Objective: To compare the predictive performance of the seasonal autoregressive integrated moving average (SARIMA) model, the Prophet model, and the Bayesian structural time series (BSTS) model in forecasting the incidence of hand, foot, and mouth disease (HFMD) , so as to provide a basis for optimizing the early warning system of this disease. Methods: Weekly incidence data of HFMD in Longgang District, Shenzhen City from 2014 to 2024 were collected. The HFMD incidence data from 2014-2019 and 2023 were used as the training set to construct SARIMA, Prophet, and BSTS models, while the data from 2024 were used as the test set to compare and evaluate the predictive performance of the three models. The technique for order preference by similarity to ideal solution (TOPSIS) method was employed to calculate the C-value. This approach integrates multiple evaluation metrics, such as the mean absolute error (MAE), mean squared error (MSE), root mean squared error (RMSE), and symmetric mean absolute percentage error (SMAPE), to comprehensively assess model performance. Results: A total of 150 111 cases of HFMD were reported in Longgang District from 2014 to 2024, with an average annual incidence of 400.72/105. The weekly incidence fluctuated between 0 and 63.78/105, exhibiting a bimodal seasonal pattern characterized by a primary peak from May to July and a secondary peak from September to October. In the training set, all three models demonstrated a good fit to the bimodal epidemic trend of HFMD, with the BSTS model achieving the best fit. The BSTS model yielded performance metrics as follows: MAE=0.124, MSE=0.050, RMSE=0.223, SMAPE=0.021, and a C-value of 1.000. In the test set, all three models, including SARIMA, Prophet, and BSTS, performed well for short-term predictions (≤16 weeks), with the Prophet model showing relatively superior predictive performance. However, the prediction accuracy of all models declined as the forecast horizon extended. During the primary peak period (May-July), the Prophet model exhibited better predictive performance, whereas the BSTS model performed relatively better during the secondary peak period (September-October). Conclusions For the short-term forecasting of weekly HFMD incidence, the Prophet model outperformed both the SARIMA and BSTS models. During the primary peak period, the Prophet model demonstrated superior predictive performance, whereas the BSTS model exhibited better accuracy in forecasting the secondary peak period.

Doxorubicin (DOX)-induced cardiotoxicity and sepsis-induced myocardial injury (SIMI) represent significant clinical challenges in patients undergoing chemotherapy, sharing a common pathological basis of oxidative stress and mitochondrial dysfunction. Ferroptosis, an iron-dependent form of regulated cell death driven by lipid peroxidation, has recently been shown to play a critical role in DOX-induced cardiotoxicity and lipopolysaccharide (LPS)-induced SIMI. This article systematically reviews the mechanisms underlying myocardial injury caused by DOX and sepsis, identifying ferroptosis as a central common pathway. DOX triggers a burst of reactive oxygen species within mitochondria and inhibits glutathione peroxidase 4 (GPX4) activity through redox cycling of its quinone group and high-affinity accumulation in mitochondrial cardiolipin. LPS, by activating pattern recognition receptors and related inflammatory signaling pathways, provokes a cytokine storm and mitochondrial dysfunction. Both can disrupt the core regulatory axis of cysteine-glutathione (GSH)-GPX4, synergistically promoting ferroptosis in cardiomyocytes. Moreover, epigenetic regulation plays a key role in DOX- and LPS-induced cardiomyocyte ferroptosis and may serve as a promising therapeutic target. A deeper understanding of the ferroptosis mechanism and its epigenetic regulatory network in the synergistic injury induced by DOX and sepsis is of great importance for developing novel strategies to mitigate chemotherapy-related cardiotoxicity and improve outcomes in cancer patients with concurrent infections.

To develop and validate a model for predicting intensive care unit (ICU) mortality risk in patients with malignant tumors complicated by acute respiratory failure (ARF) based on an explainable machine learning framework.

