Biomedical subjects

S Guo

Publications and source records attributed to S Guo.

At least 91 records · Page 5Linked to original sources

PubMed2000

[Immunotherapeutic effect of Mycobacterium vaccae on multi-drug resistant pulmonary tuberculosis].

OBJECTIVE: To evaluate the immuNotherapeutic effect of M. vaccae on multi-drug resistant (MDR) pulmonary tuberculosis. METHODS: 90 cases of MDR pulmonary tuberculosis with bacteriological positive were divided into immunotherapy (M, 28 cases), control (C, 28 cases) group at random pair and self control (S, 34 cases) group. The group M were treated by chemotherapy and M. vaccae for 6 months, the group C only treated by chemotherapy for 6 months, while group S only by chemotherapy in the first 3 months and in combination with M. vaccae in the next 6 months. RESULTS: After 6 months, the sputum negative conversion rates of group M were 43% in smear positive cases and 46% in culture positive cases, both of which were significant higher than those of group C (21%, 18%, P < 0.01). The sputum negative conversion rates of group S were 3%, 3% in smear and culture positive cases after 3-month chemotherapy, which increased to 44%, 41% respectively when M. vaccae was added for 6 months. Compared with group C, group M was better in improving of X-ray manifestation and cell-mediated immunity and closing of cavity (P < 0.05). The bacteriological relapse rates in group M, C, S were 8%, 20% and 7% respectively. CONCLUSION: As a adjunct to chemotherapy, M. vaccae is helpful for patients with MDR pulmonary tuberculosis by improving the cell-medicated immunity, sputum negative conversion and X-ray manifestation.

Adult↗

PubMed2000

[The expression of interleukin-6 mRNA and autosecretion in human leukemic cells].

OBJECTIVE: To make a comprehensive and systematic study on the constructive expression of IL-6 mRNA and IL-6 autosecretion in human leukemic cells and discuss the effect of IL-6 autosecretion on the specific binding of IL-6-PE40 fusion protein to targeted leukemic cells. METHODS: Semi-quantitative RT-PCR, sequencing and ELISA were used to detect the constructive expression of IL-6 mRNA and autosecretion level of IL-6 protein in human leukemic cell lines, such as U937, HL60, KG1, TF1, K562, HuT28, CEM and Raji. RESULTS: The relative expression level of IL-6 mRNA in myelocytic, monocytic and erythrocytic leukemic cell lines including HL60, U937, KG1 and TF1 and lymphoblastic leukemic cell lines such as CEM, HuT28 and Raji is very weak, ranging from 0.03 to 0.07. However, K562, an chronic myelocytic leukemic cell line, had the highest level 1.25 among the 8 leukemic cell lines and the level was also higher than that of the positive control U266 multiple myeloma cell line. Based on ELISA assay of IL-6, there were remarkable differences between the 8 leukemic cell lines, their secretion of IL-6 could be divided into 3 levels, i.e. high, moderate and low secretion type. CONCLUSION: These observations imply that the intrinsic expression and secretion of IL-6 differ obviously among different leukemic cell lines. Autocrine IL-6 may prevent IL-6-PE40 fusion protein from specific binding to targeted leukemic cells and consequently affect its specific killing toxicity.

Cell Line, Tumor↗

PubMed2000

[Research progression of nuclear transcription factor-kappaB].

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Animals↗

PubMed2000

[Raman spectra and IR spectra of 3-triphenylgermyl-1,1-diphenyl-1-butanol and its derivatives].

The Raman spectra and FTIR spectra of 3-triphenylgermyl-1,1-diphenyl-1-propanol (A), 3-triphenylgermyl-1,1-diphenyl-1-butanol (B) and 3-triphenylgermyl-2-methyl-1,1-diphenyl-1-propanol (C) have been measured and analyzed. In Raman spectra of these compounds, the Ge--Ph stretching vibrations are near 1,000 cm-1, and the Ge--C stretching vibrations are 594.1 (for A), 578.7 (for B), 599.2 cm-1 (for C). The spectra show that the three compounds have similar molecular vibration characteristics.

English Abstract↗

PubMed1999

Crystal structure of the helicase domain from the replicative helicase-primase of bacteriophage T7.

