Measurement of body potassium with a whole-body counter: relationship between lean body mass and resting energy expenditure

We conducted studies to determine whether the Mayo whole-body counter could be used to measure body potassium, and thus lean body mass (LBM), and whether moderate obesity alters resting energy expenditure when corrected for LBM. Twenty-four nonobese and 18 moderately obese adults underwent body potassium (40K) counting, as well as tritiated water space measurement and indirect calorimetry. LBM values predicted from 40K counting and tritiated water space measurements were highly correlated (P = 0.001; r = 0.88). Resting energy expenditure was closely related to LBM (P less than 0.0001; r = 0.78): kcal/day = 622 kcal + (LBM.20.0 kcal/kg LBM). In this relationship, the obese subjects did not differ from nonobese subjects. In summary, the Mayo whole-body counter can accurately measure LBM, and moderate obesity has no detectable effect on corrected resting energy expenditure.     

Circulating vascular endothelial growth factor and systemic inflammatory markers in patients with stable and exacerbated chronic obstructive pulmonary disease

The aim of the present study was to assess circulating levels of VEGF (vascular endothelial growth factor), a biomarker with prognostic significance in cardiovascular disease, and markers of systemic inflammation in patients with stable and exacerbated COPD (chronic obstructive pulmonary disease). Lung function parameters, arterial blood gas analysis and circulating levels of VEGF, IL-6 (interleukin-6), TNF-alpha (tumour necrosis factor-alpha), CRP (C-reactive protein), fibrinogen and the peripheral blood neutrophil cell count were assessed in 30 patients on admission to the hospital for acute exacerbation of COPD, in 30 age-, gender- and BMI (body mass index)-matched patients with stable COPD, and 30 matched controls with normal lung function. Patients with acute exacerbated COPD had higher circulating concentrations of VEGF (P<0.001), IL-6 (P<0.05) and CRP (P<0.01) and an increased blood neutrophil cell count (P<0.05) compared with patients with stable COPD and healthy controls. VEGF levels in exacerbated COPD correlated with systemic inflammatory markers, such as CRP (r=0.61, P<0.005), IL-6 (r=0.46; P<0.01) and fibrinogen (r=0.39, P<0.05). In patients with stable COPD, there was a significant relationship between circulating VEGF levels and the percentage of the predicted FEV(1) (forced expiratory volume in 1 s) (r=0.47, P<0.01). Recovery from the exacerbation resulted in a significant decrease in both circulating VEGF levels and markers of systemic inflammation. In conclusion, circulating levels of VEGF and markers of systemic inflammation are up-regulated in patients with acute exacerbated COPD and decrease after recovery from the exacerbation.     

Resting energy expenditure in chronic cardiac failure.

1. Resting energy expenditure has previously been shown to be elevated in the acute phase of heart failure, but the situation in the compensated state of chronic cardiac failure is unclear. Resting energy expenditure was assessed in 14 patients with stable chronic cardiac failure and 14 matched control subjects by using indirect calorimetry. 2. Resting energy expenditure was significantly elevated in the patients with chronic cardiac failure (112.6 +/- 18.1 versus 87.1 +/- 12.2 kJ day-1 kg-1 total body weight, P less than 0.0002; mean +/- SD) as were resting O2 consumption (3.88 +/- 0.64 versus 3.00 +/- 0.43 ml min-1 kg-1, P less than 0.0002), ventilation (164 +/- 40.3 versus 104 +/- 16.2 ml min-1 kg-1, P less than 0.0001) and heart rate (85.8 +/- 16.9 versus 66.6 +/- 6.9 beats/min, P less than 0.001). Both the resting plasma concentration of noradrenaline (4.48 +/- 1.52 versus 2.28 +/- 0.96 nmol/l, P less than 0.0001) and the serum concentration of free fatty acids (0.78 +/- 0.21 versus 0.57 +/- 0.27 mmol/l, P less than 0.03) were greater in the patients with chronic cardiac failure. Analysis of covariance indicated that most of the difference in resting energy expenditure could be accounted for by the elevated ventilation in the patients with chronic cardiac failure. Arm muscle area, an index of wasting, was lower in the patients with chronic cardiac failure (39.1 +/- 13.1 versus 50.5 +/- 9.4 cm2, P less than 0.02) and resting energy expenditure was found to account for some of this difference. 3. We conclude that an elevated basal metabolism occurs in chronic cardiac failure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Raised resting energy expenditure in Parkinson's disease and its relationship to muscle rigidity.

