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Biomedical subjects

X Yang

Publications and source records attributed to X Yang.

At least 865 records · Page 48Linked to original sources
PubMed1996

Yeast SNF1 protein kinase interacts with SIP4, a C6 zinc cluster transcriptional activator: a new role for SNF1 in the glucose response.

The SNF1 protein kinase has been widely conserved in plants and mammals. In Saccharomyces cerevisiae, SNF1 is essential for expression of glucose-repressed genes in response to glucose deprivation. Previous studies supported a role for SNF1 in relieving transcriptional repression. Here, we report evidence that SNF1 modulates function of a transcriptional activator, SIP4, which was identified in a two-hybrid screen for interaction with SNF1. The N terminus of the predicted 96-kDa SIP4 protein is homologous to the DNA-binding domain of the GAL4 family of transcriptional activators, with a C6 zinc cluster adjacent to a coiled-coil motif The C terminus contains a leucine zipper motif and an acidic region. When bound to DNA, a LexA-SIP4 fusion activates transcription of a reporter gene. Transcriptional activation by SIP4 is regulated by glucose and depends on the SNF1 protein kinase. Moreover, SIP4 is differentially phosphorylated in response to glucose availability, and phosphorylation requires SNF1. These findings suggest that the SNF1 kinase interacts with a transcriptional activator to modulate its activity and provide the first direct evidence for a role of SNF1 in activating transcription in response to glucose limitation.

Amino Acid Sequence↗
PubMed1996

A new compound heterozygous frameshift mutation in the type II 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) gene causes salt-wasting 3 beta-HSD deficiency congenital adrenal hyperplasia.

We report a new compound heterozygous frameshift mutation in the type II 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) gene in a Pakistanian female child with the salt-wasting form of 3 beta-HSD deficiency congenital adrenal hyperplasia. The child, born with clitoral enlargement, manifesting salt-wasting adrenal crisis, and public hair growth during infancy, was treated with hormonal replacement therapy. The etiology of her congenital adrenal hyperplasia, however, was not defined. Two of her siblings, as well as one paternal cousin with ambiguous genitalia and palpable gonads and another paternal cousin with normal female genitalia, had symptoms of adrenal crisis and died during early infancy. Thus, although the family history suggested possible 3 beta-HSD deficiency disorder, suppressed adrenal function caused by excess glucocorticoid therapy in this child at 7 yr of age did not allow hormonal diagnosis. To confirm 3 beta-HSD deficiency, we sequenced the type II 3 beta-HSD gene in the patient, her family, and the parents of her decreased paternal cousins. The type II 3 beta-HSD gene region of a putative promoter, exons I, II, III, and IV, and exon-intron boundaries were amplified by PCR and sequenced in all subjects. The DNA sequence of the child revealed a single nucleotide deletion at codon 318 [ACA (Thr)-->AA] in exon IV in one allele, and two nucleotide deletions at codon 273 [AAA(Lys)-->A] in exon IV in the other allele. The remaining gene sequences were normal. The codon 318 mutation was found in one allele from the father, brother, and parents of the deceased paternal cousins. The codon 273 mutation was found in one allele of the mother and a sister. These findings confirmed inherited 3 beta-HSD deficiency in the child caused by the compound heterozygous type II 3 beta-HSD gene mutation. Both codon 273 and 318 mutations yielding frameshift and premature stop codons at codons 279 and 367, respectively, are predicted to result in an altered and truncated type II 3 beta-HSD protein, thereby causing salt-wasting 3 beta-HSD deficiency in the patient. The type II 3 beta-HSD gene findings and clinical history of her family members suggest that the patient's deceased siblings were likely affected males with the same compound heterozygous mutations of the gene as in the proband, whereas the deceased cousins were likely affected with the homozygous codon 318 mutation in the gene.

3-Hydroxysteroid Dehydrogenases↗
PubMed1996

Studies of 3 beta-hydroxysteroid dehydrogenase genes in infants and children manifesting premature pubarche and increased adrenocorticotropin-stimulated delta 5-steroid levels.

