Metabolic syndromes increase significantly with the accumulation of bad dietary habits.

BACKGROUND: The association between dietary habits and metabolic syndrome (MetS) has not been well documented, due to the complexity and individualization of dietary culture in the Chinese population. OBJECTIVE: To construct a composite score from various bad dietary habits and to evaluate their comprehensive association with the prevalence of MetS and its components among Chinese men and women across various age groups. SETTING: Serial cross-sectional studies. METHODS: Twenty-three dietary habits were assessed through face-to-face interviews with 98,838 males and 83,099 females in health check-up programs from 2015 to 2021, among which eighteen bad dietary habits were observed to be associated independently with total MetS. The total score of bad dietary habits was composed of four categories via variable clustering analysis, including irregular dietary habits, unhealthy dietary flavors, unbalanced dietary structure, and high-fat diet. The 2016 Chinese guideline for the management of dyslipidemia in adults was used to define MetS. RESULTS: Men had a higher score of bad dietary habits than women (9.63 ± 3.11 vs. 8.37 ± 3.23), which decreased significantly with increasing age in both males and females (Pinteraction<0.01). The prevalence of total MetS increased significantly with the cumulative score of bad dietary habits in both males (highest quintile vs. lowest quintile: OR, 1.90; 95% confidence interval [CI], 1.80-2.00; Plinear<0.01) and females (OR, 2.23; 95% CI, 2.02-2.46; Plinear<0.01) after adjusted for age, education, smoking status, alcohol consumption, and physical activities. These linear trends were also observed for each MetS component (all Plinear<0.01). The role of irregular dietary habits and high-fat diet on MetS prevalence are much higher in males than in females, while unhealthy dietary flavors and unbalanced dietary structure had a greater influence on females. CONCLUSIONS: The accumulation of bad dietary habits contributes to the MetS developments. Thus, individualized lifestyle interventions are needed to correct bad dietary habits with regard to gender differences.

Association between dietary diversity, sedentary time outside of work and depressive symptoms among knowledge workers: a multi-center cross-sectional study.

BACKGROUND: Low-diversity diets and sedentary status are risk factors for depressive symptoms, while knowledge workers were ignored before. The purpose of this current study was to examine the relationship between dietary diversity, sedentary time spent outside of work, and depressive symptoms among knowledge workers. STUDY DESIGN AND METHODS: This was a multicenter and cross-sectional design that included 118,723 knowledge workers. Participants self-reported online between January 2018 and December 2020. Demographic information, the Dietary Diversity Scale, the Patient Health Questionnaire-9, dietary habits (which included eating three meals on time, midnight snacking, overeating, social engagement, coffee consumption, sugary drink consumption, smoking and alcohol use), sedentary time spent outside of work and physical activity were investigated. RESULTS: The relationships between demographic information, dietary habits and dietary diversity, and depressive symptoms were estimated. Compared with the first and second levels of dietary diversity, the third level of dietary diversity (OR: 0.91; 95% CI: 0.84-0.98) reduced the risk of depressive symptoms. Knowledge workers with different degrees of sedentary status (2-4 h (OR: 1.11; 95% CI: 1.07-1.14), 4-6 h (OR: 1.21; 95% CI: 1.17-1.26), and > 6 h (OR: 1.49; 95% CI: 1.43-1.56), presented a progressively higher risk of depressive symptoms. CONCLUSION: High amounts of sedentary time spent after work and low levels of dietary diversity are risk factors for depressive symptoms. In addition, an irregular diet and overeating are also major risk factors for knowledge workers.

Influence of metabolic syndrome and lifestyle factors on thyroid nodules in Chinese adult men: a cross-sectional study.

