Acupoint sensitization and deqi （得气） are key factors influencing the therapeutic efficacy of acupuncture. Acupoint sensitization serves as an important prerequisite for achieving deqi. Based on a review of recent research progress on acupoint sensitization and deqi， this study proposes that the biological basis of deqi primarily encompasses the biomechanical basis of mechanotransduction and microenvironmental changes， the energy metabolic basis of molecular events and signaling pathway activation， the neurophysiological basis of receptor activation and central integration， and the biological effect basis of bidirectional regulation within the neuro-endocrine-immune network. The extension of deqi refers to a sustained and relatively stable biological homeostasis after deqi through self-regulation and remodeling of the organism， which mainly manifests as neural reflex threshold resetting and neural functional remodeling， re-establishment of endocrine homeostasis， rebalancing of immune homeostasis， and temporal changes in gene expression. Systematic investigation into the scientific connotation and extension of deqi not only contributes to a deeper elucidation of the mechanisms underlying acupuncture's therapeutic actions， but also provides theoretical foundations and practical guidance for the optimization of clinical therapeutic regimens.

Acupoint sensitization and deqi （得气） are key factors influencing the therapeutic efficacy of acupuncture. Acupoint sensitization serves as an important prerequisite for achieving deqi. Based on a review of recent research progress on acupoint sensitization and deqi， this study proposes that the biological basis of deqi primarily encompasses the biomechanical basis of mechanotransduction and microenvironmental changes， the energy metabolic basis of molecular events and signaling pathway activation， the neurophysiological basis of receptor activation and central integration， and the biological effect basis of bidirectional regulation within the neuro-endocrine-immune network. The extension of deqi refers to a sustained and relatively stable biological homeostasis after deqi through self-regulation and remodeling of the organism， which mainly manifests as neural reflex threshold resetting and neural functional remodeling， re-establishment of endocrine homeostasis， rebalancing of immune homeostasis， and temporal changes in gene expression. Systematic investigation into the scientific connotation and extension of deqi not only contributes to a deeper elucidation of the mechanisms underlying acupuncture's therapeutic actions， but also provides theoretical foundations and practical guidance for the optimization of clinical therapeutic regimens.

Objective To investigate the biological functions of the ERG3 gene in Candida albicans and its potential value in antifungal therapy. Methods The ERG3 null mutant was constructed by the CRISPR/Cas9 technology. Gas chromatography-mass spectrometry, microbroth dilution method, hyphal induction and mouse systemic infection models were carried out to evaluate sterol metabolism, drug susceptibility, hyphal formation ability and pathogenicity in C. albicans. Results The disruption of the ERG3 gene led to disordered sterol metabolism in C. albicans with a significant increased level of episterol, 14α-methylfecosterol and ergosta-7,22-dienol. The ERG3 null mutant exhibited significantly reduced susceptibility to antifungal azole and polyene drugs, which suggested that ERG3 involve in regulating drug resistance. Although the disruption of ERG3 inhibited hyphal growth and biofilm formation, it did not significantly alter the pathogenicity of the strain in a mouse model of systemic fungal infection. Conclusion The ERG3 gene was a key regulator in the ergosterol synthesis pathway in C. albicans. Its deletion induced multi-drug resistance by reshaping sterol metabolism, while pathogenicity maintenance depended on compensatory mechanisms. This study provided critical insights for developing antifungal drugs targeting sterol metabolism and overcoming drug resistance.

