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Biomedical subjects

J Bell

Publications and source records attributed to J Bell.

At least 109 records · Page 6Linked to original sources
PubMed1999

Human immunodeficiency virus infection, inducible nitric oxide synthase expression, and microglial activation: pathogenetic relationship to the acquired immunodeficiency syndrome dementia complex.

The regional expression of immune-mediated and neurotoxic events in the human immunodeficiency virus (HIV)-infected brain in relationship to the acquired immunodeficiency syndrome (AIDS) dementia complex (ADC) and brain pathology remains uncertain. The extent of gp41, inducible nitric oxide synthase (iNOS), and HLA-DR expression was examined in the frontal lobe and basal ganglia of 25 patients at varying stages of ADC. The expression of gp41 and iNOS was present predominantly in perivascular cells and most often in the basal ganglia. Staining for gp41 correlated significantly with iNOS in the basal ganglia, whereas the severity of staining for gp41 and iNOS in the basal ganglia and white matter was significantly greater in subjects with moderate to severe dementia compared with those with milder impairment. The degree of macrophage staining in the white matter and basal ganglia also correlated significantly with ADC severity and was more abundant than gp41 or iNOS staining, particularly in the white matter. Logistic regression analysis revealed that staining for iNOS and gp41 increased linearly with ADC severity and was significantly more abundant in the basal ganglia compared with the white matter. Double-immunolabeling studies colocalized iNOS predominantly to macrophage/microglia and to gp41-positive cells. The expression of iNOS and gp41 in the basal ganglia combined with immune activation contributes to the development and progression of the clinical syndrome.

AIDS Dementia Complex↗
PubMed1999

Mannose 6-phosphate/insulin-like growth factor II receptor mediates the growth-inhibitory effects of retinoids.

Both retinoids and the mannose 6-phosphate/insulin-like growth factor-II receptor (M6P/IGF2R) have been shown to play an important role in controlling cell growth during embryonic development and oncogenesis. Our recent work (Kang et al., Proc. Natl. Acad. Sci. USA, 94: 13671-13676, 1997; Kang et al., Proc. Natl. Acad. Sci. USA, 95: 13687-13691, 1998) revealed a direct biochemical interaction between retinoic acid (RA) and the M6P/IGF2R, thereby leading us to hypothesize that the M6P/IGF2R may mediate a growth-inhibiting effect of RA. To test this hypothesis, cell growth and apoptosis in response to RA and various receptor-selective retinoids were examined in cells that lack or overexpress the M6P/IGF2R. RA and those retinoids capable of binding to the M6P/IGF2R induced a remarkable morphological change with characteristics of round shape and reduced spreading, apoptosis, and growth inhibition in stably transfected mouse P388D1 cells overexpressing the M6P/IGF2R but not in the M6P/IGF2R-deficient P388D1 cells. These effects of RA were neither blocked by a potent RA nuclear receptor (RAR) antagonist (AGN193109), nor mimicked by a selective RAR agonist (TTNPB), suggesting that the observed effects of RA are independent of RARs. Similar effects of the retinoids were observed in cultured neonatal rat cardiac myocytes that have high levels of the M6P/IGF2R. Furthermore, overexpression of the M6P/IGF2R in a RA-resistant cancer cell line (HL-60R) that lacked functional RARs gave the cells a susceptibility to RA-induced apoptosis. These data suggest that the M6P/ IGF2R may play an important role in mediating retinoid-induced apoptosis/growth-inhibition and provide insight into the similar biological effects of RA and the M6P/IGF2R on fetal development and carcinogenesis.

Actin Cytoskeleton↗
PubMed1999

Intraoperative use of the absorbable fibrin adhesive bandage: long term effects.

PURPOSE: The absorbable fibrin adhesive bandage (AFAB) reduces acute blood loss in experimental trauma models, but the effects on wound healing and subsequent function have heretofore not been investigated. Retropubic prostatectomy was selected to evaluate short and long term effects of using the AFAB intraoperatively. MATERIALS AND METHODS: Dogs undergoing prostatectomy were randomly assigned to one of four treatments: CONTROL- sponges and manual pressure were applied after transecting the prostatic pedicles. Sponges were removed when the prostate was delivered. Vessels were isolated and ligated if bleeding continued after removal. AFAB- hemostatically active bandages were applied to the prostatic bed prior to sponges and pressure. Additional bandages were applied at the urethrovesical junction after completing the anastomosis. PLACEBO- visually identical (hemostatically inert) bandages were applied in an identical fashion. LIQUID SEALANT- concentrated thrombin and fibrinogen solution was applied to the vessels prior to sponges and pressure. Additional sealant solution was applied around the anastomosis. RESULTS: Blood loss and time to achieve hemostasis were significantly less in the AFAB group compared with the other treatments. There were no differences in days to anastomotic integrity, continence, or intra-abdominal adhesions at necropsy six weeks later. CONCLUSIONS: The AFAB can reduce surgery time and blood loss, with no decrement in wound healing or subsequent function.

