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OBJECTIVE: The aim of our study was to analyze the factors influencing the occurrence of hyperuricemia and poor cardiac and renal outcomes in chronic kidney disease (CKD). PATIENTS AND METHODS: One hundred and sixteen patients with CKD admitted to our hospital from January 2022 to September 2022 were picked as the subjects. Fasting venous blood of these subjects was collected to value the serum uric acid (SUA) levels on an automatic biochemical analyzer. Patients were then grouped as the CKD-only group (n=80) and hyperuricemia group (n=36), according to the SUA results, or the good prognosis group (n=88) and poor prognosis group (n=28), according to the presence of cardiovascular diseases. The changes in laboratory indexes and clinical data were analyzed and compared. Multivariate logistic regression analysis was used to analyze the risk factors for combined hyperuricemia and the risk factors for poor cardiac and renal outcomes in patients with CKD. The correlation between SUA level and cardiac and renal indexes was analyzed by Pearson analysis. RESULTS: Patients in the CKD hyperuricemia group had markedly higher content of systolic blood pressure (SBP), diastolic blood pressure (DBP), B-type natriuretic peptide (BNP), urinary retinol-binding protein (RBP), urinary N-acetyl-ß-D glucosidase (NAG), much higher proportion of heart failure episodes history, and much lower content of total cholesterol (TC), albumin (Alb), hemoglobin (Hb), urinary a1-microglobulin (a1-MG), and glomerular filtration rate (eGFR) than the CKD-only group (p < 0 .05). S UA, B NP, SBP, and history of heart failure episodes were independent risk factors for combined hyperuricemia in CKD patients (p < 0.05). Besides, eGFR, albumin, and hemoglobin were independent protective factors for combined hyperuricemia in CKD patients (p < 0.05). Compared with the good prognosis group, the content of BNP, SBP, DBP, urinary RBP, urinary NAG, and SUA was much higher, the proportion of heart failure episodes history was obviously higher, and the levels of Alb, Hb, TC, eGFR, and urinary a1-MG were sharply lower in the poor prognosis group (p < 0.05). SUA, BNP, SBP, and history of heart failure episodes were independent risk factors for poor cardiac and renal outcomes (p < 0 .05), a nd e GFR was an independent protective factor for poor cardiac and renal outcomes in patients with CKD (p < 0.05). The SUA level in CKD patients was positively correlated with BNP and SBP (r=0.463, 0.215, p < 0 .05), b ut n egatively c orrelated w ith eGFR (r=0.463, 0.215, p < 0.05). CONCLUSIONS: The serum SUA level was elevated with the aggravation of the CKD stage. High serum SUA level is a risk factor for the development of hyperuricemia and poor cardio-renal outcomes in CKD patients, suggesting that early monitoring of changes in SUA levels may help assess the risk of cardio-renal outcomes in CKD patients. [ABSTRACT FROM AUTHOR]

The electronics properties for benzene derivatives with different side groups connected to two gold electrodes with symmetric contacts are investigated by using first-principles methods based on the density functional theory. We have found that a bias can induce a transition from the electron-withdrawing behaviors to the electron-denoting behaviors for the OH side group in a phenoldithiol molecule. The degree of asymmetry of the I-V characteristics and the magnitudes in current depend remarkably on the type and number of attached side groups. The detailed analysis illustrates that the “doping” effect of the side groups and the asymmetry of potential profile in devices under different bias polarities are intrinsic origins leading to such observed phenomena. The results show that it is feasible to import some particular characteristics to a benzene-dithiol molecular device through an attachment of different side groups. [ABSTRACT FROM AUTHOR]

Aims: To determine how the microbicide ceragenin‐13 (CSA‐13) kills Bacillus subtilis spores prepared on growth or sporulation media, and these spores' properties. Methods and Results: Spores made on Luria broth (LB) growth or double‐strength Schaeffer's‐glucose (2xSG) sporulation plates found that spores made on LB plates have coat defects as evidenced by their lower hypochlorite resistance, faster germination with dodecylamine and slower germination with Ca2+‐dipicolinic acid (CaDPA) than 2xSG plate spores. CSA‐13 triggered CaDPA release from spores, an early step in germination, but only well at 70°C and better with spores made on LB than on 2xSG plates. Approximately 90% of spores with elevated levels of SpoVA proteins that form a CaDPA release channel, released CaDPA with CSA‐13 at 70°C, and faster with spores made on LB than 2xSG plates. Levels of CSA‐13 killing of spores made on LB and 2xSG plates were similar to levels of CaDPA release triggered by this agent. Conclusions: CSA‐13 kills bacterial spores, but only at high concentrations and temperatures, and is preceded by CaDPA release. Significance and Impact of the Study: CSA‐13 is not a direct sporicide as reported previously, but most likely germinates spores via activation of spores' CaDPA channel, albeit inefficiently, and then killing the germinated spores. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the regulating roles of miR-199b in hepatocellular carcinoma (HCC). PATIENTS AND METHODS: The expression of miR-199b of 45 human HCC tissues and the corresponding para-cancerous tissue samples were detected by quantitative Real-time-polymerase chain reaction (qRT-PCR). Western blot was employed to investigate the level of JAG1. Transwell assay was used to monitor the ability of cell migration and invasion. Cell proliferation was tested by CCK-8 assay and luciferase reporter assay was done to clarify whether JAG1 was a target of mir-199b. RESULTS: miR-199b expression level was decreased in 45 paired tumor tissues in contrast with the corresponding para-carcinoma tissues. The expression level of miR-199b was closely associated with TNM stage, tumor size, and 5-year overall survival. Transwell assay result showed that miR-199b inhibited HCC cell migration and invasion. Cell counting kit-8 (CCK-8) results demonstrated that miR-199b could suppress HCC cell proliferation. Luciferase reporter assay suggested that Jagged1 (JAG1) was a direct target of miR-199b in HCC cells. miR-199b could negatively regulate JAG1 expression by targeting JAG1. CONCLUSIONS: miR-199b exerted tumor suppressive functions in HCC by targeting JAG1, and it may be a potential target treatment for hepatocellular carcinoma. [ABSTRACT FROM AUTHOR]

The clinical and genetic spectrum of hereditary sensory and autonomic neuropathy ( HSAN) is still unknown in Japan. We collected a broad cohort of 33 unrelated patients with predominant sensory and/or autonomic dysfunctions, who were referred to our genetic laboratory. A gene panel sequencing targeting 18 HSAN-related genes was performed using a next-generation sequencing system. A recurrent frame shift mutation in the WNK1/ HSN2 gene, c.3237_3238insT (p.Asp1080*), was detected in 5 patients. This mutation was homozygous in 4 cases and of a compound heterozygous genotype in 1 case. Geographic and haplotype analysis of all 5 patients suggested a founder event. In addition, a novel heterozygous nonsense variant, c. 2615C>G (p.Ser872*), was identified. All the 5 patients presented with severe sensory and autonomic dysfunctions at birth or during adolescence. In 2 patients, an uncommon phenotype of acute pathological pain presented at ~50 years of age. Here, we present the first founder mutation of WNK1/ HSN2, in addition to French Canadian, which accounts for ~15.2% of Japanese patients with HSAN in our cohort. We have also reviewed all previously described mutations in WNK1/ HSN2 and reconciled their nomenclature strategy on the basis of the current longest transcript. [ABSTRACT FROM AUTHOR]