Introduction: Given the high prevalence of thyroid nodules and the potential for malignancy, it is imperative to understand the various factors that contribute to their development. This study aimed to explore the relationship between metabolic syndrome, lifestyle, and thyroid nodules in adult men in southern China. Methods: This study enrolled a total of 183,990 subjects at a medical examination center in a general hospital in southern China between January 1, 2015, and December 31, 2020. Multivariate logistic regression analysis was utilized to evaluate the relationship between metabolic syndrome, lifestyle factors, and thyroid nodules. Furthermore, structural equation modeling elucidated the intricate relationships among these variables. Results: The prevalence of thyroid nodules among Chinese adult males was 14.9%. Several factors were identified as risk factors for thyroid nodules, including advanced age, irregular meal time, smoking or quitting smoking, quitting drinking, heavy manual labor, hypertension, diabetes, dyslipidemia and centripetal obesity, and those belonging to ethnic minorities and drinking alcohol were found to be protective factors against thyroid nodules. Structural equation modeling highlighted metabolic syndrome's mediating role amidst lifestyle influences on thyroid nodules. Conclusion: The prevalence of thyroid nodules in Chinese adult males is relatively moderate to low. The factors identified in this study can help clinicians identify high-risk patients and develop targeted screening strategies for the timely detection of thyroid nodules. However, further mechanistic research and longitudinal studies are necessary to explore the underlying causes and establish causal relationships.

Dietary diversity, physical activity and depressive symptoms among middle-aged women: A cross-sectional study of 48,637 women in China.

OBJECTIVE: Depression is the leading cause of mental health-related disease burden. This study aimed to investigate the relationship among dietary diversity, physical activity and depressive symptoms in middle-aged women. METHOD: Based on the WHO guidelines on physical activity, subjects who meet moderate-intensity aerobic physical exercise of 150-300 min per week were qualified or otherwise unqualified. The dietary diversity scores (DDS) were developed according to the balanced diet pagoda and assessed the consumption of nine food groups. The total scores ranged from 0 to 9 and could divide into three levels: insufficient [DDS-1] (score of 1-5), moderate [DDS-2] (score of 6-7), and sufficient [DDS-3] (score of 8-9). RESULTS: An age at menarche ≥12 years old (OR = 0.94; 95 % CI: 0.89-1.00; p < 0.05), a higher dietary diversity score [DDS-3] (OR = 0.59; 95 % CI: 0.55-0.63; p < 0.001), drinking coffee (OR = 0.88; 95 % CI: 0.84-0.92; p < 0.001), and qualified physical activity (OR = 0.69; 95 % CI: 0.66-0.72; p < 0.001) were protective factors for depressive symptoms, while an age at first birth ≤20 years old (OR = 1.23; 95 % CI: 1.12-1.36; p < 0.001) or ≥30 years old (OR = 1.18; 95 % CI: 1.11-1.26; p < 0.001), eating late-night snacks (OR = 1.44; 95 % CI: 1.36-1.52; p < 0.001), drinking sugar-sweetened beverages (OR = 1.15; 95 % CI: 1.06-1.24; p < 0.001), and overeating (OR = 2.30; 95 % CI: 2.069-2.56; p < 0.001) were risk factors. CONCLUSION: This study suggested that dietary diversity and physical activity are associated with depressive symptoms in middle-aged women. To improve dietary diversity, attention should be given to dietary patterns and dietary habits, instead of simply increasing the amount of food.

Iron metabolism disorder regulated by BMP signaling in hypoxic pulmonary hypertension.

