Cervical Intraepithelial Neoplasia ; diagnosis ; pathology ; surgery ; Colposcopy ; Conization ; Electrosurgery ; Female ; Humans ; Hysterectomy ; methods ; Neoplasm Regression, Spontaneous ; Uterine Cervical Neoplasms ; diagnosis ; pathology ; surgery ; Vaginal Smears

Objective To investigate the value of detecting BK virus(BKV)in urine of renal al- lograft recipients for the diagnosis and treatment of BKV infection.Methods Using polymerase chain re- action(PCR)method combined with DNA sequencing,61 urine samples from renal allograft recipients,30 u- fine samples from dialytic patients and 30 urine samples from healthy volunteers(controls)were detected. The results were compared among the 3 groups.Results The BKV positive rate in renal allograft recipi- ents was 36.1%,compared with 13.3% in dialytic patients(P＜0.05)and 0.0% in controls(P＜0.05). One renal allograft recipient who was positive for BKV developed ureteral obstruction.The BKV positive rate was 40.9%(9/22)in renal allograft recipients with rejection episode,compared with 33.3%(13/39)in the recipients without rejection episode(P＞0.05);and the BKV positive rate was 36.0%(18/50)in the recip- ients with normal graft function,compared with 36.4%(4/11)in the recipients with abnormal graft function (P＞0.05).Conclusions Renal allograft recipients are the high risk population who may develop BKV viruria.There is no correlation between recipients with or without rejection episode and BKV viruria,and also no correlation between recipients with normal or abnormal graft function and BKV viruria.Detection of BKV in the urine of renal allograft recipients is helpful in differential diagnosis of BKV induced ureteral obstruc- tion,and PCR method for detecting BKV DNA can be used to screen for BK virus-associated nephropathy (BKVAN).

Objective To explorethe relationship between serum uric acid (SUA ) and transcutaneousoxygenpressure(TcPO2)inpatientswithT2DM.Methods 622hospitalizedpatients with T2DM were recruited and divided into high SUA (HUA) group and normal SUA (T2DM) group.The differences in TcPO2 (initial value ,stable value ,initial value‐stable value ,leg‐raising initial value and leg‐raising maximum value)were compared between two groups.The correlations between SUA and TcPO2 were evaluated. Results The levels of TcPO2 were lower in HUA group than in T2DM group [initial value:left (34.05 ± 13.17) vs (39.26 ± 15.82) ,right (34.71 ± 14.90) vs (40.15 ± 16.23);stable value:left (38.93 ± 12.23) vs(45.19 ± 13.40) ,right (39.98 ± 12.34) vs (45.90 ± 16.77) ,P<0.05]. Pearson correlation analysis showed that the SUA levels negatively related with the stable TcPO2 value of leftor right side ,and with the change between the initial value and the stable value of TcPO2 (P<0.05 or P<0.01). The multiple linear regression analysis showed that SUA level was the impact factorof the left TcPO2 stable value. Conclusion HUA may be one of the risk factors microcirculation disorder in T2DM patients.

ObjectiveTo observe the preventive effect of type Ⅱ collagen on experimental rat articular cartilage damage induced by T-2 toxin,to explore molecular biomarkers of articular cartilage damage and repair,and to provide a theoretical basis for control of articular cartilage damage.MethodsEighty Wistar rats were randomly divided into 4 groups according to their body weights:negative control,positive control,high-dose intervention,and low-dose intervention groups,20 rats in each group.Animals in negative control group were fed with standard rat chow,and animals in other three groups were fed with T-2-toxin-contaminated chow( 100 ng/kgfeed).Animals in negative and positive control groups drank distilled water,animals in high-dose intervention and low-dose intervention groups drank water containing type Ⅱ collagen(0.5,5.0 g/L,respectively).These rats were sacrificed after 3 and 5 months,respectively,and bilateral knee joints were collected.Histopathologic changes in hyaline cartilage were examined by light microscope,serum levels of type Ⅱ collagen carboxyl terminal peptide (CTX-Ⅱ ),cartilage oligomeric matrix protein (COMP) and urinary deoxypyridinoline (DPD) were determined by enzyme-linked immunosorbent assay(ELISA).ResultsHE staining showed,that the positive control articular chondrocytes were disarranged,deformated,degenerated,with necrosis and extensive areas of chondrocyte loss;but the two intervention groups only showed fibril formation and swelling and surface cartilage cells became round,flat cartilage cells decreased in number,and cartilage cells clustered and so on early pathological changes of osteoarthritis.At the ends of 3 month and 5 month experiment,the levels of serum CTX- Ⅱ in different groups were,negative control[(18.77 ± 4.61),(25.07 ± 9.17)μg/L],high-dose intervention[ (21.11 ± 5.02),(33.20 ± 9.74)μg/L ],low-dose intervention [ ( 19.87 ± 4.53 ),( 29.73 ± 9.32 ) μg/L ] and positive control [ ( 24.43 ± 5.23 ),( 39.17 ±10.49 ) μg/L ] ; the levels of serum COMP were,negative control group [ (5.43 ± 2.75 ),( 6.38 ± 2.23 ) μg/L ],highdose intervention group[ (17.27 ± 4.77),(20.32 ± 4.74)μg/L],low-dose intervention group[(20.13 ± 5.07),(19.44 ± 4.92)μg/L] and positive control group[ (21.37 ± 4.72),(24.52 ± 4.26)μg/L].At the end of 3 month,compared with negative control group,the level of serum CTX- Ⅱ in other three groups increased,but only positive control group increased significantly(P ＜ 0.05) ; at the end of 5 month,compared with negative control group,the level of serum CTX-Ⅱ in other three groups increased significantly,and the difference was statistically significant (all P ＜ 0.05),and the level of CTX-Ⅱ in the two intervention groups was significantly lower compared with that of positive control group(all P ＜ 0.05).Compared with negative control group,the level of serum COMP in other groups increased significantly at the end of 3 month (all P ＜ 0.05) and only the level of serum COMP in high-dose intervention group was significantly lower compared with that of positive control group(P ＜ 0.05).At the end of 5 month,compared with negative control group,the level of serum COMP in other three groups increased significantly,the difference were statistically significant (all P ＜ 0.05) ; the levels of serum COMP in the two intervention groups were significantly lower than that of positive control group(all P ＜ 0.05).At the ends of 3 month and 5 month,the content of urinary DPD in negative control group were[ (3.47 ± 2.20),(4.14 ± 1.06)μg/L],positive control group[ (4.09 ± 2.48),(4.33 ± 3.43)μg/L],high-dose intervention group[ (3.86 ± 2.31 ),(5.72 ± 3.89)μg/L] and low-dose intervention group[ (3.58 ± 2.77),(4.23 ± 2.90)μg/L].The difference between the 4 groups were not statistically significant (F =2.608,2.436,all P ＞ 0.05).ConclusionsType Ⅱ collagen could effectively reduce the level of serum CTX-Ⅱ and COMP in experimental rats and delay the process of articular cartilage damage induced by T-2 toxin.