1. Resting energy expenditure was measured, by indirect calorimetry, in 12 patients with Parkinson's disease and in eight healthy age-matched control subjects. In the patients with Parkinson's disease measurements were made in both the untreated state and after an injection of the dopamine agonist apomorphine (treated state). In each state muscle rigidity was recorded. 2. Resting energy expenditure was higher in patients with Parkinson's disease in both the treated and untreated states than in the control subjects. Of the patients with Parkinson's disease, seven showed no difference in resting energy expenditure between the two treatment states, whereas four showed markedly increased resting energy expenditure in the untreated state. The change in resting energy expenditure in the untreated state, as compared with the treated state, was significantly related to the development of muscle rigidity in the untreated state. 3. In Parkinson's disease, even in optimally treated patients, resting energy expenditure is raised and this may contribute to the weight loss seen in this disease. Severe muscle rigidity occurring during untreated periods results in a further increase in resting energy expenditure.     

Resting energy expenditure in patients with pancreatitis

OBJECTIVE: To assess the resting energy expenditure of hospitalized patients with pancreatitis. DESIGN: Prospective, case-referent study. SETTING: Nutrition support service in a university tertiary care hospital. PATIENTS: Patients referred to the Nutrition Support Service with the diagnosis of pancreatitis. Excluded from study entry included those with cancer, obesity (greater than 150% ideal body weight), those measured within 3 postoperative days, or patients requiring ventilator support with an FIO2 of greater than 0.5. Forty-eight patients with either acute pancreatitis (n = 13), chronic pancreatitis (n = 24), acute pancreatitis with sepsis (n = 7), or chronic pancreatitis with sepsis (n = 7) were studied. The two septic groups were combined into a single pancreatitis-with-sepsis group, since no significant differences among measured variables were observed between individual septic groups. INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: Resting energy expenditure was measured by indirect calorimetry and compared with the predicted energy expenditure, as determined by the Harris-Benedict equations. Resting energy expenditure (percent of predicted energy expenditure) was significantly (p less than .02) greater for patients with pancreatitis complicated by sepsis (120 +/- 11%) compared with the nonseptic chronic pancreatitis group (105 +/- 14%). Resting energy expenditure for the nonseptic acute pancreatitis patients (112 +/- 17%) was not significantly different from the other groups. The septic pancreatitis group had the largest percentage (82%) of hypermetabolic (resting energy expenditure greater than 110% of predicted energy expenditure) patients, whereas 61% and 33% of the acute and chronic pancreatitis groups were hypermetabolic, respectively (p less than .02). CONCLUSIONS: Resting energy expenditure is variable in patients with pancreatitis (77% to 139% of predicted energy expenditure). The Harris-Benedict equations are an unreliable estimate of caloric expenditure. Septic complications are associated with hypermetabolism and may be the most important factor influencing resting energy expenditure in pancreatitis patients.     

丹参注射液对慢性阻塞性肺疾病外周血白细胞黏附分子CD11b表达的影响

目的：研究外周血白细胞黏附分子CD11b与慢性阻塞性肺疾病（COPD）发病的关系及丹参注射液对CD11b表达及肺功能的影响。方法：采用全血直接免疫荧光流式细胞术检测我院81例COPD急性发作期患者（COPD组．分为常规治疗组和丹参治疗组）和21例正常对照组外周血白细胞黏附分子CD11b的表达及其相应的肺功能（FEV1）。结果：（1）COPD组患者CD11b水平明显高于正常对照组（P〈0．01），二者肺功能差异亦有显著性（P〈0．01）。（2）常规治疗组和丹参治疗组治疗后CD11b差异有显著性（P〈0．05），二者治疗后肺功能差异亦有显著性（P〈0．05）。（3）COPD组白细胞黏附分子CD11b与肺功能呈显著负相关（治疗前r=-0．536，P〈0．01：常规治疗组治疗后r=-0．634，P〈0．01；丹参治疗组治疗后r=-0．738．P〈0．01）。结论：CD11b参与了COPD的发病。丹参明显阻抑外周血CD11b的表达．这可能是此类中药具有抗炎活性的机制之一。[著者文摘]     

