2006年 · 第119卷第08期

Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) occurs when periods of hyperventilation with waxing/waning tidal volume alternated with periods of central hypopnea/apnea. It is present in approximately 40 percent of patients with severe congestive heart failure (CHF). CSR-CSA may contribute to the progression of heart failure by causing repetitive arterial oxygen desaturation, sleep fragmentation, increased left ventricular afterload, activation of sympathetic nervous system, and oscillations in heart rate and blood pressure. There are evidences indicating that CSR-CSA is associated with a remarkable increase in mortality and is also an independent risk factor for cardiac transplantation; furthermore, treatment of CSR-CSA in combination with optimal medical therapy may influence the course of chronic heart failure, improve quality of life and the survival of patients.1 The paper by Zhang et al2 highlights the importance of recognizing this pathological breathing pattern as a potential therapeutic target.

Abstract：Background Congestive heart failure (CHF) is associated with Cheyne-Stokes respiration (CSR), which may hasten CHF. Adaptive servoventilation (ASV) is a novel method of ventilatory support designed for removal of CSF in CHF patients. This study compares the efficacy of ASV in patients with CHF and CSR with the efficacy of oxygen therapy. Methods Fourteen patients with CHF and CSR were recruited. During sleep, nasal oxygen therapy and ASV treatment were each performed for two weeks. Comparison before and after each treatment was made for the following items: a) parameters of sleep respiration, sleep structure and quality; b) left ventricle ejection fraction (LVEF) and 6-minute walk distance. Results Compared with the baseline levels of apnoea hypopnoea index of 34.5±6.1 before treatment, the apnoea hypopnoea index significantly decreased following oxygen therapy to 27.8±8.2, P<0.05 and further reduced following ASV treatment to 6.5±0.8, P<0.01. The minimal pulse oxygen saturation markedly increased following oxygen therapy from a baseline of (84.3±2.6)% to (88.6±3.7)%, P<0.05 and further increased following ASV treatment (92.1±4.9)%, P<0.01. Stages I +II sleep as percentage of total sleep time decreased from (81.9±7.1)% to (78.4±6.7)% following oxygen therapy and further to (72.4±5.0)% following ASV treatment. Stages III +IV sleep as percentage of total sleep time decreased from (8.4±5.5)% to (6.0±3.0)% following oxygen therapy and but increased to (11.9±5.4)% following ASV treatment. The arousal index of 30.4±8.1 before treatment significantly decreased following oxygen therapy to 25.6±5.7, P<0.05 and further declined following ASV treatment to 18.2±6.1, P<0.01. No significant difference was shown in above percentages between day 14 of oxygen therapy and before treatment (P > 0.05). LVEF was significantly higher on day 14 of ASV treatment (37.2±4.1)% than on day 14 of oxygen therapy (33.2±5.1)% and before treatment (30.2±4.6)% (all P<0.05). Six-minute walk distance was the shortest before treatment (226±28) m, longer on day 14 of oxygen therapy (289±26) m, and the longest on day 14 of ASV treatment (341±27) m (all P < 0.01). Conclusion ASV treatment is of better efficacy and greater clinical significance in improvement of CHF by eliminating CSR than oxygen therapy。

