Investigator initiated trial （IIT） represents a primary format for clinical research in traditional Chinese medicine （TCM）. As key implementation sites for TCM-based IIT targeting malignant tumors， western medicine institutions often face unique challenges in conducting such studies， which limit their feasibility and standardization. This paper reviews the registration status of TCM-based IIT for malignancies conducted in western medical institutions and analyzes key difficulties， including complex project initiation and management processes， limited TCM knowledge and skills among western medicine physicians， and relatively low patient acceptance of TCM. From a practical perspective， the study proposes several optimization strategies. These include improving the review and management mechanisms of TCM-related IIT within western medical institutions， establishing multidisciplinary clinical research teams that integrate TCM and western medicine， and enhancing investigators' training in TCM theory and clinical skills. Additionally， the study suggests standardizing IIT operational procedures， objectifying the collection of TCM diagnostic information， refining subject recruitment methods， and increasing TCM involvement in patient follow-up and management. These investigator-oriented， TCM-featured， and operable strategies aim to promote the high-quality development of TCM-based IIT in western medicine institutions and enhance the clinical application of TCM.

Objective To quantitatively assess the association of short-term exposure to polycyclic aromatic hydrocarbons (PAHs) in ambient fine particulate matter (PM2.5) with residents mortality. Methods A time-stratified case-crossover study was conducted from 2020 to 2022 among 10606 non-accidental residents by using the Guangzhou Cause of Death Surveillance System in Conghua District, Guangzhou. Exposure levels of PAHs in PM_2.5 and meteorological data during the study period were obtained from the Center for Disease Control and Prevention in Conghua District and the China Meteorological Administration Land Data Assimilation System (CLDAS-V2.0), respectively. Conditional Poisson regression model was used to estimate the exposure-response association between PAHs and the mortality risk. Results Fluoranthene, chrysene, benzo[k]fluoranthene, benzo[a]pyrene, and indeno[1,2,3-cd]pyrene were significantly associated with an increased risk of mortality. For every one interquartile range increase in exposure levels, the non-accidental mortality risks increased by 8.33% (95% CI: 1.80%, 15.27%), 4.67% (95% CI: 1.86%, 7.57%), 6.07% (95% CI: 2.08%, 10.21%), 4.62% (95% CI: 1.85%, 7.47%), and 4.70% (95% CI: 0.53%, 9.03%), respectively. The estimated non accidental deaths attributable to exposure to fluoranthene, chrysene, benzo[k]fluorine, benzo[a]pyrene and indine[1,2,3-cd]pyrene were 5.91%, 6.08%, 6.51%, 6.46%, and 4.21%, respectively. Conclusions Short-term exposure to PAHs in PM_2.5, including fluoranthene, chrysene, benzo[k]fluoranthene, benzo[a]pyrene and indine[1,2,3-cd]pyrene, was significantly associated with an increased risk of mortality among residents.

Background Exposure to air pollutants increases the risk of diseases in multiple systems, including respiratory and cardiovascular systems, yet its association with neurological diseases remains unclear. Objective To quantitatively evaluate the association between short-term exposure to air pollutants and outpatient and emergency visits for neurological diseases, identify potential susceptible populations, and quantify associated disease burden. Methods Daily 24-hour average concentrations of fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and carbon monoxide (CO), daily maximum 8-hour average concentration of ozone (O₃), daily meteorological data (24-hour average temperature, 24-hour average relative humidity), and data on daily outpatient and emergency department visits for neurological diseases from two hospitals in Conghua District, Guangzhou, China, were collected from 2015 to 2022. A time-stratified case-crossover design was adopted, and a conditional Poisson regression model was constructed to analyze the association between air pollution exposure and neurological disease visits. Two-pollutant models and sensitivity analysis were used to validate model stability. Stratified analyses by season (cold season: from November to March; warm season: from April to October), sex (male, female), and age (≤45 years, 46–60 years, ≥61 years) were performed to identify vulnerable group. Additionally, the number and proportion of neurological disease visits attributable to short-term air pollutant exposure were calculated. Results A total of 72 673 outpatient and emergency department visits for neurological diseases were included during the study period. Most of the patients were middle-aged and elderly individuals (69.89% were over 45 years old) and females (60.25%). The results of single-pollutant models showed that for each interquartile range (IQR) increase in exposure to PM_2.5, PM₁₀, SO₂, NO₂, CO, and O₃, the risk of outpatient and emergency department visits for neurological diseases increased by 7.54% (95%CI: 4.69%, 10.46%), 6.66% (95%CI: 3.92%, 9.46%), 16.72% (95%CI: 10.58%, 23.19%), 8.12% (95%CI: 4.82%, 11.53%), 5.60% (95%CI: 2.34%, 8.97%), and 6.11% (95%CI: 2.91%, 9.40%), respectively. The results of the two-pollutant model showed that the association between PM_2.5 and SO₂ exposure and outpatient and emergency department visits for neurological diseases were relatively stable. The stratified analyses showed that the effect of SO₂ was stronger in the cold season. It was estimated that 8.32% (95%CI: 5.55%, 10.96%) and 6.65% (95%CI: 4.27%, 8.96%) of the outpatient and emergency department visits were attributable to short-term exposure to SO₂ and PM_2.5, respectively. Conclusion Exposure to PM_2.5 and SO₂ is associated with increased risks of outpatient and emergency visits for neurological diseases. SO₂ shows stronger effects during the cold season, and exposure to air pollution contributes to up to 8.32% of neurological disease visits.

