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Biomedical subjects

H Zhu

Publications and source records attributed to H Zhu.

At least 235 records · Page 13Linked to original sources

[Effects of excessive iodine on activity of enolase in hippocampus of developing mice].

OBJECTIVE: To study the effects of excessive intake of iodine for a long term on activity of enolase in hippocampal tissues of young mice. METHODS: A hyperiodine goiter animal model was replicated with drinking water with high level of iodine. Activity of neuron specific enolase (NSE) in hippocampal tissues was determined with enzyme-linked immunosorbent assay (ELISA) for young offspring of the first and the second generations of mice with hyperiodine goiter on the 7th, 14th and 21st day of age, respectively. RESULTS: Activity of enolase in young offspring of the first and second generation of mice with hyperiodine goiter was all lower than that in controls from the day of their birth to the 30th day after birth, and that at hippocampal tissues in young mice of the second generation was significantly lower than that of the first generation on the 14th day of age. CONCLUSION: Hyperiodine can decrease activity of NSE in the brain of mice. It suggests that hyperiodine can affect NSE, and thus interfere energy supply in the brain, resulting in disturbance of neuron development and brain function.

Animals↗

[Effects of excessive iodine on apoptosis and expression of bcl-2, bax genes in the cells of brain and thyroid gland in guinea pigs].

OBJECTIVE: To investigate the effects of excessive iodine intake on apoptosis and the expression of bcl-2, bax genes in the cells of brain and thyroid gland. METHODS: Guinea pigs, divided into two groups at random, were fed with distilled water containing iodine 50 microg/L (a control group with appropriate iodine) and 10,000 microg/L (a trial group with excessive iodine), respectively for six months. Apoptosis rate and expression of bcl-2, bax gene in the cells of cerebral cortex, hippocampus and thyroid gland in guinea pigs were quantitatively determined by flow cytometry and immunofluorescent techniques. RESULTS: The proportion of apoptosis in the cells of cerebral cortex, hippocampus and thyroid gland was significantly higher in the group with excessive iodine intake than that in the control one (P < 0.01). The level of expression of bcl-2 gene was notably decreased (P < 0.05), but that of bax was notably increased (P < 0.01), in the cerebral cortex, hippocampus and thyroid gland in the group with excessive iodine than in the control one. The ratio of bcl-2 to bax in the cerebral cortex, hippocampus and thyroid gland of the group with excessive iodine was decreased significantly (P < 0.01) than that of the control one. CONCLUSION: Excessive iodine intake may induce apoptosis in the cells of cerebral cortex, hippocampus and thyroid gland. The over-expression of bax gene and the down-regulation of bcl-2, which can then cause the decrease in a ratio of bcl-2 to bax, appear to play an important role in the course of apoptosis induced by excessive iodine intake.

Animals↗

[Protective efficacy of H2 strain live attenuated hepatitis A vaccines in an outbreak of hepatitis A].

OBJECTIVE: To investigate the protective efficacy of H(2) strain live attenuated hepatitis A vaccine (H(2)-strain vaccine) locally produced in an outbreak of hepatitis A (HA). METHODS: A nonrandomized controlled design was used in a trial for HA vaccination. Five thousand five hundred and fifty-one children at preschool classes and at grades 1 - 3 of primary schools were selected in 14 villages. Epidemiological and serological methods were used to evaluate its protective efficacy of the vaccines and serum immunoglobulin M against hepatitis A virus (IgM anti-HAV) was detected with ELISA for 271 subjects in vaccinated group and 341 in the control one. RESULTS: An outbreak of HA occurred one year after the vaccination with 26 cases in the vaccinated group, including one vaccine-related case with an attack rate of 0.28% (1/356), and 25 cases in the control group with an attack rate of 5.92% (25/422). The protective efficacy of vaccines was 95.27% (95% confidence interval of 85.83% to 104.72%). Positivity of IgM anti-HAV, i.e., newly-infected cases, was 4.43% (12/271) in the vaccinated group and 13.38% (42/314) in the control group, respectively. Clinically apparent cases accounted for 8.33% (1/12) and 50.00% (21/42) in newly-infected cases in vaccinated and control groups, respectively. CONCLUSION: Vaccination with H(2) strain vaccines locally produced was effective in reducing occurrence of HA during its outbreak, but not so effective in preventing its infection. A booster dose of HA vaccine should be vaccinated for children in adequate time.

