Search PubMed⌕ Search

Biomedical subjects

J Weiss

Publications and source records attributed to J Weiss.

At least 163 records · Page 9Linked to original sources
PubMed1996

Employee injuries and convenience store robberies in selected metropolitan areas.

The number of robberies and robbery-related injuries to employees in convenience stores (C-stores) during 1992 or 1993 were estimated for selected metropolitan areas around Miami and Tampa, Florida; Atlanta, Georgia; Chicago, Illinois; Baltimore, Maryland; Boston, Massachusetts; Detroit, Michigan; Pittsburgh and Philadelphia, Pennsylvania; Charleston, Columbia, Greenville, and Spartanburg, South Carolina; and Arlington, Chesterfield, and Henrico counties, Virginia. Of the 1835 C-store robberies that occurred during 1992 or 1993 in all selected areas (excluding Atlanta and Chicago), there were 12 homicides of C-store employees; 219 nonfatal injuries of C-store employees; 1071 robberies in which there were no injuries but a weapon was used, displayed, or implied toward a C-store employee; and 132 robberies in which there was no injury and no weapon used, but an employee was struck, pushed, or shoved. Corresponding figures for the 238 robberies that occurred in Chicago during January to June 1993, and for which victim employment status was unknown (customer or employee) were three homicides, 53 nonfatal injuries, 120 attacks in which a weapon was used but there was no injury, and 57 attacks in which a person was struck, pushed, or shoved but there was no injury. The proportion of robberies that resulted in a homicide or injury to an employee varied among selected areas from .03 to .25. The proportion of homicides and injuries to an employee was. 14 or higher for target areas in Baltimore (.24), Detroit (.25), and Virginia (.14); the proportion to an employee or customer was .24 in Chicago. The conclusions from these data are that the risk of employee injury in C-store robberies was high in selected metropolitan areas. This underscores the need for effective robbery prevention programs to reduce injury. In addition, further research is needed to determine the effectiveness of prevention programs in the C-store industry and the application of these programs to other retail industries.

Commerce↗
PubMed1996

[Development of a detection system for Helicobacter pylori DNA in gastric juice].

A rapid and sensitive PCR-based microwell plate assay (PCR-MWP) system to detect the 16 S ribosome RNA gene of Helicobacter pylori was developed. Analytical sensitivity, evaluated with purified recombinant plasmid DNA and genomic DNA of H. pylori, was one copy of DNA per PCR. Specificity was validated with a panel of DNA from 75 kinds of microorganisms including Helicobacter showed weak positives, when 1 pg of DNA was input. Other microorganisms gave negative signals even when 100 pg of DNA was used for PCR. When compared with a Nested-PCR system to detect the urease A-subunit gene performed by a commercial reference laboratory, the results obtained (sensitivity 93.3% and specificity 73.3%) was almost equivalent. The PCR-MWP was rapid and easy for the detection of H. pylori DNA in gastric juice specimen.

DNA, Bacterial↗
PubMed1996

Determinants of activation by complement of group II phospholipase A2 acting against Escherichia coli.

Prompt killing of many strains of Escherichia coli during phagocytosis in vitro by isolated polymorphonuclear leukocytes (PMN) requires the presence of nonlethal doses of nonimmune serum (B. A. Mannion, J. Weiss, and P. Elsbach, J. Clin. Invest. 86:631-641, 1990). Because this requirement is bypassed in a phospholipase A (PLA)-rich mutant (pldA ) of E. coli, we have examined the effect of serum on bacteria] phospholipid (PL) degradation during phagocytosis of wild-type (pldA+) and PLA-deficient (pldA) E. coli. In parallel with increased killing, nonlethal doses of serum increased the degradation of prelabeled bacterial PL during phagocytosis by two- to fivefold, to nearly the same levels (ca. 50 to 60%) as those produced during phagocytosis of E. coli pldA in the absence of serum. The effects on the E. coli pldA mutant imply that there is a serum-mediated enhancement of granule-associated group II PMN PLA2 activity. At the same doses, serum promoted action against E. coli in the presence of purified rabbit and human group II PLA2 but did not activate bacterial PLA. Related PLA2s that lack specific structural determinants needed for optimal activity against E. coli treated with the bactericidal/permeability-increasing protein (BPI) of PMN are also less active than wild-type group II PLA2 against serum-treated E. coli. Treatment of E. coli with C7- or C9-depleted serum did not enhance bacterial killing or PL degradation during phagocytosis or the action of purified PLA2. In summary, these findings suggest that (i) nonlethal assemblies of the membrane attack complex promote intracellular killing and destruction of E. coli ingested by PMN, in part by promoting the action of granule-associated PLA2 against ingested bacteria, and (ii) structural determinants first implicated in PLA2 action against BPI-treated E. coli are also important in PLA2 action in concert with other host defense systems, such as complement.