【Objective】 To explore the effectiveness of intraovarian injection of platelet-rich plasma(PRP) in the treatment of patients with diminished ovarian reserve(DOR), aiming to provide new diagnostic and therapeutic ideas for the treatment. 【Methods】 A total of 22 patients with DOR who underwent autologous PRP ovarian injection at the Reproductive Medical and Genetic Center of Qinzhou Maternal and Child Health Hospital from January 2021 to December 2023 were collected. Among them, 12 patients underwent assisted reproductive technology for pregnancy. The patient′s anti-Müllerian hormone (AMH), antral follicle count (AFC), basal follicle-stimulating hormone (FSH), basal luteinizing hormone (LH) and basal estradiol (E2) levels were observed. 【Results】 The levels of AMH, AFC, basal FSH, basal LH and basal E2 in 22 patients improved after treatment compared with those before treatment. Of the 12 patients who received assisted reproduction, 2 had IVF cycle canceled due to poor ovarian reaction. Ten patients obtained embryos, of which 5 obtained high-quality embryos. 【Conclusion】 Intraovarian injection of autologous PRP can effectively improve ovarian reserve function in patients with DOR.

【Objective】 To evaluate the quality of laboratory testing using anti-HIV ELISA quality monitoring indicators and continuously improve laboratory testing capabilities. 【Methods】 The data of our blood testing laboratory from July 1, 2020 to December 31, 2022 using laboratory quality monitoring indicators were analyzed, including the reaction sample size and reaction rate of initial test and the reaction sample size and compliance rate of retest. The indoor quality control data of two anti HIV ELISA reagents (Xinchuang and Wantai) during the above time period were collected. A line chart or scatter box chart was drawn to monitor the long-term trends and identify the reasons. Inter-laboratory capability comparison and evaluation with the data from the quality monitoring index evaluation report of the National Health Commission′s Clinical Inspection Center and the National Blood Station Blood Testing Laboratory during the same period was conducted. 【Results】 From July 1, 2020 to December 31, 2022, the initial reaction rates of Xinchuang and Wantai anti HIV ELISA reagents were 0.052% and 0.080%, respectively (P<0.05), and the retest compliance rates were 43.97% and 73.39%, respectively (P<0.001). The linear mean trend of the retest compliance rate of innovative reagents is close to the national average retest compliance rate of the same group, while the retest compliance rate of Wantai reagents is higher than the national average retest compliance rate of the same group reagents. The usage rates of the two reagents are lower than the national average for the same group of reagents. The average dispersion of indoor quality control values between different batches of innovative reagents is greater than that of Wantai reagents, but the dispersion of indoor quality control CV between different batches of reagents is similar. 【Conclusion】 Longitudinal analysis of long-term testing data in our laboratory through laboratory quality monitoring indicators and horizontal comparison of laboratories with the same reagents nationwide are able to promptly identify problems in the laboratory, therefore help correct the problems and continuously improve the laboratory′s quality management system, further enhancing the laboratory′s testing capabilities.

