Objective:To analyze the hearing outcomes of high-risk children of diabetic mothers, especially in the subtypes of pre-pregnancy diabetes and gestational diabetes, in order to provide some reference for clinical practice. Methods:The basic characteristics and hearing levels of children whose mothers had a history of diabetes during pregnancy and underwent audiological diagnosis and evaluation at our hospital's Children's Hearing Diagnosis Center from January 2003 to June 2024 were analyzed. T-tests, Wilcoxon rank-sum tests, and chi-square tests were used for inter-group comparisons, with a significance level set at P<0.05. Results:A total of 285 children（570 ears） of diabetic mothers were included. Hearing loss was found in 310 ears, and the incidence of hearing loss was 54.39%（310/570）. The mean ABR threshold in the pregestational diabetes group was（50.01±29.29） dB HL, while that in the gestational diabetes group was（44.13±26.19） dB HL. The degree of hearing loss in the pregestational diabetes group was more severe than that in the gestational diabetes group（χ²=10.000, P=0.019）. Conclusion:Maternal history of diabetes may be one of the risk factors for hearing loss in their offspring, and the risk of hearing loss in children whose mothers had diabetes before pregnancy may be higher than that in the gestational diabetes group. It is suggested that the clinical practice should pay attention to the monitoring and follow-up management of the hearing status of such children, so as to improve the auditory outcomes of children born to diabetic mothers.
Humans ; Female ; Pregnancy ; Diabetes, Gestational ; Hearing Loss/etiology* ; Child ; Pregnancy in Diabetics ; Risk Factors ; Child, Preschool ; Mothers ; Male

Actinomycosis is a rare chronic granulomatous disease characterized by granuloma formation and tissue fibrosis with sinus tracts,often misdiagnosed due to its similarity to many infectious and non-infectious diseases.This report presents a case of a 60-year-old female with more than 10 years history of rheumatoid arthritis who developed actinomycosis infection after long-term treatment with immunosuppressants and biologics,including methotrexate,leflunomide,and infliximab,leading to recurrent joint pain,poorly controlled rheumatoid arthritis activity,and persistent elevation of white blood cell counts.Abdominal CT revealed a pelvic mass and right ureteral dilation.Pathological examination of cervical tissue showed significant neutrophil infiltration and sulfur granules,indicating actinomycosis.The patient received 18 months of doxycycline treatment for the infection and continued rheumatoid arthritis therapy with leflunomide,hydroxychloroquine sulfate,and tofacitinib,resulting in improved joint symptoms and normalized white blood cell counts.After 2 years of follow-up,the patient remained stable with no recurrence.This case highlights the importance of clinicians being vigilant for infections,particularly chronic,occult infections from rare pathogens,in rheumatoid arthritis patients on potent immunosuppressants and biologics,advocating for early screening and diagnosis.

Objective To investigate the alteration of mood and hippocampal microglia morphology in a mouse model of chronic inflammatory pain induced by complete Freund' s adjuvant (CFA). Methods Thirty-two male ICR mice were randomly divided into two groups, including normal saline control group (NS) and CFA model group (CFA). The pain model was established by right hindpaw intraplantar CFA injection. The change of mechanical pain threshold after CFA injection was measured by von Frey fiber needle, the locomotor activity and anxiety-like behavior were determined by open field test (OFT), the depression-like behavior was determined by sucrose preference test (SPT) and forced swimming test (FST). The expression of microglia marker ionized calcium binding adaptor molecule-1 (IBA-1) in the hippocampus was determined by immunohistochemistry and its morphological change was analyzed by Sholl analysis. Results Compared with the NS group, the mechanical pain threshold of CFA group decreased significantly (P<0.01). The behavior result showed that the CFA group showed remarkably reduced time in the inner area (P<0.01) compared with the NS group in the open field test; In the sucrose preference test, the percentage of sucrose preference (P<0.01) of CFA mice decreased significantly compared with the NS mice, while the immobility time of CFA mice (P<0.01) increased significantly in the forced swimming test compared with the NS mice. The immunohistochemistry showed that the number of microglia in the dentate gyrus (DG) of CFA mice increased significantly compared with the NS mice. The Sholl analysis result showed that compared with the NS mice, the number of intersections of microglia in hippocampal DG decreased significantly in CFA mice. Conclusion Our finding indicates that the negative emotions in CFA-induced chronic inflammatory pain may be related to the morphological changes of hippocampal microglia in the mice.

