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Biomedical subjects

W Guo

Publications and source records attributed to W Guo.

At least 145 records · Page 8Linked to original sources
PubMed1999

[Extra-trabeculotomy and trabeculectomy in treatment of primary infantile glaucoma].

OBJECTIVE: To compare the effectiveness and complication of extra-trabeculotomy and trabeculectomy in the treatment of primary infantile glaucoma. METHOD: Patients with primary infantile glaucoma and having undergone either of the two procedures from Jan, 1992 - June, 1996 were selected. Among them, group one (30 patients, 51 eyes) underwent extra-trabeculotomy, while group two (26 patients, 46 eyes) underwent trabeculectomy. RESULTS: The success rates in group one were 92.2% at the time of discharge and 87.5% during follow-up (mean 26.3 months); the rates in group two were 73.9% and 62.9% (mean 28.1 months) respectively, the differences being significant (P < 0.05). In group one, there was no severe complication, while in group two, two cases had vitreous prolapse. CONCLUSION: Extra-trabeculotomy is more efficacious and safer than trabeculectomy in the treatment of primary infantile glaucoma. It should be the first choice in the treatment of primary infantile glaucoma.

Child↗
PubMed1999

[An analysis of nutritional and harmful components of vegetables grown in plastic greenhouses].

OBJECTIVE: To study the changes in nutritional and harmful components of vegetables grown in plastic greenhouses. METHODS: In plastic greenhouses, microclimate and air concentrations of carbon monoxide, carbon dioxide, fluoride and respirable particulate were measured, and chlorophyll, total sugar, crude fiber, nitrite, fluoride, arsenic and some mineral elements in vegetables were determined as compared with those grown in the open-air fields. RESULTS: Greenhouse appeared a lower wind speed and darker illumination. Contents of chlorophyll a an b, total chlorophyll, reduced vitamin C, crude fiber in vegetables grown in greenhouse all were lower than those grown in open-air fields. Contents of potassium, calcium, magnesium, iron, zinc, copper and phosphorous were all lower in the vegetables grown in greenhouse than those grown in open-air fields. The contents of chlorophyll reducing Vitamin C. CONCLUSION: Lower wind speed and inadequate illumination in greenhouse affected photosynthesis and uptake of water in vegetables causing changes in their nutritional components. But, no contamination of burning coal was found in vegetables grown in greenhouse.

Air Pollutants↗
PubMed1999

[Electroencephalography and transcranial Doppler analysis in children with migraine].

Electroencephalogram(EEG) and transcranial Doppler(TCD) recordings were carried out in 25 children with migraine during ictal and interictal period. The results were that the abnormal rate of EEG and TCD was 85% and 72%, respectively; the positive rate of EEG provoked test was 60%; there was the single untypical epileptiform wave in the occipital in 3 patients by EEG. We conclude that EEG combined TCD examination in migraine can increase the correct rate of diagnosis and help to differ epilepsy from migraine.

Adolescent↗
PubMed1998

[Effect of impactor sampling on the ratio of respirable dust concentration to total dust concentration].

The aim of this study was to verify the change of the ratio of Respirable Dust Concentration (RDC) to Total Dust Concentration (TDC) taken by two-stage impactor sampling. The results showed that there was a correlation between the ratio of RDC/TDC and TDC (correlation coefficient was 0.8576, 0.8689, 0.8736 and 0.9674, respectively) under the condition of identical sampling volume, and the ratio increases along with the elevated TDC.

Air Pollutants, Occupational↗
PubMed1998

Oncogene-dependent apoptosis is mediated by caspase-9.

Understanding how oncogenic transformation sensitizes cells to apoptosis may provide a strategy to kill tumor cells selectively. We previously developed a cell-free system that recapitulates oncogene dependent apoptosis as reflected by activation of caspases, the core of the apoptotic machinery. Here, we show that this activation requires a previously identified apoptosis-promoting complex consisting of caspase-9, APAF-1, and cytochrome c. As predicted by the in vitro system, preventing caspase-9 activation blocked drug-induced apoptosis in cells sensitized by E1A, an adenoviral oncogene. Oncogenes, such as E1A, appear to facilitate caspase-9 activation by several mechanisms, including the control of cytochrome c release from the mitochondria.

Adenovirus E1A Proteins↗
PubMed1998

Identification of the binding surface on Cdc42Hs for p21-activated kinase.