Objective To understand the changing trend of Internet outpatient visits in public hospitals,and provide support for the development planning of Internet hospitals.Methods Using the data of Internet outpatient visits in a public hos-pital from January 2021 to June 2023,the ARIMA model and GM(1,1)model were constructed respectively.The mean absolute error(MAE)and root mean square error(RMSE)were used to evaluate the fitting effect,and the Internet outpatient visits from July to December 2023 were predicted based on the dominance model.Results ARIMA(1,2,1)model and GM(1,1)model were used to predict the number of return visits of Internet outpatient service.The average absolute errors were 369.86 and 978.84,and the root-mean-square errors were 479.49 and 1444.83,respectively.The ARIMA(0,1,0)model and GM(1,1)model were used to predict the number of Internet outpatient consultations.The average absolute errors were 297.23 and 369.62,and the root-mean-square errors were 413.61 and 496.30,respectively,indicating that the ARIMA model has a good prediction effect.The forecast results show that the predicted value of Internet outpatient visits in December 2023 is 14,831 cases,and the predicted value of consultation visits is 7461 cases.Conclusion The number of Internet outpatient visits in a public hospital will continue to rise from 2021 to 2023.Therefore,hospitals should fully realize the importance of Internet medical services,take ac-tive measures to continuously optimize the medical service model,and provide patients with high-quality,efficient and convenient Internet medical services.

Objective To investigate the changing trend of the current situation of Internet-based oncology outpatient treatment and provide support for the development and management of Internet hospitals.Methods The ARIMA and GM(1,1)models were constructed based on the Internet-based outpatient data of a cancer hospital from January 2021 to June 2023,and the fitting effect was evaluated by mean absolute error(MAE)and root mean square error(RMSE).Based on the model,the pro-portion of Internet-based outpatient visits and the offline outpatient visits were predicted from July to December 2023.Results ARIMA(1,1,2)and GM(1,1)models were used to predict the proportion of Internet-based outpatient visits.The average abso-lute errors were 2.06%and 2.41%,and the root-mean-square errors were 3.01%and 3.17%,respectively.The ARIMA(0,1,1)and GM(1,1)models were used to predict the proportion of Internet-based outpatient visits to the offline outpatient visits,with the rate of the average absolute errors of 0.58%and 1.08%,respectively,and the rate of the root mean square errors 0.75%and 1.31%,respectively.The figures indicated that the ARIMA model had a better prediction effect.The forecast results showed that the predicted value of Internet outpatient service in December 2023 was 90.35%,and the predicted value of Internet-based outpatient service accounted for 16.46%of the offline outpatient service.Conclusion In 2021-2023,the proportion of Inter-net-based outpatient visits in the cancer hospital showed a steady trend,and the proportion of Internet outpatient visits in the off-line outpatient visits showed a rising trend.Therefore,hospitals need to establish a continuous monitoring mechanism,constantly adjust management strategies and measures to meet the needs of patients and continue to promote the high-quality development of Internet-based medical services.

