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Background and Aims. Inflammation is involved in the pathophysiology of ischemic stroke. The aim of this prospective study was to evaluate the association of hs-CRP with incident ischemic stroke in patients with nonalcoholic fatty liver disease (NAFLD). Methods. A sample of 318 participants without previous strokes was included in this study. Hs-CRP levels and other potential confounding factors were measured at baseline. NAFLD was performed by abdominal ultrasound after excluding secondary causes for fat accumulation. According to baseline hs-CRP concentrations, participants were categorized into 3 groups: level 1 (

We propose a new method to measure production inefficiency by estimating the target and production technology of individual units using quantile regression. This method not only measures inefficiency in total factor productivity but also inefficiencies in input utilizations. We also propose two methods for decomposing the estimated inefficiency. We apply this proposed method for measuring the inefficiency of primary sector production for the Xinjiang Production and Construction Corps in China to clarify its usefulness and advantages. We specify the capital stock using the area sown and other inputs to estimate the production function with the restriction of constant returns-to-scale. Results indicate that lower labor inputs make production inefficient, and the inefficiency of labor utilization makes a large contribution to the mean and variance of total inefficiency. We also compare the proposed inefficiency measure to those employing corrected ordinary least squares and data envelopment analysis. The estimated efficiencies obtained are similar to those for existing methods. However, the proposed method provides additional advantages, including information on the inefficiencies in input utilization.

Sarcopenia has been proved to be related to the prognosis of patients with bladder cancer (BC) after radical cystectomy (RC). The relationship between sarcopenia and the occurrence of venous thromboembolism (VTE) after RC is unclear. We collected data of 252 BC patients treated with RC at our institution. Data was obtained from the electronic medical record database. Sarcopenia was defined by the third lumbar vertebra skeletal muscle index (SMI) which was measured using preoperative computed tomography. The primary outcome was the incidence of VTE within 30 days after the surgery in sarcopenia and non-sarcopenia groups. Outcomes between the two cohorts were compared using univariate analysis. Multivariate logistic regression was used to control for differences between cohorts. Two hundred fifty-two patients were enrolled, of which 85 (33.7%) patients were in sarcopenia group, while 167 (66.3%) patients were not in sarcopenia group. The incidence of total VTE in sarcopenia group was higher than that in the extended group (10.6% vs. 1.8%, p = 0.005). Sarcopenia did not cause an increase in other postoperation 30 days complications (all p > 0.05). Multivariate analysis confirmed sarcopenia was independently associated with increased odds of VTE (OR = 4.18, 95% CI [1.01–17.27]; p = 0.048). Subgroup analysis showed that patients with VTE tended to be older (76.5 vs 66.0, p = 0.025) and have higher proportion of diabetes (58.3% vs 14.2%, p

In this paper, frozen steamed bread was used as the object to study the effect of frozen storage on the protein characteristics in a steamed bread system by measuring the changes in water holding capacity, oil holding capacity, emulsifying capacity, soluble protein content, surface hydrophobicity, secondary structure and molecular weights of gluten proteins in frozen steamed bread. The results showed that with an extension of frozen storage time, the disulfide bond (S‒S) and total content of sulfydryl (-SH) decreased as a whole, and the molecular weights of steamed bread proteins were mainly distributed between 22 and 31 kDa, which were composed of a mixture of gliadin and low-molecular-weight glutenin subunits. With a decrease in frozen storage temperature, the soluble protein contents and protein water holding capacities of steamed bread first increased and then decreased, and the trend of the surface hydrophobicity was opposite. The frozen storage temperature had a significant effect on the protein properties of the steamed bread system. The changes in protein emulsification, oil holding capacity and soluble protein content were stable at -24 °C, which was suitable for long-term frozen storage.

