With water immersion, the water exerts a pressure on the body surface. Thus there is a blood volume shift from the periphery to the central circulation, resulting in marked volume loading of the thorax and heart. This article illustrated hemodynamic and hurohumoral responses of hydrotherapy, and dicussed whether patients with left ventricular dysfunction (LVD) or chronic heart failure (CHF) can immerse, take balneotherapy, exercise in the water and swimming. A positive effect of therapeutic warm-water tub bathing has been observed in patients with LVD and CHF, which was assumed to be from afterload reduction due to peripheral vasodilatation caused by the warm water. Optimal swimming as used for cardiovascular training programs may be allowed exclusively for NYHA class Ⅱ patients with myocardial infarction older than 6 weeks, myocarditis suffered more than 6 months ago, and cardiomyopathy. Patients with previous severe myocardial infarctions and/or CHF may bathe in a half sitting position, but immersed no deeper than the xiphoid process, because immersion up to the neck could produce abnormal increase in mean pulmonary pressure and pulmonary capillary wedge pressure temporarily. In coronary artery disease (CAD) patients with reduced LV function the heart is working more efficiently with mild cycling in water than cycling outside of water. Decompensated heart failure is the absolute contraindication to hydrotherapy.

The effects of mangiferin on uric acid excretion, kidney function and related renal transporters were investigated in hyperuricemic mice induced by potassium oxonate. Mice were divided into normal control group, and 5 hyperuricemic groups with model control, 50, 100, and 200 mg x kg(-1) mangiferin, and 5 mg x kg(-1) allopurinol. Mice were administered by gavage once daily with 250 mg x kg(-1) potassium oxonate for seven consecutive days to create the model. And 3 doses of mangiferin were orally initiated on the day 1 h after potassium oxonate was given, separately. Serum uric acid, creatinine and urea nitrogon levels, as well as urinary uric acid creatinine levels were measured. Mouse uromodulin (mUMOD) levels in serum, urine and kidney were determined by ELISA method. The mRNA and protein levels of related renal transporters were assayed by RT-PCR and Western blotting methods, respectively. Compared to model group, mangiferin significantly reduced serum uric acid, creatinine and urea nitrogon levels, increased 24 h uric acid and creatinine excretion, and fractional excretion of uric acid in hyperuricemic mice, exhibiting uric acid excretion enhancement and kidney function improvement. Mangiferin was found to down-regulate mRNA and protein levels of urate transporter 1 (mURAT1) and glucose transporter 9 (mGLUT9), as well as up-regulate organic anion transporter 1 (mOAT1) in the kidney of hyperuricemic mice. These findings suggested that mangiferin might enhance uric acid excretion and in turn reduce serum uric acid level through the decrease of uric acid reabsorption and the increase of uric acid secretion in hyperuricemic mice. Moreover, mangiferin remarkably up-regulated expression levels of renal organic cation and carnitine transporters (mOCT1, mOCT2, mOCTN1 and mOCTN2), increased urine mUMOD levels, as well as decreased serum and kidney mUMOD levels in hyperuricemic mice, which might be involved in mangiferin-mediated renal protective action.

To study on the phylogenetic characterization of the VP1 genes of coxsackievirus A16 (CVA16) causing hand-food-mouth disease (HFMD) isolated from Anhui province in 2014. A total of 413 throat swab specimens from HFMD patients were collected during January to November, 2014 for the isolation and identification of enteroviruses using real-time RT-PCR assays. The VP1 regions of CVA16 isolates were amplified using RT-PCR and sequenced. And the phylogenetic tree was constructed among the VP1 regions of those isolates, the different genotypes and sub-genotypes of CVA16 strains. A total of 97 enteroviruses were isolated from 413 samples, the positive rate was 23.49% (97/413), including seventeen CVA16, seventy six HEV71 and four other enteroviruses. The results of the phylogenetic tree showed that 17.CVA16 strains isolated from Anhui in 2014 clustered within B1b evolution branch of B1 genotype. The nucleotide and amino acid sequence identities were 95.30%-100% and 98.70%-100% among the isolates, respectively, but within B1b branch of 17 strains formed several small transmission chains. The nucleotide acid of 17 CVA16 isolates in Anhui province were closed to the strains isolated from Yunnan, Hunan, Guangdong, Tibet and Jiangsu, especially from Hunan in 2013 and from Shenzhen of Guangdong in 2014, the identity were 96.40%-99.70%. The CVA16 strains isolated from Anhui in 2014 were all belong to genetic subtype B1b of B1 genotype was dominant, and among those isolates, several small virus transmission chains had formed with co-circulating and evolution.
China ; Enterovirus A, Human ; classification ; genetics ; isolation & purification ; Enterovirus Infections ; virology ; Genotype ; Humans ; Molecular Sequence Data ; Phylogeny ; Viral Proteins ; genetics ; metabolism

