The biotechnology of glycolipid fermented b y a bacillus coagulans was studied and the fermentation pro cess in 10L bioreactor was conducted.Suitable medium contained 6% bean oil as ca rbon source,3 5g/L NaNO 3 as nitrogen source,0 75g/L yeast extract and some i no rganic salts.The fermentation temperature of 30℃,initial pH of 8 5,strring rev olution of 150～240r/min and fermentation period of 96h proved to be optimal.The yield of glycolipid in 10L bioreactor was 7 073g/L.

Adult ; Diagnosis, Differential ; Female ; Granulomatous Disease, Chronic ; metabolism ; pathology ; Hodgkin Disease ; metabolism ; pathology ; Humans ; Ki-1 Antigen ; metabolism ; Lewis X Antigen ; metabolism ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Young Adult

Adult ; Coloring Agents ; adverse effects ; Diagnosis, Differential ; Humans ; Lymphadenitis ; chemically induced ; Male ; Melanoma ; secondary ; Tattooing ; adverse effects

Adult ; Antigens, CD20 ; metabolism ; CD3 Complex ; metabolism ; Diagnosis, Differential ; Facial Dermatoses ; metabolism ; pathology ; surgery ; Follow-Up Studies ; Humans ; Lymphoma, B-Cell, Marginal Zone ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Male ; Pseudolymphoma ; metabolism ; pathology ; surgery ; Skin Neoplasms ; metabolism ; pathology

Actins ; metabolism ; Adult ; Diagnosis, Differential ; Granzymes ; metabolism ; Histiocytic Sarcoma ; metabolism ; pathology ; Humans ; Ki-1 Antigen ; metabolism ; Lymph Nodes ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Male ; Neoplasms, Muscle Tissue ; metabolism ; pathology ; Protein-Tyrosine Kinases ; metabolism ; Receptor Protein-Tyrosine Kinases

Adult ; Antigens, CD20 ; metabolism ; Burkitt Lymphoma ; metabolism ; pathology ; Diagnosis, Differential ; Female ; Follow-Up Studies ; Histiocytic Necrotizing Lymphadenitis ; metabolism ; pathology ; Humans ; Lymphatic Diseases ; metabolism ; pathology ; Lymphoma, Large B-Cell, Diffuse ; metabolism ; pathology ; Lymphoma, Large-Cell, Anaplastic ; metabolism ; pathology ; Neprilysin ; metabolism ; Proto-Oncogene Proteins c-bcl-6 ; metabolism ; Receptors, Complement 3d ; metabolism ; Submandibular Gland Diseases ; metabolism ; pathology ; Young Adult

This paper proposes a one-way micro valve with a simple structure and a simulation design for the engineering capsule. We have now got its design parameter selection method and its mechanic characteristic from experiments.
Capsules ; Computer Simulation ; Drug Delivery Systems ; methods ; Equipment Design ; Infusion Pumps, Implantable ; Technology, Pharmaceutical ; instrumentation ; methods

Burkitt Lymphoma ; diagnosis ; pathology ; Female ; Hodgkin Disease ; diagnosis ; pathology ; Humans ; Lymphoma ; classification ; diagnosis ; pathology ; Lymphoma, Extranodal NK-T-Cell ; diagnosis ; pathology ; Lymphoma, Follicular ; diagnosis ; pathology ; Lymphoma, Large B-Cell, Diffuse ; diagnosis ; pathology ; Male ; Precursor Cell Lymphoblastic Leukemia-Lymphoma ; diagnosis ; pathology

Objective The expression and impaired function of ion channels might be one of the pathophysiological mecha -nisms responsible for diarrhea in inflammatory bowel disease ( IBD) .Proper animal model is the key to explore detailed pathophysiolog-ical process.The purpose of this study was to build a rat model of acute colitis induced by dextran sodium sulfate (DSS) in C57BL/6 mice and evaluate diarrhea-associated clinical , histological , pathological parameters and expressions of ion channel protein . Methods C57BL/6J mice of model group were treated with 4%DSS solution for 7 days to induce acute colitis.Mice body weight, stool moisture, stool consistency and the degree of hematochezia were recorded .The histopathological changes of mice colon specimens were observed visually and microcosmically, and the ion channel SLC26A3 protein was detected by Western Blot . Results All experimental mice survived.In the experiment, compared with control group , bloody diarrhea and weight lose occurred in model group , along with increased stool moisture ([73.30 ±8.31]% after experiment vs [44.32 ±6.42]% before experiment, P=0.004), and rapidly in-creased disease activity index (DAI) of acute colitis ([3.50 ±0.87] after experiment vs [1.0 ±0.00] before experiment, P=0.000).At the end of this experiment , compared with control group , the model group resulted in higher colonic damage score and pathological inflammation score (P=0.00, P=0.002), significantly shortened co-lon (P=0.00) and decreased expression of SLC26A3. Conclusion The intestinal mucosal injury and phenotypic features of 4%DSS-induced acute colitis are very similar to those of human ulcerative colitis .Impaired expression of intestinal ion transporter SLC26 A3 coexists with diarrhea in model group mice , and this model can support the research on mechanism of functional changes of ion channels in inflammatory diarrhea .

Objective To investigate the clinical features and LRRK2 gene mutation in patients with autosomal dominant familial Parkinson's disease (PD). Methods The clinical features of 16 autosomal dominant familial PD probands were analyzed in terms of age at onset, onset symptoms, UPDRS scores, response to the levodopa treatment and drug-induced dyskinesia. The LRRK2 gene exons 5,13,31,32,35,37,41 and 48 of 16 probands were sequenced after polymerase chain reaction. The novel mutation was further screened in 24D sporadic PD patients and 214 controls using PCR-RFLP for the genotypo frequency analysis. Results Clinically, most of 16 probands had late-onset age. Resting tremor (9patients, 56. 25%,t=0.558,P=0.679)and bradykinesia (9 patients,56.25%,t=0.369,P=0.454)were common onset symptoms followed by rigidity(6 patients,37.50%,t=1.324,P=0.735)and postural instability(5 patients,31.25%,t=2.369,P=0.956).Majority of them had good response to levedopa treatment and rare occurrence of drug-induced dyskinesia. Among the 16 autosomal dominant familial PD probands,6 variants were identified:c.457 T＞C(Leu153Leu),c.1432 G＞T(Asp478Tyr),c.5457 T＞C(Gly1819Gly),c.7153 G＞A(Gly2385Arg),IVS31+28 T＞G and IVS37+162 T＞C. The c.1432G＞T(Asp478Tyr)variant was a novel mutation and it was not detected in 240 sporadic PD patients and 214 controls. The reported mutations associated with the PD, such as Arg1441 Cys/Gly/His, Arg1514Gln, Tyr1699Cys, Ile2012Thr, Gly2019Ser and Ile2020Thr,were not found in our study. Conclusions The autosomal dominant familial PD patients present with classical symptoms of PD and bear the LRRK2 variantsAsp478Tyr and Gly2385Arg.