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Biomedical subjects

J Zhu

Publications and source records attributed to J Zhu.

At least 523 records · Page 29Linked to original sources
PubMed1997

The inhibition of nitric oxide-activated poly(ADP-ribose) synthetase attenuates transsynaptic alteration of spinal cord dorsal horn neurons and neuropathic pain in the rat.

Transsynaptic alteration of spinal cord dorsal horn neurons characterized by hyperchromatosis of cytoplasm and nucleoplasm (so-called 'dark' neurons) occurs in a rat model of neuropathic pain induced by chronic constriction injury (CCI) of the common sciatic nerve. The incidence of dark neurons in CCI rats has been proposed to be mediated by glutamate-induced neurotoxicity. In the present study, we examined whether the inhibition of the nitric oxide (NO)-activated poly(ADP-ribose) synthetase (PARS), a nuclear enzyme critical to glutamate-induced neurotoxicity, would both reduce the incidence of dark neurons and attenuate behavioral manifestations of neuropathic pain in CCI rats. Dark neurons were observed bilaterally (with ipsilateral predominance) within the spinal cord dorsal horn, particularly in laminae I-II, of rats 8 days after unilateral sciatic nerve ligation as compared to sham operated rats. The number of dark neurons in the dorsal horn was dose-dependently reduced in CCI rats receiving once daily intrathecal (i.t.) treatment with the PARS inhibitor benzamide (200 or 400 nmol, but not 100 nmol benzamide or saline) for 7 days. Consistent with the histological improvement, thermal hyperalgesia, mechanical hyperalgesia, and low threshold mechano-allodynia also were reliably reduced in CCI rats treated with either 200 or 400 nmol benzamide. Neither dark neurons nor neuropathic pain behaviors were reliably affected by i.t. administration of either 800 nmol novobiocin (a mono(ADP-ribose) synthetase) or 800 nmol benzoic acid (the backbone structure of benzamide), indicating a selective effect of benzamide. Intrathecal treatment with an NO synthase inhibitor NG-nitro-L-arginine methyl ester (40 nmol, but not its inactive D-isomer) utilizing the same benzamide treatment regimen resulted in similar reductions of both dark neurons and neuropathic pain behaviors in CCI rats. These results provide, for the first time, in vivo evidence indicating that benzamide is neuroprotective and that the PARS-mediated transsynaptic alteration of spinal cord dorsal horn neurons contributes to behavioral manifestations of neuropathic pain in CCI rats. These observations may have general implications beyond treatment of neuropathic pain in that PARS-mediated neuronal alterations may play a significant role in glutamate-mediated neurotoxicity under many other circumstances.

ADP Ribose Transferases↗
PubMed1997

The effect of combined fluid percussion and entorhinal cortical lesions on long-term potentiation.

Among the pathological processes initiated by traumatic brain injury are excessive neuroexcitation and target cell deafferentation. The current study examines the contribution of these injury components, separately as well as their combined effect, on postinjury alterations in the capacity for long-term potentiation and the immunolocalization of N-methyl-D-aspartate receptors and GABA. Adult rats underwent central fluid percussion traumatic brain injury, electrolytic bilateral entorhinal cortex lesions, or a combined injury of both procedures separated by 24 h. At two or 15 days postinjury, the capacity for long-term potentiation of the Schaffer collateral-commissural input to CA1 was measured in acute electrophysiological recordings. Entorhinal cortical lesions resulted in time-dependent increases in the effectiveness of tetanic stimulation to elevate population postsynaptic potentials and population spike amplitudes. These lesions also resulted in a marked intensification in the density of N-methyl-D-aspartate receptors in the CA1 stratum lacunosum-moleculare. All injury conditions that included fluid percussion as a component (alone or in combined injuries) produced a persistent impairment in long-term potentiation of the evoked population postsynaptic potentials. Thus, in combined injuries, the presence of concussion-induced neuroexcitation attenuated deafferentation-induced response increases. Both N-methyl-D-aspartate receptor and GABA immunobinding following combined injuries were also reduced relative to those observed following entorhinal lesions alone. The present results suggest that a process of receptor plasticity, possibly involving reactive synaptogenesis, may contribute to postdeafferentation enhancements of long-term potentiation, and that a traumatic brain insult will attenuate these enhancements. This interaction of different injury components suggests that recovery of function following brain injury may be enhanced by pharmacological reduction of neuroexcitation during postinjury intervals of reactive receptor plasticity.

