55 cases of severe multiple organ failure above 60 years old were treated from April 1977 to January 1987. Each case suffered from 2 to 11 kinds of chronic diseases with an average of 3.8 kinds, and an average of 3.3 organ failures. The average mortality rate was 90.9%. The main precipitating factors were pulmonary infection(72.7%), metastatic carcinoma (14.6%), cardiac arrhythmia (7.3%) and improper medication (5.5%). Low organ infusion, endotoxin and immunological insufficiency probably contributed to their development. Diagnosis, prognosis, therapy and prevention of MOF in the elderly were discussed.

M-mode and pulsed Doppler echocardiography was used to evaluate the changes in structure and function of the left ventricle in 30 patients with chronic renal failure (CRF).The left ventricular mass index (LVMI) and systolic function were unchanged in the early stage of the CRF cases as compared with those of the controls (n = 30). However, the decrement in VE (early peak filling velocity) and the increase in VA/VE (late to early peak velocity ratio) indicated damage of the diastolic function. After 13 months follow-up, the LVMI of the CRF group elavated significantly and the VE diminished further.The ejection fraction (EF), shortening fraction (FS) and circumferencial muscular shortening velocity (mVcf) were decreased as compared with those before the follow up. 47.7% of the patients showed left ventricular heart failure.

Essential hypertension (EH) is an escalating problem for developed and developing countries.It is currently seen as a 'complex' genetic trait caused by multiple susceptibility genes which are modulated by gene-environment and gene-gene interactions.Over the past 10 years,mitochondrial defects have been implicated in a wide variety of degenerative diseases,aging,and cancer.Recently several studies showed that human essential hypertension has excess maternal transmission which suggests a possible mitochondrial involvement.However,the exact pathophysiology of mitochondrial DNA mutation (mtDNA) in essential hypertension still remains perplexing.With the application of a variety of imaging approaches and successive mouse model of mitochonddal diseases we convince that these problems will be resolved in the near future.(J Geriatr Cardiol 2008;5(1):60-64)

During aging, cardiac contractile response to β-AR stimulation is decreased in humans and animal models. Recent studies demonstrate that the positive inotropic effects of both β1-AR and β2-AR stimulation are significantly decreased with aging.This is accompanied by decreases in both β-AR subtype densities and a reduction in membrane adenylyl cyclase activity. However,neither G protein-coupled receptor kinases (GRKs) nor inhibitory G proteins (Gi) appears to contribute to the age-associated reduction in the β-AR modulation of contraction. Thus, while both aging and chronic heart failure exhibit a diminution in cardiac β-AR responsiveness, only heart failure exhibits increased GRK-mediated desensitization ofβ-Ars and an upregulation of Gi proteins.

Objective The aim of the study is to explore the relationship of lung infection(LI)and multiple organ failure in the elderly(MOFE).Methods Consecutive patients ,who were admitted to the Institute of Geriatric Cardiovascular Diseases of the PLA General Hospital and the Endocardial Department of the Air Force General Hospital,withage≥65 years old were enrolled into 5 groups retrospectively by following criteria:acute LI alone,LI with the first presentation of acute lung edema,chronic bronchitis complicated with LI,chronic heart failure complicated with LI,and nic bronchitis and heart failure complicated with LI.Results Sixty-eight patients were selected of(72.5?7.6)years old ( 38 male).There were 4 cases of pure LI(4%),12 cases of LI firstly presented with the symptoms of acute lung edema(18%),16 cases of LI complicated with chronic bronchitis(24%),15 cases of LI based on chronic heart failure(22%)and 22 cases of LI complicated with chronic bronchitis and heart failure(32%).LI initiated MOFE in 25 cases(37%).Most of them were developed on the basis of chronic bronchitis and/or heart failure(34%).Mortality of secondary LI was higher than that of the primary LI(7.4% VS 0%,P

OBJECTIVE To investigate the distribution of drug resistance of Pseudomonas aeruginosa(PAE) among neonates and analyze the characteristic of the PAE infection.METHODS API system was used for the identification of 131 PAE clinical isolates and the resistance to 17 kinds antibiotics was determined by K-B method.RESULTS Most of 131 strains were isolated from sputum(42.0%) and gastric juice(32.8%).All strains were mainly isolated from neonate intensive care unit(NICU).The sensitivity to amikacin,levofloxacin,ofloxacin,ciprofloxacin,piperacillin/tazobactam,cefoperazone/sulbactam,imipenem and meropenem was respectively over 70.0%.PAE was inferior sensitivity to piperacillin,mezlocillin,cefoperazone,ceftriaxone,ceftazidime and aztreonam.CONCLUSIONS PAE is one of the most common pathogens causing nosocomial infection especially for neonates.Its susceptibility to antibiotics showed multidrug resistance.In order to reduce or prevent the occurrence of resistant isolate,we should rationally choose and use antibiotics combining with trait of neonate.