Adolescent↗

[A comparative study on the expressions of IL-4, IFN-gamma and TNF-alpha in BMMNC of acute and chronic aplastic anemia patients].

OBJECTIVE: To detect the induced levels of IL-4, IFN-gamma and TNF-alpha in the supernatant of bone marrow mononuclear cells (BMMNC) and compare the difference of immune status between acute (SAA) and chronic (CAA) aplastic anemia patients. METHODS: Concentrations of IL-4, IFN-gamma and TNF-alpha in PHA-P-induced BMMNC supernatants were determined by ELISA assay in 11 SAA and 13 CAA patients as well as 16 controls. Concentration differences between the two groups were compared. RESULTS: (1) The IFN-gamma and TNF-alpha levels in AA patients studied were much higher than that in controls, and IL-4 levels were normal in SAA group but elevated in CAA group. (2) TNF-alpha levels were comparable between the two AA groups, but both IL-4 and IFN-gamma levels were significantly different between them. CONCLUSION: Enhanced cellular immunity seems to play an important role in the pathogenesis of SAA, and enhancement of both cellular and humoral immunity might contribute to the pathogenesis of CAA.

Acute Disease↗

[MTHFR gene expression in EB virus transformed human B lymphoblasts].

In order to detect the expression of N5, N10-methylene-tetra hydrofolate reductase(MTHFR) gene in Epstein-Barr virus(EBV) transformed human B lymphoblast, as well as the cDNA sequence, human peripheral blood was transformed by EBV to build B lymphoblast cell line. Total RNA was isolated from the cell culture. Variant segments of MTHFR cDNA were amplified using RT-PCR protocol and analysed by polyacrylamide gel electrophoresis(PAGE). One of the cDNA segments was sequenced. Results showed MTHFR gene was expressed in human B lymphoblast cell line. The cDNA sequence was almost the same as that of human liver cDNA from Genbank.

B-Lymphocytes↗

[Methionine synthase and neural tube defects].

It has been indicated lately that higher plasma homocysteine is one of the risk factors in neural tube defects(NTDs) and vascular disease. Methionine synthase is a key enzyme in homocysteine metabolism. The defects of methionine synthase activity could result in hyperhomocysteinemia and methionine auxotrophy. The gene mutations of methionine synthase with the epidemiological studies of NTDs are reviewed in this paper. It is considered that the gene mutations of methionine synthase can not make a relation to NTDs and hyperhomocysteine, but methionine synthase reductase may be a clue for the study on NTDs in the future.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

[Clinical effects of intra-arterial nitrogen mustard (NH2) chemotherapy during operation for oral cancer].

OBJECTIVE: To discuss the general and local side-effects and clinic appliance of the intra-arterial chemotherapy, and evaluate the short-time clinic effects of the intra-arterial chemotherapy. METHODS: From February, 1997 to December, 1997 11 patients with oral cancer (9 cases with lingual carcinoma, 2 cases with mouth carcinoma) were received one-shot chemotherapy during operation by NH2 catheterizing of lingual arteries (concentration of 1 mg/ml, dosage of 5 mg), and the other 16 oral cancer patients (13 cases with lingual carcinoma, 3 cases with mouth carcinoma) were only received operation as the control. At the same time, all patients were treated with Chinese flaps or Major pectoris myocutanous flaps homochronously. Then the general and local side-effects including the flap complexion were observed 1 week post-operatively and the follow-up was done in a shot time of 3-12 months. RESULTS: No obvious general and local side-effects (including blood, mal function of liver and kidney, flap complexion, vomit and hemiplegia) happened and all the 11 flaps (6 Chinese flaps, 5 major pectoris myocutanous flaps) were alive in the experimental group. The local recurrent rate of the experimental group was 9.1%, while the rate was 18.8% in the control group (following up of 3-12 months). There was no significant difference between the experiment and the control groups by Student t-test. CONCLUSION: The one-shot chemotherapy intra-operationally is a method with few side-effects, and it doesn't injure the homochronously reconstructed flaps. It might be an effective means of reducing the local recurrence of oral cancer.

