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Biomedical subjects

G Guo

Publications and source records attributed to G Guo.

At least 19 recordsLinked to original sources
PubMed2006

The molecular genetics of Marfan syndrome and related disorders.

Marfan syndrome (MFS), a relatively common autosomal dominant hereditary disorder of connective tissue with prominent manifestations in the skeletal, ocular, and cardiovascular systems, is caused by mutations in the gene for fibrillin-1 (FBN1). The leading cause of premature death in untreated individuals with MFS is acute aortic dissection, which often follows a period of progressive dilatation of the ascending aorta. Recent research on the molecular physiology of fibrillin and the pathophysiology of MFS and related disorders has changed our understanding of this disorder by demonstrating changes in growth factor signalling and in matrix-cell interactions. The purpose of this review is to provide a comprehensive overview of recent advances in the molecular biology of fibrillin and fibrillin-rich microfibrils. Mutations in FBN1 and other genes found in MFS and related disorders will be discussed, and novel concepts concerning the complex and multiple mechanisms of the pathogenesis of MFS will be explained.

Activin Receptors, Type I↗
PubMed2006

Gender differences in associations between depressive symptoms and patterns of substance use and risky sexual behavior among a nationally representative sample of U.S. adolescents.

OBJECTIVE: This study uses a cluster analysis of adolescents, based on their substance use and sexual risk behaviors, to 1) examine associations between risk behavior patterns and depressive symptoms, stratified by gender, and 2) examine gender differences in risk for depression. METHODS: Data are from a nationally representative survey of over 20,000 U.S. adolescents. Logistic regression was used to examine the associations between 16 risk behavior patterns and current depressive symptoms by gender. RESULTS: Compared to abstention, involvement in common adolescent risk behaviors (drinking, smoking, and sexual intercourse) was associated with increased odds of depressive symptoms in both sexes. However, sex differences in depressive symptoms vary by risk behavior pattern. There were no differences in odds for depressive symptoms between abstaining male and female adolescents (OR = 1.07, 95% CI 0.70-1.62). There were also few sex differences in odds of depressive symptoms within the highest-risk behavior profiles. Among adolescents showing light and moderate risk behavior patterns, females experienced significantly more depressive symptoms than males. CONCLUSIONS: Adolescents who engage in risk behaviors are at increased risk for depressive symptoms. Girls engaging in low and moderate substance use and sexual activity experience more depressive symptoms than boys with similar behavior. Screening for depression is indicated for female adolescents engaging in even experimental risk behaviors.

Adolescent↗
PubMed2006

Parathyroid hormone regulates osterix and Runx2 mRNA expression predominantly through protein kinase A signaling in osteoblast-like cells.

Runt-related transcription factor 2 (Runx2) and osterix are osteoblast-specific transcription factors essential for the development of osteoblastic cells and bone formation. PTH given intermittently has anabolic effects on bone; however, the exact role remains to be understood completely. The purpose of this study was both to investigate whether PTH regulates Runx2 as well as osterix expression and to identify the signaling used. Using RT-PCR, we confirmed that PTH (1-34) regulated Runx2 and osterix mRNA expression, in rat osteoblast-like cell line UMR 106, in a dose- and time-dependent manner. PTH in low concentrations stimulated both Runx2 and osterix mRNA expression while that in high concentrations did not. Forskolin, an adenylate cyclase activator, also enhanced Runx2 and osterix transcription, and the stimulatory effects of PTH and forskolin were blocked by the pre-treatment of the cells with H-89, a protein kinase A (PKA) inhibitor. In contrast, the protein kinase C (PKC) activator phorbol 12-myristate 13-acetate (PMA) had no effect on Runx2 transcription, but induced an increase in osterix mRNA level at the concentration of 500 nM at 12 h after treatment. Moreover, pre-treatment of the cells with calphostin C, a PKC-specific inhibitor, reduced the increase in osterix transcripts enhanced by PTH and PMA 12 h after treatment. However, these inhibitory effects were not sustained for longer terms. These observations demonstrate that PTH stimulates Runx2 and osterix expression in vitro, at least in part, at transcriptional level. Induction of Runx2 mRNA is mediated through the activation of cAMP/PKA signal transduction. In the case of osterix, although the increase in mRNA level is predominantly mediated via cAMP/PKA signaling, PKC activation might also be involved in this process.