The Wnt signaling pathway plays an important role in maintaining liver homeostasis and liver regeneration.In healthy livers,the Wnt signaling pathway is mostly inactive,but it is continuously overactivated during cell renewal or regeneration processes,as well as in certain pathological conditions,diseases,precancerous states,and cancers.Persistent liver cell injury often leads to chronic liver diseases such as liver fibrosis,liver cirrhosis,and liver cancer.This article summarizes the basic structural features of the Wnt signaling pathway and analyzes its important role in the pathological progression of various liver diseases,so as to provide new ideas for the prevention and treatment of liver diseases in clinical practice.

Objective To investigate the effects of α7 nicotinic acetylcholine receptor (α7nAChR) on CD11b, IL-1β, IL-18 and TNF-α in acute respiratory distress syndrome (ARDS) mice. Methods A total of 40 healthy and clean male Balb/C mice (6 weeks old) were randomly divided into normal group (N group), normal saline control group (NS group), ARDS group (A group), and ARDS mice treated with nicotinic acetylcholine receptor agonist after bilateral cervical vagotomy group (J group), with 10 mice in each group. The right lung structure of mice in each group was observed by hematoxylin-eosin (HE) staining, the lung tissue wet weight/body weight ratio (LWW/DW ratio) was detected, and the percentage of CD11b in the alveolar lavage fluid of mice was detected by flow cytometry. Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of IL-1β mRNA, IL-18 mRNA and TNF-α mRNA in left lung tissue. Serum IL-18 was determined by enzyme-linked immunosorbent assay (ELISA) and double antibody sandwich method. Results HE staining of the right lung of mice in group N and NS showed normal structure, while the lung interstitial of mice in group A showed a large number of inflammatory cells infiltrated, alveolar wall thickened, alveolar structure destroyed and alveolar cavity fused. The alveolar structure of mice in group J was intact, with a little damage and alveolar cavity. The percentage of CD11b in alveolar lavage fluid in group A was higher than that in the other three groups, and the difference was statistically significant compared with group N, NS and J, respectively (P<0.05). The expressions of IL-1β mRNA, IL-18 mRNA and TNF-α mRNA in the left lung of mice in group J were statistically significant compared with those in group N, NS and A (P<0.05), and the serum IL-18 level of mice in group A was higher than that in the other three groups, and the differences were statistically significant compared with groups N, NS and J, respectively (P<0.05). Conclusions Activation of α7nAChR can directly inhibit the release of CD11b in lung tissue and reduce the accumulation of inflammatory factors. Simultaneously, it can also directly inhibit the expression of IL-β1 mRNA, IL-18 mRNA and TNF-α mRNA in lung tissue and the release of IL-18, thus inhibiting the inflammatory response of ARDS and alleviating the pathological changes of ARDS.

ObjectiveTo explore the mechanism of Jiawei Wendantang in preventing and treating diabetic atherosclerosis by observing the effect of this prescription on the nuclear factor-κB / NOD-like receptor protein 3（NF-κB/NLRP3） pathway and related inflammatory cytokines in rat model of diabetic atherosclerosis. MethodFifty-four SPF-grade rats were randomized into blank， model， atorvastatin （0.9 mg·kg^-1·d^-1）， and high-， medium-， low-dose （18.2， 9.1， 4.55 g·kg^-1·d^-1， respectively） Jiawei Wendantang groups. The rats in other groups except the blank group were modeled for diabetic atherosclerosis by intraperitoneal injection of streptozotocin and feeding with a high-sugar high-fat diet， and those in the blank group were injected with an equal dose of citric acid buffer and fed with a regular diet. The drug administration lasted for 4 weeks， and the blood glucose level in the tail vein was measured every 6 days. After the last administration， the rats were anesthetized for sample collection. Enzyme-linked immunosorbent assay was employed to measure the serum levels of interleukin-18 （IL-18）， C-reactive protein （CRP）， tumor necrosis factor-α （TNF-α）， and intercellular adhesion molecule-1 （ICAM-1）. Western blot was employed to determine the relative protein levels of NF-κB p65， NLRP3， and ICAM-1 in the abdominal aorta. Real-time quantitative polymerase chain reaction was employed to determine the mRNA levels of NLRP3 and interleukin-1β （IL-1β） in the abdominal aorta. The pathological changes in the thoracic aorta were observed by hematoxylin-eosin staining. ResultCompared with the blank group， the model group showed elevated levels of IL-18， CRP， TNF-α， and ICAM-1 in the serum and blood glucose （P<0.05， P<0.01）， up-regulated protein levels of NF-κB p65， NLRP3， and ICAM-1 （P<0.01）， and up-regulated mRNA levels of NLRP3 and IL-1β （P<0.05）. Compared with model group， Jiawei Wendantang lowered the levels of IL-18， CRP， TNF-α， ICAM-1 and blood glucose （P<0.05， P<0.01）， down-regulated the protein levels of NF-κB p65， NLRP3， and ICAM-1 （P<0.01）， and down-regulated the mRNA levels of NLRP3 and IL-1β （P<0.05， P<0.01）. Moreover， Jiawei Wendantang alleviated the pathological injuries in the thoracic aorta. ConclusionJiawei Wendantang may modulate the NF-κB/NLRP3 signaling pathway to reduce the release and adhesion of inflammatory cytokines and regulate the blood glucose level to treat diabetic atherosclerosis.