Abstract：Background Leptin is a protein mainly secreted by adipocytes, and the major function of leptin was its role in body weight regulation. It is suggested that increased levels of circulating leptin may contribute to anorexia in pathologic conditions including chronic obstructive pulmonary disease (COPD). Recent studies have provided evidence for a link between leptin and proinflammatory cytokines such as tumor necrosis factor-α (TNF-α). This study aimed to explore the role of serum leptin in the malnutrition of COPD patients, and to observe the changes of serum leptin levels during acute exacerbation, also to investigate relationship between leptin and TNF-α. Methods Seventy-two COPD patients and 34 control subjects participated in this study. Seventy-two COPD patients were divided into 3 groups: group COPD IA (patients without malnutrition during acute exacerbation, n=25), group COPD IB (patients without malnutrition during stable disease, n=29), group COPD II (patients with malnutrition during stable disease, n=18). To eliminate the effect of sex differences, all patients and controls were male. Body mass index (BMI), percent ideal body weight (IBW%), triceps skin-fold thickness (TSF), mid-upper arm circumference (MAC), mid-upper arm muscle circumference (MAMC), serum leptin and TNF-α levels, serum prealbumin (PA), serum transferrin (TF), serum albumin (Alb), total lymphocytes count (TLC), forced expiratory volume in one second (FEV1), maximal inspiration pressure (MIP) and maximal expiration pressure (MEP) were measured in all participants. Leptin levels were measured by radioimmunoassay. TNF-α levels were measured by ELISA. The between group difference and correlation of these parameters were analyzed. Results Serum leptin levels were significantly lower in group COPD II [(4.07±3.42) ng/ml] than in group COPD IB [(9.72±6.67) ng/ml] and controls [(8.21±5.41) ng/ml] (P<0.05). There was no statistically significant difference in serum leptin levels between group COPD IA [(10.82±6.40) ng/ml], group COPD IB [(9.72±6.67) ng/ml] and controls [(8.21±5.41) ng/ml]. There was no statistically significant difference in serum TNF-α levels between group COPD II [(8.03±3.37) pg/ml], group COPD IA [(8.90±1.60) pg/ml], and group COPD IB [(7.25±2.08) pg/ml]. There was no significant correlation between leptin and TNF-α in any group. Conclusions Leptin was not involved in anorexia and weight loss of COPD patients. There was no statistically significant difference in serum leptin levels between COPD patients during stable stage and acute exacerbation, and there was no significant correlation between TNF-α and leptin during the regulation of the energy balance in COPD patients。

Abstract：Background Middle mediastinal masses comprise a wide variety of tumors but may also reflect lymphadenopathy, and thus remain an interesting diagnostic challenge. We performed positron emission tomography (PET) of mediastinal masses in order to evaluate the ability of PET to predict the malignancy of these tumors. We compared histologic findings, videomediastinoscopy, computed tomography (CT), and PET-CT in patients with mediastinal disease. Methods Thirty-two patients were evaluated with CT, PET-CT and videomediastionoscopy, and all studies were performed within four weeks in each patient. 11C-choline as a PET tracer was used to visualize masses. PET data were evaluated using the standardized uptake value (SUV) and were compared with pathologic data.Results There were 13 men and 19 women aged from 21 to 74 (mean 45.2) years. Among the patients with mediastinal diseases, sarcoidosis was diagnosed in 12 patients, tuberculosis in 5 patients, lymphoma in 5 patients, and noncaseating granulomata without classical "sarcoid" finding in 3 patients. N2 or N3 nodal metastasis was revealed in 6 of 7 patients who had non-small cell lung cancer or suspected lung cancer, and one was negative (the pathological diagnosis was reactive hyperplasia). The accuracies for correctly diagnosing mediastinal masses for CT, PET-CT and videomediastinoscopy were 38% (12/32), 63% (20/32), and 91% (29/32) respectively. The diagnostic accuracy of videomediastinoscopy was superior to that of PET-CT (χ2=11.130,P<0.001). The SUVs were similar among these diseases. On the other hand, if the diagnostic classification was benign vs malignancy, the accuracies for CT, PET-CT and videomediastinoscopy were 53% (17/32), 75% (24/32), 100% (32/32) respectively. The diagnostic accuracy of videomediastinoscopy was superior to that of PET-CT (χ2=22.042, P<0.001). The SUV of malignant lesions (6.9, 3.2-9.8; n=11) appeared to be higher than that of benign lesions (4.9, 2.9-8.3; n=21), however, this difference was not statistically significant (P=0.054).Conclusions To diagnose lesions located in the middle mediastinum, videomediastinoscopy possesses the highest diagnostic accuracy, and therefore remains the gold standard. PET-CT is valuable for differential diagnosis of benign vs malignant lesions, CT alone or PET alone (SUV) may provide misdiagnosis in a substantial proportion of patients with mediastinal masses.