ObjectiveTo investigate whether Shixiaosan can improve neurological function and inhibit ferroptosis in rats with cerebral ischemia-reperfusion injury （CIRI） by regulating the nuclear factor E₂-related factor 2 （Nrf2）/solute carrier family 7 member 11 （SLC7A11）/glutathione peroxidase 4 （GPX4） pathway. MethodsA rat model of CIRI was established using the intraluminal filament method. Briefly， cervical blood vessels were separated， branches of the external carotid artery were ligated， and the common carotid artery and internal carotid artery were clamped. A nylon filament was inserted through the opening of the external carotid artery to the origin of the middle cerebral artery to block blood flow and induce cerebral ischemia. After 60-120 min of ischemia， the filament was withdrawn to restore blood flow， and the external carotid artery incision was ligated. The rats were divided into a CIRI group， a Shixiaosan low-dose （-L） group （intragastric administration of 1.26 g·kg^-1 Shixiaosan）， a Shixiaosan high-dose （-H） group （intragastric administration of 2.52 g·kg^-1 Shixiaosan）， a donepezil hydrochloride tablet （DON） group （intragastric administration of 0.45 mg·kg^-1 DON）， and a Shixiaosan -H + Nrf2 inhibitor （ML385） group （intragastric administration of 2.52 g·kg^-1 Shixiaosan combined with intraperitoneal injection of 30 mg·kg^-1 ML385）. An additional 12 rats underwent cervical artery separation followed by incision suturing and served as the control group. Equal volumes of double-distilled water were administered to the CIRI and control groups. Neurological function impairment was assessed using the modified Garcia JH score. Magnetic resonance imaging was used to determine the cerebral infarct volume ratio. Hematoxylin-eosin （HE） staining and Prussian blue staining were performed to observe neuronal injury and iron accumulation in the ischemic penumbra， respectively. Transmission electron microscopy was used to examine the ultrastructure of neuronal mitochondria in the ischemic penumbra. Commercial kits were used to measure ferrous iron （Fe²⁺）， malondialdehyde （MDA）， reduced glutathione （GSH） content， and reactive oxygen species （ROS） activity in the ischemic penumbra. The BODIPY （581/591） C11 fluorescent probe was used to detect intracellular lipid peroxidation levels. Western blot was performed to detect protein expression levels of Nrf2， SLC7A11， GPX4， transferrin receptor 1 （TFRC）， ferritin heavy chain （FHC）， and ferritin light chain （FLC） in the ischemic penumbra. ResultsCompared with the control group， the CIRI group exhibited neuronal injury in the ischemic penumbra， characterized by reduced neuron numbers， nucleolar shrinkage， and interstitial edema. Marked iron accumulation was observed in the tissue. Neuronal mitochondria showed atrophy and rupture， with reduced mitochondrial cristae and increased membrane density. The cerebral infarct volume ratio， Fe²⁺ content， MDA content， ROS activity， and lipid peroxidation levels were increased， whereas the modified Garcia JH score， GSH content， and protein expression levels of Nrf2， SLC7A11， GPX4， FHC， and FLC were decreased， and TFRC protein expression was increased （P<0.05）. Compared with the CIRI group， the Shixiaosan -L group， Shixiaosan -H group， and DON group showed attenuated neuronal injury in the ischemic penumbra， reduced iron accumulation， alleviated mitochondrial damage， decreased cerebral infarct volume ratio， Fe²⁺ and MDA contents， ROS activity， and lipid peroxidation levels， as well as increased modified Garcia JH scores， GSH content， and protein expression levels of Nrf2， SLC7A11， GPX4， FHC， and FLC， while TFRC protein expression was decreased （P<0.05）. The magnitude of changes in all indicators was greater in the Shixiaosan -H group than in the Shixiaosan -L group （P<0.05）. Compared with the Shixiaosan -H group， all measured indicators in the Shixiaosan -H + ML385 group showed opposite trends （P<0.05）. ConclusionShixiaosan may inhibit ferroptosis and restore neurological function in rats with CIRI by activating the Nrf2/SLC7A11/GPX4 pathway.

