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Biomedical subjects

Q Xu

Publications and source records attributed to Q Xu.

At least 91 records · Page 5Linked to original sources

Primary transanal rectosigmoidectomy for Hirschsprung's disease: Preliminary results in the initial 33 cases.

PURPOSE: The authors describe their newly developed technique-primary transanal rectosigmoidectomy for Hirschsprung's disease (HD) and its preliminary results in neonates and infants. METHODS: Thirty-four consecutive patients (26 boys) with biopsy-proven rectosigmoid HD, aged 18 days to 4 years, underwent this new procedure. Rectal mucosectomy started 1 to 1.5 cm posteriorly and 2 to 3 cm anteriorly proximal to the dentate line. The rectal muscular sleeve below the peritoneal reflection was resected to the level of the striated muscle complex, leaving a shorter muscular cuff, into which a partial internal sphincterotomy was made posteriorly. An oblique anastomosis was constructed between the pull-through ganglionic colon and the anus canal. RESULTS: The mean time for the operation was 160 minutes, and the average length of bowel resected was 29.5 cm (range, 12.5 to 41 cm). Two children (6.06%, 2 of 33) had 2 to 5 episodes of postoperative enterocolitis (EC). One was cured by rectal irrigation and dilation, and the another by Lynn's myectomy. Eighty-four percent of patients had 1 to 6 bowel movements per day during a 6- to 18-month follow-up period. CONCLUSIONS: Primary transanal rectosigmoidectomy for HD is logical and associated with excellent early results. A long-term follow-up is required to determine bowel functions. J Pediatr Surg 36:1816-1819.

Anal Canal↗

In Caenorhabditis elegans, the RNA-binding domains of the cytoplasmic polyadenylation element binding protein FOG-1 are needed to regulate germ cell fates.

FOG-1 controls germ cell fates in the nematode Caenorhabditis elegans. Sequence analyses revealed that FOG-1 is a cytoplasmic polyadenylation element binding (CPEB) protein; similar proteins from other species have been shown to bind messenger RNAs and regulate their translation. Our analyses of fog-1 mutations indicate that each of the three RNA-binding domains of FOG-1 is essential for activity. In addition, biochemical tests show that FOG-1 is capable of binding RNA sequences in the 3'-untranslated region of its own message. Finally, genetic assays reveal that fog-1 functions zygotically, that the small fog-1 transcript has no detectable function, and that missense mutations in fog-1 cause a dominant negative phenotype. This last observation suggests that FOG-1 acts in a complex, or as a multimer, to regulate translation. On the basis of these data, we propose that FOG-1 binds RNA to regulate germ cell fates and that it does so by controlling the translation of its targets. One of these targets might be the fog-1 transcript itself.

3' Untranslated Regions↗

Metastatic melanoma cells escape from immunosurveillance through the novel mechanism of releasing nitric oxide to induce dysfunction of immunocytes.

Nitric oxide (NO) is known to facilitate tumour metastasis through the promotion of angiogenesis, vascular dilation, platelet aggregation, etc. In the present study we explored its novel role in producing dysfunction of the host immune system in the metastasis of murine metastatic melanoma B16-BL6 cells. A significant reduction in the mixed lymphocyte reaction (MLR) was observed in the spleen cells from B16-BL6-bearing mice, but not in those from mice bearing the parent cell B16. When B16-BL6 cells were added in vitro to the MLR, a significant decrease was also found, even when they were co-cultured with the lymphocytes in two compartments of a Transwell chamber separated by an 8.0 microm filter. The supernatant from cultured B16-BL6 but not B16 cells, which had a greatly increased NO activity, significantly inhibited concanavalin A- and lipopolysaccharide-induced lymphocyte proliferation. A remarkably higher expression of inducible NO synthase (iNOS) was detected in B16-BL6 cells than in B16 cells. Nomega-Nitro-l-arginine (l-NNA), a NO synthase inhibitor and superoxide dismutase, significantly antagonized the above inhibition by B16-BL6 cells, while l-arginine, a NO precursor, and S-nitroso-N-acetyl-d,l-penicillamine, a NO donor, strengthened the inhibition. Furthermore, l-NNA significantly inhibited lung metastasis of B16-BL6 cells, while l-arginine tended to enhance the metastasis. The cytotoxicity of B16-BL6-specific T-cells was significantly decreased by pre-culture with B16-BL6 cells in a Transwell chamber or the culture supernatants of B16-BL6 cells, whereas l-iminoethyl-lysine, a selective inhibitor of iNOS, showed a significant recovery from the disease. These results suggest that NO released by metastatic tumour cells may impair the immune system, which facilitates the escape from immunosurveillance and metastasis of tumour cells.