Abstract：Background Imiquimod is an imidazoquinoline, which class of compounds are known to have antiviral and antitumoural properties. In recent studies, it was shown that imiquimod modulates the T helper cell type Th1/Th2 response by inducing the production of Th1 cytokines like IFN-γ, and by inhibiting the Th2 cytokines like interleukin (IL)-4. Several investigators have shown that T-bet and GATA-3 are master Th1 and Th2 regulatory transcription factors. This study investigated whether imiquimod treatment inhibited airway inflammation by modulating transcription factors T-bet and GATA-3.Methods Thirty-six male SD rats were randomly divided into a control group, an asthmatic group, and an imiquimod group, which was exposed to an aerosol of 0.15% imiquimod. Twenty-four hours after the last ovalbumin (OVA) challenge, airway responsiveness was measured and changes in airway histology were observed. The concentrations of IL-4, IL-5 and IFN-γ in bronchoalveolar lavage fluid (BALF) and serum were measured by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of IL-4, IL-5, IFN-γ, T-bet and GATA-3 in lung and in CD4+ T cells were determined by reverse transcription polymerase chain reaction (RT-PCR). The protein expressions of T-bet and GATA-3 were measured by Western blot. Results It was demonstrated that imiquimod 1) attenuated OVA induced airway inflammation; 2) diminished the degree of airway hyperresponsiveness (AHR); 3) decreased the Th2 type cytokines and increased Th1 type cytokines mRNA and protein levels; 4) modulated the Th1/Th2 reaction by inhibiting GATA-3 production and increasing T-bet production.Conclusion Imiquimod treatment inhibits OVA induced airway inflammation by modulating key master switches GATA-3 and T-bet that result in committing T helper cells to a Th1 phenotype.

Abstract：Background One of the major causes of death in severe acute pancreatitis (SAP) is severe infection owing to bacterial translocation. Some clinical studies suggested that ecoimmunonutrition (EIN) as a new strategy had better treatment effect on SAP patients. But the experiment studies on the precise mechanism of the effect of EIN were less reported. In this study, we mainly investigated the effects of EIN on bacterial translocation in SAP model of dogs.Methods SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in healthy hybrid dogs. The SAP dogs were supported with either parenteral nutrition (PN) or elemental enteral nutrition (EEN) or EIN. The levels of serum amylase, serum aminotransferase and plasma endotoxin were detected before and after pancreatitis induction. On the 7th day after nutrition supports, peritoneal fluid, mesenteric lymph nodes (MLN), liver, and pancreas were collected for bacterial culture with standard techniques to observe the incidence of bacterial translocation. Pathology changes of pancreas were analyzed by histopathologic grading and scoring of the severity of pancreas, and the degree of intestinal mucosal damage was assessed by measuring mucosal thickness, villus height, and crypt depth of ileum.Results Compared with PN and EEN, EIN significantly decreased the levels of serum amylase, serum aminotransferase, plasma endotoxin, and the incidence of bacterial translocation. Furthermore, compared with the others, the histology scores of inflammation in pancreas and the ileum injury (ileum mocosa thickness, villus height, and crypt depth) were significantly alleviated by EIN (P<0.05). Moreover, concerning liver function, the serum levels of alanine aminotransferase, aspartate aminotransferase and albumin were ameliorating significantly in the EIN group.Conclusion Our results suggested that EIN could maintain the integrity of intestinal mucosal barrier and reducing the incidence of bacterial translocation in SAP dogs. Early EIN was safe and more effective treatment for SAP dogs.