This study explores the effects and possible mechanisms of nuclear factor E2 related factor 2 (NRF2) on ovarian granulosa cells, providing a scientific basis to prevent premature ovarian failure. An ovarian cell injury model was constructed by treating human ovarian granulosa cell (KGN cell) with 4-Vinylcyclohexene dioxide (VCD). Firstly, KGN cells were treated with different concentrations of VCD, and cell counting kit 8 (CCK-8) was used to detect ovarian cell proliferation. After determining IC 50 by CCK8, the levels of estradiol and progesterone in the cell supernatant were detected using enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) assay kit was used to detect the content of ROS in ovarian cells, real-time fluorescence quantitative polymerase chain reaction (qRT PCR) was used to detect the mRNA expression level of NRF2, and Western blot was used to detect the protein expression level of NRF2. Further, NRF2 silence (siNRF2) and overexpression (NRF2-OE) cell models were constructed through lentivirus transfection, and the effects of regulating NRF2 on VCD treated cell models were investigated by detecting hormone levels, oxidative stress indicators (ROS, SOD, GSH-Px), and autophagy (LC3B level). The results showed that VCD intervention inhibited the proliferation of ovarian granulosa cells in a time-dependent and dose-dependent manner ( F>100, P<0.05), with an IC 50 of 1.2 mmol/L at 24 hours. After VCD treatment, the level of estradiol in the cell supernatant decreased from (56.32±10.18) ng/ml to (24.59±8.75) ng/ml ( t=5.78, P<0.05). Progesterone decreased from (50.25±7.03) ng/ml to (25.13±6.67) ng/ml ( t=6.54, P<0.05). After VCD treatment, the SOD of cells decreased from (44.47±7.71) ng/ml to (30.92±4.97) ng/ml ( t=3.61, P<0.05). GSH-Px decreased from (68.51±10.17) ng/ml to (35.19±6.59) ng/ml ( t=5.73, P<0.05). Simultaneously accompanied by an increase in autophagy and a decrease in NRF2. This study successfully constructed KGN cell models that silenced NRF2 and overexpressed NRF2. Subsequently, this study treated each group of cells with VCD and found that the cell proliferation activity of the siNRF2 group was significantly reduced ( t=8.37, P<0.05), while NRF2-OE could reverse the cell activity damage caused by VCD ( t=3.37, P<0.05). The siNRF2 group had the lowest level of estradiol ( t=5.78, P<0.05), while NRF2-OE could reverse the decrease in cellular estradiol levels caused by VCD ( t=5.58, P<0.05). The siNRF2 group had the lowest progesterone levels ( t=3.02, P<0.05), while NRF2-OE could reverse the decrease in cellular progesterone levels caused by VCD ( t=2.41, P<0.05). The ROS level in the siNRF2 group was the highest ( t=2.86, P<0.05), NRF2-OE could reverse the increase in ROS caused by VCD ( t=3.14, P<0.05), the SOD enzyme content in the siNRF2 group was the lowest ( t=2.98, P<0.05), and NRF2-OE could reverse the decrease in SOD enzyme content caused by VCD ( t=4.72, P<0.05). The GSH-Px enzyme content in the siNRF2 group was the lowest ( t=3.67, P<0.05), and NRF2-OE could reverse the decrease in antioxidant enzyme content caused by VCD ( t=2.71, P<0.05). The LC3B level was highest in the siNRF2 group ( t=2.45, P<0.05), and NRF2-OE was able to reverse the LC3B elevation caused by VCD ( t=9.64, P<0.05). In conclusion, NRF2 inhibits ROS induced autophagy, thereby playing a role in reducing ovarian granulosa cell damage, which may be a potential target for premature ovarian failure.

