Search

Diabetic retinopathy, the most common complication of diabetes, is a neurodegenerative disease in the eye. And Parkinson's disease, affecting the health of 1–2% of people over 60 years old throughout the world, is the second largest neurodegenerative disease in the brain. As the understanding of diabetic retinopathy and Parkinson's disease deepens, the two diseases are found to show correlation in incidence, similarity in clinical presentation, and close association in pathophysiological mechanisms. To reveal the association between pathophysiological mechanisms of the two disease, in this review, the shared pathophysiological factors of diabetic retinopathy and Parkinson's disease are summarized and classified into dopaminergic system, circadian rhythm, neurotrophic factors, α-synuclein, and Wnt signaling pathways. Furthermore, similar and different mechanisms so far as the shared pathophysiological factors of the two disorders are discussed systematically. Finally, a brief summary and new perspectives are presented to provide new directions for further efforts on the association, exploration, and clinical prevention and treatment of diabetic retinopathy and Parkinson's disease. [ABSTRACT FROM AUTHOR]

The study of molecular derivatives of biological dyes is of great importance for the green transformation of the printing, dyeing, and textile industries. In this study, B3LYP density functional methods are used to optimize the geometric configuration of the selected molecules and to explore the relationship between the structure and color of biological dye molecules and their color mechanism. This study focuses on the analysis of polyenes, quinones, indoles, and azide biological dyes in colors commonly used in the textile industry: blue, yellow, purple, red, green, and so on. Quantum chemical investigations show that the conjugate structure of a biological dye is directly related to its color and that the group or structure affecting the conjugate structure will in many cases cause a change in color. In addition, time-dependent density functional theory spectral calculations with the CAM-B3LYP functional for UV-Vis spectra show that in the visible band, the color of the remaining band after subtracting the absorption wavelengths was exactly the same as the color of the pigment. These results indicate that the color of the pigment is exactly complementary to the light absorption color of the material. Our study provides theoretical guidance for the design of molecular derivatives of biological dyes and is expected to promote the green transformation of the textile, printing, and dyeing industries to a certain extent. [ABSTRACT FROM AUTHOR]

Let 픤 be a finite-dimensional simple Lie algebra over ℂ. A Y(픤)-module is said to be weight if it is a weight 픤-module. We give a complete classification of simple weight modules for Y(픰픩2) which admits a one-dimensional weight space. We prove that there are four classes of such modules: finite, highest weight, lowest weight and dense modules. Different from the classical 픰픩2-representation theory, we show that there exists a class of Y(픰픩2) irreducible modules which have uniformly two-dimensional weight spaces. [ABSTRACT FROM AUTHOR]

Object. Halitosis has great adverse impact on personal and social life. There is no strong evidence for the effect of Chinese medicine (CM) and combined Chinese and western medicine (CWM) on halitosis. The aim of the present study is to evaluate the effective rate of CM and CWM on halitosis. Materials and Methods. Literature search in English and Chinese was conducted in PubMed, Embase, CNKI, CBM, and Wanfang database. Study selection and data collection were conducted. Risks of bias were assessed by the Cochrane tool. Synthesis of results was done by RevMan 5.3. p<0.05 was considered significant difference. Subgroup analysis by classification of halitosis and sensitivity analysis were also conducted. Results. Seventeen studies were included. The follow-up length ranged from five days to eight weeks. CM had significantly better effect than WM on intraoral halitosis (I2 =24%; RR=1.21 (95% CI, 1.04, 1.40), P=0.01) and extraoral halitosis (I2 =0; RR=1.39 (95% CI, 1.19, 1.63), P<0.0001). CWM had significantly better effect than WM on intraoral halitosis (I2 =0; RR=1.25 (95% CI, 1.16, 1.35), P<0.00001) and extraoral halitosis (I2 =0; RR=1.19 (95% CI, 1.08, 1.31), P=0.0004). Subgroup analysis and sensitivity analysis showed insignificant results. Conclusion. With the limitation of our study, both CM and CWM have significantly better effect on halitosis than WM. More effort should be made to explore long-term effect of CM and CWM on halitosis. This study was registered with the PROSPERO (ID: CRD42018107229). [ABSTRACT FROM AUTHOR]

