Thermal effect on availability of individual amino acids (AIAA) of red kidney beans was evaluated. Sulfur amino acids (SAA), methionine and cystine (Met + Cys), are the limiting amino acids (AA) and have the lowest availability among the AAs in nine treatments. The availability of SAA (ASAA) ranged from -18.6% in raw beans to 39.8-68.0% in thermally processed beans. Autoclaving at 121 °C for 10-90 min gradually reduced ASAA values. The mean availability for each AA (MAEAA) is the average of the AIAA values for the same AA. MAEAA values ranged from 82.1% (arginine) to 50.4% (Met + Cys). The mean availability in each treatment (MAET) is the average of the AIAA values in the same treatment. The difference between MAET and true digestibility of protein (TDP) was less than 7%. However, the differences between ASAA and TDP (16-37%) and between ASAA and MAET (14-30%) were large. The ASAA-corrected amino acid score (AAS ASAA ) for raw beans was negative (-29.4%) and ranged from 61.8 to 42.1% for thermally processed beans. From a comparison among the protein quality indexes, AAS ASAA is the preferred method to evaluate protein quality of beans.

Laparoscopic donor hepatectomy (LDH), accepted as a minimally invasive approach, has become increasingly popular for living donor liver transplant. However, the outcomes of LDH remain to be fully clarified when compared with open living donor hepatectomy. Thus, our meta-analysis was designed to assess the efficacy of laparoscopic in comparison with conventional open donor hepatectomy. The PubMed, Cochrane, and Embase electronic databases were searched to identify the articles concerning the comparison of the efficacy of laparoscopic versus open surgery in treatment of living donor liver transplantation updated to March, 2020. The main search terms and medical Subject Heading terms were: “living donor,” “liver donor,” “minimally invasive,” “laparoscopic surgery,” and “open surgery.” After rigorous evaluation on quality, the data was extracted from eligible publications. The outcomes of interest included intraoperative and postoperative results. The inclusion criteria were met by a total of 20 studies. In all, 2001 subjects involving 633 patients who received laparoscopic surgery and 1368 patients who received open surgery were included. According to the pooled result of surgery duration, the laparoscopic surgery was associated with shorter duration of hospital stay (MD = −1.07, 95% CI −1.85 to −0.29; P = .007), less blood loss (MD = −57.57, 95% CI −65.07 to −50.07; P < .00001), and less postoperative complications (OR = 0.61, 95% CI 0.44–0.85; P = .003). And the open donor hepatectomy achieved a trend of shorter operation time (MD = 30.31, 95% CI 13.93–46.69; P = .0003) than laparoscopic group. Similar results were found in terms of ALT ( P = .52) as well as the AST ( P = .47) peak level between the 2 groups. LDH showed the better perioperative outcomes as compared with open donor hepatectomy. The findings revealed that LDH may be a feasible and safe procedure for the living donor liver transplantation.

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Otoferlin, an integral membrane protein implicated in a late stage of exocytosis, has been reported to play a critical role in hearing although the underlying mechanisms remain elusive. However, its widespread tissue distribution infers a more ubiquitous role in synaptic vesicle trafficking. Glutamate, an excitatory neurotransmitter, is converted to its inhibitory counterpart, γ-aminobutyric acid (GABA), by L-glutamic acid decarboxylase (GAD), which exists in soluble (GAD67) and membrane-bound (GAD65) forms. For the first time, we have revealed a close association between otoferlin and GAD65 in both HEK293 and neuronal cells, including SH-SY5Y neuroblastoma and primary rat hippocampus cells, showing a direct interaction between GAD65 and otoferlin's C2 domains. In primary rat hippocampus cells, otoferlin and GAD65 co-localized in a punctate pattern within the cell body, as well as in the axon along the path of vesicular traffic. Significantly, GABA is virtually abolished in otoferlin-knockdown neuronal cells whereas otoferlin overexpression markedly increases endogenous GABA. GABA attenuation in otoferlin-knockdown primary cells is correlated with diminished L-type calcium current. This previously unknown and close correlation demonstrates that otoferlin, through GAD65, modulates GABAergic activity. The discovery of otoferlin-GAD65 functional coupling provides a new avenue for understanding the molecular mechanism by which otoferlin functions in neurological pathways.