Evaluation of mechanisms behind elevated energy expenditure in cancer patients with solid tumours

Abstract. The aim of this study was to demonstrate significant factors behind elevated resting energy expenditure in weight-losing cancer patients. There tore, weight-losing cancer patients (n= 60), with normal liver and kidney function tests, were randomized to receive one of four drug treatments for 5 days: (a) Propranolol 80 mg × 2 (β-adreneceptor blockade); (b) Indomethacin 50 mg × 2 (prostaglandin synthesis inhibition); (c) Morphine 5 mg × 3 (pain reliet) or (d) Placebo x 2. A reterence group of healthy well-nourished individuals were examined outside the formal randomization protocol and they received Propranolol 80 mg × 2. The cancer patients were randomized by a computer based algorithm stratifying for measured resting energy expenditure (REE), body composition, biochemical tests, previous therapy, tumour type and tumour stage. Resting energy expenditure was measured by indirect calorimetry in the morning after an overnight fast betore and after drug treatment. β-blockade reduced REE significantly in cancer patients from 1416 ± 95 kcal day^-1 to 1160 ± 63 kcal day^-1 (P <0.02) and from 1472 ± 69 vs. 1398 ± 62 kcal day^-1, (P <0.01) in the well-nourished reterence individuals. The reduction found in cancer patients (10%) was significantly larger than that in the group of reterence patients (5%), (P <0.01). Indomethacin, morphine or placebo did not induce any significant alteration in energy expenditure in our cancer patients. Propranolol treatment was associated with a significant reduction in plasma concentrations of free fatty acids (FFA), but not in plasma glycerol. Our results support the suggestion that adrenergic factors are the most important mediators behind elevated resting energy expenditure in weight-losing cancer patients. Such factors were more important than inflammation and cytokine production related to prostaglandin dependent pathways.     

Total energy expenditure and the level of physical activity correlate with plasma leptin concentrations in five-year-old children.

Leptin, the product of the ob gene, is a hormone secreted by adipocytes that is known to decrease food intake and increase energy expenditure in ob/ob mice. In humans, variants in the OB gene have not been detected and very little is known about the action of leptin on food intake and energy expenditure, although circulating leptin concentrations are positively correlated to body fat stores. The purpose of this study was to assess the relationship between fasting plasma leptin concentrations and energy expenditure in 123 5-yr-old Pima Indian children (67 males/76 females). Body composition was assessed by isotopic water dilution (18O) whereas total energy expenditure (TEE) and resting metabolic rate (RMR) were measured using doubly labeled water and indirect calorimetry, respectively. The physical activity level was calculated as the ratio of TEE:RMR. Plasma leptin concentrations were positively correlated to percent body fat (r = 0.84, P < 0.0001), but were similar in boys and girls after adjusting for percent body fat. Most importantly, we found that, independent of the percentage of body fat, plasma leptin concentrations correlated with TEE (in absolute values, r = 0.37, P < 0.0001, or adjusted for body size r = 0.42; P < 0.0001) and with physical activity level (r = 0.26, P < 0.01), but not RMR. These results suggest that, as in animal models, leptin plays a role in energy expenditure in humans.     

Reduced sympathetic nervous activity. A potential mechanism predisposing to body weight gain.

The sympathetic nervous system is recognized to play a role in the etiology of animal and possibly human obesity through its impact on energy expenditure and/or food intake. We, therefore, measured fasting muscle sympathetic nerve activity (MSNA) in the peroneal nerve and its relationship with energy expenditure and body composition in 25 relatively lean Pima Indian males (means +/- SD; 26 +/- 6 yr, 82 +/- 19 kg, 28 +/- 10% body fat) and 19 Caucasian males (29 +/- 5 yr, 81 +/- 13 kg, 24 +/- 9% body fat). 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate were measured in a respiratory chamber, whereas body composition was estimated by hydrodensitometry. Pima Indians had lower MSNA than Caucasians (23 +/- 6 vs 33 +/- 10 bursts/min, P = 0.0007). MSNA was significantly related to percent body fat in Caucasians (r = 0.55, P = 0.01) but not in Pimas. MSNA also correlated with energy expenditure adjusted for fat-free mass, fat mass, and age in Caucasians (r = 0.51, P = 0.03; r = 0.54, P = 0.02; and r = 0.53, P = 0.02 for adjusted 24-h energy expenditure, sleeping metabolic rate, and resting metabolic rate, respectively) but not in Pima Indians. In conclusion, the activity of the sympathetic nervous system is a determinant of energy expenditure in Caucasians. Individuals with low resting MSNA may be at risk for body weight gain resulting from a lower metabolic rate. A low resting MSNA and the lack of impact of MSNA on metabolic rate might play a role in the etiology of obesity in Pima Indians.     