The role of O-linked N-acetylglucosamine (O-GlcNAc) modification in the cell cycle has been enigmatic. Previously, both O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) disruptions have been shown to derail the mitotic centrosome numbers, suggesting that mitotic O-GlcNAc oscillation needs to be in concert with mitotic progression to account for centrosome integrity. Here, using both chemical approaches and biological assays with HeLa cells, we attempted to address the underlying molecular mechanism and observed that incubation of the cells with the OGA inhibitor Thiamet-G strikingly elevates centrosomal distances, suggestive of premature centrosome disjunction. These aberrations could be overcome by inhibiting Polo-like kinase 1 (PLK1), a mitotic master kinase. PLK1 inactivation is modulated by the myosin phosphatase targeting subunit 1 (MYPT1)–protein phosphatase 1cβ (PP1cβ) complex. Interestingly, MYPT1 has been shown to be abundantly O-GlcNAcylated, and the modified residues have been detected in a recent O-GlcNAc–profiling screen utilizing chemoenzymatic labeling and bioorthogonal conjugation. We demonstrate here that MYPT1 is O-GlcNAcylated at Thr-577, Ser-585, Ser-589, and Ser-601, which antagonizes CDK1-dependent phosphorylation at Ser-473 and attenuates the association between MYPT1 and PLK1, thereby promoting PLK1 activity. We conclude that under high O-GlcNAc levels, PLK1 is untimely activated, conducive to inopportune centrosome separation and disruption of the cell cycle. We propose that too much O-GlcNAc is equally deleterious as too little O-GlcNAc, and a fine balance between the OGT/OGA duo is indispensable for successful mitotic divisions.

Human papillomaviruses (HPVs) cause a subset of head and neck squamous cell carcinomas (HNSCCs). Previously, we demonstrated that HPV16 oncogene E6 or E6/E7 transduction increases the abundance of O-linked β-N-acetylglucosamine (O-GlcNAc) transferase (OGT), but OGT substrates affected by this increase are unclear. Here, we focus on the effects of O-GlcNAcylation on HPV-positive HNSCCs. We found that upon HPV infection, Unc-51-like kinase 1 (ULK1), an autophagy-initiating kinase, is hyper-O-GlcNAcylated, stabilized, and linked with autophagy elevation. Through mass spectrometry, we identified that ULK1 is O-GlcNAcylated at Ser409, which is distinct from the previously reported Thr635/Thr754 sites. It has been demonstrated that PKCα mediates phosphorylation of ULK1 at Ser423, which attenuates its stability by shunting ULK1 to the chaperone-mediated autophagy (CMA) pathway. Using biochemical assays, we demonstrate that ULK1 Ser409Ser410 O-GlcNAcylation antagonizes its phosphorylation at Ser423. Moreover, mutations of Ser409A and its neighboring site Ser410A (2A) render ULK1 less stable by promoting interaction with the CMA chaperone HSC70 (heat shock cognate 70 kDa protein). Furthermore, ULK1-2A mutants attenuate the association of ULK1 with STX17, which is vital for the fusion between autophagosomes and lysosomes. Analysis of The Cancer Genome Atlas (TCGA) database reveals that ULK1 is upregulated in HPV-positive HNSCCs, and its level positively correlates with HNSCC patient survival. Overall, our work demonstrates that O-GlcNAcylation of ULK1 is altered in response to environmental changes. O-GlcNAcylation of ULK1 at Ser409 and perhaps Ser410 stabilizes ULK1, which might underlie the molecular mechanism of HPV-positive HNSCC patient survival.

Neuroinflammation, defined as an inflammatory response mediated by central nervous system astrocyte, Microglia and endothelial cells, disrupts homeostasis and is typical of many Neurodegeneration. The DA receptor family is mainly expressed in Microglia, and microglia-induced neuroinflammation is an important pathogenesis of Neurodegeneration, this article reviews the pathogenesis and treatment of neuroinflammation.

We propose a new empirical approach to analyze fiscal decentralization and apply it to Chinese intergovernmental fiscal relationships between the central government and provincial governments, using nonsymmetric Nash solution. In calculating budgetary revenue and expenditure shares, we include extra budgetary revenue and expenditure. We find that although an increase in either income inequality or real per capita GDP lowers local governments’ bargaining power within the budgetary system, local governments can offset this by obtaining more bargaining power over extra budgetary expenditures. Another finding is that although urbanization increases provincial governments’ budgetary revenues, it also restricts the scope for further budgetary expenditure.

