Purpose The purpose of this paper is to reveal the internal mechanism of the deviation of targeted poverty alleviation under the condition of asymmetric information. Design/methodology/approach Introducing a traditional signaling game theory model with dynamic asymmetric information, this study uses a dataset covering 813 poor households from Southern Xinjiang, China, to theoretically and empirically study the effect of aspiration of the poor households on poverty alleviation. Findings First, there exists asymmetric information between the poor households and village leaders. Second, the “short, arbitrary and fast” poverty alleviation approach may quickly pull people out of poverty, but it may also nurture a dependency culture where poor households lose their aspiration and ability to escape poverty through their own efforts. Third, due to long lasting universal state support, poor households in the national designated poor counties are less able and ambitious to escape poverty by themselves than their counterparts living in the national nondesignated areas. Originality/value The research results show that pro-poor development policies should be upheld to improve the residual utility that can benefit all households as a result of the poverty alleviation campaign. Relevant policy recommendations are made for China's continuous effort to fight relative poverty beyond 2020.
Aim Hepatocyte apoptosis is involved in the pathogenesis of liver diseases, while at the same time oxidative stress plays an important role in liver cell damage. This prompted us to evaluate the possible relationship between hepatocyte apoptosis and oxidative stress in patients with chronic hepatitis B. Methods CHB patients were placed in groups A (ALT >40 IU/L) and B (ALT ≤40 IU/L). Healthy controls were considered as group C (all ALT ≤40 IU/L). Serum concentrations of α-tocopherol, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were determined and liver cell apoptosis was evaluated by using terminal deoxynucleotydil transferase-mediated d-UTP biotin nick-end labeling (TUNEL). Results SOD, GSH-Px, and MDA did not differ between groups. α-Tocopherol was significantly decreased in groups A (p<0.01) and B (p<0.05) when compared with group C and it was negatively correlated with the apoptosis index (r=-0.575, p<0.01). Conclusion Only the plasma concentration of α-tocopherol rather than the other oxidative stress markers changed significantly in patients with normal alanine aminotransferase levels (ALT <40 IU/L) when compared with healthy controls and correlated significantly with the apoptosis index, suggesting that α-tocopherol may be a possible marker to reflect liver cell damage, especially in the absence of serum aminotransferase elevation.
Background: Talaromyces marneffei (TM) is the third most prevalent opportunistic infection in HIV-positive patients after tuberculosis and cryptococcosis.However, such infection of non-HIV individuals has rarely been reported.Case Presentation: We describe a very rare case of a 52-year-old male who presented with a single space-occupying lesion on the right lung and was eventually diagnosed with pulmonary TM infection.The patient was HIV-negative and had liver cirrhosis with portal vein thrombosis.Lung tissue next-generation sequencing (NGS) revealed TM infection.We successfully treated the patient with voriconazole for 8 weeks and observed lesion absorption via subsequent CT.The patient consumed wild bamboo rats two months before admission.Mutations related to congenital immune deficiency were not detected by whole-exome sequencing. Conclusion:Early and timely diagnosis is critical for improving patient prognosis.NGS plays a vital role in the diagnosis of pulmonary TM infection in patients.To our knowledge, this is the first published case of pulmonary TM infection in an HIV-negative patient with liver cirrhosis.
To investigate the characteristic of coagulation function in 303 patients with Coronavirus disease 2019 (COVID-19), we evaluated the correlation between coagulation function and disease status. We retrospectively analyzed 303 patients diagnosed with COVID-19 and evaluated the clinical data of 240 patients who were discharged. The coagulation function of the two groups (mild and severe) was compared. Compared with the mild group, majority of patients in the severe group were male (76.9% vs. 49.8%) and elderly (median age 65 vs. 50), and the proportion with chronic underlying diseases was higher (73.1% vs. 36.1%). There were 209 abnormalities (69.0%) of coagulation parameters in 303 patients admitted to hospital. Comparison of various indexes of coagulation function between the two groups in admission, the proportion of abnormal coagulation indicators in the severe group was higher than that in the mild group (100% vs. 66.1%). The median coagulation parameters in the severe group were higher than those in the mild group: international normalized ratio (1.04 vs. 1.01), prothrombin time (13.8 vs. 13.4) seconds, activated partial thromboplastin time (43.2 vs. 39.2) seconds, fibrinogen (4.74 vs. 4.33) g/L, fibrinogen degradation products (2.61 vs. 0.99) µg/mL, and D-dimer (1.04 vs. 0.43) µg/mL, the differences were statistically significant (p < 0.05). Coagulation dysfunction is common in patients with COVID-19, especially fibrinogen and D-dimer elevation, and the degree of elevation is related to the severity of the disease. As the disease recovers, fibrinogen and activated partial thromboplastin time also return to normal.