Cystic fibrosis clinical score: a new scoring system to evaluate acute pulmonary exacerbation.

Although pulmonary function tests are used to evaluate acute changes in obstructive airway disease in patients with cystic fibrosis (CF), these tests are relatively difficult to perform in young children or severely ill patients and may be costly. Other standard tests (eg, the Shwachman-Kulczycki and National Institutes of Health [NIH] scoring systems) evaluate disease severity and predict prognosis but do not measure day-to-day changes in clinical status. They thus provide little information for assessing the start of acute pulmonary exacerbation. Alternative scoring systems are needed to better identify the start of pulmonary exacerbation, to predict worsening or improvement of respiratory function after intervention, and to distinguish the scores from illness severity scores. This study was undertaken to compare a new 10-component, 50-point-maximum, acute clinical scoring system with forced expiratory volume in 1 second (FEV1) and forced vital capacity (FVC) variables in children with CF who were experiencing an acute pulmonary exacerbation before antimicrobial therapy was initiated and until the end of therapy. One hundred thirty children aged 5 to 17 years (median age, 11 years) had a median NIH score of approximately 64 (range, 39 to 85) at admission. The cystic fibrosis clinical score (CFCS) at admission was found to correlate highly with the modified NIH score at study entry (r = -.68, P = 0.0001 ). The total CFCS at entry was correlated inversely with both FEV1 (r = -.57, P = 0.0001) and FVC (r = -.55, P = 0.0001) measurements; crackles, dyspnea, sputum production, and respiratory rate were the 4 components most highly associated with either pulmonary function variable. The change in total CFCS from start to end of antimicrobial therapy also correlated with changes in FEV1 (r = -.31, P = 0.0016) and change in FVC (r = -.47, P = 0.0001). Clinical improvement was observed in all patients at the end of therapy, and only 1 patient had an increase in total CFCS. Patients who experienced clinical relapse had a mean increase of 8.5 points in the CFCS from end of therapy to 2- to 4-week follow-up, indicating worsening signs and symptoms of acute exacerbation. These data suggest that the CFCS is a predictive and optional surrogate of pulmonary function in assessing the health of patients with CF. Following further validation, this scoring system could be used to evaluate health status in the outpatient setting, the need for hospitalization, and subsequent improvement during an acute pulmonary exacerbation, as well as to compare the efficacy of therapeutic regimens.     

慢性阻塞性肺疾病患者血浆纤维蛋白原水平的临床评价

目的评价慢性阻塞性肺疾病(COPD)患者血浆纤维蛋白原(FB)水平的临床意义.方法 COPD病人113例,未合并肺心病者46例为B组;合并肺心病者67例为C组.正常健康人40例为A组.全部病例在稳定期间与急性发作期入院时各做一次FB、血流变与FEV1测定.每例患者随访2年,记录住院次数.结果 (1)FB和血流变:B组稳定期高于A组但仅FB和血浆粘度P<0.05,其余P>0.05;C组稳定期高于B组稳定期和A组(P<0.01);C组急发期高于B组急发期(P<0.01); B、C组的急发期均高于各自的稳定期(P<0.01).(2)FEV1:C组稳定期低于B组稳定期(P<0.01),C组急发期低于B组急发期P<0.01,B、C组急发期均低于各自的稳定期(P<0.01).(3)住院总次数C组高于B组(P<0.01).(4)稳定期间的FB与FEV1的关系呈非常显著的负相关(r=-0.85,P<0.01).结论血浆纤维蛋白原水平升高的COPD患者,其并发症增加和住院率上升而肺功能减退.     

