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Biomedical subjects

R Hu

Publications and source records attributed to R Hu.

At least 91 records · Page 5Linked to original sources
PubMed1996

Epidemiology of incident spinal fracture in a complete population.

STUDY DESIGN: Cross-section observational study of incident spinal fractures using an administrative data-base. OBJECTIVES: To identify and define all patients who have spinal fractures within a complete population. SUMMARY OF BACKGROUND DATA: The true incidence of spinal column and cord injury is not known. Previous studies have been institutional or practice based. Accurate information concerning the magnitude of the spinal injury population and their characteristics may provide more rational basis for public health decision making and resource allocation. METHODS: The study dates were April 1, 1981 to March 31, 1984. Using the Manitoba Health Services Insurance Plan database, all patients with ICD-9-CM coding of 805.x and 806.x (spinal column fracture with and without spinal cord injury) were identified. Incidence rates, age and gender distribution, and ambulatory and hospital contracts were identified. Hospital discharge abstracts were used to classify mechanisms of injury, associated injuries, and length of stay. RESULT: The annual incidence rate of spinal fracture was 64 per 100,000. Two thousand sixty-three patients were identified, with 944 being admitted to the hospital. There were two peaks of incidence occurring in young men and elderly women. Of the hospitalized patients, 182 had cervical injury, 286 had thoracic fracture, and 403 had injury in the lumbosacral spine Associated injuries occurred in 38% of hospitalized patients. Length of stay was an average of 38.5 days. Overall mortality was 41%. Neurologic injury occurred in 122 patients. CONCLUSIONS: Ambulatory care of spine injuries is more common than hospital care. Two peaks of incidence occur-in young men and elderly women. Future decisions for research, public health policy, and resource allocation can be based on these data.

Adolescent↗
PubMed1996

HIV-1 gp160 induces transforming growth factor-beta production in human PBMC.

Transforming growth factor-beta (TGF-beta) is a multifunctional cytokine secreted by many mononuclear cells in peripheral blood (PBMC) and has diverse effects on cellular and humoral immunity. Increased TGF-beta mRNA expression has been reported in PBMC of HIV-infected patients, but the mechanism by which HIV induces TGF-beta secretion is unknown. In this study, we observed that HIV gp160 could induce significant TGF-beta secretion and TGF-beta mRNA expression in PBMC from HIV-seronegative healthy donors. The cellular source of TGF-beta was attributed to non-T cells, presumably monocytes. Specificity of secreted TGF-beta was confirmed by the addition of anti-TGF-beta mAb which abrogated the proliferative response of CCL-64 cells by gp160-treated culture supernatants. Soluble CD4 blocked the gp160-induced TGF-beta production, suggesting that CD4-gp160 interaction is required to induce TGF-beta production. Our results suggest that HIV-1 gp160 may contribute to the immune defects in HIV infection by inducing TGF-beta secretion.

Antibodies↗
PubMed1996

Dextrorphan reduces infarct volume, vascular injury, and brain edema after ischemic brain injury.

Focal cerebral ischemia confined to the cerebral cortex in the right middle cerebral artery (MCA) territory was induced by temporary ligation of the MCA and both common carotid arteries (CCAs). Reperfusion was initiated by releasing all three arterial occlusions after 90 min of ischemia. Infarct volume was morphometrically measured after triphenyltetrazolium chloride staining 24 h postischemia. Blood-brain barrier breakdown was assessed 4 h postischemia by measuring vascular permeability to fluorescein isothiocyanate-conjugated dextran (FITC-D), a macromolecule tracer. Ischemic brain edema was measured based on percent water content, 24 h postischemia. Dextrorphan (DX) 20-10 mg/kg given ip 15 min before ischemia reduced infarct volume in a dose-dependent manner with an apparent U-shaped dose-response curve; best protection was observed at 30 mg/kg. Posttreatment at 30 min, but not 60 min, was still effective. DX (30 mg/kg, given 15 min before ischemia) also reduced the postischemic increase in vascular permeability and brain edema in the right MCA cortex. Results from this study support the idea that NMDA receptor activation contributes to blood-brain barrier breakdown and brain edema after ischemic insults

Analysis of Variance↗
PubMed1996

Entomological correlates of Babesia microti prevalence in an area where Ixodes scapularis (Acari:Ixodidae) is endemic.

