Industrial Microbiology is a stem course in the undergraduate and graduate education of Biological Engineering major; and the research and development on computer -aided education in biological fields is just at the beginning stage in China. This paper focuses on the construction and application of web-based courseware for teaching and studying of industrial microbiology.

Brain Neoplasms ; diagnosis ; metabolism ; pathology ; Child ; Diagnosis, Differential ; Female ; Glioma ; pathology ; Humans ; Immunohistochemistry ; Magnetic Resonance Imaging ; Meningioma ; diagnosis ; metabolism ; pathology ; Mucin-1 ; metabolism ; Occipital Lobe ; Vimentin ; metabolism

Objective To assess the effective length of jejunal graft when the 3~(rd) intestinal artery is u- tilized as vascular pedicle and afford a reliable theoretic base for clinical esophageal reconstruction.Methods In 32 formalin preserved and 21 fresh cadaver specimens,the diameter of 1st to 5th intestinal arteries and diameter of arterial arches are measured with linear calibre.Measure the length of jejunum that can be harves- ted as graft when the arches are extended.In the 21 fresh specimens,the 1st,2nd,4th and 5th intestinal ar- teries are ligated,acetic ester stained with red dye were injected into the lumen of 3rd intestinal artery via catheter.Extent of distribution of the arteries to the jejunum was observed.And then red ABS solution was in- jected into the 3rd intestinal artery to make into cast specimen.The blood supply distribution of jejunum through 3rd intestinal artery-arterial arch and communicating system were observed again.Results The di- ameter of the 3rd intestinal artery was the largest among the 1st to 5th intestinal arteries.The length of jejunum vascularized by 3rd intestinal artery can be as long as (142.2?62.3) (69.0～206.60cm) in acetic ester in- filtrated specimens.While in ABS east specimen,the average available extent of donor jejunum was(30.8?7.3) (23.0～37.3cm).Conclusion As observed by this applied anatomy study,the jejunum graft vascu- larized by 3rd intestinal artery alone has sufficient length to meet the need of esophageal reeonstrution.

Objective To study the effects of nitric oxide on Ca2+-activated K+ (KCa) channels in the hypothalamus neurons of newborn SD rats. Methods The data were recorded using inside-out or cell-attached configuration of patch-clamp technique and the kinetic changes of KCa channels are compared before and after 100 μmol/L sodium nitroprusside (SNP) was added into the bathing solution. Results When 100 μmol/L SNP was added to the bathing solution in cell-attached configuration, the open probability of the KCa channels increased from (7.3±1.5)% to (40.2±6.5)%, open time from (7.12±1.41) ms to (15.34±3.45) ms, frequency from (11.3±3.5) Hz to (26.6±4.2) Hz. Conclusion NO-cGMP signal pathway could greatly increase the open probability of the channels as a result of both the prolongation of open period and increase of open frequency, but the pathological or physiological roles it may play require further study.

Objective To study the effects of nitric oxide on Ca2+-activated K+ (KCa) channels in the hypothalamus neurons of newborn SD rats. Methods The data were recorded using inside-out or cell-attached configuration of patch-clamp technique and the kinetic changes of KCa channels are compared before and after 100 μmol/L sodium nitroprusside (SNP) was added into the bathing solution. Results When 100 μmol/L SNP was added to the bathing solution in cell-attached configuration, the open probability of the KCa channels increased from (7.3±1.5)% to (40.2±6.5)%, open time from (7.12±1.41) ms to (15.34±3.45) ms, frequency from (11.3±3.5) Hz to (26.6±4.2) Hz. Conclusion NO-cGMP signal pathway could greatly increase the open probability of the channels as a result of both the prolongation of open period and increase of open frequency, but the pathological or physiological roles it may play require further study.

OBJECTIVETo observe the effect of high glucose exposure on connective tissue growth factor (CTGF) expression in cultured human renal tubular epithelial cells and investigate the role of p38MAPK pathway in this process.

METHODSHuman renal tubular epithelial cells (HKC) with and without SB203580 pretreatment were cultured in the presence of high glucose levels for 24, 48, 72, 96 h and 20 days. RT-PCR, immunohistochemical staining, indirect fluorescence staining and Western blotting were used to detect the changes in CTGF mRNA and protein expressions in the cells after the treatment.