Animals↗
PubMed1997

Haemophilus influenzae and Streptococcus pneumoniae induce different intracerebral mRNA cytokine patterns during the course of experimental bacterial meningitis.

Using in situ hybridization with radiolabelled oligonucleotide probes, we studied the mRNA expression of IL-1beta, IL-4, IL-6, IL-10, IL-12, tumour necrosis factor-alpha (TNF-alpha), TNF-beta, interferon-gamma (IFN-gamma), and transforming growth factor-beta (TGF-beta) in the brain during the lethal course of experimental meningitis in a rat model inoculated intracisternally with Haemophilus influenzae type b (Hib) or Streptococcus pneumoniae and in uninfected control rats inoculated with the same volume of PBS. The production of IL-1beta, IL-4, IL-6 and IFN-gamma was also evaluated by immunohistochemistry. In the brain of Hib-inoculated rats, there was marked mRNA expression of IL-1beta, IL-6, TNF-alpha, IL-12 and IFN-gamma. IL-1beta, IL-6 and TNF-alpha were up-regulated throughout the observation period at 2, 8 and 18 h post-inoculation (p.i.), with similar patterns of induction. The Th1 cytokines IFN-gamma and TNF-beta were up-regulated within 8 h p.i. IL-10 and TGF-beta were down-regulated at 18 h p.i., while IL-4 was not detected. In contrast, the brain of S. pneumoniae-inoculated rats showed lower levels of IL-1beta, IL-6 and TNF-alpha, but higher levels of TNF-beta and detectable mRNA expression of IL-4 when compared with Hib-inoculated rats. IL-12, IFN-gamma, IL-10 and TGF-beta exhibited similar patterns of induction in the brains of Hib- and S. pneumoniae-inoculated rats. At 18 h p.i., immunohistochemistry showed similar patterns of IL-1beta, IL-4, IL-6 and IFN-gamma as mRNA expression in the brains of Hib- and S. pneumoniae-inoculated rats. The differences of cytokine profiles induced by the two bacterial strains may imply that different immunomodulating approaches should be considered, depending on etiology.

Animals↗
PubMed1997

A deficiency screen for zygotic loci required for establishment and patterning of the epidermis in Caenorhabditis elegans.

To identify genomic regions required for establishment and patterning of the epidermis, we screened 58 deficiencies that collectively delete at least approximately 67% of the Caenorhabditis elegans genome. The epidermal pattern of deficiency homozygous embryos was analyzed by examining expression of a marker specific for one of the three major epidermal cell types, the seam cells. The organization of the epidermis and internal organs was also analyzed using a monoclonal antibody specific for epithelial adherens junctions. While seven deficiencies had no apparent effect on seam cell production, 21 were found to result in subnormal, and five in excess numbers of these cells. An additional 23 deficiencies blocked expression of the seam cell marker, in some cases without preventing cell proliferation. Two deficiencies result in multinucleate seam cells. Deficiencies were also identified that result in subnormal numbers of epidermal cells, hyperfusion of epidermal cells into a large syncytium, or aberrant epidermal differentiation. Finally, analysis of internal epithelia revealed deficiencies that cause defects in formation of internal organs, including circularization of the intestine and bifurcation of the pharynx lumen. This study reveals that many regions of the C. elegans genome are required zygotically for patterning of the epidermis and other epithelia.

Animals↗
PubMed1997

Developmental quantitative genetics, conditional epigenetic variability and growth in mice.

