Publications by authors named "Wilner G"

Article Synopsis
  • The study examined the effects of off-season training on natural bodybuilders' (BB) recovery compared to recreationally active (RA) individuals, focusing on how their autonomic nervous system (ANS) responds post-exercise.
  • Despite comparing heart rate variability (HRV) metrics between the two groups, no significant differences were found at rest or during recovery, indicating similar baseline states.
  • However, the BB group exhibited significantly lower HRV recovery at 15 minutes post-exercise and did not return to baseline levels within 45 minutes, suggesting poorer recovery compared to the RA group.
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Heart rate variability (HRV) is a non-invasive indicator of the activity of the autonomic nervous system, which regulates many physiological functions including metabolism. The purpose of this study was to quantify the relationship between resting markers of HRV and oral glucose tolerance test (OGTT) response. Eighteen healthy individuals (10 males, 8 females, (23.

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Background: Adverse local tissue reaction (ALTR), characterized by a heterogeneous cellular inflammatory infiltrate and the presence of corrosion products in the periprosthetic soft tissues, has been recognized as a mechanism of failure in total hip replacement (THA). Different histological subtypes may have unique needs for longitudinal clinical follow-up and complication rates after revision arthroplasty. The purpose of this study was to describe the histological patterns observed in the periprosthetic tissue of failed THA in three different implant classes due to ALTR and their association with clinical features of implant failure.

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Adverse local tissue reactions (ALTR) associated with tribocorrosion following total hip arthroplasty (THA) have become a significant clinical concern in recent years. In particular, implants featuring metal-on-metal bearing surfaces and modular femoral stems have been reported to result in elevated rates of ALTR. These tribocorrosion-related tissue reactions are characterized by marked necrosis and lymphocytic infiltration, which contrasts sharply with the macrophagic and foreign body giant cell inflammation associated with polyethylene wear particle induced peri-implant osteolysis.

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Background: Adverse local tissue reaction (ALTR) is characterized by periprosthetic soft tissue inflammation composed of a mixed inflammatory cell infiltrate, extensive soft tissue necrosis, and vascular changes. Multiple hip implant classes have been reported to result in ALTR, and clinical differences may represent variation in the soft tissue response at the cellular and tissue levels. The purpose of this study was to describe similarities and differences in periprosthetic tissue structure, organization, and cellular composition by conventional histology and immunohistochemistry in ALTR resulting from two common total hip arthroplasty (THA) implant classes.

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Objective: To determine the level of carboxyhemoglobin found in banked blood in the Albany, NY region.

Design: A retrospective descriptive analysis of carboxyhemoglobin (COHb) levels in a series of packed red blood cell (PRBC) units.

Setting: The blood bank of a university tertiary care hospital in Albany, NY.

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Background: Chyothorax is an uncommon medical condition. To the best of our knowledge, there have been no detailed English-language report dealing with its cytopathologic findings and diagnostic pitfalls

Cases: A 12-year-old boy, hemodialysis dependent, with congenital nephrotic syndrome due to focal segmental glomerular sclerosis and a failed renal transplant, developed shortness of breath. Physical and radiologic examinations revealed a left pleural effusion.

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The hypereosinophilic syndrome (HES) is a rare yet frequently fatal disorder of unknown etiology characterized by markedly elevated eosinophil counts and subsequent multiple organ failure due presumably to eosinophil-derived protein toxicity. We describe the laboratory and anatomic findings in a 15-year-old female with extraordinarily high circulating levels of eosinophil major basic protein (MBP) who sustained a precipitous cardiac death secondary to a massive myocardial infarction. Postmortem examination showed marked cardiomegaly with extensive recent left ventricular infarction.

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The binding and mitogenic properties of thrombin have been established in various transformed cell lines. In such systems, thrombin induces cell division in the absence of exogenous growth factors, and the enzyme is considered to act directly as a mitogen. This study explores thrombin's interaction with nontransformed, growth factor-dependent cells.

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Esterolytically inactive diisopropyl fluorophosphate-conjugated thrombin (DIP-alpha-thrombin) stimulated 3H-thymidine incorporation and proliferation of growth-arrested vascular smooth muscle cells (SMCs), similar to native alpha-thrombin. Half-maximal mitogenic response of SMCs was obtained at 1 nM thrombin and was specifically blocked by the leech-derived, high-affinity thrombin inhibitor, hirudin. Native thrombin and a variety of thrombin species that were chemically modified to alter thrombin procoagulant or esterolytic functions were found to induce 3H-thymidine incorporation to a similar extent.

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Previous studies have indicated that Factor IX/IXa interacts in a specific and high affinity manner with a binding site on the endothelial cell surface. In this study, the contributions of the gamma-carboxyglutamic acid-containing (GLA) and growth factor domains to the finding of Factor IX to the endothelium were assessed. While GLA-containing peptides from Factors IX, X, and prothrombin were inhibitors of 125I-Factor IX-endothelial cell binding, the GLA peptide from Factor IX was about 250-800-fold more effective than those from prothrombin and Factor X, respectively.