Alkaline Phosphatase↗
PubMed2006

Congenital lumbosacral limb duplication: a case report.

We report a case of congenital lumbosacral limb duplication at the pelvis, lower limb, and foot of a 4-year-old boy. The patient presented with a supernumerary lower limb joined at the lumbosacral region by a bony connection. A pseudo-navel and a pseudo-penis were found on the supernumerary limb and foot duplication was noted at the end. Radiography and a 3-dimensional computed-tomography reconstruction revealed duplication of an inversely oriented pelvis dorsal to the normal pelvis, semi-vertebrae in T7 to T9, thoracolumbar scoliosis, lumbosacral vertebral dysplasia, and dislocation of the left hip. Magnetic resonance imaging demonstrated a tethered spinal cord and an adipoma in the sacral canal. Motor conduction velocity was reduced in the left peroneal nerve. Surgery to remove the supernumerary limb was successfully performed. The patient recovered well and further surgery is planned for functional reconstruction of the left lower limb.

Abnormalities, Multiple↗
PubMed2001

Contributions of angiotensin II and tumor necrosis factor-alpha to the development of renal fibrosis.

Angiotensin II upregulates tumor necrosis factor-alpha (TNF-alpha) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-alpha receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT(1a) or the TNF-alpha receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vv(int)) in the C57BI/6 wild-type mouse was decreased in the AT(1a) KO from 32.8 +/- 4.0 to 21.0 +/- 3.7% (P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 +/- 2.1% (P < 0.005). The Vv(int) of the TNFR1/TNFR2 KO was further decreased to 15.2 +/- 3.7% (P < 0.01) by enalapril compared with no treatment. The induction of TNF-alpha mRNA and transforming growth factor-beta1 (TGF-beta1) mRNA in the kidney with UUO was significantly blunted in the AT(1a) or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-alpha and TGF-beta1 mRNA and their proteins to near normal levels. Also, alpha-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT(1a) or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-alpha systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy.

Actins↗
PubMed2000

A genome scan in families from Australia and New Zealand confirms the presence of a maternal susceptibility locus for pre-eclampsia, on chromosome 2.

Epidemiological studies have shown that genetic factors contribute to the etiology of the common and serious pregnancy-specific disorder pre-eclampsia (PE)/eclampsia (E). Candidate-gene studies have provided evidence (albeit controversial) of linkage to several genes, including angiotensinogen on 1q42-43 and eNOS on 7q36. A recent medium-density genome scan in Icelandic families identified significant linkage to D2S286 (at 94.05 cM) on chromosome 2p12 and suggestive linkage to D2S321 (at 157.5 cM) on chromosome 2q23. In the present article, the authors report the results of a medium-density genome scan in 34 families, representing 121 affected women, from Australia and New Zealand. Multipoint nonparametric linkage analysis, using the GENEHUNTER-PLUS program, showed suggestive evidence of linkage to chromosome 2 (LOD=2.58), at 144.7 cM, between D2S112 and D2S151, and to chromosome 11q23-24, between D11S925 and D11S4151 (LOD=2.02 at 121.3 cM). Given the limited precision of estimates of the map location of disease-predisposing loci for complex traits, the present finding on chromosome 2 is consistent with the finding from the Icelandic study, and it may represent evidence of the same locus segregating in the population from Australia and New Zealand. The authors propose that the PE/E-linked locus on chromosome 2p should be designated the "PREG1" (pre-eclampsia, eclampsia gene 1) locus.

Australia↗
PubMed2000

Maternal child-rearing behaviors and correlates in rural minority areas of Yunnan, China.

An epidemiological survey of maternal child-rearing behaviors was conducted in the rural minority areas of Yunnan, China. An interview of 2019 rural mothers of Hani, Yi, Hui, Miao, and Han and 544 urban mothers with children younger than 7 years of age showed that 51.7% of these rural mothers placed their infants in swaddling clothes. In the rural sample, exclusive breastfeeding occurred at frequency rates of 76.7% and 34.2% during 3 and 6 months postpartum, respectively. Maternal training and playing behaviors were reported less frequently, whereas physical punishment for children's misbehavior was more commonly found in the child-rearing behavior of rural mothers. Maternal child-rearing behaviors differed significantly among ethnic groups as well as between urban and rural areas. Maternal child-rearing behaviors were significantly associated with maternal education level, family type, family income, maternal age at delivery, and number of children in the family. Children's gender had no significant association with maternal child-rearing behaviors.

