Measuring Productivity and Relative Efficiency of Public Tertiary Traditional Chinese Medicine Hospitals in Hubei, China.

Improving the productivity and relative efficiency of traditional Chinese medicine (TCM) hospitals is pivotal for hospital managers and policymakers to optimize the utilization of TCM resources in China. This study aimed to measure the productivity and relative efficiency of public tertiary TCM hospitals in Hubei Province. The input and output indicators data were extracted from the Health Commission of Hubei Province (HCHP) from 2019 to 2021. The Bootstrap-Malmquist-DEA model was employed to measure the productivity and relative efficiency of the hospitals. The statistical significance was set at P < .05. The numbers of total diagnostic patients and discharged patients declined by 23.44% and 28.34% from 2019 to 2020, and then increased by 25.76% and 20.44% respectively from 2020 to 2021. The average bias-corrected technical efficiency (TE) scores of the TCM hospitals from 2019 to 2021 were 0.8391, 0.8048, and 0.8559, indicating good efficiency. The average total factor productivity (TFP) in 2020 and 2021 decreased compared to that in 2019, with scores of 0.7479 and 0.8996, respectively. Between 2019 and 2020, the TFP changes among 19 out of 21 (90.48%) TCM hospitals and the technological changes (TC) among 20 out of 21 (95.24%) were less than 1.0000 (P < .05). The TFP changes of 17 out of 21 (80.95%) TCM hospitals and the TC of 20 out of 21 (95.24%) were less than 1.0000 (P < .05) between 2019 and 2021. COVID-19 might have constrained the provision of healthcare services by the public tertiary TCM hospitals in Hubei Province. Priority should be given to the utilization of healthcare resources, performance evaluation, information system strengthening, and internal hospital management to boost technical efficiency. TCM hospitals need to focus further on technology innovation to improve their technological progress.

A histidine cluster determines YY1-compartmentalized coactivators and chromatin elements in phase-separated enhancer clusters.

As an oncogenic transcription factor, Yin Yang 1 (YY1) regulates enhancer and promoter connection. However, gaps still exist in understanding how YY1 coordinates coactivators and chromatin enhancer elements to assemble enhancers and super-enhancers. Here, we demonstrate that a histidine cluster in YY1's transactivation domain is essential for its formation of phase separation condensates, which can be extended to additional proteins. The histidine cluster is also required for YY1-promoted cell proliferation, migration, clonogenicity and tumor growth. YY1-rich nuclear puncta contain coactivators EP300, BRD4, MED1 and active RNA polymerase II, and colocalize with histone markers of gene activation, but not that of repression. Furthermore, YY1 binds to the consensus motifs in the FOXM1 promoter to activate its expression. Wild-type YY1, but not its phase separation defective mutant, connects multiple enhancer elements and the FOXM1 promoter to form an enhancer cluster. Consistently, fluorescent in situ hybridization (FISH) assays reveal the colocalization of YY1 puncta with both the FOXM1 gene locus and its nascent RNA transcript. Overall, this study demonstrates that YY1 activates target gene expression through forming liquid-liquid phase separation condensates to compartmentalize both coactivators and enhancer elements, and the histidine cluster of YY1 plays a determinant role in this regulatory mechanism.

Antidepressive Effect of Arctiin by Attenuating Neuroinflammation via HMGB1/TLR4- and TNF-α/TNFR1-Mediated NF-κB Activation.

Inflammation is a potential factor in the pathophysiology of depression. A traditional Chinese herbal medicine, arctiin, and its aglycone, arctigenin, are the major bioactive components in Fructus arctii and exhibit neuroprotective and anti-inflammatory activities. Arctigenin has been reported to have antidepressant-like effects. However, the antidepressant-like effects of arctiin, its precursor, remain unknown. In this study, we investigated the antidepressant-like effects of arctiin and its underlying mechanisms by in vivo and in vitro experiments in mice. Our results showed that arctiin significantly attenuated sucrose consumption and increased the immobility time in tail suspension and forced swimming tests. Arctiin decreased neuronal damage in the prefrontal cortex (PFC) of the brain. Arctiin also attenuated the levels of three inflammatory mediators, indoleamine 2,3-dioxygenase, 5-hydroxytryptamine, and dopamine, that were elevated in the PFC or serum of chronic unpredictable mild stress (CUMS)-exposed mice. Arctiin reduced excessive activation of microglia and neuroinflammation by reducing high mobility group box 1 (HMGB1)/toll-like receptor 4 (TLR4)- and tumor necrosis factor-α (TNF-α)/TNF receptor 1 (TNFR1)-mediated nuclear factor-kappa B (NF-κB) activation in the PFC of CUMS-exposed mice and HMGB1- or TNF-α-stimulated primary cultured microglia. These findings demonstrate that arctiin ameliorates depression by inhibiting the activation of microglia and inflammation via the HMGB1/TLR4 and TNF-α/TNFR1 signaling pathways.