Abstract：Background Transforming growth factor (TGF) β1-Smads signal plays an important role in cardiac remodeling following myocardial infarction (MI). In addition, both angiotensin converting enzyme inhibitor (ACEI) and angiotensin II type I receptor blocker (ARB) can effectively prevent left ventricular remodeling. The current study focused on whether the combination of ACEI and ARB is more beneficial for preventing ventricular remodeling and whether Smad proteins mediate this beneficial effect.Results VW/BW significantly increased in the placebo groups compared with that in the control group (P<0.01). This increase was limited in ACEI, ARB, and combined groups (P<0.01 compared with placebo group). There was no significant difference among the three actively treated groups. Collagen was increased in placebo group (5.68±0.5)% compared with that in control group (P<0.01). ACEI, ARB and combined treatment attenuated this increase of collagen [(4.3±0.5)%, (3.5±0.5)%, (3.2±0.4)%] in comparison with that in placebo group (P<0.01 respectively). Combined treatment showed more significant effect on collagen deposition. EF and FS significantly decreased, LVDd and E/A significantly increased in placebo group compared with that in control group (P<0.01 respectively). ACEI, ARB and combined treatment ameliorated these indexes (P<0.01 compared with placebo group). The mRNA expression of TGFβ1, Smad 2, and Smad 3 (0.700±0.045, 0.959±0.037 and 0.850±0.051) increased in placebo group compared with that in control group (P<0.01). ACEI, ARB and combined treatment normalized the increase (P<0.01). Furthermore, ARB and combined treatment proved to be more effective in decreasing TGF β1 and Smad mRNA expression than ACEI treatment (P<0.01). The expression of Smad 2 and Smad 3 protein increased in placebo group compared with that in control group (P<0.01). ACEI, ARB and combined treatment normalized the increase (P<0.01). Furthermore, ARB and combined treatment proved to be more effective than ACEI alone (P<0.01).Conclusions TGFβ1-Smads signal activation is correlated with ventricular remodeling following MI. ACEI and ARB treatment prevents ventricular remodeling by inhibiting expression of Smad 2 and Smad 3. ARB and combined treatment are more effective than ACEI alone。

Abstract：Background Fibrinogen-depleting agents are promising in the treatment of cerebral ischemic disease. They were studied by many trials, and the outcomes were different because of different regimens and different doses. In this study, we assessed the efficacy and safety of defibrase on acute cerebral infarction in China.Methods A search using Chinese hospital knowledge database (CHKD) and MEDLINE database for randomized controlled trials was carried out. A CHKD (1994 June 2005) search was performed with the keyword "defibrase", then a second search for the keyword "acute cerebral infarction"; a MEDLINE search (1950 June 2005) was performed with the following keywords: [(cerebral ischemia), OR (acute cerebral infarction), OR (stroke)], AND [defibrase]. Meta-analysis was performed with RevMan software 4.2.Results Included were 14 studies comparing the efficiency and safety of defibrase with other drugs in the treatment of acute cerebral infarction. Patients' records were pooled (total 646 patients; defibrase, n=328, no defibrase n=318). Neurological deficit score (NDS) before treatment showed weighted mean differences (WMD)=0.95, 95% confidence interval (CI)= (-0.60, 2.50), P=0.23; NDS after treatment showed WMD=-2.20, 95% CI= (-4.21, -0.18), P=0.03; Barthel index at 3 months showed WMD=4.45, 95% CI= (-0.13, 9.03), P=0.06; the plasma fibrinogen level before treatment showed WMD=0.02, 95% CI= (-0.16, 0.19), P=0.86; plasma fibrinogen level after treatment showed WMD=-1.51, 95% CI= (-1.88, -1.15), P<0.00 001. Conclusions With the given dose and regimen of defibrase in China, defibrase may play a role of anticoagulation. It might inhibit the progression of stroke and prevent the recurrence of stroke.

The medical community should, by now, be well aware of the importance of chronic obstructive pulmonary disease (COPD), an increasingly common condition with high morbidity and mortality. In modern terms, COPD has come to signify concurrent chronic bronchitis, asthmatic bronchitis and emphysema. Cigarette smoking has long been recognized as the predominant aetiological agent. Arterial hypoxaemia, a frequent complication of COPD, can lead to pulmonary hypertension and cor pulmonale. COPD affects over 5% of the adult population and is the only major cause of death whose morbidity and mortality are increasing in several countries.1 In China, it is difficult to quantify how many people are affected with COPD. However, a recent epidemiological survey indicated that COPD prevalence was 8.2% in China. COPD prevalence in men was significantly higher than in women (12.4% cf 5.1%). The prevalence in rural areas was higher than that in urban areas (8.8% cf 7.8%). Of patients with COPD, 61.5% were smokers. The report also stated that COPD is the major cause of death in rural areas in China and the fourth leading cause of death in urban areas, rising to the third leading cause of death by 2020.2 The prevalence of the disease increases with age with highest rates seen in people over the age of 70 years. COPD is the only major cause of mortality with a rising incidence and prevalence worldwide, rendering it an increasingly worrisome

