Search PubMed⌕ Search

Biomedical subjects

E Rubinstein

Publications and source records attributed to E Rubinstein.

At least 145 records · Page 8Linked to original sources
PubMed1992

Therapy of experimental murine brucellosis with streptomycin, co-trimoxazole, ciprofloxacin, ofloxacin, pefloxacin, doxycycline, and rifampin.

Mice infected with Brucella melitensis were treated with streptomycin, co-trimoxazole, ciprofloxacin, doxycycline, and rifampin intraperitoneally and with ciprofloxacin, ofloxacin, pefloxacin, doxycycline, and rifampin orally for 14 to 21 days. Doxycycline- and rifampin-treated animals (either route) demonstrated a cure rate significantly better than that of controls. Longer therapy periods were associated with a significantly better outcome. Therapy failure was observed in all mice treated with ciprofloxacin, ofloxacin, and pefloxacin administered orally as well as in mice treated intraperitoneally with ciprofloxacin. Our findings demonstrate that treatment of experimental brucellosis in mice with doxycycline and rifampin yields therapeutic results that are superior to those yielded by treatment with quinolones.

Administration, Oral↗
PubMed1992

Prevalence of HIV antibodies in transsexual and female prostitutes.

Human immunodeficiency virus (HIV) prevalence was studied in an unselected group of 216 female and transsexual prostitutes. Subjects were asked about age, biological sex, marital status, children, length of occupation, sexual practices, and drug abuse history. Blood was drawn on site. All 128 females who did not admit to drug abuse were seronegative; 2 of the 52 females (3.8%) who admitted to intravenous drug abuse were seropositive. In contrast, 11.1% of the 36 male transsexuals (including 3 out of 32 non-drug abusers) were seropositive. The results support the notion that vaginal transmission of HIV is less effective than anal transmission.

Adolescent↗
PubMed1992

Teicoplanin--domiciliary use in surgical infections.

This is an ongoing study designed to evaluate the role of teicoplanin in the therapy of sternal wound infections following cardiac surgery caused by Gram-positive microorganisms. Intravenous teicoplanin therapy is begun in the hospital, but once the patients return home it is given as a single intramuscular dose of 400 mg/day. Only a limited number of patients have been recruited so far, but in these, the clinical success rate and the bacteriological elimination rate are 85%. Only one patient had to be withdrawn from the study due to intolerable side-effects. These preliminary results suggest that teicoplanin is suitable for the therapy of chest wound infections following cardiac surgery; a major part of the course can be administered at home in a single daily intramuscular injection. This novel therapy regimen is expected to reduce considerably the hospital costs involved in the therapy of sternal wound infections.

Ambulatory Care↗
PubMed1992

[Where is the diagnosis of anthrax?].

The large use of antibiotics entailed a dizzy fall of the bacteriological positivity in diagnosis of acute anthrax, from 98-100% to 25% in average. Common serological methods are of low sensitivity and not so confluent. The more sophisticated methods (ELISA, EITB) are of a much better sensitivity but their employment in field epidemiological investigations is difficult and does not be suitable for a retrospective diagnosis. These inconveniences can be successfully surmounted by use of the anthraxin skin test. This test allows to diagnose acute anthrax in 98-100% of cases, and retrospectively (from 45 days to 30 years after recovery) in an average of 86.2% of cases. This skin test is simple for use, and does not requires a special medical competence.

Anthrax↗
PubMed1991

Fc gamma receptor-mediated interplatelet activation by a monoclonal antibody against beta 2 microglobulin.

