Paracoccus albicereus sp. nov., isolated from the shallow-sea hydrothermal system off Kueishantao Island.

Strain designated TK19116T was isolated from the shallow-sea hydrothermal systems off Kueishantao Island in Taiwan, China. The bacterium was Gram-stain-negative, aerobic, oxidase-positive and catalase-positive. Cells of the strain TK19116T were short-rod-shaped and non-motile. The results of phylogenetic analysis of 16S rRNA gene sequences indicated that strain TK19116T belonged to the genus Paracoccus, with the highest sequence similarity to Paracoccus alkanivorans 4-2T (97.1 %). The average nucleotide identity values between the strain TK19116T with Paracoccus alkanivorans 4-2T, Paracoccus zhejiangensis J6T, Paracoccus siganidrum M26T and Paracoccus tegillarcae BM15T were 75.3, 76.7, 76.7 and 75.8%, respectively. The digital DNA-DNA hybridization value between the strain TK19116T with Paracoccus alkanivorans 4-2T, Paracoccus zhejiangensis J6T, Paracoccus siganidrum M26T and Paracoccus tegillarcae BM15T were 19.7, 20.3, 20.5 and 20.0%, respectively. The main respiratory quinone of strain TK19116T was ubiquinone 10. The polar lipids include aminolipid, phosphatidylcholine, diphosphatidylglycerol, glycolipid, phosphatidylglycerol and phospholipid. The principal fatty acid of strain TK19116T was summed feature 8 (C18 : 1 ω6c and/or C18 : 1 ω7c). The G+C content of the chromosomal DNA was 64.2 %. The combination of the results of the phylogenetic, phenotypic and chemotaxonomic analysis, strain TK19116T represents a novel species of the genus Paracoccus, for which the name Paracoccus albicereus sp. nov. is proposed. The type strain is TK19116T (= MCCC 1K08025T=JCM 35527T).

Effects of M currents on the persistent activity of pyramidal neurons in mouse primary auditory cortex.

Neuronal persistent activity (PA) is a common phenomenon observed in many types of neurons. PA can be induced in neurons in the mouse auditory nucleus by activating cholinergic receptors with carbachol (CCh), a dual muscarinic and nicotinic receptor agonist. PA is presumed to be associated with learning-related auditory plasticity at the cellular level. However, the mechanism is not clearly understood. Many studies have reported that muscarinic receptor agonists inhibit muscarinic-sensitive potassium channels (M channels). Potassium efflux through M channels produces potassium currents, called M currents, that play an essential role in regulating neural excitability and synaptic plasticity. Further study is needed to determine whether M currents affect the PA of auditory central neurons and provide additional analysis of the variations in electrophysiological properties. We used in vitro whole cell patch-clamp recordings in isolated mouse brain slices to investigate the effects of M currents on the PA in pyramidal neurons in layer V of the primary auditory cortex (AI-L5). We found that blocking M currents with XE991 depolarized the AI-L5 pyramidal neurons, which significantly increased the input resistance. The active threshold and threshold intensity were significantly reduced, indicating that intrinsic excitability was enhanced. Our results also showed that blocking M currents with XE991 switched the neuronal firing patterns in the AI-L5 pyramidal neurons from regular spiking to intrinsic bursting. Blocking M currents facilitated PA by increasing the plateau potential and enhancing intrinsic excitability. Our results suggested that blocking M currents might facilitate the PA in AI-L5 pyramidal neurons, which underlies auditory plasticity.NEW & NOTEWORTHY Persistent activity (PA) in AI-L5 pyramidal neurons plays an essential role in acoustic information processing. We used in vitro whole cell patch-clamp recordings to investigate the effects of M currents on the PA in AI-L5 pyramidal neurons. Blocking M currents with XE991 facilitated PA by increasing the plateau potential and enhancing intrinsic excitability, causing the firing patterns of AI-L5 pyramidal neurons to become more bursting. These results provide new insight into our understanding of the cellular mechanisms that govern learning-induced auditory plasticity.

Age-dependent association of high urinary iodine concentration with major depression in adults: NHANES 2007-2020.

Excessive iodine exposure can have detrimental effects on thyroid function and overall health. This study aimed to investigate the age-dependent association between high urinary iodine concentration (UIC) and major depression symptoms in adults, using data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2020. To perform stratified analysis by age, we utilized a rolling window method with a 15-year window width to examine the trend of the odds ratios (ORs) of UIC on depression symptoms with age. Full-factor and one-factor multinomial logistic regression models were employed to calculate the ORs, and violin plots were utilized to depict the ORs of UIC on major depression. The LASSO regression was applied to select variables for one-factor models. The bootstrap method was utilized to ensure the robustness of the results, and the Games-Howell test was applied to compare the differences in the bootstrapped ORs of different UIC groups. Our results indicate that, after age 46, the ORs of high UIC (≥ 300 µg/L) on major depression are significantly higher than those of normal UIC (100-199 µg/L). The bootstrapped ORs of high UIC on major depression calculated by the full-factor and one-factor multinomial logistic regression models are 1.9 (1.28, 2.82) and 1.42 (1.02, 1.93) among participants aged 46 and older, respectively. Based on these findings, we conclude that major depressive symptoms are significantly associated with high UIC among older individuals aged 46 and above.

