Objective To investigate the impact of overweight and obesity on left atrial (LA) function in healthy subjects with excess body weight.Methods Conventional echocardiography and tissue Doppler imaging were performed in 30 obese subjects (BMI≥28 kg/m2),30 overweight subjects (BMI,24to 28 kg/m2) and 30 age-matched normal subjects (BMI＜24kg/m2).Strain (S),peak systolic strain rate (SSR),peak early diastolic strain rate (ESR) and peak late diastolic strain rate (ASR) values were used to evaluating LA function.Results Compared with controls,mean S,SSR and ESR were decreased in obese subjects,while mean SSR,ESR and ASR were decreased in overweight subjects.Compared with overweight subjects,mean ESR was decreased in obese subjects.Conclusions An impaired LA function is found in overweight and obese subjects who has no other clinically appreciable cause of heart disease by using strain and SR imaging.

Objective To assess left ventricular synchronicity in patients with metabolic syndrome(MS)by tissue Doppler imaging.Methods Twenty-two patients with MS and left ventricular hypertrophy(LVH)(MS-LVH group),69 patients with MS and non-LVH(MS-NLVH group)and 33 healthy subjects(control group) were included.Left ventricular(LV)systolic and diastolic synchronicity were determined by measuring the maximal difference in time to peak myocardial systolic contraction(Ts-diff)and time to peak myocardial early diastolic relaxation(Te-diff),and the standard deviation of time to peak myocardial systolic contraction(Ts-SD)and early diastolic relaxation(Te-SD)with 6 basal and 6 middle LV segments.Results Compared with control group,patients with MS in MS-NLVH and MS-LVH group showed significantly prolonged Ts-diff,Ts-SD,Te-diff and Te-SD.Furthermore,Te-diff and Te-SD were much more prolonged in MS-LVH group than in MS-NLVH group.Conclusions Patients with MS have impaired L V systolic and diastolic synchronicity.LVH impacts the LV diastolic synchronicity much more obviously than systolic synchronicity in the patients with MS and LVH.

BACKGROUND AND OBJECTIVES: Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. METHODS: Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-κB was determined by western blot. RESULTS: BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68+ macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-κB in the infarcted hearts. CONCLUSIONS: These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.
Animals ; Blotting, Western ; Cytokines ; Echocardiography ; Enzyme-Linked Immunosorbent Assay ; Eosine Yellowish-(YS) ; Fluorescent Antibody Technique ; Heart ; Hematoxylin ; Interleukin-6 ; Interleukins ; Macrophages ; Mice ; Monocytes ; Mortality ; Myocardial Infarction ; Phosphorylation ; Recovery of Function ; Rhodophyta ; Tumor Necrosis Factor-alpha

Objective To observe the changes of adiponectin (APN),chemerin and tumor necrosis factor-α (TNF-α) in subclinical hypothyroidism (SCH) rats,and to clarify the effect of L-thyroxine (L-T4) replacement therapy.Methods Sixty-five male Wistar rats were randomly divided into five groups via the random number table method:control group (n =10),SCH group A (n =15),SCH group B (n =15),SCH group C (n =15) and L-T4 treatment group (SCH + L-T4,n =10).Rats in groups SCH A,B and C were fed with 5,15 and 20 mg·kg-1·d-1 methimazole (MMI) once daily by gavage.The rats in SCH + L-T4 group were given 20 mg·kg-1·d-1 MMI once daily through gavage,after 8 weeks,6 μg·kg-1· d-1 of L-T4 was intragastrically added (50 μg/tablet) and the model was completed at the 16th week.The levels of serum APN,chemerin and TNF-α were measured via the enzyme linked immunosorbent assay (ELISA) method.The mRNA and protein levels of APN,chemerin and TNF-α in visceral adipose tissue of 5 groups were determined by real-time PCR (RT-PCR) and Western blotting,respectively.Results Compared with the control group [(202.20 + 17.27) ng/L,(143.70 ± 18.46) ng/L,(114.69 ± 4.18) μg/L],the serum chemerin levels in the SCH A,B,C groups were significantly higher [(314.33 ± 16.80),(355.00 ± 17.10),(365.00 ± 11.63) ng/L,P ＜0.05] and TNF-α levels also increased significantly [(222.60 ± 14.13),(279.20 ± 12.79),(288.30 ± 15.89) ng/L,P ＜0.05],and APN levels were significantly decreased [(77.21 ± 3.08),(68.58 ± 2.92),(59.45 ± 2.41) μg/L,P ＜0.05];but compared with SCH group C,the levels of chemerin and TNF-α in the SCH + L-T4 group were decreased [(260.07 ± 10.80),(178.40 ± 10.29) ng/L] and the level of APN [(102.35 ± 3.17) μg/L] was increased (P＜ 0.05).The mRNA and protein levels of APN in SCH A,B,C groups were significantly lower than those in the control group (P ＜0.05).The APN mRNA and protein levels in the SCH + L-T4 group were significantly higher than those in the SCH group C (P ＜ 0.05).The mRNA and protein levels of chemerin and TNF-α in the SCH A,B,C groups were higher than those in the control group (P ＜ 0.05).However,the mRNA and protein levels of chemerin and TNF-α in the SCH + L-T4 group were significantly lower than those in the SCH group C (P ＜ 0.05).Conclusion The expression levels of serum chemerin and TNF-α in SCH rats have increased,and APN levels decreased,but L-T4 can ameliorate these changes.

