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Biomedical subjects

X J Zeng

Publications and source records attributed to X J Zeng.

At least 19 recordsLinked to original sources

The prevalence of dental erosion in preschool children in China.

OBJECTIVE: To describe the prevalence of dental erosion and associated factors in preschool children in Guangxi and Hubei provinces of China. METHODS: Dental examinations were carried out on 1949 children aged 3-5 years. Measurement of erosion was confined to primary maxillary incisors. The erosion index used was based upon the 1993 UK National Survey of Children's Dental Health. The children's general information as well as social background and dietary habits were collected based on a structured questionnaire. RESULTS: A total of 112 children (5.7%) showed erosion on their maxillary incisors. Ninety-five (4.9%) was scored as being confined to enamel and 17 (0.9%) as erosion extending into dentine or pulp. There was a positive association between erosion and social class in terms of parental education. A significantly higher prevalence of erosion was observed in children whose parents had post-secondary education than those whose parents had secondary or lower level of education. There was also a correlation between the presence of dental erosion and intake of fruit drink from a feeding bottle or consumption of fruit drinks at bedtime. CONCLUSION: Erosion is not a serious problem for dental heath in Chinese preschool children. The prevalence of erosion is associated with social and dietary factors in this sample of children.

Beverages↗

Role of protein kinase A in GABAA receptor dysfunction in CA1 pyramidal cells following chronic benzodiazepine treatment.

One-week treatment with the benzodiazepine (BZ) flurazepam (FZP), results in anticonvulsant tolerance, associated with reduced GABAA receptor (GABAR) subunit protein and miniature inhibitory post-synaptic current (mIPSC) amplitude in CA1 neurons of rat hippocampus. Because protein kinase A (PKA) has been shown to modulate GABAR function in CA1 pyramidal cells, the present study assessed whether GABAR dysfunction is associated with changes in PKA activity. Two days after 1-week FZP treatment, there were significant decreases in basal (- 30%) and total (- 25%) PKA activity, and a 40% reduction in PKA RIIbeta protein in the insoluble fraction of CA1 hippocampus. The soluble component of CA1 showed a significant increase in basal (100%) but not total PKA activity. Whole-cell recording in vitro showed a 50% reduction in mIPSC amplitude in CA1 pyramidal cells, with altered sensitivity to PKA modulators. Neurons from FZP-treated rats responded to 8-bromo-cAMP with a significant increase (31%) in mIPSC amplitude. Likewise, vasoactive intestinal polypeptide (VIP), an endogenous PKA activator, caused a significant 36% increase in mIPSC amplitude in FZP-treated cells. Neither agent had a significant effect on mIPSC amplitude in control cells. This study supports a role for PKA in GABAR dysfunction after chronic FZP treatment.

8-Bromo Cyclic Adenosine Monophosphate↗

Role of bicarbonate ion in mediating decreased synaptic conductance in benzodiazepine tolerant hippocampal CA1 pyramidal neurons.