Thirty-six patients with acetabular fracture undergoing Kocher-Langenbeck approach surgery in Beijing Jishuitan Hospital between January 2001 and December 2005 were selected.All patients underwent tibial tubercle or femoral upper condyle traction before surgery.People with traumatic arthritis or other lower limb injury on postoperative X-ray were excluded.Using Biodex system to test the abduction and extension muscle at 60( ?)/s and 180( ?)/s.Peak torque,total work,and mean power were used for evaluation.The difference between bilateral limbs ≤ 10% was normal,≥ 20% was abnormal and 11%-19% was suspected.The muscle strength in fast test was more than the slow test(t=2.21,P

Objective To study acute toxicity of nanometer titanium dioxide to the liver and kidney of mice. Methods 20 KM mice (22-26 g) were randomly divided into two groups, the control group and the experimental group, TiO2 (20-30 nm) suspension (single dose of 5 g/kg body weight) was given to mice by a single oral gavage, the mice in the control group were given the physiologicalsaline. 14 days after the treatment, the mice were sacrificed and the serum were collected to evaluate the levels of ALT(alanine amino transferase), AST(aspartate aminotransferase), ALP(alkaline phosphatase), UA(uric acid), Cr(creatinine),BUN(blood urea nitrogen), CK(creatine kinase), LDH(lactate-dehydrogenase), ?-HBDH(alpha-hydroxybutyrate dehydrogenase), TBIL(total bilirubin levels). The tissues of the liver and kidney were excised and were embedded in paraffin blocks, hematoxylin-eosin (HE) staining for further histopathological diagnosis. Results The serum ALT, ALT/AST, BUN, LDH and ?-HBDH of the TiO2 group were statistically higher than those in the control group (P

Objective To investigate calcification of cultured aortic medial cells in vitro and acceleration by 25 hydroxycholesterol or ? glycerophosphate. Methods Aortic medial cells were obtained by explantation, and the calcification was observed by von Kossa staining. Insoluble calcium precipitation in cellular layer was determined by biochemical method , and osteocalcin in the media was analyzed with radioimmunoassay. Results Two different types of primary cells were shown from culture: one with parallel cellular growth and being negative by von Kossa staining, the other cell type formed cellular nodules with positive von Kossa staining. After 28 days of cell passages, cell growth appeared no nodule formation. However, many cellular nodules and positive von Kossa staining were observed in the passaged cells treated with 25 hydroxycholesterol or ? glycerophosphate, and both insoluble calcium 〔(57 80?18 50)?g/pool, (67 50?15 30)?g/pool〕and osteocalcin 〔(0 886?0 063)?g/L, (0 895?0 061)?g/L〕in the medium were significantly increased than that of the untreated cells. Conclusions Cultured aortic medial cells could be divided into two subtypes, one with the characters of smooth muscle cells, the other with the micro vascular pericytes which could calcify the extracellular matrix. 25 hydroxycholesterol and ? glycerophosphate promoted the in vitro calcification, and osteocalcin secretion was increased in the process of calcification of aortic medial, suggesting that osteocalcin might participate in the aortic calcification.

To investigate the mechanism of aldosterone in the induction of hypertensive myocardial fibrosis, we compared the changes of the incorporation rate of 3H proline, the contents of cardiac tissue collagen, and the activities of the cardiac mitogen activated protein kinase (MAPK) in the spontaneous hypertensive rats (SHRs) untreated and treated with a competitive antagonist of the aldosterone receptorspironolactone (spiron), and also in normotensive rats. The results showed that the incorporation of 3H proline incubating with the myocardial tissue slices significantly increased at three time points (at 4,6,8 h), that the tissue collagen contents and the activities of tissue MAPK also increased in SHRs than in SHRs treated with spiron and in normotensive rats. It suggests that aldosterone stimulates the cardiac MAPK through specific recepter, thus increases the absorption of proline and synthesis of collagen in the cardiac fibroblasts, and in turn, is responsible for the myocardial fibrosis.