The development and validation of clinical prediction models based on artificial intelligence (AI) and machine learning methods have become increasingly widespread. However, the prediction model bias risk and applicability evaluation tool developed in 2019 (i.e., PROBAST-2019) has shown significant limitations. Therefore, an expanded and updated version of the PROBAST-2019 tool was released in 2025, known as the PROBAST+AI tool. The tool is divided into two parts including model development and model evaluation. It aims to comprehensively and systematically evaluate potential methodological quality issues in model development, bias risks in model evaluation, and the applicability of models, regardless of the modeling method used. This paper provides a systematic interpretation of the PROBAST+AI tool's items and case analyses, with the aim of guiding and assisting researchers engaged in related studies and promoting the high-quality development of clinical predictive model research.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Objective To investigate the mechanism by which apelin inhibits the transition from acute kidney injury(AKI)to chronic kidney disease(CKD).Methods Human proximal tubular epithelial cells were cultured in vitro and divided into control,cisplatin,cisplatin+apelin,cisplatin+apelin+Sirt3 siRNA,and apelin groups.Cells were transfected with Sirt3 siRNA and incubated with a medium containing cisplatin(10 μmol/L)and/or apelin-13(1 μmol/L).Mitochondrial morphology was observed using MitoTracker? probes;mito-chondrial membrane potential was detected using the JC-1 assay kit;and the expression of the fibrogenic cytokine,transforming growth factor β1(TGF-β1)was measured by Western blotting.Forty 10-week-old male C57BL/6J mice were divided into control,cisplatin,cisplatin+apelin,cisplatin+apelin+Sirt3 knockdown,and empty adenovirus groups,with eight mice per group.Except for the control and empty adenovirus groups,all the other groups were intraperitoneally injected with cisplatin(20 mg/kg)to establish the AKI model.The cis-platin+apelin group was intraperitoneally injected with apelin-13(0.1 μg·kg-1·d-1);the control group was injected with an equal volume of saline;the cisplatin+apelin+Sirt3 knockdown group was injected with Sirt3 knockdown adenovirus(2 × 109 pfu/mL)via the tail vein and intraperitoneal injection of apelin-13(0.1 μg·kg-1·d-1);and the empty adenovirus group was injected with adenovirus(2 × 109 pfu/mL)via the tail vein.The mice were sacrificed after 2 weeks.Kidney fibrosis was assessed by Masson's trichome staining.Type Ⅰ collagen(Col-Ⅰ)expression was observed by immunohistochemical staining.Plasma creatinine(Cr)and blood urea nitrogen(BUN)levels were measured by ELISA.Results In vitro experiments showed that,compared with the control group,the cisplatin group exhibited reduced mitochondrial fluorescence staining,decreased mitochondrial membrane potential,and increased TGF-β1 expression(all P＜0.05).Compared with the cisplatin group,the cisplatin+apelin group showed increased fluorescence staining,elevated mitochondrial membrane potential,and reduced TGF-β1 expression(all P＜0.05);however,these effects were counteracted after Sirt3 siRNA transfection.In vivo experiments showed that,compared with the control group,the cisplatin group exhibited significant renal tubular atrophy and interstitial fibrosis,increased Col-Ⅰ positive expression,and elevated plasma Cr and BUN levels(all P＜0.05).Compared with the cisplatin group,the cisplatin+apelin group showed a significant improvement in all the above indicators(all P＜0.05).Compared with the cisplatin+apelin group,the cisplatin+apelin+Sirt3 knockdown group showed a significant reduction in the renal protective effects of apelin.Conclusion The polypeptide apelin inhibits the transition from AKI to CKD by regulating Sirt3 expression to maintain mitochondrial structure and function,which can reduce renal fibrosis and improve renal function.