Chronic flurazepam treatment substantially impairs the function of GABAergic synapses on hippocampal CA1 pyramidal cells. Previous findings included a significant decrease in the synaptic and unitary conductance of CA1 pyramidal neuron GABA(A) receptor channels and the appearance of a GABA(A)-receptor mediated depolarizing potential. To investigate the ionic basis of the decreased conductance, whole-cell voltage-clamp techniques were used to record evoked, GABA(A) receptor-mediated IPSCs carried by HCO(3)(-)-Cl(-) or Cl(-) alone. Hippocampal slices were prepared from rats administered flurazepam orally for 1 week, 2 days after ending drug treatment. Slices were superfused with HCO(3)(-)-aCSF or with HEPES-aCSF (without HCO(3)(-)) plus 50 microM APV and 10 microM DNQX. The micropipette contained 130 mM CsCl and 1 microM QX-314. GABA(A) receptors located on pyramidal cell somata or dendrites were activated monosynaptically by maximal stimulation of GABAergic terminals at the stratum oriens-pyramidale (SO-SP) or stratum lacunosum-molecular (S-L-M) border, respectively. In HCO(3)(-)-aCSF, there was a significant reduction in synaptic-conductance in flurazepam-treated neurons following both SO-SP (control: 1058 pS, flurazepam: 226 pS, P<0.01) and S-L-M (control 998 pS, flurazepam: 179 pS, P<0.01) stimulation, as well as the total charge transfer, indicating a decreased HCO(3)(-)-Cl(-) flux. In HEPES-aCSF, the synaptic conductance and total charge transfer, and thus Cl(-) flux, was unchanged in flurazepam-treated neurons (SO-SP: control 588 pS, flurazepam: 580 pS, P>0.05; S-L-M: control 595 pS, flurazepam: 527 pS, P>0.05). Taken together, these findings suggest that a reduction in HCO(3)(-) flux may play a prominent role in mediating the action of GABA and that a loss of HCO(3)(-) conductance may significantly contribute to impaired GABA(A) receptor function after chronic benzodiazepine treatment.

Animals↗

Long-term efficacy of plasma-derived hepatitis B vaccine: a 15-year follow-up study among Chinese children.

To determine necessity and timing of booster of hepatitis B vaccine, we need to observe the duration of its protection. We report the results of a 15-year follow-up of a cohort of 649 children who participated a randomized, double blind, placebo-controlled trial on a plasma-derived hepatitis B vaccine in 1982. During the 15 years after vaccination, more vaccinated children had anti-HBs of 10 S/N ratios or over, compared with the controls, at all nine observations. At 15 years 50.0% (26/52) of the participants studied in the vaccinated group and 33.3% of the tested controls (18/54) retained anti-HBs levels of S/N ratios> or =10 (P < 0.09). However, since 5 years after vaccination, median S/N ratios of anti-HBs among the vaccinated children with detectable anti-HBs were lower than those of the controls except that detected at 15 years. 16.7% (9/54) of the tested children in the control group were HBsAg positive at 15 years after vaccination, in comparison with 1.9% (1/52) of the tested children in the vaccinated (P < 0.02). 28 chronic HBsAg carriers were identified in the control cohort over the 15 years, whereas only 1 case was noted in the vaccinated group (8.2% vs. 0.3%, P < 0.00001), corresponding to an efficacy of 96%.

Double-Blind Method↗

Benzodiazepine tolerance at GABAergic synapses on hippocampal CA1 pyramidal cells.

Modulation of GABA function following 1 week oral administration of flurazepam (FZP) was investigated in chloride-loaded, rat hippocampal CA1 pyramidal neurons. Rats were sacrificed 2 or 7 days after ending drug treatment, when anticonvulsant tolerance was present or absent in vivo, respectively. Spontaneous (s)IPSCs and miniature (m)IPSCs were recorded using whole-cell voltage-clamp techniques. s/mIPSCs were bicuculline-sensitive, voltage-dependent, and reversed their polarity at 0 mV, the predicted E(Cl-). Comparisons of s/mIPSCs between FZP-treated and control groups were made at Vh = -90, -70, and -50 mV. The frequency of sIPSCs, but not mIPSCs, was significantly decreased in FZP-treated neurons 2 days, but not 7 days, after FZP treatment, suggesting a decrease in interneuron activity. These conclusions were supported by the negative findings of additional studies of [3H]GABA release from hippocampal slices and [3H]GABA uptake from hippocampal synaptosomes. The lack of change in the paired-pulse depression of GABA(B)-mediated IPSPs suggested that autoreceptor function was also not impaired following chronic FZP treatment. A large reduction in both sIPSC and mIPSC amplitude (60%) in FZP-treated neurons, the absence of mIPSCs in one-third of FZP-treated cells, and a measurable reduction in synaptic and unitary conductance confirmed that postsynaptic GABA(A) receptor function was profoundly impaired in FZP-treated CA1 neurons. Zolpidem, an alpha1-selective benzodiazepine receptor ligand, enhanced mIPSC amplitude and decay, but its ability to prolong mIPSC decay was reduced in FZP-treated neurons. Several pre- and postsynaptic changes at GABAergic synapses on CA1 pyramidal cells might be related to the decreased tonic GABA inhibition in FZP-treated CA1 neurons associated with the expression of benzodiazepine anticonvulsant tolerance.

