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Biomedical subjects

I Rabinowitz

Publications and source records attributed to I Rabinowitz.

At least 19 recordsLinked to original sources
PubMed2005

An unusual reoccurrence of Waldenstrom's macroglobulinemia as pleural effusions that had a discordant response with treatment.

A 77-year-old female with a past medical history of Waldenstrom's macroglobulinemia presented with progressive shortness of breath and a newly diagnosed left pleural effusion. Numerous diagnostic studies were performed on the patient and finally a pleural biopsy confirmed pulmonary involvement of Waldenstrom's macroglobulinemia. As past studies have shown, Waldenstrom's involvement as a pulmonary process is uncommon. Unexpectedly, treatment with rituximab and fludarabine did decrease the patient's serum immunoglobulin M levels, but her pleural effusions never improved.

Aged↗
PubMed2005

A randomized trial assessing the utility of a test-dose program with taxanes.

OBJECTIVE: Taxanes are commonly used anticancer agents with a potential of producing an allergic or hypersensitivity reaction (HSR). We performed a randomized study to evaluate the value of a test dose given prior to the full dose of either paclitaxel or docetaxel. RESEARCH DESIGN AND METHODS: Patients were randomly assigned to either the administration of the full dose or to the prior administration of a 1 mg intravenous test dose of either paclitaxel or docetaxel. The primary endpoints were severity of the HSR and the cost of drug wastage due to a HSR. RESULTS: Two hundred and eighteen patients were randomized from three different treatment sites. The overall incidence of HSR was 6.5% and there was no significant difference in the incidence of HSR in either group. The mean HSR severity grade was 2.8 for patients without a test dose and 2.3 for those receiving a test dose. There was, however, a reduction in the wastage of taxane in the test dose arm. Wastage avoided in the test dose arm was $1573 per patient who had a HSR and $104 per patient treated with a taxane. CONCLUSION: Although a test dose may not reduce the severity of a HSR with the administration of a taxane, it does reduce the cost associated with drug wastage.

Adult↗
PubMed2000

Physician compliance with warfarin prophylaxis for central venous catheters in patients with solid tumors.

PURPOSE: There is an established benefit of prophylactic warfarin in cancer patients with central venous catheters. This study assessed the compliance rate of prophylactic low-dose warfarin prescription in cancer patients with central venous catheters at a single institution. PATIENTS AND METHODS: Oncology patients with central venous catheters were identified by a retrospective chart review. Information retrieved included whether prophylactic warfarin had been prescribed and whether the patient had suffered a thrombotic or bleeding event. After the initial chart review, physicians were notified of the benefits of warfarin prophylaxis, and subsequently, a physician-independent mechanism of prescribing prophylactic warfarin was instituted. After each of these interventions, we retrospectively reviewed a further two cohorts of patients to assess compliance with warfarin prophylaxis. RESULTS: During the baseline study, only 10% of patients were prescribed prophylactic warfarin. After physician notification, the compliance rate increased to only 20% (P =.3). After instituting the physician-independent mechanism of prescribing prophylactic warfarin, the compliance rate increased to 95% (P <.001). The rate of catheter-related thrombosis was 11% for patients who were prescribed warfarin compared with 21% in those who were not anticoagulated (P =.2). CONCLUSION: At our institution, the rate of prescribing prophylactic warfarin was low in this patient population, and there was a reluctance of treating physicians to change their prescribing practice. Mechanisms exist to improve the rate of anticoagulant prophylaxis in this clinical setting. We recommend that institutions review their rate of compliance with prophylactic anticoagulation for patients with central venous catheters and solid tumors.

Anticoagulants↗
PubMed1999

Factitious methemoglobinemia.

We report the case of a 26 year-old female who was treated on numerous occasions for methemoglobinemia believed secondary to surreptitious abuse of dapsone as part of a factitious disorder.

Adult↗
PubMed1998

Bleeding in a patient with lupus anticoagulant without associated hemostatic abnormalities.

Bleeding is very rare in patients with lupus anticoagulants in the absence of associated hemostatic abnormalities. Few cases have been reported with attention given to work-up for other coagulation defects. We report a case of spontaneous hematoma in a patient with lupus anticoagulant, immunoglobulin (Ig)M anticardiolipin antibodies, and no other associated abnormalities.

Aged↗
PubMed1998

The "door-to-needle blitz" in acute myocardial infarction: the impact of a CQI project.