Objective: To analyze the one year follow up changes and influencing factors of anisometropia among primary school students in Beihai, so as to provide data support for formulating targeted prevention and control strategies. Methods: In 2023 and 2024, visual acuity and refractive screening were conducted on primary school students in Beihai. A cohort matching method was used based on unique identifiers to link data from 2023 (baseline) Grades one to five with those from 2024 (follow up) Grades two to six, obtaining a total of 59 743 complete datasets. McNemar test and generalized estimating equations(GEE) model were employed to analyze the changing patterns of anisometropia. Results: The detection rate of anisometropia among primary school students in Beihai increased from 10.88% in 2023 to 12.30% in 2024 ( χ 2=97.12, P <0.01). Among them, the detection rate in Grade 1 decreased from 8.82% in 2023 to 7.50% in 2024, Grade 3 increased from 10.15% to 11.52%, Grade 4 increased from 12.10 % to 15.22%, Grade 5 increased from 14.61% to 17.88% ( χ 2=16.51,18.03,95.52,95.95,all P <0.05). The GEE results showed that the risk of anisometropia development was higher in girls than in boys ( OR =1.15), the risk of anisometropia increased by 16% with each 1 year increment in age ( OR =1.16) among primary school students, the risk of anisometropia development in Grade 5 was 2.20 times higher than that in Grade 1 ( OR =2.20)(all P <0.05). In lower grades, only the baseline anisometropia status in lower grades had a statistically significant effect on anisometropia among primary school students( OR =59.09), while the positive effects of gender and age difference gradually emerged and strengthened in middle and higher grades (all P ＜0.05). Conclusions The detection rate of anisometropia among primary school students in Beihai shows dynamic changes and influencing factors vary by grade level. It is necessary to develop stratified prevention and control strategies tailored to different grades.

Objective: To analyze characteristics of hepatitis B infection in HBsAg-/HBV DNA+ blood donors in Taiyuan, so as to provide evidence for adjusting blood screening strategies. Methods: Blood samples of HBsAg-/HBV DNA+ donors were tested using enzyme-linked immunosorbent assay (ELISA), chemiluminescence assay, nucleic acid qualitative test, and nucleic acid quantitative test. Data on HBsAg-/HBV DNA+ donors in Taiyuan region from January 1, 2016 to December 31, 2024 were statistically analyzed to evaluate the detection rate, demographic characteristics, influencing factors of detection rate, nucleic acid quantitative results, and serological patterns of HBsAg-/HBV DNA+ donors. Results: From January 1, 2016 to December 31, 2024, 991 565 donor samples underwent nucleic acid testing in Taiyuan. A total of 309 HBsAg-/HBV DNA+ samples were detected, resulting in an HBsAg-/HBV DNA+ detection rate of 3.12 per 10 000. The detection rate varied significantly across different years (P<0.05). Males had a significantly higher HBsAg-/HBV DNA+ detection rate than females, first-time donors had a higher rate than repeat donors, and whole blood donors had a higher rate than apheresis donors (P<0.05). The detection rate also differed significantly among age groups (P<0.05). Logistic regression analysis showed that gender, age, donation frequency, and donation type were all influencing factors for HBsAg-/HBV DNA+ detection (all P<0.05). The predominant serological patterns among HBsAg-/HBV DNA+ donors were HBsAb+/HBcAb+ (43.69%, 135/309) or HBcAb+ alone (24.27%, 75/309). Viral load was detectable in 53.40% (165/309) of the HBsAg-/HBV DNA+ donors. Among these, 61.21% (101/165) donors had a viral load<20 IU/mL, and 94.55% (156/165) had a viral load<200 IU/mL. Donors with viral load<200 IU/mL primarily exhibited HBsAb+/HBcAb+ (41.67%, 65/156) or HBcAb+alone (36.54%, 57/156) serological patterns. Conclusion: The prevalence of HBsAg-/HBV DNA+ is low among blood donors in Taiyuan. Higher detection rates were observed in the 46-55 years age group, males, first-time donors, and whole blood donors. HBsAg-/HBV DNA+ donors exhibit specific serological patterns and generally have low viral loads, indicating a potential residual transfusion risk. It is recommended to add HBcAb testing, together with high-sensitivity nucleic acid testing technologies and donor follow-up, to ensure blood safety and guide donor reentry.