Objective To investigate the mechanism by which apelin inhibits the transition from acute kidney injury(AKI)to chronic kidney disease(CKD).Methods Human proximal tubular epithelial cells were cultured in vitro and divided into control,cisplatin,cisplatin+apelin,cisplatin+apelin+Sirt3 siRNA,and apelin groups.Cells were transfected with Sirt3 siRNA and incubated with a medium containing cisplatin(10 μmol/L)and/or apelin-13(1 μmol/L).Mitochondrial morphology was observed using MitoTracker? probes;mito-chondrial membrane potential was detected using the JC-1 assay kit;and the expression of the fibrogenic cytokine,transforming growth factor β1(TGF-β1)was measured by Western blotting.Forty 10-week-old male C57BL/6J mice were divided into control,cisplatin,cisplatin+apelin,cisplatin+apelin+Sirt3 knockdown,and empty adenovirus groups,with eight mice per group.Except for the control and empty adenovirus groups,all the other groups were intraperitoneally injected with cisplatin(20 mg/kg)to establish the AKI model.The cis-platin+apelin group was intraperitoneally injected with apelin-13(0.1 μg·kg-1·d-1);the control group was injected with an equal volume of saline;the cisplatin+apelin+Sirt3 knockdown group was injected with Sirt3 knockdown adenovirus(2 × 109 pfu/mL)via the tail vein and intraperitoneal injection of apelin-13(0.1 μg·kg-1·d-1);and the empty adenovirus group was injected with adenovirus(2 × 109 pfu/mL)via the tail vein.The mice were sacrificed after 2 weeks.Kidney fibrosis was assessed by Masson's trichome staining.Type Ⅰ collagen(Col-Ⅰ)expression was observed by immunohistochemical staining.Plasma creatinine(Cr)and blood urea nitrogen(BUN)levels were measured by ELISA.Results In vitro experiments showed that,compared with the control group,the cisplatin group exhibited reduced mitochondrial fluorescence staining,decreased mitochondrial membrane potential,and increased TGF-β1 expression(all P＜0.05).Compared with the cisplatin group,the cisplatin+apelin group showed increased fluorescence staining,elevated mitochondrial membrane potential,and reduced TGF-β1 expression(all P＜0.05);however,these effects were counteracted after Sirt3 siRNA transfection.In vivo experiments showed that,compared with the control group,the cisplatin group exhibited significant renal tubular atrophy and interstitial fibrosis,increased Col-Ⅰ positive expression,and elevated plasma Cr and BUN levels(all P＜0.05).Compared with the cisplatin group,the cisplatin+apelin group showed a significant improvement in all the above indicators(all P＜0.05).Compared with the cisplatin+apelin group,the cisplatin+apelin+Sirt3 knockdown group showed a significant reduction in the renal protective effects of apelin.Conclusion The polypeptide apelin inhibits the transition from AKI to CKD by regulating Sirt3 expression to maintain mitochondrial structure and function,which can reduce renal fibrosis and improve renal function.

Body weight abnormalities, including overweight, obesity, and underweight, have become a dual public health challenge in Chinese adults: overweight and obesity lead to a variety of chronic complications, while underweight increases the risks of malnutrition, sarcopenia, and organ dysfunction. To systematically address these issues, multidisciplinary experts in endocrinology, sports science, nutrition, and psychiatry from various regions have held multiple weight management seminars. Based on the latest epidemiological data and clinical evidence, they expanded the guideline to include assessment and intervention strategies for underweight, in addition to the core content of obesity management. This guideline outlines the etiological mechanisms, evaluation methods, and multidimensional management strategies for overweight and obesity, covering key areas such as diagnosis and assessment, medical nutrition therapy, exercise prescription, pharmacological intervention, and psychological support. It is intended to provide a scientific and standardized approach to weight management across the adult population, aiming to curb the rising prevalence of obesity, mitigate complications associated with abnormal body weight, and improve nutritional status and overall quality of life.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.

Objective To generate and identify the Itgbl1(integrin beta-like)promoter-driven Cre knock-in mouse line.Methods Itgbll-Cre knock-in mice were generated using clustered regularly interspaced short palindromic repeats(CRISPR)/CRISPR-associated protein 9(Cas9)gene editing.The Itgbl1-Cre mice were crossed with the Cre reporter ROSALSL-tdTomato)mice to detect the expression profile of Cre activity.The tdTomato expression pattern across tissues and cell-specific markers were used to identify the cell types of Itgbl1-expressing cells and their progeny.Results and Conclusion tdTomato was specifically expressed in mucous acinar cells of the sublingual gland,pancreatic islet cells,and gastric endocrine cells.In addition,tdTomato expression was also found in some of the neurons of the retina and brain,as well as in a few cells in the serosal layer of the intestine,articular cartilage,periosteum,and bone marrow.The first Itgbl1-Cre recombinase transgenic mouse line was established,which can specifically label the mucous acinar cells of the sublingual gland.