BACKGROUNDS AND AIMS: Unexplained iron deficiency is associated with poorer survival in patients with pulmonary hypertension (PH). Bone morphogenetic protein (BMP) signaling and BMP protein type II receptor (BMPR2) expression are important in the pathogenesis of PH. BMP6 in hepatocytes is a central transcriptional regulator of the iron hormone hepcidin that controls systemic iron balance. This study aimed to investigate the effects of BMP signaling on iron metabolism and its implication in hypoxia-induced PH. METHODS AND RESULTS: PH was induced in Sprague-Dawley Rats under hypoxia for 4 weeks. Compared with the control group, right ventricular systolic pressure and right ventricle hypertrophy index were both markedly increased, and serum iron level was significantly decreased with iron metabolic disorder in the hypoxia group. In cultured human pulmonary artery endothelial cells (HPAECs), hypoxia increased oxidative stress and apoptosis, which were reversed by supplementation with Fe agent. Meanwhile, iron chelator deferoxamine triggered oxidative stress and apoptosis in HPAECs, and treatment with antioxidant alleviated iron-deficiency-induced apoptosis by reducing reactive oxygen species production. Expression of hepcidin, BMP6 and hypoxia-inducible factor (HIF)-1α were significantly upregulated, while expression of BMPR2 was downregulated in hepatocytes in the hypoxia group, both in vivo and in vitro. Expression of hepcidin and HIF-1α were significantly increased by BMP6, while pretreatment with siRNA-BMPR2 augmented the enhanced expression of hepcidin and HIF-1α induced by BMP6. CONCLUSIONS: Iron deficiency promoted oxidative stress and apoptosis in HPAECs in hypoxia-induced PH, and enhanced expression of hepcidin regulated by BMP6/BMPR2 signaling may contribute to iron metabolic disorder.

Hydroxychloroquine alleviates the neurotoxicity induced by anti-ribosomal P antibodies.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by a wide spectrum of autoantibodies, among which anti-ribosomal P (anti-P) antibodies are considered to be closely related to the neuropsychiatric SLE (NPSLE). Hydroxychloroquine (HCQ) has been proven to be effective against a variety of autoimmune diseases and is an essential drug for the treatment of SLE. In this study, we investigated the effects of anti-ribosomal P (anti-P) antibodies on neural cells and determined whether hydroxychloroquine (HCQ) influenced the anti-P antibodies-induced changes. The results showed that the binding of anti-P antibodies with mouse neuroblastoma- 2a (N2a) cells and rat primary neurons resulted in elevated intracellular calcium levels, inducing decreased cell viability and cell apoptosis. These inhibitory effects were alleviated by HCQ in a concentration-dependent manner by reducing the intracellular calcium levels and modulating the expression of apoptotic proteins. In summary, our study demonstrates that anti-P antibodies induce neural cell damage. HCQ could ease the damage effects and may play a neuroprotective role in NPSLE.

Rapamycin Modulates the Proinflammatory Memory-Like Response of Microglia Induced by BAFF.

Background: Recently trained immunity of microglia provided an opportunity to study the chronic effect of microglial activation and its metabolic rewiring in neuroimmunological diseases. Since elevated levels of B cell-activating factor (BAFF) have been proved to be associated with some chronic neuroimmunological disorders. Here, we used the trained innate immunity model to analyze the effect of BAFF, a vital regulator of the adaptive immune system, on long-term microglial activation and metabolic reprogramming in vitro and in vivo. Methods and results: In vitro, BV2 cells and mouse primary microglial cells were incubated with BAFF for 24 h (BAFF priming). After 5 days of resting, microglia were restimulated with LPS (LPS restimulation) or BAFF (BAFF restimulation). BAFF priming induced a pro-inflammatory trained immunity-phenotype of both BV2 cells and primary microglial cells, which was indicated by morphological change, secretion of pro-inflammatory cytokine and chemokine upon LPS restimulation or BAFF restimulation. The production of lactate and NAD+/NADH ratio were elevated 5 days after BAFF priming. The activation of the Akt/mTOR/HIF-1α pathway was induced by BAFF priming and lasted for 5 days. Pretreating the BV2 cells or mouse primary microglial cells with rapamycin blocked mTOR/HIF-1α activation and cellular metabolic reprogramming induced by BAFF training. Consistently, rapamycin efficiently suppressed the trained immunity-like responses of microglia triggered by BAFF. In vivo, adult male mice were treated with BAFF by intracerebroventricular injection for priming and 7 days later with BAFF for restimulation. BAFF training activated microglia in the cortex and hippocampus. The production of proinflammatory cytokines and chemokines was elevated after BAFF training. Conclusion: Our current data, for the first time, demonstrate that BAFF priming induces a proinflammatory memory-like response of microglia not only to LPS but also to BAFF itself. Rapamycin inhibits microglial priming triggered by BAFF through targeting the mTOR/HIF-1α signaling pathway. Our data reveal a novel role of BAFF in trained immunity and that rapamycin may be a potential therapeutic target of neuroimmunological diseases.