Objective:To investigate the expression of serum matrix metalloproteinase 3 (MMP-3) in patients with rheumatoid arthritis (RA) and analyze its correlation with bone erosion and disease activity.Methods:100 RA patients diagnosed in the First People's Hospital of Changde from July 2018 to December 2019 were selected as the RA group, and 35 healthy volunteers who came to the hospital for physical examination at the same time were selected as the control group. The clinical data of the patients were collected, and the serum MMP-3 levels of the patients and healthy volunteers were detected by enzyme-linked immunosorbent assay (ELISA). The serum MMP3 levels of RA patients with different disease activity, different imaging stages and different bone mineral density were compared, and the correlation with clinical indicators were analyzed.Results:⑴ RA patients were grouped according to the Disease Activity Score (DAS) 28. Serum MMP-3 levels in the highly active group (300.87±15.93)ng/ml and in the moderately active group (213.78±12.79)ng/ml were higher than those in the clinical remission group (82.87±8.19)ng/ml increased significantly. ⑵ The serum MMP3 level in the RA group (190.98±13.43)ng/ml was significantly higher than that in the healthy control group (69.97±10.63)ng/ml. ⑶ There were significant differences in serum MMP-3 levels among RA patients with different imaging stages ( P<0.05). The level of MMP-3 in stage Ⅲ (206.18±13.58)ng/ml and stage Ⅳ (301.72±13.43)ng/ml were significantly higher than those in stage Ⅰ (89.16±10.13)ng/ml. ⑷ RA patients were divided into normal group, osteopenia group, and osteoporosis group according to bone mineral density. The serum MMP-3 level in the osteopenia group (180.87±12.69)ng/ml and osteoporosis group (289.54±13.28)ng/ml were significantly higher than that in the normal group (121.05±8.45)ng/ml. ⑸ Serum MMP-3 levels were positively correlated with C-reaction (CRP), erythrocyte sedimentation rate (ESR), DSA 28, rheumatoid factor (RF), joint swelling index, joint tenderness index, and platelet count in the RA group ( P<0.05). Conclusions:The serum MMP-3 plays an important role in the progression of RA, and is closely related to RA disease activity and bone erosion. It is expected to become a serological indicator for predicting RA bone erosion and radiological progress.

Objective:To explore the effect and involved mechanism of naringenin on acute kidney injury (AKI) induced by ischemia-reperfusion (IR).Methods:The IR-AKI rat model was constructed using the classic bilateral renal pedicle clamping method, then renal function and pathological change were assessed, as well as inflammation-associated genes were detected by quantitative real-time PCR. The hub genes were selected through differential gene analysis and protein-protein interaction network analysis, and their transcription factors were predicted, which constructed a protein library together. The proteins binding to naringenin were selected by reverse molecular docking analysis and further their binding patterns were predicted to explore the mechanism of naringenin. Finally, the results of bioinformatics were verified by experimental methods.Results:Compared with the AKI group, the kidney pathology of the rats in the naringenin pretreatment group was significantly improved, and the renal tubular injury score was reduced ( P<0.01); meanwhile the serum creatinine level and the mRNA expression of the kidney injury molecule 1 (KIM-1) were significantly decreased (both P<0.05). Compared to sham group, IR-AKI increased the level of nuclear factor κB (NF-κB), tumor necrosis factor-α and interleukin-1β (all P<0.05), which reversed by naringenin indicated that naringenin inhibited inflammation in IR-AKI. Differential gene analysis was performed on the GSE98622 data set, and 359 differential genes were obtained. In reverse molecular docking, the proteins with smallest binding energy including NFKBIA, BCL3, NFKB2 and RELA were considered to be related to the preventive effect of naringenin, which were mainly enriched in NF-κB-related inflammation pathways. Domain functional analysis of NF-κB-related genes showed that naringenin could stably bind to its key domain. According to quantitative real-time PCR results, naringenin increased BCL3 level after AKI ( P<0.05), and further decreased the expression level of RELA and NFKB2 (both P<0.05). Conclusion:Naringenin protects IR-AKI by alleviating inflammation, and its mechanism is related to increasing BCL3 and thereby inhibiting the NF-κB pathway.

