Purpose:To explore the effect of anti-FasL on ADM resistance of K562/ADM cell subline and its possible mechanism.Methods:Control group,untreated with VER or anti-FasL ,VER-treated group,anti-FasL-treated group and anti-FasL +VER-treated group were set up. MTT、FCM、TUNEL、S-P immunechemistry and RT-PCR assay were used for detection.Results:Anti-FasL or VER treatment was capable of strengthening sensitivity of K562/ADM cells to ADM,ID 50 of anti-FasL and VER was 200ng/ml and 6?g/ml,respectively;DNA content of apoptosis from cycling analysis curve of K562/ADM cell was 7.42%,32.10%,49.29%,56.26%,respectively,and positive rate in situ apoptosis was 4.5%,36%,45%,58%,respectively,which represented a tendency of gradual increase. Anti-FasL was capable of effecting FasL and bcl-2 expression,but not Pgp.Conclusions:Anti-FasL alone or synergically with VER was capable of reversing ADM resistance of K562/ADM cell,which may be used as a novel reversor of multidrug resistance.

Objective Through comparision of Her-2 gene in invasive breast carcinoma tissues assayed by IHC, CISH and FISH respectively, to explore an optimal detective methods. MethodsIHC, CISH and FISH were used in detection for Her-2 gene of 100 cases, respectively.ResultsCISH identified no Her-2 gene amplification in IHC score negative rumors (6/6) and gene amplication in 7.1%(1/14) of IHC score (+) and in 32 % of IHC score (++) tumors(l6/50) and in 80 % of IHC score (+++) (24/80), Concordant rate between CISH and FISH was 100 %(20/20). ConclusionThere are advantage and disadvantage among IHC,CISH and FISH. CISH is an accurate and dependable methods and would be easy to apply for detection of Her-2 gene.

Objective To evaluate the impact of total parenteral nutrition(TPN)on nutrition status and inflammatory markers in hospitalized fasted patients with inflammatory bowel disease(IBD).Methods A retrospective study was performed and 82 hospitalized fasted IBD patients [male/female=58/24,(39.4±14.5)years] who received TPN entered the study.Among them,38 patients had ulcerative colitis(UC)and 44 patients suffered from Crohn`s disease(CD).Clinical data(gender,age,duration of disease,history of disease,prednisone,immuno-suppressor,and antibiotics)were obtained from medical records.Nutritional parameters,C-creative protein(CRP),and erythrocyte sedimentation rate(ESR)before and after TPN were also obtained.Average caloric supplementation by TPN was(4 437.3±1 199.1)kJ/d and the nitrogen amount was(9.9±1.7)g/d.Median PN length was 15 days(7-54 days).67 IBD patients received a TPN formula with glutamine(≥14 d,25 patients vs.0-14 d,42 patients)and 15 IBD subjects received TPN without glutamine.Malnutrition was diagnosed by body mass index(BMI)and serum albumin level.Results The prevalence of undernutrition was 90.2％(74/82)in the study population.CD patients had a significantly longer history of disease [84(3-288)months vs.24(1-324)months,P<0.001] and a significantly lower BMI [(15.6±1.8)kg/m2 vs.(19.1±3.5)kg/m2,P<0.001] compared with those in UC patients.TPN improved nutritional parameters [serum albumin:(28.7±6.6)g/L before TPN vs.(31.7±5.8)g/L after TPN,P<0.001;pre-albumin:(174.1±85.5)mg/L before TPN vs.(227.2±82.8)mg/L after TPN,P<0.001].Conclusions TPN improves nutritional status in hospitalized fasted IBD patients.However,prospective randomized controlled trials are required to estimate the role of low-to-middle dosage of glutamine in IBD patients.

Objective:To analyze the splicing mutation site of COL4A5 gene in a family with X-linked dominant Alport syndrome and explore the possibility of exon specific U1 small nuclear RNA (snRNA) gene therapy. Methods:The clinical data of the proband and family members of Alport syndrome were collected, and the gene mutations in the whole exon of a series of nephropathy genes in the proband were detected by high-throughput sequencing. The splice site changes and pathogenicity caused by COL4A5 c.546+5G>A mutation were analyzed by online software. Minigene experiment was used to verify and analyze the effect of COL4A5 gene mutation site c.546+5G>A in the proband of Alport syndrome family, and transient transfection and introduction of modified U1 snRNA to correct splicing mutation. Results:The results of gene sequencing showed that there was a hemizygous variation of COL4A5 gene in the proband and his half brother, and the variation site was c.546+5G>A. The results of online software for analyzing the pathogenicity of splice variation showed that the original donor splicing site could not be detected after mutation, suggesting that there was a great possibility of affecting splicing. The abnormal splicing mode of COL4A5 gene with c.546+5G>A mutation—deletion of exon 9 was verified by hybridized small gene detection. The abnormal splicing mutation could be partially corrected by the modified U1 snRNA. The correction ratios of ExSpeU1 (MT), ExSpeU1(E9+1), ExSpeU1(E9+9) and ExSpeU1(E9+11) to exon 9 deletion caused by c.546+5G>A were 0, 43.81%, 52.09% and 48.12%, respectively. Conclusions:The pathogenicity of the new splicing mutation of COL4A5 is verified, and the modified U1 snRNA can partially correct the abnormal splicing.

Objective:To investigate the familial inheritances, clinical features, treatments and outcomes of familial Waldenstrom macroglobulinemia (WM) patients.Methods:The clinical manifestations, laboratory examinations, diagnosis and treatments, and follow-up data of 6 familial WM patients who were admitted to Yancheng No.1 People's Hospital from June 2002 to July 2019 were retrospectively analyzed, and the literature was reviewed.Results:Among 6 WM patients, 4 patients had dizziness and fatigue at the onset, 1 patient had recurrent low-grade fever and abnormal sweating as the first manifestations, 1 patient was hospitalized due to pulmonary infection, and WM was found later. Two brothers of the patients were diagnosed with WM, another 2 brothers of the patients had IgM-type monoclonal gammopathy of undetermined significance (MGUS) during the physical examination. All the 6 patients were middle-aged/elderly men, with a median age of 63 years old (51-70 years old). The median follow-up time were 71.5 months (4-217 months), and by the end of the follow-up (June 2020), 2 cases died of pulmonary infection, and 1 of them developed acute myeloid leukemia; the other 4 cases were in regular chemotherapy. Two IgM-MGUS patients were followed up without symptoms.Conclusions:WM patients have familial aggregation, and their clinical manifestations are highly heterogeneous. Patients with family history may have poor prognosis. It is necessary to strengthen the awareness of WM and family history screening.