A Gram staining negative, rod-shaped, aerobic bacterial strain J5-3T with a single polar flagellum was isolated from coking wastewater collected from Shaoguan, Guangdong, China. It was motile and capable of optimal growth at pH 6–8, 30 °C, and 0–2 % (w/v) NaCl. Its predominant fatty acids were 11-methyl C18:1ω7c (29.2 %), C16:0 (20.6 %), C19:0 cyclo ω8c (18.2 %), C18:0 (11.0 %), and C18:1ω7c/C18:1ω6c (10.9 %) when grown on trypticase soy agar. The major polar lipids were diphosphatidylglycerol, phosphatidylglycerol, two unknown glycolipids (GL1, GL2), and two unknown phospholipid (PL1, PL2). The predominant ubiquinone was Q-10, and the genome DNA G+C content was 61.7 mol %. Phylogenetic analysis based on the 16S rRNA gene sequences indicated that strain J5-3T belonged to the family Hyphomicrobiaceae in Alphaproteobacteria. It shared the 16S rRNA gene sequence similarities of 93.8–96.1 % with the genus Devosia, 94.5–94.8 % with the genus Pelagibacterium, and <92.0 % with all the other type strains in family Hyphomicrobiaceae. It can be distinguished from the closest phylogenetic neighbors based on several phenotypic and genotypic features, including α-galactosidase activity, tetracycline susceptibility, major fatty acid composition, polar lipid profile, DNA gyrase B subunit (gyrB) gene sequence, and random-amplified polymorphic DNA profile. Therefore, we consider strain J5-3T to represent a novel species of a novel genus within the family Hyphomicrobiaceae, for which the name Paradevosia shaoguanensis gen. nov., sp. nov. is proposed. The type strain of Paradevosia shaoguanensis is J5-3T (=CGMCC 1.12430T =LMG 27409T). 相似文献
A protein-free, isothermal, self-amplified nucleic acid sensing system which was a G-quadruplex integrated hybridization chain reaction (GQ-HCR) system was developed. The G-quadruplex was closed two-thirds in the loop and one-third in the stem of one of the GQ-HCR hairpin probes. In the absence of the target molecule, the GQ-HCR probes stayed as inactive meta-stable hairpin structures and the G-quadruplex was inert. Reversely, the GQ-HCR probes could be cross-opened to start a hybridization chain reaction and the closed G-quadruplex could be released to be free when the GQ-HCR probes came across the target molecule. The GQ-HCR nucleic acid sensing system could detect as low as 7.5nM ssDNA or RNA by the colorimetric method and 4nM ssDNA by the fluorometric method. Less than 10 copies of dsDNA template could also be detected when PCR was combined with the GQ-HCR system (PCR+GQ-HCR). Because of these advantages, the GQ-HCR system was also studied for application in visual chip detection to obtain a satisfactory repeatable and specific result. 相似文献
Podocyte injury plays a key role in the occurrence and development of kidney diseases. Decreased autophagic activity in podocyte is closely related to its injury and the occurrence of proteinuria. Liver X receptors (LXRs), as metabolic nuclear receptors, participate in multiple pathophysiological processes and express in several tissues, including podocytes. Although the functional roles of LXRs in the liver, adipose tissue and intestine are well established; however, the effect of LXRs on podocytes function remains unclear. In this study, we used mouse podocytes cell line to investigate the effects of LXR activation on podocytes autophagy level and related signaling pathway by performing Western blotting, RT-PCR, GFP-mRFP-LC3 transfection, and immunofluorescence staining. Then, we tested this effect in STZ-induced diabetic mice. Transmission electron microscopy and immunohistochemistry were employed to explore the effects of LXR activation on podocytes function and autophagic activity. We found that LXR activation could inhibit autophagic flux through blocking the formation of autophagosome in podocytes in vitro which was possibly achieved by affecting AMPK, mTOR, and SIRT1 signaling pathways. Furthermore, LXR activation in vivo induced autophagy suppression in glomeruli, leading to aggravated podocyte injury. In summary, our findings indicated that activation of LXRs induced autophagy suppression, which in turn contributed to the podocyte injury.
