Objective:To investigate the iodine nutrition level of different populations in Daxing District of Beijing, and to provide a basis for implementation of "tailored measures, classified guidance, and scientific iodine supplementation" for prevention and control of iodine deficiency disorders.Methods:From 2020 to 2023, Daxing District of Beijing was divided into 5 districts from April to September each year based on east, west, south, north, and center. One township (street) was selected from each district, and 20 pregnant women, 40 women of childbearing age, 40 adult males, and 40 non boarding children aged 8 to 10 from one primary school were selected from each township (street). At the same time, 100 pregnant women with current addresses in Daxing District, Beijing were selected from one obstetrics hospital in Daxing District every year. Once random urine sample was collected from all survey subjects, and the household edible salt samples were collected from children and 400 pregnant women for determination of urinary iodine and salt iodine levels.Results:From 2020 to 2023, a total of 3 022 urine samples were collected, including 920, 700, 702, and 700 samples from children aged 8 - 10, pregnant women, women of childbearing age, and adult males, respectively. The median urinary iodine levels were 181.1, 135.0, 144.0, and 140.0 μg/L, respectively. There were statistically significant differences in urinary iodine levels among children aged 8 - 10, pregnant women, and women of childbearing age in different years ( H = 77.88, 9.40, 22.11, P < 0.05). A total of 1 320 household edible salt samples were collected from children aged 8 - 10 and pregnant women. Among them, 920 salt samples were collected from children, the median salt iodine was 21.3 mg/kg, the iodized salt coverage rate was 88.48% (814/920), and the qualified iodized salt consumption rate was 80.76% (743/920). Four hundred salt samples were collected from pregnant women, the median salt iodine was 21.8 mg/kg, the coverage rate of iodized salt was 90.25% (361/400), and the consumption rate of qualified iodized salt was 77.50% (310/400). The results of correlation analysis showed there was no correlation between urinary iodine level of children aged 8 to 10 and pregnant women with their salt iodine level ( r = 0.06, 0.07, P = 0.055, 0.142). Conclusions:Pregnant women in Daxing District, Beijing are at a deficiency level in iodine nutrition, with children aged 8 - 10, women of childbearing age, and adult males all at an appropriate level of iodine nutrition. We should strengthen health education for pregnant women and ensure that they receive sufficient iodine nutrition. At the same time, relevant departments should increase the supervision and management of iodized salt.

AIM:To explore the role and mechanism of calcium-sensing receptor(CaSR)in regulating macro-phage polarization in hypertensive rats.METHODS:Male spontaneously hypertensive rats(SHR)and Wistar-Kyoto(WKY)rats were categorized into WKY group,SHR group,SHR+R568(CaSR agonist)group,and SHR+NPS2143(CaSR inhibitor)group.The thoracic aorta was isolated,and the expression of CaSR and macrophage polarization markers in the aorta was observed through immunofluorescence staining.The primary peritoneal macrophages of SHR and WKY rats were aseptically extracted following anesthesia.After intervention with R568 and NPS2143,the expression levels of M1 and M2 markers of peritoneal macrophages were observed by Western blot and immunofluorescence staining.The levels of interleukin(IL)-1β and IL-10 were measured by ELISA.The concentration of Ca2+in peritoneal macrophages was mea-sured by immunofluorescence.Western blot was employed to identify the expression of CaSR and nucleotide-binding oligo-merization domain-like receptor protein 3(NLRP3)inflammasome components.Following anesthesia,vascular smooth muscle cells(VSMCs)were isolated from SHR using an adherent method.Subsequently,a co-culture system was estab-lished with macrophage supernatant.The optimal action time for this co-culture system was determined through CCK-8 as-say.RESULTS:Compared with SHR group,activation of CaSR resulted in a significant decrease in the protein expres-sion of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers in the aorta(P<0.05).Compared with SHR group,administration of R568 led to a significant decrease in the protein ex-pression of M1 polarization markers(P<0.05)and a concomitant increase in the protein expression of M2 polarization markers(P<0.05)in peritoneal macrophages.Additionally,there was a notable reduction in the protein levels of NLRP3 inflammasome components(P<0.05).Furthermore,the fluorescence intensity of intracellular Ca2+was significantly en-hanced following R568 treatment(P<0.05).After administration of MCC950,an NLRP3 inflammasome inhibitor,the re-sults were consistent with those observed following R568 treatment,demonstrating statistical significance(P<0.05).This effect was reversed by the combined intervention of U73122,a phospholipase C(PLC)inhibitor(P<0.05).Compared with the control(0 h),the 24-h peritoneal macrophage supernatant exhibited the strongest capacity to enhance the viabili-ty of VSMCs after 24 h of culture(P<0.05).CONCLUSION:In hypertensive rats,the CaSR inhibits NLRP3 inflamma-some activation via the PLC-Ca2+signaling pathway,thereby mediating an increase in macrophage polarization towards the M2 phenotype and a decrease towards the M1 phenotype.

