Characterization and correlation analysis of microbial flora and flavor profile of stinky acid, a Chinese traditional fermented condiment.

To explore the microbial diversity and flavor profiles of stinky acid, we utilized high-throughput sequencing, culture-based techniques, and bionic E-sensory technologies. The results revealed a significant correlation between the acidity levels of stinky acid and the richness of its microbial community. Ten core bacterial genera and three core fungal genera exhibited ubiquity across all stinky acid samples. Through E-nose analysis, it was found that sulfides constituted the principal odor compounds responsible for stinky acid's distinct aroma. Further insights arose from the correlation analysis, indicating the potential contribution of Debaryomyces yeast to the sour taste profile. Meanwhile, three genera-Rhizopus and Thermoascus and Companilactobacillus-were identified as contributors to aromatic constituents. Interestingly, the findings indicated that Rhizopus and Thermoascus could reduce the intensity of the pungent odor of stinky acid. In summary, this investigation's outcomes offer new insights into the complex bacterial diversity of stinky acid.

[Expression of matrix metalloproteinases and their inhibitors in fetal skin and their biological significance].

OBJECTIVE: To investigate the expression characteristics of matrix metalloproteinases (MMP-2, MMP-3, MMP-9) and tissue inhibitor of metalloproteinase (TIMP-1, TIMP-2) in developing fetal skin and their potential biological significance. METHODS: Skin of 24 cases of fetuses with different gestational age (12-40 weeks) were obtained, embedded with paraffin wax, and sectioned. Immunohistochemistry and pathological methods were used to detect the expression intensity and distribution of MMP-2, MMP-3, MMP-9, TIMP-1 and TIMP-2. RESULTS: Positive immunohistochemical signals of MMPs and TIMPs could be found in fetal skin at different gestational periods. These proteins mainly located in the cytoplasm of epidermal cells, fibroblasts, epithelial cells of hair follicles and sweat glands and vascular endothelial cells. In earlier gestational fetal skin (12-18 weeks), the expression levels of MMP-2, MMP-3 and MMP-9 were high. Along with the advancement in gestational age, the positive rates of these three proteins in skin were lowered, and in later gestational fetal skin (27-40 weeks) the expression rates were significantly decreased compared with those in earlier gestational fetal skin (all P<0.05). On the contrary, protein expression levels of TIMP-1 and TIMP-2 were apparently lower in earlier versus later gestational skin (both P<0.05). CONCLUSION: MMP-2, MMP-3, MMP-9, TIMP-1 and TIMP-2 might be involved in the skin development and maintenance of cutaneous structure and function. Higher expression of MMP-2, MMP-3 and MMP-9 and lower protein levels of TIMP-1 and TIMP-2 may provide an antiscarring signal in healing of wound during early periods of gestation.

[Effect of selenium dioxide on proliferation, apoptosis, and elomerase activity of human lung cancer cell line in vitro].

BACKGROUND & OBJECTIVE: It was reported that selenium could induce apoptosis of cancer cells; moreover, apoptosis of cancer cells and telomerase activity were closely related to the development of cancer. This study was designed to investigate the effect of selenium dioxide on human pulmonary adenocarcinoma GLC-82 cell to reveal its probable mechanism and the relationship between apoptosis and telomerase activity. METHODS: Methyl thiazolyl tetrazolium(MTT) method was used to determine the growth inhibition rates of lung cancer GLC-82 cells by various concentrations of selenium dioxide at different time. TRAP-PCR-ELISA assay was used to examine the changes of GLC-82 cells treated with selenium dioxide. The cell apoptotic rate was measured by flow cytometry (FCM). DNA ladder was showed by DNA agarose gel electrophoresis. The morphological changes of the cancer cells were examined under light and electron microscope. RESULTS: After being treated with 3, 10, 30 micromol/L selenium dioxide, the proliferation and telomerase activity of GLC-82 cells were markedly inhibited. The growth inhibition rates in GLC-82 cells for 24 hours were 0.7%, 12.8%, and 31.8%; for 72 hours were 15.1%, 51.2%, and 61.1%, respectively. Telomerase activity of GLC-82 cells for 24 hours were 1.173+/-0.029,1.127+/-0.067, and 1.050+/-0.098(P< 0.05); for 48 hours were 1.150+/-0.026, 1.047+/-0.060, and 0.950+/-0.036(P< 0.05), respectively (control group: 1.227+/-0.032 and 1.167+/-0.023, respectively). An apoptosis peak appeared before diploid peak in FCM. Agarose gel electrophoresis showed overt ladder-shape band of cell apoptosis. GLC-82 cells treated by selenium dioxide showed morphological characteristics of apoptotic cells. CONCLUSION: Selenium dioxide could significantly inhibit the growth of lung cancer GLC-82 cells through inducing apoptosis and inhibiting the telomerase activity. Selenium dioxide has strong growth inhibitory effect in a dose-and time-dependent manner.

[Relation of heparanase mRNA expression and angiogenesis to the progression of gastric carcinoma].

OBJECTIVE: To investigate the relation of heparanase gene and angiogenesis with the progress of gastric carcinoma (GC). METHODS: Expression of heparanase mRNA in 52 GC tissue was detected by in situ hybridization assay. Microvessel density (MVD) was examined by immunohistochemical method. MVD and heparanase mRNA expression were analysed with their relation to histological grade, invasion depth,lymph node metastasis and organ metastasis. RESULTS: MVD was 73.2 +/- 22.8 in 25 (48.1%) tissue with positive heparanase mRNA. It was 44.8 +/- 11.9 in 27 (51.9%) tissues with negative heparanase mRNA, between which the difference was significant (P < 0.001). MVD and heparanase mRNA expression were related with lymph node metastasis and depth of serosal invasion in GC (P < 0.005). CONCLUSION: Heparanase, being related to angiogenesis in gastric cancer, promotes growth, invasion and metastasis. Heparanase mRNA expression is an important predictor of the biological behavior of human gastric carcinoma.