The Ras superfamily of GTP-binding proteins is involved in a number of cellular signaling events including, but not limited to, tumorigenesis, intracellular trafficking, and cytoskeletal organization. The Rho subfamily, of which Cdc42Hs is a member, is involved in cell morphogenesis through a GTPase cascade which regulates cytoskeletal changes. Cdc42Hs has been shown to stimulate DNA synthesis as well as to initiate a protein kinase cascade that begins with the activation of the p21-activated serine/threonine kinases (PAKs). We have determined previously the solution structure of Cdc42Hs [Feltham et al. (1997) Biochemistry 36, 8755-8766] using NMR spectroscopy. A minimal-binding domain of 46 amino acids of PAK was identified (PBD46), which binds Cdc42Hs with a KD of approximately 20 nM and inhibits GTP hydrolysis. The binding interface was mapped by producing a fully deuterated sample of 15N-Cdc42Hs bound to PBD46. A 1H,15N-NOESY-HSQC spectrum demonstrated that the binding surface on Cdc42Hs consists of the second beta-strand (beta2) and a portion of the loop between the first alpha-helix (alpha1) and beta2 (switch I). A complex of PBD46 bound to 15N-Cdc42Hs.GMPPCP exhibited extensive chemical shift changes in the 1H,15N-HSQC spectrum. Thus, PBD46 likely produces structural changes in Cdc42Hs which are not limited to the binding interface, consistent with its effects on GTP hydrolysis. These results suggest that the kinase-binding domain on Cdc42Hs is similar to, but more extensive than, the c-Raf-binding domain on the Ras antagonist, Rap1 [Nassar et al. (1995) Nature 375, 554-560)].

Amino Acid Sequence↗
PubMed1998

The upstream, direct repeat sequence of Prague A Rous sarcoma virus is deficient in mediating efficient Gag assembly and particle release.

Rous sarcoma virus (RSV) contains two approximately 135-nt imperfect direct repeats composed of smaller repeats, dr1 (approximately 100 nt) and dr2 (approximately 36 nt), that are between the env and src genes and downstream of src in the 3' untranslated region, respectively. It has previously been shown that a Prague A RSV mutant in which both dr1 sequences are deleted is defective at several points in the virus life cycle, including unspliced RNA and env mRNA stability, unspliced RNA transport, and virus particle assembly. A defect in unspliced RNA transport occurs because a cytoplasmic transport element is present within the dr1. We have suggested that the defect of particle production may arise from the failure of the unspliced RNA to be targeted to sites in the cytoplasm where its translation is favorable for Gag protein assembly. In this report, we have further investigated the function of the direct repeats by comparing virus mutants containing either a single upstream or downstream dr1 sequence. Both mutants were delayed in replication compared to the wild-type; the mutant with a single upstream dr1 (delta DDR) is significantly more defective than the mutant with a single downstream dr1 (delta UDR). While both mutants appear capable of efficiently transporting unspliced RNA to the cytoplasm, the delta DDR mutant with only the upstream dr1 is defective in its ability to support Gag assembly and particle release. The replication defect cannot be repaired by placing the upstream dr1 at the location of the downstream dr1 in the 3' untranslated region. A single point mutation in the upstream dr1 (U to C) restored replication and particle production to near normal levels. The results suggest that unspliced RNA transport and Gag assembly functions may be mediated by different elements within the dr1 and that the Prague A upstream dr1 is defective in the latter but not the former function.

Animals↗
PubMed1998

Regulatory mechanisms of growth hormone secretion are sexually dimorphic.

Sexually dimorphic growth hormone (GH) secretory pattern is important in the determination of gender-specific patterns of growth and metabolism in rats. Whether GH secretion in humans is also sexually dimorphic and the neuroendocrine mechanisms governing this potential difference are not fully established. We have compared pulsatile GH secretion profiles in young men and women in the baseline state and during a continuous intravenous infusion of recombinant human insulin-like growth factor I (rhIGF-I). During the baseline study, men had large nocturnal GH pulses and relatively small pulses during the rest of the day. In contrast, women had more continuous GH secretion and more frequent GH pulses that were of more uniform size. The infusion of rhIGF-I (10 microg/kg/h) potently suppressed both spontaneous and growth hormone-releasing hormone (GHRH)-induced GH secretion in men. In women, however, rhIGF-I had less effect on pulsatile GH secretion and did not suppress the GH response to GHRH. These data demonstrate the existence of sexual dimorphism in the regulatory mechanisms involved in GH secretion in humans. The persistence of GH responses to GHRH in women suggests that negative feedback by IGF-I might be expressed, in part, through suppression of hypothalamic GHRH.