Animals↗
PubMed1999

Implementation of a pet visitation program in critical care.

We have no quantitative research data to document that these visits are actually helpful to patients in any measurable way, although we certainly hope to have some soon. However, observations of staff members and evaluations from participants in the program have been quite positive thus far. The program has been in place for more than 2 years, and about 30 pets have visited so far, including 28 dogs and 2 cats. Implementing a pet visitation program for critically ill patients affords healthcare providers the opportunity to offer a unique and humanistic therapeutic intervention to appropriate patients. Although it is a time-consuming endeavor, it has been well received by those patients and families that have participated in pet visits. Critically ill patients are often denied many simple pleasures because they are in physiological crisis. Such patients experience loneliness, isolation, depression, and lack of emotional support. Pet visitation is one way to address these common problems of ICU patients. For this reason, pet visitation will remain a therapeutic option for the support of our critically ill patients.

Animals↗
PubMed1998

Retinoic acid alters the intracellular trafficking of the mannose-6-phosphate/insulin-like growth factor II receptor and lysosomal enzymes.

Previously, we showed that retinoic acid (RA) binds to the mannose-6-phosphate/insulin-like growth factor II receptor (M6P/IGF2R) with high affinity, suggesting that M6P/IGF2R may be a receptor for RA. Here, we show that RA, after 2-3 h of incubation with cultured neonatal-rat cardiac fibroblasts, dramatically alters the intracellular distribution of M6P/IGF2R as well as that of cathepsin B (a lysosomal protease bearing M6P). Immunofluorescence techniques indicate that this change in intracellular distribution is characterized by a shift of the proteins from the perinuclear area to cytoplasmic vesicles. The effect of RA was neither blocked by an RA nuclear receptor antagonist (AGN193109) nor mimicked by a selective RA nuclear-receptor agonist (TTNPB). Furthermore, the RA-induced translocation of cathepsin B was not observed in M6P/IGF2R-deficient P388D1 cells but occurred in stably transfected P388D1 cells expressing the receptor, suggesting that the effect of RA might be the result of direct interaction with M6P/IGF2R, rather than the result of binding to the nuclear receptors. These observations not only support the idea that M6P/IGF2R mediates an RA-response pathway but also indicate a role for RA in control of intracellular trafficking of lysosomal enzymes. Therefore, our observations may have important implications for the understanding of the diverse biological effects of retinoids.

Animals↗
PubMed1998

Emergence and epidemiology of vancomycin-resistant enterococci in Australia.

Enterococci with acquired resistance to vancomycin and other glycopeptides (VRE) have emerged and spread rapidly through Europe and the United States since 1988. The first isolate of VRE in Australia occurred in 1994. Only one case was noted in 1995. Since March 1996 there has been a steady increase in the number of reports of VRE throughout the country. To August 1998 there have been 69 documented strains or clusters of strains detected in patients with documented infection, and about 3 times as many strains have been detected through screening procedures of contacts or in risk groups. 19% of strains whose source was known were blood isolates, while 34% came from urine and 47% came from other specimens. The strains have been found in 26 institutions in 10 widely separated cities or regions of the country (in 6/8 states or territories), without any obvious temporal associations in their appearance. All strains appear to have arisen locally except for one strain imported from the United Kingdom. Furthermore there was no direct evidence of interhospital transfer of strains. All clinical strains were examined by PCR to confirm species and to test for the presence of known vancomycin-resistance genes. Of the 69 strains, 42 were vanB E. faecium, 12 were vanA E. faecium, 9 were vanB E. faecalis, 3 were vanA E. faecalis. Three were negative for vanA, vanB, vanC1, vanC2/C3 and vanD. PGFE profiles on 38 strains have revealed at least 8 types of vanB E. faecium, 6 of vanA E. faecium, 4 of vanB E. faecalis and 2 of vanA E. faecalis. Isolates containing vanA always had different profiles from those containing vanB. Clinical clustering was confirmed by PFGE, and supported by extended antibiogram. 14 of 15 E. faecalis were ampicillin susceptible compared to only 2 of 54 E. faecium. One E. faecalis strain was beta-lactamase positive. The epidemiology of VRE in Australia appears to be different from that of Europe or the United States, since vanB E. faecium predominates and strains have appeared in diverse locations independently and are highly polyclonal.