Classic 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) deficiency congenital adrenal hyperplasia (CAH) results from a mutation in the type II 3 beta HSD gene encoding adrenal and gonadal 3 beta HSD. We investigated the type II and type I 3 beta HSD gene sequences in 15 infants and children with premature pubarche (PP; mean/range of age at PP, 4/0.08-9 yr) and elevated ACTH-stimulated delta 5 precursor steroid levels. Compared to Tanner I control subjects of similar age, ACTH-stimulated hormonal levels were at 2.3-10.7 SD for 17-hydroxypregnenolone (delta 5-17P) in all PP subjects, at 2.2-17 SD for dehydroepi-androsterone (DHEA) and 2.4-5.6 SD for the delta 5-17P/cortisol (F) ratio in all PP subjects except 1 infant, and at 2.3-10 SD for the DHEA/ androstenedione (delta 5-A) ratio in 8 PP subjects. Compared to Tanner II normal children, the hormonal levels were at 3-8 SD for delta 5-17P in all 13 PP children, at 2.3-4.7 SD for the delta 5-17P/F ratio in 6 PP children, and at 2.3-6.5 SD for DHEA and 3.5-9 SD for the DHEA/delta 4-A ratio in 7 PP children. Type II 3 beta HSD gene sequences, including regions of a putative promoter, all exons (I, II, III, and IV), and exon-intron boundaries, were normal in all subjects. Sequences of the type I 3 beta HSD gene encoding extraadrenal and extragonadal 3 beta HSD were normal in the 6 patients tested. The ACTH-stimulated delta 5-17P levels and delta 5-17P/F ratios in the PP children without type II 3 beta HSD gene mutation were exceedingly lower than the respective reported hormonal data for children with 3 beta HSD deficiency CAH with proven type II 3 beta HSD gene mutation. The ACTH-stimulated DHEA levels and DHEA/delta 4-A ratios were not exceedingly different between the children with and without type II 3 beta HSD gene mutation. These findings suggest that the degree of ACTH-stimulated delta 5 precursor steroid abnormality, such as delta 5-17P levels up to 10 SD above the normal mean level found in our PP patients, is not caused by a mild variant of 3 beta HSD deficiency CAH resulting from type II or type I 3 beta HSD gene mutation. The hormonal criterion for ACTH-stimulated delta 5-17P levels in patients with mild variant 3 beta HSD deficiency, therefore, is predicted to be higher than 10 SD above the normal mean value.

17-alpha-Hydroxypregnenolone↗
PubMed1996

Association of HLA class II alleles in patients with juvenile myoclonic epilepsy compared with patients with other forms of adolescent-onset generalized epilepsy.

Reports have suggested an association of juvenile myoclonic epilepsy (JME) with an HLA-DR allele. We examined the HLA-DR and DQ frequencies in two populations of epilepsy patients: (1) JME patients and (2) patients with other forms of adolescent-onset, idiopathic generalized epilepsy (IGE). We did DNA-based HLA typing on 24 JME patients and 24 patients with non-JME forms of adolescent-onset IGE, forms that are clinically similar to JME. In typing the HLA region, we paid particular attention to the alleles contributing to the HLA-DR13 type and also to the DQB1 locus alleles that are in linkage disequilibrium with the alleles that comprise the DR13 type. We also examined the HLA-AP locus, which is centromeric to the DR locus. The frequency of DR13 was significantly higher in JME compared with the non-JME patients. Nine JME patients, compared with two non-JME patients, carried that type (chi 2 = 5.78 [p < 0.017, 1 df]). The odds ratio was 6.6. Furthermore, the DQB1 alleles in linkage disequilibrium with the alleles contributing to the DR13 type were also more frequent in JME than in non-JME epilepsy patients. The chi 2 is highly significant (8.1, p < 0.005) with an odds ratio of 13.8. These results confirm that JME is an HLA-associated form of epilepsy. They also show that the JME locus probably lies within the HLA region, most likely between the HLA-DP and HLA-B loci. The association studies also confirm linkage results showing that JME is genetically different from some other IGEs and emphasize that careful diagnosis is critical to genetic studies of the epilepsies.

