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Biomedical subjects

M Weinberg

Publications and source records attributed to M Weinberg.

At least 37 records · Page 2Linked to original sources
PubMed1995

Two rapidly growing fatty tumors of the upper limb in children: lipoblastoma and infiltrating lipoma.

One case of lipoblastoma and another case of infiltrating lipoma of the upper limb in infancy are reported. These rare benign fatty tumors may be congenital and may grow rapidly soon after birth. The classification of these fatty tumors and their management are presented to increase awareness of the benign nature of these tumors despite their rapid growth and to demonstrate that complete surgical excision should be done to prevent local recurrence.

Arm↗
PubMed1994

Continuous esophageal pH monitoring during laparoscopic cholecystectomy.

Gastro-esophageal regurgitation (GER) and eventual aspiration is considered a major risk during general anesthesia. High intraperitoneal pressure produced during laparoscopic cholecystectomy (LC) is a possible source of increased GER. We investigated the incidence of GER using continuous esophageal pH monitoring in 14 patients undergoing elective LC. Only two brief episodes of acid reflux (pH < 4) occurred during LC. Apparently the high intraperitoneal pressure during LC carries no increased risk of regurgitation and aspiration.

Adult↗
PubMed1994

Pulmonary hemorrhage risk in infants with a clinically diagnosed patent ductus arteriosus: a retrospective cohort study.

OBJECTIVE: To determine if an early, clinically detectable patent ductus arteriosus (PDA) was associated with pulmonary hemorrhage (PH) in infants who received rescue artificial surfactant therapy. METHODS: This retrospective cohort study of 233 low birth weight infants (< or = 1700 g) who received artificial surfactant therapy for respiratory distress syndrome compared antenatal and postnatal characteristics of infants with PH and without PH. Pulmonary hemorrhage was defined by an onset of bright red blood from the endotracheal tube in quantities that resulted in increased ventilatory support and a new infiltrate on a chest radiograph. RESULTS: Pulmonary hemorrhage occurred in 6% (15/233) of the infants. Thirty-three percent (5/15) of the infants with PH died within 14 days of the hemorrhage. Of the 15 PH, 73% occurred within 48 hours of the first surfactant dose. Pulmonary hemorrhage was more common in male infants and infants of mothers who received antibiotic therapy during labor (P < or = .04). Infants with PH received surfactant earlier than those without PH (P = .04). Nursery events or therapies occurring following surfactant therapy that were associated with PH included: little improvement in ventilatory efficiency index (P = .01), dopamine infusion (P = .04), and the presence of a clinically detectable PDA before, or at the time of, the PH [60% (9/15) vs 33% (71/217), P = .03]. After adjusting for severity of illness before surfactant therapy, risk of PH remained greater in infants who developed symptoms of a PDA. Dopamine support appeared to modify the association between PDA and PH. CONCLUSIONS: In this retrospective cohort study, pulmonary hemorrhage, was associated with the presence of a clinically detectable patent ductus arteriosus before, or at the time of, pulmonary hemorrhage.

Cohort Studies↗
PubMed1994

A new intratracheal stent made from nitinol, an alloy with "shape memory effect".

Temporary or permanent tracheal splinting in pediatric patients may be indicated in tracheomalacia or bronchomalacia, repair of congenital tracheal stenosis, and after tracheal resection. This study presents the results of the development of a new intraluminal airway stent made from titanium alloy, a metal with "shape memory effect". At low temperatures (martensitic state) the titanium alloy stent can be fashioned into a specific shape; then when heated to a higher temperature (austenitic state) the stent alters its shape, only to regain its original shape when recooled to the lower temperature. The stent, connected to a small electric power supply, was introduced into 20 young rabbits with the use of a 2.5 cm rigid bronchoscope. After implantation in the martensitic state the stent was warmed to 40 degrees C, the austenitic state, by an electric current of 1.5 to 3 ampere for 1 to 2 seconds. After a period of 8 to 10 weeks the stent was removed (in its martensitic state) through the same-sized bronchoscope after being cooled with 3 to 4 ml of 80% alcohol solution at 6 degrees C. No signs of airway obstruction developed in any of the animals after implantation or extraction of the stent. The biomechanical properties of the trachea, as shown by strain measurements with the use of incremental forces, showed significant differences between the stented and unstented segments (p < 0.005). The titanium alloy intratracheal stent adequately fulfilled the requirements of a temporary intraluminal airway splint, and because of its unique feature of shape memory effect the stent could be inserted, fixed, and removed easily, even in very small airways.