BACKGROUND AND OBJECTIVES: Appropriate inflammatory response is necessary for cardiac repairing after acute myocardial infarction (MI). Three-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a potent antioxidant and natural bromophenol compound derived from red algae. Although BDB has been shown to have an anti-inflammatory effect, it remains unclear whether BDB affects cardiac remolding after MI. The aim of this study was to investigate the potential role of BDB on cardiac function recovery after MI in mice. METHODS: Mice were intraperitoneally injected with BDB (100 mg/kg) or vehicle control respectively 1 hour before MI and then treated every other day. Cardiac function was monitored by transthoracic echocardiography at day 7 after MI. The survival of mice was observed for 2 weeks and hematoxylin and eosin (H&E) staining was used to determine the infarct size. Macrophages infiltration was examined by immunofluorescence staining. Enzyme-linked immunosorbent assay (ELISA) was used to test the production of cytokines associated with macrophages. The phosphorylation status of nuclear factor (NF)-κB was determined by western blot. RESULTS: BDB administration dramatically improved cardiac function recovery, and decreased mortality and infarcted size after MI. Treatment with BDB reduced CD68+ macrophages, M1 and M2 macrophages infiltration post-MI, and suppressed the secretion of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-1β, monocyte chemoattractant protein (MCP)-1, and IL-6 in the injured hearts. Furthermore, BDB inhibited the phosphorylation of NF-κB in the infarcted hearts. CONCLUSIONS These data demonstrate, for the first time, that BDB treatment facilitated cardiac healing by suppressing pro-inflammatory cytokine secretion, and indicate that BDB may serve as a therapeutic agent for acute MI.

Objective To investigate whether a stable and reliable hyperuricemia model can be established in mice with an ICR background via a triple-modeling method(combined potassium oxazine,hypoxanthine,and 30％yeast paste),and to evaluate the effect of the positive drug febuxostat on the model.Methods A hyperuricemia model of ICR mice was established using a single drug or double-or triple-drug combinations.Serum uric acid and creatinine concentrations,xanthine oxidase(XOD)and urate oxidase(UOX)activity,and uric acid transporter(URAT)1,glucose transporter(Glut)9,anion transporter(OAT)1,and ATP-binding box subfamily G member(ABCG)2 mRNA levels were detected to evaluate whether the hyperuricemia model was formed successfully.Results The serum uric acid levels of ICR mice were not significantly changed by potassium oxazine alone,as they showed an increase but were not significantly different to those of the 30％yeast paste diet or hypoxanthine combined groups.Serum uric acid levels in the triple administration group were significantly increased at 7 days(P＜0.01),while XOD enzyme activity had increased(P＜0.01)and UOX enzyme activity decreased(P＜0.001)at the same timepoint.There were increased expression levels of URAT1 and Glut9(P＜0.05,P＜0.001),and decreased expression levels of OAT1 and ABCG2(P＜0.001).During dynamic monitoring,the blood uric acid levels of triple administration-induced ICR mice peaked at 7 days.In addition,triple administration-induced hyperuricemia in ICR mice was sensitive to the positive drug febuxostat,which caused a significant decrease in blood uric acid levels(P＜0.001).Conclusions A hyperuricemia model in ICR mice can be stably induced by triple administration for 7 days.

Objective:To investigate the distribution of pathogens and the antibiotic resistance profile of bloodstream infections in adult patients with hematological diseases in the period 2014-2018 to provide evidence for the rational use of antibiotics.Methods:We retrospectively analyzed the bloodstream infections in patients with hematological diseases from January 2014 to December 2018 at the institute of Hematology & Blood Diseases Hospital; this included an assessment of the clinical characteristics, distribution of pathogens, and antibiotic resistance data.Results:There were 1935 episodes of BSIs in the 1478 patients who were studied; among these, 1700 episodes occurred in the neutropenic phase. The 7-day and 30-day all-cause mortality rates were 5.5% and 8.2%, respectively. Bloodstream infection was usually accompanied by respiratory tract, perianal zone mucositis, and digestive tract symptoms; the respective proportions were 12.4%, 12.3%, and 9.1%, respectively. Total 2025 strains were isolated; 1551 (76.6%) of the pathogens were gram-negative bacteria, mainly Escherichia coli, Klebsiella pneumonia, and Pseudomonas aeruginosa; 423 (20.9%) were gram-positive bacteria, mainly Staphylococcus spp. and Streptococcus spp. Viridans; 51 (2.5%) were fungi, mainly Candida tropicalis. The resistance rates of Enterobateriaceae to piperacillin/tazobactam, carbapenems, amikacin were <10%. The resistance rates of K. pneumoniae to cefepime, piperacillin/tazobactam and meropenem increased annually. The resistance rates of Pseudomonas aeruginosa to piperacillin/tazobactam, quinolones, Aminoglycosides were <5% even when compared to carbapenems. Eleven stains of methicillin-resistant S. aureus and 1 stain of vancomycin-resistant Enterococcus faecium were detected.Conclusion:The pathogens of bloodstream infection in adult patients with hematological diseases are widely distributed. The resistance rates of different strains vary; the rates in some species had a tendency to increase. Antibiotics should be selected rationally as per the distribution of pathogens and resistance to antibiotics in different patient groups.

Epigenomic imbalance drives abnormal transcriptional processes,promoting the onset and progression of cancer.Although defective gene regulation generally affects carcinogenesis and tumor suppression networks,tumor immunogenicity and immune cells involved in antitumor responses may also be affected by epigenomic changes,which may have significant implications for the development and application of epigenetic therapy,cancer immunotherapy,and their combinations.Herein,we focus on the impact of epigenetic regulation on tumor immune cell function and the role of key abnormal epigenetic processes,DNA methylation,histone post-translational modification,and chromatin structure in tumor immunogenicity,and introduce these epigenetic research methods.We emphasize the value of small-molecule inhibitors of epigenetic modulators in enhancing antitumor immune responses and discuss the challenges of developing treatment plans that combine epigenetic therapy and immuno-therapy through the complex interaction between cancer epigenetics and cancer immunology.