Objective:To compare the 1-year effects of Roux-en-Y gastric bypass (RYGB) and sleeve gastrectomy with Roux-en-Y duodenal bypass (SG+RYDJB) on weight loss, remission of diabetes, and postoperative complications in patients with obesity and type 2 diabetes.Methods:A single-center retrospective cohort study was conducted at the First Affiliated Hospital of Nanjing Medical University from January 2020 to December 2020. Sixty-four patients with type 2 diabetes and body mass index (BMI) of 27.5-40.0 kg/m 2 were included in this study and divided into the RYGB group ( n=34) and the SG+RYDJB group ( n=30). In both procedures, the biliopancreatic branch was measured 100 cm distal to the Treitz ligament, and the food branch was measured 100 cm distal to the gastric or duodenojejunal anastomosis. Patients were followed up by telephone or WeChat, a free messaging and calling app at 1, 3, 6, and 12 months postoperatively to determine their weight loss and remission of diabetes. The primary outcomes were the weight loss and reduction in blood glucose concentrations at 1 year after surgery and postoperative complications. Other postoperative changes, including body weight, BMI, percentage of total weight loss (%TWL), percentage of excess weight loss (%EWL), glycated hemoglobin A1c (HbA1c), and fasting blood glucose at 1 year after surgery were also assessed. Results:There were no significant differences in baseline data between the two groups (all P>0.05). No conversion to open surgery or death occurred in either group. Operation time was longer in the SG+RYDJB than the RYGB group (137.8±22.1 minutes vs. 80.0±24.9 minutes, t=9.779, P<0.001) and the incidence of perioperative complications was higher in the SG+RYDJB than the RYGB group (20% [6/30] vs. 2.9% [1/34], χ 2=4.761, P=0.029). However, the postoperative hospital stay was similar between the two groups [3.0 (3.0, 4.3) days vs. 3.0 (4.0, 6.0) days, U=641.500, P=0.071]. Perioperative complications comprised small gastric pouch anastomotic leakage in one patient in the RYGB group and leakage (three patients) and bleeding (two patients with gastrointestinal bleeding and one with trocar site bleeding) in the SG+RYDJB group. Long-term complications were as follows. The incidence of anemia was significantly higher in the RYGB than the SG+RYDJB group (26.5% [9/34] vs. 3.3% [1/30], χ 2=6.472, P=0.011). However, there were no significant differences in incidences of postoperative reflux, dumping syndrome, alopecia, diarrhea, constipation or foul-smelling flatus between the two groups (all P>0.05). Compared with 1 year before surgery, the body weights and fasting plasma glucose concentrations of patients in the SG+RYDJB and RYGB group (72.4±10.6 kg vs. 98.5±14.2 kg, respectively; 68.2±10.0 kg vs. 91.9±14.8 kg, respectively), BMI (25.2±2.9 kg/m 2 vs. 34.3±4.2 kg/m 2, respectively; 24.3±2.4 kg/m 2 vs. 32.7±3.7 kg/m 2, respectively) (5.5±1.6 vs. 10.6±3.3, respectively; 5.8±2.1 vs. 9.0±3.4, respectively); HbA1c (5.7±0.8 vs. 9.7±1.2, respectively; 9.1±1.9 vs. 5.9±0.9, respectively) were significantly lower at 1 year after surgery (all P<0.05). However, the % TWL (26.5%±6.0% vs. 25.6%±4.4%, t=0.663, P=0.510) and % EWL (109.1%±38.2% vs. 109.4%±40.3%, t=-0.026, P=0.026), rate of complete remission of diabetes at 1 year (80.0% [24/30] vs. 82.4% [28/34], χ 2=0.058, P=0.810] did not differ significantly between the two groups (all P>0.05). Conclusions:Although SG+RYDJB surgery compared with RYGB is more difficult to perform, it can achieve similar weight loss and remission of diabetes and is associated with a lower incidence of anemia because of the preservation of the pylorus.

Somatostatin (SST) is an inhibitory polypeptide hormone that plays an important role in a variety of biological processes. Somatostatin receptor 2 (SSTR2) is the most widely expressed somatostatin receptor. However, the specific cell types expressing Sstr2 in the tissues have not been investigated. In this study, we detected the expression pattern of SSTR2 protein in mouse at different development stages, including the embryonic 15.5 days and the postnatal 1, 7, 15 days as well as 3 and 6 months, by multicolour immunofluorescence analyses. We found that Sstr2 was expressed in some specific cells types of several tissues, including the neuronal cells and astrocytes in the brain, the mesenchymal cells, the hematopoietic cells, the early hematopoietic stem cells, and the B cells in the bone marrow, the macrophages, the type Ⅱ alveolar epithelial cells, and the airway ciliated cells in the lung, the epithelial cells and the neuronal cells in the intestine, the hair follicle cells, the gastric epithelial cells, the hematopoietic stem cells and the nerve fibre in the spleen, and the tubular epithelial cells in the kidney. This study identified the specific cell types expressing Sstr2 in mouse at different developmental stages, providing new insights into the physiological function of SST and SSTR2 in several cell types.
Mice ; Animals ; Receptors, Somatostatin/metabolism* ; Hematopoietic Stem Cells/metabolism* ; Epithelial Cells