Alloys↗
PubMed1993

Effects of intravenous magnesium sulfate on arrhythmias in patients with congestive heart failure.

Intravenous magnesium is an effective treatment for ventricular tachycardia of some etiologies, and in patients with congestive heart failure low serum magnesium concentrations are associated with frequent arrhythmias and high mortality. This suggests that magnesium administration may decrease the frequency of ventricular arrhythmias in patients with heart failure. We therefore assessed the impact of an intravenous magnesium infusion upon the frequency of ventricular premature depolarizations in 40 patients with New York Heart Association (NYHA) class II to IV heart failure and serum magnesium < or = 2.0 mg/dl. Within 1 week of a baseline 6-hour ambulatory electrocardiographic recording, an infusion of 0.2 mEq/kg of MgSO4 was given over 1 hour and a repeat 6-hour recording was obtained. There was an inverse relationship between the change in magnesium concentration and the change in frequency of premature ventricular depolarizations; premature ventricular depolarizations declined by 134 +/- 207 hr-1 in patients in whom serum magnesium concentration increased > or = 0.75 mg/dl, but increased by 72 +/- 393 hr-1 in patients with a change < 0.75 mg/dl (p < 0.05). For all patients, the frequency of premature ventricular depolarizations was 283 +/- 340 hr-1 pretreatment and 220 +/- 269 hr-1 following magnesium infusion (p = 0.21). Patients with > or = 300 premature ventricular depolarizations hr-1 demonstrated a decrease from 794 +/- 309 to 369 +/- 223 hr-1 (p < 0.001). Intravenous magnesium administration decreased the frequency of couplets from 233 +/- 505 to 84 +/- 140 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Identical mutations in unrelated families with generalized resistance to thyroid hormone occur in cytosine-guanine-rich areas of the thyroid hormone receptor beta gene. Analysis of 15 families.

Generalized resistance to thyroid hormone (GRTH) is a syndrome of variable reduction of tissue responsiveness to thyroid hormone. 28 different point mutations in the human thyroid hormone receptor beta (TR beta) gene have been associated with GRTH. These mutations are clustered in two regions of the T3 binding domain of the TR beta (codons 310-347 and 417-453). We now report point mutations in the TR beta gene of six additional families with GRTH and show that three mutations occurred each in three families with GRTH, and that three other mutations were each present in two families. In 11 of these 15 families, lack of a common ancestor could be confirmed by genetic analysis. 28 of the 38 point mutations so far identified, including all those occurring in more than one family, are located in cytosine-guanine-rich areas of the TR beta gene. Differences in clinical and laboratory findings in unrelated families harboring the same TR beta mutation suggest that genetic variability of other factors modulate the expression of thyroid hormone action.

Base Composition↗
PubMed1993

Human thyroxine-binding globulin gene: complete sequence and transcriptional regulation.

T4-binding globulin (TBG) is a glycoprotein of hepatic origin which transports thyroid hormone in serum. To characterize the human TBG (hTBG) gene, we studied its genomic organization, promoter activity, and regulation. To this purpose, we isolated from liver a complete hTBG cDNA clone containing the 5'-untranslated region and localized the transcription start site (TSS). The analysis of genomic clones revealed that the hTBG gene consists of five exons and that its exon-intron organization is similar to that of other members of the serine protease inhibitor family. The first exon (exon 0) is a short noncoding sequence located 1.62 kilobase pairs (kbp) upstream from exon 1. Potential cis-acting transcriptional regulatory elements including a TATA box, a CAAT box, and a hepatocyte nuclear factor-1 binding motif were identified in the upstream region. A reporter gene in which 3.2 kbp of the 5'-flanking region, including exon 0, was inserted upstream of the bacterial chloramphenicol acetyltransferase gene showed significant activity when transfected into a hepatblastoma-derived (HepG2) cell line. The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate, down-regulated the promoter activity by more than 80% and completely inhibited hTBG synthesis, whereas thyroid hormone, glucocorticoid, estrogen, and nicotinic acid had little, if any, effect. A series of 5'-deletions revealed that the fragment -218 to +4 from the TSS had the highest promoter activity, nearly 1000-fold greater than the promoterless chloramphenicol acetyltransferase construct. When nonhepatocyte-derived cell lines (CV-1 and CHO) were tested, promoter activity was reduced by a factor of 100, showing that the promoter works in liver-specific manner. The region -218 to -102 contains liver-specific enhancer elements, since deletion to nucleotide -101 resulted in a profound reduction of the promoter activity in HepG2 cells but not in CV-1 or CHO cells. On the other hand, mutational disruption of the putative hepatocyte nuclear factor-1 site (located 65 bp upstream of the TSS) completely abolished the promoter activity in all cell lines, indicating that this site is absolutely required for the transcription of the hTBG gene.