Urinary ferritin creatinine ratio, a potential biomarker for lupus nephritis activity.

INTRODUCTION/OBJECTIVE: Ferritin has gained increasing attention in systemic lupus erythematosus (SLE).This study aimed to investigate the clinical significance of urinary ferritin/creatinine ratio in lupus nephritis (LN). METHOD: Samples from 62 SLE patients (35 with LN and 27 without LN) and 62 healthy controls were evaluated. There were nine patients who underwent renal biopsy. The amount of urinary ferritin was measured by enzyme-linked immunosorbent assay (ELISA) and normalized by the amount of urinary creatinine to obtain the urinary ferritin/creatinine ratio (UFCR). The relationships between UFCR and inflammatory markers, laboratory indicators, as well as the activity index (AI), and chronicity index (CI) of KBs were also investigated by correlation analysis. RESULTS: UFCR level in severe active SLE patients was significantly higher than that in inactive SLE patients (P < 0.01) or healthy controls (P < 0.01). In addition, UFCR level was significantly increased in the patients with LN when compared with those without LN (P < 0.01).Correlation analysis showed that UFCR level is positively correlated with Systemic Lupus Erythematosus Disease Activity Index (SLEDAI) (P < 0.01), 24 h urine protein quantitation, serum creatinine, serum cystatin C, and GFR. The UFCR levels was significantly positively correlated with AI (P < 0.05) but not CI (P = 0.614) of KBs. CONCLUSIONS: UFCR level is a potential biomarker for the kidney injury in LN. Key Points • UFCR level is significantly increased in LN patients. • UFCR level is positively correlated with SLEDAI. • UFCR level is closely related to kidney injury indicators. • UFCR level is a potential biomarker for the kidney injury in LN.

Lupus serum IgG induces microglia activation through Fc fragment dependent way and modulated by B-cell activating factor.

BACKGROUND: Neuropsychiatric manifestations are frequent in patients with systemic lupus erythematosus (SLE), yet the etiology and pathogenesis of brain damage in SLE remains unclear. Because the production of autoantibodies, formation and deposition of immunocomplexes are major serological characteristics of SLE, the elevated level of serum immunoglobulin may contribute to brain tissue injury of SLE. To testify this, in this study, we examined whether immunoglobulin G (IgG) in the serum of SLE patients affects the cellular functions in central nervous system and the potential mechanism. METHODS: In vivo intracerebral injection of SLE-serum in mouse was used to activate microglia and the production of pro-inflammatory cytokine was assessed by ELISA. Sera was divided into IgG and IgG depleted fractions, while IgG was further divided into Fc and Fab fragments to examine which part has an effect on microglia. Flow cytometry, immunofluorescence and quantitative PCR (qPCR) were used to verify the synergistic effect of B-cell activating factor (BAFF) on IgG stimulation of microglia. RESULTS: We found that IgG in lupus sera can induce M1 activation of brain microglia following intraventricular injection into normal mice, and BAFF facilitates this process. In vitro, we identified that IgG bound to microglia through Fc rather than Fab fragments, and BAFF up-regulated the expression of Fc receptors (FcγR) on the surface of microglia, consequently, promote IgG binding to microglia. CONCLUSION: Our results suggest that lupus serum IgG causes inflammatory responses of microglia by involving the Fc signaling pathway and the activity could be up-regulated by BAFF. Accordingly, disruption of the FcγR-mediated signaling pathway and blockade of microglia activation may be a therapeutic target in patients with neuropsychiatric lupus erythematosus.

Imbalance of circulating Tfr/Tfh ratio in patients with rheumatoid arthritis.