Animals↗

Promoters of the CATG-specific methyltransferase gene hpyIM differ between iceA1 and iceA2 Helicobacter pylori strains.

Helicobacter pylori strains can be divided into two groups, based on the presence of two unrelated genes, iceA1 and iceA2, that occupy the same genomic locus. hpyIM, located immediately downstream of either gene, encodes a functional CATG-specific methyltransferase. Despite the strong conservation of the hpyIM open reading frame (ORF) among all H. pylori strains, the sequences upstream of the ORF in iceA1 and iceA2 strains are substantially different. To explore the roles of these upstream sequences in hpyIM regulation, promoter analysis of hpyIM was performed. Both deletion mutation and primer extension analyses demonstrate that the hpyIM promoters differ between H. pylori strains 60190 (iceA1) and J188 (iceA2). In strain 60190, hpyIM has two promoters, P(a) or P(I), which may function independently, whereas only one hpyIM promoter, P(c), was found in strain J188. The XylE assay showed that the hpyIM transcription level was much higher in strain 60190 than in strain J188, indicating that regulation of hpyIM transcription differs between the H. pylori iceA1 strain (60190) and iceA2 strains (J188). Since the iceA1 and iceA2 sequences are highly conserved within iceA1 or iceA2 strains, we conclude that promoters of the CATG-specific methylase gene hpyIM differ between iceA1 and iceA2 strains, which leads to differences in regulation of hpyIM transcription.

Acetyltransferases↗

Local gene transfer of tissue inhibitor of metalloproteinase-2 influences vein graft remodeling in a mouse model.

Recently, we established a new mouse model of vein graft arteriosclerosis by grafting vena cava to carotid arteries. In many respects, the morphological features of this murine vascular graft model resemble those of human venous bypass graft disease. Using this model, we studied the effects of local gene transfer of tissue inhibitor of metalloproteinase-2 (TIMP-2) on vein graft remodeling. Mouse isogeneic vessels of the vena caval veins were grafted end to end into carotid arteries, then enveloped with the replication-defective recombinant adenoviruses overexpressing human TIMP-2 (RAdTIMP-2) or beta-galactosidase (RAdLacZ) at 1x10(10) plaque-forming units/mL in a total volume of 50 microL, and incubated at room temperature for 20 minutes. In the untreated group, vessel wall thickening was observed as early as 1 week after surgery and progressed to 4- to 10-fold the original thickness in grafted veins at 4 and 8 weeks, respectively. RAdLacZ vector treatment significantly enhanced neointimal lesions at 8 weeks, which was completely blocked by RAdTIMP-2 gene overexpression. Interestingly, RAdTIMP-2 gene transfer resulted in a reduction in vessel diameter of grafted veins compared with ungrafted veins (819+/-96 versus 624+/-67 microm, respectively; P<0.05). Maximal beta-galactosidase activity was found at 2 weeks and was detectable until 4 weeks after gene transfer. Double immunofluorescence studies demonstrated that cells overexpressing TIMP-2 were mostly localized in the adventitia and were MAC-1-positive monocytes/macrophages but not smooth muscle cells. Furthermore, the activity of matrix metalloproteinases was markedly decreased in the vessel walls treated with RAdTIMP-2 compared with that in the untreated control group and the RAdLacZ-treated group. Thus, this mouse model has been proven to be useful in gene transfer studies. Our findings demonstrate that local TIMP-2 gene transfer significantly reduces vein graft diameter, ie, remodeling to an artery-like vessel via inhibition of matrix metalloproteinase activity.

Adenoviridae↗

Exacerbated vein graft arteriosclerosis in protein kinase Cdelta-null mice.