Amino Acid Sequence↗
PubMed1992

Sequencing of the variant thyroxine-binding globulin (TBG)-San Diego reveals two nucleotide substitutions.

Thyroxine-binding globulin (TBG) is a liver glycoprotein that transports thyroid hormone in serum. In 1989, a variant TBG was reported with reduced binding affinity for thyroxine (T4) and triiodothyronine (T3) which results in low serum T4 and T3 levels. This variant, TBG-San Diego (TBG-SD), also displays reduced heat stability but has a normal isoelectric focusing pattern. We now report the sequence of the entire coding region of TBG-San Diego. It reveals two nucleotide substitutions: one located in exon 1 which results in the replacement of the normal Ser-23 (TCA) with threonine (ACA) and the other, located in exon 3, changes the normal codon 283 of TTG (leucine) with that of TTT, (phenylalanine). Allele specific amplification was used to search for both nucleotide substitutions in four affected members of the family. Results confirmed the co-segregation of these nucleotide substitutions with the TBG-SD phenotype. The substitution in codon 283 has been previously described and exists as a polymorphism in some ethnic groups or in combination with other TBG variants with different physical characteristics. Thus, it appears that the replacement of Ser-23 with threonine is responsible for the observed alterations in physical properties of TBG-San Diego.

Amino Acid Sequence↗
PubMed1992

Cardiodepressant effects of mexiletine in patients with severe left ventricular dysfunction.

Mexiletine is thought to exert minimal negative inotropic actions, but its effects have not been evaluated in patients with severe congestive heart failure. The haemodynamic response to an oral loading dose of mexiletine (400 mg) was assessed in 20 patients with severe chronic heart failure. Mexiletine caused marked haemodynamic deterioration, with stroke work index decreasing in 18 of the patients. Two hours after mexiletine, mean cardiac and stroke work indexes decreased by 15% and 25%, respectively (both P less than 0.001), while heart rate and systemic vascular resistance increased by 10% and 20%, respectively (both P less than 0.05). Simultaneously, left ventricular filling pressure and right atrial pressure increased by 37% and 36%, respectively (both P less than 0.001), but mean arterial pressure did not change. Furthermore, clinical deterioration, with onset of dyspnoea at rest, developed in five patients at the time of peak haemodynamic effect. Plasma mexiletine concentrations were within the accepted therapeutic range of 0.5 to 2.0 micrograms.ml-1 in all but two of the patients. Nevertheless, the plasma concentration was an important determinant of haemodynamic effect. The stroke work index decreased by 38% in the patients with a mexiletine level above the median value of 1.3 micrograms.ml-1 (range 25 to 56%), but only 13% (range 15 to 43) in patients with lower plasma concentrations. In conclusion, although mexiletine may cause cardiodepressant effects in any patient with severe left ventricular dysfunction, dosing which results in a high (but still therapeutic) plasma level is more likely to cause haemodynamic deterioration.

Adult↗
PubMed1992

Elevated concentrations of endogenous ouabain in patients with congestive heart failure.

BACKGROUND: An endogenous digitalis-like compound in mammals has long been postulated, but only recently has a substance indistinguishable from ouabain been identified in human plasma. Because of the potential significance of such a substance in patients with congestive heart failure, we sought to evaluate the pathophysiology of endogenous ouabain in these individuals. METHODS AND RESULTS: Using an immunoassay, we determined plasma ouabain concentrations in 51 patients with heart failure and in 19 control subjects. Plasma ouabain concentrations in control subjects ranged from 0.16 to 0.77 nM (mean, 0.44 +/- 0.20 nM). In 19 matched heart failure patients receiving digoxin, the mean ouabain was significantly elevated at 1.59 +/- 2.2 nM (range, 0.17-8.76 nM, p less than 0.05 versus control subjects). The ouabain concentration correlated inversely with both cardiac index (r = -0.62, p less than 0.005) and mean arterial pressure (r = -0.51, p less than 0.05). However, there was no correlation between ouabain and left ventricular filling (r = 0.19, NS) or right atrial pressures (r = 0.20, NS). In 16 heart failure patients not receiving digoxin, the mean ouabain was 1.52 +/- 2.58 nM. No relation between renal function and ouabain was detected. CONCLUSIONS: The unanticipated lack of correlation of ouabain with atrial pressures indicates that volume is not the chief determinant of ouabain concentration in patients with congestive heart failure. However, the significant relations of plasma ouabain concentration with cardiac index and mean arterial pressure imply that endogenous ouabain may be an important homeostatic factor in humans.