Ontogenetic variation in the causal components of phenotypic variability and covariability is described for body weight and tail length in mice derived from a full 7 x 7 diallel cross. Age-related changes in additive, dominance, sex-linked and maternal variance and covariance between 14 and 70 days of age are described. Age-specific variance components at time t are conditioned on the causal genetic effects at time (t - 1). This procedure demonstrates the generation of significant episodes of new genetic variation arising at specific intervals during ontogeny. These episodes of new genetic variation are placed in the context of epigenetic models in developmental quantitative genetics. These results are also concordant on recent findings on age-specific gene expression in mouse growth as shown by QTL analyses.

Animals↗
PubMed1997

Influence of crossing a line selected for increased shank width and a commercial sire line on performance and walking ability of turkeys.

The present study was initiated to determine whether walking ability (WA) could be markedly improved without seriously compromising growth rate and body conformation by crossing a relatively unimproved commercial sire line (UC) with a line (FL) selected for increased shank width and backcrossing F1 females to UC line males. Body weights at 8, 16, and 20 wk of age were generally similar for both lines at the time of the initial cross. The UC line had inferior WA, shorter and narrower shanks, and wider breasts compared with the FL line. The F1 birds exhibited overdominance for BW at all ages. Heterosis in BW ranged from 3.2 to 7.8%. At 16 wk of age, the WA scores decreased (indicating improved WA) in the F1 relative to the average of the parental lines. Heterosis of WA scores was -10.5% (P > or = 0.05) for males and -23.5% (P < or = 0.05) for females. Heterosis was observed in the F1 for shank length but not for other shank measurements (width and depth). No heterosis was observed for breast width. Mortality from 8 through 20 wk of age was reduced in the F1 relative to the parental lines. The backcross of the F1 females to UC males still exhibited heterosis for male BW at 16 and 20 wk of age and for WA scores, although the magnitude was reduced 50% or more. Mortality from 8 to 20 wk of age decreased in the backcross compared with the parental lines. The results suggest that a line exhibiting improved leg structure and WA, and poor conformation, such as FL, can be used to greatly improve the WA of a cross involving a sire line with poor WA but excellent conformation. A portion of the gains in BW and breast width obtained in the F1 was retained in a backcross to the sire line, making such a crossing scheme commercially feasible.

Animals↗
PubMed1997

Thalidomide suppresses T- and B-cell responses to myelin antigen in experimental allergic neuritis.

The effects of thalidomide and, for reference, dexamethasone on T- and B-cell functions were assayed in vitro in Lewis rats with experimental allergic neuritis induced by active immunization with bovine peripheral nerve myelin (BPM) and complete Freund's adjuvant. Thalidomide and dexamethasone at the concentration ranges 10(-5)-10(-7) g/ml and 4 x 10(-5)-4 x 10(-9) g/ml, respectively, both inhibited phytohemagglutinin (PHA)- and BPM-induced T-cell proliferation as well as levels of PHA- and BPM-reactive interferon (IFN)-gamma-secreting cells, reflecting the suppression of Th1-like cells. The effect of dexamethasone was most pronounced on PHA-induced T-cell proliferation and IFN-gamma secretion, whereas the effect of thalidomide was most pronounced on BPM-induced T-cell proliferation and IFN-gamma secretion. Thalidomide reduced the B-cell responses to both BPM and Mycobacterium tuberculosis purified protein derivative, but to a lesser extent than dexamethasone. The in vitro design described could be useful to evaluate compounds with putative immunomodulatory activities. The inhibitory effects of thalidomide on autoantigen-induced Th1-cell functions may warrant the use of this substance in T-cell-mediated autoimmune diseases.

Animals↗
PubMed1997

Survival and functional outcome of children requiring endotracheal intubation during therapy for severe traumatic brain injury.