Plasmacytoid dendritic cells (pDCs) represent a unique and crucial immune cell population capable of producing large amounts
of type I interferons (IFNs) in response to viral infection. The function of pDCs as the professional type I IFN-producing
cells is linked to their selective expression of Toll-like receptor 7 (TLR7) and TLR9, which sense viral nucleic acids within
the endosomal compartments. Type I IFNs produced by pDCs not only directly inhibit viral replication but also play an essential
role in linking the innate and adaptive immune system. The aberrant activation of pDCs by self nucleic acids through TLR signaling
and the ongoing production of type I IFNs do occur in some autoimmune diseases. Therefore, pDC may serve as an attractive
target for therapeutic manipulations of the immune system to treat viral infectious diseases and autoimmune diseases. 相似文献
Acute respiratory distress syndrome (ARDS) is characterized by increased pulmonary inflammation and endothelial barrier permeability. Omentin has been shown to benefit obesity-related systemic vascular diseases; however, its effects on ARDS are unknown. In the present study, the level of circulating omentin in patients with ARDS was assessed to appraise its clinical significance in ARDS. Mice were subjected to systemic administration of adenoviral vector expressing omentin (Ad-omentin) and one-shot treatment of recombinant human omentin (rh-omentin) to examine omentin''s effects on lipopolysaccharide (LPS)-induced ARDS. Pulmonary endothelial cells (ECs) were treated with rh-omentin to further investigate its underlying mechanism. We found that a decreased level of circulating omentin negatively correlated with white blood cells and procalcitonin in patients with ARDS. Ad-omentin protected against LPS-induced ARDS by alleviating the pulmonary inflammatory response and endothelial barrier injury in mice, accompanied by Akt/eNOS pathway activation. Treatment of pulmonary ECs with rh-omentin attenuated inflammatory response and restored adherens junctions (AJs), and cytoskeleton organization promoted endothelial barrier after LPS insult. Moreover, the omentin-mediated enhancement of EC survival and differentiation was blocked by the Akt/eNOS pathway inactivation. Therapeutic rh-omentin treatment also effectively protected against LPS-induced ARDS via the Akt/eNOS pathway. Collectively, these data indicated that omentin protects against LPS-induced ARDS by suppressing inflammation and promoting the pulmonary endothelial barrier, at least partially, through an Akt/eNOS-dependent mechanism. Therapeutic strategies aiming to restore omentin levels may be valuable for the prevention or treatment of ARDS.Acute respiratory distress syndrome (ARDS) is a devastating condition with a 30–60% mortality rate.1, 2 Although the pathogenesis of ARDS is complex, the inflammatory response and endothelial barrier disruption play important roles in the development of ARDS.3, 4, 5 Therefore, in addition to conventional anti-inflammatory treatments, therapeutic strategies aim to restore pulmonary endothelial barrier integrity and function through regulating inter-endothelial AJs and the endothelial cytoskeleton to minimize protein leakage and leukocyte infiltration under ARDS conditions.6, 7Obesity, especially visceral obesity, has clearly been shown to impair systemic vasculature and to lead to the initiation and progression of vascular disorders.8, 9, 10 Although different from the well-documented impacts of obesity on cardiovascular disease, the relationships between obesity and ARDS have not been well elucidated. Clinical and experimental data focused on pertinent physiological changes in obesity indicate that the obesity may alter ARDS pathogenesis by ‘priming'' the pulmonary endothelial barrier for insult and amplifying the early inflammatory response, thus lowering the threshold to initiate ARDS.11, 12 Contrary to conventional dogma, adipose tissue is now appreciated as an important endocrine tissue that secretes various bioactive molecules called adipokines, which contribute to the progression of diverse vascular diseases, including hypertension, cardiovascular disease and atherosclerosis.13, 14, 15, 16 Although ARDS is not a classified pulmonary vascular disease, it is a severe inflammatory lung condition with widespread pulmonary endothelial breakdown. Clinical evidence has indicated that the obesity might be an emerging risk factor for ARDS and that circulating adipokines levels are associated with the initiation and progression of ARDS.11, 12, 17, 18 Moreover, experimental studies have suggested that some anti-inflammatory adipokines, such as adiponectin and apelin, exert beneficial actions on ARDS.19, 20, 21Omentin is an anti-inflammatory adipokine that is abundant in human visceral fat tissue.22, 23 Paradoxically, higher circulating omentin-1 levels are present in lean and healthy individuals compared with the obese and diabetic patients. Moreover, as a novel biomarker of endothelial dysfunction, reduced circulating omentin levels are related to the pathological mechanism of obesity-linked vascular disorders, including type 2 diabetes, atherosclerosis, hypertension and cardiovascular disease.24, 25, 26, 27, 28 Furthermore, experimental studies have found that omentin stimulates vasodilation in isolated blood vessels and suppresses cytokine-stimulated inflammation in endothelial cells (ECs).29, 30, 31 Thus, these data suggest that omentin may protect against obesity-related vascular complications through its anti-inflammatory and vascular-protective properties; however, little