RESULTSLow levels of CTGF mRNA and protein were detected in cultured HKC cells, and after high glucose treatment, the mRNA expression increased gradually and reached the peak level at 48 h, then followed by gradual decrease till recovering the baseline level at 96 h. Prolonged high glucose treatment for 20 days resulted in persisted high CTGF mRNA expression twice the level in the control group. The expression level of CTGF protein also increased progressively as the treatment time then prolonged, and long-term (20 days) treatment increased the expression by 4 folds in comparison with the expression in the control cells. SB203580 significantly inhibited the increase in the expressions of CTGF mRNA and protein stimulated by high glucose treatment.

CONCLUSIONHigh glucose treatment can increase CTGF mRNA and protein expressions in cultured human renal tubular epithelial cells, suggesting that increased CTGF levels is a key event in the pathogenesis of renal tubulo-interstitial fibrosis in patients with diabetic nephropathy. p38MAPK pathway may also participate in this process.

Cells, Cultured ; Connective Tissue Growth Factor ; genetics ; metabolism ; Diabetic Nephropathies ; pathology ; Epithelial Cells ; cytology ; metabolism ; Glucose ; pharmacology ; Humans ; Kidney Tubules ; cytology ; RNA, Messenger ; genetics ; metabolism ; Signal Transduction ; p38 Mitogen-Activated Protein Kinases ; metabolism

OBJECTIVETo explore the relations between fasting blood glucose (FBG), glycosylated hemoglobin A1c (HbA1c) and glycosylated serum protein (GSP).

METHODSFBG, HbA1c and GSP were measured in 303 patients with diabetic nephropathy and in 167 non-diabetic patients with comparable baseline data, and the correlations between FBG, HbA1c and GSP were analyzed.

RESULTSGSP levels were significantly higher in patients with diabetic nephropathy than in the non-diabetic patients (P<0.01). In patients with diabetic nephropathy, GSP levels were found to positively correlate to FBG (r=0.606) and HbA1c (r=0.733).

CONCLUSIONPatients with diabetic nephropathy show strong correlations between FBG, HbA1c and GSP. GSP detection is convenient, stable, and practical in evaluating the average FBG over a short term, which reduces the interference by FBG fluctuations in conventional blood glucose monitoring.

Adult ; Aged ; Aged, 80 and over ; Blood Glucose ; analysis ; Blood Proteins ; analysis ; Case-Control Studies ; Diabetes Mellitus, Type 2 ; blood ; Diabetic Nephropathies ; blood ; Female ; Glycated Hemoglobin A ; analysis ; Glycoproteins ; analysis ; Humans ; Male ; Middle Aged ; Serum ; metabolism

OBJECTIVETo investigate the immunohistochemical expression of isocitrate dehydrogenase 1 gene (IDH1) R132H in glioma and its diagnostic utility.

METHODSImmunohistochemical study of IDH1R132H expression was performed on formalin-fixed paraffin-embedded tissue samples of 75 gliomas, including 33 cases of grade II, 20 cases of grade III and 22 cases of grade IV tumors. Six cases of pilocytic astrocytoma and 12 cases of gliosis were used as controls.

RESULTSNineteen in 33 cases of grade II (57.6%), 8 in 20 cases of grade III (40.0%), 6 in 22 cases of grade IV (27.3%) showed positive cytoplasmic staining of IDH1R132H. Scattered invasive glioma cells at the tumor periphery also expressed IDH1R132H. Gliomas involving the frontal lobe showed more strong IDH1R132H staining. In contrast, none of the pilocytic astrocytomas and gliosis showed IDH1R132H staining. Moreover, the rate of p53 immunopositivities were 42.4% (14/33) in grade II, 65.0% (13/20) in grade III and 77.3% (17/22) in grade IV gliomas. There were no statistic correlations between expression of IDH1R132H and p53.

CONCLUSIONIDH1R132H tends to express preferentially in low-grade gliomas, and it thus may serve as a valuable marker in distinguishing low grade gliomas from gliosis.