Three different mAb directed against beta 2 microglobulin (two IgG1 and one IgG2a) were tested for their ability to activate human platelets. Although all three antibodies bound to platelets, only one of them, B2.62.2, of the IgG1 subclass, induced platelet activation. This activation is similar to the activation by SYB-1, a CD9 antibody of the same subclass previously described as activating platelets through platelet Fc gamma R. These similarities include serotonin secretion, a lag time preceding aggregation and the induction of a strong intracellular calcium mobilization from storage pools. As with CD9 antibodies, the F(ab')2 fragments of B2.62.2 did not induce activation but blocked the activation by the native antibody, by preventing the binding to beta 2 microglobulin. Also, this activation was inhibited by pretreating the platelet with IV-3, a mAb that blocks the Fc binding site of the FcR. Inasmuch as the same antibody does not prevent the binding of B2.62.2 on platelets, we conclude that the activation by B2.62.2 is mediated by the FcR. Nevertheless, there were differences with the activation by SYB-1. B2.62.2 activation was more dependent on thromboxane A2 formation and no cytoplasmic alkalinization was detected. Finally, contrary to SYB-1, B2.62.2 activation proved to be sensitive to platelet count, suggesting that it involves the formation of immune complexes consisting of antibodies and platelets, that activate nearby platelets.

Antibodies, Monoclonal↗
PubMed1991

Interaction of two GPIIb/IIIa monoclonal antibodies with platelet Fc receptor (Fc gamma RII).

We have previously used the IV-3 monoclonal antibody specific for Fc gamma RII to demonstrate that platelet activation by CD9 monoclonal antibodies such as ALB-6 is mediated by the Fc gamma RII. Here, we show that platelet activation following addition of a monoclonal antibody directed against GPIIb/IIIa, P256 is completely blocked by IV-3, as monitored by serotonin release, calcium and pH modifications. However, aggregation was only partially inhibited. D3GP3 is another monoclonal antibody directed against GPIIIa which has been shown to induce platelet aggregation by exposure of the fibrinogen binding site. The present study demonstrates that this phenomenon is not accompanied by calcium flux or pH modification, nor is it blocked by pretreatment of platelet by IV-3. Despite its apparent independence from the Fc gamma RII activation pathway, D3GP3, but not its Fab fragment, was able to inhibit ALB-6 induced activation, including serotonin release, calcium flux and pH modifications. Binding studies demonstrated that D3GP3 (20 micrograms/ml, 0.13 microM) does not block ALB-6 binding to CD9 antigen but completely blocks IV-3 binding to the Fc receptor for concentrations of IV-3 ranging from 0 to 15 nM. Together, these results suggest an interaction between GPIIb/IIIa, Fc gamma RII and GPIIb/IIIa monoclonal antibodies which in some cases can result in activation of platelets through Fc gamma RII.

Antibodies, Monoclonal↗
PubMed1991

In vitro susceptibility of Brucella melitensis to antibiotics.

The in vitro susceptibilities of 86 recent clinical isolates of Brucella melitensis to minocycline, streptomycin, co-trimoxazole, rifampin, and six fluoroquinolones were determined. Minocycline exhibited the lowest MIC and was followed by rifampin and streptomycin. Among the quinolones, WIN 57273 and ciprofloxacin were the most active agents. No antibiotic combination of these agents exhibited synergy against 15 selected isolates. In killing rate experiments, streptomycin exhibited the most rapid kill (less than 12 h), while a complete kill with minocycline, rifampin, and ciprofloxacin was delayed up to 48 h. The combinations of streptomycin with each of minocycline, rifampin, or ciprofloxacin exhibited the fastest kills (within 2 h), while with the other combinations, a complete kill was delayed up to 96 h. These results demonstrate the discrepancy between the results of various in vitro methods in evaluating the antibiotic susceptibility of B. melitensis.

Anti-Bacterial Agents↗
PubMed1991

Pancreatic secretion of zinc and copper in normal subjects and in patients with chronic pancreatitis.