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PTH stimulates osteoblast-like cells to produce a product(s) capable of increasing cellular bone resorption. We have investigated this phenomenon using primary cultures of osteoblasts and the clonal osteoblast-like cell line ROS 17/2. Conditioned medium from PTH-stimulated populations of either culture increases bone resorption compared to conditioned medium measured in three independent assay systems; the isolated osteoclast assay system, elicited macrophages, and the fetal bone rudiment system.

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Activation of prothrombin to alpha-thrombin generates not only the catalytic site and associated regions but also an independent site (an exosite) which binds anionic substances, such as Amberlite CG-50 resin [cross-linked poly(methylacrylic acid)]. Like human alpha-thrombin with high fibrinogen clotting activity (peak elution at I = 0.40 +/- 0.

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Right ventricular hypertrophy produced in rats exposed to 10% oxygen for 3 weeks resulted in a ninefold increase in atriopeptin immunoreactivity (APir) and a 160-fold increase in atriopeptin messenger RNA (AP mRNA) in the right ventricular myocardium. A small but significant increase in left ventricular APir and AP mRNA was also present, probably representing the interventricular septum. Right atrial APir was decreased by 50%, but left atrial APir was not different from normoxic controls.

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The formation and degradation of fibrin play a central role in hemostasis, but other activities have been associated with fibrin(ogen)-derived peptides, which suggests that products of fibrin(ogen) turnover may be involved in inflammation and wound healing. The present study was undertaken to determine whether the plasmic fibrinogen-derived peptide B beta 1-42 has effects on inflammatory cells and fibroblasts (FB). B beta 1-42 was found to be a potent chemotaxin for neutrophils (PMN) and FB, maximally stimulating PMN migration at 10(-9) mol/L peptide.

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We have previously established that the mitogenic effect of fibrinogen on hemopoietic cell lines Raji and JM is mediated via a specific receptor (Levesque, J.-P. et al.

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Thrombin, a major procoagulant enzyme and growth factor, is also selectively chemotactic for monocytes and macrophages but not for neutrophils. This effect stands in contrast to other well-known chemotactic agents such as fMet-Leu-Phe, C5a fragments, and LTB4, which stimulate directed cell movement in both cell types, and have important physiological implications. The human leukemic cell line HL-60, which is capable of differentiating either along granulocytic or monocytic lineages, was therefore used to explore the development of this selective monocyte/macrophage chemotactic response to thrombin.

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In the Beta Blocker Heart Attack Trial, a double blind, randomized, controlled study, patients taking propranolol (180 or 240 mg/day) initiated 5-21 days post myocardial infarction had 26% fewer deaths than those taking placebo over a 25 month (mean) followup. Detailed analysis of the circumstances surrounding the BHAT deaths failed to reveal any striking difference between propranolol and placebo in the type of clinical event preceding death, the incidence and type of acute and prodromal signs and symptoms, the location of death, the activity preceding death or the percentage of deaths that were sudden or instantaneous, suggesting that propranolol may exert an "across the board" effect and improve survival by a combination of mechanisms. An unexpected finding was that the protective effect of propranolol appeared to occur during the hours of 10 p.

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Our studies to date have clearly demonstrated the existence of a unique cell interactive exosite region in thrombin, which mediates specific biologic effects on cells of monocytic-macrophage lineage. These findings are of potential physiologic significance, since even proteolytically degraded forms of thrombin (beta- and gamma-thrombin) or fragments of thrombin arising due to breakdown of thrombin-thrombomodulin complexes are potentially biologically active and are not subject to inhibition by inhibitors such as antithrombin III. Such degraded thrombin forms and proteolytic fragments are likely to be present at sites of inflammation and wound repair where they may be important modulators of macrophage-monocyte responsiveness.

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Fibrin formation and turnover are intimately associated with inflammation and wound healing. To explore whether fibrin(ogen)-derived peptides exert direct effects upon cells involved in inflammation and tissue repair we examined the capacity of human fibrinopeptide B (hFpB), a thrombin-derived proteolytic cleavage product of the fibrinogen B beta-chain, to stimulate neutrophils (PMN), monocytes, and fibroblasts. hFpB caused directed cell migration of PMN and fibroblasts that was optimal at approximately 10(-8) M.

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In contrast to fibroblasts, the exposure of G0/G1-arrested J774 cells, a murine macrophage-like tumor cell line, with either active or esterolytically inactive diisopropyl phosphorofluoridate-conjugated alpha-thrombin (the enzymatically active form of thrombin, EC 3.4.21.

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Simplified procedures were developed to produce and isolate the plasmin-derived B beta 1-42 fragment from human fibrinogen. Peptides generated from fibrinogen by plasmin were separated by reverse phase HPLC chromatography. Two distinct peaks were identified as having amino acid compositions identical to B beta 1-42.

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