Breast Feeding↗
PubMed2000

Osteogenic protein-1 prevents renal fibrogenesis associated with ureteral obstruction.

Unilateral ureteral obstruction (UUO) is a model of renal injury characterized by progressive tubulointerstitial fibrosis and renal damage, while relatively sparing the glomerulus and not producing hypertension or abnormalities in lipid metabolism. Tubulointerstitial fibrosis is a major component of several kidney diseases associated with the progression to end-stage renal failure. Here we report that when a critical renal developmental morphogen, osteogenic protein-1 (OP-1; 100 or 300 microg/kg body wt), is administered at the time of UUO and every other day thereafter, interstitial inflammation and fibrogenesis are prevented, leading to preservation of renal function during the first 5 days after obstruction. Compared with angiotensin-converting enzyme inhibition with enalapril treatment, OP-1 was more effective in preventing tubulointerstitial fibrosis and in preserving renal function. The mechanism of OP-1- induced renal protection was associated with prevention of tubular atrophy, an effect not shared with enalapril, and was related to preservation of tubular epithelial integrity. OP-1 blocked the stimulation of epithelial cell apoptosis produced by UUO, which promoted maintenance of tubular epithelial integrity. OP-1 preserved renal blood flow (RBF) during UUO, but enalapril also stimulated RBF. Thus OP-1 treatment inhibited tubular epithelial disruption stimulated by the renal injury of UUO, preventing tubular atrophy and diminishing the activation of tubulointerstitial inflammation and fibrosis and preserving renal function.

Actins↗
PubMed2000

The mechanisms mediating the effects of poverty on children's intellectual development.

Although adverse consequences of poverty for children are documented widely, little is understood about the mechanisms through which the effects of poverty disadvantage young children. In this analysis we investigate multiple mechanisms through which poverty affects a child's intellectual development. Using data from the NLSY and structural equation models, we have constructed five latent factors (cognitive stimulation, parenting style, physical environment, child's ill health at birth, and ill health in childhood) and have allowed these factors, along with child care, to mediate the effects of poverty and other exogenous variables. We produce two main findings. First, the influence of family poverty on children's intellectual development is mediated completely by the intervening mechanisms measured by our latent factors. Second, our analysis points to cognitive stimulation in the home, and (to a lesser extent) to parenting style, physical environment of the home, and poor child health at birth, as mediating factors that are affected by lack of income and that influence children's intellectual development.

Adolescent↗
PubMed2000

Stimulatory activity of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic receptors.

OBJECTIVE: To study the activity of anti-peptide antibodies against the second extracellular loop of human M2 muscarinic receptors on cAMP production and inward calcium currents (Ica) in guinea pig ventricular myocytes. A comparison was also made with those of a muscarinic receptor agonist. METHODS: cAMP content was determined by radioimmunoassay and the Ica in guinea pig single ventricular cells were recorded by the whole-cell patch clamp technique. RESULTS: Both the muscarinic receptor agonist, carbachol (Carb 10 mumol/L), and anti-peptide antibodies (Abs 100 nmol/L) could decrease basal cAMP levels (by 46.9% +/- 4.2% and 60.2% +/- 4.6%, respectively) and basal Ica. Both Carb (10 mumol/L) and Abs (100 nmol/L) could also inhibit the isoprenaline-induced (Iso 0.8 mumol/L) increases in cAMP production (from 108.2 +/- 7.0 to 88.4 +/- 7.2 pmol/mg.protein/min for Carb and 88.6 +/- 5.1 pmol/mg.protein/min for Abs, respectively) and the increases in Ica. The muscarinic receptor antagonist atropine (Atr) was able to prevent these effects of Carb and Abs. CONCLUSIONS: Anti-peptide antibodies against an epitope located in the second extracellular loop of human M2 muscarinic receptors, similar to muscarinic receptor agonist, could decrease the basal Ica and beta-receptor agonist stimulated increase of Ica by decreasing the basal and beta-receptor agonist stimulated increase of cAMP production, and therefore could have an effect on their target receptor. These results further suggest that autoimmunity may participate in the pathogenesis of human cardiomyopathy and the second extracellular loop of human M2 muscarinic receptor could be the main immunodominant region.

