ObjectiveTo explore the mechanism by which Xianglian Huazhuo prescription ameliorates chronic atrophic gastritis （CAG） through regulating the Golgi protein 73 （GP73）/protein kinase R-like endoplasmic reticulum kinase （PERK）/activating transcription factor 4 （ATF4） signaling pathway and modulating endoplasmic reticulum stress （ERS）. MethodA mouse model of CAG was induced by multiple factors， including ranitidine， N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， and irregular feeding. The CAG mice were randomized into five groups： model， Morodan （2.0 g·kg^-1）， and high-dose， medium-dose， and low-dose （7.6， 3.8， 1.9 g·kg^-1， respectively） Xianglian Huazhuo prescription， with 10 mice in each group. At the same time， 10 mice in normal group were set up. The mice in the Morodan group and the high-dose， medium-dose， and low-dose groups of Xianglian Huazhuo prescription were administrated with corresponding agents by gavage， and those in the normal group and the model group were administrated with an equal volume of normal saline. All the mice were intervened once a day for 60 consecutive days. After the last administration， the overall morphological changes of the gastric tissue were observed. Hematoxylin-eosin （HE） staining and transmission electron microscopy （TEM） were used to evaluate the pathological morphology and the endoplasmic reticulum ultrastructure in the gastric tissue. The serum levels of pepsinogen Ⅰ （PGⅠ）， pepsinogen Ⅱ （PGⅡ）， gastrin-17 （G-17）， and GP73 were determined by enzyme-linked immunosorbent assay （ELISA）. The pepsinogen ratio （PGR， PGⅠ/PGⅡ） was calculated. The protein levels of GP73， PERK， phosphorylated （p）-PERK， glucose-regulated protein 78 （GRP78）， ATF4， CCAAT enhancer-binding protein homologous protein （CHOP）， cysteinyl aspartate-specific protease-12 （Caspase-12）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were assessed by Western blot. The expression of GRP78 was detected by immunofluorescence （IF） assay， and the location of Bcl-2 and Bax by immunohistochemistry （IHC）. ResultsCompared with the normal group， the model group showed pale gastric mucosa with flattened folds and reduced and loosely arranged gastric mucosal glands， declined serum levels of PGI， PGR， G-17， and GP73 （P<0.01）. downregulated protein levels of GP73， p-PERK， ATF4， GRP78， CHOP， Caspase-12， and Bax in the gastric tissue， and upregulated protein level of Bcl-2 （P<0.01）. Compared with the model group， the Morodan group and each Xianglian Huazhuo prescription group exhibited red gastric mucosa with increased folds， alleviated pathological damage， swelling endoplasmic reticulum， elevated serum levels of PGI， G-17， and GP73 （P<0.05， P<0.01）， and upregulated protein levels of Caspase-12 and Bax and downregulated protein level of Bcl-2 in the gastric tissue （P<0.05， P<0.01）. The Morodan group and the high-dose and medium-dose Xianglian Huazhuo prescription groups exhibited increased serum level of PGR （P<0.05， P<0.01） and upregulated protein levels of GP73， p-PERK， ATF4， GRP78， and CHOP in the gastric tissue （P<0.05， P<0.01）. ConclusionXianglian Huazhuo prescription can activate the GP73/PERK/ATF4 signaling pathway and induce ERS-mediated apoptosis to alleviate the pathological damage of the gastric mucosa， thereby demonstrating a protective effect against CAG in mice.

