Objective To evaluate the diagnostic value of glycosylated hemoglobin A1c (HbA1c)and glycated albumin(GA) in hyperglycemia patients with liver cirrhosis (LCH).Methods One hundred LCH patients were divided into anemia and no-anemia group by Hb 110 g/L The no-anemia group was further divided into low albumin (serum albumin ＜ 30 g/L),and high albumin group (serum albumin 30-＜40 g/L).One hundred type 2 diabetes without liver cirrhosis were included as control group (T2DM).HbA1c,GA,fasting plasma glucose (FPG),postprandial 2h plasma glucose (2hPG) were collected for statistical analysis.Results (1) The HbA1c level in LCH with anemia tended lower than that in T2DM subjects [(6.76 ±2.20)％ vs (7.34 ± 1.23)％,P =0.06];though the level of GA [(19.10 ±7.47)％vs (16.68 ±2.90)％,P＜0.01] and 2hPG [(12.09 ±3.39) mmol/L vs (10.84 ±2.95) mmol/L,P＜0.05] were significantly higher than that in T2DM group.(2) No-anemia subjects in LCH group with albumin ＜ 30 g/L had obviously higher GA levels than those with albumin 30-＜ 40 g/L and T2DM (albumin≥40 g/L) [(18.79 ±2.28)％ vs (16.71 ±2.42)％ and (16.73 ±2.96)％,P＜0.01];though the level of HbA1c of three groups above has no significant difference.(3) The level of HbA1c between LCH without anemia group and T2DM group had no significant difference (P ＞ 0.05);and the level of GA between LCH without anemia group with albumin 30-＜ 40 g/L and T2DM group had no significant difference(P ＞0.05).(4) The HbA1c has a positive correlation with FPG and 2hPG in LCH (FPG∶r =0.45,P＜0.001;2hPG∶r =0.33,P=0.001) and T2DM subjects (FPG∶ r =0.76,P＜0.001;2hPG∶r =0.81,P ＜ 0.001).GA also has a positive correlation with FPG and 2hPG in LCH (FPG∶ r =0.48,P ＜0.001;2hPG:r=0.39,P ＜0.001) and T2DM subjects (FPG∶ r =0.74,P ＜0.001;2hPG∶ r =0.76,P ＜0.001).Conclusion It is unfavorable to use HbA1c to evaluate the blood glucose level in liver cirrhosis patients with Hb ＜ 110 g/L and to use GA in patients with serum albumin ＜ 30 g/L.

Objective To explore the efficiency of endoscopic septoplasty with submucous resection for the treatment of 220 patients with deviated nasal septum and report our experience in this field. Methods From May 2006 to May 2010, 220 patients with deviated nasal septum were treated by endoscopic septoplasty with submucous resection to decompress the stress points, resect the deviated parts and implant the reshaped bone of nasal septum, while retaining the normal structure of nasal septum with minimally invasive technique. Results Satisfactory effects were achieved in all the 220 patients, showing centered septal structure and disappeared symptoms such as nasal obstruction, headache and nasal hemorrhage, but no complications including perforation of nasal septum, depressed nasal bridge and septal chalasia and flaring. Conclusion Rhino-endoscopic septoplasty with submucous resection can substantially retain the original structure of nasal septum and thus is proven to be a desirable operation with multiple advantages including minimal invasiveness, quicker healing and fewer complications.

Ataxia Telangiectasia Mutated Proteins ; Breast ; metabolism ; pathology ; Breast Neoplasms ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; metabolism ; pathology ; Carcinoma, Intraductal, Noninfiltrating ; metabolism ; pathology ; Cell Cycle Proteins ; metabolism ; Checkpoint Kinase 2 ; DNA-Binding Proteins ; metabolism ; Female ; Humans ; Lymphatic Metastasis ; Neoplasm Grading ; Protein-Serine-Threonine Kinases ; metabolism ; Tumor Burden ; Tumor Suppressor Protein p53 ; metabolism ; Tumor Suppressor Proteins ; metabolism