Follicular helper T(Tfh) cells and follicular regulatory T(Tfr) cells are critical for the development and maintenance of germinal center and humoral immune responses. Accumulating evidence has demonstrated that the dysregulation of either Tfh or Tfr cells contributes to the pathogenesis of autoimmune diseases. The aim of this study was to examine the numbers of Tfh and Tfr cells in patients with rheumatoid arthritis (RA). Twenty-four patients with RA patients and 20 health controls (HCs) were enrolled in this study. We analyzed the numbers of Tfh (CD4+ CXCR5+ PD-1hi) cells and Tfr (CD4+ CXCR5+CD127lo) cells in 24 RA patients via flow cytometry. The level of the soluble PD-1 and its ligands (sPD-L1 and sPDL-2) were examined by ELISA. Flow cytometry revealed that both circulating Tfh and Tfr cells were increased in RA patients compared with HCs. More importantly, the ratio of Tfr/Tfh was decreased, indicating a disruption of the balance between Tfh and Tfr. The Tfr/Tfh ratio was inversely correlated with level of serum CRP, ESR, RF, anti-CCP, IgG and DAS28 index. We also found that the serum level of sPD-1 was significantly elevated in the RA patients, which was positively correlated with CRP, ESR and the number of Tfh cells. These results indicate that an imbalance of circulating Tfr and Tfh cells may be involved in the immunopathogenesis of RA and may provide novel insight for the development of RA therapies.

Anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus

Abstract: Background: The clinical significance of anti-neutrophil cytoplasmic antibodies in patients with new-onset systemic lupus erythematosus, especially in systemic disease accompanied by interstitial lung disease remains to be elucidated. Objectives: This study was designed to investigate the role of anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus patients. Methods: A hundred and seven patients with new-onset SLE were enrolled. Presence of anti-neutrophil cytoplasmic antibodies in the sera was assessed by indirect immunofluorescence as well as enzyme linked immunosorbent assay against proteinase-3 and myeloperoxidase. Clinical features and laboratory parameters of patients were also recorded. All patients were subjected to chest X-ray, chest high-resolution computed tomography and pulmonary function test. Results: Forty-five systemic lupus erythematosus patients (45/107, 42%) were seropositive for anti-neutrophil cytoplasmic antibodies. Compared with anti-neutrophil cytoplasmic antibodies-negative patients, the anti-neutrophil cytoplasmic antibodies-positive patients had significantly higher incidence of renal involvement, anemia, and Raynaud's phenomenon as well as decreased serum level of complement 3/complement 4 and elevated erythrocyte sedimentation rate. In addition, there was a positive correlation between serum anti-neutrophil cytoplasmic antibodies level and disease activity of systemic lupus erythematosus. Furthermore, prevalence of interstitial lung disease in the anti-neutrophil cytoplasmic antibodies -positive patients (25/45, 55.6%) was obviously higher than that in the anti-neutrophil cytoplasmic antibodies-negative patients (15/62, 24.2%). Study limitations: The sample size was limited and the criteria for screening new-onset systemic lupus erythematosus patients might produce bias. Conclusions: The level of anti-neutrophil cytoplasmic antibodies in new-onset systemic lupus erythematosus patients correlates positively with the disease activity and the prevalence of interstitial lung disease.

Long-term exposure to high air pollution induces cumulative DNA damages in traffic policemen.

The specific effects of long-term exposure to high air pollution on human health and biological remain unclear. To explore the adverse health effects as well as biological mechanisms and biomarkers for durative exposure to air pollution, 183 traffic policemen and 88 office policemen were enrolled in this study. The concentration of PM2.5 in both the traffic and office policemen's working environments were obtained. Detailed personal questionnaires were completed and levels of inflammation, oxidative stress and DNA damage markers of all participants were analyzed in this study. The average PM2.5 concentration of the intersections of main roads and the offices of control group were 132.4±48.9µg/m3 and 50.80±38.6µg/m3, respectively. The traffic policemen, who stably exposed to at least 2 times higher PM2.5 in their work area as compared with the control group, have a median average duration of 7.00years, and average cumulative intersection duty time reached 8030h. No statistically significant differences in the levels of inflammation markers were observed between the traffic and office policemen. However, the DNA damage markers in traffic policemen shared significant positive correlation with cumulative intersection duty time and higher than those in the office policemen. Multiple linear regression analysis demonstrated that the increase of cumulative intersection duty time by 1h per day for one year was associated with the increase in 8-hydroxy-20-deoxyguanosine of 0.329% (95% CI: 0.249% to 0.409%), tail DNA of 0.051% (95% CI: 0.041% to 0.061%), micronucleus frequency of 0.036‰ (95% CI: 0.03‰ to 0.043‰), and a decrease in glutathione of 0.482% (95% CI: -0.652% to -0.313%). These findings suggest that long-term exposure to high air pollution could induce cumulative DNA damages, supporting the hypothesis that durative exposure to air pollution is associated with an increased risk of cancer.

