Objective To investigate the status of self-management of elderly patients with chronic heart failure (CHF) in Xinjiang Region,and to explore the effects of different demographic factors on self-management.Methods A total of 704 patients with chronic heart failure were randomly selected from Urumqi,Kashgar,Khotan,Changji,Shihezi,Yili Hazakh in Xinjiang Uygur Autonomous Region via convenience sampling method and were investigated using heart failure self-management scale.Results The total score of self-management of chronic heart failure elderly patients was(47.6±11.1) and scoring rate was 59.5％.There were statistically significant differences(P＜0.01) in self-management score among patients with different ethnicity,religion,self-care ability,per capita income.The influencing factors of self-management were self-care ability,NYHA class and per capita monthly income(P＜0.05).Conclusion The overall level of self-management of elderly patients with chronic heart failure in Xinjiang Region is low,and self-management is affected by self-care ability,NYHA class and per capita monthly income.Tailored culture-based education should be provided to improve patients' self-management.

Objective To examine the distribution of systemic inflammation and risk factors of cardiovascular disease (CVD) in patients with psoriatic arthritis (PsA) by comparing with healthy controls.Methods Forty PsA patients and 44 controls were recruited into this cross-sectional study.We evaluated the disease activity and severity [erythrocyte sedimentation rate (ESR),C reactive protein(CRP) and Disease Activity Score (DAS)28],functional ability in patients with predominant axial involvement [Bath AS disease activity index (BASDAI) and Bath AS functional index (BASH)],traditional CVD risk factors and inflammation between these two groups of patients.Then,we compared risk factors for CVD between 40 consecutive PsA patients and 44 controls,adjusted for body mass index (BMI).The frequencies were compared using chi-square tests for categorical variables.Student's t-tests or Mann-Whitney U-tests were used forcontinuous variables where appropriate.Association between the traditionaland metabolic risk factors and the hs-CRP level were assessed using Spearman correlations.Finally,we also assessed the role of inflammation on the CVD risk factor by using a BMI and hs-CRP-adjusted model.Results The BMI of PsA patients was significantly higher than that of the controls.After adjusting for the BMI,PsA patients had a higher prevalence of hypertension (OR=5.615,95％CI 1.844-17.099) and diabetes mellitus (OR=10.655,95％CI 1.150-98.683) than the controls.PsA patients had significantly increased systolic and diastolic blood pressures [(SBP) and (DBP)],total cholesterol (TC)/high density lipoprotein cholesterol (HDL),insulin resistance,inflammatory markers (hsCRP,white cell count and platelet) and decreased HDL compared to the controls.As excepted,the hsCRP level [4.0 (2.1-13.9) vs 1.7 (1.3-2.2)],platelet and white cell counts were significantly increased in the PsA group reflecting underlying inflammation.Further adjustment for hsCRP level rendered the differences in the prevalence of hypertension (OR=3.544,95％CI 1.151-10.914);but the DBP,HDL and sugar levels were non-significantly different between the two groups,while the differences in other parameters were significant.Conclusion The data support the hypothesis that PsA may be associated with hypertension,obesity and dyslipidemia because of the shared inflammation pathway.

OBJECTIVETo explore the influence of lanthanum chloride on the TNFalpha expression of murine peritoneal macrophages stimulated by lipopolysaccharide (LPS).

METHODSMurine peritoneal macrophages (Mphi) were isolated, cultured and then stimulated by LPS. The influence of lanthanum chloride on the TNFalpha secretion and TNFalphamRNA expression of murine Mphi stimulated by LPS was determined by ELISA method and SYBR green fluorescence quantitative RT-PCR. Forty BALB/C mice were randomly divided into two groups and were treated by lethal dose of LPS and lanthanum chloride processed LPS, respectively. The mortality within 7 days was observed.

RESULTSThe TNFalpha secretion and TNFalphamRNA expression level of the Mphi from mice treated by lanthanum chloride processed LPS were obviously lower than those by LPS only (P < 0.01). The mortality of the mice treated by lethal dose of LPS which has been processed by lanthanum chloride was significantly lower than that by lethal dose of LPS only.

CONCLUSIONLanthanum chloride possessed the capacity of lowering down the toxicity of LPS and inhibiting the TNFalpha secretion and TNFalphamRNA expression in murine Mphi stimulated by LPS.

Animals ; Cells, Cultured ; Female ; Gene Expression Regulation ; drug effects ; Lanthanum ; pharmacology ; Lipopolysaccharides ; pharmacology ; toxicity ; Macrophages, Peritoneal ; cytology ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred BALB C ; RNA, Messenger ; drug effects ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha ; genetics ; secretion

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lycium barbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl4). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl4 solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl4-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase Ⅱ detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I?V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.