Objective:To analyze the risk factors of acute kidney injury (AKI) in hospitalized patients with infective endocarditis (IE), construct prediction model, and discuss its predictive value.Methods:The clinical data of 402 adult inpatients diagnosed with IE admitted to the Affiliated Hospital of Qingdao University from January 2010 to January 2020 were retrospectively analyzed. The patients were divided into the AKI group and the non-AKI group. The clinical data, such as gender, age, presence of diabetes, basic estimated glomerular filtration rate (eGFR), laboratory indexes at admission, involvement of valves, presence of sepsis, medication during hospitalization, surgery and outcome of the two groups were compared. Multivariate Logistic regression analysis was used to screen the risk factors of AKI in IE inpatients. A predictive model was constructed, and receiver operating characteristic (ROC) curve was used to analyze the predictive value of the model.Results:A total of 290 patients with IE were enrolled, including 198 non-AKI patients and 92 AKI patients. The incidence of AKI was 31.7%. Among the 92 AKI patients, 46 patients were at AKI stage 1 (50.0%), while 46 patients were at AKI stage 2 and stage 3 (50.0%). Compared with the non-AKI group, patients in the AKI group were older [years old: 64 (55, 71) vs. 55 (46, 63)], and had lower basic eGFR (mL·min -1·1.73 m -2: 64.6±13.6 vs. 82.9±19.5), higher proportion of diabetic and incidence of sepsis (16.3% vs. 8.6%, 38.0% vs. 13.1%), more frequent use of angiotensin converting enzyme inhibitors/angiotensin Ⅱ receptor antagonists (ACEI/ARB), diuretics and non-steroidal anti-inflammatory drugs (NSAIDs; 25.0% vs. 15.2%, 82.6% vs. 63.1%, 58.7% vs. 24.2%), more abnormal urine test results (hematuria or proteinuria, 35.9% vs. 22.7%), higher pathogen culture negative rate (73.9% vs. 51.5%), lower Gram positive (G +) cocci infection rate and surgery rate (22.8% vs. 40.4%, 60.9% vs. 81.8 %), with significant differences (all P < 0.05). There were no significant differences in the gender, number and location of involved valves, and laboratory indexes at admission between the two groups. Compared with the non-AKI group, the inpatient mortality rate of the AKI group was higher (30.4% vs. 8.6%, P < 0.01), and the inpatient mortality rate of patients with AKI stage 2 and stage 3 was significantly higher than that of patients with AKI stage 1 (43.5% vs. 17.4%, P < 0.01). In multivariate Logistic regression analysis, the lower basic eGFR [hazard ratio ( HR) = 0.136, 95% confidence interval (95% CI) was 0.066-0.280], sepsis ( HR = 6.100, 95% CI was 2.394-15.543), demand for NSAIDs ( HR = 2.990, 95% CI was 1.184-7.546) and radiocontrast agent ( HR = 3.153, 95% CI was 1.207-8.238) were independent risk factors for AKI in hospitalized patients with IE (all P < 0.05). A prediction model was constructed based on the above risk factors, and ROC curve analysis showed that the area under the ROC curve (AUC) of prediction model for AKI was 0.888 (95% CI was 0.833-0.943, P < 0.01) with sensitivity of 86.4% and specificity of 80.9%. Conclusions:In the IE-susceptible population, low basic eGFR, sepsis, the need for NSAIDs and contrast agent are independent risk factors to AKI. The predictive model constructed by the above risk factors has certain predictive value for the occurrence of AKI in the IE inpatients.

Objective To study the predictive value of evaluation in oxygen partial pressure[p(O2)] and carbon dioxide partial pressure[p(CO2)] of pleural cavity to the closure of visceral pleura in primary spontaneous pneumothroax (PSP) pa-tients. Methods Seventy-six hospitalized pneumothroax patients were divided into two groups:closed pneumothroax group (n=40) and open pneumothroax group (n=36), according to the radiographic information.To collect the expiratory gas by the device which we designed and produced, to collect the gas in the pleural cavity by thoracentesis. To detect the p(O2)and p(CO2)respectively, and the blood gas analysis of radial artery was done at same time. Results There was significantly low-er value of p(O2)of the gas in the pleural cavity in patients of closed pneumothroax than that of open pneumothroax (P <0.05). The level of p(CO2)was higher in patients of closed pneumothroax than that of open pneumothroax ( P<0.05). There were no significant differences in values of p(O2)and p(CO2)in expiratory gas and the blood gas analysis between two groups (P>0.05). There was significantly higher value of the expiratory gas/the pleural cavity gas p(O2) and a significantly lower value of p(CO2), in closed pneumothroax group than those of open pneumothroax group (P<0.05). Logistic regression analy-sis showed that values of the expiratory gas/the pleural cavity gas p(O2) and p(CO2) were the effective factors for the closure of visceral pleura. ROC curve showed that the areas under ROC curve (AUC) for the expiratory gas/the pleural cavity gas p(O2) and p(CO2) was 0.985 and 0.867, the sensitivities were 92.5% and 77.8%, the specificities were 100%and 85.0%and the reference values were 1.81 and 0.97. Conclusion To utilize the evaluation of gas partial pressure can predict whether the leakage of the visceral pleura is closed.

