Objective: To investigate if high glucose (HG) exacerbates Porphyromonas gingivalis (P.g) lipopolysaccharide (LPS)-induced inflammatory response in human gingival fibroblasts (HGFs) and to explore the underlying mechanisms. To provide a basis for the mechanism of diabetes aggravating periodontitis. Methods: HGFs were divided into four groups: the control group (basal medium), the LPS group (treated with 5 μg/mL P.g-LPS for 24 h), the HG group (treated with 25 mmol/L glucose for 24 h), and the HG+LPS group (treated with 25 mmol/L glucose + 5 μg/mL P.g-LPS for 24 h). After culturing for 24 h in the respective media, the cells were harvested for experiments. Intracellular reactive oxygen species (ROS) and mitochondrial reactive oxygen species (mtROS) were detected using 2 ', 7' - dichlorodihydrofluorescein diacetate (DCFH-DA) and MitoSOX Red staining, respectively. Fluorescence intensity was analyzed by confocal fluorescence microscopy and directly measured in cell suspension. Immunofluorescence was used to detect changes in mitochondrial DNA (mtDNA) content of HGFs. Real-time fluorescence quantitative PCR was used to detect the content of mtDNA in cytoplasm and cell supernatant. Protein expression of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) pathway was assessed by western blot, while mRNA expression levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were detected by PCR. Results: Compared to the control group, both the LPS group and the HG group exhibited a significant increase in ROS and mtROS, with a more pronounced elevation in the HG+LPS group, demonstrating a synergistic effect (ROS: F = 396.5, P < 0.001; mtROS: F = 29.38, P < 0.001, CI < 1). The cytoplasmic mtDNA content was significantly elevated in the LPS group, with a more marked increase in the HG+LPS group (F = 27.85, P < 0.001). The supernatant mtDNA levels were significantly higher in both the LPS and HG groups, with a more pronounced elevation in the HG+LPS group (F = 15.26, P < 0.001). The phosphorylated proteins p-STING, p-TBK1, and p-P65 in the cGAS-STING pathway showed varying degrees of activation in the LPS and HG groups, reaching the highest levels in the HG+LPS group (p-STING: F = 52.67, P < 0.001; p-TBK1: F = 15.67, P = 0.001; p-P65: F = 9.83, P = 0.005), while p-IRF3 showed no significant differences among the groups (P = 0.072). Pro-inflammatory cytokine TNF-α was significantly higher in the HG+LPS group compared to the control group (F = 15.05, P < 0.001), and IL-1β increased in both the LPS and HG groups, with a more pronounced rise in the HG+LPS group (F = 30.98, P < 0.001). IL-6 showed no significant differences among the groups (P = 0.847). Conclusion High glucose and LPS act synergistically to enhance oxidative stress, accompanied by increased mtDNA release, which activates the cGAS-STING pathway, thereby amplifying the inflammatory response in HGFs.

A 65-year-old male was admitted to Peking Union Medical College Hospital. The patient had intermittent fever for 2 months with a maximum body temperature of 39.3 ℃ and elevated serum creatinine levels for 1 week. He had no other suggestive symptoms or positive signs. Laboratory test results suggested acute kidney injury and a sharp elevation in serum lactic dehydrogenase levels. Abdominal enhanced computed tomography (CT) revealed multiple low-density lesions, and further biopsy pathology demonstrated chronic inflammation. Thereafter, positron emission tomography (PET)/CT showed abnormally elevated uptake value for the bones throughout the entire body, in addition to the liver and brain. Repeated bone marrow biopsy finally confirmed metastatic bone cancer, which possibly originated from the kidney according to immunohistochemical staining. In this rare case of fever of unknown origin, the primary lesion was a renal tumor with bone, liver, and brain metastases. Enhanced CT and PET/CT provided negative results, and the diagnosis was eventually confirmed by repeated bone marrow pathology.

A 65-year-old male was admitted to Peking Union Medical College Hospital. The patient had intermittent fever for 2 months with a maximum body temperature of 39.3 ℃ and elevated serum creatinine levels for 1 week. He had no other suggestive symptoms or positive signs. Laboratory test results suggested acute kidney injury and a sharp elevation in serum lactic dehydrogenase levels. Abdominal enhanced computed tomography (CT) revealed multiple low-density lesions, and further biopsy pathology demonstrated chronic inflammation. Thereafter, positron emission tomography (PET)/CT showed abnormally elevated uptake value for the bones throughout the entire body, in addition to the liver and brain. Repeated bone marrow biopsy finally confirmed metastatic bone cancer, which possibly originated from the kidney according to immunohistochemical staining. In this rare case of fever of unknown origin, the primary lesion was a renal tumor with bone, liver, and brain metastases. Enhanced CT and PET/CT provided negative results, and the diagnosis was eventually confirmed by repeated bone marrow pathology.

Acute idiopathic maculopathy(AIM)is an inflammatory lesion of unknown cause that primarily affects the macula. It follows a unique natural course, distinct from other maculopathy, often manifesting as a sudden loss of visual acuity followed by flu-like symptoms that gradually resolve as the disease subsides. A comprehensive understanding of the unique history, multimodal imaging, and a thorough systematic examination are crucial in determining the final diagnosis of AIM. The treatment and prognosis of AIM remain controversial. Meanwhile, it presents similar clinical manifestations and pathological changes to various chorioretinopathy, posing challenges for clinical differentiation. This article provides a review of its pathogenesis, clinical symptoms, multimodal imaging features, diagnosis and differential diagnosis, treatment and prognosis, in order to reduce misdiagnosis and mistreatment while enhancing comprehension of AIM.