Zoonotic prevalence of Babesia microti Franca piroplasms infecting white-footed mice, Peromyscus leucopus Rafinesque, was determined at 34 sites in Rhode Island where nymphal blacklegged tick, Ixodes scapularis Say, densities ranged from low to hyperabundant (1.7-525.3 nymphs per hour of flagging). Babesia was only detected at sites where tick abundance was moderate to high (> 20 nymphs per hour of flagging) and appeared to exhibit a clumped distribution. Where B. microti was detected, the mean number of nymphal ticks collected per hour of flagging was 229.2 compared with a mean of 40.1 at sites where Babesia was not detected. By combining the spatial occurrence of Babesia with a tick density database in a geographic information system, it may be possible to predict the pattern of zoonotic and human infection with B. microti.

Animals↗
PubMed1996

Very delayed infarction after mild focal cerebral ischemia: a role for apoptosis?

The temporal evolution of cerebral infarction was examined in rats subjected to transient occlusion of both common carotid arteries and the right middle cerebral artery. After severe (90-min) ischemia, substantial right-sided cortical infarction was evident within 6 h and fully developed after 1 day. After mild (30-min) ischemia, no cortical infarction was present after 1 day. However, infarction developed after 3 days; by 2 weeks, infarction volume was as large as that induced by 90-min ischemia. These data suggest that infarction after mild focal ischemia can develop in a surprisingly delayed fashion. Some evidence of neuronal apoptosis was present after severe ischemia, but only to a limited degree. However, 3 days after mild ischemia, neurons bordering the maturing infarction exhibited prominent TUNEL staining, and DNA prepared from the periinfarct area of ischemic cortex showed internucleosomal fragmentation. Furthermore, pretreatment with 1 mg/kg cycloheximide markedly reduced infarction volume 2 weeks after mild ischemia. These data raise the possibility that apoptosis, dependent on active protein synthesis, contributes to the delayed infarction observed in rats subjected to mild transient focal cerebral ischemia.

Animals↗
PubMed1996

Small versus large diameter closed-section femoral nails for the treatment of femoral shaft fractures: is there a difference?

UNLABELLED: A retrospective series of 99 femoral shaft fractures treated by small diameter (10 and 11 mm) and large diameter (> 11 mm) closed section femoral nails from November 1989 to September 1993 was analyzed. No significant differences in the parameters of bony union and time to full weight bearing were seen between the two groups nor were there significant differences between the rate of secondary procedures. There were no broken nails in either group and there was no difference in the overall respiratory complication rate. CONCLUSION: No statistically significant differences existed between the small and large diameter groups except for the mean age and mean follow-up period. Small diameter nails can be used safely without the risk of nail breakage.

Adult↗
PubMed1996

Experimental Babesia microti infection in golden hamsters: immunoglobulin G response and recovery from severe hemolytic anemia.

We described the parasitemia, hematologic changes, and immunity developed by golden hamsters during 8 wk of infection with Babesia microti following experimental inoculation. All 8 hamsters used in this study were readily infected. Animals attained peak parasitemias asynchronously but within a 2-wk period. Most of the animals reached their peak parasitemia by 4 wk postinoculation, attaining a mean +/- SD of 21.9 +/- 9.4% infected erythrocytes (range = 20-35%). Red blood cell count, packed cell volume, and hemoglobin level were used to monitor the course of the hemolytic anemia experienced by infected hamsters. All 3 measures corresponded inversely to the parasitemia; significant hematologic changes (P = 0.0001) were observed during the 8 wk of monitoring. Although all hamsters suffered from severe hemolytic anemia, they also recovered within the same period. Golden hamsters developed a detectable anti-B. microti IgG response by 2 wk postinoculation. Individual animals typically attained peak antibody levels (> or = 1:8, 192) 1 wk after the peak parasitemia. Hamsters retained a high IgG titer (> or = 1:4,096), although parasitemias fell dramatically, fluctuating thereafter at low levels (< 5%).

Analysis of Variance↗
PubMed1996

[Changes in brain monoamine neurotransmitter in iron deficiency nonanemic rats].

