Preparation and microscopy examination of alginate-poly-L-lysine-alginate microcapsules.

Ca-alginate-poly-l-lysine-alginate (APA-Ca) and Ba-alginate-poly-l-lysine-alginate (APA-Ba) microcapsules were prepared and their thickness and surface were examined by light microscopy and scanning electron microscopy. Specifically, light microscopy with frozen section was used to visualize and quantify the thickness of APA membrane, and monitor temporal changes in the thickness of microcapsules during a month long culture in vitro. The section graph of APA microcapsule represents the accurate measurement of layer thickness of APA-Ca with diameter 900 ± 100 and 500 ± 100 µm at 6.01 ± 1.02 and 9.54 ± 2.42 µm (p < 0.05), and layer thickness of APA-Ba with diameter 900 ± 100 and 500 ± 100 µm at 5.47 ± 0.90 and 8.21 ± 1.97 µm (p < 0.05), regardless of the alginate composition used to generate the microcapsules. The microcapsule was stable during the culture for 30 days in vitro. Field emission scanning electron microscopy with freeze drying method was used to detect the surface and thickness of dried microcapsules. From the results, the outer surface of APA-Ca and APA-Ba membrane were smooth and dense, the film thickness of the APA-Ca was about 450-690 nm, while the APA-Ba was approximately 335 nm. In vivo experiment, little significant difference was seen in the change of film thickness of microcapsules in intrapertioneal site for 30 days after transplantation (p > 0.05), except that the recovery of APA-Ba was higher than the APA-Ca microcapsules. The paper showed an easy method to prepare APA-Ca and APA-Ba, and examine their thickness and surface, which could be utilized to study other types of microcapsules.

G6PD deficiency-induced hemolysis in a Chinese diabetic patient: a case report with clinical and molecular analysis.

A 59-year-old Chinese male patient was admitted at diagnosis of type 1 diabetes with ketoacidosis. During the normalization of blood glucose with insulin, the patient developed acute hemolysis. The factors predisposing to hemolysis were not found, except the significantly diminished activity of glucose-6-phosphate dehydrogenase (G6PD). DNA analysis did not show any coding or intronic mutation in the G6PD gene. This is the first reported case of a Chinese patient in diabetic ketoacidosis with hemolysis induced by G6PD deficiency in the absence of mutations in the G6PD gene.

[The role of JNK in apoptosis of renal tubular epithelial cells in diabetic rats with fluctuant high blood glucose].

OBJECTIVE: To explore the signal transduction mechanisms of apoptosis in renal tubular epithelial cells in diabetic rats with fluctuant high blood glucose. METHODS: Healthy SD rats were randomly divided into 3 groups: normal control group (A), stable high blood glucose group (B) and fluctuant high blood glucose group (C). Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65 mg/kg), and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of ordinary insulin and glucose at different time point every day. The superoxide dismutase (SOD) activity and the content of malonaldehyde (MDA) in renal tissue homogenate were detected with colorimetry. The protein expression of Nox4 and JNK were examined by immunohistochemistry and Western blot. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL). RESULTS: After 12 experimental weeks, significantly increased cell apoptosis, up-regulation of Nox4 and P-JNK expression in renal tubular epithelial cells were observed in B and C groups compared with those in A group. The MDA content increased and SOD activity decreased in renal tissue in B and C groups. Above effects were more obviously shown in C group. CONCLUSION: Fluctuant high blood glucose induced more apoptosis of renal tubular epithelial cell than stable high blood glucose in diabetic kidney, which might be related to the activation of JNK signal transduction pathway.

[Online diagnosis of the conversion of methane to C2 hydrocarbons under glow discharge plasma at atmospheric pressure].

Optical emission spectroscopy (OES) was adopted for the first time by our group for in situ diagnosis of the conversion of CH4-H2 under glow discharge plasma at atmospheric pressure with rotary electrodes. The emission of excited species such as excited radicals and atoms (C, CH, C2, H and H2) was detected in the spectra range of 300-700 nm. The spectrum of hydrogen atom was used to figure out the plasma excitation temperature by a Boltzmann plot scheme. It was evaluated that the excitation temperature of hydrogen plasmas under varied discharge conditions is in the range of 6300-6600 K. The electron density was calculated based on spectral profile of H lines and its order is about 10(20) m(-3).

[Study on the mitochondrial DNA variation in patients with type 2 diabetes mellitus].

OBJECTIVE: To explore the relationship between type 2 diabetes mellitus (T2DM) and the mutations in the fragment of mitochondrial DNA (mtDNA) from nucleotides 3153 to 3551, which have shown high frequency of point mutation. METHODS: One hundred and ninety-one normal controls and 222 patients with T2DM were screened by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), T-A cloning sequencing and denatured high performance liquid chromatography (DHPLC) techniques. RESULTS: The prevalence of mtDNA mutations in the patient group (24.32%) was significantly higher than that in the control group (7.33%) (P < 0.05). Three novel mutations of A3209T, T3253G and A3467C were found, and C3497T was first reported in DM. Onset age, body mass index, fasting blood glucose, HbA1C, high density lipoprotein-cholesterol and diabetic nephropathy could be related to occurrence of mtDNA mutations (P < 0.05). CONCLUSION: Mitochondrial DNA mutations might implicate T2DM in Wenzhou population, which should play an important role in the pathogenesis of T2DM.

[Detecting of mtDNA mutations at position A3243G and G3316A in patients with type 2 diabetes mellitus in Wenzhou].

To investigate the frequencies of mitochondria DNA (mtDNA) tRNA(Leu (UUR)) point mutation A3243G and NADH dehydronase subunit 1(ND1) gene point mutation G3316A in Wenzhou area of Zhejiang Province, and to explore the correlation between these mutations and the clinical manifestations in patients with type 2 mellitus diabetes(T2DM). Two hundreds and forty-four unrelated patients with T2DM and 156 healthy subjects without family history of T2DM were enrolled in Wenzhou area in this study and screened for the point mutations mentioned above with polymerase chain reaction (PCR) and restricted fragment length polymorphism(RFLP) analysis. The heterogeneous mutations were confirmed with DNA sequencing and denaturing high performance liquid chromatography (DHPLC) following T-A cloning of PCR products. The percentage of A3243G mutation in group of patients with T2DM and control were 0.410% and 0.0% (1/244 vs 0/156), respectively; however, there's not any significant difference between these two groups in frequency of A3243G mutation (P>0.05). G3316A mutation was detected in 4 of 244 cases with T2DM (1.639%) and 2 of 156 healthy controls (1.282%), showing that there's also no statistic difference between these two groups in frequency of G3316A mutation (P>0.05). It's shown that the frequency of mtDNA tRNA(Leu (UUR)) A3243G mutation is fairly low in patients with T2DM in Wenzhou area. Thus it's reasonable to assume that this mutation may not be involved in the development and progression of T2DM. Furthermore, it's demonstrated that the rate of G3316A mutation of mtDNA ND1 gene is rare in patients with T2DM in Wenzhou area and this mutation also happened in healthy control. It's suggested that G3316A mutation is just a gene polymorphism of mtDNA and not related to the pathogenesis of T2DM.