Association of Combined Healthy Lifestyle Factors With Incident Dementia in Participants With and Without Multimorbidity: A Large Population-Based Prospective Cohort Study.

BACKGROUND: The effect of a healthy lifestyle on dementia associated with multimorbidity is not well understood. Our objective is to examine whether the adoption of a healthy lifestyle could potentially reduce the elevated risk of dementia in individuals with and without multimorbidity. METHODS: We utilized data from the UK Biobank cohort. A comprehensive healthy lifestyle score, ranging from 0 to 6, was generated. Cox proportional hazards models were used to examine the associations between multimorbidity, the healthy lifestyle score, and the incidence risk of dementia. RESULTS: Over a median follow-up period of 12.5 years, 5 852 all-cause dementia were recorded. Multimorbidity including cardiovascular, metabolic, neuropsychiatric, and inflammation-related diseases was associated with a higher risk of subsequent dementia. Each additional chronic disease was associated with a hazard ratio (HR) of 1.38 (95% CI: 1.33, 1.44). Compared to individuals without multimorbidity and a healthy lifestyle score of 5-6, patients with multimorbidity and a lifestyle score of 0-1 had a significantly higher risk of dementia (HR: 3.13; 95% CI: 2.64, 3.72), but the risk was markedly attenuated among those with multimorbidity and a lifestyle score of 5-6. Among patients with 3 or more diseases, the HR for dementia was 0.53 (95%CI: 0.42, 0.68) when comparing a lifestyle score of 5-6 to 0-1. And we observed more pronounced association between them among people younger than 60 years old. CONCLUSIONS: Adherence to a combination of healthy lifestyle factors, especially at a young age, was associated with a significantly lower risk of dementia among participants with multimorbidity.

Expression and role of anti-oxidative damage factors in the placenta of preterm infants with premature rupture of membranes. / æŠ—æ°§åŒ–æŸä¼¤å› å­åœ¨èƒŽè†œæ—©ç ´æœªè¶³æœˆå„¿èƒŽç›˜ä¸­çš„è¡¨è¾¾åŠä½œç”¨.

OBJECTIVES: To study the association of the anti-oxidative damage factors nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NAD(P)H:quinone oxidoreductase-1 (NQO1) with preterm premature rupture of membranes (PPROM). METHODS: A prospective study was conducted. The neonates who were hospitalized in Yanbian Hospital from 2019 to 2020 were enrolled as subjects, among whom there were 30 infants with PPROM, 32 infants with term premature rupture of membranes (TPROM), and 35 full-term infants without premature rupture of membranes (PROM). Hematoxylin and eosin staining was used to observe the inflammatory changes of placental tissue. Immunohistochemical staining was used to measure the expression of Nrf2, HO-1, and NQO1 in placental tissue. Western blot was used to measure the protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue. RESULTS: Compared with the PPROM group, the TPROM group and the non-PROM full-term group had significantly higher positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue (P<0.05). There were no significant differences in the positive expression rates and relative protein expression levels of Nrf2, HO-1, and NQO1 in placental tissue between the TPROM and non-PROM full-term groups (P>0.05). CONCLUSIONS: The low expression levels of Nrf2, HO-1, and NQO1 in placental tissue may be associated with PPROM, suggesting that anti-oxidative damage is one of the directions to prevent PPROM.

[Impact of subchronic exposure to low-dose nano-nickel oxide on the reproductive function and offspring of male rats].