Sulfoquinovose is a widespread organosulfur substrate for Roseobacter clade bacteria in the ocean.

Sulfoquinovose (SQ) is one of the most abundant organosulfur compounds in the biosphere, and its biosynthesis and degradation can represent an important contribution to the sulfur cycle. To data, in marine environments, the microorganisms capable of metabolising SQ have remained unidentified and the sources of SQ are still uncertain. Herein, the marine Roseobacter clade bacteria (RCB) Dinoroseobacter shibae DFL 12 and Roseobacter denitrificans OCh 114 were found to grow using SQ as the sole source of carbon and energy. In the presence of SQ, we identified a set of highly up-regulated proteins encoded by gene clusters in these two organisms, of which four homologues to proteins in the SQ monooxygenase pathway of Agrobacterium fabrum C58 may confer the ability to metabolise SQ to these marine bacteria. The sulfite released from SQ desulfonation by FMN-dependent SQ monooxygenase (SmoC) may provide bacteria with reduced sulfur for assimilation, while proteins associated with sulfite production via assimilatory sulfate reduction were significantly down-regulated. Such SQ catabolic genes are restricted to a limited number of phylogenetically diverse bacterial taxa with the predominate genera belonging to the Roseobacter clade (Roseobacteraceae). Moreover, transcript analysis of Tara Oceans project and coastal Bohai Sea samples provided additional evidence for SQ metabolism by RCB. SQ was found to be widely distributed in marine phytoplankton and cyanobacteria with variable intracellular concentrations ranging from micromolar to millimolar levels, and the amounts of SQ on particulate organic matter in field samples were, on average, lower than that of dimethylsulfoniopropionate (DMSP) by one order of magnitude. Together, the phototroph-derived SQ actively metabolised by RCB represents a previously unidentified link in the marine sulfur cycle.

The Potential Role of Voltage-Dependent Anion Channel in the Treatment of Parkinson's Disease.

Parkinson's disease (PD) is a neurodegenerative disease second only to Alzheimer's disease in terms of prevalence. Previous studies have indicated that the occurrence and progression of PD are associated with mitochondrial dysfunction. Mitochondrial dysfunction is one of the most important causes for apoptosis of dopaminergic neurons. Therefore, maintaining the stability of mitochondrial functioning is a potential strategy in the treatment of PD. Voltage-dependent anion channel (VDAC) is the main component in the outer mitochondrial membrane, and it participates in a variety of biological processes. In this review, we focus on the potential roles of VDACs in the treatment of PD. We found that VDACs are involved in PD by regulating apoptosis, autophagy, and ferroptosis. VDAC1 oligomerization, VDACs ubiquitination, regulation of mitochondrial permeability transition pore (mPTP) by VDACs, and interaction between VDACs and α-synuclein (α-syn) are all promising methods for the treatment of PD. We proposed that inhibition of VDAC1 oligomerization and promotion of VDAC1 ubiquitination as an effective approach for the treatment of PD. Previous studies have proven that the expression of VDAC1 has a significant change in PD models. The expression levels of VDAC1 are decreased in the substantia nigra (SN) of patients suffering from PD compared with the control group consisting of normal individuals by using bioinformatics tools. VDAC2 is involved in PD mainly through the regulation of apoptosis. VDAC3 may have a similar function to VDAC1. It can be concluded that the functional roles of VDACs contribute to the therapeutic strategy of PD.

Cuproptosis-Related MiR-21-5p/FDX1 Axis in Clear Cell Renal Cell Carcinoma and Its Potential Impact on Tumor Microenvironment.

