Objective To investigate the clinical application of fecal calprotectin in inflammatory bowel disease (IBD).Methods Colonoscopy took 79 patients with IBD that were diagnosed with pathology,including 47 cases of ulcerative colitis (UC) patients,32 cases of Crohn's disease (CD).Moreover,42 cases of IBD patients without abdominal pain,diarrhea and other intestinal inflammation were used as disease control group,and 34 cases of healthy people were used as healthy control group.The level of fecal calprotectin in each group was detected by enzyme-linked immunosorbent assay (ELISA).Results The positive rate of fecal Calprotectin in IBD group,disease control group and the healthy control group was 57.0％,19.0％,and 0,respectively; each positive rate in IBD group was significantly higher than the other two groups (P ＜ 0.05).The serum concentration of fecal calprotectin in IBD group [(493.86 ±204.18) μg/g] was significantly higher than the disease control group [(71.46 ± 60.51) μg/g] and the healthy control group [(36.19 ± 13.46) μg/g] (P ＜ 0.05) ; IBD active calprotection [(1015.23 ± 324.96) μg/g] was significantly higher than resting [(52.69 ±34.71) μg/g] (P ＜0.01).Conclusions Fecal calprotectin test benefits early diagnosis of IBD,and may be taken as the diagnostic index of IBD activity.It has extensively clinical value.

Objective To obtain the Cyclin D1 through cloning and prokaryotic expression of Cyclin D 1 gene.Methods The total RNA was extracted from liver cancer tissue .The Cyclin D1 cDNA was obtained by reverse transcriptase polymerase chain reaction (RT-PCR).The Cyclin D1 cDNA was sequenced, and sub-cloned to the PET32a+.The prokaryotic expressed was used to obtain the Cyclin D1.Results The 483 bp Cyclin D1 cDNA was obtained.The sequence of Cyclin D1 was corrected.The 36 KD CyclinD1 was obtained by prokaryotic expression .Conclusions The Cyclin D1 cDNA was obtained.Cyclin D1 was expressed in BL21.

Objective To establish the rheumatoid arthritis (RA) mouse model induced by glucose-6-phosphate isomerase (GPI),and explore the mechanism of GPI in RA.Methods Totally 36 DBA/1 mice were randomly divided into three groups:test group (injection GPI),positive group (injection of bovine collagen Ⅱ),and negative group (saline).The rates and changes of weight were observed.The score of the arthritis,the ankle histopathological changes and serum GPI content were detected.Results Toes swollen slightly,joint swelling,deformity and accompanied by block were appeared at 35th day in the test group.Compared to the control group,the rates and changes of weight in test group showed a significant difference (P ＜ 0.05).The score of arthritis was showed by x ± s.Compared to the negative group,the test group and positive group were showed significant difference (P ＜ 0.05).A lot of lower synovial lining exudate macrophages,fibroblasts,and other inflammatory cells were increased in the test group.The GPI content in the test group [(0.39 ±0.11)μg/ml] was significantly higher than the negative group [(0.10± 0.06) μg/ml,P ＜ 0.05].Conclusions GPI could induce rheumatoid arthritis in mice.It provides the experimental basis to diagnose RA.

Objective To analyze the relationship between the expression of protection of telomeres 1 (POT1) and the pathogenesis of acute myeloid leukemia (AML). Methods 62 patients with de novo AML (case group) and 10 patients with iron deficiency anemia (control group) were enrolled in this study. The quantitative real-time polymerase chain reaction (PCR) and Western blot were used to detect the expression of POT1 in AML patients. Results There were 62 de novo AML patients, including 2 cases M1, 14 cases M2, 12 cases M3, 14 cases M4, 17 cases M5, 2 cases M6 and 1 case AML without classification. According to the risk stratification, high risk group (24 cases), medium risk group (22 cases) and low risk group (16 cases) were divided. Compared with that in the controls, POT1 expression levels in patients with AML were significantly decreased both in mRNA and protein level (P< 0.05). The relative expression levels of POT1 mRNA and protein in patients with M2, M4 and M5 were significantly lower than those in the controls (P< 0.05). The expression levels of POT1 in high risk group, medium risk group and low risk group were significantly decreased than those in the controls (P<0.05). Compared with that in the controls, The relative POT1 mRNA expression was significantly decreased in M3 patients (P< 0.05), but not in protein level. POT1 protein expression was showed both in the cytoplasm and nucleus. There was no significant difference of the expression of POT1 protein between cytoplasm and nucleus (P> 0.05). Conclusions POT1 may be involved in the pathogenesis of AML. POT1 protein expresses in both cytoplasm and nucleus, and the regulatory mechanism may be related to the telomere length.

Objective To investigate the value of urinary trehalase (T) in patients with renal proximal tubular damage.Methods 134 patients with kidney disease (male:66 female:68 age:18-59 ; 31cases with acute renal failure,30 cases with chronic renal failure,20 cases with drug-induced renal impairment,21 cases with renal transplantation and 32 cases with nephritic syndrome) and 101 healthy controls (58 males and 43 females) were selected.Urinary T,N-acetyl-D-glucosaminidase (NAG),β2-MG,gamma-glutamyl transferase (GGT) were detected.Data were analyzed by SPSS 11.5,including nonparametric rank test,ROC analysis.Results The level of urinary trehalase in control group was normally distributed (7.1 ± 4.1) μmol/h · g Cr (0-25 μmol/h · g Cr).There was no significant difference between men and women (t =0.63,P =0.53).Urinary T levels were significant higher in all kidney disease groups than in control group (Z =6.80,5.90,5.23,6.00,8.04,P ＜0.01).According to ROC curve,the area of urinary T under the ROC curve (AUC) in 134 patients was 0.9,significantly different with NAG,β2-MG,GGT area (P ＜ 0.01),the AUCs of T were 0.94,0.85,0.90,0.90,0.91 in acute and chronic renal failure group,drug-induced renal impairment group,renal transplantation group and nephritic syndrome group,respectively; Youden index were 0.85,0.65,0.77,0.66,0.72 respectively.Corresponding to the Youden index,sensitivity and specificity were 90.3％ and 95.1％,73.3％ and 92.1％,85.0％ and 92.1％,81.0％ and 85.2％,87.5％ and 84.2％ respectively.Conclusions The Urinary trehalase is better than other markers in the diagnosis of the proximal renal tubular damage.It was better to evaluate the proximal tubular function early in time.The diagnostic value of urinary trehalase played a key role in diagnosis,treatment and prognosis of kidney diseases.

Occupational chromium rhinopathy is chronic nasal damage caused by chromic anhydride, chromate and dichromate 6-valent chromium compounds. In 2016, 700 people who were exposed to chromium slag in steel plant were checked out. 24 people were found to have nasal injuries. The expert group confirmed 1 case of occupational severe chromium rhinosis and 23 cases of occupational mild chromium rhinosis.There was no significant difference in the incidence, type of work and duration of injury among 24 patients (P>0.05) . Active measures should be taken to prevent chromium rhinopathy and the technological process should be reformed. Occupational health education and occupational health monitoring should be strengthened to avoid exposure of chromium and its compounds through nose and respiratory tract, and to reduce or eliminate the occurrence of chromium rhinosis.