BACKGROUND: A continuous quality improvement (CQI) project was conducted at Soroka Medical Center in Beer-Sheva, Israel, in an effort to identify and address causes of delays in thrombolytic therapy in patients arriving at a high-volume (160,000 patients per year) emergency department with acute myocardial infarction and thereby reduce the "door-to-needle time" (DTNT). The study had four phases: preintervention survey, peri-intervention process redesign, postintervention evaluation, and follow-up evaluation. CQI TEAM: The CQI team followed a seven-step protocol: problem definition, present-state screening, factors analysis, solution development, outcome evaluation, standardization, and conclusions. RESULTS: A DTNT of 45 minutes was considered acceptable for this data set, and accordingly, patients were divided into an "early" group (n = 50, DTNT < 45 minutes), and a "late" group (n = 50, DTNT > or = 45 minutes). After the CQI intervention, the mean DTNT decreased from 61.8 +/- 32.5 (mean +/- standard deviation) to 47.6 +/- 18.5 minutes (p < 0.029). The prolonged DTNT time intervals of the late versus the early groups was primarily due to extended decision-making time (36.0 +/- 22.7 versus 13.6 +/- 6.7 minutes, p < 0.003), followed by time until therapy was initiated (26.2 +/- 14.2 versus 11.1 +/- 5.8 minutes, p < 0.002). CONCLUSIONS: Results suggest that the 30-minute DTNT suggested by the American College of Cardiology/American Heart Association is appropriate for patients with a clear diagnosis and no contraindications for thrombolysis, but when the risk-benefit ratio of thrombolytic therapy raises concerns, a 45- to 60-minute DTNT may still be acceptable. Further CQI projects should address technical triage of simple cases and clinical estimation of risk-benefit ratio in complicated patients.

Emergency Service, Hospital↗
PubMed1994

Adhesion receptor activation of phosphatidylinositol 3-kinase. von Willebrand factor stimulates the cytoskeletal association and activation of phosphatidylinositol 3-kinase and pp60c-src in human platelets.

The cytoskeleton participates in the coordinated regulation of intracellular signaling molecules, following agonist stimulation of cells. We have demonstrated that von Willebrand factor (vWF) induced the cytoskeletal association and activation of phosphatidylinositol 3-kinase (PtdIns 3-kinase) in human platelets. The activation of PtdIns 3-kinase coincided with the tyrosine phosphorylation of multiple platelet proteins, as assessed by anti-phosphotyrosine immunoblotting. One of these tyrosine-phosphorylated proteins, pp60c-src, became specifically enriched in the cytoskeletal fraction of vWF-stimulated platelets. The vWF-stimulated cytoskeletal association of PtdIns 3-kinase and pp60c-src required platelet stirring and aggregation, was specifically blocked by an anti-GPIb monoclonal antibody, and was not observed in platelets lacking the glycoprotein Ib/IX complex (Bernard-Soulier syndrome). Pretreatment of normal platelets with 5 mM EDTA (37 degrees C for 90 min) or RGDS (2 mM), which disrupts the binding of various adhesive proteins to platelet integrins and inhibits fibrinogen-mediated platelet aggregation, did not alter the vWF-stimulated activation and cytoskeletal association of PtdIns 3-kinase and pp60c-src. Pretreatment of platelets with acetylsalicylic acid (1 mM) completely abolished vWF-stimulated production of thromboxane A2, dense granule release, and the activation of protein kinase C, without altering the activation and cytoskeletal translocation of PtdIns 3-kinase and pp60c-src. Our results suggest that vWF binding to the platelet adhesion receptor glycoprotein Ib/IX can mediate activation and translocation of both tyrosine and lipid kinase(s) independent of other agonists.

Aspirin↗
PubMed1994

Interviewing prepubertal children about suicidal ideation and behavior.

OBJECTIVE: Much of the literature on assessment of suicidal children has focused on identifying risk factors associated with suicidal ideation and behavior in this population. Unique problems encountered in interviewing prepubertal children about suicidal ideation and behavior are examined in this paper. METHOD: Observations of problems encountered in interviewing prepubertal children about suicidal ideation and behavior were gleaned in the context of interviews of children admitted to a child psychiatry inpatient unit and interviews of the parents of these children. RESULTS: Unique problems include difficulties in assessment of suicidal intent, impact of cognitive development, particularly of the concept of death, interaction between current emotional state and memory of previous suicidal episodes, characteristics of play associated with suicidal states, effects of parents' attitudes toward assessment on information gathering, and the impact of certain risk factors on cognition and behavior during the interview. CONCLUSION: Interviewing children about suicidal ideation and behavior necessitates that the clinician attend to multiple elements of the interview simultaneously. These interviews are further complicated by the stressful thoughts and feelings that can be raised in both clinician and child in reaction to exploring the child's suicidal ideation and behavior. Additional research is needed to refine the process of reliable interviewing of children about suicidal ideation and behavior and to develop instruments both to quantitate the different elements of these interviews and to guide the clinicians conducting them.

Adolescent↗
PubMed1993

Type IIB mutation His-505-->Asp implicates a new segment in the control of von Willebrand factor binding to platelet glycoprotein Ib.