Helicases that unwind DNA at the replication fork are ring-shaped oligomeric enzymes that move along one strand of a DNA duplex and catalyze the displacement of the complementary strand in a reaction that is coupled to nucleotide hydrolysis. The helicase domain of the replicative helicase-primase protein from bacteriophage T7 crystallized as a helical filament that resembles the Escherichia coli RecA protein, an ATP-dependent DNA strand exchange factor. When viewed in projection along the helical axis of the crystals, six protomers of the T7 helicase domain resemble the hexameric rings seen in electron microscopic images of the intact T7 helicase-primase. Nucleotides bind at the interface between pairs of adjacent subunits where an arginine is near the gamma-phosphate of the nucleotide in trans. The bound nucleotide stabilizes the folded conformation of a DNA-binding motif located near the center of the ring. These and other observations suggest how conformational changes are coupled to DNA unwinding activity.

Amino Acid Sequence↗

PubMed1999

The linker region between the helicase and primase domains of the bacteriophage T7 gene 4 protein is critical for hexamer formation.

The gene 4 protein of bacteriophage T7, a functional hexamer, comprises DNA helicase and primase activities. Both activities depend on the unidirectional movement of the protein along single-stranded DNA in a reaction coupled to the hydrolysis of dTTP. We have characterized dTTPase activity and hexamer formation for the full-length gene 4 protein (gp4) as well as for three carboxyl-terminal fragments starting at residues 219 (gp4-C219), 241 (gp4-C241), and 272 (gp4-C272). The region between residues 242 and 271, residing between the primase and helicase domains, is critical for oligomerization of the gene 4 protein. A functional TPase active site is dependent on oligomerization. During native gel electrophoresis, gp4, gp4-C219, and gp4-C241 migrate as oligomers, whereas gp4-C272 is monomeric. The steady-state k(cat) for dTTPase activity of gp4-C272 increases sharply with protein concentration, indicating that it forms oligomers only at high concentrations. gp4-C219 and gp4-C241 both form a stable complex with gp4, whereas gp4-C272 interacts only weakly with gp4. Measurements of surface plasmon resonance indicate that a monomer of T7 DNA polymerase binds to a dimer of gp4, gp4-C219, or gp4-C241 but to a monomer of gp4-C272. Like the homologous RecA and F(1)-ATPase proteins, the oligomerization domain of the gene 4 protein is adjacent to the amino terminus of the NTP-binding domain.

Bacteriophage T7↗

PubMed1999

Phosphorylation of the transcription factor forkhead family member FKHR by protein kinase B.

Protein kinase B lies "downstream" of phosphatidylinositide (PtdIns) 3-kinase and is thought to mediate many of the intracellular actions of insulin and other growth factors. Here we show that FKHR, a human homologue of the DAF16 transcription factor in Caenorhabditis elegans, is rapidly phosphorylated by human protein kinase Balpha (PKBalpha) at Thr-24, Ser-256, and Ser-319 in vitro and at a much faster rate than BAD, which is thought to be a physiological substrate for PKB. The same three sites, which all lie in the canonical PKB consensus sequences (Arg-Xaa-Arg-Xaa-Xaa-(Ser/Thr)), became phosphorylated when FKHR was cotransfected with either PKB or PDK1 (an upstream activator of PKB). All three residues became phosphorylated when 293 cells were stimulated with insulin-like growth factor 1 (IGF-1). The IGF-1-induced phosphorylation was abolished by the PtdIns 3-kinase inhibitor wortmannin but not by PD 98059 (an inhibitor of the mitogen-activated protein kinase cascade) or by rapamycin. These results indicate that FKHR is a physiological substrate of PKB and that it may mediate some of the physiological effects of PKB on gene expression. DAF16 is known to be a component of a signaling pathway that has been partially dissected genetically and includes homologues of the insulin/IGF-1 receptor, PtdIns 3-kinase and PKB. The conservation of Thr-24, Ser-256, and Ser-319 and the sequences surrounding them in DAF16 therefore suggests that DAF16 is also a direct substrate for PKB in C. elegans.

3-Phosphoinositide-Dependent Protein Kinases↗

PubMed1999

Phosphorylation of serine 256 by protein kinase B disrupts transactivation by FKHR and mediates effects of insulin on insulin-like growth factor-binding protein-1 promoter activity through a conserved insulin response sequence.