ObjectiveTo explore the mechanism by which Xianglian Huazhuo prescription ameliorates chronic atrophic gastritis （CAG） through regulating the Golgi protein 73 （GP73）/protein kinase R-like endoplasmic reticulum kinase （PERK）/activating transcription factor 4 （ATF4） signaling pathway and modulating endoplasmic reticulum stress （ERS）. MethodA mouse model of CAG was induced by multiple factors， including ranitidine， N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， and irregular feeding. The CAG mice were randomized into five groups： model， Morodan （2.0 g·kg^-1）， and high-dose， medium-dose， and low-dose （7.6， 3.8， 1.9 g·kg^-1， respectively） Xianglian Huazhuo prescription， with 10 mice in each group. At the same time， 10 mice in normal group were set up. The mice in the Morodan group and the high-dose， medium-dose， and low-dose groups of Xianglian Huazhuo prescription were administrated with corresponding agents by gavage， and those in the normal group and the model group were administrated with an equal volume of normal saline. All the mice were intervened once a day for 60 consecutive days. After the last administration， the overall morphological changes of the gastric tissue were observed. Hematoxylin-eosin （HE） staining and transmission electron microscopy （TEM） were used to evaluate the pathological morphology and the endoplasmic reticulum ultrastructure in the gastric tissue. The serum levels of pepsinogen Ⅰ （PGⅠ）， pepsinogen Ⅱ （PGⅡ）， gastrin-17 （G-17）， and GP73 were determined by enzyme-linked immunosorbent assay （ELISA）. The pepsinogen ratio （PGR， PGⅠ/PGⅡ） was calculated. The protein levels of GP73， PERK， phosphorylated （p）-PERK， glucose-regulated protein 78 （GRP78）， ATF4， CCAAT enhancer-binding protein homologous protein （CHOP）， cysteinyl aspartate-specific protease-12 （Caspase-12）， B-cell lymphoma-2 （Bcl-2）， and Bcl-2-associated X protein （Bax） were assessed by Western blot. The expression of GRP78 was detected by immunofluorescence （IF） assay， and the location of Bcl-2 and Bax by immunohistochemistry （IHC）. ResultsCompared with the normal group， the model group showed pale gastric mucosa with flattened folds and reduced and loosely arranged gastric mucosal glands， declined serum levels of PGI， PGR， G-17， and GP73 （P<0.01）. downregulated protein levels of GP73， p-PERK， ATF4， GRP78， CHOP， Caspase-12， and Bax in the gastric tissue， and upregulated protein level of Bcl-2 （P<0.01）. Compared with the model group， the Morodan group and each Xianglian Huazhuo prescription group exhibited red gastric mucosa with increased folds， alleviated pathological damage， swelling endoplasmic reticulum， elevated serum levels of PGI， G-17， and GP73 （P<0.05， P<0.01）， and upregulated protein levels of Caspase-12 and Bax and downregulated protein level of Bcl-2 in the gastric tissue （P<0.05， P<0.01）. The Morodan group and the high-dose and medium-dose Xianglian Huazhuo prescription groups exhibited increased serum level of PGR （P<0.05， P<0.01） and upregulated protein levels of GP73， p-PERK， ATF4， GRP78， and CHOP in the gastric tissue （P<0.05， P<0.01）. ConclusionXianglian Huazhuo prescription can activate the GP73/PERK/ATF4 signaling pathway and induce ERS-mediated apoptosis to alleviate the pathological damage of the gastric mucosa， thereby demonstrating a protective effect against CAG in mice.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

Chronic atrophic gastritis （CAG）， a common digestive system disease， has an unclear pathogenesis. Currently， it is mostly believed to be related to Helicobacter pylori （Hp） infection， immune factors， dietary factors， bile reflux， long-term use of antibiotics and anti-inflammatory drugs， and other factors. Ferroptosis is a regulated cell death mechanism that is iron-dependent and characterized by disruption of iron metabolism and accumulation of lipid peroxides. More and more studies have found that ferroptosis is closely related to the onset of CAG. Professor LI Diangui， a master of traditional Chinese medicine， first proposed the turbid toxin theory， which holds that spleen deficiency and turbid toxin is the main pathogenic mechanism of CAG. Abnormal iron metabolism regulation is a prerequisite for the accumulation of turbid toxin in CAG， and ferroptosis is in accordance with the pathogenic mechanism （spleen deficiency and turbid toxin） of CAG. This article explores the pathological mechanism of spleen deficiency and turbid toxin in CAG from the perspectives of iron metabolism， oxidative stress， and lipid peroxidation， providing theoretical support of traditional Chinese medicine for the modern research on CAG. It enriches the modern scientific connotation of the turbid toxicity theory and provides new ideas and breakthrough points for the clinical treatment of CAG.