Objective To investigate mutations of CSMD3 gene in a pedigree of familial cortical myoclonic tremor with epilepsy (FCMTE).Methods Peripheral blood (5 ml) was obtained from FCMTE patients (7 cases),suspected cases,and control individuals.Polymerase chain reaction (PCR) and purification of PCR products for sequencing were used to detect the existence of mutations in 73 exons of gene CSMD3.The resulting products were subjected to agarose gel electrophoresis and gel-imaging system.The PCR amplification products were sequenced.Results The sequencing results of 73 exons were compared with CSMD3gDNA sequence in human GenBank.We neither found any DNA sequence variation nor disease-related mutations.Conclusions The family does not have a mutation in the CSMD3 gene.We need to further find the disease genes and the mutations in this family.

Objective To evaluate the guiding values of different lung compressed forms in the choice of the treat?ment of spontaneous pneumothorax. Methods Based on lung compressed forms on anterior-posterior chest X-ray , a total of 219 spontaneous pneumothorax patients were divided into the periphery shape group (n=127) and irregular shape group (n=92). We observe the relationship between lung compressed form with the times of previous closed thoracic drainage,the cure rate of closed chest drain at the 7th day,length that closed thoracic drainage cure pneumothorax and the incidences of the surgical pleural adhesion. Results We found that the incidence of irregular lung compression in 0, 1 and 2 times of re?ceiving previous drainage were 11.71%(13/111), 57.89%(22/57) and 90.19%(46/51) respectively. Its incidence increased with the times of previous closed chest drain (χ2=96.339, P<0.01). In total, 94 patients (85 of which were cured until the 7th day) and 30 patients (11 of which were cured until the 7th day) were cured using close chest drain in peripheral shape and ir?regular shape group. And the 7th day cure rate is lower in irregular group than that in the peripheral shape. [36.7%(11/30) vs 90.4%(85/94),χ2=37.596, P<0.01]. What’s more, patients in irregular group need longer time to cure pneumothorax than patients in peripheral shape did [d:10.1±4.87 vs 4.00±2.07, t=9.806, P<0.01]. Among the 95 patients who underwent surgi?cal treatment in both groups, the incidence of pleural adhesion is higher in irregular shape group than that in peripheral shape group [91.9%(57/62)vs18.2%(6/33),χ2=52.445, P<0.01]. Conclusion The 7th day cure rate in patients with pe?ripheral shape lung compressed form is higher than patients in irregular lung compressed form using closed chest drain with fewer incidence of pleural adhesion and shorter cure time. Those with irregular lung compression is more appropriate for sur?gical treatment.

Objective To establish the pathogenic gene loci on 8q23.3-24.1 and 10p15 in this benigh adult familial myoclonic epilepsy (BAFME) pedigree.Methods After obtaining informed consent, peripheral blood samples were obtained from 7 BAFME patients and 13 control individuals;amplified polymerase chain reaction (PCR) and short tandem repeat (STR) method were employed to conduct linkage analysis;five STRs on chromosomal segments 8q23.3-q24.1 and three STRs on chromosomal segments 10p1 5 were chosen at genetic distances appropriate.Results Negative signal was all obtained for 8q23.3-q24.1 and 10p15 (LOD scores less than-2 for these STRs, respectively;θ=0.0), excluding involvement of these regions in the BAFME pedigree analyzed.Conclusion STR linkage analysis of 8q23.3-q24.1 and 10p 15 does not support linkage to these regions, indicating that the pathogenic gene in the pedigree we studied is not in these chromosome segments.