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Biomedical subjects

R Bick

Publications and source records attributed to R Bick.

15 recordsLinked to original sources
PubMed2001

Vascular thrombohemorrhagic disorders: hereditary and acquired.

This review has summarized the more important diseases that may be accompanied by or lead to a disorder of hemostasis or thrombosis via alterations of the vasculature. It is to be stressed that the vascular component of hemostasis is often overlooked by clinicians caring for patients with disorders of hemostasis and thrombosis. It should be appreciated that the vasculature is intricately related to the coagulation protein system and to platelets when involved in thrombohemorrhagic diatheses. Although many vascular disorders may lead to hemorrhage or thrombosis, it must be appreciated that often it is impossible to discern between a primary vascular defect/damage and a defect that has been induced by platelet activation/dysfunction or procoagulant abnormalities.

Amyloidosis↗
PubMed2000

L-asparaginase-provoked seizures as singular expression of central nervous toxicity.

Patients treated with L-asparaginase may present with hemorrhagic and thrombotic cerebrovascular events. This syndrome generally occurs after a few weeks of therapy and may occur after L-asparaginase therapy is completed. Complications appear to result from depletion of plasma proteins involved in coagulation and fibrinolysis. Seizures are uncommon symptoms, and are always caused by cerebrovascular events. We report a case of seizure associated with L-asparaginase therapy but no evidence of hemorrhagic or thrombotic cerebrovascular events.

Adult↗
PubMed1998

Useful laboratory tests for studying thrombogenesis in acute cardiac syndromes.

We review laboratory tests that evaluate thrombogenesis during acute coronary syndromes. These tests have been found to be valuable research tools in more clearly understanding the pathophysiology of acute coronary syndromes. In particular, we describe tissue factor, tissue factor pathway inhibitor, prothrombin fragment 1.2, thrombin-antithrombin complex, fibrinopeptide A, tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), t-PA-PAI complex, Bbeta 15-42-related peptides, fibrinogen degradation products, fibrin degradation products, D-dimer, platelet factor 4, beta-thromboglobulin, 5-hydroxytryptamine, thromboxane B2, prostacyclin, endothelin, angiotensin-converting enzyme, soluble thrombomodulin, C1-esterase inhibitor, anaphylotoxins C3a, C4a, and C5a, bradykinin, tumor necrosis factor, leukotriene C4, platelet activating factor, anti-phospholipid antibody, and von Willebrand factor. Some of these tests may prove to be useful in clinical diagnosis and management of acute coronary syndromes. Clinical outcome studies are needed to determine which tests may be cost effective and medically useful.

Acute Disease↗
PubMed1996

Response of the neonatal rat cardiomyocyte in culture to energy depletion: effects of cytokines, nitric oxide, and heat shock proteins.

Cytokines exert autocrine and paracrine effects on the heart, some of which may be mediated by inducible nitric oxide synthase (i-NOS) expression. We studied the effects of cytokine-mediated NO synthesis on cell injury in the presence of deoxyglucose (DOG) and cyanide (CV)(20 mM DOG and 2 mM CN) for up to 3 hours and during recovery (18 hours). The influence of heat shock protein-70 on the extent of myocyte damage was also assessed. IL-1 beta and gamma-IFN act synergistically to enhance NO synthesis by cardiac myocytes. When these cytokines are present, the rate of ATP depletion after DOG and CN is significantly greater than in their absence. When IL-1 beta and gamma-IFN are added with the NOS inhibitor, L-monomethyl-L-arginine (L-NMMA), or when a cytokine that does not produce NO (TNF-alpha) is present, the rate of ATP depletion is no different from the rate seen with DOG and CN alone. After recovery for 18 hours, myocytes that were exposed to IL-1 beta and gamma-IFN release more lactic dehydrogenase and have significantly lower levels of ATP. L-NMMA decreases lactic dehydrogenase release and maintains ATP at levels similar to metabolically inhibited cells in the absence of these cytokines. Consistent with the decreased recovery in ATP with cells incubated with DOG and CN plus IL-1 beta and gamma-IFN is a decrease in cytochrome oxidase activity. Decreases in cellular ATP correspond to increased levels of heat shock protein-70 measured in myocytes after 18 hours of recovery after metabolic inhibition in the presence of IL-1 beta and gamma-IFN. In contrast, prior induction of heat shock protein-70 reduces the rate of ATP depletion in myocytes treated with DOG and CN and maintains ATP at levels that are significantly higher than those seen in non-heat-shocked cells. Recovery of cells exposed to heat shock is also greater, as seen by decreased lactic dehydrogenase and citrate synthase release. The heat-shocked myocytes contain significantly more glycogen than the cells that were not heat shocked. The increased cellular glycogen is likely responsible for the greater lactate production and slower rates of ATP depletion in the heat-shocked, metabolically inhibited cells. Cell survival under conditions of metabolic inhibition is closely related to cellular ATP preservation.

Adenosine Triphosphate↗
PubMed1989

Free-standing cancer centers: rationale for improving cancer care delivery.

Free-standing cancer centers (FSCC) represent a growing trend in cancer care delivery within community practice. The critical components to FSCC are multidisciplinary cancer care, a complete menu of direct care and support services, a commitment to clinical trials and clinical investigation, and a comprehensive program for quality assurance. The advantages of FSCC to the community, to hospital programs, to the practicing surgical, medical, and radiation oncologists, and to the third-party carriers, including health maintenance organizations, are detailed. The development of an FSCC depends on the resolution of issues of (a) competition (between hospitals, hospitals and physicians, therapeutic disciplines, regional comprehensive cancer centers and FSCCs) and (b) concerns about conflict of interest. The ideal model of FSCC may well be represented by the joint venture of community hospital(s) and the community oncologists.