Animals↗
PubMed1996

Potent CD14-mediated signalling of human leukocytes by Escherichia coli can be mediated by interaction of whole bacteria and host cells without extensive prior release of endotoxin.

How invading microorganisms are detected by the host has not been well defined. We have compared the abilities of Escherichia coli and lipopolysaccharides (LPS) purified from these bacteria to prime isolated neutrophils for phorbol myristate acetate-stimulated arachidonate release, to trigger respiratory burst in 1% blood, and to increase steady-state levels of tumor necrosis factor alpha mRNA in whole blood. In all three assays, bacteria were > or = 10-fold more potent than equivalent amounts of LPS and could trigger maximal cellular responses at ratios as low as one bacterium per 20 to 200 leukocytes. Both E. coli and LPS-triggered responses were enhanced by LPS-binding protein and inhibited by an anti-CD14 monoclonal antibody and the bactericidal/permeability-increasing protein (BPI). However, whereas O polysaccharide did not affect the potency of isolated LPS, intact E. coli carrying long-chain LPS (O111:B4) was less potent than rough E. coli (J5). Furthermore, material collected by filtration or centrifugation of bacteria incubated under conditions used to trigger arachidonate release or chemiluminescence was 5- or 30-fold less active, respectively, than whole bacterial suspensions. Extracellular BPI (not bound to bacteria) inhibited bacterial signalling, but BPI bound to bacteria was much more potent. Taken together, these findings indicate that E. coli cells can strongly signal their presence to human leukocytes not only by shedding LPS into surrounding fluids but also by exposing endotoxin at or near their surface during direct interaction with host cells.

Acute-Phase Proteins↗
PubMed1996

Inhibin A and inhibin B are inversely correlated to follicle-stimulating hormone, yet are discordant during the follicular phase of the rat estrous cycle, and inhibin A is expressed in a sexually dimorphic manner.

Inhibin A and inhibin B are related dimeric protein hormones and endocrine regulators of the reproductive axis. Specifically, inhibin inhibits FSH secretion from the anterior pituitary. The inhibins are synthesized by the gonads and are themselves modulated by FSH. Although the activity of these ligands has been well characterized, the circulating concentrations of dimeric inhibin A and dimeric inhibin B have not previously been reported for the rat. Our group examined the serum concentration of inhibin A and inhibin B in normally cycling female rats, male rats, and in gonadectomized animals. Both inhibin isoforms are detected in intact female rat serum. Interestingly, inhibin B, but not inhibin A, is detected in intact male rat serum. Neither inhibin isoform is detected in long-term castrate female or male rats. In normally cycling female rats, inhibin A was low on the morning of metestrus and rose steadily to a peak on proestrus. In contrast, inhibin B was elevated on the mornings of metestrus, diestrus, and proestrus. Both ligands persisted in the serum until proestrus evening. Serum inhibins then declined beginning at 2100 h (inhibin A) or 1800 h (inhibin B) on proestrus, and the concentrations reached a nadir on the morning of estrus (0600 h). The nadir coincided with the peak of the secondary FSH surge. Both inhibins rebounded later on the morning of estrus. The results of this study demonstrate that dimeric, ovarian-derived inhibin A and inhibin B circulate in the female rat. The inverse relationship of the inhibins during the secondary FSH surge is consistent with the hypothesis that they participate in the regulation of reproductive cyclicity. The differing patterns of inhibin A and inhibin B during the period of follicular development on metestrus and diestrus suggest different follicle sources or regulation of these molecules during this period. We further demonstrate that inhibin B is the dominant form of FSH regulating protein in the male rat.