OBJECTIVE: To investigate the influence of subchronic exposure to low-dose subchronic nano-nickel oxide (NNO) on the reproductive function of male rats and embryonic development of the pregnant rats. METHODS: Fifty normal healthy male SD rats weighing 180－220 g were randomly divided into five groups of equal number, negative control, 4 mg/ml micro-nickel oxide (MNO), and 0.16, 0.8 and 4 mg/ml NNO, those of the latter four groups exposed to MNO or NNO by non-contact intratracheal instillation once every 3 days for 60 days, and then all mated with normal adult female rats in the ratio of 1∶2. After the female animals were confirmed to be pregnant, the males were sacrificed and the weights of the body, testis and epididymis obtained, followed by calculation of the visceral coefficients, determination of epididymal sperm concentration and viability and the nickel contents in the blood and semen by atomic fluorescence spectrometry. The female rats were killed on the 20th day of gestation for counting of the implanted fertilized eggs and live, dead and resorbed fetuses. RESULTS: After 60 days of exposure, the rats of the NNO groups showed no statistically significant differences from those of the negative control and MNO groups in the weights of the body, testis and epididymis or visceral coefficients. Compared with the negative control group, the animals of the 0.8 and 4 mg/ml NNO groups exhibited markedly decreased sperm concentration (ï¼»9.36 ± 0.98ï¼½ vs ï¼»7.49 ± 1.46ï¼½ and ï¼»6.30 ± 1.36ï¼½ ×106/ml, P < 0.05) and viable sperm (ï¼»85.35 ± 9.16ï¼½% vs ï¼»68.26 ± 16.63ï¼½% and ï¼»65.88 ± 14.68ï¼½ %, P < 0.05), increased morphologically abnormal sperm (ï¼»8.30 ± 2.47ï¼½% vs ï¼»13.99 ± 4.87ï¼½% and ï¼»15.38 ± 8.86ï¼½ %, P < 0.05), and elevated rate of dead and resorbed fetuses (1.18% vs 6.89% and 7.37%, P < 0.05), blood nickel content (ï¼»0.13 ± 0.16ï¼½ vs ï¼»0.52 ± 0.34ï¼½ and ï¼»0.82 ± 0.44ï¼½ mg/L, P < 0.05) and semen nickel content (ï¼»0.08 ± 0.13ï¼½ vs ï¼»0.35 ± 0.23ï¼½ and ï¼»0.63 ± 0.61ï¼½ mg/L, P < 0.05). The nickel level in the semen was correlated significantly with that in the blood (r = 0.912, P <0.01), negatively with the rate of viable sperm (r = －0.879, P <0.01) and positively with the percentage of morphologically abnormal sperm (r = －0.898, P <0.01). CONCLUSIONS: Sixty-day exposure to nano-nickel oxide at 0.8 and 4 mg/ml can produce reproductive toxicity in male rats and result in fetal abnormality in the females, while that at 0.16 mg/ml has no significant toxic effect on the reproductive function of the males.

Effect of smoking cessation intervention for pregnant smokers.

This study retrospectively evaluated the effect of smoking cessation intervention in pregnant women with smoking.A total of 176 pregnant smokers were included in this study. Ninety-five participants received smoking cessation intervention plus physical activity, and were assigned into a treatment group. Eighty-one participants underwent physical activity only, and were assigned into a control group. Primary outcomes included the number of participants quit smoking, daily cigarettes consumption, and quit attempts. The secondary outcomes included infant outcomes. All primary outcomes were measured after 12-week treatment and at delivery. Secondary outcomes were measured at delivery only.After 12-week treatment, participants in the treatment group did not significantly reduce the number of participants quit smoking; decrease daily cigarettes consumption, and quit attempts in pregnant smokers, compared with subjects in the control group. At delivery, the comparison also did not show significant differences in the number of participants quit smoking, decreasing daily cigarettes consumption, and quitting attempts in pregnant smokers, as well as all infant outcomes between 2 groups.The results of this retrospective study did not found that smoking cessation intervention may help to quit smoking for pregnant smokers.

A retrospective study of smoking cessation intervention among university students.

This retrospective study investigated the effect of smoking cessation intervention (SCI) among university students in China.Around 192 eligible smokers among university students were included, and were assigned to an intervention group (n = 100), and a control group (n = 92). All included subjects in both groups were recommended to increase fruits and vegetables consumptions. Additionally, participants in the intervention group also underwent SCI therapy for a total of 4 weeks. The outcome measurements consisted of a number of students quit smoking, daily cigarettes, quit attempts, mean days of smoking in the past 30 days, and also stage of change.After 4-week treatment, SCI neither can decrease the number of students quit smoking (P = .21), daily cigarettes (P = .21), quit attempts (P = .07), and mean days of smoking in past 30 days (P = .77), nor can enhance the stage of change (precontemplation, P = .18; contemplation, P = .59; preparation, P = .46).The results of this study showed that after 4-week therapy, SCI may be ineffective for smokers among university students in Chinese.

Methylation of the suppressor of cytokine signaling 3 gene (SOCS3) in bladder cancer.