Adult↗
PubMed1998

Electrochemical immunoassay based on catalytic conversion of substrate by labeled metal ion and polarographic detection of the product generated.

In a new electrochemical immunoassay based on the conversion of a substrate catalyzed by a labeled metal ion and the polarographic detection of the product generated, metal copper ion was used to label model antigen human serum albumin through the bifunctional chelating agent diethylenetriaminepentaacetic acid. After heterogeneous competitive immunoreaction, the labeled copper ion was released or activated by acidification and chemically catalyzed the conversion of the substrate o-phenylenediamine to the electroactive product 2,3-diaminophenazine (DAP). The DAP was quantified using linear-potential scan polarography. The sensitivity of the proposed assay was 100 times higher than that of the previous methods based on direct detection of the metal ion labels. This immunoassay can be used to detect any protein of interest.

Catalysis↗
PubMed1998

Identification of different lipid phases and calcium phosphate deposits in human carotid artery plaques by MAS NMR spectroscopy.

Accumulation of lipids in atherosclerotic plaques causes progressive narrowing of the arterial lumen, often followed by thrombosis and ischemia. Currently several different methods, most requiring disruption of the plaque, are used to study the physical properties of lipids accumulated in plaques, and lipid composition is typically determined by chemical analysis of completely disrupted plaques. In this study, 13C magic angle spinning NMR spectroscopy (MAS NMR) was used to determine in situ the lipid composition and molecular organization of all lipid phases in human carotid artery plaques (ex vivo). Protocols were developed to observe signals from one lipid phase without interference from other phases. In addition, 31P MAS NMR detected calcification in plaques by the signals from inorganic phosphate complexed to calcium. Together, 13C and 31P MAS NMR comprise a powerful nondisruptive approach for determining the quantity and phase state of components in arterial plaques.

Calcium Phosphates↗
PubMed1998

Regulation of cardiac Kv1.5 K+ channel expression by cardiac fibroblasts and mechanical load in cultured newborn rat ventricular myocytes.

Of the six voltage-gated K+ channel alpha subunits detected in rat heart, the Kv1.5 channel is abundantly expressed, and its gene transcription and protein expression are reduced during cardiac remodeling. Since cardiac fibroblasts and mechanical load have been known to play important roles in myocardial hypertrophy, we studied the regulation of Kv1.5 K+ channel protein expression by these factors in cultured newborn rat ventricular myocytes, using immunofluorescent cytochemistry and Western blot analysis. Ventricular cells were isolated from 1-day-old Wistar rats and cultured for a period of 5 days. The effect of cardiac fibroblasts was examined by co-culturing myocytes with fibroblasts or incubating pure myocytes in fibroblast-conditioned growth medium (FCGM) for 72 h. In addition, a 48-h cyclic stretch at 0.5 Hz with 20% elongation in length was applied to pure myocyte cultures to mimic mechanical load. With a polyclonal antibody against rat Kv1.5 K+ channel protein, single cultured myocytes showed a weak and uniform antibody labeling. Co-culturing with fibroblasts or incubating pure myocytes in FCGM both induced a significant increase in myocyte size implying cell hypertrophy, but neither allowed normal expression of the Kv1.5 K+ channel as indicated by almost negative anti-Kv1.5 labeling. Western blots of cell proteins prepared from ventricular myocyte cultures revealed a single protein band at 75 kD recognized by the anti-Kv1.5 antibody and a 45% decrease in Kv1.5 immunoreactive protein level in the FCGM-treated preparations. Application of 1 microM losartan, an angiotensin II type I receptor blocker, significantly attenuated the FCGM-induced myocyte hypertrophy and reduction of Kv1.5 K+ channel expression. On the other hand, although no cell hypertrophy was stimulated by mechanical stretch, intense punctate antibody labeling with a 48% increase in Kv1.5 protein level was observed in the stretched myocytes. These results suggest that the protein expression of cardiac Kv1.5 K+ channel is differentially regulated by cardiac fibroblasts and mechanical load. Some soluble factors produced from cardiac fibroblasts contribute to the depressed Kv1.5 K+ channel expression in myocardial hypertrophy. This channel regulation may be mediated by angiotensin II type I receptor.

Animals↗
PubMed1998

Cell cycle-related changes in the voltage-gated Ca2+ currents in cultured newborn rat ventricular myocytes.