The role of O-linked N-acetylglucosamine (O-GlcNAc) modification in the cell cycle has been enigmatic. Previously, both O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) disruption have been shown to derail the mitotic centrosome numbers, suggesting that mitotic O-GlcNAc oscillation needs to be in concert with mitotic progression to account for centrosome integrity. Here we attempted to address the underlying molecular mechanism by both chemical approaches and biological assays, and observed that Thiamet-G (OGA inhibitor) incubation strikingly elevated centrosomal distances, suggestive of premature centrosome disjuction. These aberrancies could be overcome by inhibiting Polo-like kinase 1 (Plk1), a mitotic master kinase. Plk1 inactivation is modulated by the Myosin Phosphatase Targeting Subunit 1 (MYPT1)-Protein Phosphatase 1 cβ (PP1cβ) complex. Interestingly, MYPT1 is abundantly O-GlcNAcylated and the modified residues have been detected in a recent O-GlcNAc profiling screen utilizing chemoenzymatic labeling and bioorthogonal conjugation. We demonstrate that MYPT1 is O-GlcNAcylated at T577, S585, S589 and S601, which antagonizes CDK1-dependent phosphorylation at S473, subsequently attenuating the association between MYPT1 and Plk1, and promoting PLK1 activity. Thus under high O-GlcNAc, Plk1 is untimely activated, conducive to inopportune centrosome separation and disrupting the cell cycle. We propose that too much O-GlcNAc is equally deleterious as too little O-GlcNAc, and a fine balance between the OGT/OGA duo is indispensible for successful mitotic divisions.

Checkpoint kinase 2 (Chk2) is a pivotal effector kinase in the DNA damage response, with an emerging role in mitotic chromosome segregation. In this study, we show that Chk2 interacts with myosin phosphatase targeting subunit 1 (MYPT1), the targeting subunit of protein phosphatase 1cβ (PP1cβ). Previous studies have shown that MYPT1 is phosphorylated by CDK1 at S473 during mitosis, and subsequently docks to the polo-binding domain of PLK1 and dephosphorylates PLK1. Herein we present data that Chk2 phosphorylates MYPT1 at S507 in vitro and in vivo, which antagonizes pS473. Chk2 inhibition results in failure of γ-tubulin recruitment to the centrosomes, phenocopying Plk1 inhibition defects. These aberrancies were also observed in the MYPT1-S507A stable transfectants, suggesting that Chk2 exerts its effect on centrosomes via MYPT1. Collectively, we have identified a Chk2-MYPT1-PLK1 axis in regulating centrosome maturation. Abbreviations: Chk2: checkpoint kinase 2; MYPT1: myosin phosphatase targeting subunit 1; PP1cβ: protein phosphatase 1c β; Noc: nocodazole; IP: immunoprecipitation; IB: immunoblotting; LC-MS/MS: liquid chromatography-tandem mass spectrometry; Chk2: checkpoint kinase 2; KD: kinase domain; WT: wild type; Ub: ubiquitin; DAPI: 4',6-diamidino-2-phenylindole; IF: Immunofluorescence; IR: ionizing radiation; siCHK2: siRNA targeting CHK2.

We overcome the problems of data availability and investigate the fiscal multipliers in autonomous prefectures in China. We first estimate the long-run elasticity of gross regional production with respect to fiscal expenditure in autonomous prefectures, using autoregressive distributed lag models. The estimated long-run elasticity is much less than unity, however, and the estimated fiscal multipliers for prefectures are between 0.61 and 4.93, with an average of 1.93. These results indicate that additional fiscal expenditure is still effective in increasing local income and promoting economic growth for most of the autonomous prefectures.

Estrogen signals have been suggested to modulate the progression and metastasis of nonsmall cell lung cancer (NSCLC), which is one of the leading causes of cancer deaths worldwide. While there are limited data concerning the roles and effects of G-protein-coupled estrogen receptor (GPER) on the progression of NSCLC, our present study reveals that the expression of GPER in NSCLC cells is obviously greater than that in lung fibroblast cell line MRC-5. Activation of GPER via its specific agonist G-1 decreases the in vitro motility of A549 and H358 cells and the expression of matrix metalloproteinase 2 (MMP-2) and MMP-9. Further, G-1 treatment can rapidly decrease the phosphorylation, nuclear translocation, and promoter activities of NF-κB in NSCLC cells. BAY 11-7082, the inhibitor of NF-κB, also inhibits the expression of MMP-2/9, while overexpression of p65 significantly attenuates G-1-induced downregulation of MMP-2/9. It suggests that inhibition of NF-κB mediates G-1-induced MMP-2/9 downregulation. G-1 treatment significantly down regulates the phosphorylation of IκB kinase β (IKK-β) and IκBα, while not IKK-α, in both 549 and H358 cells. ACHP, the specific inhibitor of IKK-β, can reinforce G-1-induced MMP-2/9 downregulation and invasion suppression of A549 cells. Collectively, our results suggest that activation of GPER can inhibit the migration of human NSCLC cells via suppression of IKK-β/NF-κB signals. These findings will help to better understand the roles and mechanisms of GPER as a potential therapy target for NSCLC patients.