Pancreatic secretion of zinc and copper in duodenal juice were measured in 7 healthy persons and in 9 patients with chronic pancreatitis. Stimulation with cholecystokinin and secretin increased secretion of zinc in healthy persons but not in patients. Copper secretion was not influenced. In patients with chronic pancreatitis, the correlations between zinc secretion, and amylase and trypsin secretion were significant while in healthy subjects they were not. Possibly pancreatic zinc secretion in the duodenal juice might be used as a measure of exogenic pancreatic function, and determination of zinc in duodenal juice may replace enzyme determinations in the diagnosis of chronic pancreatitis.

Adult↗
PubMed1991

Ciprofloxacin inhibits human hematopoietic cell growth: synergism with tumor necrosis factor and interferon.

The cytokines tumor necrosis factor (TNF) and interferon (IFN) induce antiproliferative and cytotoxic activity in a variety of cell types. Ciprofloxacin (CFN)--a new fluoroquinolone antibiotic--has also been described, at high concentrations, to suppress hematopoietic cell growth and to affect cytokine production. This study examines the possible relationship between TNF alpha and IFN gamma, as components of host defense mechanisms, and CFN. To investigate the effect of CFN, either alone or combined with TNF or IFN, on normal human hematopoiesis, we examined in vitro changes in hematopoietic progenitor cell growth. We also studied the effect of CFN on human cytokine production by determining TNF, IFN, and colony-stimulating factor (CSF) production by human mononuclear leukocytes (MNC). Granulocyte and monocyte colony formation (granulocyte-macrophage colony-forming cells, GM-CFC) as well as erythroid burst formation (erythroid burst-forming units, BFU-E) were inhibited only by high nontherapeutic levels of CFN. Lower CFN concentrations, however, were inhibitory in the presence of low, noninhibitory concentrations of human recombinant (r)IFN gamma or rTNF alpha. CFN induced a striking dose-dependent increase in IFN gamma production and a decrease in CSF production by mitogen-stimulated MNC. No effect was observed, however, on TNF production by stimulated MNC. The synergistic inhibition of hematopoietic progenitor cell proliferation, achieved by combining low doses of CFN and of antiproliferative cytokines, may explain the occasional case of leukopenia or anemia observed in infected patients receiving CFN. This effect may also indicate the applicability of such a combination against malignant cell growth.

Cell Division↗
PubMed1991

The intravitreal penetration of orally administered ciprofloxacin in humans.

To evaluate the penetration of ciprofloxacin, a new wide-spectrum oral antibiotic, into the vitreous, ciprofloxacin was administered orally to 21 patients who were scheduled to undergo vitreal surgery. Seven patients received 750 mg ciprofloxacin 4 hr before surgery (group I), seven patients received this dose 8 hr before surgery (group II), and seven patients received two 750-mg doses of oral ciprofloxacin every 12 hr. The last dose was administered 12 hr before surgery (group III). Vitreous and blood samples were collected simultaneously and assayed for ciprofloxacin concentrations by bioassay and high-performance liquid chromatography.

Administration, Oral↗
PubMed1990

Extensive C1q-complement initiated lysis of human platelets by IgG subclass murine monoclonal antibodies to the CD9 antigen.

Several monoclonal antibodies (MAbs) to CD9, a surface membrane glycoprotein of 24 kDa found on platelets as well as several other hematopoietic and nonhematopoietic tissues, have the property of activating platelets. We have recently shown that with two of these MAbs (ALB-6 and SYB-1) this activation is mediated by interaction of the Fc portion of these IgG1 subclass MAbs with the Fc gamma II receptor (FcRII) and is blocked by a MAb to this receptor (IV-3). In this report we show that several MAbs to the CD9 antigen (BA-2, BU-16, MM2/57) also cause extensive and rapid platelet lysis in plasma. This lysis is mediated by the classical complement pathway dependent on C1q fixation. Lysis was not blocked by inhibiting platelet activation with prostaglandin E1 or by the MAb to FcRII (IV-3). The CD9 MAb BU-16 can also activate platelets through the FcRII when complement lysis is prevented by removal of C1q using specific antisera or by isolation of the platelets from plasma.

Animals↗