Amino Acid Sequence↗
PubMed2000

[The effects of different patterns of mechanical ventilation on the respiratory mechanics and gas exchange in dogs severely injured by steam inhalation].

OBJECTIVE: To study the effects of conventional mechanical ventilation (CMV), high-frequency jet ventilation (HFJV) and high-frequency bidirectional jet ventilation (HFTJV) on the respiratory mechanics and gas exchange in dogs inflicted severely by steam inhalation injury. METHODS: Nine mongrel dogs inflicted by steam inhalation to severe inhalation injury were served as the model. Indices of respiratory mechanics, hemodynamics and blood gas analysis were monitored respectively with the above three patterns of mechanical ventilation. RESULTS: (1) Total respiratory resistance (Rrs) and resistance of lungs (R(L)) were evidently higher with the ventilations than those in control (P < 0.01). And total respiratory compliance (Crs) and compliance of lungs (C(L)) were obviously lower with the ventilations than those in control (P < 0.05) but with no significant differences among the changes of Rrs, R(L), Crs and C(L). (2) Carbon dioxide (CO(2)) retention could be induced by CMV and HFJV. HFTJV was much more effective than HFJV in enhancing the expiration of CO(2) (P < 0.01). (3) There was no remarkable difference in functional residual capacity (FRC) and PaO2 between dogs with three patterns of ventilations. CONCLUSION: All these three patterns of ventilations could overcome the respiratory resistance and help respiration, but they couldn't restore the high airway resistance and low compliance of lungs already established postburn. The efficiency of CMV was similar to that by HFJV, but that of HFTJV was much better than that of HFJV.

Animals↗
PubMed2000

[Coordination chemistry and Raman spectra of acetylide dianion].

This paper shows the syntheses of double salts of silver acetylide with various soluble silver salts, investigations on the coordination modes of acetylide dianion and their Raman spectra, discussion of the relationship between the coordination chemistry of acetylide dianion and the bind mode of N2 molecule in the FeMoco factor of nitrogenase. The results present that the bind mode of N2 molecule inside the FeMoco factor of nitrogenase is more reasonable.

English Abstract↗
PubMed2000

[Infrared spectra and Raman spectra of monoclinic RblnS2 and CsInS2].

Monoclinic RbInS2 and CsInS2 were prepared by the traditional flux method and their IR and Raman spectra were studied. The IR and Raman absorption bands of CsInS2 shift to lower frequency compared with RbInS2. IR and Raman spectra show that monoclinic RbInS2 and CsInS2 exhibit good infrared transmission.

English Abstract↗
PubMed1999

Genetic susceptibility to pre-eclampsia and chromosome 7q36.

Pre-eclampsia is the most common serious medical disorder of human pregnancy. The human endothelial cell nitric oxide synthase (eNOS) gene is a candidate for pre-eclampsia/eclampsia (PE/E) susceptibility. A linkage study was performed on Australian PE/E families using 25 microsatellite markers from chromosome 7, one of which (eNOS-CA) resides within the eNOS gene. No significant linkage was found for the eNOS-CA marker using either parametric or non-parametric analysis. However, D7S 1805 from the eNOS gene region on 7q36, gave a suggestion of linkage using parametric analysis (maximum LOD score =2.143 at theta=0.14) and non-parametric APM analysis (T1/sqrt(p)=3.53; P=0.002). Further, an association study was performed on unrelated PE/E cases and controls from both Chinese and Australian populations to test for a relationship between the eNOS gene and PE/E. No association was found between the eNOS-CA marker and PE/E in either population. However, there was a significant difference in the allelic distribution of eNOS-CA between the two ethnic groups. The linkage results support the possibility that a susceptibility locus for pre-eclampsia resides in the 7q36 region, however, there is no definitive evidence to support the notion that the eNOS gene itself is responsible for susceptibility to pre-eclampsia.

Asian People↗
PubMed1999

Prevalence and correlates of malnutrition among children in rural minority areas of China.