Competing endogenous RNAs (ceRNAs) are a newly discovered class of molecular regulators involved in many diseases, especially tumors. Therefore, exploration of the potential ceRNA regulatory network regarding the occurrence and development of pancreatic cancer will provide a new theoretical basis for its diagnosis and treatment. Based on the above background, we applied a bioinformatics approach to mine the public database The Cancer Genome Atlas (TCGA) and performed a series of subsequent molecular biology assays to confirm the hypothesis that HOXA10-AS/ miR-340-3p/HTR1D axis could modulate the malignant progression of pancreatic cancer. Here, our present study demonstrated that the expression level of HTR1D, positively correlated with the level of lncRNA HOXA10-AS and negatively associated with the level of miR-340-3p, was significantly increased in pancreatic cancer cell lines (PCs) compared with that in normal HPDE6-C7 cells. Knocking down HTR1D obviously inhibited the proliferation and migration of PCs and promoted apoptosis by upregulating p-AKT. Elevated miR-340-3p blocked the progression of pancreatic cancer by downregulating HTR1D. Lessened level of lncRNA HOXA10-AS reduced the sponging of miR-340-3p, resulting in an increase of miR-340-3p and a subsequent decrease of HTR1D to ultimately suppress the malignant biological behaviors of cancer. These data illustrated that the HOXA10-AS/miR-340-3p/HTR1D ceRNA axis acted a crucial part in the malignant biological behavior of pancreatic cancer in an AKT-dependent manner.

The small nucleolar RNA (snoRNA) is a type of small non-coding RNA widely distributed in the nucleoli of eukaryotic cells, promoting cancer development. The aim of this study was to assess box C/D snoRNA 89 (SNORD89) dysregulations in endometrial cancer. According to the TCGA database as well as the International Federation of Gynecology and Obstetrics (FIGO), higher SNORD89 expression is found in endometrial cancer tissues. In addition, the SNORD89 expression level was higher in endometrial carcinoma with lymph node metastasis than in endometrial carcinoma without lymph node metastasis. By interacting with the conservative chaperone protein methylase fibrillarin (Fbl), SNORD89 inhibits the translation process of the Bim gene, leading to a decrease in Bim protein. Cancer-promoting effect of SNORD89 can be reversed by Fbl knockdown or Bim overexpressing. What’s more, ASO-mediated silencing of SNORD89 could inhibit endometrial cancer cell proliferation and migration ability. Taken together, SNORD89 can modify Bim through 2′-O-methylation and affect downstream signaling pathways to promote endometrial cancer occurrence and development. The role of methylation modification in the prevention and treatment of endometrial cancer provides a new understanding and SNORD89 may be a new diagnostic and therapeutic target for endometrial cancer.

Circular RNAs (circRNAs) play important roles in cancer tumorigenesis and progression, representing prognostic biomarkers and therapeutic targets. In this case, we demonstrated the role of circ-NOLC1 in epithelial ovarian cancer (EOC). Our results have shown that Circ-NOLC1 expression was higher in EOC tissues than in normal tissues, and was positively associated with FIGO stage, differentiation. Among ovarian cancer cell lines, circ-NOLC1 expression was the highest in A2780, and lowest in CAOV3. Overexpression of circ-NOLC1 in CAOV3 cells increased cell proliferation, migration, and invasion ability, whereas silencing of circ-NOLC1 in A2780 cells had the opposite effect: however, neither circ-NOLC1 downregulation nor overexpression influenced NOLC1 mRNA expression. In nude mice with subcutaneous tumors, circ-NOLC1 downregulation decreased tumor growth. Bioinformatic analysis and RNA-binding protein immunoprecipitation showed that circ-NOLC1 could bind to ESRP1. In addition, the overexpression of circ-NOLC1 significantly increased ESRP1, RhoA, and CDK1 protein and mRNA expression level; circ-NOLC1 downregulation had the opposite effects. The tumor-promoting effect of circ-NOLC1 was inhibited by knockdown of ESRP1, CDK1, or RhoA expression in circ-NOLC1-overexpressing cells, which might act by modulating RhoA and CDK1 expression. In conclusion, our study demonstrated that Circ-NOLC1 might promote EOC tumorigenesis and development by binding ESRP1 and modulating CDK1 and RhoA expression.