Objective: To develop a model incorporating radiomic features and clinical factors to accurately predict acute ischemic stroke (AIS) outcomes. Materials and Methods: Data from 522 AIS patients (382 male [73.2%]; mean age ± standard deviation, 58.9 ± 11.5 years) were randomly divided into the training (n = 311) and validation cohorts (n = 211). According to the modified Rankin Scale (mRS) at 6 months after hospital discharge, prognosis was dichotomized into good (mRS ≤ 2) and poor (mRS > 2); 1310 radiomics features were extracted from diffusion-weighted imaging and apparent diffusion coefficient maps. The minimum redundancy maximum relevance algorithm and the least absolute shrinkage and selection operator logistic regression method were implemented to select the features and establish a radiomics model. Univariable and multivariable logistic regression analyses were performed to identify the clinical factors and construct a clinical model. Ultimately, a multivariable logistic regression analysis incorporating independent clinical factors and radiomics score was implemented to establish the final combined prediction model using a backward step-down selection procedure, and a clinical-radiomics nomogram was developed. The models were evaluated using calibration, receiver operating characteristic (ROC), and decision curve analyses. Results: Age, sex, stroke history, diabetes, baseline mRS, baseline National Institutes of Health Stroke Scale score, and radiomics score were independent predictors of AIS outcomes. The area under the ROC curve of the clinical-radiomics model was 0.868 (95% confidence interval, 0.825–0.910) in the training cohort and 0.890 (0.844–0.936) in the validation cohort, which was significantly larger than that of the clinical or radiomics models. The clinical radiomics nomogram was well calibrated (p > 0.05). The decision curve analysis indicated its clinical usefulness. Conclusion The clinical-radiomics model outperformed individual clinical or radiomics models and achieved satisfactory performance in predicting AIS outcomes.

Phosphoinositide 3-kindase,an important signal transduction molecule in cells,plays a key role in the process of cell survival,proliferation and differentiation.Significant progress has been made in the treatment of cancer with PI3K inhibitors,yet the drug resistance of PI3K inhibitors affects their long-term efficacy in clinical treatment.In order to overcome the drug resistance,a variety of rational combined therapies have been developed.In this paper,the research progress of phosphoinositide-3 kinase inhibitors in combination with other drugs to overcome the drug resistance were reviewed.

Objective:To investigate age related changes in urodynamic parameters of women with uri-nary incontinence.Methods:From May 2008 to October 2015,a total of 214 patients diagnosed with urinary incontinence in Peking University People’s Hospital was involved in this study.Average age was (56.97 ±10.68)years,ranging from 30 to 82 years,and average history was (8.44 ±8.85)years, ranging from one month to 50 years.Urodynamic examinations of each patient were taken before operation routinely in Department of Urology,Peking University People’s Hospital.The urodynamic study was composed of non-invasive and invasive procedures.Analysis included maximal flow rate (Qmax ),average flow rate,time to Qmax ,voiding time,detrusor pressure at Qmax ,maximal detrusor pressure,voided volume,post-void residual urine volume (PVR),the total capacity of bladder,first-,strong-,and urge-desire to void,cough leak point pressure (CLPP),and Valsalva leak point pressure (VLPP).Patients were divided into four groups according to age,Kolmogorov-Smirnov test and one-way ANOVA were used for data analysis.Results:A total of 214 patients were enrolled in this study.The data of Qmax ,average flow rate,voided volume,and total capacity of bladder decreased with statistical significance.The value of residual urine volume and voiding time increased without statistical significance,while the value of maximal detrusor pressure decreased.Conclusion:Urodynamic examination data of females with urinary incontinence changes along with the elapse of age,which was mainly observed as age ascends,and the changes in urodynamic parameters of women with urinary incontinence suggest that the value of Qmax , average flow rate,voided volume,and total capacity of bladder decreased significantly,while the value of PVR and the voiding time increased and the value of maximal detrusor pressure decreased.

Objective:To investigate the role and probable mechanism of moderate activation of hypoxia‐inducible factor(HIF) in slowing chronic kidney disease progression of remnant kidney .Methods :Rat models of remnant kidney were established by 5/6 subtotal nephrectomy in male Sprague‐Dawley rats . And then they were randomly allocated to L‐mimosine (L‐Mim ) treatment group ,in which the rats were treated with intraperitoneal injections of L‐Mim during 5‐12 week after operation ,and untreated remnant kidney group .Meanwhile ,sham operated rats were set as control group .All rats were sacrificed at the end of week 12 ,and the specimens were collected .Results:The serum creatinine level in L‐Mim treatment group was lower than that in untreated remnant kidney group(82 .4 ± 6 .3 vs .130 .1 ± 24 .1 μmol/L ,P<0 .05) ,as well as the 24 h Ualb level (0 .7 ± 0 .1 vs .1 .7 ± 0 .5 g/d , P< 0 .05) .And the pathological changes in in L‐Mim treatment group was slightly improved while compared to untreated remnant kidney group .The result of miRNA microarray analysis showed that miR‐29c in renal cortex was up‐regulated in L‐Mim group compared with untreated remnant group and meanwhile the expressions of HIF‐1αand HIF‐2αincreased .Tropomyosin 1 (TPM1) met the sequence criteria for microRNA‐target interaction ,which was later confirmed by luciferase reporter system and mutation test in vitro .HK2 cell transfected with pre‐miT‐29c oligonucleotide could inhibit the tropomyosin up‐regulation induced by TGF‐β1 treatment (3 ng/mL ,24 h) , P<0 .05 or 0 .01 .Conclusions :Renal interstitial fibrosis in rat remnant kidney was significant ,and it was accompanied by the miR‐29c down‐regulation .Moderate activation of HIF level may attenuate the deterioration of renal function by up‐regulating miR‐29c expression .