OBJECTIVE To explore the effect of hydrogen peroxide disinfectant on terminal disinfection in wards of medical institutions.METHODS The surfaces of highly frequent contact objects of the wards of the First Affilia-ted Hospital of Nanchang University from which the public health center patients were discharged between Apr.2024 and Jun.2024 were respectively disinfected with 0.5％(low)and 5％(high)concentrations of hydrogen peroxide disinfecting wipes,totally 180 samples were randomly collected before and after the disinfection,and the pathogens were detected.The air of the wards from which the public health center patients were discharged be-tween Jul.2024 and Aug.2024 were disinfected with hydrogen peroxide dry mist disinfection device,and 90 sam-ples were respectively collected before and after the disinfection.Geobacillus stearothermophilus was used as the biological indicator and placed at various points within the air-disinfected wards to evaluate the disinfection level.The environmental sampling results and distribution of bacteria were observed and compared.RESULTS The qualified rates of disinfection of the object surfaces were 95.56％(86/90)and 98.89％(89/90)respectively for the low and high concentratioins of hydrogen peroxide disinfecting wipes,and there was no significant difference in the disinfection effect.Totally 120 strains of pathogens were isolated from unqualified samples before the disinfection,among which gram-negative bacteria(69.17％)were dominant,and the isolation rate of multidrug-resistant or-ganisms was 22.50％(27/120);only 1 strain of carbapenem-resistant Acinetobacter baumannii was isolated after the disinfection.The qualified rate of disinfection of air in the wards was 96.00％by 7.5％hydrogen peroxide dry mist disinfection device,the average bacterial colony counts in the air were 2 CFU/(5 min·vsl)after the dis-infection,and the killing rate of Geobacillus stearothermophilus was 100.00％by the air disinfection.CONCLUSION The hydrogen peroxide disinfectant can meet the requirement for terminal disinfection of the wards of the medical institutions,and it is portable and highly efficient.

Cystic renal mass(CRM)is common in clinic,covering a variety of diseases,and the differentiation of benign and malignant CRM is crucial for treatment decisions.Imaging technologies had their own advantages for diagnosis of CRM,while new grading systems and diagnostic methods kept emerged.The definition of CRM,the application and diagnostic progresses of imaging,especially ultrasound for CRM,and the characteristics and shortcomings of existing diagnostic methods were reviewed in this article,aiming to provide reference for accurate diagnosis and treatment of CRM.

Objective:To analyze the clinical features and genetic sequencing results of a patient with Kallmann syndrome(KS) carrying digenic mutations who initially presented with osteoporosis, and to enhance awareness of this disease phenotype.Methods:Clinical data were collected, and peripheral blood DNA was extracted for whole-exome sequencing. Relevant literature was reviewed to summarize phenotypes associated with digenic/oligogenic variants involving CHD7.Results:The patient exhibited back pain, delayed development of secondary sexual characteristics, and hyposmia. Laboratory tests revealed reduced sex hormones and gonadotropin levels, while pituitary imaging was unremarkable. Bone mineral density imaging confirmed osteoporosis, and thoracolumbar X-rays showed multiple vertebral compression fractures. Genetic analysis identified a heterozygous splice-site mutation in CHD7(c.2698-1G>T) and a heterozygous missense mutation in WDR11(c.439G>A: p.D147N). According to ACMG criteria, the CHD7 mutation was classified as pathogenic, while the WDR11 variant was defined as a variant of uncertain significance(VUS). Literature review indicated that 40% of KS patients with digenic/oligogenic variants involving CHD7 presented with hearing or ocular abnormalities.Conclusion:This study reports a novel CHD7 mutation and a previously undescribed digenic combination of CHD7 and WDR11 variants in a KS patient. CHD7 variants may be implicated in auditory or ocular involvement in KS cases with digenic/oligogenic inheritances. KS patients may also manifest skeletal abnormalities in addition to hypogonadotropic hypogonadism. Tailored management of sex hormones and osteoporosis therapies across life stages is essential for optimizing bone health in KS.

