The market role of local governments in urbanization

This research explores from the perspective of new institutional economics the role played by local governments in the Chinese urbanization process. In conventional wisdom of city planning and economics, government is often considered as the opposite of the market: the public goods can only be supplied in special ways, different from that of the common goods. Institutions, planned economy or market economy, are often labelled by how much the government intervenes in its economy. However, theories based on such paradigms can hardly explain the behaviours of governments in the real world. This research argues that government is a part of the market mechanism, but not the opposite of market. A city government is in nature an enterprise that sells its products and services within its territory. Correspondingly, a city is in nature a place to trade public services, which makes the key institutional difference between a city and a village. In light of his argument, the theoretical debate on public goods is first examined. Then the behaviours of Chinese local governments are investigated and explained with a new framework, which cannot be achieved with traditional theory. Case studies in China demonstrate that the rapid growth of Chinese cities in recent years results mainly from the success of the business model of Chinese local governments. Lastly the inadequacies and mistakes of traditional urban planning theories in the Chinese context are analyzed and suggestions are made to transfer planning theory to the new paradigm, which is based mainly on the assumption that the behaviours of governments is to maximise their surplus. In the appendix a new pricing theory is formulated to extend the theoretical ground of this research. With this theory, the public goods can be supplied on a competitive market without substantial distinction from other good

The diagnostic performance of machine learning based on resting-state functional magnetic resonance imaging data for major depressive disorders: a systematic review and meta-analysis

ObjectiveMachine learning (ML) has been widely used to detect and evaluate major depressive disorder (MDD) using neuroimaging data, i.e., resting-state functional magnetic resonance imaging (rs-fMRI). However, the diagnostic efficiency is unknown. The aim of the study is to conduct an updated meta-analysis to evaluate the diagnostic performance of ML based on rs-fMRI data for MDD.MethodsEnglish databases were searched for relevant studies. The Quality Assessment of Diagnostic Accuracy Studies (QUADAS-2) was used to assess the methodological quality of the included studies. A random-effects meta-analytic model was implemented to investigate the diagnostic efficiency, including sensitivity, specificity, diagnostic odds ratio (DOR), and area under the curve (AUC). Regression meta-analysis and subgroup analysis were performed to investigate the cause of heterogeneity.ResultsThirty-one studies were included in this meta-analysis. The pooled sensitivity, specificity, DOR, and AUC with 95% confidence intervals were 0.80 (0.75, 0.83), 0.83 (0.74, 0.82), 14.00 (9, 22.00), and 0.86 (0.83, 0.89), respectively. Substantial heterogeneity was observed among the studies included. The meta-regression showed that the leave-one-out cross-validation (loocv) (sensitivity: p < 0.01, specificity: p < 0.001), graph theory (sensitivity: p < 0.05, specificity: p < 0.01), n > 100 (sensitivity: p < 0.001, specificity: p < 0.001), simens equipment (sensitivity: p < 0.01, specificity: p < 0.001), 3.0T field strength (Sensitivity: p < 0.001, specificity: p = 0.04), and Beck Depression Inventory (BDI) (sensitivity: p = 0.04, specificity: p = 0.06) might be the sources of heterogeneity. Furthermore, the subgroup analysis showed that the sample size (n > 100: sensitivity: 0.71, specificity: 0.72, n < 100: sensitivity: 0.81, specificity: 0.79), the different levels of disease evaluated by the Hamilton Depression Rating Scale (HDRS/HAMD) (mild vs. moderate vs. severe: sensitivity: 0.52 vs. 0.86 vs. 0.89, specificity: 0.62 vs. 0.78 vs. 0.82, respectively), the depression scales in patients with comparable levels of severity. (BDI vs. HDRS/HAMD: sensitivity: 0.86 vs. 0.87, specificity: 0.78 vs. 0.80, respectively), and the features (graph vs. functional connectivity: sensitivity: 0.84 vs. 0.86, specificity: 0.76 vs. 0.78, respectively) selected might be the causes of heterogeneity.ConclusionML showed high accuracy for the automatic diagnosis of MDD. Future studies are warranted to promote the potential use of these classification algorithms in clinical settings

CcGSDMEa functions the pore-formation in cytomembrane and the regulation on the secretion of IL-lβ in common carp (Cyprinus carpio haematopterus)