Sleep disorders is one of the most frequent and severe complications in patients with tinnitus and is highly correlated with the severity of tinnitus.Sleep disorders and tinnitus influence each other,forming a vicious circle.While in-terventions have been developed to alleviate tinnitus distress,these interventions are usually not effective in improving sleep in patients with tinnitus and sleep disorders.Helping tinnitus patients to resolve sleep disorders is the key to breaking the cycle and improving their quality of life.In this narrative review,we studyed the current state of research on sleep disorders in patients with tinnitus through three aspects:epidemiology,physiological and psychological mechanisms,and existing psychological,physical,and pharmacological interventions,and to provide a basis for further research on the relationship between tinnitus and sleep disorders and the precise treatment of tinnitus.

Objective This study mainly focuses on the relationship between the serum glycoprotein non-metastatic melanoma protein B(GPNMB)concentration and the degree of neurological damage and prognosis in patients with acute ischemic stroke(AIS),and screens potential biomarkers to provide a reference for clinical diagnosis and treatment.Methods A total of 105 AIS patients hospitalized in the Department of Neurology of the Hospital 2 of Nantong University from June 2023 to March 2024 were selected as the sample group.In this study,the patients were divided into mild group(n=42)and moderate to severe group(n=63)according to the National Institutes of Health Strobe Scale(NIHSS)score within 24 hours of admission.The Modified Rankin Scale(mRS)was used to evaluate the functional recovery 3 months after discharge.The samples were subdivided into good prognosis group(n=34)and poor prognosis group(n=71).The serum GPNMB protein level was detected by ELISA,and the correlation between serum GPNMB protein level and NIHSS and mRS scores was analyzed.The binary Logistic regression model was used to evaluate the predictive value and prognostic evaluation value of serum GPNMB protein level for AIS neurological function damage.Results The serum GPNMB protein concentration in patients with moderate to severe neurological impairment and poor prognosis was significantly lower than that in patients with mild and good prognosis(P<0.05).The serum GPNMB protein level was significantly negatively correlated with the NIHSS score(r=-0.196,P<0.05)and the mRS score(r=-0.334,P<0.05).Multivariate regression analysis showed that GPNMB was still a key independent risk factor for AIS(P<0.05).The evaluation results obtained based on the receiver operating characteristic curve(ROC)showed that the serum GPNMB protein level had diagnostic value in predicting neurological impairment and poor prognosis(sensitivity reached 55.6%,specificity was 81.8%,and the overall accuracy was 63.81%,P<0.05).Conclusion There is a significant positive correlation between the decrease in serum GPNMB protein concentration and the degree of neurological damage in AIS patients,and it is likely to become an important biological indicator for measuring the severity of the disease and long-term prognosis.

Objective:To analyze the etiological characteristics of Clostridium ramosum DZS3717106 isolated from the blood of a patient with septic shock secondary to perianal abscess and the immunological characteristics of the patient. Methods:The isolate was subjected to morphological observation, mass spectrometry, antibiotic susceptibility testing, and 16S rRNA sequencing. Biochemical and cytological test results of the patient were collected. Flow cytometry was used to detect T cell subsets. Impacts of the virulence factors of the isolate on the host immune system were evaluated.Results:DZS3717106 was an anaerobic Clostridium with pleomorphic rod-shaped cells and spores. It was sensitive to penicillin G, piperacillin/tazobactam, and metronidazole, but resistant to clindamycin. It carried various virulence and resistance genes. The patient was immunocompromised with abnormal IL-6, IL-8, and IL-10 levels. Conclusions:Septic shock caused by Clostridium ramosum is rare, and more research is needed on the causes and epidemiology. DZS3717106 infection triggers over-activated inflammatory response in the patient, which may be closely related to the occurrence and development of septic shock.

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.

This article reported a case of a newborn with congenital absence of the penis. The prenatal examinations were unremarkable. Physical examination of the newborn revealed abnormal external genitalia, with well-developed scrotum and fully descended testicle in normal size, but without the penis. Postnatal ultrasound showed no obvious signals of uterus and ovaries in pelvis and had normal bilateral testicles and urinary system. The diagnosis was congenital absence of the penis.