The development of acute liver injury can result in liver cirrhosis, liver failure, and even liver cancer, yet there is currently no effective therapy for it. The purpose of this study was to investigate the protective effect and therapeutic mechanism of Lyciumbarbarum polysaccharides (LBPs) on acute liver injury induced by carbon tetrachloride (CCl₄). To create a model of acute liver injury, experimental canines received an intraperitoneal injection of 1 mL/kg of CCl₄ solution. The experimental canines in the therapy group were then fed LBPs (20 mg/kg). CCl₄-induced liver structural damage, excessive fibrosis, and reduced mitochondrial density were all improved by LBPs, according to microstructure data. By suppressing Kelch-like epichlorohydrin (ECH)-associated protein 1 (Keap1), promoting the production of sequestosome 1 (SQSTM1)/p62, nuclear factor erythroid 2-related factor 2 (Nrf2), and phase II detoxification genes and proteins downstream of Nrf2, and restoring the activity of anti-oxidant enzymes like catalase (CAT), LBPs can restore and increase the antioxidant capacity of liver. To lessen mitochondrial damage, LBPs can also enhance mitochondrial respiration, raise tissue adenosine triphosphate (ATP) levels, and reactivate the respiratory chain complexes I‒V. According to serum metabolomics, the therapeutic impact of LBPs on acute liver damage is accomplished mostly by controlling the pathways to lipid metabolism. 9-Hydroxyoctadecadienoic acid (9-HODE), lysophosphatidylcholine (LysoPC/LPC), and phosphatidylethanolamine (PE) may be potential indicators of acute liver injury. This study confirmed that LBPs, an effective hepatoprotective drug, may cure acute liver injury by lowering oxidative stress, repairing mitochondrial damage, and regulating metabolic pathways.
Animals ; Dogs ; Antioxidants/metabolism* ; Carbon Tetrachloride ; Chemical and Drug Induced Liver Injury/drug therapy* ; Kelch-Like ECH-Associated Protein 1/metabolism* ; Liver ; Metabolic Networks and Pathways ; Mitochondria/metabolism* ; NF-E2-Related Factor 2/metabolism* ; Oxidative Stress ; Polysaccharides/pharmacology* ; Lycium/chemistry*

BACKGROUNDNicotine is primarily rsponsible for the highly addictive properties of cigarettes. Similar to other substances, nicotine dependence is related to many important brain regions, particular in mesolimbic reward circuit. This study was to further reveal the alteration of brain function activity during resting state in chronic smokers by fractional amplitude of low frequency fluctuation (fALFF) based on functional magnetic resonance imaging (fMRI), in order to provide the evidence of neurobiological mechanism of smoking.

METHODSThis case control study involved twenty healthy smokers and nineteen healthy nonsmokers recruited by advertisement. Sociodemographic, smoking related characteristics and fMRI images were collected and the data analyzed.

RESULTSCompared with nonsmokers, smokers showed fALFF increased significantly in the left middle occipital gyrus, left limbic lobe and left cerebellum posterior lobe but decreases in the right middle frontal gyrus, right superior temporal gyrus, right extra nuclear, left postcentral gyrus and left cerebellum anterior lobe (cluster size >100 voxels). Compared with light smokers (pack years ≤ 20), heavy smokers (pack years >20) showed fALFF increased significantly in the right superior temporal gyrus, right precentral gyrus, and right occipital lobe/cuneus but decreased in the right/left limbic lobe/cingulate gyrus, right/left frontal lobe/sub gyral, right/left cerebellum posterior lobe (cluster size >50 voxels). Compared with nonsevere nicotine dependent smokers (Fagerstrőm test for nicotine dependence, score ≤ 6), severe nicotine dependent smokers (score >6) showed fALFF increased significantly in the right/left middle frontal gyrus, right superior frontal gyrus and left inferior parietal lobule but decreased in the left limbic lobe/cingulate gyrus (cluster size >25 voxels).

CONCLUSIONSIn smokers during rest, the activity of addiction related regions were increased and the activity of smoking feeling, memory, related regions were also changed. The resting state activity changes in many regions were associated with the cumulative amount of nicotine intake and the severity of nicotine dependence.

Adult ; Brain ; physiology ; Case-Control Studies ; Female ; Humans ; Magnetic Resonance Imaging ; methods ; Male ; Smoking ; adverse effects ; Young Adult