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| 1 | Phosphine production in anaerobic wastewater treatment under tetracycline antibiotic pressure显示文摘The influence of tetracycline(TC) antibiotics on phosphine(PH_3) production in the anaerobic wastewater treatment was studied. A lab-scale anaerobic baffled reactor with three compartments was employed to simulate this process. The reactor was operated in a TC-absence wastewater and 250 μg/L TC-presence wastewater for three months after a start-up period,respectively. The responses of p H, oxidation–reduction potential(ORP), chemical oxygen demand(COD), total phosphorus(TP), enzymes activity(dehydrogenase and acid phosphatase),and microbial community were investigated to reveal the effect of TC on PH_3 production.Results suggested that the dehydrogenase(DH) activity, acid phosphatase(ACP) activity and COD have positive relationship with PH_3 production, while p H, ORP level and the TP in liquid phase have negative relationship with PH_3 production. With prolonged TC exposure, decrease in p H and increase in DH activity are beneficial to PH_3 production, while decrease in COD and ACP activity are not the limiting factors for PH_3 production. | Meiqing Lu Xiaojun Niu Weiyi Chen Zhu Liang Sheng You Xiaohong Gu | 2018 | Journal of Environmental Sciences2018，30，7： | 5 |
| 2 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 0 |
| 3 | Efficacy of comprehensive cognitive health management for Shanghai community older adults with mild cognitive impairment显示文摘Background The management of modifiable risk factors and comorbidities may impact the future trajectory of cognitive impairment,but easy-to-implement management methods are lacking.Aims This study investigated the effects of simple but comprehensive cognitive health management practices on the cognitive function of older adults in the community with normal cognition(NC)and mild cognitive impairment(MCI).Methods The comprehensive cognitive health management programme included a psychiatric assessment of the cognitive risk factors for those in the intervention groups and individualised recommendations for reducing the risks through self-management supported by regular medical professional follow-up.The intervention groups for this study included 84 elderly participants with NC and 43 elderly participants with MCI who received comprehensive cognitive health management.The control groups included 84 elderly participants with NC and 43 elderly participants with MCI who matched the intervention group’s general characteristics and scale scores using the propensity matching score analysis.The Montreal Cognitive Assessment(MoCA)scale and Geriatric Depression Scale(GDS)scores were compared after a 1-year follow-up.Results For older adults with MCI in the intervention group,MoCA scores were higher at the 1-year followup than at baseline(24.07(3.674)vs 22.21(3.052),p=0.002).For the MoCA subscales,the intervention group’s abstract and delayed memory scores had significantly increased during the 1-year follow-up.Furthermore,in a generalised linear mixed model analysis,the interaction effect of group×follow-up was statistically significant for the MCI group(F=6.61,p=0.011;coefficients=5.83).Conclusions After the comprehensive cognitive health management intervention,the older adults with MCI in the community showed improvement at the 1-year follow-up.This preliminary study was the first to demonstrate an easy-to-implement strategy for modifying the cognitive risk factors of elderly individuals with MCI in the community,providing new insight into early-stage intervention for dementia. | Jiayuan Qiu Lu Zhao Shifu Xiao Shaowei Zhang Ling Li Jing Nie Li Bai Shixing Qian Yang Yang Michael Phillips Meiqing Sheng Yuan Fang Xia Li | 2022 | General Psychiatry2022，35，4： | 0 |
| 4 | Identification of a hotspot on PD-L1 for pH-dependent binding by monoclonal antibodies for tumor therapy显示文摘Dear Editor,Monoclonal antibody(mAb)-based tumor immune checkpoint therapy(ICT)has gained particular interest in recent years.1 The molecular basis of binding between mAbs and PD-1 or PD-L1 has been reported,providing clear information of the binding“hotspots”for mAbs.2,3 Tumor suppression efficacy of PD-L1 specific mAbs relies on not only the blocking of PD-1/PD-L1 interaction to restore T cell reactivity,but also Fc-mediated tumor cell cytotoxity.PD-L1 antibody drug conjugate(ADC)for selective chemo-guided immune modulation of tumor has also been developed which has shown promising tumor suppression potency.4 MAbs that could bind to antigen in a pH-dependent manner would improve recycling of the antibodies and engineered IL-6R mAbs with pH-dependent binding properties have displayed increased lysosomal delivery and therapeutic potency.5 However,no PD-L1 specific mAb with pH-dependent binding property has been reported,and whether the binding to a specific region on PD-L1 would induce pH-dependent interaction remains unknown. | Hongchuan Liu Xiaoshan Bi Yuehua Zhou Rui Shi Sheng Yao Jianxun Qi Hui Feng Meiqing Feng Jinghua Yan Shuguang Tan | 2020 | Signal Transduction and Targeted Therapy2020，5，1： | 0 |
| 5 | Kindlin-2 regulates skeletal homeostasis by modulating PTH1R in mice显示文摘In vertebrates,the type 1 parathyroid hormone receptor(PTH1R)is a critical regulator of skeletal development and homeostasis;however,how it is modulated is incompletely understood.Here we report that deleting Kindlin-2 in osteoblastic cells using the mouse 10-kb Dmp1-Cre largely neutralizes the intermittent PTH-stimulated increasing of bone volume fraction and bone mineral density by impairing both osteoblast and osteoclast formation in murine adult bone.Single-cell profiling reveals that Kindlin-2 loss increases the proportion of osteoblasts,but not mesenchymal stem cells,chondrocytes and fibroblasts,in non-hematopoietic bone marrow cells,with concomitant depletion of osteoblasts on the bone surfaces,especially those stimulated by PTH.Furthermore,haploinsufficiency of Kindlin-2 and Pth1r genes,but not that of either gene,in mice significantly decreases basal and,to a larger extent,PTH-stimulated bone mass,supporting the notion that both factors function in the same genetic pathway.Mechanistically,Kindlin-2 interacts with the C-terminal cytoplasmic domain of PTH1R via aa 474–475 and Gsα.Kindlin-2 loss suppresses PTH induction of cAMP production and CREB phosphorylation in cultured osteoblasts and in bone.Interestingly,PTH promotes Kindlin-2 expression in vitro and in vivo,thus creating a positive feedback regulatory loop.Finally,estrogen deficiency induced by ovariectomy drastically decreases expression of Kindlin-2 protein in osteocytes embedded in the bone matrix and Kindlin-2 loss essentially abolishes the PTH anabolic activity in bone in ovariectomized mice.Thus,we demonstrate that Kindlin-2 functions as an intrinsic component of the PTH1R signaling pathway in osteoblastic cells to regulate bone mass accrual and homeostasis. | Xuekun Fu Bo Zhou Qinnan Yan Chu Tao Lei Qin Xiaohao Wu Sixiong Lin Sheng Chen Yumei Lai Xuenong Zou Zengwu Shao Meiqing Wang Di Chen Wenfei Jin Youqiang Song Huiling Cao Ge Zhang Guozhi Xiao | 2021 | Signal Transduction and Targeted Therapy2021，6，1： | 0 |
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