An iron deficiency nonanemic rat model was established by feeding with low-iron diet (11.9 mg/kg) to study if there exists biochemical abnormality in brain tissues. Iron contents of the brain, activities of monoamine oxidase (MAO) in the corpus striatum, and the contents of monoamine neurotransmitter and its metabolite in the cerebral cortex and hippocampus were determined by DCP-AES technique, enzyme histochemical method, and high performance liquid chromatography with electrochemical detection (HPLC-ECD), respectively. Results showed that iron contents and activities of MAO in brain tissues of iron deficiency nonanemic rats reduced significantly, and contents of norepinephrine (NE) and 5-hydroxytryptamine (5-HT) in cerebral cortex were significantly higher than those of controls, while 5-hydroxydroxytryptamine acid (5-HIAA) metabolite of 5-HT in the hippocampus was lower than that of controls. It indicated that there existed metabolic abnormality of monoamine neurotransmitter in the brain tissues of iron deficiency nonanemic rats. Also, this study laid a biochemical basis for abnormal mental and behavioral development caused by iron deficiency.

Animals↗
PubMed1995

HIV gp120 inhibits T cell activation by interfering with expression of costimulatory molecules CD40 ligand and CD80 (B71).

One mechanism of the immune suppression in HIV infection has been postulated as being caused by the interaction of HIV envelope glycoprotein gp120 with CD4 molecules. Thus, pretreatment of purified peripheral blood T cells or CD4+ T cell clones with gp120 (or an anti-CD4 mAb) results in inhibition of anti-CD3 mAb-induced proliferative responses. In this study, we have analyzed the role of the interacting pairs of costimulatory molecules, CD28-B71 (CD80) and CD40 ligand (CD40L)-CD40, to elucidate further the mechanism of HIV gp120-induced inhibitory effects on T cell functions. Interactions between CD28-B71 and CD40L-CD40 were found to be essential for the anti-CD3 mAb-induced T cell proliferation, as demonstrated by up-regulation of B71 and CD40L and the ability of anti-B71 and anti-CD40L mAbs to inhibit this response. Pretreatment of CD4+ T cells with gp120 before CD3 ligation with anti-CD3 mAb resulted in failure of up-regulation of CD40L on T cells and B71 on APC. Exogenous addition of anti-CD28 mAb overcame the inhibitory effect of gp120 on anti-CD3 mAb-induced T cell proliferation. We conclude that binding of gp120 to CD4 molecules on T cells may interrupt the sequential cascade of intercellular interaction involving 1) Ag/MHC class II-TCR/CD4, 2) CD40L-CD40, and 3) B71-CD28. These studies indicate that the CD4-gp120 interaction results in dysregulation of expression of costimulatory molecules, CD40L, and B71 expression on T cells and APC, respectively, thereby contributing to the T cell hyporesponsiveness in HIV infection.

Antibodies, Monoclonal↗
PubMed1995

Mechanism of apoptosis in peripheral blood mononuclear cells of HIV-infected patients.

Lymphocytes from patients with HIV-infection have been shown to undergo accelerated spontaneous apoptosis. Binding of CD4 molecules by HIV envelope protein gp120 and anti-gp120 antibodies can lead to crosslinking of CD4 molecules (CD4XL) in vitro and conceivably in vivo. We have recently shown that CD4XL in vitro, when performed in unfractioned peripheral blood mononuclear cells (PBMC) on normal HIV seronegative donors, is by itself sufficient to induce T cell apoptosis (Blood 82:3392, 1993). To further examine the mechanisms involved in apoptosis, we have examined the expression of Fas antigen (Fas) using 3 color flow cytometry. Fas is a cell surface molecule known to mediate apoptosis-triggering signals. We induced CD4XL in PBMC obtained from normal donors, either by anti-CD4 mAb Leu3a or by HIV-1 envelope protein gp160. PBMC subpopulations were examined for Fas Ag expression and for apoptosis induction by flow cytometry. CD4XL was found to result in increased Fas expression as well as Fas mRNA in lymphocytes and the up-regulated Fas Ag was closely correlated with apoptotic cell death. CD4XL in PBMC also resulted in induction of the cytokines INF-tau and TNF-alpha in the absence of IL-2 and IL-4 secretion. Both these cytokins contributed to Fas Ag up-regulation and antibodies to TNF-alpha and INF-tau abrogated CD4XL-induced Fas up-regulation and T-cell apoptosis. These findings suggest that CD4XL occurring in vivo might play an important role in inducing an abberant cytokine profile (which has been observed in HIV infected individuals) and also in triggering of T-cell apoptosis.

Apoptosis↗
PubMed1995

Binding of human plasminogen and urokinase-type plasminogen activator to the Lyme disease spirochete, Borrelia burgdorferi.