Smooth muscle cell (SMC) accumulation is a key event in the development of atherosclerosis, including vein bypass graft arteriosclerosis. Because members of the protein kinase C (PKC) family signal cells to undergo proliferation, differentiation, or apoptosis, we generated PKCdelta knockout mice and performed vein bypass grafts on these animals. PKCdelta(-/-) mice developed normally and were fertile. Vein segments from PKCdelta(-/-) mice isografted to carotid arteries of recipient mice of either genotype led to a more severe arteriosclerosis than was seen with PKCdelta(+/+) vein grafts. Arteriosclerotic lesions in PKCdelta(-/-) mice showed a significantly higher number of SMCs than were found in wild-type animals; this was correlated with decreased SMC death in lesions of PKCdelta(-/-) mice. SMCs derived from PKCdelta(-/-) aortae were resistant to cell death induced by any of several stimuli, but they were similar to wild-type SMCs with respect to mitogen-stimulated cell proliferation in vitro. Furthermore, pro-apoptotic treatments led to diminished caspase-3 activation, poly(ADP-ribose) polymerase cleavage, and cytochrome c release in PKCdelta(-/-) relative to wild-type SMCs, suggesting that their apoptotic resistance involves the loss of free radical generation and mitochondrial dysfunction in response to stress stimuli. Our data indicate that PKCdelta maintains SMC homeostasis and that its function in the vessel wall per se is crucial in the development of vein graft arteriosclerosis.

Animals↗

Ruscogenin glycoside (Lm-3) isolated from Liriope muscari improves liver injury by dysfunctioning liver-infiltrating lymphocytes.

The effects of ruscogenin 1-O-[beta-D-glucopyranosyl(1 --> 2)] [beta-D-xylopyranosyl(1 --> 3)]-beta-D-fucopyranoside (Lm-3) and its aglycone, ruscogenin, on liver injury induced in mice by delayed-type hypersensitivity to picryl chloride have been investigated. Lm-3 and ruscogenin significantly decreased liver injury when given during the effector phase of the delayed-type hypersensitivity reaction. The pretreatment of nonparenchymal cells, but not hepatocytes, with Lm-3 or ruscogenin in-vitro caused a concentration- and time-dependent inhibition against the damage. Lm-3 showed a stronger inhibition against the damage than ruscogenin (IC50: Lm-3 6.3 x 10(-10) M, ruscogenin 3.9 x 10(-7) M). However, neither Lm-3 nor ruscogenin blocked the hepatotoxic potential of CCl4, when used to pretreat hepatocytes. Moreover, Lm-3 and ruscogenin inhibited concanavalin A-induced lymphocyte proliferation only at high concentrations. These results suggested that Lm-3 and ruscogenin improved the immunological liver injury by selectively causing dysfunction of the liver-infiltrating cells rather than by protecting hepatocyte membranes. Such characteristics would be significant for treating immunologically related liver diseases as well as for developing new drugs.

Animals↗

Elements in erythrocytes of population with different thyroid hormone status.

The contents of elements K, Ca, Fe, Cu, Zn, Se, and Rb in erythrocytes of 78 cases with different thyroid hormone status have been measured by proton-induced X-ray emission and neutron activation analysis. According to the status of thyroid hormones T3, T4, TSH, FT3, and FT4 detected by radioimmunoassay, the experiment subjects were divided into four groups (i.e., hyperthyroid, hypothyroid, critical [one of thyroid hormones was abnormal], and normal). Elements contents and hormones levels of four groups were analyzed by one-way analysis of variance and correlation using an SPSS/PC statistical package. The results showed that the Se contents of four groups were not significantly different (p<0.05). Zn content of hypothyroid group was significantly higher than those of hyperthyroid and critical groups. The Zn content of the normal group was higher than that of the hypothyroid group and lower than that of the hyperthyroid and critical groups. In the hyperthyroid group, there were significant correlations between elements contents and thyroid hormones levels (except TSH), but not between elements contents and levels of thyroid hormones. However, in the hypothyroid group, relatively strong correlations have been found between elements contents and thyroid hormones levels, especially between Zn and the T3/T4 ratio, and between Zn and TSH.

Animals↗

An improved optimization strategy and its application to clustering analysis.