BACKGROUND: It has been identified consequences of dysregulation of JAK-STAT signalling, particularly in regard to JAK-STAT signalling that has been shown to have roles in the oncogenesis of several cell types. SOCS3 protein, the negative regulatory protein of JAK-STAT signaling pathway, may also plays critical regulatory roles in cancer initiation and progression. SOCS3 promoter hypermethylation has often been identified in human cancers; however, the precise role of SOCS3 in bladder cancer is unclear. METHODS: The methylation status of the SOCS3 was analyzed in an age (±5 years) and sex-matched case-control study, including 112 bladder cancer cases and 118 normal controls, using the MassARRAY EpiTYPER system. RESULTS: Methylation rate of JAK2, SOCS3 and STAT3 gene were shown to vary among different CpG island. The methylation rate of SOCS3 gene was also much higher in BCa than in normal control participants, but the methylation rate of JAK2, STAT3 gene weren't different in Bca and normal control participants. CONCLUSIONS: Our study demonstrates that promoter hypermethylation of SOCS3 gene is associated with BCa and thus, may serve as an independent prognostic biomarker.

Association of selenoprotein S gene polymorphism with ischemic stroke in a Chinese case-control study.

Previous studies showed that selenoprotein S (SELS) was associated with a range of inflammatory markers, and its gene expression was influenced by a polymorphism in the promoter region. The genetic basis of the ischemic stroke has now been largely determined, so the aim of the study was to examine the role of SELS genetic variants in the ischemic stroke risk in a Chinese population. We conducted a case-control study with 239 ischemic stroke patients and 240 controls. Two single-nucleotide polymorphisms (SNPs) in SELS genes were analyzed for association with the risk of ischemic stroke in the Chinese Han population. No evidence of ischemic stroke association was observed with the SNP rs34713741. Interestingly, the strongest evidence showed that SELS SNP rs4965814 was associated with ischemic stroke (P < 0.05). We found a significant association with increased ischemic stroke risk in women carrying the CC genotype of rs4965814 [hazard ratio: 2.43(1.03-5.75)]; a similar trend was also found in men carrying the TC genotype of rs4965814 [hazard ratio: 1.81(1.06-3.08)]. SNP rs4965814 of SELS may affect the susceptibility to ischemic stroke. Understanding the inflammatory mechanisms of ischemic stroke may give new therapeutic targets to pharmacologists.

Neuroprotective effects of hydrogen sulfide and the underlying signaling pathways.

Hydrogen sulfide (H2S) is an endogenously produced gas that represents a novel third gaseous signaling molecule, neurotransmitter and cytoprotectant. Cystathionine ß-synthase (CBS), cystathionine γ-lyase (CSE), 3-mercaptopyruvate sulfur transferase with cysteine aminotransferase (3-MST/CAT) and 3-mercaptopyruvate sulfur transferase with d-amino acid oxidase (3-MST/DAO) pathways are involved in the generation of endogenous H2S despite the ubiquitous or restricted distribution of those enzymes. CBS, 3-MST/CAT and 3-MST/DAO can be found in the brain, while CSE is widely located in other organs. There also exist up-taking or recycling and scavenging mechanisms in H2S metabolism to maintain its persistence for physiological function. In recent years, investigating the role that H2S plays in the central nervous system and cardiovascular system has always been a hotspot. To date, effects of H2S are at least partially verified in multiple animal models or neuron cell lines of Alzheimer's disease, Parkinson's disease, cerebral ischemia, major depression disorders and febrile seizure, although subsequent studies are still badly needed. This article presents an overview of current knowledge of H2S focusing on its neuroprotective effects and corresponding signaling pathways, together with connections to potential therapeutic strategies in the clinic.

Antidepressant-like and anxiolytic-like effects of hydrogen sulfide in behavioral models of depression and anxiety.

Depression is a common and debilitating mental illness and is often comorbid with anxiety disorders. Altered synaptic plasticity is considered to be an important mechanism underlying antidepressant drug action. It has been reported that hydrogen sulfide (H2S), the third gaseous transmitter, facilitates the induction of hippocampal long-term potentiation and augments synaptic neurotransmission, involved in the regulation of synaptic plasticity. The aim of this study was to clarify the antidepressant-like and anxiolytic-like effects of H2S. H2S (NaHS, 1.68 or 5.6 mg/kg, intraperitoneally, for 7 days) exerts a specific antidepressant-like effect in the forced swimming test of mice and rats and the tail suspension test of mice, and reduces the anxiety-like behaviors of both mice and rats in the elevated plus-maze test. These results reveal a unique antagonistic action of H2S in depressive-like and anxiety-like behaviors and suggest that elevating H2S signaling in the brain may represent a novel approach for the treatment of depressive and anxiety disorders.