Insulin inhibits the expression of multiple genes in the liver containing an insulin response sequence (IRS) (CAAAA(C/T)AA), and we have reported that protein kinase B (PKB) mediates this effect of insulin. Genetic studies in Caenorhabditis elegans indicate that daf-16, a forkhead/winged-helix transcription factor, is a major target of the insulin receptor-PKB signaling pathway. FKHR, a human homologue of daf-16, contains three PKB sites and is expressed in the liver. Reporter gene studies in HepG2 hepatoma cells show that FKHR stimulates insulin-like growth factor-binding protein-1 promoter activity through an IRS, and introduction of IRSs confers this effect on a heterologous promoter. Insulin disrupts IRS-dependent transactivation by FKHR, and phosphorylation of Ser-256 by PKB is necessary and sufficient to mediate this effect. Antisense studies indicate that FKHR contributes to basal promoter function and is required to mediate effects of insulin and PKB on promoter activity via an IRS. To our knowledge, these results provide the first report that FKHR stimulates promoter activity through an IRS and that phosphorylation of FKHR by PKB mediates effects of insulin on gene expression. Signaling to FKHR-related forkhead proteins via PKB may provide an evolutionarily conserved mechanism by which insulin and related factors regulate gene expression.

Amino Acid Sequence↗

PubMed1999

SAC1-like domains of yeast SAC1, INP52, and INP53 and of human synaptojanin encode polyphosphoinositide phosphatases.

The SAC1 gene product has been implicated in the regulation of actin cytoskeleton, secretion from the Golgi, and microsomal ATP transport; yet its function is unknown. Within SAC1 is an evolutionarily conserved 300-amino acid region, designated a SAC1-like domain, that is also present at the amino termini of the inositol polyphosphate 5-phosphatases, mammalian synaptojanin, and certain yeast INP5 gene products. Here we report that SAC1-like domains have intrinsic enzymatic activity that defines a new class of polyphosphoinositide phosphatase (PPIPase). Purified recombinant SAC1-like domains convert yeast lipids phosphatidylinositol (PI) 3-phosphate, PI 4-phosphate, and PI 3,5-bisphosphate to PI, whereas PI 4,5-bisphosphate is not a substrate. Yeast lacking Sac1p exhibit 10-, 2.5-, and 2-fold increases in the cellular levels of PI 4-phosphate, PI 3,5-bisphosphate, and PI 3-phosphate, respectively. The 5-phosphatase domains of synaptojanin, Inp52p, and Inp53p are also catalytic, thus representing the first examples of an inositol signaling protein with two distinct lipid phosphatase active sites within a single polypeptide chain. Together, our data provide a long sought mechanism as to how defects in Sac1p overcome certain actin mutants and bypass the requirement for yeast phosphatidylinositol/phosphatidylcholine transfer protein, Sec14p. We demonstrate that PPIPase activity is a key regulator of membrane trafficking and actin cytoskeleton organization and suggest signaling roles for phosphoinositides other than PI 4,5-bisphosphate in these processes. Additionally, the tethering of PPIPase and 5-phosphatase activities indicate a novel mechanism by which concerted phosphoinositide hydrolysis participates in membrane trafficking.

Fungal Proteins↗

PubMed1999

Mutations in the zebrafish unmask shared regulatory pathways controlling the development of catecholaminergic neurons.

The mechanism by which pluripotent progenitors give rise to distinct classes of mature neurons in vertebrates is not well understood. To address this issue we undertook a genetic screen for mutations which affect the commitment and differentiation of catecholaminergic (CA) [dopaminergic (DA), noradrenergic (NA), and adrenergic] neurons in the zebrafish, Danio rerio. The identified mutations constitute five complementation groups. motionless and foggy affect the number and differentiation state of hypothalamic DA, telencephalic DA, retinal DA, locus coeruleus (LC) NA, and sympathetic NA neurons. The too few mutation leads to a specific reduction in the number of hypothalamic DA neurons. no soul lacks arch-associated NA cells and has defects in pharyngeal arches, and soulless lacks both arch-associated and LC cell groups. Our analyses suggest that the genes defined by these mutations regulate different steps in the differentiation of multipotent CA progenitors. They further reveal an underlying universal mechanism for the control of CA cell fates, which involve combinatorial usage of regulatory genes.