Annexin A3 (ANXA3), a member of Annexin family, is reported to mediate membrane transport and cancer development. However, the effect of ANXA3 on osteoclast formation and bone metabolism is still unclear. In this study, we found that knockdown of ANXA3 can significantly inhibit receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast formation through NF-κB signaling. ANXA3 downregulation abrogated the expression of osteoclast-specific genes, including Acp5, Mmp9 and Ctsk in osteoclast precursors. Moreover, lentiviral of shRNA against ANXA3 reversed the bone loss in osteoporosis using ovariectomized mice model. Mechanistically, we found that ANXA3 directly bound to RANK and TRAF6 to accelerate osteoclast differentiation by promoting their transcription and limiting degradation. In conclusion, we propose a fundamentally novel RANK-ANXA3-TRAF6 complex to effectively modulate the formation and differentiation of osteoclast to manipulate bone metabolism. The ANXA3-targeted therapeutic strategy may provide new insight for bone degrading-related diseases prevention and treatment. • ANXA3 promotes RANKL-induced osteoclast differentiation. • ANXA3 silencing relieves the bone loss in OVX mice. • ANXA3 directly binds to RANK and TRAF6, promoting their expression. [ABSTRACT FROM AUTHOR]

A set of ullazine-derived D–π–A–π–A photosensitisers were considered and selected for a potential dye with the best performance via computational approaches. The designed dyes HJ1–HJ13, which originated from dye YZ7, were constructed with different π-linking motifs and two kinds of auxiliary withdrawing groups. The photoelectric and photovoltaic parameters were determined by density functional theory approaches, and PBE0 optimisation with the TD-cam-B3LYP method was shown to be the best choice of functional in these designed dyes, with the calculated maximum absorption wavelength and excited lifetime in accordance with the experimental findings for YZ7. Replacement of the C≡C bond by the C＝C bond could reduce aggregation and improve the photoelectronic property. In addition, the D–π–A–π–A-type photosensitiser was found to achieve higher light-harvesting efficiency and higher performance for dye-sensitised solar cells (DSSCs). HJ8 was selected as the potential dye for DSSCs, as it had a 69 nm redshift in the maximum absorption wavelength and a 66% increment in the maximum extinction coefficient compared to YZ7, and achieved 99.9% light-harvesting efficiency, the longest excited time of 2.82 ns, a suitable driving force of injection and regeneration, the largest short-circuit current density and the largest open-circuit voltage. Our theoretical results provide strong guidance for discovering new efficient D–π–A–π–A-type organic dyes in DSSCs. [ABSTRACT FROM AUTHOR]

The relationship patterns of organizations participating in disaster response projects have a significant impact on their performance. However, research on appropriate relationship patterns of disaster response organizations is lacking both in theory and practice. To fill this gap, we conducted a comparative study on three interorganizational relationship patterns: government-centric, decentralized participatory, and partially collaborative. Drawing on the complex network modeling method, the mechanism of the interorganizational network composed of participating organizations in disaster response projects are conceptualized to depict different relationship patterns. Then, we conducted numerical simulation to further explore the optimal relationship pattern from the perspective of disaster response project effectiveness, efficiency, and fairness. The results reveal that the optimal organizational relationship pattern varies with changes in disaster response conditions. In the initial situation of an emergency with insufficient resources, government agencies should coordinate nongovernmental organizations (NGOs) to participate in disaster response in an orderly manner. When the demand for emergency resources drops, or the supply of emergency resources gradually becomes sufficient as disaster response projects progress, the government-centric pattern becomes the optimal relationship pattern. Moreover, the relationship between the response network structure and disaster response performance turns out to be inconsistent. At the early stage, response performance can be improved by reducing the number of steps to complete disaster relief and by appropriately increasing the connections between government agencies and NGOs. When a disaster situation is mitigated, the centralization of response power and unified coordination should be emphasized to improve emergency response performance. This study contributes to improving disaster response performance from the organizational relationship perspective and enriching disaster management theories. [ABSTRACT FROM AUTHOR]