Animals↗
PubMed1996

Gonadotropin-releasing hormone regulation of pituitary follistatin gene expression during the primary follicle-stimulating hormone surge.

Follistatin is produced in the gonadotrope and folliculostellate cells of the pituitary gland and is thought to indirectly regulate FSH biosynthesis and secretion through its ability to bind activin. Recent measurements of follistatin gene expression during the rat estrous cycle revealed a marked increase in pituitary follistatin messenger RNA (mRNA) levels at the time of the preovulatory FSH surge. This finding suggests a role for follistatin in the regulation of FSH at this dynamic time of the cycle. The aim of the present study was to identify the hormonal control mechanisms responsible for stimulating follistatin gene expression on proestrus. In particular, the roles of estrogen (E) and GnRH were assessed using an in vivo ovariectomized (OVX) animal model in which steroid priming results in daily gonadotropin surges. Follistatin mRNA and serum FSH levels were unchanged throughout the day in untreated OVX rats. E priming of OVX rats elicited a 2-fold elevation in follistatin mRNA levels between 1600-2000 h coincident with the peak of the E-induced FSH surge. To determine whether this effect of E on follistatin mRNA levels was the result of the direct or indirect effects of E on the pituitary, follistatin mRNA levels were examined in E-primed OVX rats that had been treated with pentobarbital at 1430 h (to block hypothalamic neurosecretion). Pentobarbital treatment prevented the E-induced increase in follistatin mRNA levels, suggesting that the effects of E are mediated via GnRH or other hypothalamic factors. The effects of GnRH on follistatin gene expression were examined further using an in vitro perifusion model. Proestrous or metestrous pituitaries were perifused for 8 h with pulsatile GnRH (one pulse per h), continuous GnRH, or medium only. Continuous GnRH treatment resulted in a significant elevation in follistatin mRNA levels in both proestrous and metestrous pituitaries, whereas pulsatile GnRH had no effect at either cycle stage. These results suggest that the proestrous GnRH surge is responsible at least in part for the elevation in pituitary follistatin mRNA levels that is associated with the primary FSH surge. GnRH-induced follistatin production on proestrus probably plays a role in the dynamic regulation of FSH at this time of the ovulatory cycle.

Animals↗
PubMed1996

Gonadotropin-releasing hormone regulates follicle-stimulating hormone-beta gene expression through an activin/follistatin autocrine or paracrine loop.

The FSH beta gene is stimulated by low frequency pulses of GnRH, but is unaffected or suppressed when GnRH is applied at higher frequencies or continuously. The current studies explored the hypothesis that GnRH frequency-dependent regulation of FSH beta may be mediated by pituitary expression of activin, which stimulates FSH beta messenger RNA (mRNA), and follistatin, which blocks activin. Using a system of perifused male rat pituitary cells, a reciprocal relationship was observed between FSH beta and follistatin mRNAs in response to different patterns of GnRH treatment. Pulses of GnRH (5 min; 10 nM) applied every 60 min stimulated FSH beta mRNA 14.0-fold with no change in follistatin mRNA. Pulses of GnRH applied every 30 and 15 min elicited stepwise increases in follistatin mRNA and decreases in FSH beta mRNA, and continuous GnRH stimulated follistatin mRNA 4.1-fold, with no significant increase in FSH beta mRNA. Stimulation of FSH beta mRNA by hourly GnRH pulses (3.7-fold) was blocked in the presence of 30 ng/ml recombinant follistatin (0.8-fold), suggesting that GnRH stimulation of FSH beta mRNA requires endogenous activin. Treatment of plated pituitary cells with continuous GnRH for 24 h confirmed that secretion of follistatin protein rises (1.5-fold) coincident with follistatin mRNA (1.7-fold) under conditions that suppress FSH beta mRNA (9% of the control value). When male rats were infused through arterial cannulas for 6 h with continuous GnRH (100 nM) or recombinant follistatin (5 micrograms/h), continuous GnRH suppressed FSH beta mRNA levels to 50% of the control value, and follistatin decreased expression to 61% of the control value. We conclude that GnRH stimulation of FSH beta mRNA is activin dependent, and pituitary follistatin production is a major pathway by which higher GnRH pulse frequencies suppress FSH beta mRNA. Changes in activin or follistatin tone, therefore, provide a mechanism by which LH and FSH can be differentially regulated by GnRH in a variety of physiological and pathophysiological conditions.