Objective This study mainly focuses on the relationship between the serum glycoprotein non-metastatic melanoma protein B(GPNMB)concentration and the degree of neurological damage and prognosis in patients with acute ischemic stroke(AIS),and screens potential biomarkers to provide a reference for clinical diagnosis and treatment.Methods A total of 105 AIS patients hospitalized in the Department of Neurology of the Hospital 2 of Nantong University from June 2023 to March 2024 were selected as the sample group.In this study,the patients were divided into mild group(n=42)and moderate to severe group(n=63)according to the National Institutes of Health Strobe Scale(NIHSS)score within 24 hours of admission.The Modified Rankin Scale(mRS)was used to evaluate the functional recovery 3 months after discharge.The samples were subdivided into good prognosis group(n=34)and poor prognosis group(n=71).The serum GPNMB protein level was detected by ELISA,and the correlation between serum GPNMB protein level and NIHSS and mRS scores was analyzed.The binary Logistic regression model was used to evaluate the predictive value and prognostic evaluation value of serum GPNMB protein level for AIS neurological function damage.Results The serum GPNMB protein concentration in patients with moderate to severe neurological impairment and poor prognosis was significantly lower than that in patients with mild and good prognosis(P<0.05).The serum GPNMB protein level was significantly negatively correlated with the NIHSS score(r=-0.196,P<0.05)and the mRS score(r=-0.334,P<0.05).Multivariate regression analysis showed that GPNMB was still a key independent risk factor for AIS(P<0.05).The evaluation results obtained based on the receiver operating characteristic curve(ROC)showed that the serum GPNMB protein level had diagnostic value in predicting neurological impairment and poor prognosis(sensitivity reached 55.6%,specificity was 81.8%,and the overall accuracy was 63.81%,P<0.05).Conclusion There is a significant positive correlation between the decrease in serum GPNMB protein concentration and the degree of neurological damage in AIS patients,and it is likely to become an important biological indicator for measuring the severity of the disease and long-term prognosis.

Although clinical evidence suggests that nonalcoholic fatty liver disease is an established major risk factor for heart failure, it remains unexplored whether sleep disorder-caused hepatic damage contributes to the development of cardiovascular disease (CVD). Here, our findings revealed that sleep fragmentation (SF) displayed notable hepatic detrimental phenotypes, including steatosis and oxidative damage, along with significant abnormalities in cardiac structure and function. All these pathological changes persisted even after sleep recovery for 2 consecutive weeks or more, displaying memory properties. Mechanistically, persistent higher expression of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4) in the liver was the key initiator of SF-accelerated damage phenotypes. SF epigenetically controlled the acetylation of histone H3 lysine 27 (H3K27ac) enrichment at the Nox4 promoter and markedly increased Nox4 expression in liver even after sleep recovery. Moreover, fine coordination of the circadian clock and hepatic damage was strictly controlled by BMAL1-dependent Sirtuin 1 (Sirt1) transcription after circadian misalignment. Accordingly, genetic manipulation of liver-specific Nox4 or Sirt1, along with pharmacological intervention targeting NOX4 (GLX351322) or SIRT1 (Resveratrol), could effectively erase the epigenetic modification of Nox4 by reducing the H3K27ac level and ameliorate the progression of liver pathology, thereby counteracting SF-evoked sustained CVD. Collectively, our findings may pave the way for strategies to mitigate myocardial injury from persistent hepatic detrimental memory in diabetic patients.

A major obstacle in type 2 diabetes mellitus (T2DM) is sleep fragmentation (SF), which negatively affects testicular function. However, the underlying mechanisms remain to be elucidated. In this study, we demonstrate that SF induces testicular damage through a mechanism involving lipid metabolism, specifically mediated by melatonin (MEL) receptor 1a (MT1). T2DM mice with SF intervention displayed several deleterious phenotypes such as apoptosis, deregulated lipid metabolism, and impaired testicular function. Unexpectedly, sleep recovery (SR) for 2 consecutive weeks could not completely abrogate SF's detrimental effects on lipid deposition and testicular function. Interestingly, MEL and MT1 agonist 2-iodomelatonin (2IM) effectively improved lipid homeostasis, highlighting MEL/2IM as a promising therapeutic drug for SF-trigged testicular damage. Mechanistically, MEL and 2IM activated FGFR1 and sequentially restrained the crosstalk and physical interaction between TAB1 and TAK1, which ultimately suppressed the phosphorylation of TAK1 to block lipid deposition and cell apoptosis caused by SF. The ameliorating effect of MEL/2IM was overtly nullified in Fgfr1 knockout (Fgfr1-KO ^+/- ) diabetic mice. Meanwhile, testicular-specific overexpression of Tak1 abolished the protective effect of FGF1^mut on diabetic mouse testis. Our findings offer valuable insights into the molecular mechanisms underlying the testicular pathogenesis associated with SF and propose a novel therapeutic approach for addressing male infertility in T2DM.