Adult↗

[Pharmacognostical studies on the stem and leaf of Mussaenda pubescens].

Morphological and microscopic chracteristics of Mussaenda pubescens Ait. f, a traditional Chinese medicine were described and illustrated with line drawings. TLC and UV analysis of the medicinal material were also undertaken. These studies provide referential information for identification and development of this medicinal material.

Chromatography, Thin Layer↗

The effect of basic fibroblast growth factor slow-release microcapsules on angiogenesis in infarcted rabbit myocardium.

OBJECTIVES: To observe the effect of basic fibroblast growth factor (bFGF) slow-release microcapsules on angiogenesis in infarcted myocardial regions. METHODS: Myocardial infarction was induced in 24 New Zealand rabbits by ligating the root of left anterior descending coronary artery. Group I (n = 8) served as control, group II (n = 8) as a blank microcapsule group, group III (n = 8, each microcapsule contains 1 microg bFGF) as microcapsule group. In group II and III, 5 blank microcapsules or bFGF slow-release microcapsules were implanted into myocardium underneath the epicardium between the left anterior descending coronary artery and left circumflex artery. Infarct size was evaluated by infarcted weight/left ventricle weight ratio and angiogenesis was evaluated by immunohistochemical examinations 5 weeks later. RESULTS: As compared with group I and II, rabbits treated with bFGF slow-release microcapsules showed higher microvessel counts (group I 37.75 +/- 4.50, group II 38.37 +/- 4.98, vs x group III 135.50 +/- 4.81, P < 0.001) and less infarcted weight/left ventricle weight (group I 16.8% +/- 0.4%, group II 16.7% +/- 0.5%, vs x group III 7.0% +/- 0.2%, P < 0.001). CONCLUSIONS: Subepicardial administration of bFGF slow-release microcapsule in the infarcted rabbit model results in effective angiogenesis and reduction in infarct size.

Animals↗

[Study on the infrared spectra of metallic clusters containing R2dtc ligand and V = O group].

This paper reports the features and regularities of the infrared spectra for two kinds of complexes containing R2dtc ligand. The cubane-like clusters containing R2dtc ligand possess weak and wide peaks at 400-500 cm-1 assigned to M-mu 3S vibration, while the peaks at 330-380 cm-1 and 1,470-1,510 cm-1 can be assigned to M-Sdtc and C-N vibrations, respectively. The nu(C-N) and nu(C = S) vibrations for Me2dtc-cubane cluster exhibit blue shift and red shift, respectively, when compared with those of other R2dtc ones. This would be attributed to the strong super-conjugation of the methyl group. The M-mu 3S vibrations for both types of complexes [V2Cu2S4(R2dtc)2(PhS)2]2- and [VCu4S4(R2dtc)n(PhS)4-n]3- (n = 0, 1, 2) occur at 480 and 465 cm-1, respectively. This small difference becomes a useful indication to distinguish the two types of clusters. Cluster complexes containing (R2dtc)2V2O2(mu-S)2 structural unit show the V = O vibration in the range of 844-970 cm-1. It is noted that (Et4N)[V3S2O3(Et2dtc)3] contains two sets of the V = O bonds corresponding to two sets of V = O vibrations at 970 and 844 cm-1. An additional coordination of the V = O bond to another metal atom obviously weakens the V = O bond to give rise to the red shift of the infrared frequency. Similar red shifts were also observed for other complexes and were discussed.

English Abstract↗

Identification of a cytochrome b-type NAD(P)H oxidoreductase ubiquitously expressed in human cells.

