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您的检索式：作者名="Rafi Mazor"
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| 1 | In vivo analysis of intestinal permeability following hemorrhagic shock显示文摘AIM: To determine the time course of intestinal permeability changes to proteolytically-derived bowel peptides in experimental hemorrhagic shock. METHODS: We injected fluorescently-conjugated casein protein into the small bowel of anesthetized Wistar rats prior to induction of experimental hemorrhagic shock. These molecules, which fluoresce when proteolytically cleaved, were used as markers for the ability of proteolytically cleaved intestinal products to access the central circulation. Blood was serially sampled to quantify the relative change in concentration of proteolytically-cleaved particles in the systemic circulation. To provide spatial resolution of their location, particles in the mesenteric microvasculature were imaged using in vivo intravital fluorescent microscopy. The experiments were then repeated using an alternate measurement technique, fluorescein isothiocyanate(FITC)-labeled dextrans 20, to semi-quantitatively verify the ability of bowel-derived low-molecular weight molecules(< 20 k D) to access the central circulation.RESULTS: Results demonstrate a significant increase in systemic permeability to gut-derived peptides within 20 min after induction of hemorrhage(1.11 ± 0.19 vs 0.86 ± 0.07, P < 0.05) compared to control animals. Reperfusion resulted in a second, sustained increase in systemic permeability to gut-derived peptides in hemorrhaged animals compared to controls(1.2 ± 0.18 vs 0.97 ± 0.1, P < 0.05). Intravital microscopy of the mesentery also showed marked accumulation of fluorescent particles in the microcirculation of hemorrhaged animals compared to controls. These results were replicated using FITC dextrans 20 [10.85 ± 6.52 vs 3.38 ± 1.11 fluorescent intensity units(× 105, P < 0.05, hemorrhagic shock vs controls)], confirming that small bowel ischemia in response to experimental hemorrhagic shock results in marked and early increases in gut membrane permeability. CONCLUSION: Increased small bowel permeability in hemorrhagic shock may allow for systemic absorption of otherwise retained proteolytically-generated peptides, with consequent hemodynamic instability and remote organ failure. | Tom Alsaigh Marisol Chang Michael Richter Rafi Mazor Erik B Kistler | 2015 | World Journal of Critical Care Medicine2015，4，4： | 1 |
| 2 | Primed polymorphonuclear leukocytes constitute a possible link between inflammation and oxidative stress in hyperlipidemic patients显示文摘 | Rafi Mazor Revital Shurtz-Swirski Raymond Farah Batya Kristal Galina Shapiro Faina Dorlechter Meital Cohen-Mazor Edna Meilin Snitkovski Tamara Shifra Sela | 2007 | Atherosclerosis2007，，2： | 1 |
| 3 | New Applications for Cryotherapy显示文摘Cryotherapy,or more commonly known as cold therapy,is the use of low temperatures in medical treatment.The most prominent use of cryotherapy is for cryosurgery where application of very low temperatures is used to ablate diseased tissue(e.g.,most commonly in dermatology).Recent research,however,shows that low temperature may modulate collagen fibers beyond the already known effects of extreme cooling on joint pain relieve and inflammation.The goal of this brief review is to outline the known effects of extreme cooling on molecular,fiber and cell physiology and to leverage these properties in various potential medical applications.Specially,we will discuss potential cryotherapies for treatment of osteoarthritis and destruction of fat cells(i.e.,cryolipolysis)for treatment of diabetes.Osteoarthritis(OA)is a degenerative disease,where joint pain and stiffness worsen over time.One of the most effective ways to relief joint pain is cooling the joint.Indeed,when evaluating different strategies to externally cool affected joints,it was found that reducing the internal joint temperature by~10o C has beneficial effects in terms of pain reduction and regression in local inflammation.Moreover,collagen,whose deterioration is a major part of OA pathophysiology,regains elasticity after several freeze-thaw cycle.Finally,cartilage cells response to cold by increasing collagen formation and reducing matrix enzyme production,and adipose tissue within the joint that promote OA by supporting inflammation is susceptible to cold temperatures.Obesity is also a devastating disease that contributes to OA.Reduction of the temperature within the joint results in reduced inflammation,renewed collagen synthesis and reduced pain.Similarly,induction of extreme low temperatures in adipose tissue results in adipocytes loss without damage to surrounding tissues.Hence,cryotherapy has applications to modulation of collagen and fat cells for various therapies. | Rafi Mazor Meital Mazor Ali EDabiri Bhavesh Patel Ghassan S.Kassab | 2020 | Molecular & Cellular Biomechanics2020，17，2： | 0 |
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