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Rural collective entrepreneurship poverty alleviation within the university participation context is regarded as a “socio-technical-economic” hybrid system, which aims to generate long-term economic benefits and social well-being for rural collectives through the knowledge of universities and realize the effect of poverty alleviation. However, the existing research has largely overlooked the dynamic mechanisms involved, especially how rural collectives transition from a passive response to a proactive creation in the context of university participation. Thus, we employ Complex Adaptive Systems (CAS) theory’s “detectors-IF/THEN rules-effectors” framework through a longitudinal case study. These findings demonstrate that (1) detectors have transitioned from “specialized knowledge embedding” to “diverse knowledge embedding,” which enables broader information scanning; (2) IF/THEN rules undergo cognitive destructuring to cognitive restructuring, fostering adaptive knowledge orchestration strategies; and (3) effectors shift from exploiting vertically related opportunities to horizontally related opportunities. (4) Cross-phase evolution: The knowledge flow mechanism of “knowledge spillover-organizational learning-knowledge absorption” propels “detectors, IF/THEN rules, and effectors” from the passive response phase to the proactive creation phase. This study advances theoretical understanding of CAS and research on entrepreneurship for poverty alleviation.

Idiopathic granulomatous mastitis is a benign chronic inflammatory breast disease and a confused treatment plan may result in worsening of the disease, unacceptable cosmetic damage for the patient and even mastectomy. We report a case of a 39-year-old Chinese woman with a two-month history of painful, solid, diabrotic, left breast lesions that measured 10 × 15 cm. Misdiagnosis had led to delayed wound healing with extensive ulcerative skin lesions. The patient was successfully treated with oral corticosteroids and bromocriptine without requirement for surgery.

The relationship between employee mental health and job performance has been one of the key concerns in workplace. However, extant studies suffer from incomplete results due to their focus on developed economies’ contexts and the unclear path of employee mental health’s impact on performance. In this paper, we investigate the mechanism of employee mental health influencing job performance. We use the data of Chinese firms to test these hypotheses. Drawing on a sample of 239 firms from China, we find that employee mental health positively impacts job performance, and such relationship is mediated by innovative behavior and work engagement. The findings not only enrich the discipline’s knowledge on mental health in an emerging economy setting but also extend the implications of mental health, innovative behavior, and work engagement to job performance.

Background: Long non-coding RNAs have suppressive or oncogenic effects in various types of cancers by serving as competing endogenous RNAs for specific microRNAs. In the present study, we aim to delineate the underlying mechanism by which the LINC00473/miR-29a-3p/Robo1 axis affects cell proliferation, migration, invasion, and metastasis in hepatocellular carcinoma (HCC). Methods: The level of Robo1 was examined in HCC tissues and cells, along with its regulatory effects on proliferation, migration, and invasion of HCC cells. Afterwards, the possible involvement of the PI3K/AKT/mTOR signaling pathway was determined. Next, miR-29a-3p expression was overexpressed or inhibited to investigate its regulatory role on HCC cell activities. The interaction among miR-29a-3p, Robo1, and LINC00473 was further characterized. Finally, a xenograft tumor in nude mice was conducted to measure tumorigenesis and metastasis in vivo. Results: miR-29a-3p was downregulated while Robo1 was upregulated in HCC tissues and cells. miR-29a-3p targeted Robo1 and negatively regulated its expression. In response to miR-29a-3p overexpression, Robo1 silencing or LINC00473 silencing, HCC cell proliferation, migration, invasion, tumor progression, and metastasis were impeded, which was involved with the inactivation of the PI3K/AKT/mTOR signaling pathway. Notably, LINC00473 could competitively bind to miR-29a-3p to upregulate Robo1 expression. Conclusion: LINC00473 might be involved in HCC progression by acting as a miR-29a-3p sponge to upregulate the expression of Robo1 that activates the PI3K/AKT/mTOR signaling pathway, which leads to enhanced cell proliferation, migration, invasion, tumor progression, and metastasis in HCC.