Adolescent ; Adult ; Aged ; Astrocytoma ; metabolism ; pathology ; Brain Neoplasms ; metabolism ; pathology ; Child ; Diagnosis, Differential ; Female ; Glioma ; metabolism ; pathology ; Gliosis ; metabolism ; pathology ; Humans ; Isocitrate Dehydrogenase ; genetics ; metabolism ; Male ; Middle Aged ; Mutation ; Tumor Suppressor Protein p53 ; metabolism ; Young Adult

OBJECTIVETo investigate the protective effect of losartan against angiotensin II (AngII)-induced beta cell (RIN-m) impairment and explore its mechanism.

METHODSIn vitro cultured RIN-m cells were divided into control group, 100 nmol/L AngII group and losartan pretreatment group. After cell incubation with the corresponding agents for 24 h, the amount of basal (3.3 mmol/L) and glucose-stimulated (16.7 mmol/L) insulin secretion (GSIS) was detected by radioimmunoassay, and the cellular reactive oxygen species (ROS) was assayed by flow cytometry with DCFH-DA staining; the mRNA and protein expressions of uncoupling protein 2 (UCP2) were determined by RT-PCR and Western blotting, respectively.

RESULTSThe basal insulin secretion showed no significant differences between the 3 groups (P>0.05). The GSIS in 100 nmol/L AngII group was significantly lower than that of the control group (P<0.001), but losartan pretreatment markedly restored the insulin secretion function to a level comparable to that of the control group (P<0.05). Compared with the control group, 100 nmol/L AngII significantly increased the cellular ROS level and the mRNA and protein expressions of UCP2 (P<0.05), and these changes were eliminated by losartan pretreatment.

CONCLUSIONSLosartan pretreatment offers protective effect against AngII-induced impairment of the GSIS of beta cells possibly by antagonizing the effects of AngII that causes increased ROS level and UCP2 expressions in beta-cells.

Angiotensin II ; adverse effects ; antagonists & inhibitors ; Animals ; Antihypertensive Agents ; pharmacology ; Cell Line, Tumor ; Insulin-Secreting Cells ; drug effects ; physiology ; Insulinoma ; pathology ; Ion Channels ; genetics ; metabolism ; Losartan ; pharmacology ; Mitochondrial Proteins ; genetics ; metabolism ; Protective Agents ; pharmacology ; RNA, Messenger ; genetics ; metabolism ; Rats ; Uncoupling Protein 2

OBJECTIVETo study the mRNA expression of the tumor suppressor gene thyroid stimulating hormone receptor (TSHR) gene in papillary thyroid carcinoma (PTC) and the correlation between aberrant promoter methylation of TSHR gene and the tumorigenesis of PTC.

METHODSRT-PCR was used to detect the mRNA expression of TSHR gene in 50 PTC cases, 20 cases of nodular goiter and 12 cases of thyroid adenoma tissue. The status of TSHR gene promoter methylation was determined using methylation-specific PCR technique.

RESULTSOf the 50 PTC patients, 34 (68%) were found to have hypermethylation of TSHR gene promoter region, as compared to 7 out of the 32 control patients (21.9%) positive for TSHR gene promoter hypermethylation, suggesting a significantly higher rate of TSHR promoter methylation of in PTC patients than in the control patients (chi(2) = 16.61, P<0.05). Of the 34 PTC patients with TSHR promoter methylation, 14 (41.2%) showed the absence of TSHR mRNA expression; in the 16 PTC patients without TSHR promoter methylation, only 2 (12.5%) were negative for TSHR mRNA expression, showing a significant difference in the rate of negative TSHR mRNA expression with regard to TSHR promoter methylation. The PTC patients had a significantly lower TSHR mRNA expression than the control patients (chi(2) = 4.02, P<0.05).

CONCLUSIONMethylation of TSHR gene in the promoter region is a common molecular event, which might be associated with the tumorigenesis and progression of human PTC.

Adult ; Base Sequence ; Carcinoma, Papillary ; genetics ; DNA Methylation ; Female ; Humans ; Male ; Middle Aged ; Molecular Sequence Data ; Promoter Regions, Genetic ; RNA, Messenger ; genetics ; Receptors, Thyrotropin ; genetics ; Thyroid Neoplasms ; genetics ; Transcription, Genetic