Activins↗
PubMed1996

Latex allergens in tire dust and airborne particles.

The prevalence and severity of latex allergy has increased dramatically in the last 15 years due to exposure to natural rubber products. Although historically this health risk has been elevated in hospital personnel and patients, a recent survey has indicated a significant potential risk for the general population. To obtain a wide-spread source for latex exposure, we have considered tire debris. We have searched for the presence of latex allergens in passenger car and truck tire tread, in debris deposited from the atmosphere near a freeway, and in airborne particulate matter samples representative of the entire year 1993 at two sites in the Los Angeles basin (California). After extraction of the samples with phosphate buffered saline, a modified-ELISA inhibition assay was used to measure relative allergen potency and Western blot analyses were used to identify latex allergens. The inhibition studies with the human IgE latex assay revealed inhibition by the tire tread source samples and ambient freeway dust, as well as by control latex sap and latex glove extracts. Levels of extractable latex allergen per unit of protein extracted were about two orders of magnitude lower for tire tread as compared to latex gloves. Western blot analyses using binding of human IgE from latex-sensitive patients showed a band at 34-36 kDa in all tire and ambient samples. Long Beach and Los Angeles, California, air samples showed four additional bands between 50 and 135 kDa. Alternative Western blot analyses using rabbit IgG raised against latex proteins showed a broad band at 30-50 kDa in all samples, with additional bands in the urban air samples similar to the IgE results. A latex cross-reactive material was identified in mountain cedar. In conclusion, the latex allergens or latex cross-reactive material present in sedimented and airborne particulate material, derived from tire debris, and generated by heavy urban vehicle traffic could be important factors in producing latex allergy and asthma symptoms associated with air pollution particles.

Air Pollutants↗
PubMed1996

Aging of the brain-testicular axis: reproductive systems of healthy old male rats with or without endocrine stimulation.

To test the hypothesis that endocrine declines in males are incidental to disease, 24 gonadally intact old (22-24 months) rats were selected on the basis of good general health and assigned to one of three groups. One group of aged males was left untreated for comparison with an untreated control group of young adult males. Results from multiple measures of sociosexual behavior and reproductive physiology indicated that endocrine declines in males are not simply a by-product of increased disease incidence with aging. The untreated old animals showed clear decrements on all 13 measures of hypothalamic-pituitary- testicular (HPT) activity. The other two groups of old males were used to compare responsiveness of the aging HPT axis in healthy males to supplements with a typical exogenous (ExT) androgen regimen (300 micrograms testosterone/kg body wt/SC/daily/6 weeks) or to social stimulation (brief daily exposure to an inaccessible estrous female) for additional episodes of endogenous (EnT) hormone. Neither treatment restored our disease-free old male rats to levels approximating those of untreated young adults. Nonetheless, both treatments activated the aging HPT axis. EnT males showed increases in sociosexual behaviors, growth of androgen-sensitive bulbospongiosus muscle, and elevation of epididymal sperm reserves. ExT males, on the other hand, experienced a more foreboding hypertrophy of the ventral prostate gland. Our conclusion is that endocrine aging in males is ubiquitous and inevitable. Still, aged androgen-sensitive systems of healthy old rats retain notable capacity, particularly, for endogenous activation. Evidence points to functional responses by healthy aged males to the presence of sexually receptive females that, although not quantitatively the same, are qualitatively similar to the responses of young adult males.