Background Coronavirus disease 2019 (COVID-19) is a newly emerging infectious disease and rapidly escalating epidemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The pathogenesis of COVID-19 remains to be elucidated. We aimed to clarify correlation of systemic inflammation with disease severity and outcomes in COVID-19 patients. Methods In this retrospective study, baseline characteristics, laboratory findings, and treatments were compared among 317 laboratory-confirmed COVID-19 patients with moderate, severe, or critically ill form of the disease. Moreover, the longitudinal changes of serum cytokines, lactate dehydrogenase (LDH), high-sensitivity C-reactive protein (hsCRP), and hsCRP to lymphocyte count ratio (hsCRP/L) as well as their associations with disease severity and outcomes were investigated in 68 COVID-19 patients. Results Within 24 h of admission, the critically ill patients showed higher concentrations of inflammatory markers including serum soluble interleukin (IL)-2 receptor, IL-6, IL-8, IL-10, tumor necrosis factor alpha (TNF-α), ferritin, procalcitonin, LDH, hsCRP, and hsCRP/L than patients with severe or moderate disease. The severe cases displayed the similar response patterns when compared with moderate cases. The longitudinal assays showed the levels of pro-inflammatory cytokines, LDH, hsCRP, and hsCRP/L gradually declined within 10 days post admission in moderate, severe cases or those who survived. However, there was no significant reduction in cytokines, LDH, hsCRP, and hsCRP/L levels in critically ill or deceased patients throughout the course of illness. Compared with female patients, male cases showed higher serum concentrations of soluble IL-2R, IL-6, ferritin, procalcitonin, LDH, and hsCRP. Multivariate logistic regression analysis revealed that IL-6 > 50 pg/mL and LDH > 400 U/L on admission were independently associated with disease severity in patients with COVID-19. Conclusion Exuberant inflammatory responses within 24 h of admission in patients with COVID-19 may correlate with disease severity. SARS-CoV-2 infection appears to elicit a sex-based differential immune response. IL-6 and LDH were independent predictive parameters for assessing the severity of COVID-19. An early decline of these inflammation markers may be associated with better outcomes.

Background Cirrhosis complicated by sepsis is a common reason for intensive care unit (ICU) admission and is associated with a markedly increased risk of short-term mortality. However, early assessment of 28-day mortality risk at ICU admission remains uncertain in this population. Existing scoring systems often rely on subjective assessments or clinical variables that may not be readily available at the time of admission, highlighting the need for a simple and objective model based on routinely obtainable data for early risk stratification. Methods Data from the Medical Information Mart for Intensive Care (MIMIC)-IV database were used for model development and internal validation, while MIMIC-III and the multicenter eICU Collaborative Research Database (eICU) were used for external validation. Predictors were selected using least absolute shrinkage and selection operator regression combined with Boruta feature selection and clinical judgment. Multiple machine learning algorithms were compared, and logistic regression was selected as the final model. Results In the MIMIC-IV cohort, 3,670 patients were screened, of whom 1,615 met the inclusion criteria and were used for model development and internal validation. External validation included 207 patients from MIMIC-III and an additional multicenter cohort from eICU. Six predictors were retained: age, white blood cell count, total bilirubin, glucose, international normalized ratio, and lactate. In internal validation, the logistic regression model achieved an area under the receiver operating characteristic curve (AUROC) of 0.785 (95% CI 0.741–0.830), outperforming SOFA 0.671 (95% CI 0.617–0.725) and MELD 0.728 (95% CI 0.679–0.777). In the MIMIC-III external validation cohort, the AUROC was 0.756 (95% CI 0.690–0.821), compared with 0.663 (95% CI 0.588–0.737) for SOFA and 0.731 (95% CI 0.663–0.799) for MELD. In the multicenter eICU cohort, the model demonstrated an AUROC of 0.745 (95% CI 0.657–0.833). Conclusions A logistic regression model based on six routinely available variables within the first 24 h of ICU admission demonstrated stable discriminative performance for predicting 28-day mortality in patients with cirrhosis and sepsis. The model provides a simple and objective tool to support early mortality risk stratification at ICU admission in this high-risk population.