Adolescent↗
PubMed1996

Strategic effects of early season treatments with Moxidectin on trichostrongylosis in young calves.

This study was conducted to evaluate the effects of strategic early season treatments with Moxidectin on trichostrongyles in first-season grazing heifer calves on a permanent pasture. Three groups of Black-Pied Friesian heifer calves were turned out in early May on a permanent pasture naturally infected with trichostrongyle larvae. Two of these groups were treated with Moxidectin at turnout or at turnout and again 8 weeks later, while one group served as untreated controls. For the first three weeks of the experiment all animals grazed together in one flock on one pasture. Subsequently, the pasture was divided into three comparable plots, which from then and until housing in mid October were grazed by each calf group. The results showed that the treatments significantly suppressed faecal egg excretion in the early part of the season, leading to reduced herbage infectivity and parasitism over the rest of the season. Results from faecal egg counts determined at genus level revealed that the persistent activity of Moxidectin appeared to be longer against Ostertagia spp. than against Cooperia spp. Two Moxidectin treatments, given at turnout and on week 8, protected the calves to a higher degree than a single Moxidectin treatment given at turnout. However, there was also a significant effect of only one Moxidectin treatment which possibly could be explained by a low overwintered larval population and a drought period in the early summer.

Animals↗
PubMed1996

Nicotine-induced inhibition in medial septum involves activation of presynaptic nicotinic cholinergic receptors on gamma-aminobutyric acid-containing neurons.

Neuronal responses to drugs acting on nicotinic cholinergic receptors (nAChRs) were examined in the rat medial septal area by using an in vivo extracellular single-unit recording technique. In the medial septal area, iontophorectically applied nicotine inhibited neuronal activity in 45% of the neurons, but had no effect on the remaining neurons. Dihydro-beta-erythroidine application to neurons in the medial septal area not only blocked nicotine-induced inhibition, but also reduced spontaneous neuronal activity of the neurons. When Mg++ was applied iontophoretically to block presynaptic neurotransmitter release, a significant reduction in spontaneous neural activity also was observed. No further reduction of spontaneous activity by dihydro-beta-erythroidine occurred in the presence of Mg++, suggesting an apparent tonic excitatory input to the majority of neurons in the medial septal area under the control of presynaptic nAChRs. Mg++ abolished the nicotine-induced inhibition in the medial septal area without having an effect on nicotine-induced inhibition in the cerebellum. Thus, these data provide evidence that the inhibitory effects of nicotine in the medial septum are due to an action on presynaptic nAChRs, controlling the release of an inhibitory neurotransmitter. Of the medial septal neurons which showed no response to nicotine, nicotine produced excitation in 21% of the cells after Mg++ application, indicating that nicotine can have a direct action on postsynaptic nAChRs, in addition to its presynaptic action, in the medial septum. Finally, application of the gamma-aminobutyric acid antagonist bicuculline reduced the nicotine-induced inhibition on the majority of medial septal neurons tested, but was without effect on the inhibition produced by nicotine on cerebellar Purkinje neurons. Consequently, it can be concluded that the nicotine-induced inhibition in the medial septum is the result of gamma-aminobutyric acid release due to its action on presynaptic nAChRs present on gamma-aminobutyric acid-containing terminals.

Animals↗
PubMed1996

Limiting dilution analysis of CD4 T-cell cytokine production in mice administered native versus polymerized ovalbumin: directed induction of T-helper type-1-like activation.