US hospitals are required to publicly post their prices for specified shoppable services online. However, the extent to which a hospital's prices posted online correlate with the prices they give to a telephone caller is unknown.
Protein-protein interaction analysis in crude bacterial lysates using combinational method of 19 F site-specific incorporation and 19 F NMR Dear Editor, Protein-protein interactions (PPI) are essential for a variety of cellular functions.Many PPI analyses were conducted in vitro, using purified proteins.In this report, the unnatural amino acid tfmF was site-specifically incorporated into several different sites of two Phox-Bem1 (PB1) domains from two mitogen activated protein kinases (MEKK3 and/ or MEK5) in the E. coli cells.Solution NMR 19 F chemical shift and side chain relaxation analysis demonstrated that MEKK3-PB1-I57, MEKK3-PB1-F77, and MEK5-PB1-I70 sites were located in the interaction interface of the MEKK3/ MEK5 complex, which was consistent with the crystal structure of MEKK3-PB1/MEK5-PB1 complex.Furthermore, crude lysates from E. coli cells with co-expressed tfmF incorporated MEKK3-PB1 and MEK5-PB1 were applied for 19 F NMR analysis.The successful implementation of in situ PPI analysis using the combinational method of site-specific tfmF incorporation and 19 F NMR demonstrated that this method could be a valuable general method for conformation and function studies of soluble multi-domain proteins or protein complexes in bacterial crude lysate, without procedures of protein purification.Protein-protein interactions (PPI) play essential roles in cellular functions, such as DNA transcription, signal transduction, or cytoskeleton formation.Currently, a variety of techniques, including co-immunoprecipitation, isothermal titration calorimetry, and surface plasma resonance are frequently applied for PPI studies (Syafrizayanti et al., 2014).However, these methods can only provide the overall interaction pattern or internal motion of purified protein complexes, and have many limitations such as low specificity, high background or false positives (Syafrizayanti et al., 2014).Structure determination methods (such as X-ray crystallography and electron cryo-microscopy) can precisely illustrate protein interaction interface, while these structural methods require high concentration of purified proteins.Recently, it has been reported that the cytoplasmic environment might have profound effects in regulating protein-protein and/or protein-ligand interactions that were hardly observed in vitro (Smith et al., 2014).The crucial
<div>Abstract<p>p16 is a tumor suppressor encoded by the <i>CDKN2A</i> gene whose expression is lost in approximately 50% of all human cancers. In its canonical role, p16 inhibits the G<sub>1</sub>–S-phase cell cycle progression through suppression of cyclin-dependent kinases. Interestingly, p16 also has roles in metabolic reprogramming, and we previously published that loss of p16 promotes nucleotide synthesis via the pentose phosphate pathway. However, the broader impact of p16/<i>CDKN2A</i> loss on other nucleotide metabolic pathways and potential therapeutic targets remains unexplored. Using CRISPR knockout libraries in isogenic human and mouse melanoma cell lines, we determined several nucleotide metabolism genes essential for the survival of cells with loss of p16/<i>CDKN2A</i>. Consistently, many of these genes are upregulated in melanoma cells with p16 knockdown or endogenously low <i>CDKN2A</i> expression. We determined that cells with low p16/<i>CDKN2A</i> expression are sensitive to multiple inhibitors of <i>de novo</i> purine synthesis, including antifolates. Finally, tumors with p16 knockdown were more sensitive to the antifolate methotrexate <i>in vivo</i> than control tumors. Together, our data provide evidence to reevaluate the utility of these drugs in patients with p16/<i>CDKN2A</i><sup>low</sup> tumors as loss of p16/<i>CDKN2A</i> may provide a therapeutic window for these agents.</p>Significance:<p>Antimetabolites were the first chemotherapies, yet many have failed in the clinic due to toxicity and poor patient selection. Our data suggest that p16 loss provides a therapeutic window to kill cancer cells with widely-used antifolates with relatively little toxicity.</p></div>
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