Objective:To investigate the clinical characteristics and independent risk factors of severe disease in patients with anti-nuclear matrix protein (NXP) 2 antibody-positive juvenile dermatomyositis (JDM).Methods:A retrospective cohort study was conducted, including 219 anti-NXP2 antibody-positive JDM patients admitted to 23 children′s hospitals across China from July 2011 to July 2023. Patients were classified into severe and non-severe groups based on classification criteria for severe dermatomyositis. Demographic characteristics, clinical manifestations, and laboratory parameters were compared between the 2 groups using independent sample t-test, Mann-Whitney U test, or χ2 test. Univariate and multivariate Logistic regression analyses were performed to identify risk factors for severe disease. The receiver operating characteristic curve was employed to calculate optimal cut-off values. Results:Among the 219 patients, 108 were male and 111 were female, with an age at onset of 6.3 (3.5, 9.4) years. The severe group comprised 69 patients, and the non-severe group 150 patients. The severe group had significantly higher rates of fever, heliotrope rash, subcutaneous edema, periorbital edema, anti-Ro52 antibody positivity, as well as elevated levels of ferritin-to-albumin ratio (FAR), creatine kinase (CK), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) (all P<0.05). Multivariate analysis identified anti-Ro52 antibody positivity ( OR=13.26, 95% CI 1.37-128.29) and elevated FAR ( OR=1.90, 95% CI 1.09-2.31) as independent risk factors for severe anti-NXP2 antibody-positive JDM (both P<0.05). Receiver operating characteristic curve analysis revealed that a FAR cutoff value of 6.82 predicted severe disease with an area under the curve of 0.87 (95% CI 0.81-0.94, P<0.001), sensitivity of 0.85, and specificity of 0.70. All patients received glucocorticoid therapy, and the severe group received higher proportions of steroid pulse therapy, cyclophosphamide, mycophenolate mofetil, intravenous immunoglobulin, biologics, and adjuvant treatments compared to the non-severe group (all P<0.05). In terms of outcomes, 2 patients (2.9%) in the severe group died (due to neurological involvement and intestinal perforation, respectively), while the remaining patients achieved complete clinical response or remission. All patients in the non-severe group achieved remission. Conclusions:The primary clinical features of anti-NXP2 antibody-positive JDM included fever, heliotrope rash, subcutaneous edema, periorbital edema, anti-Ro52 antibody positivity, and elevated levels of CK, AST, LDH, and FAR. Furthermore, anti-Ro52 antibody positivity and a FAR>6.82 were identified as independent risk factors.