OBJECTIVE: To determine the predictors of survival and functional outcome of pediatric patients with traumatic brain injury severe enough to require endotracheal intubation and mechanical ventilation. DESIGN: Retrospective, observational cohort study. SETTING: Pediatric intensive care unit (ICU) at a tertiary care children's hospital. PATIENTS: All children (n = 105) admitted over a 5-yr period with traumatic brain injury severe enough to require endotracheal intubation and mechanical ventilation. The median age was 43 months (range 1 month to 14 yrs). Of these children, 74% were male and 70% were white. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Variables studied included vital signs during the first 24 hrs of admission, Pediatric Risk of Mortality (PRISM) score, Glasgow Coma Score, duration of mechanical ventilation, and number of pediatric ICU and hospital days. Functional status was graded as normal, independent, partially dependent, or dependent in the areas of locomotion, self-care, and communication. This status was assessed at hospital discharge by chart review and at follow-up by telephone interview. The median Glasgow Coma Score was 6 (range 3 to 14) and the median PRISM score was 13 (range 1 to 51). There were 19 (18.1%) deaths, 17 in the pediatric ICU and two after hospital discharge. Of the patients who survived to hospital discharge, 39 (37.1%) patients were completely normal or independent, 42 (40%) patients were partially dependent, and seven (6.7%) patients were dependent in all three areas of function. Follow-up evaluations were available for 80 patients, with a median follow-up time of 24.5 months (range 8 to 70). Of the 78 patients who survived and were available for follow-up, the number who were functionally normal or independent increased to 69 (65.7%). At follow-up, there were eight (7.6%) patients remaining with partial dependency in at least one area of function while one (0.9%) patient continued to be dependent in all three areas of function. Mortality and dependent functional outcome were more likely in patients with younger age, lower Glasgow Coma Score, and higher PRISM score at hospital admission. Of the 27 patients with a Glasgow Coma Score of < or = 5, 11 (40.7%) survived with normal or independent functional status at follow-up. Of the 24 patients with PRISM scores of > 20, only five (20.8%) were functionally normal or independent at follow-up. The relative risk of a bad outcome for patients with a Glasgow Coma Score of < or = 5 and a PRISM score of > or = 20 was ten times higher than the group of patients with a Glasgow Coma Score of < or = 5 but a PRISM score of < 20. CONCLUSIONS: Children with severe traumatic brain injury who survive to hospital discharge will continue to improve in their functional status over the next few years. Although low Glasgow Coma Score is strongly associated with death or poor functional outcome after therapy for traumatic brain injury, many patients with Glasgow Coma Score of < or = 5 can survive with good function. PRISM scores add to the power of Glasgow Coma Score to predict survival and functional outcome in tracheally intubated pediatric patients with Glasgow Coma Score of < or = 5.

Activities of Daily Living↗
PubMed1997

Startle reflex modulation by pleasant and unpleasant odors in a between-subjects design.

Participants were presented with an acoustic startle probe while they smelled either a pleasant odor or an unpleasant odor (n = 40 per condition). Within each condition, participants were presented with four blocks in which odor was present and four in which odor was not present (no-odor control). Significant differences were found in both conditions between the odor and no-odor blocks. In the unpleasant odor condition, blink magnitude was greater during the odor blocks; in the pleasant odor condition, blink magnitude was smaller during the odor blocks.

Acoustic Stimulation↗
PubMed1997

Expression of osteocalcin in cementoblasts forming acellular cementum.

To determine the phenotypic expression of cementoblasts responsible for acellular cementum, an immunohistochemical study was performed using a polyclonal antibody raised against the aminoterminal peptide of rat osteocalcin (OC). Maxillary first molars of Wistar male rats aged 2 and 3 wk were used for observations. Serial sections of decalcified paraffin embedded specimens were stained either with hematoxylin and eosin or with the anti-OC antibody. In 2-wk-old rats, apical roots were lined with the epithelial root sheath. A thin layer of acellular cementum was seen at most of the root surface, but was not seen near to root apex. In 3-wk-old rats, cellular cementum began to be formed at root apex, and acellular cementum became more thick than in 2-wk-old rats. Acellular and cellular cementum were lined with the fibroblast-like cells. Osteocalcin staining was detected in cells lining root surface in both 2- and 3-wk-old rats. Almost all cells lining cellular cementum were positive for OC. In contrast OC positive cells lining acellular cementum and root surface devoid of cementum appeared at a specific site of the root. The cells at the interradicular area of root surface were positive but the cells at the outer area (the opposite side of the interradicular area) were negative for OC. Osteoblasts and odontoblasts were positive with the antibody. The present results suggest that the OC expression of cementoblasts forming acellular cementum is similar to that of cells forming cellular cementum as well as osteoblasts and odontoblasts, and has a role for calcification of acellular cementum.