Protein ubiquitin-like modification of Neddylation is an important post-translational modification mode of protein to widely regulate cell cycle, growth, development and other biological processes. Recent studies have found that MLN4924, small molecule inhibitor of Neddylation modification, has a significant anti-tumor effect, which can inhibit the tumor growth by inducing cell cycle arrest, senescence and apoptosis, and inhibiting tumor angiogenesis. This paper reviews the related mechanism research of cell programmed death induced by Neddylation modification pathway inhibitor MLN4924.

Objective To investigate the dynamic alterations of parameters of platelet in newborns with pulmonary hemorrhage(PHN).Methods One hundred and forty-eight cases were selected into research group,within 48 hours after admission,every 3 hours at the time of pulmonary bleeding,peripheral arterial blood were collected and tint deal blood samples were examined with full-automatic blood cell analyzer in order to monitor dynamically changes of platelet and its parameters.Results The blood platelet count(BPC),thronbocytocrit and PDW were greatly changed at 6 hours before occuring pulmonary hemorrhage(all P

This study examined the effect of P85 (a pluronic block copolymer) and microbubble (MB) ultrasound contrast agents under ultrasound irradiation on gene transfection and expression. The pEGFP plasmids that can encode enhanced green fluorescent protein (pEGFP) served as a report gene and were mixed with different concentrations of MB/0.05% (w/v) P85. Then the plasmids were transfected into human hepatoma G2 (HepG2) cells. The HepG2 cells treated with MB/P85 or without treatment were exposed to ultrasound (US parameters: 1 MHz, 1.0 W/cm(2), 20 s, 20% duty cycle). Twenty-four hours later, the transfection efficiency was assessed by fluorescence microscopy and fluorescence activated cell sorting (FACS) analysis. The cell viability was evaluated by Trypan blue exclusion test. The results showed that the gene transfection efficiency in HepG2 cells under ultrasound irradiation was significantly higher than that without ultrasound irradiation. HepG2 cells in the MB or P85 group in the absence of ultrasound expressed less amount of green fluorescent protein. The expression efficiency reached (22.14±3.06)% and the survival rate was as high as (55.73±3.32)% in the 30% MB plus P85 group. It was concluded that MB and P85 in the presence of ultrasound can enhance gene transfection and expression.

Objective To observe the inhibitive effect of electro-acupuncture (EA)at Zusanli points (ST36)on inflammatory mediators of postoperative intra-abdominal adhesions and study the relationship between EA and cholinergic anti-inflammatory pathway.Methods Forty-eight male Wistar rats were divided into 6 groups (each =8):Group A (control),Group B(abdominal adhesions model),Group C (abdominal adhesions plus EA),Group D(sham acu-point control),Group E (abdominal adhesions plus α-bungarotoxin )and Group F (abdominal adhesions plus EA after α-bungarotoxin).Animal models of abdominal adhesion were produced by Chiang’s path.Bilateral Zusanli points (ST36) and shame acupoints were electro-acupunctured at a constant voltage for 1 hour while rats were awake.The ɑ-BGT(1 μg/kg)was injected into the abdominal cavity after surgery.All the rats were sacrificed on the 3rd day,and the levels of inflammatory mediators (TNF-ɑ,NO and NOS)in tissues were evaluated.Results Three days after surgery,the damaged cecum of abdominal adhesion groups developed obvious edema that did not adhere with other tissues.Compared with sham control,the abdominal adhesion resulted in significant elevation of inflammatory mediators (TNF-ɑ,NO and NOS).EA at Zusanli points obviously lowered the elevated levels of inflammatory mediators (P <0.01 and P <0.05).EA at Zusanli points following the injection of ɑ-BGT showed less anti-inflammatory effect(P <0.01).Conclusion EA at Zusanli points significantly lowers the elevated levels of inflammatory mediators after abdominal adhesion challenge.The activation of cholinergic anti-inflammatory pathway might be one of the mechanisms by which Zusanli points exert anti-inflammatory effects.