Many bacteria that spread in the skin produce enzymes that digest extracellular matrix components. Borrelia burgdorferi spreads from a skin inoculation site to form the characteristic erythema migrans skin lesion. It was determined that B. burgdorferi does not produce collagenase, elastase, hyaluronidase, or other enzymes that digest extracellular matrix components. However, B. burgdorferi bound human plasmin, plasminogen (Pgn), and urokinase-type plasminogen activator (uPA). When spirochetes were sequentially incubated with Pgn and uPA, bioactive plasmin was generated on the surface of B. burgdorferi. B. burgdorferi did not produce an endogenous Pgn activator. Fluorochrome-conjugated uPA and Pgn colocalized to the terminus of the spirochete. In a mouse model, uPA-treated B. burgdorferi were more infectious than control spirochetes. Binding of host uPA and Pgn to form a bioactive extracellular matrix protease on B. burgdorferi represents a mechanism that could facilitate dissemination and localization of spirochetes to sites of vascular injury.

Animals↗
PubMed1995

Determining the duration of Ixodes scapularis (Acari: Ixodidae) attachment to tick-bite victims.

The duration of tick attachment is one factor associated with risk for human infection caused by several tick-borne pathogens. We measured tick engorgement indices at known time intervals after tick attachment and used these indices to determine the length of time that ticks were attached to tick-bite victims in selected Rhode Island and Pennsylvania communities where the agents of Lyme disease and human babesiosis occur. The total body length and width as well as the length and width of the scutum were measured on nymphal and adult female Ixodes scapularis Say removed from laboratory animals at 0, 12, 24, 36, 48, 60, and 72 h after their attachment. Three engorgement indices were calculated at each time interval. In addition, engorgement indices measurements were recorded for 504 ticks submitted to a commercial laboratory for pathogen detection testing between 1990 and 1992. No detectable change was observed in the average engorgement indices for either nymphal or adult ticks between 0 and 24 h of attachment using any of the engorgement indices. After 24 h of tick attachment, all engorgement indices continuously increased: average indices for nymphs attached 36, 48, and 60 h were significantly different from those attached < or = 24 h and from each other. Similarly, average engorgement indices for adult ticks attached < or = 36 h were significantly different from those attached for 48 h or more. More than 60% of tick-bite victims removed adult ticks by 36 h of attachment, but only 10% found and removed the smaller nymphal ticks within the first 24 h of tick feeding. The duration of tick attachment may serve as a useful predictor of risk for acquiring various infections, such as Lyme disease and babesiosis, transmitted by I. scapularis. Regression equations developed herein correlate tick engorgement indices with duration of feeding. A table containing specific engorgement index prediction intervals calculated for both nymphs and adults will allow the practitioner or clinical laboratory to use easily measured tick engorgement indices to predict transmission risk by determining the duration of feeding by individual ticks.

Animals↗
PubMed1995

Bone graft harvest site as a determinant of iliac crest strength.

Bone graft harvest site fracture can occur after removal of bone from the anterior iliac crest. No biomechanically proven guidelines for safe removal of bone exist. Cadaveric hemipelves were tested in a materials testing system machine, with the harvest site occurring 15-mm posterior to the anterosuperior iliac spine in 8 specimens and 30-mm posterior in 7 specimens. These pelves were then tested to failure by simulating avulsion fractures caused by the forces of the flexors of the hip. Average force at failure was 783 N (standard deviation, +/- 333 N) in the 15-mm group and 1917 N (standard deviation, +/- 735) in the 30-mm group. This study provides objective data which demonstrate that harvest 30 mm posterior to the anterosuperior iliac spine weakens the iliac crest less than harvest 15 mm posterior to the anterosuperior iliac crest. To minimize the possibility of iliac crest fracture after bone graft harvest, bone should be removed at least 30 mm from the anterior superior iliac spine.

Fractures, Bone↗
PubMed1995

mRNA expression of vimentin gene in lens of transgenic mouse and DNA amplification in human cataracts.