Animals↗
PubMed1997

Effects of substitutions D73E, D73N, D103N and V106M on signaling and pH titration of sensory rhodopsin II.

Several mutations in the repellent phototaxis receptor sensory rhodopsin II (SRII), in residues homologous to residues important in the related proton pump bacteriorhodopsin, were expressed in Pho81Wr-, a Halobacterium salinarum strain deficient in production of SRII and its transducer protein HtrII. The lack of production of SRII and HtrII is shown to be due to insertion of an ISH2 transposon into the promoter region upstream of the htrII-sopII gene pair. Near wild-type phototaxis responses are rescued in Pho81Wr- by expression of HtrII with D73E, D103N or V106M receptors. Partial responses are restored by the HtrII-D73N pair. From absorption spectroscopy of his-tag-purified receptor protein from mutants D73N and D73E we conclude that Asp73 is the primary counterion to the protonated Schiff base in SRII, like the corresponding Asp85 in bacteriorhodopsin. The absorption maximum of SRII (487 nm) is shifted to 514 nm in mutant D73N, a 1080 cm-1 shift identical to that caused by D85N in bacteriorhodopsin. Acid titration of SRII also induces the red shift with a pK of 3.0 in wild type. The absorption shift and the pK are nearly the same in V106M and D103N, but the pK is raised to 5.1 in D73E, confirming that Asp73 is the residue responsible for this spectral transition.

Archaeal Proteins↗
PubMed1997

Chronic treatment with prazosin causes a subtype-specific increase in the alpha 1-adrenoceptor density of the stressed rat cerebral cortex.

The effects of chronic treatment with prazosin and of immobilization stress on the alpha 1-adrenoceptor subtypes in rat cerebral cortex have been examined. Prazosin-treated rats were allowed free access to tap water containing two different concentrations of prazosin (16 or 156 mg L-1) for 5 weeks. The mean plasma concentrations of prazosin were 5 ng mL-1 in groups treated with a low dose and 8 or 14 ng mL-1 in those treated with a high dose. Immobilization stress (2 h day-1, 2 weeks) or chronic treatment with a low dose of prazosin caused no significant change in the affinity for [3H]prazosin or in the maximum number of alpha 1-adrenoceptor sites (Bmax). However, treatment with prazosin (low dose) combined with stress increased the density of alpha 1-adrenoceptors with low affinity for prazosin. Treatment with a high dose of prazosin increased the density of alpha 1L-adrenoceptors, irrespective of stress loading. The densities of alpha 1A- and alpha 1B-adrenoceptors with high affinity for prazosin were increased only after treatment with a high dose of prazosin in combination with stress. These results indicate that three distinct alpha 1-adrenoceptor subtypes, alpha 1A, alpha 1B and alpha 1L, might be affected differently by treatment with prazosin and by stress.

Adrenergic alpha-Antagonists↗
PubMed1997

A role for tissue transglutaminase in hepatic injury and fibrogenesis, and its regulation by NF-kappaB.

This study was undertaken to delineate a possible role for tissue transglutaminase (tTG), an enzyme that catalyzes protein cross-linking, in hepatic fibrogenesis. Rats were treated with CCl4 solution and then killed at different stages of liver injury and fibrogenesis. Liver tTG mRNA levels were markedly increased as early as 6 h after the first injection, peaked at 4 days and 1 wk, and remained increased for 8 wk. The enzymatic activity of tTG was increased in livers of rats treated with CCl4, in a fashion that paralleled the Northern blot results. Cell isolation experiments indicated that all hepatic cell types synthesize tTG mRNA. Increased binding to the nuclear factor-kappaB (NF-kappaB) motif of the tTG promoter was found in the nuclear extracts prepared from CCl4-treated samples. These data demonstrate an increase in tTG gene expression during hepatic injury and fibrosis, suggesting a possible role for this enzyme in stabilizing the fibrotic bands during hepatic fibrogenesis. Moreover, increased NF-kappaB binding to the tTG promoter may represent one of the mechanisms by which cell injury induces tTG transcription and thus potentiates the process of fibrogenesis.

