Homocysteine ( Hcy) is an independent risk factor for a variety of diseases and closely related to cardiac-cerebralvascu-lar diseases, neurological diseases, diabetes and diabetic com-plications. High homocysteine levels can significantly increase the recurrence risks of cardiac-cerebralvascular events and stroke in patients with stroke, leading to high all-cause mortality. The risk of Alzheimer’s disease is increased by 1. 8 fold when the concentration of Hcy is over 14 μmol·L-1 . For each 5 μmol· L-1 increase in plasma Hcy in diabetes patients, the mortality rate increases by 5 fold in the next five years. High Hcy triggers the pathogenesis of diseases via multiple mechanisms including oxidative stress, lesions of vascular endothelial cells, prolifera-tion of vascular smooth muscle cells, dysfunction of coagulation and lipid metabolism and genomic hypomethylation etc.

Objective To study the clinical value of combined detection of CA125 and CA153 for diagnosis of endometrial carcinoma.Methods The combimed detection of CA125 and CA153 were performed in 36 patients with endometrial carcinoma,confirmed by pathological examination,on admission and 2-3 months after operation.Fifty-seven patients with uterine myoma,admitted for laparotomy in the same period and confirmed by pathology,were as controls.Results The sensitivity of combined detection of CA125 and CA153 for diagnosing endometrial carcinoma increased to 82.3% and the specificity decreased.Total accuracy rate of diagnosis reached 75.1%.There was statistical difference between the group of endometrial carcinoma and controls(P

OBJECTIVE:To establish a microbial limit test method for povidone iodine solution.METHODS:Validation on methodology of the microbial limit test of povidone iodine solution was performed using plating method(Ⅰ),culture agent dilution method(Ⅱ),membrane-filter procedure method(Ⅲ)and sodium thiosulfate neutralization in combination with membrane-filter procedure method(Ⅳ).RESULTS:The recovery rates of all of the test organisms in method Ⅰ and method Ⅱ approached zero,less than 70% in method Ⅲ but above 85% in method Ⅳ.The growth of the control bacteria was abnormal in method Ⅱand method Ⅲ,but normal in method Ⅳ.CONCLUSION:It is advisable to adopt the method Ⅳ for microbial limit test of povidone iodine solution.

Objective To investigate the correlation between the expression changes of brain-derived neurotrophic factor (BDNF) in colon mucosa and abdominal pain in irritable bowel syndrome (IBS). The density of nerve fiber in colon mucosa and ultrastructural alterations of nerve fiber in IBS were also observed. Methods From September 2008 to January 2010,the IBS patients who visited the department of gastroenterology of our hospital and met the Rome Ⅲ diagnosis criteria were selected and divided into IBS with diarrhea (D-IBS) and IBS with constipation (C-IBS) according to their clinical features. The patients with colon polyps detected by colonoscopy in our hospital were selected as control group. All subjects were asked to fill in Self-Rating abdominal pain or abdominal uncomfortable Scale according to abdominal symptom in the last 2 weeks before visit and underwent colonoscopy. Four biopsy specimens were taken from the colon mucosa of rectosigmoid junction. Ofwhich,two specimens were for protein isolation and detection of BDNF expression level,one specimen was used for PGP 9. 5 immunohistochemistry staining in paraffin slices. Another specimen was used to observe the ultrastructure changes of nerve fiber in colon mucosa under transmission electron microscopy. Results Total 40 IBS patients were enrolled in this study,of those 21 were D-IBS patients,19 were C-IBS patients,and 21 were controls. The abdominal pain severity score and frequency score of IBS patients were (2. 3±0. 8) and (2. 1±0. 7),which were significantly higher than those of control group (0. 4±0. 7 and 0. 3±0. 5,P＜0. 001). Compared with the control group,the BDNF expression in colon mucosa was significantly elevated in IBS patients (P= 0. 003 ),and which correlated with the severity and frequency of abdominal pain/discomfort (r=0. 57,P＜0. 001and r=0. 46,P= 0. 003,respectively). The immunohistochemistry result indicated that the nerve fiber density in colon mucosa of IBS patients was significantly higher than that of controls,and there were ultrastructural changes of colon mucosal nerve fibers in IBS patients. Conclusion Increased colon mucosal BDNF expression may be associated with abdominal pain symptom in IBS patients. The impaired ultrastructural of mucosal nerve fibers may cause the increased BDNF expression in colon mucosa,and result in the increased mucosal nerve fiber density in IBS patients.

levels are elevated in patients with NAFL and correlated with HOMA-IR, suggesting RBP4 may participate in the development of IR and NAFL.

Objective To investigate the risk factors of central lymph node metastasis and significance of prophylactic central lymph node dissection for clinical N0 (cN0) patients with papillary thyroid carcinoma (PTC).Methods The clinical data of 315 patients with cN0 PTC in Department of General surgery,the Second Affiliated Hospital of Dalian Medical University from Jan.2012 to Jan.2014 were analyzed retrospectively.Results (Iumor size,infiltration of thyroid capsule,and tumor number were associated with central lymph node metastasis in patients with cN0 PTC(P＜0.05),and the high risk factors of central lymph node metastasis were infiltration of thyroid capsule and multiple lesions (P＜0.05);()The overall complication rate was 3.17％ (10/315),the rate of transient recurrent laryngeal nerve paralysis was 0.63％ (2/315),and the rate of transient hypoparathyroidism was 2.54％ (8/315).All patients with complications recovered after treatment.No patient developed permanent recurrent laryngeal nerve paralysis or hypoparathyroidism;()The follow-up time was 6 to 30 months,and 2 cases were lost.No patient developed local tumor recurrence,distant metastasis,or death.Conclusions The high risk factors of central lymph node metastasis in patients with cN0 PTC were infiltration of thyroid capsule and multiple lesions.No patient developed local tumor recurrence,distant metastasis,or death.It is preferable and necessary to perform prophylactic central lymph node dissection in patients with cN0 PTC.