Digoxin↗
PubMed1991

Hemodynamic and neurohormonal effects of quinidine in patients with severe left ventricular dysfunction secondary to coronary artery disease or idiopathic dilated cardiomyopathy.

Quinidine causes vasodilation directly and by inhibition of adrenergic vasoconstriction, but it also exerts negative inotropic activity. Although this drug is often administered to patients with severe congestive heart failure, the net consequences of these opposing actions have not been evaluated in such patients. The hemodynamic and neurohormonal response to oral quinidine (600 mg) in 19 patients with severe chronic heart failure was therefore determined. Vasodilation was the predominant effect of quinidine, with reductions in mean arterial, left ventricular filling and right atrial pressures of -9% (confidence interval [CI] -5 to -13), -8% (CI -19 to 3), -15% (CI -26 to -4), respectively. The quinidine-induced vasodilation increased plasma norepinephrine and epinephrine concentrations by 44% (CI +17 to +72) and 47% (CI +2 to +91), respectively. No change in cardiac performance was noted, with the cardiac index slightly increased (+10%, CI +2 to +17) and stroke work index unchanged (0%, CI -11 to +11) after quinidine. Although the mean serum quinidine concentration was within the therapeutic range or lower in all patients, the serum quinidine concentration and the change in mean arterial pressure did correlate (r2 = 0.64). In conclusion, vasodilation is the predominant hemodynamic effect of oral quinidine in patients with congestive heart failure. However, potential adverse effects may be caused by consequent neurohormonal activation.

Adult↗
PubMed1991

Comparative hemodynamic effects of mexiletine and quinidine in patients with severe left ventricular dysfunction.

Mexiletine and quinidine are often administered to patients with severe congestive heart failure, but their hemodynamic effects have not been adequately studied in these individuals. In a randomized, crossover study, the hemodynamic responses to single oral doses of quinidine (600 mg) and mexiletine (400 mg) were compared in 20 patients with marked left ventricular dysfunction. Quinidine predominantly caused vasodilation, with mean arterial, left ventricular filling, and right atrial pressures all decreasing (-7 +/- 2, -2.3 +/- 1.0, and -1.1 +/- 0.5 mm Hg, respectively) and the systemic vascular resistance also declining (-308 +/- 84 dynes.sec.cm5). In contrast, the systemic vascular resistance increased (314 +/- 84 dynes.sec.cm-5) and the mean arterial, left ventricular filling, and right atrial pressures also increased (+2 +/- 2, +6.1 +/- 1.8, and +1.8 +/- 0.6 mm Hg, respectively) after mexiletine. Cardiac performance declined with mexiletine (cardiac and stroke work indexes decreasing -0.3 +/- 0.1 L/min/m2 and -5 +/- 1 gm.m/m2, respectively), but there was no significant change in cardiac or stroke work indexes with quinidine (+0.1 L/min/m2 and -0.3 +/- 0.9 gm.m/m2, respectively). The response to the two agents significantly differed for all parameters measured (p less than 0.005). These hemodynamic changes were accompanied by clinical effects. Mexiletine induced increased dyspnea in five patients and quinidine led to symptomatic hypotension in two patients. Plasma concentrations of mexiletine and serum concentrations of quinidine were within or below the therapeutic range in all patients. In conclusion, mexiletine and quinidine exert different hemodynamic effects when given to patients with severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1991

Immunoglobulins A, G, and M to cytomegalovirus during recurrent infection in recipients of allogeneic bone marrow transplantation.