In this paper, a new optimization strategy is put forward which locates as many potential unimodal regions as possible in the search space. The potential optima can be further explored by a global optimization method for searching in the identified unimodal regions. The proposed strategy was evaluated by the optimization of test functions. The results obtained by this approach are comparable with those achieved by variable step size generalized simulated annealing (VSGSA) and a genetic algorithm (GA). Finally, we used this strategy in a clustering analysis of a tobacco data set.

Algorithms↗

[Study on polymorphism of D gene exons among RhD-negative Chinese Han population].

OBJECTIVE: To explore the genomic structure of 8 exons in D gene of RhD(-) Chinese Han population. METHODS: Polymerase chain reaction-sequence specific primers(PCR-SSP) were used to study genomic DNA from 50 samples of RhD(-) Chinese Han donors. Exons 2, 3, 4, 5, 6, 7, 9, 10 of RHD gene and exons 1, 2, 4, 5 of RHCE gene were specifically amplified, also intron 4 of them was amplified. RESULTS: Phenotypes of the 50 RhD(-) donors were: 22 ccdee, 22 Ccdee, 3 CcdEe, 3 CcdEe. The 8 exons of RHD gene were completely absent in 25 donors with ccdee or ccdEe phenotype, while polymorphisms of D gene exons were found in 25 donors with Ccdee or CcdEe phenotype: the presence of all 8 exons of D gene in 9 donors, the absence of the 8 exons in 7 donors, the presence of exon 2 in 5 donors, the presence of exon 6 in 3 donors and the presence of exons 2, 6, 10 in 1 donor were demonstrated. CONCLUSION: Polymorphisms of RHD gene exons were present among RhD(-) Chinese Han blood donors. The 8 exons of RHD gene were completely absent in donors with Rhesus cc phenotype, while 5 polymorphisms of RHD gene exons were found in donors with Rhesus Cc phenotype. The discrepancy of the RHD gene in RhD(-) individuals between Chinese Hans and Caucasians indicates that care should be exercised by clinicians in the use of the RhD genotyping results.

China↗

Sensitive blood-retinal barrier breakdown quantitation using Evans blue.

PURPOSE: This study investigated whether a nonradioactive dye, Evans blue, can be adapted as a safe alternative to the isotope-dilution method for quantitating blood-retinal barrier breakdown. METHODS: Blood-retinal barrier breakdown was induced in rats with vascular endothelial growth factor (VEGF) or through the induction of diabetes. After allowing Evans blue to circulate in the vasculature, the dye was cleared from the bloodstream with saline, citrate, or citrate-buffered paraformaldehyde, and the efficacies of the perfusion solutions were compared. Extravasated dye was detected at 620 nm and was normalized against the time-averaged Evans blue plasma concentration, the circulation time, and also against wet and dry retina weights. RESULTS: Evans blue leakage from retinas treated with VEGF was 4.0-fold higher than that of contralateral untreated eyes (n = 6 rats, P: < 0.05). Retinal Evans blue leakage of eyes from 1-week diabetic animals (n = 11 retinas) was 1.7-fold higher (P: < 0.05) than that of nondiabetic controls (n = 10 retinas). Intra-animal, inter-retina weights showed significantly less variability (P: < 0.05) with the use of dry weights (11.2%, n = 74 retina pairs) than with wet weights (20.5%, n = 93 retina pairs). CONCLUSIONS: The Evans blue dye technique can be modified to be as sensitive and quantitative as the isotope-dilution method for measuring blood-retinal barrier breakdown. The advantages of the Evans blue technique are its safety, relative simplicity, and economy.

Animals↗

[Ultrafiltration of micropolluted water in combination with coagulation and PAC process].

The experiments of ultrafiltration of Huangpu River water with coagulation and powered activated carbon (PAC) combinations was evaluated. The results showed that coagulation and PAC pretreatment effectively remove dissolved organic matters (DOM), of which coagulation removes high molecular weight (MW) DOM and PAC removes low MW DOM. Coagulation and PAC are effective treatment for removing Trihalomethane Formation Potential (THMFP). In terms of low MW THMEP, coagulation removes poorly and PAC removes effectively. The results also showed that addition of coagulant and PAC reduce cake resistance greatly. At coagulant dosage 4 mg/L (as Al), cake resistance was minimized.