BACKGROUND: Child growth retardation and malnutrition remain a matter of uttermost public concern in economically disadvantaged areas of China. The present study aimed to estimate the prevalence of protein-energy malnutrition with various anthropometric indices and examine its correlates in a large sample of poor rural minority children. METHODS: A total of 2019 children under 7 years of age belonging to the Hani, Yi, Hui, Miao ethnic minority groups and the Han major group were drawn from four poor rural minority counties in the Yunnan Province of China. Well-trained investigators completed child physical measurements and maternal interviews. Protein-energy malnutrition was defined as being underweight (weight for age), wasting (weight for height) and stunting (height for age) on the basis of reference data from the National Center of Health Statistics (NCHS)/World Health Organization (WHO). RESULTS: The respective prevalence of moderate and severe protein-energy malnutrition was 15.8 and 3.1% for underweight children, 31.8 and 19.2% for stunting and 0.9 and 0.5% for wasting. Stunting was most common in children aged 2 years. Boys were more likely to suffer from malnutrition. Logistic regression analyses showed that lower family income, lower parental height, belonging to the Miao, Yi and Hani ethnic groups compared with Han and poorer maternal child-rearing behavior significantly increased the risk for stunting of children. CONCLUSIONS: Protein-energy malnutrition is relatively high in the rural minority children of China. Chronic socioeconomic underdevelopment and genetic effects, rather than a severe or immediate lack of food, may lead to protein-energy malnutrition.

Child↗
PubMed1999

Role of TNFR1 and TNFR2 receptors in tubulointerstitial fibrosis of obstructive nephropathy.

Unilateral ureteral obstruction (UUO) results in tubulointerstitial fibrosis of the obstructed kidney. In this study, we report the contribution of tumor necrosis factor-alpha (TNF-alpha) to the fibrosis that develops after ureteral obstruction. Mice in which individual TNF-alpha receptors TNFR1 or TNFR2 had been genetically knocked out were used, and results were compared with mice of C57Bl/6 background after 5 days UUO. Both kidneys were removed and examined histologically for changes in interstitial volume (Vv(int)), collagen IV deposition, alpha-smooth muscle actin (alpha-SMA) matrix score, nuclear factor-kappaB (NF-kappaB) activity, and TNF-alpha mRNA levels. We found that the Vv(int) of contralateral unobstructed kidneys averaged approximately 7% and was indistinguishable among the three genotypes of mice. Vv(int) of ureteral obstructed kidney of C57Bl/6 mice averaged 33 +/- 3.9% after 5 days of UUO. Vv(int) of obstructed kidneys of TNFR1 mice was significantly reduced to 19.4 +/- 3.1%, whereas that of TNFR2 mice was significantly decreased to 25.4% +/- 4.8%. There was a modest but significant difference between Vv(int) of TNFR1 and TNFR2 (P < 0. 047). Both collagen IV and alpha-SMA matrix scores were decreased significantly in obstructed kidney of TNFR1 mouse compared with that of C57Bl/6 and TNFR2 mice. Nuclear extracts prepared from kidney cortex were found to have a significant increase in NF-kappaB binding activity in obstructed kidney compared with contralateral kidney. Individual knockout of the TNFR1 or TNFR2 genes resulted in significantly less NF-kappaB activation compared with the wild type, with TNFR1 being less than TNFR2 knockout. There was a significant increase in TNF-alpha mRNA in the kidney with ureteral obstruction in all three genotypes. TNFR1 knockout displayed a significant reduction in amount of TNF-alpha mRNA induced compared with wild-type or TNFR2 knockout mice. Treatment of TNFR1 knockout mice with an angiotensin converting enzyme inhibitor further decreased Vv(int) and TNF-alpha mRNA induction, suggesting an interaction of ANG II and TNF-alpha systems. These results suggest that TNF-alpha contributes, in part, to changes in interstitial volume, myofibroblast differentiation, and NF-kappaB activation in the kidney during ureteral obstruction. These changes appear to be mediated through both TNFR1 and TNFR2 gene products with effects through the TNFR1 receptor predominating. Furthermore, ANG II appears to stimulate TNF-alpha pathophysiological events leading to renal fibrosis.

Actins↗