The expression of T-type Ca2+ current (ICa,T) has been reported to change during postnatal heart development and myocardial hypertrophy, which are characterized respectively by the arrest of the cell cycle soon after birth and a switching on of DNA synthesis in the terminally differentiated cardiac myocytes. The hypothesis that there are cell cycle-related changes in cardiac Ca2+ channel expression was tested by performing whole-cell voltage-clamp recording and BromodeoxyUridine (BrdU) immunolabeling to determine the S phase of the cell cycle in the same single cultured newborn rat ventricular cells. Myocytes were isolated from 1-day-old Wistar rats and cultured for 15 days. ICa,T was detected in 27% of the 5-day cultured myocytes. The progressive loss of ICa,T during the period of 15-day incubation, which resembles the developmental changes in vivo, paralleled the decrease in the percentage of cells showing BrdU labeling. At day 5 of cell culture, the fraction of myocytes expressing ICa,T was significantly higher in the BrdU-labeled population (95%) as compared with the non-labeled cells (19%). In addition, a 72-h treatment with 20 microM nickel, an ICa,T blocker, revealed no effect on the percentage of BrdU-positive cells. L-type Ca2+ current (ICa,L) was constantly expressed throughout the 15-day cell culture. The frequency of ICa,L expression was identical between the BrdU-labeled and the non-labeled myocytes, although the latter cell population demonstrated a relatively greater current density. No differences in the inactivating kinetics of ICa,L and their reaction to beta-adrenoceptor stimulation were observed between the two groups. These findings provide convincing evidence for the cell cycle-related expression of cardiac Ca2+ channel. Cardiomyocytes at the S phase of the cell cycle predominantly express ICa,T, while the major properties of ICa,L' are unchanged during the cell cycle. Such a cell cycle-related channel expression may play a critical role in regulating the cardiac electrophysiological properties during heart development and myocardial remodeling.

Animals↗
PubMed1998

Regulation of Kv4.2 and Kv1.4 K+ channel expression by myocardial hypertrophic factors in cultured newborn rat ventricular cells.

Postnatal development and myocardial hypertrophy are associated with alterations in cardiac voltage-gated K+ channels. To investigate mechanisms underlying this K+ channel remodeling, expression of Kv4.2 and Kv1.4 K+ channel alpha-subunits was examined in cultured newborn rat ventricular myocytes by Western blot analysis using polyclonal antibodies against each of the subunits. At day 5 of cell culture, Kv1.4 protein was expressed at higher level than Kv4.2; as the age of culture progressed, Kv1.4 was significantly diminished while Kv4.2 increased with time in culture and became the predominant K+ channel protein. Such K+ channel isoform switch from Kv1.4 to Kv4.2 resembles that of the development in vivo. A 72-h treatment with exogenous triiodothyronine (T3, 0.1 microM) to cultured neonatal myocytes enhanced the expression of Kv4.2 by 73% and decreased the Kv1.4 expression by 22%. The effects of T3 were associated with an increase in the protein-to-DNA ratio indicating myocyte hypertrophy. On the other hand, a 72-h treatment with cardiac non-myocyte cell (NMC)-conditioned growth medium (NCGM) or phenylephrine (20 microM) induced similar cell hypertrophy, but in sharp contrast to T3, both markedly suppressed the Kv4.2 channel protein level. In addition, the trophic and the Kv4.2-downregulating effects of NCGM could be mimicked by exogenous endothelin-1 (0.1 microM), a paracrine factor secreted from cardiac NMCs. Our observations for the first time suggest that cardiac Kv4.2 and Kv1.4 K+ channel alpha-subunits are differentially regulated by a variety of myocardial hypertrophic factors. That T3 accelerated the developmental K+ channel isoform switch from Kv1.4 to Kv4.2 in vitro indicates the critical importance of thyroid hormone in postnatal K+ channel remodeling. Cardiac NMCs and alpha-adrenoceptor activation may contribute to the reduced outward K+ channel density in hypertrophied cardiomyocytes.

Adrenergic alpha-Agonists↗
PubMed1998

alpha1-adrenoceptor agonists and IGF-1, myocardial hypertrophic factors, regulate the Kv1.5 K+ channel expression differentially in cultured newborn rat ventricular cells.