Charcoal↗

[Primary study on heart rate variability of non-linear dynamics in patients with coronary artery disease and diabetes].

This is a comparative study on the non-linear dynamics between 30 healthy controls and three groups of patients with single coronary artery disease(n = 20), multi-coronary disease(n = 8), and diabetic patients with diabetic autonomic neuropathy (DAN)(n = 18), respectively. We selected and adopted six quantity indices of dispersed-dot plot, including the area of plot (SQ), long-axis (LA), short-axis (SA), the angle of long-axis and short-axis (ALS), vector length index (VLI) and vector angle index (VAI), and Kolmogorov entropy and fractal dimension. We found that the non-linear indices in healthy control had obvious day-to-night change, while the change in coronary artery disease patients decreased and disappeared in diabetics. By the findings that both coronary artery disease patients and diabetic patients had the turbulence of vegetal nerve system, we concluded that the vegetal nerve activity might be an important factor in heart non-linear dynamics. And marked differences in the non-linear indices were seen between the normal control, the single-vessel, multi-vessel coronary artery disease patients, and the diabetic patients, thus suggesting that these indices may be used in clinical practice.

Adult↗

VEGF-initiated blood-retinal barrier breakdown in early diabetes.

PURPOSE: The objectives of this study were to (1) determine whether endogenous vascular endothelial growth factor (VEGF) triggers diabetic blood-retinal barrier breakdown, and (2) identify the site as well as phenotype of the hyperpermeable diabetic retinal vessels. METHODS: Retinal VEGF mRNA levels were quantified in 1-week diabetic rats using the RNase protection assay. VEGF bioactivity was blocked via the systemic administration of a highly specific VEGF-neutralizing soluble Flt/F(c) construct (VEGF TrapA(40)). An inactive IL6 receptor/F(c) construct (IL6R Trap) was used as an isotype control. Blood-retinal barrier breakdown was quantified using the Evans blue technique and was spatially localized with fluorescent microspheres. RESULTS: Retinal VEGF mRNA levels in 1-week diabetic animals were 3.2-fold higher than in nondiabetic controls (P < 0.0001). Similarly, retinal vascular permeability in 8-day diabetic animals was 1.8-fold higher than in normal nondiabetic controls (P < 0.05). Diabetes-induced blood-retinal barrier breakdown was dose-dependently inhibited with VEGF TrapA(40), with 25 mg/kg producing complete inhibition of the diabetes-induced increases (P < 0.05). Blood-retinal barrier breakdown in diabetic animals treated with solvent alone or IL6R Trap did not differ significantly from untreated diabetic animals (P > 0.05). Spatially, early blood-retinal barrier breakdown was localized to the retinal venules and capillaries of the superficial retinal vasculature. CONCLUSIONS: Early blood-retinal barrier breakdown in experimental diabetes is VEGF dependent and is restricted, in part, to the venules and capillaries of the superficial inner retinal vasculature. VEGF inhibition should prove a useful therapeutic approach in the treatment of early diabetic blood-retinal barrier breakdown.

Animals↗

[Effects of nitric oxide and prostaglandin on gastric mucosal perfusion in rats with portal hypertensive gastropathy].

OBJECTIVE: To observe the effects of nitric oxide (NO) and prostaglandin on gastric mucosal perfusion in rats with portal hypertensive gastropathy (PHG). METHODS: Two weeks after partial portal vein ligation, gastric mucosal blood flow (GMBF) was measured with the neutral red clearance method and the changes of portal venous pressure (PVP) were observed. RESULTS: GMBF and PVP were significantly higher in rats with PHG than in sham operated rats (P<0.01). Low dose inhibitor of NO synthesis N(-nitro-L-arginine methyl ester (L-NAME 1mg/kg, 4mg/kg) caused a significant and dose dependent reduction in GMBF in PHG rats, but had no effect on sham operated rats. High dose L-NAME (12 mg/kg) significantly decreased GMBF in both PHG and sham operated rats. The inhibition of prostaglandin synthesis with indomethacin significantly decreased GMBF in rats with PHG, but had no effect in sham operated rats. In sham operated rats pretreated with indomethacin, GMBF was not modified after and before injection of low dose L-NAME (4mg/kg); likewise, high dose of L-NAME (12mg/kg) did not alter the significant reduction in GMBF as compared with pretreatment without indomethacin. In PHG rats the significant dose dependent reduction in GMBF induced by L-NAME (4mg/kg, 12mg/kg) was not significantly different between pretreatment with and without indomethacin. CONCLUSIONS: NO and prostaglandins play an important role in the regulation of GMBF in rats with PHG, but no synergistic interactions between them.