Anti-Bacterial Agents↗
PubMed1998

Doctors detected self-administering opioids in New South Wales, 1985-1994: characteristics and outcomes.

OBJECTIVE: To describe the characteristics and outcomes of doctors whose drug authorities were withdrawn as a result of self-administering opioids for non-medical purposes. DESIGN: Retrospective review of New South Wales Health Department information relating to all doctors whose authorities to possess, supply, prescribe or administer drugs of addiction had been withdrawn in the period 1985 to 1994 as a result of confirmed self-administration of opioids. OUTCOME MEASURES: Age, sex, geographical location and practice category at the time of intervention; drugs used; period of opioid use before authority withdrawal; means of detection; and registration status as at August 1995. RESULTS: From 1985 to 1994, 79 doctors had their drug authorities withdrawn (0.4% of the NSW medical profession in 1994). The groups significantly over-represented were general practitioners and those aged 30-39 years. Pethidine was the main drug used (66 doctors; 84%). Drug use for more than two years before detection was reported by 34 (43%) doctors. Community pharmacists were the source of reports leading to detection of 28 (35%) doctors. As at August 1995, 27 (34%) of the study group were not practising; 10 (13%) had died. CONCLUSION: Outcomes for these doctors were poor. There was substantial attrition from practice and a high mortality rate.

Adult↗
PubMed1998

Hydrogen peroxide activates mitogen-activated protein kinases and Na+-H+ exchange in neonatal rat cardiac myocytes.

Reperfusion of cardiac tissue after an ischemic episode is associated with metabolic and contractile dysfunction, including reduced tension development and activation of the Na+-H+ exchanger (NHE). Oxygen-derived free radicals are key mediators of reperfusion abnormalities, although the cellular mechanisms involved have not been fully defined. In the present study, the effects of free radicals on mitogen-activated protein (MAP) kinase function were investigated using cultured neonatal rat ventricular myocytes. Acute exposure of spontaneously beating myocytes to 50 micromol/L hydrogen peroxide (H2O2) caused a sustained decrease in contraction amplitude (80% of control). MAP kinase activity was measured by in-gel kinase assays and Western blot analysis. Acute exposure to H2O2 (100 micromol/L, 5 minutes) resulted in sustained MAP kinase activation that persisted for 60 minutes. Catalase, but not superoxide dismutase, completely inhibited MAP kinase activation by H2O2. Pretreatment with chelerythrine (10 micromol/L, 45 minutes), a protein kinase C inhibitor, or genistein (75 micromol/L, 45 minutes) or herbimycin A (3 micromol/L, 45 minutes), tyrosine kinase inhibitors, caused significant inhibition of H2O2-stimulated MAP kinase activity (51%, 78%, and 45%, respectively, at 20 minutes). Brief exposure to H2O2 also stimulated NHE activity. This effect was completely abolished by pretreatment with the MAP kinase kinase inhibitor PD 98059 (30 micromol/L, 60 minutes). These results suggest that low doses of H2O2 induce MAP kinase-dependent pathways that regulate NHE activity during reperfusion injury.

Animals↗
PubMed1998

Young people in transition: the relationship between homesickness and self-disclosure.

Whilst the majority of new students cope well with the transition to university, a number experience levels of homesickness which can adversely affect the process of adaptation. In this study the relationship between homesickness and self-disclosure, seen as a possible mediating factor, was assessed in a sample of 83 students (mean age 18.0541 years, s.d.=7.055 months) at the start of their first semester and then 6 weeks later. The results showed that homesickness declined during the semester whilst levels of self-disclosure increased. A significant negative association was found between levels of self-disclosure and homesickness at both time periods. High self-disclosers experienced a significantly greater reduction in homesickness than low self-disclosers. The results showed the importance of the socially-mediated and supportive benefits of self-disclosure during this life transition.