Minocycline attenuates interferon-α-induced impairments in rat fear extinction.

BACKGROUND: Extinction of conditioned fear is an important brain function for animals to adapt to a new environment. Accumulating evidence suggests that innate immune cytokines are involved in the pathology of psychotic disorders. However, the involvement of cytokines in fear dysregulation remains less investigated. In the present study, we investigated how interferon (IFN)-α disrupts the extinction of conditioned fear and propose an approach to rescue IFN-α-induced neurologic impairment. METHODS: We used a rat model of auditory fear conditioning to study the effect of IFN-α on the fear memory process. IFN-α was infused directly into the amygdala of rats and examined the rats' behavioral response (freezing) to fear-conditioned stimuli. Immunohistochemical staining was used to examine the glia activity status of glia in the amygdala. The levels of the proinflammatory cytokines interleukin (IL)-1ß and tumor necrosis factor (TNF)-α in the amygdala were measured by enzyme-linked immunosorbent assay. We also administrated minocycline, a microglial activation inhibitor, before the IFN-α infusion to testify the possibility to reverse the IFN-α-induced effects. RESULTS: Infusing the amygdala with IFN-α impaired the extinction of conditioned fear in rats and activated microglia and astrocytes in the amygdala. Administering minocycline prevented IFN-α from impairing fear extinction. The immunohistochemical and biochemical results show that minocycline inhibited IFN-α-induced microglial activation and reduced IL-1ß and TNF-α production. CONCLUSIONS: Our findings suggest that IFN-α disrupts the extinction of auditory fear by activating glia in the amygdala and provides direction for clinical studies of novel treatments to modulate the innate immune system in patients with psychotic disorders.

Metabolic Syndrome and Risk of Cervical Human Papillomavirus Incident and Persistent Infection.

Few studies have been conducted on the relationship between metabolic syndrome (MetS) and cervical human papillomavirus (HPV) incidence and persistent infection. We performed a prospective cohort study including 8598 female employees in Hunan, China. First, the subjects were stratified into HPV-negative (N = 7282) and HPV-positive (N = 1316) subgroups, according to the results of an HPV DNA test at baseline. Second, comparisons of the risks of HPV incident and persistent infection between MetS-positive (exposed) and MetS-negative (unexposed) groups were conducted among the HPV-negative and -positive subgroups, respectively. There were 976 (11.39%) subjects diagnosed with MetS and 1316 subjects diagnosed with HPV infection at baseline. The 12-month cumulative incidence of any type of HPV and high-risk type HPV were 7.28% (530/7282) and 6.26% (456/7282), respectively. Obesity was a modifier of the association between MetS and HPV incident infection. As long as obesity presented, MetS and hypertriglyceridemia were significantly associated with an increased risk of HPV incident infection (any-type or high-risk type) (adjusted risk ratios (RR) were 2.88 (95% confidence interval (CI): 1.16, 7.19) and 3.29 (95% CI: 1.47, 7.38), respectively). Among those infected with HPV at baseline, the 12-month type-specific persistence rates were 51.67% and 53.38% for any-type and high-risk type HPV, respectively. No interaction was found between obesity and MetS with regard to the risk of HPV persistence. After adjustment for confounding factors, MetS was still associated with increased risk of any-type HPV persistence (RRadj = 1.21, 95% CI: 1.05, 1.41) and high-risk type HPV persistence (RRadj = 1.25, 95% CI: 1.09, 1.46). No single metabolic component was associated with the risk of HPV persistence. The prevalence of MetS was 11.39% among the Hunan female occupational population. MetS was associated with an increased risk of persistent cervical HPV infection and also with an increased risk of HPV incident infection when obesity presented as well.