PURPOSE: To investigate the role of vimentin gene in cataractogenesis. METHODS: The 12.7kb chicken vimentin genes were microinjected into the male pronuclei of 918 fertilized mice eggs. 841 injected embryos were transferred into oviducts of pseudopregnant recipient females, of which 12 pregnant mice gave birth to 49 offspring mice. The integration and expression of exogenous gene in the offspring were analysed by Southern and Northern blot hybridizations. In the human senile cataract, the lens vimentin gene was analyzed with the chicken vimentin gene probe. RESULTS: It showed that four of F1 offspring were transgenic mice in which the chicken vimentin gene was integrated in their genomes. The transgenic band was 12kb, similar to the 12.7kb chicken vimentin fragment injected. One 2kb vimentin mRNA was visualized on E2 mouse lens blot, which revealed that the chicken vimentin gene was efficiently expressed in this transgenic mouse. In the human senile cataract lens, 12kb BamHI-restricted vimentin fragments displayed a stronger hybridization signal than that of the control lens in Southern blot analysis. It implies that the formation of human senile cataract may be associated with the amplification of vimentin gene. CONCLUSIONS: We have successfully developed four transgenic mice bearing chicken vimentin gene and having mRNA expression which can be used for further study. It is to be observed if the normal lens cell function is affected by the expressed product and cataract occurs in our transgenic mice. The cause of the gene amplification in human cataract remains for further investigation.

Adult↗
PubMed1994

Cross-linking of CD4 molecules upregulates Fas antigen expression in lymphocytes by inducing interferon-gamma and tumor necrosis factor-alpha secretion.

We have recently shown that, in unfractioned peripheral blood mononuclear cells (PBMCs), the cross-linking of CD4 molecules (CD4XL) is sufficient to induce T-cell apoptosis. However, the underlying mechanism for the CD4XL-mediated T-cell apoptosis is largely unknown. Several recent studies have shown that Fas antigen (Ag), a cell-surface molecule, mediates apoptosis-triggering signals. We show here that cross-linking of CD4 molecules, induced either by anti-CD4 monoclonal antibody (MoAb) Leu3a or by human immunodeficiency virus-1 (HIV-1) envelope protein gp160, upregulates Fas Ag expression as well as Fas mRNA in normal lymphocytes. Addition of the tyrosine protein kinase inhibitor genistein or of the immunosuppressive agent cyclosporin A abrogated these effects. The upregulation of Fas Ag closely correlated with apoptotic cell death, as determined by flow cytometry. In addition, CD4XL resulted in the induction of interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha) in the absence of interleukin-2 (IL-2) and IL-4 secretion in PBMCs. Both INF-gamma and TNF-alpha were found to contribute to Fas Ag upregulation and both anti-IFN-gamma and anti-TNF-alpha antibodies blocked CD4XL-induced Fas Ag upregulation and lymphocyte apoptosis. These findings strongly suggest that aberrant cytokine secretion induced by CD4XL and consequent upregulation of Fas Ag expression might play a critical role in triggering peripheral T-cell apoptosis and thereby contribute to HIV disease pathogenesis.

Antibodies↗
PubMed1994

Envelope glycoproteins of HIV-1 interfere with T-cell-dependent B cell differentiation: role of CD4-MHC class II interaction in the effector phase of T cell help.

T-cell-dependent B cell differentiation involves two phases: an inductive phase of T cell activation followed by an effector phase, which involves stimulation of B cells by activated T cells. We have previously demonstrated that anti-CD3 mAb and antigen-induced T-cell-dependent B cell functions are inhibited by HIV-1 envelope glycoprotein, gp120, at the inductive phase of T-cell-dependent B cell response. In this study we have investigated whether gp120 also inhibits the effector phase of interactions involved in T-cell-dependent-B cell differentiation response. For these studies, CD4+ T cells were first activated with antigen or pokeweed mitogen, cultured with soluble HIV-gp120 or medium for 2 hr, and washed. Coculture of gp120-treated preactivated T cells with autologous B cells resulted in impairment of IgG secretion, but did not affect IgM secretion significantly. The IgG secretion was restored by the addition of PMA (activator of protein kinase C) or forskolin (activator of adenylate cyclase), but not by the addition of ionomycin (inducer of intracellular calcium) to the T plus B cell cultures. A similar pattern of Ig secretion (IgM, no IgG) was observed with B cells of a patient with bare lymphocyte syndrome, indicating a requirement for MHC class II molecule interaction with T cells. These studies suggest that the effector phase of T-B cell interactions are impaired by gp120, and that the mechanism involves a signal transducing event(s), which is dependent upon cyclic AMP and/or protein kinase C. Furthermore, these latter reactions occur subsequent to T-B cell contact-dependent interactions at the effector phase, which involve MHC class II molecules on B cells and CD4 molecules on T cells.

Antigen Presentation↗
PubMed1994

Severe spinal degeneration in Wilson's disease.

This case report is the first to report severe spinal degeneration and destruction in Wilson's disease. The presentation, assessment, and decision making for treatment are discussed. This condition should be considered in patients with Wilson's disease who present with back pain.

Adult↗