Allergic diseases of the airway, which include seasonal rhinitis, chronic perennial rhinitis and asthma, are recognized as inflammatory disorders of the airway mucosa,1-3 but differ in the location of the inflammatory reaction and clinical manifestations of the disease. Asthma and allergic rhinitis frequently coexist in the same patient and are thought to share common predisposing genetic factors which interact with the environmental influences. Both diseases have increased in prevalence over recent decades4,5 particularly in westernized countries. This increase has been largely attributed to environmental factors such as exposure to aerial pollutants,4,6 and early life events, including the degree of exposure to infectious agents which might affect IgE production,5,7 since there has been insufficient time for a significant change in the gene pool。

Bronchodilator reversibility, a response of airway to bronchodilator, occurred in 64% of stable patients with chronic obstructive pulmonary disease (COPD).1 In patients with COPD who have a significant response to bronchodilators, a clinical and functional response to inhaled corticosteroids is similar to that in asthmatics.2

An X-ray film is capable of showing that bacterial infection, viral infection, and non-microbial antigens may all cause infiltrations in the chest. To judge what reason is exactly responsible for the shadows in the film poses a challenge for medical staffs, and this problem can be further complicated by newly discovered pathogens and microbes that need to be further discovered.

Mycobacterium tuberculosis (M. tuberculosis) is a pathogen associated with the deaths of millions of people worldwide annually. Although tuberculosis is a treatable disease, the emergence and increasing prevalence of multi-drug resistant bacterial pathogens emphasizes the need for new and innovative anti-microbial strategies. Effective therapeutic regimens, which have existed, are limited by the emergence of drug resistance and the inability of antibiotics to kill dormant or intracellular organisms。

The most common interventional therapies for liver cancer at present include transcatheter hepatic arterial chemoembolization (TACE),1 percutaneous ethanol injection2 and radiofrequency ablation,3 but all these therapies have some intrinsic disadvantages. Since the advent of electrochemo- therapy (EChT), it has been accepted as a safe and effective therapy for malignant tumors4,5 There are only a few experimental studies reporting the use of EChT in the treatment of liver cancer in the foreign medical literature.6-8 However, there have been some clinical studies, and even fewer reports of experimental studies on EChT for liver cancer in China. We used a rat implanted liver cancer animal model to monitor changes in tumour size, tumour necrosis, cellular apoptosis, expression of peripheral immunological markers (IL-2, sIL-2R, IL-6 and TNF-α) and survival.

Toxoplasma gondii (T. gondii) is one of the intracellular parasitized protozoa and may cause severe medical complications in fetus or immunocompromised individuals. T. gondii existed as tachyzoite during acute stage while as bradyzoite during chronic phase in human cells. To improve understanding of the prevention, diagnosis, and treatment of the disease, it is important to explore the distribution and fluctuation and other biological features of T. gondii in host. The trophozoite had been found in the saliva, blood or urine of the host.1-4 Some studies suggested the dynamic changes of circulating antibody and toxoplasma circulating antigen (TCA) either in blood or in urine.5,6 T. gondii in tissue or blood cannot be counted exactly under the microscope because it was only several micrometers in size and thus most of the studies were performed qualitatively by mouse inoculation or immunology methods. The quantitative fluorescent polymerase chain reaction (QF-PCR) and its application raised the possibility for dynamic observation of the polypide in the host.7,8 In this study, blood and semen were collected from the male rabbit model infected with toxoplasma tachyzoites and T. gondii was detected by QF-PCR quantitatively。