Objective To study the damage to striatum in patients perorally addicted to compound codeine phosphate solution by using the brain dopamine transporter SPECT imaging. Methods Patients p erorally addicted to compound codeine phosphate solution ( n = 29 ) and addicted to heroin ( n = 27 ), as well as healthy volunteers (n = 31 ) were included in the study. Each of them underwent dopamine transporter (DAT) SPECT imaging with 99Tcm-2β-[N, N'-bis-( 2- mercaptoethyl ) ethylenediamino] methyl, 3β-(4-chlorophenyl)tropane (99Tcm-TRODAT-1). The striatum volume (V, cm3), mass (m, g) and radiactivity ratio (Ra) of striatum to whole brain were calculated using physio-mathematical modeling method.R esults Bilateral striatum of healthy volunteers showed typical "panda eyes" pattern and the distribution of DAT was uniform and symmetrical. Bilateral striatum of patients addicted to compound codeine phosphate showed impaired tracer uptake, similar to those addicted to heroin. The V, m and Ra of bilateral striatum of patients addicted to compound codeine phosphate were (23.68 ±4.94) cm3, (24.87 ±5.19) g and (5.01 ±0. 88 ) %, respectively, which were significantly lower than those of healthy controls: ( 35.39 ± 4.42 ) cm3,(37.16 ±4.64) g and (7.93 ±0.86)% (t = -9.69, -9.69, - 13.01, all P =0.000), but significantly higher than those addicted to heroin: ( 18.87 ± 4.66 ) cm3, ( 19.81 ± 4.90 ) g and (4.26 ± 1.02 ) % ( t =3.74, 3.74, 2.96, P = 0.000, 0.000, 0.005 ). Conclusion Long-term peroral intake of compound codeine phosphate solution may damage the function of cerebral striatum, which is someway similar to though less severe than, the impairment caused by heroin.

Objective To construct an expression plasmid carrying the specific siRNA of survivin gene,and to evaluate its silencing effect on the expression of survivin gene and its inhibition effect on the growth of gastric cancer cells.Methods The specific siRNA of survivin gene was designed and synthesized,and an expression plasmid pAdGFP-siRNA was constructed.Gastric cancer cell line SGC-7901 was cuhured and transferred with pAdGFP-siRNA,then the silencing of survivin gene expression and the growth inhibition of cancer cell mediated by pAdGFP-siRNA were identified.Results The growth of gastric cancer cells was inhibited after transferring the pAdGFP-siRNA,with the inhibition rate of 68.2% compared to the control group.Immunohistochemistry showed that the specific siRNA markedly silenced the expression of survivin gene in cancer cells.Conclusions The overexpression of survivin gene in gastric cancer cells results in the high proliferation and the resistance to the chemo- and radio-therapy of the cancer cells.The specific siRNA can markedly silence the expression of survivin gene and inhibit the growth of cancer cells.

OBJECTIVETo explore the influence of the DNA repair gene ERCC2 single nucleotide polymorphisms (SNPs) rs13181, rs1618536, and rs1799793 on male idiopathic infertility in Ningxia, China.

METHODSUsing MassArray, we conducted a case-control study and genotyped three ERCC2 SNPs rs13181, rs1618536, and rs1799793 for 351 males (aged 31.0 +/- 4.2 years) with idiopathic infertility and another 327 normal fertile men (aged 33.0 +/- 5.9 years) as controls.

RESULTSThe ERCC2 AnyG-anyA-anyA genotypes were significantly associated with an increased risk of idiopathic infertility (OR 0.414, 95% CI 0.176 - 0.970), while the three single ERCC2 SNPs rs13181, rs1618536, and rs1799793 showed no significant differences between the cases and controls (P > 0.05).

CONCLUSIONThe ERCC2 SNPs rs13181, rs1618536, and rs1799793 play a role of interaction in male idiopathic infertility in Ningxia, contributing to the risk of the disease.

Adult ; Case-Control Studies ; China ; DNA Repair ; Genotype ; Humans ; Infertility, Male ; genetics ; Male ; Polymorphism, Single Nucleotide ; Xeroderma Pigmentosum Group D Protein ; genetics

Objective: To study the effect of arsenic trioxide (As2O3) on human pancreatic cancer cell proliferation and apoptosis (mainly early stage) in vitro. Methods: SW1990 cells line were trea ted with As2O3 at different concentration. Cell proliferation was evaluated by MTT and apoptosis by Annexin-Ⅴ-fluostaining, electron-microscopy, flow cytometry and immunocytochemical staining of Bcl-2 and Bax. Results: As2O3 and cisplatin had the same cytotoxity on SW1990. The cytotoxic effe ct on tumor cell was produced by induction of apoptosis. Twelve hours after cult ure with 10 μg/ml As2O3, much more SW1990 cells went into apoptosis than t he control. The apoptosis rate reached 24% after 48 h with the similar concentra tion of As2O3. Immunohistochemical study revealed that the expression of Bcl -2 was decreased after treated with As2O3. Conclusion: As 2O3 can depress the proliferation of SW1990 in vitro, mainly through the i nduction of apoptosis, and it is a potential agent for pancreatic cancer chemoth erapy.