Gastric variceal rupture and bleeding and hepatic encephalopathy are common and life-threatening complications in decompensated cirrhosis. As a minimally invasive interventional technique， balloon-occluded retrograde transvenous obliteration （BRTO） has made significant progress in the clinical management of gastric varices and hepatic encephalopathy in recent years. This article systematically reviews the technical principles， indications （e.g.， isolated gastric varices and refractory hepatic encephalopathy）， clinical efficacy （an acute hemostasis rate of 85% — 95%， a 1-year rebleeding rate of <15%， and an improvement rate of 60% — 80% for hepatic encephalopathy）， and safety （including complications such as renal impairment and elevated portal vein pressure） of BRTO. Meanwhile， this article discusses the advantages and disadvantages of BRTO and conventional treatment modalities （e.g.， transjugular intrahepatic portosystemic shunt and endoscopic treatment） and reviews the latest technological improvements in recent years， such as coil-assisted retrograde transvenous obliteration and plug-assisted retrograde transvenous obliteration. Future research should focus on the precision of patient selection （e.g.， stratification based on hemodynamic parameters）， the optimization of embolic materials （e.g.， application of new biodegradable embolic agents）， and the development of individualized treatment regimens， so as to improve efficacy and reduce the risk of complications.

High myopia has become a major public health concern worldwide, particularly in China and Southeast Asia. It is associated not only with a variety of fundus diseases but also with earlier onset and greater severity of cataracts, resulting in significant visual impairment. Phacoemulsification is currently the main surgical treatment for cataracts. However, intraoperative fluctuations in perfusion pressure and exposure to ultrasonic energy may affect the vitreoretinal structures, potentially accelerating the progression of fundus pathology after surgery in highly myopic eyes. This article summarizes current evidence on the progression of posterior scleral staphyloma, myopic maculopathy, and retinal detachment following phacoemulsification in highly myopic eyes.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.

Diabetic kidney disease （DKD） is one of the more common chronic kidney diseases，and its causes are complex. DKD is very easy to progress to end-stage renal disease，and the current therapeutic effect still needs to be improved. As an important excretive organ of the human body， the kidney has physiological functions such as discharging metabolic waste， regulating fluid balance， and maintaining the stability of the body's internal environment. These highly complex biochemical processes all depend on the energy support provided by mitochondria. Mitochondrial dysfunction is a key factor causing kidney injury， and the imbalance of mitochondrial homeostasis is an important link leading to mitochondrial dysfunction. The occurrence and development of DKD are often accompanied by the imbalance of mitochondrial homeostasis in renal cells. Mitochondrial autophagy， as a means of regulating mitochondrial homeostasis， is very important for the prevention and treatment of DKD. The PTEN-induced putative kinase 1 （PINK1）/Parkin pathway is one of the most classical pathways to regulate mitochondrial autophagy. Recent studies have found that some drugs can regulate the PINK1/Parkin signaling pathway to target mitochondrial homeostasis and exert renoprotective effects. In particular， traditional Chinese medicine has a significant effect on early and middle stage DKD by regulating PINK1/Parkin pathway-mediated mitochondrial autophagy. This article discussed the mechanism of PINK1/Parkin pathway in mitochondrial autophagy and DKD and reviewed the effect of PINK1/Parkin pathway-mediated mitochondrial autophagy on DKD. At the same time， it explored the therapeutic effect of traditional Chinese and western medicine on DKD mediated by PINK1/Parkin-mediated mitochondrial autophagy， aiming to broaden the ideas of traditional Chinese and western medicine for the prevention and treatment of DKD from the perspective of PINK1/Parkin regulating mitochondrial autophagy.