway (Bristow et al., 2008, Houghton et al., 2010, Talukdar et al., 2012). Elucidation of interactions with other proteases such as proteinase-3 and cathepsin G in the β cell and its potential role in regulating insulin sensitivity will further assist in deciphering the signaling pathways activated by SerpinB1. Alternative possibilities that require further investigation include interactions with protease-activated receptors (PARs), which are expressed in islets (J.S., A.E.O., and R.N.K., unpublished data).
Using zebrafish, we determined that serpinB1’s ability to potentiate β cell proliferation is conserved from fish to mammals. Moreover, in zebrafish we showed that serpinB1 can potentiate β cell proliferation in vivo analogous to the in vivo effects we observed in mouse and human islets. By ablating the β cells in zebrafish, we also observed that serpinB1 can stimulate β cell regeneration and warrants studies to examine its role during β cell development.
In sum, the identification of SerpinB1 as a conserved endogenous secretory protein that promotes proliferation of β cells across species constitutes an important step to achieve regeneration of functional β cells. While it is likely that additional factors will be identified, the next challenge will be to explore whether one or a combination of these factors can safely, specifically, and reversibly enhance human β cell mass with the long-term goal of restoring normoglycemia in patients with diabetes.
SOURCE
http://www.cell.com/cell-metabolism/fulltext/S1550-4131(15)00616-6
2012pharmaceutical
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