Type IIB von Willebrand disease is characterized by increased affinity of mutant von Willebrand factor (vWF) for platelet glycoprotein Ib. Eight different missense mutations that cause this phenotype have been reported within the disulfide loop defined by Cys-509 and Cys-695 of the mature vWF subunit; this disulfide loop is required for normal binding of vWF to platelet glycoprotein Ib. A new mutation was identified in a patient with type IIB von Willebrand disease (vWD) characterized by a lifelong bleeding disorder, mild thrombocytopenia, normal levels of factor VIII, vWF antigen, and ristocetin cofactor activity but increased ristocetin-induced platelet agglutination at low concentrations of ristocetin. Exon 28 of the patient's vWF gene was amplified, cloned, and sequenced. At nucleotide 3802 (numbering the cDNA from translation initiation), a C to G transversion was identified, which changes the encoded amino acid sequence from His-505 to Asp. The corresponding mutant recombinant vWF was expressed in transiently transfected COS cells. Relative to wild type vWF, the mutant vWF exhibited markedly increased binding to platelets at low concentrations of ristocetin, confirming the association between the His-505-->Asp substitution and the type IIB vWD phenotype. The His-505-->Asp mutation lies outside the disulfide loop affected by other type IIB vWD mutations and implicates a new segment of vWF in the regulation of platelet glycoprotein Ib binding.

Alleles↗
PubMed1993

New variant of von Willebrand disease type II with markedly increased levels of von Willebrand factor antigen and dominant mode of inheritance: von Willebrand disease type IIC Miami.

A variant of von Willebrand disease (vWD) was identified in six members of a kindred spanning four generations. The proband was a 46-year-old woman with a lifelong history of bleeding, a prolonged bleeding time (> 15 minutes), markedly elevated von Willebrand factor (vWF) antigen (vWF:Ag = 2.09 U/mL), slightly reduced ristocetin cofactor activity, and a plasma vWF multimer pattern similar to that of vWD type IIC. Similar findings were observed in her three children, mother, and brother. In affected family members, platelet and plasma vWF multimer patterns were discrepant with higher molecular weight multimers observed in platelet vWF. Following a 1-Des-amino-8-D-arginine vasopressin (DDAVP) challenge, the proband failed to normalize her bleeding time even though vWF: Ag rose by 70% and higher molecular weight multimers were increased slightly. Genetic studies were consistent with autosomal dominant inheritance of a mutation within the vWF gene. By sequencing of cloned genomic DNA, mutations were excluded in exons 4, 5, 14, and 15, which encode regions of the vWF propeptide proposed to be important in multimer biosynthesis. Mutations also were excluded in exons 28 to 31, which encompass the known mutations that cause vWD types IIA, IIB, and B. This new variant of vWD, characterized by autosomal dominant inheritance, a qualitative defect that resembles vWD type IIC, and increased plasma vWF:Ag, was tentatively designated vWD type IIC Miami.

Base Sequence↗
PubMed1993

The effectiveness of a remote access hotline service for the handling of night shift calls.

In order to justify dedicated staff for night calls, improve the quality of our handling of these calls, and qualify for certification by the AAPCC, we sought an alternative to hiring dedicated night staff. We offered our certified staff members the opportunity to fulfill part of their regular duties answering night calls from home. We set them up with a computer system, dedicated telephone line, texts and consultant information. They were able to access the Poison Center hotline computer via a remote access program. A significant increase took place in the number of documented calls to the Poison Center during the midnight to 8:00 am shift. Quality of documentation also improved significantly and level of service has been complemented by callers. The remote access method is a viable way for a small Poison Center to cover the night shift with certified, reliable, capable staff. This method of call answering has solved our major problem of hiring night staff who would satisfy requirements and provide excellent service.

Hotlines↗
PubMed1992

von Willebrand disease type B: a missense mutation selectively abolishes ristocetin-induced von Willebrand factor binding to platelet glycoprotein Ib.

von Willebrand factor (vWF) is a multimeric glycoprotein that mediates the adhesion of platelets to the subendothelium by binding to platelet glycoprotein Ib. For human vWF, this interaction can be induced in vitro by the antibiotic ristocetin or the snake venom protein botrocetin. A missense mutation, Gly-561-->Ser, was identified within the proposed glycoprotein Ib binding domain of vWF in the proband with von Willebrand disease type B, a unique variant characterized by no ristocetin-induced, but normal botrocetin-induced, binding to glycoprotein Ib. The corresponding mutant recombinant protein, rvWF(G561S), formed normal multimers and exhibited the same functional defect as the patient's plasma vWF, confirming that this mutation causes von Willebrand disease type B. These data show that botrocetin and ristocetin cofactor activities of vWF can be dissociated by a point mutation and confirm that these mediators promote vWF binding to platelets by different mechanisms. The normal botrocetin-induced binding and the defective ristocetin-induced binding of rvWF(G561S) suggest that the primary defect in von Willebrand disease type B may be a failure of normal allosteric regulation of the glycoprotein Ib binding function of vWF.