Analysis of pulmonary function test results in a health check-up population.

BACKGROUND: To explore the incidences of chronic obstructive pulmonary disease (COPD), obstructive ventilatory dysfunction, and obstructive small airway disease and their risk factors in a health check-up population, with an attempt to inform the early diagnosis and treatment of COPD. METHODS: Subjects who aged 20 years and older and received health check-up in the Health Management Center, Third Xiangya Hospital, Central South University from June 2013 to June 2015 were enrolled in this study. The results of detection and survey for COPD, obstructive ventilatory dysfunction, and obstructive small airway disease were analyzed. RESULTS: Among 6,811 subjects enrolled in this study, the detection rate of COPD, obstructive ventilator dysfunction, and obstructive small airway disease was 0.8%, 2.6%, and 4.0%, respectively, which showed a positive correlation with male gender, age, and smoking index. CONCLUSIONS: Health check-up is an important approach for screening COPD, obstructive ventilator dysfunction, and obstructive small airway disease. Smoking cessation and controlling of relevant risk factors are helpful to lower the incidences of these conditions.

[Association of metabolic syndrome with serum cystatin C in people undergoing health examination].

OBJECTIVE: To investigate the relationship between metabolic syndrome (MetS) and cystatin C in people undergoing healthy examination.
 METHODS: A total of 6 783 subjects were analyzed. They were divided into MetS group (n=1 578), metabolic disturbance (MetD) group (n=3 617) and healthy control (HC) group (n=1 588). The general information, anthropometry, blood sample and urine sample were collected for all the subjects. Multiple logistic regression analysis was used to identify risk factors for MetS and analysis of covariance was used to investigate the correlation between the number of metabolic disturbance components and cystatin C.
 RESULTS: Compared with the HC group, the level of cystatin C significantly increased in MetS and MetD group; compared with MetD group, the level of cystatin C significantly increased in MetS group (P<0.05). After correction by age, sex, smoking, alcohol intake, menopause, waist circumference, body mass index, blood pressure, plasma cholesterol, fasting plasma glucose, estimated glomerular filtration rate, serum uric acid, microalbuminria, high sensitive C-reaction protein and homocysteine, the cystatin C was closely related with MetS (OR=1.951, 95% CI 1.265-3.009, P<0.05). Similarly, the OR value of risk with MetS was increased with the quartile of cystatin C level (P<0.05). In addition, with the increase in metabolic disturbance components, the level of cystatin C was also increased significantly (P<0.01).
 CONCLUSION: Serum cystatin C in our study was significantly associated with MetS. Moreover, the level of cystatin C may be correlated with severity of MetD.

Intra-amygdala microinjection of TNF-α impairs the auditory fear conditioning of rats via glutamate toxicity.

During an inflammatory or infectious process, innate immune cells produce large amount of pro-inflammatory cytokines that act on the brain to cause cognitive dysfunctions. Tumor necrosis factor alpha (TNF-α) is one of the main pro-inflammatory cytokines. Thus, it is important to study how the excessive TNF-α affects the cognitive functions of central nervous system and possible antagonists to its effects. In the present study, we conducted behavioral experiments of rats to determine whether murine TNF-α administered directly into the brain would elicit behavioral effects related to learning and memory impairments. Rats subjected to single-dose intra-amygdala TNF-α infusion showed a significant delay in the acquisition and extinction of auditory fear conditioning. Accordingly, the glutamate level of the tissue samples from amygdala was elevated after the TNF-α treatment. Furthermore, pharmacological blockade of NMDAR before the TNF-α treatment reversed the TNF-α induced impairments in fear learning. Our findings suggest that TNF-α can impair the learning and memory functions through glutamate-NMDAR neurotoxicity, and present the possibility to develop therapeutic modalities directing at glutamate transmission for the treatment of neuro-inflammative dysfunctions.