ObjectiveTo study the impact of jogging mode on T-2 toxin-induced articular cartilage injury in rats,and to evaluate the role of movement in the development of bone and joint disease.MethodsA hundred Wistar rats were randomly divided into five groups:negative control group(free activities in the cage),positive control group(firee activities in the cage),high-regulation group(regular exercise,the treadmill speed of 24 m/min),lowregulation group (regular exercise,the treadmill speed of 12 m/min) and the random group(random exercise,the treadmill speed of 12 or 24 n/min).The negative control group was fed on commercial grain fodder and other groups were fed on grain fodder contaminated with T-2 toxin.At the end of 5,10 weeks,the histopathological changes of hyaline cartilage were detected by optical microscope,and the level of serum cartilage oligomeric matrix protein (COMP) was determined.ResultsArticular cartilage lesions in each experimental group was evident,presented as cartilage cell degeneration,necrosis,karyopyknosis deeply stained,cells arranged in disorder and cell proliferation,articular dryness,and so on.Compared with the positive control group,the cartilage surface cells of rats in the movement groups showed degeneration,necrosis and loss of cells obviously.The injury in high-regulation group was the most serious than that in other movement groups,with the surface and the middle layer lesions,and a large area of cartilage necrosis,and loss of matrix collagen; cartilage degeneration,polarity disappeared,cell proliferation-based disorder showed in random group.The pathological changes of rat articular cartilage damage worsened with the extension of experimental period.The serum levels of COMP at week 5 in experimental groups were higher than that of both the negative control group and the positive control group,and the difference was statistically significant (F =15.733,P ＜ 0.05 ); compared with negative control group [ (11.55 ± 0.89)μg/L],the COMP levels in high-regulation group,low-regulation group,random group[(13.95 ± 1.23),(14.96 ± 1.29),( 12.99 ± 1.43)μg/L] were significantly higher(all P ＜ 0.05); compared with the positive control group[(12.32 ± 1.38) μg/L],the COMP levels in high-regulation group and low-regulation group were significantly higher(all P ＜ 0.05) ; and compared between the exercise groups,the COMP levels in low-regulatinn group were higher than that of random group(P ＜ 0.05).At week 10,the changes were in the same trend as that of week 5,and the difference between groups was statistically significant (F =6.144,P ＜ 0.05) ; and compared with the negative control group [(10.59 ± 1.93)μg/L],the COMP levels in high-regulation group,low-regulation group,random group [ ( 13.72 ± 2.67 ),( 14.94 ± 1.06 ),( 13.21 ± 1.58 ) μg/L] were significantly higher(all P ＜ 0.05) ; compared with the positive control group[ (11.45 ± 0.12)μg/L],the COMP levels in low-regulation group were significantly higher (P＜0.05); but compared with the exercise groups,the difference were not statistically significant(all P＞0.05).ConclusionsHigh-intensity regular running and irregular intensity running can increase the articular cartilage damage,and injury of articular cartilage by low-intensity treadmill exercise is not significant.