Interest has arisen concerning the importance of alpha-adrenergic function and insulin-like growth factor-1 (IGF-1) in cardiac remodelling. The hypothesis that these two factors may underlie the regulation of voltage-gated K+ channel expression in hypertrophied cardiomyocytes was tested by performing Western blot analysis of the Kv1.5 K+ channel alpha-subunit in cultured newborn rat ventricular cells. Myocyte size was quantified by surface area and total cell protein concentration. Cell exposure to the alpha1-adrenoceptor agonist phenylephrine (PE, 20 microM) and IGF-1 (60 ng/ml) for 72 h both induced a significant increase of cell size indicating myocyte hypertrophy, which could be separately blocked by the protein kinase C inhibitor staurosporine (20 nM) and the tyrosine kinase inhibitor genistein (15 microM). Western blots of cell proteins prepared from myocyte cultures showed a single protein band at 75 kD recognized by the anti-Kv1.5 antibody, and demonstrated a 56% reduction in the Kv1. 5 immunoreactive protein level in the PE-treated cell preparations. This suppression was not affected by staurosporine, but was remarkably attenuated by W7 (20 microM), a selective calmodulin antagonist. In contrast to PE, a 48% enhancement of the protein expression of Kv1.5 channel was induced by IGF-1 and this stimulation was specifically blocked by genistein. Our findings suggest that the differential regulation of cardiac Kv1.5 K+ channel expression can be produced by alpha1-adrenoceptor activation and IGF-1 via distinctive signalling pathways. Calmodulin-dependent kinase and tyrosine kinase contribute importantly to the alpha1-adrenoceptor-mediated decrease and the IGF-1-mediated increase in cardiac Kv1.5 K+ channel expression, respectively.

Adrenergic alpha-1 Receptor Agonists↗
PubMed1998

A 13C nuclear magnetic resonance study of free fatty acid incorporation in acylated lipids in differentiating preadipocytes.

To understand the role of free fatty acid (FFA) incorporation in the accumulation of lipids in the adipocyte and ultimately in the development of obesity, 13C nuclear magnetic resonance was used to study lipid metabolism in differentiating preadipocytes. The incorporation of 13C=O-labeled FFA into cellular lipids in primary cultured rat preadipocytes and 3T3L1 preadipocytes at different stages of differentiation was monitored by the 13C carbonyl chemical shift. Significant incorporation of palmitic acid into phosphatidylcholine in both the alpha and beta acyl chain positions was found in cells at early stages of differentiation. At later differentiation stages or after extended incubation periods, most of the 13C=O signals were found in the triacylglycerol (TG) molecules. Unsaturated 13C=O-labeled acyl chains were detected in the TG molecules when cells were incubated with saturated 13C=O-labeled FFA, indicating that intracellular dehydrogenation had occurred in the 13C=O-labeled palmitoyl chain. By using 13C-labeled methyl myristate as an internal intensity reference, incorporation of 13C FFA into each acyl chain position of the major intracellular lipids was determined quantitatively.

3T3 Cells↗
PubMed1998

Favorable response to lymphoblastoid interferon-alpha in children with chronic hepatitis C.

BACKGROUND/AIMS: We investigated the efficacy of interferon therapy for the treatment of children with chronic hepatitis C virus infection. METHODS: Twenty-four out of 26 children completed the 6-month treatment with lymphoblastoid interferon-alpha and were followed for 12 months or longer. Response to interferon therapy was defined by assaying for circulating HCV-RNA, using a nested PCR, at 6-month intervals after the end of the therapy. RESULTS: At the end of treatment circulating HCV-RNA was undetectable in 18/24 patients and at 6 months in 12/24. Ten of these 12 primary responders have remained virus free for more than 2 years. One patient remained negative at 12 months. The remaining patient relapsed at 12 months. At 24 months 10 of 18 patients tested negative for HCV-RNA. Serum alanine aminotransferase was normal in 11/24 patients at the end of treatment, at 6 months 12/24 were normal, and at 12 months 11/12 were normal. In eight children with sustained response, repeated liver biopsies revealed a reduction in Knodell's scores for inflammation in the hepatic lobules and in the portal areas. In three of them neither plus nor minus strand of HCV-RNA was detectable in the liver tissue. Responders had a significantly lower level of viremia than non-responders. Side effects of interferon including fever, hair loss, neutropenia, and thrombocytopenia were not serious enough to warrant cessation of interferon treatment. CONCLUSIONS: Interferon therapy in children with chronic hepatitis C may be beneficial as evaluated by sustained loss of viremia as well as by primary response.

Adolescent↗