Cytochrome b-type NAD(P)H oxidoreductases are involved in many physiological processes, including iron uptake in yeast, the respiratory burst, and perhaps oxygen sensing in mammals. We have identified a cytosolic cytochrome b-type NAD(P)H oxidoreductase in mammals, a flavohemoprotein (b5+b5R) containing cytochrome b5 (b5) and b5 reductase (b5R) domains. A genetic approach, using BLAST searches against DBEST for FAD-, NAD(P)H-binding sequences followed by reverse transcription-PCR, was used to clone the complete cDNA sequence of human b5+b5R from the hepatoma cell line Hep 3B. Compared with the classical single-domain b5 and b5R proteins localized on endoplasmic reticulum membrane, b5+b5R also has binding motifs for heme, FAD, and NAD(P)H prosthetic groups but no membrane anchor. The human b5+b5R transcript was expressed at similar levels in all tissues and cell lines that were tested. The two functional domains b5* and b5R* are linked by an approximately 100-aa-long hinge bearing no sequence homology to any known proteins. When human b5+b5R was expressed as c-myc adduct in COS-7 cells, confocal microscopy revealed a cytosolic localization at the perinuclear space. The recombinant b5+b5R protein can be reduced by NAD(P)H, generating spectrum typical of reduced cytochrome b with alpha, beta, and Soret peaks at 557, 527, and 425 nm, respectively. Human b5+b5R flavohemoprotein is a NAD(P)H oxidoreductase, demonstrated by superoxide production in the presence of air and excess NAD(P)H and by cytochrome c reduction in vitro. The properties of this protein make it a plausible candidate oxygen sensor.

Amino Acid Sequence↗

Cloning of novel splice variants of mouse mGluR1.

Three splice variants of the mouse metabotropic glutamate receptor 1, mGluR1E55, mGluR1a and mGluR1b, have been isolated from mouse brain cDNA libraries. The sequences of mGluR1a and mGluR1b are similar to those from rat and human. mGluR1E55 is a novel splice variant. mGluR1E55 has two additional exons. One is 80-bp long at the 5' untranslational region. The other (E55) is 110-bp long at the cysteine-rich region after the ligand-binding domain and before the seven-transmembrane domain. Insertion of the E55 exon results in an inframe stop codon. The predicted protein product contains only the extracellular domain of the receptor and may be secreted.

Alternative Splicing↗

Mechanistic aspects of iontophoresis in human epidermal membrane.

A large number of factors are involved in the movement of ions and molecules across human epidermal membrane (HEM) under the influence of an electric field. These factors and their interplay need to be understood if our knowledge of iontophoretic transport of drugs across HEM is to reach a point where physical models and strategies may be employed for useful quantitative predictions. In a typical in vitro experiment, the fully hydrated HEM is positioned between aqueous compartments of a two-chamber diffusion cell. When a low electric field is applied across the HEM under these conditions, the transport enhancement of ions in the pre-existing pores of the stratum corneum is the result of, (a) the direct interaction of the electric field with the charge of the ion in question, and (b) convective solvent flow (electroosmosis); in the case where the permeant is non-ionic under these circumstances, transport enhancement is by convective solvent flow only. At moderate-to-high voltage iontophoresis (> or = around 1.0 V applied across a single HEM), in addition to the direct field effect and convective solvent flow in the pre-existing pores, there can generally be a significant (e.g. 10- to 100-fold enhancement) contribution to transport enhancement arising from new pore induction (electroporation). Much of the recent work in our laboratory has been devoted to defining and quantifying HEM electroporation, and an especially difficult aspect has been that of dealing with the large HEM membrane-to-membrane variabilities with regard to, (a) the extent of new pore induction, and (b) the characteristics of the newly induced pores. Recently we discovered that the extent of relevant (i.e. permeant accessible) pore induction may be correlated to the change in HEM electrical conductance (and quantifiable) if an appropriate matching background electrolyte can be selected having ion sizes comparable to that of the permeant. For example, employing tetraethylammonium (TEA) pivalate (PIV) for which the ion sizes are approximately 3.5 A, but not KCl (ion sizes approximately 1.9 A), as the background electrolyte for TEA (as the permeant) gave very good results; in this example, the sizable contribution of pore induction to iontophoresis was quantitatively factored out from the total iontophoretic enhancement. Experiments with a large number of HEM samples gave good agreement with the Nernst-Planck (N-P) predictions of the direct field effect when TEA-PIV was used as the background electrolyte for TEA transport, but large variations (up to 300%) between N-P predictions and experimental results were observed with KCl as the background electrolyte. Another area of recent effort has been HEM pore size determinations, both at low voltages (i.e. for pre-existing pores) and at voltages where the newly induced pores dominate HEM permeability. The sizes of pre-existing pores of HEM have been determined with the hindered diffusion theory (using experimental fluxes of several probe permeants of different known molecular sizes) to be generally in the range, 10-20 A, by a number of investigators in our laboratory for a large number HEM samples. Deducing pore sizes of electric field induced pores under steady electroporation conditions has been a more challenging task. We succeeded recently in developing a novel method for 'passively' determining pore sizes (i.e. by passive diffusion with hindered diffusion theory) under steady electroporation conditions: by using low frequency (12.5 Hz) a.c. at 2-5 V. We have been able to sustain electroporation at a nearly constant state of electroporation long enough to carry out a set of 'passive' diffusion experiments with relatively good precision to obtain the sizes of the newly induced pores. Studies to date have revealed that the sizes of pores induced with 2-5 V are of the same order of magnitude as those of the pre-existing pores (i.e. 10-20 A). Finally, another research question of interest has been that of pore charge