This study explores the effects and possible mechanisms of nuclear factor E2 related factor 2 (NRF2) on ovarian granulosa cells, providing a scientific basis to prevent premature ovarian failure. An ovarian cell injury model was constructed by treating human ovarian granulosa cell (KGN cell) with 4-Vinylcyclohexene dioxide (VCD). Firstly, KGN cells were treated with different concentrations of VCD, and cell counting kit 8 (CCK-8) was used to detect ovarian cell proliferation. After determining IC 50 by CCK8, the levels of estradiol and progesterone in the cell supernatant were detected using enzyme-linked immunosorbent assay (ELISA), reactive oxygen species (ROS) assay kit was used to detect the content of ROS in ovarian cells, real-time fluorescence quantitative polymerase chain reaction (qRT PCR) was used to detect the mRNA expression level of NRF2, and Western blot was used to detect the protein expression level of NRF2. Further, NRF2 silence (siNRF2) and overexpression (NRF2-OE) cell models were constructed through lentivirus transfection, and the effects of regulating NRF2 on VCD treated cell models were investigated by detecting hormone levels, oxidative stress indicators (ROS, SOD, GSH-Px), and autophagy (LC3B level). The results showed that VCD intervention inhibited the proliferation of ovarian granulosa cells in a time-dependent and dose-dependent manner ( F>100, P<0.05), with an IC 50 of 1.2 mmol/L at 24 hours. After VCD treatment, the level of estradiol in the cell supernatant decreased from (56.32±10.18) ng/ml to (24.59±8.75) ng/ml ( t=5.78, P<0.05). Progesterone decreased from (50.25±7.03) ng/ml to (25.13±6.67) ng/ml ( t=6.54, P<0.05). After VCD treatment, the SOD of cells decreased from (44.47±7.71) ng/ml to (30.92±4.97) ng/ml ( t=3.61, P<0.05). GSH-Px decreased from (68.51±10.17) ng/ml to (35.19±6.59) ng/ml ( t=5.73, P<0.05). Simultaneously accompanied by an increase in autophagy and a decrease in NRF2. This study successfully constructed KGN cell models that silenced NRF2 and overexpressed NRF2. Subsequently, this study treated each group of cells with VCD and found that the cell proliferation activity of the siNRF2 group was significantly reduced ( t=8.37, P<0.05), while NRF2-OE could reverse the cell activity damage caused by VCD ( t=3.37, P<0.05). The siNRF2 group had the lowest level of estradiol ( t=5.78, P<0.05), while NRF2-OE could reverse the decrease in cellular estradiol levels caused by VCD ( t=5.58, P<0.05). The siNRF2 group had the lowest progesterone levels ( t=3.02, P<0.05), while NRF2-OE could reverse the decrease in cellular progesterone levels caused by VCD ( t=2.41, P<0.05). The ROS level in the siNRF2 group was the highest ( t=2.86, P<0.05), NRF2-OE could reverse the increase in ROS caused by VCD ( t=3.14, P<0.05), the SOD enzyme content in the siNRF2 group was the lowest ( t=2.98, P<0.05), and NRF2-OE could reverse the decrease in SOD enzyme content caused by VCD ( t=4.72, P<0.05). The GSH-Px enzyme content in the siNRF2 group was the lowest ( t=3.67, P<0.05), and NRF2-OE could reverse the decrease in antioxidant enzyme content caused by VCD ( t=2.71, P<0.05). The LC3B level was highest in the siNRF2 group ( t=2.45, P<0.05), and NRF2-OE was able to reverse the LC3B elevation caused by VCD ( t=9.64, P<0.05). In conclusion, NRF2 inhibits ROS induced autophagy, thereby playing a role in reducing ovarian granulosa cell damage, which may be a potential target for premature ovarian failure.

Objective:To investigate the risk factors affecting in-hospital mortality in patients with acute mesenteric ischemia (AMI).Methods:From January 1, 2014 to June 30, 2022, the clinical data of 67 patients diagnosed with AMI at Renmin Hospital of Wuhan University were retrospectively analyzed, which included basic data (age, gender, past medical history and comorbidities, etc.), laboratory results (white blood cell count (WBC), alanine aminotransferase (ALT), aspartate aminotransferase (AST), creatinine, prothrombin time (PT), etc.), and imaging manifestations (intestinal pneumatosis, intestinal wall thickening, intestinal dilation, ascites). The clinical data of AMI patients who died during hospitalization were compared with that of AMI patients who survived. Binary logistic regression was used to analyze the independent risk factors of in-hospital mortality in patients with AMI. Mann-Whitney U test and chi-square test were used for statistical analysis. Results:Among the 67 patients with AMI, 17 died and 50 survived. There were significant differences between died and survived patients with AMI in age, the proportion of patients with organ failure, WBC, ALT, AST, creatinine, PT, and the proportion of patients with intestinal dilatation and ascites (76 years old(68 years old, 79 years old) vs. 61 years old (50 years old, 74 years old), 12/17 vs.12.0%(6/50), 15.8×10 9/L(13.5×10 9/L, 23.7×10 9/L) vs. 12.1×10 9/L (9.1×10 9/L, 19.4×10 9/L), 32.0 U/L(19.0 U/L, 88.5 U/L) vs. 20.5 U/L(14.8 U/L, 29.0 U/L), 64.0 U/L(33.8 U/L, 117.0 U/L) vs. 26.0 U/L (18.5 U/L, 36.8 U/L), 135.0 μmol/L(61.5 μmol/L, 198.5 μmol/L) vs. 73.5 μmol/L(60.5 μmol/L, 85.0 μmol/L), 13.7 s(12.9 s, 16.3 s) vs. 12.7 s (11.9 s, 13.6 s), 13/17 vs. 38.0%(19/50), 10/17 vs. 24.0% (12/50); Z=3.06, χ2=22.16, Z=2.01, 2.69, 4.08, 2.45 and 2.78, χ2=7.53 and 6.98; P=0.002, <0.001, =0.044, =0.007, <0.001, =0.014, =0.006, =0.006 and =0.008). The results of binary logistic regression analysis showed that age ( OR=1.224, 95% confidence interval 1.011 to 1.482, P=0.038), organ failure ( OR=113.989, 95% confidence interval 1.353 to 9 604.644, P=0.036), and ascites ( OR=348.289, 95% confidence interval 1.676 to 72 357.934, P=0.032) were independent risk factors of in-hospital mortality in AMI patients. Conclusion:Age, organ failure and ascites are independent risk factors of in-hospital mortality in AMI patients.