is known regarding its role in lung tissue. It was reported that decreased circulating omentin-1 levels could be regarded as an independent predictive marker for the obstructive sleep apnea syndrome and that omentin protects against pulmonary arterial hypertension through inhibiting vascular structure remodeling and abnormal contractile reactivity.32, 33, 34 However, to our knowledge, no study has assessed the impact of omentin on ARDS.Akt-related signaling pathways function as an endogenous negative feedback mechanism in response to the injurious stimulus. Our prior studies have demonstrated that Akt-related signaling contributes to protection against ARDS.35, 36 Moreover, omentin has been reported to exert anti-inflammatory, pro-survival and pro-angiogenic functions in various cells via an Akt-dependent mechanism.30, 31, 37, 38, 39, 40, 41, 42Collectively, given that ARDS is ultimately an obesity-related disorder of vascular function and that omentin is a favorable pleiotropic adipokine capable of anti-inflammatory, pro-angiogenic and anti-apoptotic abilities; omentin may exert beneficial effects on ARDS. In the present study, we first aimed to appraise the clinical significance of omentin in ARDS and then specifically evaluated its impact on inflammation and the endothelial barrier. Furthermore, we mechanistically investigated the role of Akt-related signaling pathways in these effects induced by omentin in vivo and in vitro. 相似文献
The increasing prevalence of HIV-1 among men having sex with men (MSM) calls for an investigation of HIV-1 prevalence and incidence in MSM by early diagnosis to assist with early preventive interventions in Hong Kong. The participants were recruited randomly from MSM communities within a one-year period. Rapid HIV Test (RHT) and real-time dried blood spot (DBS)-based quantitative polymerase chain reaction (DBS-qPCR) were used for the early diagnosis of 474 participants. Risk behavior analysis was performed by studying information obtained from the participants during the study period. The HIV-1 prevalence and incident rates in the studied MSM population were 4.01% (19/474) and 1.47% (7/474), respectively. Three infected participants were found at the acute phase of infection by DBS-qPCR. Only 46.4% (220/474) MSM were using condoms regularly for anal sex. HIV infection significantly correlated with unprotected receptive anal sex and syphilis infection. An increased number of infections was found among foreign MSM in Hong Kong. This study is the first to use DBS-qPCR to identify acutely infected individuals in a community setting and to provide both the prevalence and incident rates of HIV-1 infection among MSM in Hong Kong. The risk analysis provided evidence that behavior intervention strengthening is necessary to fight against the increasing HIV-1 epidemic among MSM in Hong Kong and surrounding regions in Asia. 相似文献
A terthieno[3,2‐b]thiophene ( 6T ) based fused‐ring low bandgap electron acceptor, 6TIC , is designed and synthesized for highly efficient nonfullerene solar cells. The chemical, optical, and physical properties, device characteristics, and film morphology of 6TIC are intensively studied. 6TIC shows a narrow bandgap with band edge reaching 905 nm due to the electron‐rich π‐conjugated 6T core and reduced resonance stabilization energy. The rigid, π‐conjugated 6T also offers lower reorganization energy to facilitate very low VOC loss in the 6TIC system. The analysis of film morphology shows that PTB7‐Th and 6TIC can form crystalline domains and a bicontinuous network. These domains are enlarged when thermal annealing is applied. Consequently, the device based on PTB7‐Th : 6TIC exhibits a high power conversion efficiency (PCE) of 11.07% with a high JSC > 20 mA cm?2 and a high VOC of 0.83 V with a relatively low VOC loss (≈0.55 V). Moreover, a semitransparent solar cell based on PTB7‐Th : 6TIC exhibits a relatively high PCE (7.62%). The device can have combined high PCE and high JSC is quite rare for organic solar cells. 相似文献
One hundred twenty crossbred piglets (Duroc × Landrace × Yorkshire) were used to determine the effects of dietary zinc glycine
chelate on growth performance, tissue mineral concentrations, and serum enzyme activity. All pigs were allotted to four treatments
and fed with basal diets supplemented with 0, 50, and 100 mg/kg Zn as zinc glycine chelate or 3,000 mg/kg Zn as zinc oxide
(ZnO). After the 35-day feeding trial, results of the study showed that, compared to the control, average daily gain was improved
(P < 0.05) for pigs fed 100 mg/kg Zn from zinc glycine chelate or 3,000 mg/kg Zn from ZnO and Zn concentrations in serum and
M. longissimus dorsi were significantly enhanced by 100 mg/kg dietary zinc glycine chelate and 3,000 mg/kg ZnO. In addition, supplementation of
100 mg/kg zinc glycine chelate decreased (P < 0.05) the liver Fe level, liver Zn level, spleen Cu level, and kidney Cu level compared to that of the 3,000-mg/kg ZnO
group. For feces mineral excretion, 3,000 mg/kg Zn from ZnO greatly increased the concentration of fecal Zn (P < 0.01) and Mn (P < 0.05) compared to that of the control or the 100-mg/kg zinc glycine chelate group. Moreover, alkaline phosphatase and Cu/Zn
superoxide dismutase activities of pigs in 100 mg/kg zinc glycine chelate and ZnO treatments were greatly higher than that
of the control. The results of present study showed that supplementation with zinc glycine chelate could improve growth and
serum enzyme activities and could also decrease zinc excretion in feces in weanling pig compared to high dietary ZnO. 相似文献