Animals↗

Benzodiazepine-mediated regulation of alpha1, alpha2, beta1-3 and gamma2 GABA(A) receptor subunit proteins in the rat brain hippocampus and cortex.

Prolonged flurazepam exposure regulates the expression of selected (alpha1, beta2, beta3) GABA(A) receptor subunit messenger RNAs in specific regions of the hippocampus and cortex with a time-course consistent with benzodiazepine tolerance both in vivo and in vitro. In this report, the immunostaining density of six specific GABA(A) receptor subunit (alpha1, beta2, beta1-3 and gamma2) antibodies was measured in the hippocampus and cortex, among other brain areas, in slide-mounted brain sections from flurazepam-treated and control rats using quantitative computer-assisted image analysis techniques. In parallel with the localized reduction in alpha1 and beta3 subunit messenger RNA expression detected in a previous study, relative alpha1 and beta3 subunit antibody immunostaining density was significantly decreased in flurazepam-treated rat hippocampal CA1, CA3 and dentate dendritic regions, and in specific cortical layers. Quantitative western blot analysis showed that beta3 subunit protein levels in crude homogenates of the hippocampal dentate region from flurazepam-treated rats, an area which showed fairly uniform decreases in beta3 subunit immunostaining (16-21%), were reduced to a similar degree (18%). The latter findings provide independent support that relative immunostaining density may provide an accurate estimate of protein levels. Consistent with the absence of the regulation of their respective messenger RNAs immediately after ending flurazepam administration, no changes in the density of alpha2, beta1 or beta2 subunit antibody immunostaining were found in any brain region. gamma2 subunit antibody staining was changed only in the dentate molecular layer. The selective changes in GABA(A) receptor subunit antibody immunostaining density in the hippocampus suggested that a change in the composition of GABA(A) receptors involving specific subunits (alpha1 and beta3) may be one mechanism underlying benzodiazepine anticonvulsant tolerance.

Animals↗

Antagonist-induced reversal of functional and structural measures of hippocampal benzodiazepine tolerance.

One week oral flurazepam (FZP) administration in rats results in anticonvulsant tolerance in vivo, tolerance measured in vitro in hippocampal CA1 pyramidal cells, and regulation of hippocampal gamma-aminobutyric acid(A)-receptor subunit protein expression. A single injection (4 or 20 mg/kg i.p) of the benzodiazepine antagonist flumazenil (FLM) was given 1 day after FZP treatment, and tolerance and subunit protein expression were evaluated 1 day later. In vivo tolerance was measured by a reduced ability of the alpha(1)-subunit-selective agonist zolpidem to suppress pentylenetetrazole-induced seizures. This tolerance was reversed by 20 but not 4 mg/kg FLM. In in vitro hippocampal slices, there was tolerance to the effect of zolpidem to prolong the decay of pyramidal cell miniature inhibitory postsynaptic currents, which was reversed by FLM (4 mg/kg) pretreatment. A reduction in miniature inhibitory postsynaptic current amplitude ( approximately 50%) was also restored by FLM injection. [(3)H]Zolpidem binding measured 0, 2, and 7 days after FZP treatment was significantly decreased in the hippocampus and cortex at 0 days but not thereafter. Changes in alpha(1)- and beta(3)-subunit protein expression were examined via quantitative immunohistochemical techniques. alpha(1)-Subunit protein levels were down-regulated in the CA1 stratum oriens and beta subunit levels were up-regulated in the stratum oriens and stratum radiatum of the CA3 region. Chronic FZP effects on alpha(1)- and beta(3)-subunit protein levels were also reversed by prior FLM injection. FLM's effect on both functional and structural correlates of benzodiazepine tolerance suggests that each of these measures plays an interdependent role in mediating benzodiazepine tolerance.