Ambulatory Care Facilities↗
PubMed1988

Unsuspected adrenal masses in the neonate: adrenal cortical carcinoma and neuroblastoma. A report of two cases.

Masses involving the adrenal in the neonate are most commonly due to hemorrhage. The literature involving the neonatal adrenal reflects this propensity. Although there have been reports of newborns with neuroblastoma [1, 2] and other tumors [3], which are more common in older children, ultrasonographic descriptions of masses involving the adrenal secondary to such tumors are rare [1]. Within a 6-month span we have discovered a clinically unsuspected adrenal carcinoma and adrenal neuroblastoma.

Adrenal Cortex Neoplasms↗
PubMed1986

Roussel award for cardiology. The mechanism of nucleotide induced calcium translocation across sarcoplasmic reticulum membranes: evidence for a non-translocated intermediate pool of calcium.

Our previous data suggested that, in cardiac muscle sarcoplasmic reticulum fragments, GTP hydrolysis occurs by an alternative enzyme cycle of the Ca2+ ATPase which is insensitive to (Ca2+) and does not involve an acyl phosphate intermediate. Despite this, GTP induces the incorporation of calcium into a membrane pool that is not translocated to the vesicular lumen. The present study suggests that this GTP-induced intermediate calcium pool is identical to a modulable component of the calcium translocation process in that: it has an identical pH sensitivity; the initial incorporation of calcium in response to GTP eliminates the initial rapid burst and lag component of the typical ATP-induced calcium uptake curve when ATP is added during GTP-induced calcium accumulation. Instead, the addition of ATP during GTP-induced calcium accumulation results in the prompt onset of the linear phase of calcium translocation; GTP-induced calcium accumulation directly affects the pH sensitivity of subsequent ATP-induced calcium accumulation. We suggest that the intermediate calcium pool is in series with calcium translocation and is the site of the pH sensitivity observed in calcium flux.

4-Nitrophenylphosphatase↗
PubMed1980

Phosphorylation of a 100 000 dalton component and its relationship to calcium transport in sarcoplasmic reticulum from rabbit skeletal muscle.

Sarcomplasmic reticulum from rabbit fast skeletal muscle contains intrinsic protein kinase activity (ATP:protein phosphotransferase, EC 2.7.1.37) and a substrate. The protein kinase activity was Mg2+ dependent and could also phosphorylate exogenous protein substrates. Autophosphorylation of sarcoplasmic reticulum vesicles was not stimulated by cyclic AMP, neither was it inhibited by the heat-stable protein kinase inhibitor protein. The phosphorylated membranes had the characteristics of a protein with a phosphoester bond. An average of 73 pmol Pi/mg protein were incorporated in 10 min at 30 degrees C. Addition of exogenous cyclic AMP-dependent protein kinase increased the endogenous level of phosphorylation by 25-100%. Sarcoplasmic reticulum membrane phosphorylation, mediated by either endogenous cyclic AMP-independent or exogenous cyclic AMP-dependent protein kinase, occurred on a 100 000 dalton protein and both enzyme activities resulted in enhanced calcium uptake and Ca2+-dependent ATPase (ATP phosphohydrolase, EC 3.6.1.3), in a manner similar to cardiac microsomal preparations. Regulation of Ca2+ transport in skeletal sarcoplasmic reticulum may be mediated by phosphorylation of a 100 000 dalton component of these membranes.

Animals↗
PubMed1978

[Bending and torsion stability of healed metatarsus osteotomy after plate osteosynthesis].

UNLABELLED: 72 transversal osteotomies on metatarsus of sheep were stabilized under contact or gap conditions with three different thicknesses of bone plates. After 16 weeks we measured bending or torsion break loading, moment of inertia of bone by transmission methode and calculated moments of bending and torsion strength. RESULTS: ultimate bending strength on osteotomied bone 100.4 +/- 14.4 N/mm2 under contact, and 77.4 +/- 11.4 N/mm2 under gap condition, torsion bending strength 26.1 +/- 4.9 N/mm2 under contact, and under gap condition 21.5 +/- 4.3 N/mm2. The best results were given by the 2.8 mm plate with the same moment of inertia like the small ASIF plate.

Animals↗
PubMedDate not supplied

Issues of thrombosis and hemorrhagic events in patients with cancer.

It is clear that patients with malignancy, particularly adenocarcinomas, have an increased propensity to thrombosis. It also appears that patients with malignancy and thrombosis are relatively refractory to warfarin therapy and some may not respond ideally to heparin preparations. Occult malignancy in patients with unexplained thrombosis is of concern; however, the incidence varies with the age of the patient approaching 10% in those over 50 years of age. The extent of the evaluation for an underlying occult malignancy should be dictated by clinical judgment. Recurrent unexplained DVT, resistance to warfarin, and thrombosis of unusual sites are the major clues to significantly enhance the suspicion of an occult malignancy. In general, patients with thrombosis and malignancy need not be evaluated for hereditary or acquired hemostasis defects; finding one of these defects is both unlikely and will probably not alter antithrombotic therapy. Hemorrhage in cancer patients is usually due to thrombocytopenia related to chemotherapy (particularly solid tumors) or bone marrow failure (usually leukemias), or disseminated intravascular coagulation (DIC). DIC is usually seen in M-3 and M-4 leukemia or in septic patients with solid tumors. Finally, catheter thrombosis is a common problem in patients with cancer and can be significantly decreased with the routine use of low-dose warfarin therapy.

Catheterization↗