GSDME is the only direct executor of caspase-dependent pyroptosis in both canonical and non-canonical inflammasomes known to date in fish, and plays an important role in anti-bacterial infection and inflammatory response. In order to determine the regulation of GSDMEa on antibacterial infection in innate immune response, the CcGSDMEa gene in common carp (Cyprinus carpio haematopterus) was first identified and characterized, and then its function related to immune defense was investigated. Our results showed that the expressions of CcGSDMEa at the mRNA and protein levels were both significantly increased after Aeromonas hydrophila intraperitoneal infection at the early stage than that in the control group. We found that CcGSDMEa could be cleaved by inflammatory caspase (CcCaspase-1b) and apoptotic caspases (CcCaspase-3a/b and CcCaspase-7a/b). Interestingly, only the CcGSDMEa-NT (1-252 aa) displayed bactericidal activity to Escherichia coli and could punch holes in the membrane of HEK293T cells, whereas CcGSDMEa-FL (1-532 aa) and CcGSDMEa-CT (257-532 aa) showed no above activity and pore-forming ability. Overexpression of CcGSDMEa increased the secretion of CcIL-1β and the release of LDH, and could reduce the A. hydrophila burdens in fish. On the contrary, knockdown of CcGSDMEa reduced the secretion of CcIL-1β and the release of LDH, and could increase the A. hydrophila burdens in fish. Taken together, the elevated expression of CcGSDMEa was a positive immune response to A. hydrophila challenge in fish. CcGSDMEa could perform the pore-formation in cell membrane and the regulation on the secretion of IL-lβ, and further regulate the bacterial clearance in vivo. These results suggested that CcGSDMEa played an important role in immune defense against A. hydrophila and could provide a new insight into understanding the immune mechanism to resist pathogen invasion in teleost

bifA Regulates Biofilm Development of Pseudomonas putida MnB1 as a Primary Response to H2O2 and Mn2+

Pseudomonas putida (P. putida) MnB1 is a widely used model strain in environment science and technology for determining microbial manganese oxidation. Numerous studies have demonstrated that the growth and metabolism of P. putida MnB1 are influenced by various environmental factors. In this study, we investigated the effects of hydrogen peroxide (H2O2) and manganese (Mn2+) on proliferation, Mn2+ acquisition, anti-oxidative system, and biofilm formation of P. putida MnB1. The related orthologs of 4 genes, mco, mntABC, sod, and bifA, were amplified from P. putida GB1 and their involvement were assayed, respectively. We found that P. putida MnB1 degraded H2O2, and quickly recovered for proliferation, but its intracellular oxidative stress state was maintained, with rapid biofilm formation after H2O2 depletion. The data from mco, mntABC, sod and bifA expression levels by qRT-PCR, elucidated a sensitivity toward bifA-mediated biofilm formation, in contrary to intracellular anti-oxidative system under H2O2 exposure. Meanwhile, Mn2+ ion supply inhibited biofilm formation of P. putida MnB1. The expression pattern of these genes showed that Mn2+ ion supply likely functioned to modulate biofilm formation rather than only acting as nutrient substrate for P. putida MnB1. Furthermore, blockade of BifA activity by GTP increased the formation and development of biofilms during H2O2 exposure, while converse response to Mn2+ ion supply was evident. These distinct cellular responses to H2O2 and Mn2+ provide insights on the common mechanism by which environmental microorganisms may be protected from exogenous factors. We postulate that BifA-mediated biofilm formation but not intracellular anti-oxidative system may be a primary protective strategy adopted by P. putida MnB1. These findings will highlight the understanding of microbial adaptation mechanisms to distinct environmental stresses

iTRAQ-Based Differential Proteomic Analysis Reveals the Pathways Associated with Tigecycline Resistance in Acinetobacter baumannii

Background/Aims: Acinetobacter baumannii is an aerobic and Gram-negative bacterial pathogen with high morbidity and mortality. It remains a serious public health problem arising from its multidrug-resistant and extensive antibiotic resistance spectrum. Methods: In the present study, iTRAQ coupled with 2D LC-MS/MS was used to evaluate the proteome in standard Acinetobacter baumannii standard strains and tigecycline-resistant strains. Results: A total of 3639 proteins were identified and 961 proteins were identified to be differentially expressed in tigecycline-resistant Acinetobacter baumannii strains compared to the standard strains. 506 (52.6%) proteins were up-regulated and 455 (47.4%) proteins were down-regulated. Based on the GO enrichment analysis and KEGG pathway analysis, we concluded that most differentially expressed proteins were associated with stress responses, cellular component organization, proteins synthesis, degradation and function. Moreover, β-lactam resistance, the longevity regulating pathway and other related pathways were also involved in the regulation of tigecycline-resistant Acinetobacter baumannii. The differential expression of key proteins were evaluated by transcript analysis using quantitative RT-PCR. Conclusion: These results may provide new insights into the mechanisms of drug resistance in Acinetobacter baumannii