Energy expenditure and severity of injury and illness indices in multiple trauma patients

OBJECTIVE: To determine whether the energy expenditure of mechanically ventilated multiple trauma patients correlates with the severity of injury and illness indices before important systemic infection has complicated the clinical course, and to compare the energy expenditure with the energy expenditure expected from the Harris-Benedict equation adjusted with correction factors for trauma. DESIGN: Prospective, clinical study. SETTING: General intensive care unit of a university teaching hospital. PATIENTS: Immediate multiple trauma adult patients who required mechanical ventilation. INTERVENTIONS: Metabolic cart connected to the ventilator. MEASUREMENTS AND MAIN RESULTS: Data on admission to the emergency department and during the first 24 hrs of intensive care unit admission were collected for computation of severity of injury and illness indices, respectively. Resting and total energy expenditures were derived at least 48 hrs after intensive care unit admission by continuous indirect calorimetry. Predicted basal energy expenditure was obtained using the Harris-Benedict equation and predicted total energy expenditure was calculated using the Harris-Benedict value adjusted with correction factors for trauma. Twenty-six multiple trauma adult patients completed the study. No statistically significant correlations were observed between both the resting energy expenditure and the total energy expenditure and the Injury Severity Score, Revised Trauma Score, Simplified Acute Physiologic Score II, Acute Physiology and Chronic Health Evaluation II score, and Glasgow Coma Scale score. A regression model of total energy expenditure was developed with the following variables: Harris-Benedict equation, heart rate, and minute ventilation (p = .01; r2 = .74). The resting energy expenditure/predicted basal energy expenditure ratio was 1.17+/-0.2 and the total energy expenditure/predicted total energy expenditure ratio was 0.76+/-0.1. CONCLUSIONS: In mechanically ventilated multiple trauma patients the energy expenditure is not correlated to the severity of injury and illness indices but is dependent on the Harris-Benedict equation in addition to heart rate and minute ventilation. Furthermore, this patient population is characterized by a moderate state of hypermetabolism, and the Harris-Benedict prediction modified with correction factors for trauma systematically overestimates the total energy expenditure.     

lnterleukin-8 and neutrophil activation in acute pancreatitis

It has been suggested that leucocytes play an important role in the pathogenesis of complicated pancreatitis. Indeed, increased plasma concentrations of neutrophil elastase as a marker of neutrophil activation could be detected in patients with a severe course of the disease. Recently, interleukin-8 (IL-8) has been described as a novel neutrophil activating peptide. To determine the role of IL-8 in acute pancreatitis we measured its serum concentrations by a specific enzyme-linked immunosorbent assay in 10 patients with acute pancreatitis daily during the first week of hospitalization. IL-8 levels were compared with plasma concentrations of neutrophil elastase and the clinical course of the disease. Three of the patients had uncomplicated pancreatitis, while seven showed various extrapancreatic complications. Patients with complicated pancreatitis had statistically significant (P less than 0.05) higher mean values of IL-8 (121 +/- 41 pg/ml-1 vs. 13 +/- 6 pg ml-1, mean +/- SEM) and neutrophil elastase (547 +/- 35 ng ml-1 vs. 250 +/- 20 ng ml-1) than patients with uncomplicated disease. There was a positive correlation (r = 0.52, P less than 0.0001) between IL-8 and neutrophil elastase in the lower concentration range of IL-8 (less than 100 pg ml-1). At IL-8 levels greater than 100 pg ml-1 neutrophil elastase was always greatly elevated; however, under these conditions the relationship between IL-8 and elastase was no longer linear. No measurable IL-8 concentrations were found when plasma elastase was less than 200 ng ml-1. During follow-up, initially elevated IL-8 concentrations decreased in correlation with clinical improvement.(ABSTRACT TRUNCATED AT 250 WORDS)     

Transient elevation of neutrophil proteinases in induced sputum during COPD exacerbation