We investigate the effects of urban and rural populations and area sizes on the expenditures of the prefecture-level local government. We found the following three results. The first relates to the expenditure for urban populations. At around 220,000 people, per capita local government expenditure is minimized in our simulation. The second is that the expenditure for rural populations is proportional to the population size. The third finding is that the expenditure in accordance with the areas is also proportional to the area size. This cost structure is the reason why China fs recent rapid urbanization increases prefectural government fs fiscal distress.

We propose a new empirical approach to analyzing fiscal decentralization and apply it to Chinese intergovernmental fiscal relationships between the central government and provincial governments. In calculating budgetary revenue and expenditure shares, we include extra budgetary revenue and expenditure. We find that although an increase in either income inequality or real per capita GDP lowers local governments f bargaining power within the budgetary system, local governments can offset this by obtaining more bargaining power over extra budgetary expenditures. Another finding is that although urbanization increases provincial governments f budgetary revenues, it also restricts the scope for further budgetary expenditure.

We overcome the problems of data availability and investigate the fiscal multipliers in autonomous prefectures in China. We first estimate the long-run elasticity of gross regional production with respect to fiscal expenditure in autonomous prefectures, using autoregressive distributed lag models. The estimated long-run elasticity is much less than unity, however, and the estimated fiscal multipliers for prefectures are between 0.61 and 4.93, with an average of 1.93. These results indicate that additional fiscal expenditure is still effective in increasing local income and promoting economic growth for most of the autonomous prefectures.

Background:Noninvasive ventilation (NIV) is a promising therapeutic strategy after cardiothoracic surgery. This study aimed to meta-analyze the efficacy and safety of NIV as compared to conventional management after cardiothoracic surgery.Methods:PubMed, EMBASE, and Cochrane Library database

To investigate potential pathogens in waters of Xiamen from Jiulong River, and to provide useful information for the prevention and control of potential pathogen infections.All samples were spread on Thiosulfate Citrate Bile Salts Sucrose (TCBS) agar plates, and then incubated at 26 +/- 1 degrees C for 24 +/- 2 h. In total 158 TCBS strains were isolated from TCBS agar plates and pure-cultivated on 2216E agar plates. All strains were identified using the 16S rRNA gene- Restriction fragment length polymorphism (RFLP), 16S rRNA sequence analysis, GenBank database Basic Local Alignment Search Tool (BLAST) and phylogenetic analysis.The results show that 158 TCBS strains from the sediments of Jiulong River estuary were classfied as 7 genus, which were Pseudomonas (28%), Aeromonas (24%), Pseudoalteromonas (19%), Shewanella (13%), Bacillus (11%), Vibrio (4%) and Psychrobacter (1%). The composition and distribution of TCBS bacteria groups varied with stations. Non-halophilic or haloduric bacteria groups were dominant in the upper area of Jiulong River estuary, and halophilic and haloduric bacteria were dominant in the lower area, which characterized a typical estuary feature. The salinity played a key role in the distribution of TCBS groups. Vibrios did not constitute a significant proportion (6% - 19%) of the total TCBS strains at different stations, and most of the them distributed at the lower region.There were a lot of potential pathogens in Jiulong River estuary. Aeromonas, a typical genus of halotolerant bacteria, was the potentially terrigenous bacteria contamination to the waters of Xiamen. Most Vibrio specieses were marine aborigines, which was not directly contaminated from the runoff of Jiulong River.

Background: China has five layers of government including the central government. Recently, some prefectural governments meet fiscal distress. Methods: We investigate the effects of urban and rural populations and area sizes on the expenditures of the prefecture-level local government by estimating quintile regression. Results: At around 220,000 people, per capita local government expenditure for urban populations is minimized in our simulation. The expenditure for rural populations is proportional to the population size. The expenditure in accordance with the areas is also proportional to the area size. Conclusions: The cost structure is the reason why China's recent rapid urbanization increases prefectural government's fiscal distress.