Polarized expression of T-helper type-1 (Th1)- or Th2-like patterns of cytokine production frequently correlates with disease outcome. Previously, we have described the long-lived reciprocal regulation of ovalbumin (OVA)-specific IgE (> 95% inhibition) and IgG2a (300-800-fold increased) production following administration of high MW OVA polymers (OVA-POL), in both de novo and ongoing OVA (alum)-induced responses. Here, limiting dilution analysis (LDA) was used to compare precursor frequencies of CD4 T cells producing interferon-gamma (IFN-gamma), interleukin-4 (IL-4) or IL-10 following OVA versus OVA-POL exposure in vivo. Adjuvants were not used, so as to circumvent their impact on measurement of precursor frequencies. We found that the two forms of antigen elicited T-cell activation of comparable intensity, as indicated by equivalent precursor frequencies of clonogenic antigen-specific CD4 T cells. However, they elicited qualitatively different cytokine responses. OVA-POL treatment led to 10-fold higher (mean of six independent LDA experiments) frequencies of IFN-gamma-producing cells, and a mean fivefold lower frequency of IL-10-producing cells, than was observed following in vivo administration of unmodified OVA. Thus, the high MW polymerized form of antigen acted to steer commitment of naive (for this antigen) CD4 T-cell activation from a situation in which IL-10 producers outnumbered IFN-gamma-producing cells by a factor of 4:1 (found in mice administered OVA), to one where IFN-gamma producers dominated by a factor of 11:1 (in mice given OVA-POL), i.e. a qualitative shift in the nature of the OVA-specific response induced from Th2-like to Th1-like. In vivo co-administration of anti-IFN-gamma monoclonal antibody (mAb) abolished the capacity of OVA-POL to preferentially elicit Th1-like dominance. Interestingly, although the ratios of IFN-gamma:IL-4 and IFN-gamma:IL-10 OVA-specific precursor frequencies were strongly increased following OVA-POL exposure (mean 18- and 47-fold higher), the frequency of IL-4-producing CD4 T cells did not differ significantly. The data suggest that this modified antigen promotes in vivo commitment of naive T cells towards a Th1-like response, with consequent inhibition of IgE and enhancement of IgG2a responses, not through direct effects on IL-4 production, but via decreased frequencies of IL-10 and increased frequencies of IFN-gamma-producing OVA-specific CD4 cells. Collectively, the data (1) demonstrate the ability to manipulate commitment of antigen-driven CD4 T-cell populations in naive mice to specific patterns of cytokine gene expression, and (2) provide in vivo evidence of the regulatory role played by IFN-gamma in limiting induction and/or expansion of IL-4- and IL-10-producing CD4 cells to protein allergens.

Animals↗
PubMed1996

[The cytochemical observation of inosine effect on glucose metabolism of BGC-823 human gastric carcinoma cell line].

The activity of intracellular lactic acid dehydrogenase (LDH) and succinic acid dehydrogenase (SDH) was studied by cytochemistry in BGC-823 gastric carcinoma cell line treated with inosine. Cytoplasmic granules of LDH were found decreased or completely disappeared, while little change of SDH was observed. The tumor cells were decreased in number and became atrophic, especially when the cells were treated with high concentrations of inosine. The results suggest that inosine can play a role in suppressing the activity of intracellular LDH, thus blocking the major source of energy supply of cancer cells.

Energy Metabolism↗
PubMed1996

Selective arterial embolization in the management of internal bleeding caused by trophoblastic diseases.

OBJECTIVE: To evaluate the efficacy and safety of selective arterial embolization in the management of internal bleeding caused by trophoblastic diseases. PATIENTS AND METHODS: Four patients with internal bleeding caused by trophoblastic diseases were diagnosed with arteriography and treated with selective arterial embolization as a life-saving measure. Effect of controlling bleeding was assessed by follow-up arteriogram and clinical observation. RESULTS: The embolization successfully controlled the bleeding in all patients. Operation time was short with a mean of 42 minutes. The shock was corrected dramatically. Fever and pain were common complications. CONCLUSION: Selective arterial embolization is a life-saving measure in the management of internal bleeding caused by trophoblastic diseases.