Objective To investigate whether and how candesartan treatment can attenuate the deleterious influence of hyperglycemia in diabetic(db/db) mice.Methods Eight-week-old db/db mice were randomized into candesartan eilexetil (1 mg/kg) or placebo group via gavage for 6 weeks.Their age-matched nondiabetie littermates db/m mice were treated with placebo and acted as non-diabetic control group.After 6 weeks' treatment, intraperitoneal glucose tolerance test,immunohistochemical stainings of oxidative stress markers [8-(OH) dG,4- HNE,NADPH oxidase],insulin,CD31,Azan staining and electron microscopy observation of islet?-cells were perfermed.Results As compared with placebo group,the improvement in glucose tolerance and marked saving of islet?-cell mass with candesartan for 6 weeks were noted.There were also notably decreased staining intensity in oxidative stress markers,such as 8-(OH) dG,4-HNE,p22~(phox),gp91~(phox),as well as attenuated intra-islet Azan staining and enhanced endothelium marker CD31 staining in islet.Under electron microscope,candesartan-treated mice showed significantly increased granulation of insulin and ameliorated proliferations of endoplasmic reticulum and Golgi bodies.Furthermore,swelling of mitochondria was relieved to nearly normal.Conclusion After diabetic onset,candesartan treatment does not reverse the state of diabetes but may effectively improve glucose tolerance and protect?-cell function by attenuating oxidative stress,islet fibrosis,sparsity of blood supply and uhrastructure disruption,and thus delays the?-cell failure.

Pathological cardiac hypertrophy is a maladaptive response in a variety of organic heart disease(OHD),which is characterized by mitochondrial dysfunction that results from disturbed energy metabolism. SIRT3, a mitochondria-localized sirtuin, regulates global mitochondrial lysine acetylation and preserves mitochondrial function. However, the mechanisms by which SIRT3 regulates cardiac hypertrophy remains to be further elucidated. In this study, we firstly demonstrated that expression of SIRT3 was decreased in AngiotensionⅡ(AngⅡ)-treated cardiomyocytes and in hearts of AngⅡ-induced cardiac hypertrophic mice. In addition, SIRT3 overexpression protected myocytes from hypertrophy, whereas SIRT3 silencing exacerbated Ang II-induced cardiomyocyte hypertrophy.In particular,SIRT3-KO mice exhibited significant cardiac hypertrophy. Mechanistically, we identified NMNAT3 (nicotinamide mononucleotide adenylyltransferase 3), the rate-limiting enzyme for mitochondrial NAD biosynthesis, as a new target and binding partner of SIRT3.Specifically,SIRT3 physically interacts with and deacety-lates NMNAT3,thereby enhancing the enzyme activity of NMNAT3 and contributing to SIRT3-mediated anti-hypertrophic effects.Moreover,NMNAT3 regulates the activity of SIRT3 via synthesis of mitochon-dria NAD.Taken together,these findings provide mechanistic insights into the negative regulatory role of SIRT3 in cardiac hypertrophy.Sirtuin 3(SIRT3),a mitochondrial deacetylase that may play an impor-tant role in regulating cardiac function and a potential target for CHF

Objective To explore the activation and function of Janus protein-tyrosine kinase (JAK)/ signal transducer and activator of transcription (STAT1) signal transduction pathway in kidney,lung and brain of MRL/lpr mice.Methods MRL/lpr mice with systemic lupus erythematosus (SLE) were studied at the age of 12 weeks up.Non-SLE MRL/lpr mice were used as controls.We used phosphospecific antibodies to detect STAT1 activation in kidney,lung and brain by immunohistochemistry and Western blots.Gene expression of the STAT induced feedback inhibitors of cytokine signaling 1 (SOCS-1) was investigated by SYBR green I real-time reverse transcriptase polymerase chain reaction (PCR).Results Phosphorylation of STAT1 protein was markedly activated in these three organs,although renal and pulmonary STAT1 activation were much more evidently activated.SOCS-1 gene expression increased in all three organs,while renal SOCS-1 gene expres- sion increased less than lung and brain.Conclusion The activation of JAK/STATI signal transduction path- way may be pathogenic in the organ involvement and progression of SLE.The pathogenesis of lupus nephritis may also be associated with the down-regulation of SOCS-1 feedback inhibition.