Objective: Type 2 diabetes mellitus (T2DM) seriously affects human life and health. The aim of this study is to investigate the molecular mechanisms underlying the pathogenesis of T2DM through functional studies of pancreatic β-cell line in vitro.In this study, a high-glucose- and high-fat-induced model of Min6 cells was constructed, and their cellular functions and insulin secretion levels were detected. Transcriptome sequencing and differentially expressed genes (DEGs) screening and identification were eventually performed.We successfully constructed a T2DM model of high-fat- and high-glucose-treated Min6 cells and found that their migration rate, survival rate, and insulin secretion capacity were reduced. Through transcriptome sequencing and bioinformatics analysis, we finally selected the glutathione S-transferase A2 (Gsta2) and neuropilin-2 (Nrp2) genes. After overexpressing Nrp2, we found that PARP1 protein levels were elevated and apoptotic pathways were activated. Cell viability and survival were significantly reduced, apoptosis was increased, and insulin secretion capacity was reduced. Overexpression of Gsta2 significantly increased the apoptosis of Min6 cells, but no increase in Nrp2 expression was observed.The results suggest that Nrp2 regulates apoptosis in Min6 cells and that there may be a link between this molecule and pathological apoptosis of pancreatic β-cells in T2DM patients. However, Gsta2 was not found to be an upstream regulator of Nrp2 in our cell line. Therefore, Gsta2 regulation of apoptosis in Min6 cells may be achieved through other apoptotic pathways.Methods: Type 2 diabetes mellitus (T2DM) seriously affects human life and health. The aim of this study is to investigate the molecular mechanisms underlying the pathogenesis of T2DM through functional studies of pancreatic β-cell line in vitro.In this study, a high-glucose- and high-fat-induced model of Min6 cells was constructed, and their cellular functions and insulin secretion levels were detected. Transcriptome sequencing and differentially expressed genes (DEGs) screening and identification were eventually performed.We successfully constructed a T2DM model of high-fat- and high-glucose-treated Min6 cells and found that their migration rate, survival rate, and insulin secretion capacity were reduced. Through transcriptome sequencing and bioinformatics analysis, we finally selected the glutathione S-transferase A2 (Gsta2) and neuropilin-2 (Nrp2) genes. After overexpressing Nrp2, we found that PARP1 protein levels were elevated and apoptotic pathways were activated. Cell viability and survival were significantly reduced, apoptosis was increased, and insulin secretion capacity was reduced. Overexpression of Gsta2 significantly increased the apoptosis of Min6 cells, but no increase in Nrp2 expression was observed.The results suggest that Nrp2 regulates apoptosis in Min6 cells and that there may be a link between this molecule and pathological apoptosis of pancreatic β-cells in T2DM patients. However, Gsta2 was not found to be an upstream regulator of Nrp2 in our cell line. Therefore, Gsta2 regulation of apoptosis in Min6 cells may be achieved through other apoptotic pathways.Results: Type 2 diabetes mellitus (T2DM) seriously affects human life and health. The aim of this study is to investigate the molecular mechanisms underlying the pathogenesis of T2DM through functional studies of pancreatic β-cell line in vitro.In this study, a high-glucose- and high-fat-induced model of Min6 cells was constructed, and their cellular functions and insulin secretion levels were detected. Transcriptome sequencing and differentially expressed genes (DEGs) screening and identification were eventually performed.We successfully constructed a T2DM model of high-fat- and high-glucose-treated Min6 cells and found that their migration rate, survival rate, and insulin secretion capacity were reduced. Through transcriptome sequencing and bioinformatics analysis, we finally selected the glutathione S-transferase A2 (Gsta2) and neuropilin-2 (Nrp2) genes. After overexpressing Nrp2, we found that PARP1 protein levels were elevated and apoptotic pathways were activated. Cell viability and survival were significantly reduced, apoptosis was increased, and insulin secretion capacity was reduced. Overexpression of Gsta2 significantly increased the apoptosis of Min6 cells, but no increase in Nrp2 expression was observed.The results suggest that Nrp2 regulates apoptosis in Min6 cells and that there may be a link between this molecule and pathological apoptosis of pancreatic β-cells in T2DM patients. However, Gsta2 was not found to be an upstream regulator of Nrp2 in our cell line. Therefore, Gsta2 regulation of apoptosis in Min6 cells may be achieved through other apoptotic pathways.Conclusions: Type 2 diabetes mellitus (T2DM) seriously affects human life and health. The aim of this study is to investigate the molecular mechanisms underlying the pathogenesis of T2DM through functional studies of pancreatic β-cell line in vitro.In this study, a high-glucose- and high-fat-induced model of Min6 cells was constructed, and their cellular functions and insulin secretion levels were detected. Transcriptome sequencing and differentially expressed genes (DEGs) screening and identification were eventually performed.We successfully constructed a T2DM model of high-fat- and high-glucose-treated Min6 cells and found that their migration rate, survival rate, and insulin secretion capacity were reduced. Through transcriptome sequencing and bioinformatics analysis, we finally selected the glutathione S-transferase A2 (Gsta2) and neuropilin-2 (Nrp2) genes. After overexpressing Nrp2, we found that PARP1 protein levels were elevated and apoptotic pathways were activated. Cell viability and survival were significantly reduced, apoptosis was increased, and insulin secretion capacity was reduced. Overexpression of Gsta2 significantly increased the apoptosis of Min6 cells, but no increase in Nrp2 expression was observed.The results suggest that Nrp2 regulates apoptosis in Min6 cells and that there may be a link between this molecule and pathological apoptosis of pancreatic β-cells in T2DM patients. However, Gsta2 was not found to be an upstream regulator of Nrp2 in our cell line. Therefore, Gsta2 regulation of apoptosis in Min6 cells may be achieved through other apoptotic pathways. [ABSTRACT FROM AUTHOR]