As a newly identified type of programmed cell death, cuproptosis may have an impact on cancer development, including clear cell renal cell carcinoma (ccRCC). Herein, we first noticed that the expression levels of cuproptosis regulators exhibited a tight correlation with the clinicopathological characteristics of ccRCC. The cuproptosis-sensitive sub-type (CSS), classified via consensus clustering analysis, harbored a higher overall survival rate compared to the cuproptosis-resistant sub-type (CRS), which may have resulted from the differential infiltration of immune cells. FDX1, the cuproptosis master regulator, was experimentally determined as a tumor suppressor in ccRCC cells by suppressing the cell growth and cell invasion of ACHN and OSRC-2 cells in a cuproptosis-dependent and -independent manner. The results from IHC staining also demonstrated that FDX1 expression was negatively correlated with ccRCC tumor initiation and progression. Furthermore, we identified the miR-21-5p/FDX1 axis in ccRCC and experimentally verified that miR-21-5p directly binds the 3'-UTR of FDX1 to mediate its degradation. Consequently, a miR-21-5p inhibitor suppressed the cell growth and cell invasion of ACHN and OSRC-2 cells, which could be compensated by FDX1 knockdown, reinforcing the functional linkage between miR-21-5p and FDX1 in ccRCC. Finally, we evaluated the ccRCC tumor microenvironment under the miR-21-5p/FDX1 axis and noted that this axis was strongly associated with the infiltration of immune cells such as CD4+ T cells, Treg cells, and macrophages, suggesting that this signaling axis may alter microenvironmental components to drive ccRCC progression. Overall, this study constructed the miR-21-5p/FDX1 axis in ccRCC and analyzed its potential impact on the tumor microenvironment, providing valuable insights to improve current ccRCC management.

Second dorsal metacarpal artery flap from the dorsum of the middle finger for coverage of volar thumb defect.

PURPOSE: The second dorsal metacarpal artery flap from the middle finger is a reconstructive technique that can be used to repair extensive volar defects in a normal-length thumb. However, few reports advocate using it for coverage of volar thumb defects. In this article, an anatomic study of 9 flaps used for resurfacing thumb defects is presented along with the clinical experience of the authors. METHODS: From 2004 to 2006, 9 patients (6 men and 3 women; mean age, 33 years; range, 18-51 years) with extensive volar defects of their normal-length thumbs had reconstruction using the described technique. In all cases, the first dorsal metacarpal artery flap technique was unable to be used because of injury. Donor sites were covered using full-thickness skin grafts. After surgery, the thumb was immobilized with a splint, followed by rehabilitation. During the follow-up period, which lasted 24 to 30 months, flap-site skin quality, scar contractures, and finger mobility were assessed. The range of motion of the hand was measured by a goniometer. Sensibility was evaluated by the 2-point discrimination test and the Semmes-Weinstein monofilament test. Cold intolerance was also assessed. RESULTS: Patient postoperative courses were uneventful, and all flaps survived completely without complication. Good coverage was obtained in all cases. Full active range of motion was observed in all patients in both the donor finger and the thumb. The mean Semmes-Weinstein sensitivity and 2-point discrimination scores of the flap were 4.02 g and 8.4 mm, respectively. Mild cold intolerance was observed in all of the thumbs. CONCLUSIONS: The second dorsal metacarpal artery flap from the middle finger is a single-stage flap that produces good results. Although its pedicle length is limited, it is reliable and can be used as an alternative for reconstruction of extensive thumb-pulp defects, especially when the first dorsal metacarpal artery flap cannot be used. TYPE OF STUDY/LEVEL OF EVIDENCE: Therapeutic IV.

Overexpression of HOXC10 promotes glioblastoma cell progression to a poor prognosis via the PI3K/AKT signalling pathway.

OBJECTIVE: The HOX gene is expressed in neoplasias occurred in multiple tissues, such as the colon, lung and breast. However, the effects of the HOX gene on glioblastoma (GBM) remain poorly understood. We examined HOXC10 expression in GBM tissues and cells, analysed its effect on GBM prognosis, and finally assessed its possible underlying mechanisms in this study. METHODS: HOXC10 expression levels and its prognostic effects on GBM tissues were analysed based on The Cancer Genome Atlas (TCGA) and ONCOMINE database. Overall survival (OS) analysis was performed using the Kaplan-Meier method and log rank test. Then, the expression of HOXC10 was detected in four GBM cell lines using quantitative real-time reverse transcription-PCR (qRT-PCR). In addition, small interfering RNA (si-RNA) was utilised in the U87 cell line with the highest HOXC10 expression to facilitate subsequent in vitro cell experiment. Cell proliferation, migration and invasion were assessed using the Cell Counting Kit-8 (CCK-8) and colony formation assay, wound healing, Transwell assay, respectively in GBM U87 cell after HOXC10 knockdown. Key proteins related to the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signalling pathway were measured by western blotting. RESULTS: HOXC10 expression was significantly increased in GBM tissues and cell lines, leading a poor OS in GBM patients. Knockdown of HOXC10 could inhibit the GBM U87 cells proliferation, migration and invasion, as well as decreased expression levels of key proteins in PI3K/AKT signalling pathway. CONCLUSION: HOXC10 was overexpressed in GBM tissues and cells, and associated with poor prognosis in GBM patients. Moreover, HOXC10 knockdown inhibited U87 cell proliferation, migration and invasion, which were potentially related to PI3K/AKT signalling pathway activation. Our findings revealed that HOXC10 represent a promising biological target for GBM treatment in the future.