Objective To explore the value of prenatal diagnosis and sonographic features of lenticulostriate vasculopathy (LSV). Methods Prenatal ultrasonographic features of three cases of fetal lenticulostriate vasculopathy were retrospectively analysed associated with maternal TORCH screen, fetal magnetic resonance imaging, neonatal physical examination and TORCH screen. Results Prenatal sonographic diagnosis of case 1 demonstrated fetal LSV as well as fetal growth restriction (FGR), periventricular hemorrhage, mitral and tricuspid regurgitation, hydropericardium and catatact. Prenatal sonographic diagnosis of case 2 demonstrated fetal LSV, FGR, periventricular hemorrhage, mitral and tricuspid regurgitation. Prenatal sonographic diagnosis of case 3 showed fetal LSV and intraventricular hemorrhage. Maternal TORCH screens of case 1 and case 3 was negative, while in case 2 was positive. Neonatal examinations of case 1 showed cataract, hearing impairment and congenital infection. Case 3 showed prompted retinal hemorrhage, sinus bradycardia, hyperbilirubinemia and congenital infection. In case 2, maternal teratogenic pathogen screen was positive and the baby did not survive because the mother decided to stop pregnancy in 34 weeks. Conclusions Fetal LSV could be imaged by prenatal ultrasonography. Fetal LSV might indicate intrauterine infection when other abnormalities were accompanied. Ultrasound might be useful for the cases with negative maternal TORCH screen results.

Objective To observe the impact of IL-1β on the expression of lectin-like oxidized LDL receptor 1 (LOX-1) and ATP-binding cassette transporter A1 (ABCA1) in human mesangial cell line (HMCL), and its association with cholesterol homeostasis of HMCL. Methods Levels of LOX-1 and ABCA1 of HMCL induced by IL-1β were examined by using real-time PCR and Western blot. Results IL-1β up-regulated LOX-1 mRNA and protein expression. Treated with 5 μg/L IL-1β, the levels of LOX-1 mRNA and protein reached the peak after 6 h and 24 h of stimulation and were 6.87 folds and 1.88 folds of control rspectively. The expression of ABCA1 mRNA and protein of lipid-loaded HMCL was down-regulated by IL-1β Stimulated with 5 μg/L IL-1β the expression of ABCA1 mRNA and protein decreased to the lowest level, 19.0% and 50.62% of the baseline respectively. Conclusions The expression of LOX-1 can be up-regulated while the expression of ABCA1 can be decreased by the stimulation of IL-1β. IL-1β can enhance dyslipidemia and influence the balance of cholesterol homeostasis of HMCL.

Objective To study the chemical constituents from the wing twigs of Euonymus alatus. Methods Compounds were isolated and purified repeatedly on silica gel, Sephadex LH-20, open RP-C18 column chromatographies and PTLC, and their chemical structures were elucidated by their physicochemical properties and spectral data, such as 1H-NMR, 13C-NMR, and EI-MS. Results Nine compounds were obtained and identified as: epifriedelinol (Ⅰ), stigmast-4-en-3-one (Ⅱ), 6?-hydroxy-stigmast-4-en-3-one (Ⅲ), ?-sitosterol (Ⅳ), methyl 2, 4-dihydroxy-3, 6-dimethyl benzoate (Ⅴ), methyl 2, 4-dihydroxy-6-methyl benzoate (Ⅵ), 7-methoxy-4-methylphthalide (Ⅶ), vanillin (Ⅷ), n-octacosanol (Ⅸ). Conclusion Compound Ⅶ is first reported as a natural product. Compounds Ⅴ-Ⅷ are reported from plants of Euonymus L. for the first time.

0.05 ) when two doctors measured the same group patients with the same method. The coefficient of variation of IVRTd was bigger than that of IVRTm when two doctors measured the same group patients with two different methods. In four sets of data, three ones showed significant difference(P

Objective To investigate the predictive value of combined analysis on single nucleotide polymorphisms (SNPs) of X-ray cross-complementing1 ( XRCC1 ) gene 194 and 399 codon,xeroderma pigmentosum group D (XPD) gene 312 codon and glutathione S-transferase P1 (GSTP1) gene 105 codon in platinum based chemotherapy.Methods Direct sequencing was performed to detect XRCC1,XPD and GSTP1 genotypes in peripheral blood from 50 cancer patients receiving platinum-based chemotherapy.Genetic polymorphisms of these genes related to sensitivity of platinum were reviewed.Results Favorable genotypes were Arg/Trp and Trp/Trp in XRCC1 194 codon,Arg/Arg in XRCC1 399 codon,Asn/Asn in XPD 312 codon and Val/Val in GSTP1 105 codon.The response rate to chemotherapy was 57.1％,75.0％,60.9％,85.7％ and 87.5％,respectively.The response rate for patients possessing ≥2 favorable genotypes and those possessing 1 or 0 favorable genotype was 78.9％,36.4％ and 0,respectively.Patients possessing ≥2 favorable genotypes demonstrated higher sensitivity to platinum based chemotherapy,compared with those possessing 1 or 0 favorable genotype ( x2 =25.79,P ＜ 0.01 ).Conclusions Combination analysis of genomic polymorphisms of XRCC1,XPD and GSTP1 may be useful in predicting sensitivity of platinum based chemotherapy.