Biological Transport↗

A transient, neuron-wide form of CREB-mediated long-term facilitation can be stabilized at specific synapses by local protein synthesis.

In a culture system where a bifurcated Aplysia sensory neuron makes synapses with two motor neurons, repeated application of serotonin (5-HT) to one synapse produces a CREB-mediated, synapse-specific, long-term facilitation, which can be captured at the opposite synapse by a single pulse of 5-HT. Repeated pulses of 5-HT applied to the cell body of the sensory neuron produce a CREB-dependent, cell-wide facilitation, which, unlike synapse-specific facilitation, is not associated with growth and does not persist beyond 48 hr. Persistent facilitation and synapse-specific growth can be induced by a single pulse of 5-HT applied to a peripheral synapse. Thus, the short-term process initiated by a single pulse of 5-HT serves not only to produce transient facilitation, but also to mark and stabilize any synapse of the neuron for long-term facilitation by means of a covalent mark and rapamycin-sensitive local protein synthesis.

Animals↗

Dietary restriction protects hippocampal neurons against the death-promoting action of a presenilin-1 mutation.

Alzheimer's disease (AD) is an age-related disorder that involves degeneration of synapses and neurons in brain regions involved in learning and memory processes. Some cases of AD are caused by mutations in presenilin-1 (PS1), an integral membrane protein located in the endoplasmic reticulum. Previous studies have shown that PS1 mutations increase neuronal vulnerability to excitotoxicity and apoptosis. Although dietary restriction (DR) can increase lifespan and reduce the incidence of several age-related diseases in rodents, the possibility that DR can modify the pathogenic actions of mutations that cause AD has not been examined. The vulnerability of hippocampal neurons to excitotoxic injury was increased in PS1 mutant knockin mice. PS1 mutant knockin mice and wild-type mice maintained on a DR regimen for 3 months exhibited reduced excitotoxic damage to hippocampal CA1 and CA3 neurons compared to mice fed ad libitum; the DR regimen completely counteracted the endangering effect of the PS1 mutation. The magnitude of increase in levels of the lipid peroxidation product 4-hydroxynonenal following the excitotoxic insult was lower in DR mice compared to mice fed ad libitum, suggesting that suppression of oxidative stress may be one mechanism underlying the neuroprotective effect of DR. These findings indicate that the neurodegeneration-promoting effect of an AD-linked mutation is subject to modification by diet.

Alzheimer Disease↗

Mutagenic drinking water and risk of male esophageal cancer: a population-based case-control study.