Animals↗

PubMed1999

[HLA-DQA1 genes involved in the genetic susceptibility to duodenal ulcer in Wuhan Hans]

OBJECTIVE: To study the genetic susceptibility of HLA-DQA1 alleles to duodenal ulcer in Chinese Hans from Wuhan and its nearby regions. METHODS: Seventy patients with duodenal ulcer and fifty healthy controls were examined for HLA-DQA1 genotypes. HLA-DQA1 typing was carried out by digesting the locus specific polymerase chain reaction amplified products with alleles specific restriction enzymes (PCR-RFLP), Apal I, Basj I, Hph I, Fok I, Mbo II and Mnl I. RESULTS: The allele frequency of DQA1 0301 in patients with duodenal ulcer (64.3%) was significantly higher than that in healthy controls (36%). In contrast, the allele frequency of DQA1 0102 in patients with duodenal ulcer (8.6%) was significantly lower than that in healthy controls (26%). CONCLUSION: These findings suggest that DQA1 0301 is a susceptible gene for duodenal ulcer in Wuhan Hans while DQA1 0102 is its resistant gene, and there are immunogenetic differences in HLA-DQA1 locus between duodenal ulcer patients and healthy controls.

Journal Article↗

PubMed1999

Maternal psychological distress and parenting stress after the birth of a very low-birth-weight infant.

CONTEXT: Few studies document how parents adapt to the experience of a very low-birth-weight (VLBW; <1500 g) birth despite societal concerns about the ethics and justification of intensive care for these infants. OBJECTIVE: To determine the degree and type of stress experienced over time by mothers whose infants vary in degree of prematurity and medical and developmental risk. DESIGN: Longitudinal prospective follow-up study of a cohort of mothers of high- and low-risk VLBW and term infants from birth to 3 years. SETTING: All level III neonatal intensive care units from a large midwestern metropolitan region. PARTICIPANTS: Mothers and infants prospectively and consecutively enrolled in a longitudinal study between 1989 and 1991. High-risk VLBW infants were diagnosed as having bronchopulmonary dysplasia, and comparison groups were low-risk VLBW infants without bronchopulmonary dysplasia and term infants (>36 weeks, >2500 g). MAIN OUTCOME MEASURES: Standardized, normative self-report measures of maternal psychological distress, parenting stress, family impact, and life stressors. RESULTS: Mothers of VLBW infants (high risk, n = 122; low risk, n = 84) had more psychological distress than mothers of term infants (n=123) at 1 month (13% vs 1%; P = .003). At 2 years, mothers of low-risk VLBW infants did not differ from term mothers, while mothers of high-risk infants continued to report psychological distress. By 3 years, mothers of high-risk VLBW children did not differ from mothers of term children in distress symptoms, while parenting stress remained greater. Severity of maternal depression was related to lower child developmental outcomes in both VLBW groups. CONCLUSIONS: The impact of VLBW birth varies with child medical risk status, age, and developmental outcome. Follow-up programs should incorporate psychological screening and support services for mothers of VLBW infants in the immediate postnatal period, with monitoring of mothers of high-risk VLBW infants.

Adult↗

PubMed1999

Development of noradrenergic neurons in the zebrafish hindbrain requires BMP, FGF8, and the homeodomain protein soulless/Phox2a.

We report that the zebrafish mutation soulless, in which the development of locus coeruleus (LC) noradrenergic (NA) neurons failed to occur, disrupts the homeodomain protein Phox2a. Phox2a is not only necessary but also sufficient to induce Phox2b+ dopamine-beta-hydroxylase+ and tyrosine hydroxylase+ NA neurons in ectopic locations. Phox2a is first detected in LC progenitors in the dorsal anterior hindbrain, and its expression there is dependent on FGF8 from the mid/hindbrain boundary and on optimal concentrations of BMP signal from the epidermal ectoderm/future dorsal neural plate junction. These findings suggest that Phox2a coordinates the specification of LC in part through the induction of Phox2b and in response to cooperating signals that operate along the mediolateral and anteroposterior axes of the neural plate.

Amino Acid Sequence↗

PubMed1999

Pleiotropic alterations in lipid metabolism in yeast sac1 mutants: relationship to "bypass Sec14p" and inositol auxotrophy.