Aging↗
PubMed1996

A unique case of long-term survival in a male patient with malignant melanoma of the distal urethra.

Primary malignant melanoma of the urethra in male patients is a rare entity, noted to have a dismal prognosis in recent reviews. No case of long-term disease-free survival in patients with primary malignant melanoma has been previously reported. We report the first such case, and review briefly the factors that could have contributed to our patient's long-term survival. We also illustrate the precursor lesion present six years prior to diagnosis.

Disease-Free Survival↗
PubMed1996

The gonadotropin genes: evolution of distinct mechanisms for hormonal control.

The glycoprotein hormones (TSH, FSH, LH, CG) are structurally related proteins with diverse physiologic functions. This family of hormones offers an opportunity to address fundamental questions concerning how gene expression is regulated in a cell-specific manner and in response to different hormones. For example, the alpha-subunit gene is expressed in several different pituitary cell types (gonadotropes and thyrotropes) as well as in the placenta. Because it must be coordinantly expressed with the different beta-subunit genes, the alpha-gene provides an interesting model for multihormonal control which varies in a cell-type specific manner. Many of the promoter regulatory DNA sequences and cognate transcription factors in the alpha-gene have been identified. These studies reveal a remarkable series of composite regulatory elements that interact with families of transcription factors that are still being characterized. In contrast, the beta-subunit genes are notable for restricted cell-type expression and more limited hormonal regulation that reflects their individual physiologic roles. The TSH beta gene is expressed only in thyrotropes where, in conjunction with the alpha-gene, it is subject to transcriptional repression by thyroid hormone. The FSH beta gene is expressed in gonadotropes where its expression is controlled primarily by activin and inhibin, with additional regulation by GnRH. The LH beta gene is also expressed in gonadotropes, but it is more dependent upon GnRH input and its expression is unaffected by the activin/inhibin system. The CG beta gene evolved recently from the LH beta gene and in the process, the CG beta promoter acquired new regulatory elements that favor its expression in the placenta rather than the pituitary gland. Less is known about the regulatory elements in the beta genes, in part because highly differentiated cells are required for their normal regulation. This chapter reviews the regulation of this family of genes with an emphasis on recent studies from our laboratory involving the gonadotropins (LH, FSH, CG). Concomitant with our advancing understanding of how the gonadotropin genes are regulated, we are also learning about genetic causes of gonadotropin deficiency syndromes.

Base Sequence↗
PubMed1995

Overall and site-specific risk of malignant melanoma associated with nevus counts at different body sites: a multicenter case-control study of the German Central Malignant-Melanoma Registry.

A large number of benign melanocytic nevi is the major risk factor for malignant melanoma (MM). In a multicenter case-control study, the number of common (CN) and clinically atypical (AN) nevi were counted separately at individual sites in 278 melanoma patients and 278 age- and gender-matched non-melanoma controls. Relative risk (RR) adjusted for age and sex was calculated. In men as well as women, the number of CN on the legs was the best predictor of overall melanoma risk. In men, RR for developing MM when > or = 1 AN were present on the trunk was 4-fold (vs. none). In women, presence of AN on the arms increased RR 9.5-fold. For men and women combined, after adjusting for age and gender, the RR for developing MM on the trunk and on the legs was best predicted by counts of CN at the respective body region. However, high counts of CN on the arms were associated with high melanoma risk on the legs (somewhat lower on the trunk). For AN, no site-specificity of melanoma risk was found. Our data suggest that nevus counts of the legs are the best predictor of overall melanoma risk if total body nevus counts are not feasible. Although high counts of CN on the trunk and legs are associated with a higher risk of developing MM at the respective site than at another site, our data do not unequivocally support a direct site-specific melanoma risk.