Amino Acid Sequence↗
PubMed1992

Characterization of three mutations causing von Willebrand disease type IIA in five unrelated families.

Von Willebrand disease (vWD) type IIA is characterized by decreased ristocetin-induced platelet aggregation, and by the absence from plasma of high molecular weight multimers of von Willebrand factor (vWF). Most mutations causing vWD type IIA are clustered within the A2 domain of the mature vWF subunit that is encoded by exon 28. Using the polymerase chain reaction (PCR), the entire exon 28 from patients with vWD type IIA and normal controls was amplified and sequenced. Three missense mutations were detected that result in the amino acid substitutions were detected that result in the amino acid substitutions Arg(834)----Trp, Gly(742)----Glu, and Ser(743)----Leu. The first mutation occurred independently in three unrelated families; each of the latter mutations was found in one family. By restriction endonuclease analysis and allele-specific oligonucleotide (ASO) hybridization the mutations were confirmed in affected family members and excluded in unaffected members and 50 normal controls. The apparently high frequency of identical independent mutations among patients with vWD type IIA suggests that a precise diagnosis may be possible in a majority of patients using relatively simple recombinant DNA screening assays.

Alleles↗
PubMed1991

Molecular basis of von Willebrand disease type IIB. Candidate mutations cluster in one disulfide loop between proposed platelet glycoprotein Ib binding sequences.

Many variants of von Willebrand disease (vWD) with qualitatively abnormal von Willebrand factor (vWF) are recognized. In vWD type IIB, the abnormal protein displays enhanced affinity for a platelet vWF receptor, the glycoprotein Ib-IX complex. 14 patients from 7 unrelated families with vWD type IIB were studied to determine the molecular basis for this phenotype. Specific oligonucleotide primers were used to amplify portions of vWF exon 28 encoding a domain that interacts with the platelet glycoprotein Ib-IX complex. Candidate missense mutations were identified for all 14 patients by DNA sequencing, allele specific oligonucleotide hybridization, and restriction endonuclease digestion. These sequence changes occur in an 11 amino acid segment within a single disulfide loop bounded by Cys(509) and Cys(695). All of these sequence changes are C----T transitions within CG dinucleotides. Six patients from two unrelated families were heterozygous for the encoded sequence Arg(543)----Trp. Seven patients from four unrelated families were heterozygous for the encoded sequence Arg(545)----Cys; this sequence change appears to have occurred independently three times, once as a new spontaneous mutation. One patient with apparently sporadic vWD type IIB was heterozygous for the encoded sequence Val(553)----Met, and this appears to be a new mutation. None of these sequence changes was found in 100 normal alleles. These findings suggest that vWD type IIB may be caused by relatively few distinct mutations, that these mutations may cluster within a specific region of one disulfide loop in vWF domain A1, and that this region can modulate the affinity of vWF for the platelet glycoprotein Ib-IX complex.

Alleles↗
PubMed1985

Accuracy of radiation field alignment in clinical practice.

We present an analysis of simulator and portal films of 71 patients. Twenty-five were analyzed retrospectively, 39 prospectively, but without changing routine filming practice, and 7 had daily portal films taken. Treatment-to-treatment variations in anatomy with respect to the field were determined by comparing sequential portal films. The standard deviation of the variations was approximately normally distributed with an average value of 3 mm independent of site and field shaping technique. Discrepancies between the portal and simulator films were greater and depended on the site of treatment. The mean worst-case discrepancy averaged over all sites was 7.7 mm; the lowest value was 3.5 mm in the head and neck region; the highest value was 9.2 mm in the thorax.

Humans↗
PubMed1976

The role of prostaglandin E, cyclic AMP, and cyclic GMP in the proliferation of guinea-pig ear skin stimulated by topical application of vitamin A acid.

Daily treatment of guinea-pig ear skin with topical 0.5% retinoic acid in acetone produced erythematous scaly dermatitis. Histologic sections revealed bandlike thickening of the epidermis on days 2 to 4, psoriasiform acanthosis, papillomatosis and increased mitotic activity on days 5 to 6. Also seen were dilatation of the upper dermal blood vessels and a fibroblastic, histiocytic reaction in the dermis. Prostaglandin E, cyclic AMP, and cyclic GMP levels were increased in the treated skin and thymidine incorporation was enhanced. Cyclic AMP and GMP levels peaked on day 5 simultaneous with maximal epidermal hyperplasia, increased mitotic activity and dermal reaction. Tritiated thymidine uptake peaked on days 4 and 5, and prostaglandin E levels continued to increase up to day 6. Cyclic AMP phosphodiesterase activity of treated skin on day 5 did not appear to be significantly different from control.

3',5'-Cyclic-AMP Phosphodiesterases↗