Animals↗
PubMed1997

A 120 kilobase resolution contig map of the rice genome.

92% of the rice genome (4.3 x 10(8) bp, 2n = 24) was covered by 631 contigs of various length, which were generated by fingerprinting from a representative and genetically stable bacterial artificial chromosome (BAC) library of the Guang Lu Ai 4 (a O. Sativa variety) genome with the average insert of 120 kb in length. To form the contig map, 565 molecular markers of RFLP, STS, cDNA and anchor set derived from two O. Sativa varieties were by colony hybridization mapped to the contigs, which were then assigned to and ordered along the particular chromosomes according to the marker colinearity. Being highly conserved DNA sequences shared among the genomes of rice, barley, wheat, oat, maize, sorghum and sugar cane, 89 anchor markers mapped help to identify the rice genes through the information provided by the maps of relative genomes, and vice versa. Numerous repeated DNA sequences of various length were identified and mapped to the chromosomes. Physical distances have been determined for hundreds pairs of adjacent markers, which would facilitate the identification by map-based cloning the rice genes of interest. The accuracy of clone overlaps in contigs was further confirmed by the existence in contigs of well fit stacks of marker-lodged clones independently identified by hybridization. Large scale DNA sequencing of individual chromosomes could now be initiated simply by selecting and sequencing the minimally overlapped BAC clones of the contigs.

Alkyl and Aryl Transferases↗
PubMed1997

[Astrogliosis and basic fibroblast growth factor].

OBJECTIVE: To study the relationship between reactive astrogliosis and its autocrine bFGF. METHODS: On the primary astrocyte culture with mechanical scratch, the dynamic expression of bFGF, PCNA, GFAP and GFAP-mRNA were determined by immunocytochemistry and in situ hybridization. RESULT: Astrocytes at the edge of the injury began to express bFGF 2 hours after scratching and reached its peak by the 12th hour, then declined after 2 days. GFAP-mRNA was detectable in astrocytes near the injury from the 6th hour and reached its peak within 24 hours. A few hypertrophic astrocytes in the injured area expressed GFAP-mRNA on the 3rd day. Enhanced GFAP expression of astrocytes was observed with hypertrophy of cytoplasma which extended wide processes into the injured area from the day of the scratch and reached its peak on the 2nd day. On the 3rd day, the previously injured area was covered with hypertrophic astrocytes. PCNA was expressed 2 hours after damage by some of the astrocytes in the vicinity of injury. CONCLUSION: Autocrine bFGF was the early response of reactive astrocytes and bFGF may act as promoter of reactive astrogliosis. Enhanced GFAP expression was the result of upregulation of GFAP-mRNA. The prominent event of reactive astrogliosis was the hypertrophy of astrocytes.

Animals↗
PubMed1997

[Protective effects of 15-methyl-prostaglandin F2 alpha on primary cultured rat hepatocyte against CCl4-induced injury].

The effect of 15-Mt-PGF2 alpha on CCl4-induced injury of primary cultured hepatocytes was studied. 15-Mt-PGF2 alpha treatment (2 mg/L) significantly decreased CCl4 (10 mmol/L)-induced damages of primary cultured rat heptocytes as indicated by decreases GPT and GOT leakage and LPO production. 15-Mt-PGF2 alpha significantly promoted 3H-uridine incorporation into RNA and [3H]-thymidine incorporation into DNA of the rat hepatocytes. Cytopathology study showed that 15-Mt-PGF2 alpha attenuated damages of mitochondria, endoplasmic reticulum and ribosome caused by CCl4. 15-Mt-PGF2 alpha appeared to maintain the stability of rat hepatocytes by inhibiting lipid peroxidation. These results indicated that 15-Mt-PGF2 alpha has notable protective effect on primary cultured rat hepatocytes against CCl4-induced damage by reducing lipid peroxidation and promoting synthesis of RNA and DNA.

Animals↗