Arm↗
PubMed1995

A defined region of loss of heterozygosity at 11q23 in cutaneous malignant melanoma.

Karyotypic and molecular data indicate that genetic alterations of the long arm of chromosome 11 (11q) may be involved in malignant melanoma. To test this we analyzed 5 polymorphic microsatellite repeats on 11q using a PCR-based assay for loss of heterozygosity in normal and tumor tissues from 24 individuals with cutaneous malignant melanoma of various stages. Our findings indicate that a tumor suppressor gene that plays a role in malignant melanoma is located on the long arm of chromosome 11, likely within a 51 cM region at 11q23. Its loss appears to be a late event in tumor progression and may serve as an indicator for a less favorable clinical outcome.

Adult↗
PubMed1995

Antibacterial proteins of granulocytes differ in interaction with endotoxin. Comparison of bactericidal/permeability-increasing protein, p15s, and defensins.

Bactericidal/permeability-increasing protein (BPI), antibacterial 15-kDa protein isoforms (p15s), and defensins (neutrophil peptides or NPs) are granule-associated antibacterial proteins of polymorphonuclear leukocytes (PMN) that have both direct and synergistic growth inhibitory activity against Gram-negative bacteria. In this study, we have compared in vitro the abilities of these antibacterial proteins, alone and in combination, to inhibit the endotoxic activity of isolated LPS and whole bacteria. All three proteins blocked endotoxin activity in: 1) the Limulus amoebocyte lysate assay, 2) priming of PMN for enhanced arachidonate release, and 3) stimulating leukocyte oxidase activity in 1% blood. However, the proteins differ markedly in both relative potency (BPI >> p15s = NP1) in the presence of the plasma LPS-binding protein and in the range of LPS chemotypes that can be inhibited. BPI potently neutralizes LPS of any chemotype, but p15s and defensins are less active against long-chain (S-type) LPS. In whole blood ex vivo, the p15s and NP1 are approximately 1000-fold less potent than BPI, but at subinhibitory doses act in synergy with BPI to inhibit the TNF-inducing activity of a serum-resistant encapsulated strain of Escherichia coli (K1/r). The anti-endotoxic effects of p15 and NP1 against E. coli K1/r in whole blood appear secondary to growth arrest, because, in marked contrast to BPI, they are not evident against nonviable bacteria (pretreated with antibiotic) nor isolated LPS. Thus, BPI stands out for its ability to inhibit isolated or bacterial LPS under physiologic conditions. However, p15s and defensins may also contribute to suppression of endotoxic signaling by Gram-negative bacteria via synergistic (with BPI) growth inhibition upon extracellular release of these proteins from PMN during inflammation.

Animals↗
PubMed1995

Mutation and expression of TP53 in malignant melanomas.

Mutations of the TP53 gene are the most common genetic alterations in human malignancies. Overexpression of the p53 protein has been reported in high frequencies in all types of skin cancer. To determine the role of TP53 in the pathogenesis of malignant melanoma, we investigated the expression of p53 in 12 cell lines and 145 primary and metastatic lesions by immunohistochemistry. Overexpression of p53 was predominantly detected in the cytoplasm of the cells in 96 (66%) tumor and 12 (93%) cell lines. In contrast to findings in other tumor types, in melanomas immunoreactive cells were found in clusters or as scattered single cells. In primary melanomas, the frequency of p53 overexpression did not correlate with tumor thickness. Nucleotide sequencing of TP53 genes of 24 melanoma tumors/cell lines demonstrated point mutations in seven samples, all coding for mutant p53 protein species. The frequency of TP53 alterations of 20%-30% is lower than in other skin tumor types. Notably, immunohistochemistry was not a suitable method to distinguish overexpression of wild-type p53 from mutant species, since cell lines/tumors with TP53 mutations did not show distinctive staining patterns. The mutation pattern in six out of seven lesions was similar to that caused by ultraviolet light damage. This finding may be regarded a further indication for a pathogenetic role of UV light damage in at least a subgroup of malignant melanomas.

Antibodies, Monoclonal↗