Adult↗
PubMed1996

[Inhibitory action of Chinese compound prescription for reinforcing vital energy and invigorating blood circulation on cancer cell multiplication].

Experiments have proved that the Chinese compound prescription for reinforcing vital energy and invigorating blood circulation markedly helps to improve the morphology of cancer cell nucleolus and membrane surface microvillus, amend the composition of microtubulin and facilitate intercellular gap junctional communication. Cell cycle kinetics shows that the multiplication of cancer cells in human stomach is checked mainly at G2M stage.

Adenocarcinoma, Mucinous↗
PubMed1996

[Selective arterial catheterization in the management of drug-resistant choriocarcinoma].

OBJECTIVE: In order to save the life of the patients with drug-resistant choriocarcinoma due to improper treatment, selective arterial catheterization was used. METHODS: All the 71 cases were treated with systemic chemotherapy together with pelvic selective arterial chemotherapy. 5 of them had arterial chemotherapy plus arterial embolization for hemorrhage. In 13 patients who had lung metastasis, intraarterial injection of methotrexate (MTX) through bronchial arterial was added. RESULTS: 55 of 71 (77.8%) achieved complete remission and 10 (14.1%) had partial remission. One patient failed to follow-up. 5 died of various causes during hospitalization. On Follow-up 12 had survived for more than 5 years with no signs of recurrence. 2 of them had childbirth after recovery. CONCLUSION: Systemic intravenous infusion chemotherapy in combination with arterial chemotherapy is useful for drug-resistant choriocarcinoma. In patients with intraperitoneal hemorrhage caused by tumor rupture, selective arterial embolization should be used as emergency treatment to effectively control the bleeding, in order that patients will have a chance for further chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

[Cardiotoxicity of 5-fluorouracil].

OBJECTIVE: To determine the possibility and magnitude of cardiotoxicity following high dose intravenous infusion of fluorouracil (5-FU). METHODS: A prospective clinical study was performed on 104 patients with choriocarcinoma and invasive mole. 5-FU was administered by slow intravenous infusion in 5% glucose 500 ml for 8 hours at doses of 28-30 mg.kg-1.day-1 when used as a single agent treatment or 24-26 mg.kg-1.day-1 when used in combination with kengshengmycin (KSM). The total cycles of treatment with 5-FU + KSM were 109 and those of 5-FU or KSM each used as a single agent were 71 and 12 respectively. The cardiac functions were monitored by cardiac symptoms, ECG and serum cardiac enzymes before and after 5-FU infusion. RESULTS: Among the 192 treatment cycles tachycardia, palpitation or cardiac distress were observed in 14 cycles. ECG showed changes of ST or T waves in 8 cycles, sinus tachycardia in 3 cycles. The results of serum cardiac enzyme determinations were variable. The diagnostic criteria of cardiotoxicity were appearances of abnormalities manifested in any two of the three monitor items. The incidence of cardiotoxicity was 4.2% in 5-FU group, 4.6% in 5-FU + KSM group and 0% in KSM group. All episodes were mild, reversible spontaneously after cessation of chemotherapy and did not reappear in subsequent chemotherapeutic cycles. Seven patients with definite cardiac diseases before chemotherapy were given 5-FU treatment, but no obvious aggravation of cardiotoxicities were observed even with repeated 5-FU treatments. CONCLUSION: Only occasional cardiotoxicities were observed in 5-FU treatments. They were rather mild and reversible. The incidence of cardiotoxicity might be reduced with emphasis on strict observance of the treatment regimen in regard to the dosage used, the speed of the infusion and attention to the treatment of any side-effects.

Adult↗
PubMed1996

Comparison of dark- and light-adapted carp retinas with NADPH diaphorase staining.