Correlations between brachial endothelial function and cardiovascular risk factors: a survey of 2,511 Chinese subjects.

OBJECTIVE: We examined the relationship of several cardiovascular risk factors (CVRF) to brachial artery flow-mediated dilatation (FMD) in Chinese subjects. METHODS: This was a cross-sectional study. In 2,511 Chinese adults (age 46.86±9.52 years, 1,891 men and 620 women) recruited from people who underwent health screening at The Third Xiangya Hospital, patients' CVRF [age, body mass index (BMI), waist circumference (WC), blood pressure (BP), cholesterol parameters, creatinine (Cr), uric acid (UA), glucose level and smoking] and prevalence of present disease (hypertension, diabetes mellitus, coronary heart disease and hyperlipidemia) were investigated. RESULTS: Multivariate analysis revealed that FMD negative correlated with age (ß=-0.29, P<0.001), gender (ß=-0.12, P<0.001), BMI (ß=-0.12, P=0.001), WC (ß=-0.10, P=0.011), systolic BP (SBP) (ß=-0.12, P<0.001), fasting glucose (ß=-0.04, P=0.009), total cholesterol (TC) (ß=-0.04, P=0.014), smoking (ß=-0.05, P=0.003), and baseline brachial artery diameter (ß=-0.35, P<0.001). FMD decreased with increasing age in both genders. In women, FMD was higher than men and age-related decline in FMD was steepest after age 40; FMD was similar in men above 55 years old. CONCLUSIONS: In Chinese subjects, FMD may be a usefully marker of CVRF. Age, gender, BMI, WC, SBP, fasting glucose, TC, smoking, and baseline brachial artery diameter were independent variables related to the impairment of FMD. The influence of CVRF on endothelial function is more in women than men.

[Application of serum thymidine kinase 1 of 26 055 cases in health screening for early detection of premalignant/early malignant tumors].

OBJECTIVE: To determine the application of serum thymidine kinase 1 (STK1) in general health screening for early detection of premalignant/early malignant tumors. METHODS: A cross sectional study was carried out in 26 055 health screenings from 8 centers of Changsha in 2011. The concentration of STK1 was determined by a sensitive chemiluminescent dot blot ECL assay. RESULTS: In the elevated STK1 group 60.35% showed diseases with a higher risk of premalignant/ early cancerous progression. The positive rate of elevated STK1 (>2.0 pmol/L) was 2.61%. There was a significantly higher rate with moderate/severe type of hyperplasia of breasts and prostate with elevated STK1 than people with normal STK1 values. CONCLUSION: STK1 may be a reliable marker for risk assessment of premalignant/early malignant tumors.

Intra-amygdala microinfusion of IL-6 impairs the auditory fear conditioning of rats via JAK/STAT activation.

Though accumulating literature implicates that cytokines are involved in the pathophysiology of mental disorders, the role of interleukin-6 (IL-6) in learning and memory functions remains unresolved. The present study was undertaken to investigate the effect of IL-6 on amygdala-dependent fear learning. Adult Wistar rats were used along with the auditory fear conditioning test and pharmacological techniques. The data showed that infusions of IL-6, aimed at the amygdala, dose-dependently impaired the acquisition and extinction of conditioned fear. In addition, the results in the Western blot analysis confirmed that JAK/STAT was temporally activated-phosphorylated by the IL-6 treatment. Moreover, the rats were treated with JSI-124, a JAK/STAT3 inhibitor, prior to the IL-6 treatment showed a significant decrease in the IL-6 induced impairments of fear conditioning. Taken together, our results demonstrate that the learning behavior of rats in the auditory fear conditioning could be modulated by IL-6 via the amygdala. Furthermore, the JAK/STAT3 activation in the amygdala seemed to play a role in the IL-6 mediated behavioral alterations of rats in auditory fear learning.