Objective:To investigate the influencing factors for gastroesophageal reflux disease (GERD) after laparoscopic Heller-Dor surgery for esophageal achalasia.Methods:The retrospective case-control study was conducted. The clinical data of 210 patients with esophageal achalasia who were admitted to Shanxi Provincial Cancer Hospital from January 2021 to December 2023 were collected. There were 119 males and 91 females, aged (47±12)years. All patients underwent laparoscopic Heller-Dor surgery. Observation indicators: (1) surgical situations; (2) follow-up; (3) influencing factors for GERD after laparoscopic Heller-Dor surgery; (4) development and evaluation of a predictive model for GERD after laparoscopic Heller-Dor surgery. Univariate and multivariate analyses were performed using stepwise Logistic regression. Results of multivariate analysis were used to construct a nomogram in predicting GERD. The predictive performance was assessed using the area under the receiver operating characteristic curve. The calibration curve was used to evaluate the accuracy of the model, and the decision curve was used to assess the overall net benefit of the model.Results:(1) Surgical situations. All 210 patients underwent laparoscopic Heller-Dor surgery. The operation time was (128±31)minutes, volume of intraoperative blood loss was (25±9)mL, and length of lower esophageal sphincter (LES) myotomy was (5±3)cm. The length of low esophageal myotomy >6 cm was performed in 49 patients, and length of gastric fundus myotomy >2 cm was performed in 58 patients. Intraoperative mucosal perforation occurred to 3 patients and was repaired intraoperatively. One patient required conversion to open surgery. Postoperative complications occurred in 18 patients. The duration of postoperative hospital stay was (4.3±2.4)days. (2) Follow-up. All 210 patients were followed up for 4(range,7-33)months after surgery. During follow-up, 32 pati-ents had GERD, including 17 cases presenting dysphagia and 25 cases presenting acid regurgitation and heartburn (the same patient may have two symptoms). There were 29 cases with body mass index (BMI) >28 kg/m2. Symptom severity scores of 210 patients showed heartburn of 0.6(range, 0-3.0), reflux of 0.7(range, 0-3.0), chest pain of 0.4(range, 0-2.0), cough and hoarseness of 0.5(range, 0-2.0), nausea and vomiting 0.3(range, 0-2.0), dysphagia 0.8(range, 0-3.0). The LES pressure was (15±8)mmHg (1 mmHg=0.133 kPa), LES relaxation rate was 81%±13.0%, and integrated relaxation pressure was (9±6)mmHg. Esophageal manometry classification showed type Ⅰ, Ⅱ, and Ⅲ in 0, 8, and 0 patients, respectively. There were 208 patients achieved symptom relief after drug or symptomatic treatment. Only two patients with severe symptoms were unresponsive to medication and subsequently underwent surgery at another hospital, with symptoms improving postoperatively. (3) Influen-cing factors for GERD after laparoscopic Heller-Dor surgery. Results of multivariate analysis showed that male, smoking history, length of lower esophageal myotomy >6 cm, and postoperative BMI >28 kg/m2 were independent risk factors for GERD after laparoscopic Heller-Dor surgery ( odds ratio=4.02, 6.34, 5.41, 7.38, 95% confidence interval as 1.50-10.78, 3.31-12.31, 1.77-13.47, 2.80-15.42, P<0.05). (4) Development and evaluation of a predictive model for GERD after laparoscopic Heller-Dor surgery. A predictive nomogram model for GERD was constructed based on the results of multivariate analysis. The receiver operating characteristic curve of predictive nomogram model for GERD had an area under curve of 0.91 (95% confidence interval as 0.82-0.97), demonstrating good discrimination. The calibration curve showed good agreement between predicted and observed probabilities, with a mean absolute error of 0.033. The decision curve demonstrated that within a threshold probability range of 0.2-0.8, the predictive model had greater net benefit than "treat-all" or "treat-none" strategies, indicating clinical utility of this model in clinical decision. Conclusions:Male, smoking history, length of lower esophageal myotomy >6 cm, and postoperative BMI >28 kg/m2 are independent risk factors for GERD after laparoscopic Heller-Dor surgery for esophageal achalasia. The predictive model for GERD after laparoscopic Heller-Dor surgery based on these factors shows strong predictive accuracy.