Variants of the interleukin-1β (IL-1β) gene have been associated with type 2 diabetes (T2D) and coronary artery diseases (CAD). However, association of IL-1β polymorphisms with diabetic patients having CAD clinical manifestation has not been studied yet. In this study, we aim to decipher the role of IL-1β common promoter variants with susceptibility/resistance to development of CAD in T2D patients. T2D patients with (n = 134) or without CAD (n = 533) were enrolled. A total of 513 essentially healthy individuals from the same population were included in this study as control. Plasma levels of IL-1β were quantified by enzyme-linked immunosorbent assay (ELISA) kit as per instructions from the manufacturer. IL-1β promoter variants (T-31C and C-511T) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). T2D patients displayed higher level of plasma IL-1β in comparison to healthy controls. Prevalence of variants for IL-1β (C-511T) polymorphism was higher in diabetic patients compared to controls (CT: P < 0.0001, OR = 3.01; TT: P < 0.0001, OR = 2.45). IL-1β (C-511T) polymorphism was linked with plasma IL-1β levels. Interestingly, heterozygous mutants (CT) were most prevalent in T2D individuals with CAD compared to those without CAD (P = 0.03, OR = 1.82). Furthermore, low-density lipoprotein (LDL) and triglycerides were elevated in T2D patients with CAD than in patients without heart-related disorder. No significant association of other polymorphism (T-31C) was noticed with susceptibility to T2D or diabetic patients with heart disorders. IL-1β (C-511T) variants are associated with elevated plasma IL-1β levels. Mutation at the IL-1β promoter region (C-511T) predisposed subjects to the development of T2D and CAD manifestation in diabetic patients. [ABSTRACT FROM AUTHOR]

Variants of the interleukin-1β (IL-1β) gene have been associated with type 2 diabetes (T2D) and coronary artery diseases (CAD). However, association of IL-1β polymorphisms with diabetic patients having CAD clinical manifestation has not been studied yet. In this study, we aim to decipher the role of IL-1β common promoter variants with susceptibility/resistance to development of CAD in T2D patients. T2D patients with (n = 134) or without CAD (n = 533) were enrolled. A total of 513 essentially healthy individuals from the same population were included in this study as control. Plasma levels of IL-1β were quantified by enzyme-linked immunosorbent assay (ELISA) kit as per instructions from the manufacturer. IL-1β promoter variants (T-31C and C-511T) were genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). T2D patients displayed higher level of plasma IL-1β in comparison to healthy controls. Prevalence of variants for IL-1β (C-511T) polymorphism was higher in diabetic patients compared to controls (CT: P < 0.0001, OR = 3.01; TT: P < 0.0001, OR = 2.45). IL-1β (C-511T) polymorphism was linked with plasma IL-1β levels. Interestingly, heterozygous mutants (CT) were most prevalent in T2D individuals with CAD compared to those without CAD (P = 0.03, OR = 1.82). Furthermore, low-density lipoprotein (LDL) and triglycerides were elevated in T2D patients with CAD than in patients without heart-related disorder. No significant association of other polymorphism (T-31C) was noticed with susceptibility to T2D or diabetic patients with heart disorders. IL-1β (C-511T) variants are associated with elevated plasma IL-1β levels. Mutation at the IL-1β promoter region (C-511T) predisposed subjects to the development of T2D and CAD manifestation in diabetic patients. [ABSTRACT FROM AUTHOR]

The role of different isoforms of Fibroblast growth factor-2 (FGF2) in tubular epithelial-to-mesenchymal transition (EMT) in diabetic nephropathy remains unknown. We aimed to evaluate the role of FGF2 isoforms in the pathogenesis of EMT. Western blot and immunofluorescence were used to assess the expression of FGF2 isoforms in db/db mice and high glucose-stimulated HK2 cells. The effects of specific FGF2 isoforms on EMT were explored via overexpression or knockdown of the corresponding isoform in HK2 cells cultivated in high glucose. Expression of low molecular weight (LMW) FGF2 was up-regulated while high molecular weight (HMW) FGF2 was down-regulated in the kidney of db/db mice and HK2 cells cultured in high glucose that underwent EMT. Overexpression of the LMW FGF2 enhanced EMT changes, while overexpression of the HMW FGF2 attenuated EMT. Knockdown of HMW FGF2 in HK2 cells promoted the EMT process. The expression and function of LMW and HMW FGF2 differed in the process of EMT in tubular cells. LMW FGF2 contributed to EMT, while HMW FGF2 played a protective role in the EMT process. [ABSTRACT FROM AUTHOR]