Animals↗

[Effects of emodin on hepatic fibrosis in rats].

OBJECTIVE: To investigate the effect of emodin on hepatic fibrosis in rats and study its possible mechanism. METHODS: The rat hepatic fibrotic model was induced by the subcutaneous injection of 40% CCl(4) (twice a week for 6 weeks). The fibrotic rats were treated with low-dose, mediate-dose and high-dose emodin (20, 40 and 80 mg/kg body weight, once a day for 42 days). Liver function, serum hyaluronic acid, laminin, and liver hydroxyproline were determined, Histopathological changes were examined by optical microscopy. The expression of alpha-smooth muscle actin (alpha-SMA) in liver tissue were detected by immunohistochemical techniques. RESULTS: Compared with model group, it revealed that in emodin-treated rats: (1) Liver functions was improved, alanine transaminase (ALT) and alkaline phosphatase (AKP) obviously reduced (P<0.05 or <0.01), total protein (TP) and albumin (ALB) significantly increased (P<0.05 or <0.01). (2) Serum hyaluronic acid and laminin markedly reduced (P<0.05 or <0.01). (3) Liver hydroxyproline were significantly decreased (P<0.05 or <0.01). (4) The degrees of fibrosis were reduced (P<0.05). (5) The expression of alpha-SMA in liver tissue were ameliorated. CONCLUSIONS: Emodin has an effect on hepatic fibrosis in rats. The effect may be related to slowing hepatocyte injury and inhibiting liver alpha-SMA expressions.

Actins↗

[Association between dopamine transporter gene polymorphism and Parkinson's disease].

OBJECTIVE: To detect the association between dopamine transporter gene polymorphism and Parkinson's disease (PD). METHODS: The authors analyzed the difference in the distribution of the variable number tandem repeat (VNTR ) polymorphism within the 3' untranslated region of the DAT gene between 85 normal controls and 128 PD patients that were further divided into the senile subgroup (aged >50 years at onset of PD ) and the early-onset subgroup (aged </=50 years). RESULTS: There were significant differences in genotypic and allelic distribution between the control group and the PD group. The senile PD was strongly associated with the 7-copy allele and weakly with the 10-copy allele, and the early onset PD was mainly associated with the 9-copy allele. CONCLUSION: The findings not only support an association between DAT gene and PD but also suggest the relationship of the 3'VNTR polymorphism of DAT gene with the age at the onset of PD.

Adolescent↗

[Pathological changes between HBeAg and anti-HBe in patients with chronic hepatitis B].

OBJECTIVE: To observe the differences of pathological changes between HBeAg and anti-HBe in chronic hepatitis B. METHODS: Liver biopsy was performed in patients with chronic hepatitis B. The histopathological grading and staging were carried out. Serum markers of viral hepatitis were tested. RESULTS: (1) The histopathological grading and staging were closely correlated with the appearance of serum HBeAg and anti-HBe. The number of G(3-4) and S(3-4) in anti-HBe cases was significantly higher than that of G(1-2) and S(1-2), respectively. The number of G(1-2) and S(1-2) in HBeAg cases was significantly higher than that of G(3-4) and S(3-4), respectively. Significant differences were found between the group of anti-HBe cases and the group of HBeAg cases (P<0.005). (2) HBV DNA was detected in 126 of 151 HBeAg positive patients (83.4%), and the positive rate of HBV DNA in anti-HBe positive patient was 29% only. CONCLUSIONS: (1) Severe inflammatory, necrosis and fibrosis of hepatic tissue are observed in patients with anti-HBe positive chronic hepatitis B. (2) Although HBV DNA is positively correlated to HBeAg, HBV-DNA can be detected in part of anti-HBe positive patients.

Biomarkers↗