Using panel data from 30 provinces and cities in China over the period 2013–2019, we intend to explore the mechanism and regional heterogeneity of the influence of digital economy development on carbon emissions. Specifically, this relationship is analyzed by including the geographical variable coefficient model into the chain mediation effect model, taking spatial correlation and heterogeneity into account. The results indicate that the digital economy decreases carbon emissions by enhancing energy intensity, but raises carbon emissions by fostering economic expansion, making digital economy a net contribution to carbon emissions. Moreover, the effect of the digital economy on carbon emissions varies by geographic location. For instance, the total impact is the greatest in northern China, followed by the southwest and southeast, and relatively minor in the northwest and south. Our findings contribute to the existing research and offer policymakers with a theoretical reference, allowing them to customize carbon reduction plans to local conditions.

SWI/SNF, an evolutionarily conserved ATP-dependent chromatin-remodeling complex, has an important role in transcriptional regulation 1 . In Saccharomyces cerevisiae , SWI/SNF regulates the expression of ∼6% of total genes through activation or repression 2 . Swi1, a subunit of SWI/SNF, contains an N-terminal region rich in glutamine and asparagine, a notable feature shared by all characterized yeast prions—a group of unique proteins capable of self-perpetuating changes in conformation and function 3 . Here we provide evidence that Swi1 can become a prion, [ SWI + ]. Swi1 aggregates in [ SWI + ] cells but not in nonprion cells. Cells bearing [ SWI + ] show a partial loss-of-function phenotype of SWI/SNF. [ SWI + ] can be eliminated by guanidine hydrochloride treatment, HSP104 deletion or loss of Swi1. Moreover, we show [ SWI + ] is dominantly and cytoplasmically transmitted. Our findings reveal a novel mechanism of 'protein-only' inheritance that results in modification of chromatin-remodeling and, ultimately, global gene regulation.

Endothelin receptors (ETRs) are activated by vasoactive peptide endothelins and involved in the pathogenesis of hepatic fibrosis. However, less is known about the role of ETRs in Schistosoma (S.) japonicum-induced hepatic fibrosis. Here, we show that the expression of ETRs is markedly enhanced in the liver and spleen tissues of patients with schistosome-induced fibrosis, as well as in murine models. Additional analyses have indicated that the expression levels of ETRs in schistosomiasis patients are highly correlated with the portal vein and spleen thickness diameter, both of which represent the severity of fibrosis. Splenomegaly is a characteristic symptom of schistosome infection, and splenic abnormality may promote the progression of hepatic fibrosis. We further demonstrate that elevated levels of ETRs are predominantly expressed on splenic B cells in spleen tissues during infection. Importantly, using a well-studied model of human schistosomiasis, we demonstrate that endothelin receptor antagonists can partially reverse schistosome-induced hepatic fibrosis by suppressing the activation of splenic B cells characterized by interleukin-10 (IL-10) secretion and regulatory T (Treg) cell-inducing capacity. Our study provides insights into the mechanisms by which ETRs regulate schistosomiasis hepatic fibrosis and highlights the potential of endothelin receptor antagonist as a therapeutic intervention for fibrotic diseases.

MicroRNA-mediated gene regulation is important in many physiological processes. Here we explore the roles of a microRNA, miR-941, in human evolution. We find that miR-941 emerged de novo in the human lineage, between six and one million years ago, from an evolutionarily volatile tandem repeat sequence. Its copy-number remains polymorphic in humans and shows a trend for decreasing copy-number with migration out of Africa. Emergence of miR-941 was accompanied by accelerated loss of miR-941-binding sites, presumably to escape regulation. We further show that miR-941 is highly expressed in pluripotent cells, repressed upon differentiation and preferentially targets genes in hedgehog- and insulin-signalling pathways, thus suggesting roles in cellular differentiation. Human-specific effects of miR-941 regulation are detectable in the brain and affect genes involved in neurotransmitter signalling. Taken together, these results implicate miR-941 in human evolution, and provide an example of rapid regulatory evolution in the human linage. miRNAs simultaneously regulate a range of genes, making them potential master players in evolution. Hu et al. identify a human-specific miRNA called miR-941, whose copy number remains polymorphic in modern humans, and show that miR-941 is expressed in the brain and could regulate important signalling pathways.