The carp retina was examined by NADPH diaphorase histochemistry to determine if the staining pattern of retinal cells was changed depending on the adaptation state of the retina. When dark-adapted for 5 h, ellipsoids of inner segments of both rods and cones and some horizontal cells were heavily stained. Staining was also found in subpopulations of amacrine cells and ganglion cells. In addition, Müller cells were strongly positive for NADPH diaphorase. When light-adapted for 5 h, ellipsoids of photoreceptors and ganglion cells were less intensely stained, whereas Müller cells and horizontal cells became negative for NADPH diaphorase. Furthermore, rod ON-center bipolar cells were clearly stained. The difference of staining of amacrine cells between dark- and light-adapted retinas was not significant. The differences in diaphorase-staining pattern between dark- and light-adapted retinas suggest that Müller cells, some horizontal cells and rod ON-center bipolar cells contain inducible nitric oxide synthase, whose induction depends on the adaptation state.

Adaptation, Ocular↗
PubMed1996

Cobalt ions enhance light responsiveness of carp cone horizontal cells in low calcium.

Effects of cobalt ions (Co2+) on horizontal cells in low extracellular calcium were examined in isolated, superfused carp retinas. While 0.1 mmol/L Co2+ completely suppressed both rod- and cone-driven horizontal cells in normal Ringer's solution, it enhanced light responses of cone horizontal cells in low (0.1 mmol/L) calcium. The enhancement of the cone horizontal cell response by Co2+ was not caused by changes in light responsiveness of cone photoreceptors. Moreover, application of 50 mumol/L IBMX, an inhibitor of phosphodiester enzyme, reduced the suppressive effect of 0.1 mmol/L Co2+ in normal Ringer's solution. In consequence, the above-described enhancement of the cone horizontal cell light responsiveness may be due to a depolarization of cones caused by low calcium, which increases the activity of voltage-dependent calcium channels at cone terminals.

1-Methyl-3-isobutylxanthine↗
PubMed1996

Evidence for a selective effect of ethanol on N-methyl-d-aspartate responses: ethanol affects a subtype of the ifenprodil-sensitive N-methyl-d-aspartate receptors.

An extracellular electrophysiological approach was used to determine the effect of ethanol on responses to N-methyl-D-aspartate (NMDA) across several brain regions in urethane-anesthetized rats. The results indicated that, in most brain regions, ethanol inhibited the NMDA-induced increases in firing rate for some, but not all, spontaneously active neurons. Ethanol functioned as an NMDA antagonist for some neurons in the medial septum, red nucleus, deep mesencephalic nucleus, substantia nigra reticulata, ventral tegmental area and cerebellum. In the hippocampus, ethanol inhibited NMDA responses from all neurons. However, ethanol was not found to be active against NMDA responses in the lateral septum, suggesting that there is a degree of regional specificity for ethanol inhibition of NMDA responses. It was then established in unanesthetized rats that ethanol also antagonized responses to NMDA in some, but not all, neurons in the medial septum and cortex, indicating that the differential action of ethanol on NMDA responses obtained in the urethane-anesthetized rats was not due to the anesthetic. Based on an earlier study showing that the effects of ifenprodil and ethanol on NMDA responses were correlated, the ability of ethanol to inhibit NMDA responses was compared with changes produced by ifenprodil on the same neurons, where ethanol did or did not affect NMDA responses. In the several brain regions investigated, ethanol inhibited NMDA responses in a subgroup of neurons in which ifenprodil inhibited NMDA-induced increases in firing. For all neurons investigated, if a cell was insensitive to ifenprodil antagonism of NMDA responses then ethanol also was ineffective against the response to NMDA. These results suggest that ethanol acts on an ifenprodil-sensitive NMDA receptor subtype. Given that previous investigations have suggested that the NMDA receptor type 2B subunit is essential for the action of ifenprodil, the positive relationship between the actions of ifenprodil and ethanol on responses to NMDA is consistent with the hypothesis that the combination of specific receptor subunits forming an NMDA receptor on a neuron determines the ability of ethanol to antagonize an NMDA response.

Animals↗