Radiation-induced brain injury (RBI) is the most serious complication of head and neck tumor after radiotherapy. The pathogenesis of RBI is complicated, and the clinical course is irreversible, while no effective treatment available. The activation of glial cells is one of the main theories of RBI, and the prevention and treatment of RBI by targeting glial cells is the focus of current research. As a post-transcriptional regulatory factor, microRNA (miRNA) has been confirmed to be involved in regulatingglial cell radiosensitivity, inflammation type transformation, autophagy, exosomatic, long non-coding RNA (lncRNA), circular RNA (circRNA) and other related pathways, thereby mediating the occurrence and development of cascade reaction of inflammatory injury and neurological function repair of central nervous system (CNS) disease. Therefore, the establishment of miRNA - glial regulatory network may provide a new strategy for the prevention and treatment of RBI.

Objective:To investigate the effect of an improved hydro-colloid dressing sticking method on preventing protective equipment induced facial pressure injuries among medical staff through a prospective, single-arm trial.Methods:According to the size of the edge of N95 mask, four pieces of hydro-colloid dressing with a size of 2 cm×5 cm were cut, and the edges of the mask were tension-free stuck. This improved sticking method was applied to the nurses working in the isolation ward. The follow-up was continued for two weeks, skin condition was reported daily, and the occurrence of pressure ulcers was analyzed after two weeks of follow-up.Results:Twenty percent (4/20) of subjects experienced increase grades of nasal and twenty five percent (5/20) in cheek pressure ulcers during a two-week follow-up. The incidence of the increased stage of cheek pressure ulcer in normal/dry skin was higher than in oily skin. Stage 2 pressure ulcers occurred in only five percent (1/20) of subjects, and no subjects had stage 3 or higher stage pressure ulcers. The incidence of increased cheek pressure ulcer grade in patients with neutral / dry skin was (5/11), higher than 0 in patients with oily skin ( χ2 value was 5.378, P = 0.02). The stage of nasal pressure ulcer was positively correlated with the disappearance time of the indentation of protective equipment ( r value was 0.615, P=0.004). The rate of increase in nasal pressure sore grade was higher in subjects who required more than 120 minutes of indentation recovery time (2/8) than in subjects who required 30 to 60 minutes 1/5 ( χ2 value was 4.382, P<0.05) and 60-120 minutes 1/5 ( χ2 value was 6.472, P<0.05). Conclusions:This improved hydro-colloid dressing sticking method can effectively prevent pressure injuries related to wearing N95 masks for a long time. However, skin evaluation of medical staff should be done properly, moisture protection for normal/dry skin should be emphasized, and skin blood flow recovery after compression should be strengthened. This method can reduce the risk of infection of medical staff, and it is worthy of clinical application.