Objective To observe the clinical effects of Zaobo decoction combined bisoprolol treating premature ventricular contractions.Methods 108 patients of ventricular premature beat were recruited intoa control group and an observation group (n=54) according to the random number table method.The control group was treated with bisoprolol, while the observation group was treated with Zaobo decoction on the basis of the control group, and both groups were treated for 8 weeks.24 h dynamic electrocardiogram (ECG), renin activity plasma (PRA), angiotensin Ⅱ (angiotensionⅡ) and ALD (Ang) were observed before and after treatment.The clinical effects were evaluated.Results The total effective rate showed significant difference between the observation group and the control group (75.9％ vs.57.4％;x2=4.167, P=0.041) after the treatment.After treatment, Ang-Ⅱ (56.22 ± 12.7 pg/ml vs.68.45 ± 12.7 pg/ml, t=5.004) in the observation group was significantly lower than the control group (P＜0.01);24 h sinus RR interval standard deviation (129.16 ± 28.56 ms vs.116.13 ± 17.38 ms, t=2.864), every 5 min sinus RR interval mean standard deviation within 24 h (123.57 ± 25.24 ms vs.112.46 ± 18.23 ms, t=2.622), and within 24 h of sinus RR interval difference rms (31.76 ± 11.42 ms vs.22.64 ± 10.32 ms, t=4.354) in the observation group were significantly higher than the control group (P＜0.01).Conclusion Zaobo decoction combined with bisoprolol can effectively improve heart rate variability, regulate rernin vascular angiotensin system, and improve the clinical efficacy of the patients with ventricular premature beat.

Objectives To assess the effects of long-term angiotensin-converting enzyme(ACE) inhibitor treatment with captopril on cardiac function in acute myocardial infarction (AMI).Methods One hundred and one patients with AMIwho were admitted to hospital within 72 hours of the onset of symptoms with no cardiogenic shock were randomly allocated to captopril (n=52; group Ⅰ) and conventional treatment (n=49; group Ⅱ). Left ventricular (LV) systolic performance and diastolic transmitral flow velocity profiles were assessed by Doppler echocardiography at admission (1.2±1.1 days), before discharge (27±10 days) and during follow-up (363±31 days).Results At one year follow-up, in group Ⅰ LV end-diastolic volume decreased, and ejection fraction increased due to a disproportionate decrease in end-systolic volume. The incidence of cardiac dilatation was reduced. LV early diastolic filling velocity (E)increased and late atrial filling velocity (A) decreased, resulting in an elevation of E/A ratio.However, the mean values of LV systolic and diastolic functional parameters were unchanged in group Ⅱ.Conclusions Long-term treatment with captopril exerts a beneficial effect on cardiac protection for patients with AMI.

The atherosclerotic plaque vulnerability may be related to inflammation,immunity,metabolism and blood clotting.One of the key factors affecting plaque stability is inflammatory reaction.This study was to investigate the relationship between vulnerability of coronary artery plaque evaluated with coronary angiography (CAG),intravascular ultrasound (IVUS) and the levels of plasma inflammatory markers.Methods Fifty-eight consecutive patients with acute coronary syndrome who had coronary lesion of a single vessel were divided into 3 groups based on angiographic morphology of the lesions:type Ⅰ lesion group (n =16),type Ⅱ lesion group (n =25) and type Ⅲ lesion group (n =17).The control group consisted of 17 patients with stable angina.Plasma levels of high sensitivity C reaction protein (hs-CRP),matrix metalloproteinase (MMP,including MMP-2 and MMP-9),CD40 ligand (CD40L) and pregnancy associated plasma protein-A (PAPP-A) were measured by ELISA.A subgroup of 28 patients (including 18 ACS patients and 10 stable angina control patients) who underwent IVUS study,were analyzed.Results The plasma levels of MMP-2,MMP-9 and PAPP-A in type Ⅱ lesion group were significantly higher than those in other groups (all P＜0.05).In type Ⅱ lesion group,linear correlation analyses showed significant positive correlation between levels of hs-CRP and MMP-2 (r=0.508);MMP-2 and MMP-9,CD40L,PAPP-A (r=0.647,0.704 and 0.751,respectively);MMP-9 and CD40L,PAPP-A (r=0.491 and 0.639,respectively);CD40L and PAPP-A (r=0.896).IVUS subgroup analysis showed that the area of plaques and plaque burden in culprit lesion,the incidence of high-risk plaques,remodeling index (RI) and positive remodeling percentage in ACS patients were significantly greater than those in control subgroup (P=0.000,0.037,0.028,0.015 and 0.040,respectively).Compared with control subgroup,the plasma levels of hs-CRP,MMP-2,MMP-9 and PAPP-A were markedly elevated (P=0.033,0.000,0.000 and 0.027,respectively).Conclusions CAG and IVUS combined with study on plasma levels of inflammation mediators are helpful in judging the vulnerability of coronary artery plaques.(J Geriatr Cardiol 2008;5:207-211)