Occurrence and significance of specific IgA and IgM to cytomegalovirus (CMV) in recurrent CMV infection was evaluated in 21 allogeneic T lymphocyte-depleted bone marrow transplantation (BMT) recipients who had been previously CMV seropositive. Of 17 patients with CMV infection, viruria was detected in 94%, CMV-specific IgA in 88% and IgM in 76%, and a fourfold rise in IgG in 65%. The median time between BMT and detection of viruria was 69 days, of IgA 70, of IgM 62, and of IgG 88 days. The IgM and IgA responses lasted for 14 and 30 days (median time), whereas high IgG titers persisted. Twelve patients developed CMV disease; in these the appearance of viruria, IgA, and IgM preceded the rise of IgG (P less than .02). CMV-specific IgA and IgM are valuable diagnostic tools in BMT recipients with recurrent CMV infection.

Adolescent↗
PubMed1991

Prevalence of sexually transmitted pathogens among women attending a methadone clinic in Israel.

OBJECTIVE: To assess the prevalence of sexually transmitted pathogens in drug-addicted women in Tel Aviv, Israel. DESIGN: A prospective study conducted between March and July 1987. SETTING: A methadone clinic in Tel Aviv, Israel. SUBJECTS: Sixty four asymptomatic female drug addicts were studied; 38 of them were declared practising prostitutes. METHODS: Cervical specimens were obtained for cultures, and blood samples were drawn for serological tests. Demographic data and sexual histories were obtained using a standard questionnaire. RESULTS: Chlamydia trachomatis was detected in the cervix of 25% of women; 98% had antibody titres (greater than 1:64). Mycoplasma hominis and Ureaplasma urealyticum were isolated in 57% and 65% respectively. Gardnerella vaginalis was detected in 17% of women, and herpes simplex virus was cultured from two prostitutes. Five per cent of women were carriers of HBsAg, while 57% had HBSs and/or HBc antibodies. Only one prostitute had specific treponemal antibodies. In no case were gonococci or group B streptococci isolated, and HIV serology was invariably negative. CONCLUSION: Chlamydia and genital mycoplasmas appear to be the prevailing pathogens in Israeli drug-addicted women, while gonococci and Treponema pallidum occur only rarely.

Adult↗
PubMed1990

Cytogenetic investigations on a cell line derived from a carcinoma arising in a salivary gland pleomorphic adenoma.

This article discusses the results of cytogenetic investigations of a cell line derived from a malignant tumor arising in a benign salivary gland pleomorphic adenoma. Initial karyotypic studies became possible with cells of the second in vitro passage and revealed the existence of hypertetraploidy. Furthermore, a marked polysomy 7 and a translocation involving 12q13-15, a breakpoint also frequently seen in benign pleomorphic adenomas, were noteworthy. During long term culture, the number of chromosomes per cell decreased as well as the number of copies of chromosome 7. Cell tumorigenicity was proved by heterotransplantation to nude mice. The resulting tumors were karyotyped again. No significant changes of the chromosome number or of the degree of polysomy 7 were found compared to the cells before heterotransplantation. In contrast, the cells from the nude mice tumors showed a remarkable number of different isochromosomes probably indicating an unknown factor supporting the generation of isochromosomes. The consistent presence of the t(12;?)(q13-15;?) makes the cell line well suited for molecular studies of this breakpoint region.

Adenoma, Pleomorphic↗
PubMed1989

Limitations to the use of a sensitive assay for serum thyrotropin in the assessment of thyroid status.

In the majority of clinical settings, a suppressed serum thyrotropin (s-TSH) level determined by the new sensitive assays is diagnostic of thyrotoxicosis. This has led to its proposed use as a screen for thyroid disease. However, s-TSH may be suppressed in conditions other than thyrotoxicosis. We retrospectively reviewed s-TSH measurements made in a large heterogeneous population to determine in which settings a suppressed value could potentially lead to misdiagnosis. We found that a suppressed s-TSH level was useful in making the diagnosis of autonomous thyroid function and in the assessment of thyroid hormone replacement therapy in patients with primary, but not central, hypothyroidism. Hyperthyroidism caused by either intrinsic thyroid disease or thyroid hormone administration accounted for 83% (111/134) of suppressed values; however, central hypothyroidism, nonthyroidal illness, acute psychiatric illness, or the administration of medication was responsible for this finding in 17% (23/134). While a suppressed s-TSH level is generally excellent in the diagnosis of pituitary suppression by thyroid hormone, in specific clinical settings, a suppressed s-TSH level may be seen in the absence of thyroid hormone excess. The limitations of its use as a first-line screen in those conditions must be recognized.

Adult↗