Adaptation, Psychological↗
PubMed1998

Help-seeking decisions among men with impotence.

OBJECTIVES: There is a paucity of valid contemporary data concerning the proportion of impotent men who seek treatment. The aim of this study was to determine the proportion of impotent men who sought treatment, from whom they sought treatment, and their reasons for seeking or not seeking treatment. METHODS: A self-administered survey of 5198 randomly selected men between 50 and 76 years old, living in four rural counties in central New York State, was used. RESULTS: The sample included 649 men who reported having experienced impotence in the 6 months preceding the study period (November 1996 to June 1997). The mean age of these men and mean duration of impotence were 64.5+/-7.2 and 4.9+/-4.6 years, respectively. Two hundred five men (31.6%) had sought treatment, 432 (66.6%) had not, and 12 (1.8%) neglected to answer the question. Most first consulted with either their primary care provider (44.7%) or a urologist (40.7%). Among those who had sought treatment, 36.3% were satisfied, 48.4% were dissatisfied, and 15.2% were neither satisfied nor dissatisfied with the results. The primary reasons for seeking treatment were to improve their self-esteem (44.8%), awareness of a new treatment (33.4%), partner insistence ( 11.3%), and coverage by their health insurance (10.4%). The reasons for not seeking treatment were embarrassment (29.8%), ignorance or misinformation (45.2%), and lack of affordability (25.0%). CONCLUSIONS: Despite increased availability of effective treatment, most men with impotence do not seek treatment, and among those who do, only 36.3% are satisfied with the results.

Aged↗
PubMed1998

Medical implications of understanding complex disease traits.

The application of genetic mapping to human disease gene identification has led to the definition of many linkages and a few disease genes in complex traits over the past two years. Its application has also increased to include aspects of pharmacogenetics relating to pharmacokinetics and pharmacodynamics.

Animals↗
PubMed1998

Manoalide, a phospholipase A2 inhibitor, inhibits arachidonate incorporation and turnover in brain phospholipids of the awake rat.

The Fatty Acid method was used to determine whether incorporation of plasma radiolabeled arachidonic acid into brain phospholipids is controlled by phospholipase A2. Awake rats received an i.v. injection of a phospholipase A2 inhibitor, manoalide (10 mg/kg), and then were infused i.v. with [1-(14)C]arachidonate or [3H]arachidonate. Animals were killed after infusion by microwave irradiation, and tracer distribution was analyzed in brain phospholipid, neutral lipid and acyl-CoA pools. Calcium-independent phospholipase A2 activity in brain homogenate was reduced by manoalide, whereas phospholipase C activity was unaffected. At 60 min but not at 20 or 40 min after its injection, manoalide had significantly decreased by 50% incorporation of unesterified arachidonate into and turnover within brain phospholipids, taking into account dilution of the brain arachidonoyl-CoA pool by recycled arachidonate. Manoalide also increased by 100% the net rate of unesterified arachidonate incorporation into brain triacylglycerol. This study indicates that manoalide can be used to inhibit brain phospholipase A2 in vivo, and that phospholipase A2 plays a critical role in arachidonate turnover in brain phospholipids and neutral lipids.

Acyl Coenzyme A↗
PubMed1998

Selective acceleration of arachidonic acid reincorporation into brain membrane phospholipid following transient ischemia in awake gerbil.

Awake gerbils were subjected to 5 min of forebrain ischemia by clamping the carotid arteries for 5 min and then allowing recirculation. Radiolabeled arachidonic or palmitic acid was infused intravenously for 5 min at the start of recirculation, after which the brains were prepared for quantitative autoradiography or chemical analysis. Dilution of specific activity of the acyl-CoA pool was independently determined for these fatty acids in control gerbils and following 5 min of ischemia and 5 min of reperfusion. Using a quantitative method for measuring regional in vivo fatty acid incorporation into and turnover within brain phospholipids and determining unlabeled concentrations of acyl-CoAs following recirculation, it was shown that reperfusion after 5 min of ischemia was accompanied by a threefold increase compared with the control in the rate of reincorporation of unlabeled arachidonate that had been released during ischemia, whereas reincorporation of released palmitate was not different from the control. Selective and accelerated reincorporation of arachidonate into brain phospholipids shortly after ischemia may ameliorate specific deleterious effects of arachidonate and its metabolites on brain membranes.

Acyl Coenzyme A↗