SacIp dysfunction results in bypass of the requirement for phosphatidylinositol transfer protein (Sec14p) function in yeast Golgi processes. This effect is accompanied by alterations in inositol phospholipid metabolism and inositol auxotrophy. Elucidation of how sac1 mutants effect "bypass Sec14p" will provide insights into Sec14p function in vivo. We now report that, in addition to a dramatic accumulation of phosphatidylinositol-4-phosphate, sac1 mutants also exhibit a specific acceleration of phosphatidylcholine biosynthesis via the CDP-choline pathway. This phosphatidylcholine metabolic phenotype is sensitive to the two physiological challenges that abolish bypass Sec14p in sac1 strains; i.e. phospholipase D inactivation and expression of bacterial diacylglycerol (DAG) kinase. Moreover, we demonstrate that accumulation of phosphatidylinositol-4-phosphate in sac1 mutants is insufficient to effect bypass Sec14p. These data support a model in which phospholipase D activity contributes to generation of DAG that, in turn, effects bypass Sec14p. A significant fate for this DAG is consumption by the CDP-choline pathway. Finally, we determine that CDP-choline pathway activity contributes to the inositol auxotrophy of sac1 strains in a novel manner that does not involve obvious defects in transcriptional expression of the INO1 gene.

Bacterial Proteins↗

PubMed1999

The behaviors of some heritability estimators in the complete absence of genetic factors.

Heritability is an important concept in quantitative genetics and is widely used in human genetics. A high or even a moderate value of heritability estimate is usually taken as evidence for a genetic component for a quantitative trait. In this paper, the behaviors of some correlation-based heritability estimators are reexamined under the assumption of complete absence of any genetic factors. It turns out that when monozygotic (MZ) twins (or full sibs) are environmentally more similar than dizygotic twins (or half sibs), or when there is placement bias in MZ twins reared apart, those correlation-based heritability estimates can lead to nonnegligible or even high heritability values, even when genetic factors are completely absent. These alarming results suggest that extreme care should be exercised when using these heritability estimators.

Data Interpretation, Statistical↗

PubMed1999

Contributors to violent behavior among elementary and middle school children.

OBJECTIVE: To examine the relative contributions of exposure to violence, parental monitoring, and television-viewing habits to children's self-reported violent behaviors. The study hypothesized that: 1) children's exposure to violence would be associated positively with self-reported violent behaviors; 2) parental monitoring would be associated negatively with children's violent behaviors; and 3) the number of daily television-viewing hours and a preference for watching violent television shows would be associated positively with children's violent behaviors. METHODS: The study used a survey design with an anonymous self-report questionnaire administered to students (grades 3-8) in 11 public schools. A total of 2245 students participated in the study, representing 80% of the students attending the participating schools during the survey. The subjects were from 7 to 15 years of age; 51% were male, 57% were white, 33% percent were black, and 5% were Hispanic. RESULTS: Hierarchical multiple regression analysis of the total sample revealed that the combination of demographic variables, parental monitoring, television-viewing habits, and exposure to violence explained 45% of students' self-reported violent behaviors. Violence exposure and parental monitoring were the most influential contributors in explaining children's violent behaviors, accounting for 24% and 5% of the variance in violent behaviors, respectively. CONCLUSIONS: All three hypotheses were supported. A significant association was demonstrated linking violence exposure, lack of parental monitoring, and television-viewing habits with children's self-reported violent behaviors within a diverse sample of elementary and middle school students. Our findings support the importance of parental monitoring of children and emphasize the need to identify and to provide services to youth who are exposed to violence.

Adolescent↗

PubMed1999

[HLA-DQA1 genes involved in the genetic susceptibility to duodenal ulcer in Wuhan Hans].

Adolescent↗

PubMed1999

[Measurement of tibia bone content and fracture threshold by quantitative ultrasonography in normal and fractured women in Taiyuan].

OBJECTIVE: To establish the reference range of tibia bone content in normal female of Taiyuan area and to explore the diagnostic criterion for osteoporotic fracture threshold by quantitative ultrasonography (QUS). METHODS: The tibia bone contents (QUS value) of 1,681 normal women (aged 7-92 years) and 63 fractured women (aged 46-91) in Taiyuan were measured by QUS. RESULTS: The QUS value increased with age in normal women before age 30, and peaked at age 30-40, then decreased and reached significance after age 50. There was a negative correlation between QUS value and duration after menopause (P < 0.01). Taken the mean QUS value of normal female aged 20-40 years minus 2.5 s (3,667 m/s) as a cutoff threshold, 93.7% of the 63 fractured women had their QUS value below this threshold. CONCLUSION: It is suggested that the above cutoff QUS value may be considered as the risk threshold of osteoporotic fracture in women.

Adolescent↗