Objective To explore whether the glomerular podocytes can be damaged by aristolochic acid. Methods Thirty-two male SD rats were equally divided into the following 2 groups:model group in which the rats received the extract of Aristolochia manshuriensis Kom (AmK) by gavage; control group only received tap water by gavage.24 h urinary protein excretion was measured at the end of the 1st and 4th week,and SDS-PAGE gel electrophoresis was performed to detect the protein in urine.At the end of the 4th week,all the rats were sacrificed and the glomeruli were isolated by laser capture microdissection technique.The mRNA expression of nephrin,podocin,CDA2P,podocalyxin and podoplanin in isolated glomeruli was determined by RT-PCR,and the average width of glomerular foot process was measured by electron microscopy and image analysis. Results At the end of the 4th week,24 h urinary protein excretion in the model group was significantly higher than that in the control group (P＜0.01) and the urinary albumin content in model group was also obviously increased.The average width of glomerular foot process in the model group was significantly larger than that in control group (P＜0.01).The mRNA expressions of nephrin,podocin,CDA2P,podocalyxin and podoplanin in glomeruli were significantly down-regulated in the model group compared with the control group,which decreased by 34％,62％,56％,50％(P＜0.01) and 27％ (P＜0.05),respectively. Conclusions Aristolochic acid can damage the glomerular podocytes,resulting in the down-regulation of nephrin,podocin,CD2AP,podoplanin and podocalyxin mRNA expression, the segmental widening of foot process, and increased urinary protein excretion.

Aurora-B as an important kinase to adjust the cell normal mitosis is a potent target for cancer treatment. Aurora-B is overexpressed in a broad range of tumor and tumor cells are more sensitive while Aurora-B is inhibited. Due to the key role of the Aurora-B in cell mitosis, the development of its inhibitors is becoming more and more important. Several small molecules inhibit with a similar efficacy both Aurora-A and Aurora-B, however, in most cases the effects resemble Aurora-B disruption by genetic methods, indicating that Aurora-B represents an effective therapeutic target. There were several Aurora-B kinase inhibitors which had entered the clinics and displayed good antitumor activity. In this review, we will outline the functions of Aurora kinase B in normal cell division and in malignancy. We will focus on recent preclinical and clinical studies that have explored the mechanism of action and clinical effect of Aurora-B inhibitors in cancer treatment.

Objective To examine whether aldosterone contribute to obesity related glomerular disease. Methods C57BL/6J mice were randomly divided into three groups: a control group (low?fat?diet, n=10), a model group (high?fat?diet, n=10) and a intervention group (high?fat?diet, n=12). After 8 weeks intervention group were treated with a mineralocorticoid receptor antagonist, spirolactone (SPL).The physicochemical indexes and the renal pathology of the three groups were all detected. The mRNA and protein expressions of podocyte marker protein were determined by real?time PCR and Western blotting, respectively. Results Compared with the control group, body weight, kidney weight, Lee ’s index, fat index, blood cholesterol, blood triglyceride, creatinine clearance rate, urinary protein excretion, glomerular average diameter, glomerular foot process average width were significantly up ? regulated (P<0.05); The mRNA and protein expression of nephrin, podocin, podoplanin and podocalyxin were significantly down?regulated in model group (P<0.05). Meanwhile, these changes were attenuated by SPL. Conclusion Aldosterone can participate in the process of obesity? related renal injury, and these can be attenuated by mineralocorticoid receptor antagonist, spirolactone. This gives us preliminary clues to treat ORG.

Objective To evaluate the effect of hydrogen ( H2 ) inhalation on mitochondrial bio?synthesis in lung tissues during acute lung injury in mice with sepsis. Methods One hundred and four male ICR mice, aged 6 weeks, weighing 20-25 g, were divided into 4 groups ( n=26 each) using a ran?dom number table: sham operation group ( group S) , sham operation + H2 group ( group S+H2 ) , sepsis group ( group Sep) and sepsis + H2 group ( group Sep+H2 ) . Sepsis was produced by cecal ligation and puncture. In S+H2 and Sep+H2 groups, the mice inhaled 2% H2 for 1 h starting from 1 and 6 h after opera?tion. Twenty mice in each group were selected, and the survival rates on postoperative days 1, 2, 3, 5 and 7 were recorded. On the postoperative day 1, 6 mice in each group were selected, and blood samples were collected from the common carotid artery for measurement of arterial oxygen partial pressure, and the oxygenation index was calculated. The pulmonary specimens were obtained for examination of the pathologi?cal changes which were scored and for determination of the expression of peroxisome proliferator?activated re?ceptor gamma coactivator?1α ( PGC?1α) in lung tissues by Western blot. The pulmonary mitochondria were isolated for determination of mitochndrial membrane potential ( MMP ) and ATP contents using spectropho?tometry and a bioluminescence technique, respectively. Results Compared with group S, the survival rate, oxygenation index and MMP and ATP content in lung tissues were significantly decreased, and the pathological scores and PGC?1α expression in lung tissues were significantly increased in Sep and Sep+H2 groups (P<0.05). Compared with group Sep, the survival rate, oxygenation index, and MMP, ATP content and PGC?1α expression in lung tissues were significantly increased, and the pathological scores were significantly decreased in group Sep+H2 ( P<0.05) . Conclusion H2 inhalation can ameliorate acute lung injury in mice with sepsis, and the mechanism is associated with the enhanced function of PGC?1αand promoted mitochondrial biosynthesis in lung tissues.