Objective:To investigate the influencing factors for gastroesophageal reflux disease (GERD) after laparoscopic Heller-Dor surgery for esophageal achalasia.Methods:The retrospective case-control study was conducted. The clinical data of 210 patients with esophageal achalasia who were admitted to Shanxi Provincial Cancer Hospital from January 2021 to December 2023 were collected. There were 119 males and 91 females, aged (47±12)years. All patients underwent laparoscopic Heller-Dor surgery. Observation indicators: (1) surgical situations; (2) follow-up; (3) influencing factors for GERD after laparoscopic Heller-Dor surgery; (4) development and evaluation of a predictive model for GERD after laparoscopic Heller-Dor surgery. Univariate and multivariate analyses were performed using stepwise Logistic regression. Results of multivariate analysis were used to construct a nomogram in predicting GERD. The predictive performance was assessed using the area under the receiver operating characteristic curve. The calibration curve was used to evaluate the accuracy of the model, and the decision curve was used to assess the overall net benefit of the model.Results:(1) Surgical situations. All 210 patients underwent laparoscopic Heller-Dor surgery. The operation time was (128±31)minutes, volume of intraoperative blood loss was (25±9)mL, and length of lower esophageal sphincter (LES) myotomy was (5±3)cm. The length of low esophageal myotomy >6 cm was performed in 49 patients, and length of gastric fundus myotomy >2 cm was performed in 58 patients. Intraoperative mucosal perforation occurred to 3 patients and was repaired intraoperatively. One patient required conversion to open surgery. Postoperative complications occurred in 18 patients. The duration of postoperative hospital stay was (4.3±2.4)days. (2) Follow-up. All 210 patients were followed up for 4(range,7-33)months after surgery. During follow-up, 32 pati-ents had GERD, including 17 cases presenting dysphagia and 25 cases presenting acid regurgitation and heartburn (the same patient may have two symptoms). There were 29 cases with body mass index (BMI) >28 kg/m2. Symptom severity scores of 210 patients showed heartburn of 0.6(range, 0-3.0), reflux of 0.7(range, 0-3.0), chest pain of 0.4(range, 0-2.0), cough and hoarseness of 0.5(range, 0-2.0), nausea and vomiting 0.3(range, 0-2.0), dysphagia 0.8(range, 0-3.0). The LES pressure was (15±8)mmHg (1 mmHg=0.133 kPa), LES relaxation rate was 81%±13.0%, and integrated relaxation pressure was (9±6)mmHg. Esophageal manometry classification showed type Ⅰ, Ⅱ, and Ⅲ in 0, 8, and 0 patients, respectively. There were 208 patients achieved symptom relief after drug or symptomatic treatment. Only two patients with severe symptoms were unresponsive to medication and subsequently underwent surgery at another hospital, with symptoms improving postoperatively. (3) Influen-cing factors for GERD after laparoscopic Heller-Dor surgery. Results of multivariate analysis showed that male, smoking history, length of lower esophageal myotomy >6 cm, and postoperative BMI >28 kg/m2 were independent risk factors for GERD after laparoscopic Heller-Dor surgery ( odds ratio=4.02, 6.34, 5.41, 7.38, 95% confidence interval as 1.50-10.78, 3.31-12.31, 1.77-13.47, 2.80-15.42, P<0.05). (4) Development and evaluation of a predictive model for GERD after laparoscopic Heller-Dor surgery. A predictive nomogram model for GERD was constructed based on the results of multivariate analysis. The receiver operating characteristic curve of predictive nomogram model for GERD had an area under curve of 0.91 (95% confidence interval as 0.82-0.97), demonstrating good discrimination. The calibration curve showed good agreement between predicted and observed probabilities, with a mean absolute error of 0.033. The decision curve demonstrated that within a threshold probability range of 0.2-0.8, the predictive model had greater net benefit than "treat-all" or "treat-none" strategies, indicating clinical utility of this model in clinical decision. Conclusions:Male, smoking history, length of lower esophageal myotomy >6 cm, and postoperative BMI >28 kg/m2 are independent risk factors for GERD after laparoscopic Heller-Dor surgery for esophageal achalasia. The predictive model for GERD after laparoscopic Heller-Dor surgery based on these factors shows strong predictive accuracy.