Animals↗

Patterns and determinants of use of antibiotics for acute respiratory tract infection in children in China.

BACKGROUND: Use of antibiotics for acute respiratory infection (ARI) of presumed viral etiology is a worldwide problem. The World Health Organization (WHO) has provided guidelines for diagnosis and treatment of ARI for developing countries. METHODS: Specially trained observers applied the WHO criteria to study the diagnosis and treatment of ARI given by 100 randomly selected health care workers (HCWs) in a rural county in China. A total of 750 cases of ARI were evaluated. RESULTS: Before the parents sought medical care, 47% of children in the county hospitals, 25% of those in the townships and 18% of those in the villages had already received antibiotics, available without prescription. Among the HCWs antibiotic abuse (antibiotics for presumably viral disease) was detected in the treatment of 97% of cases, and severe abuse (such as prescription of two incompatible antibiotics) was detected in 37%. Most (197 of 200) patients with bacterial disease received antibiotics, but inappropriate antibiotic treatment (dose or type) was observed in 63% of these cases. HCWs with university training and those with higher test scores on knowledge and attitude prescribed antibiotics more judiciously than those lacking those attributes. CONCLUSIONS: Abuse of antibiotics for ARI is a serious and costly problem in rural China, potentially leading to widespread antibiotic resistance. Educating HCWs in the management of ARI and proper use of antibiotics has high priority in China.

Acute Disease↗

[Effects of tripchlorolide (T4) of Tripterygium Wilfordii Hook on the production of immunoglobulins by peripheral blood mononuclear cells and by synovial cells of rheumatoid arthritis patients in vitro].

Tripchlorolide(T4) is an active ingredient recently isolated from Tripterygium Wilfordii Hook. The in vitro effects of T4 on the peripheral blood mononuclear cells(PBMC) of healthy persons(n = 10), the digested single synovium cells(DSSC) (n = 3) and PBMC(n = 6) from RA patients on production of immunoglobulins (Ig) were studied using Elisa method. The results showed that T4 at concentrations from 5 ng.ml-1 to 35 ng.ml-1 significantly reduced the production of Ig by PWM-stimulated PBMC of healthy persons in a dose dependent manner. At concentration of 25 ng.ml-1, T4 also reduced the Ig secretion of RA-PBMC and DSSC. It is hoped that T4 would be an encouraging new drug of herbal nature for the treatment of RA.

Adult↗

Insulinoma: 31 years of tumor localization and excision.

This report is based on 31 years of experience with 116 cases of hyperinsulinism. Six cases had hypertrophy of the islets of Langerhans, 3 had widespead metastasis from malignant insulinomas, and 107 were benign adenoma cases. An immunoreactive insulin to glucose ratio of 0.3 of the peripheral venous blood before operation is of great value in diagnosing hyperinsulinism. Intraoperatively, immunoreactive insulin assay of the portal blood (IRI) is very valuable in determining if an insulinoma remains. The dividing line is 100 microU.ml-1. In localizing the tumor, "differential" PTPC is important before operation. During the operation, fine needle aspiration cytology may assist in ascertaining if the palpable tumor is an insulinoma. Multiple fine needle aspiration cytology examinations can sometimes reveal an insulinoma in an indurated pancreas. Portal vein blood IRI and blood sugar assays may serve to confirm if removal of the insulinoma is complete. Removal of the insulinoma controls hypoglycemia satisfactorily, but the brain damage incurred by prolonged hypoglycemia cannot be significantly altered. Removal of the tumor should be by enucleation, and the raw surface of the pancreas should be drained not sutured.

Adenoma, Islet Cell↗