Drinking mutagenic downstream water from the Huangpu River was hypothesized to have increased the risk for male esophageal cancer in Shanghai, China. The authors conducted a population-based case-control study of a total of 71 esophageal cancer deaths and 1,122 controls collected during a 5-year follow-up period, 1984-1988, from four male cohorts born before January 1, 1944, living in four communities consuming water with different mutagenicities in the Shanghai area. The controls represented a 1% random sample of the defined living cohorts selected at the end of each of the 5 years of follow-up. Logistic regression showed an odds ratio of 2.77 (95% confidence interval: 1.52, 5.03) for drinking mutagenic downstream water from the river versus drinking nonmutagenic upstream water after controlling for possible confounders including age, disease history (hepatitis, cirrhosis, schistosomiasis, digestive tract ulcer), hazardous occupational history, pesticide exposure, lifestyle factors (cigarette smoking, tea intake, and alcohol intake), dietary habits (intake of pickled vegetables, maize, peanuts, and cured meat), education, poverty, urban environment, and water chlorination.

Adult↗

Role of p53 and p21waf1/cip1 in senescence-like terminal proliferation arrest induced in human tumor cells by chemotherapeutic drugs.

Exposure of human tumor cell lines to moderate doses of anticancer agents induces terminal proliferation arrest accompanied by morphologic and enzymatic changes that resemble senescence of normal cells. We have investigated the role of p53 and p21waf1/cip1 in the induction of this response in drug-treated tumor cells. Doxorubicin treatment induced the senescence-like phenotype (SLP) and its associated terminal growth arrest in wild-type HCT116 colon carcinoma cells; this response was strongly decreased but not abolished in HCT116 lines with homozygous knockout of p53 or p21. Transduction of HT1080 fibrosarcoma cells with a genetic inhibitor of p53 also decreased the induction of SLP and increased drug-induced mitotic cell death. To determine if drug-stimulated p21 expression was responsible for senescence-like growth arrest, we have expressed different levels of p21 from an inducible promoter. While high-level overexpression of p21 was sufficient to induce SLP in HT1080 cells, the levels of p21 expressed in doxorubicin-treated cells could account for only a fraction of doxorubicin-induced SLP. Our results indicate that p53 and p21 act as positive regulators of senescence-like terminal proliferation arrest, but their function is neither sufficient nor absolutely required for this treatment response in tumor cells.

Antineoplastic Agents↗

Biochemical characterization of lucigenin (Bis-N-methylacridinium) as a chemiluminescent probe for detecting intramitochondrial superoxide anion radical production.

Direct detection of intramitochondrial superoxide anion radical (O(-*)(2)) production is of critical importance for investigating the pathophysiological consequences resulting from altered cellular reactive oxygen homeostasis. The purpose of this study with isolated mitochondria was to characterize the biochemical basis for lucigenin as a chemiluminescent probe to detect intramitochondrial O(-*)(2) production. Incubation of isolated mitochondria with lucigenin at non-redox cycling concentration produced lucigenin-derived chemiluminescence (LDCL), which was increased markedly by mitochondrial substrates, pyruvate/malate or succinate. The LDCL was reduced greatly by the membrane permeable superoxide dismutase (SOD) mimetics, 2,2,6,6-tetramethylpiperidine-N-oxyl and Mn(III)tetrakis(1-methyl-4-pyridyl)porphyrin, but not by Cu,Zn-SOD. With an ion-pair HPLC method, a concentration-dependent accumulation of lucigenin was detected within mitochondria. The accumulation of lucigenin by mitochondria was reduced markedly in the presence of carbonyl cyanide p-(trifluoromethoxy)phenyhyldrazone, an uncoupler known to dissipate the mitochondrial membrane potential. With submitochondrial particles, we observed that both complexes I and III of the mitochondrial electron transport chain appear to be able to catalyze the one electron reduction of lucigenin, a critical step involved in LDCL. After incubation of mitochondria with lucigenin at non-redox cycling concentrations, formation of N-methylacridone, the proposed end product of the reaction pathway leading to LDCL, within the mitochondrial fraction was also detected. In addition, a significant linear correlation was observed between the LDCL and either the lucigenin accumulation or the N-methylacridone formation within the mitochondria. Taken together, our results conclusively demonstrate that when properly used LDCL can reliably detect intramitochondrial O(-*)(2) production.

Acridines↗