Objective To investigate the changes in the levels of serum high-sensitivity C-reactive protein(hs-CRP)and soluble fms-like tyrosine kinase-1(sFlt-1)in hypertensive disorder of pregnancy(HDP)patients with fetal growth restriction(FGR),and to evaluate their predictive value for FGR.Methods A total of 137 HDP patients admitted to the Obstetrics De-partment of Ganzhou Maternal and Child Health Hospital from December 2021 to May 2023 were selected as the study subjects.According to whether their fetuses had growth restriction,they were divided into the restricted group(n=46)and the non-re-stricted group(n=91).The general information and serum levels of hs-CRP and sFlt-1 were collected and analyzed.Multiple lo-gistic regression analysis was used to identify the influencing factors for fetal growth restriction in HDP patients,and receiver oper-ating characteristic(ROC)curve was plotted to evaluate the predictive value of serum hs-CRP and sFlt-1 levels for fetal growth restriction in HDP patients.Results Univariate analysis showed that the serum levels of folic acid(FA),vitamin B12(VitB12),and placental growth factor(PIGF)in the restricted group were lower than those in the non-restricted group,while the serum lev-els of hs-CRP and sFlt-1 were higher than those in the non-restricted group,with statistically significant differences(P＜0.05).Multivariate analysis showed that serum hs-CRP,sFlt-1,and PIGF levels were independent risk factors for fetal growth restriction in HDP patients.The H-L test of the model showedx2=7.014,P=0.535,indicating a good fit.The area under the ROC curve(AUC)was 0.932,with a 95％CI of 0.889-0.975(P＜0.05),a sensitivity of 93.50％,and a specificity of 89.00％.Conclusion Serum hs-CRP and sFlt-1 levels are upregulated in HDP patients with fetal growth restriction,indicating their good predictive value for the occurrence of fetal growth restriction.

Arsenic, as a toxic substance that can affect human health, can cause various neurological disorders, including cognitive impairment, when excessive. Relevant epidemiological surveys and animal experimental studies have shown that exposure to arsenic can not only cause intellectual impairment and peripheral neuropathy in humans, but also lead to abnormal behavior in humans and animals. However, so far, the mechanism of arsenic induced damage to the nervous system is still unclear. Peroxisome proliferator activated receptor γ auxiliary activation factor 1α (PGC-1α), as a nuclear transcription coactivator, can interact with transcription factors or other coactivators and plays a role in biological processes such as mitochondrial biogenesis and energy metabolism. PGC-1α, by activating mitochondrial biogenesis, affecting energy metabolism, activating oxidative stress regulatory factors [catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), etc.], mitigates the damage to the central nervous system (CNS), peripheral nervous system (PNS), and blood-brain barrier (BBB) caused by arsenic. This article summarize the research progress of arsenic-induced neurological injury and the mechanism of PGC-1α's role in arsenic-induced neurological injury to provide a theoretical basis for further prevention and treatment of neurological diseases caused by arsenic.