Objective. Patients with chronic obstructive pulmonary disease (COPD) are prone to acute exacerbations associated with increased morbidity and mortality. One potential group of enzymes causing tissue destruction in this disease includes neutrophil proteinase elastase (NE), collagenase‐2 (matrix metalloproteinase‐8 (MMP‐8)) and gelatinase B (MMP‐9). We investigated the activity of NE and the levels of MMP‐8 and MMP‐9 in a longitudinal setting at and after COPD exacerbation using a non‐invasive technique, i.e. induced sputum, to ascertain whether these proteinases play a role in COPD exacerbation. Material and methods. The study included healthy non‐smokers (n = 32), healthy smokers (n = 28), patients with stable COPD (n = 15), COPD patients with acute exacerbations (exa) (n = 10) and their recovery (n = 8) after 4 weeks. NE activity by synthetic peptide substrate and spectrophotometry, MMP‐8 levels by immunofluorometry and MMP‐9 levels by ELISA were analysed from induced sputum supernatants. Results. NE activity and the level of MMP‐8 increased highly significantly in patients with COPD exacerbation compared to stable COPD and controls (NE: p = 0.001 and p<0.0001; MMP‐8: p<0.001 and p<0.0001). Paired samples showed a decrease of these proteinases during the recovery period after exacerbation (p = 0.03, p = 0.04). The proteinase levels correlated not only with the percentage and number of neutrophils but also with the lung function parameters (FEV1/FVC and diffusion capacity). Conclusions. COPD exacerbations are associated with neutrophil recruitment into the airways but also transient activation and/or elevation of tissue destruction proteinases, such as NE and MMP‐8, which can be detected from the induced sputum supernatants of these COPD patients.     

Spirometric correlates of dyspnea improvement among emergency department patients with chronic obstructive pulmonary disease exacerbation

OBJECTIVE: To examine whether change in slow vital capacity (SVC) correlates to dyspnea improvement during emergency department (ED) treatment of chronic obstructive pulmonary disease (COPD) exacerbation. METHODS: We performed a prospective cohort study and enrolled consecutive patients during a 3-week period. ED patients > or = 55 years old with COPD exacerbation were asked to perform bedside spirometry shortly after ED arrival and again at discharge. SVC was measured first, then forced expiratory volume in the first second (FEV1), peak expiratory flow (PEF), and forced vital capacity (FVC). Concurrent with spirometry, patients rated their dyspnea on a 10-cm visual analogue scale. RESULTS: Thirty-six patients were enrolled. The median ED stay was 271 min (interquartile range 219-370 min). Seventy-one percent of the patients reported dyspnea improvement during their ED stay. Change in SVC was significantly higher among the patients whose dyspnea improved than among those whose did not (median increase of 0.15 L vs median decrease of 0.25 L, respectively, p < 0.01). By contrast, the change in spirometry values were similar for FEV1, PEF, and FVC (all p > 0.30). Spearman correlation supported these findings: SVC r = 0.45 (p = 0.02) versus nonsignificant correlation with FEV(1) (r = 0.33), PEF (r = -0.22), and FVC (r = 0.35). CONCLUSIONS: Increase in SVC significantly correlated with dyspnea improvement among ED patients with moderate-to-severe COPD exacerbation. Change in SVC merits consideration when evaluating therapeutic response during COPD exacerbation.     

水陆二仙丹通过增加精液中PMNE抑制剂含量抑制精子氧化损伤的发生

目的评价水陆二仙丹对男性不育患者精子氧化损伤的影响,并探讨其可能的作用途径。方法将80例不育患者采用随机双盲平行安慰剂对照的方法分为治疗组和对照组,每组各40例,两组均服用抗氧化剂,在此基础上,治疗组服用水陆二仙丹水煎剂,对照组服用安慰剂,疗程为3个月。同时收集20例健康捐精者的精液作为正常对照组。对精子基本参数(精子密度、精子活动率及正常精子形态)的变化及精液中超氧化歧化酶(SOD)、丙二醛(MDA)、中性粒细胞弹性蛋白酶(NE)及α1抗胰蛋白酶的水平进行比较。结果 1治疗前,治疗组和对照组的精子密度、精子活动率及正常精子形态均低于正常对照组(P0.05)。治疗后,治疗组和对照组的精子基本参数(精子密度、精子活动率及正常精子形态)均显著改善(P0.0001),且治疗组改善精子基本参数的程度显著高于对照组(P0.0001)。2治疗前,治疗组和对照组NE及MDA的水平均明显高于正常对照组,而α1抗胰蛋白酶和SOD水平均低于正常对照组(P0.05)。治疗后,治疗组和对照组NE和MDA的水平较治疗前均显著降低(P0.0001),而α1抗胰蛋白酶及SOD的水平则显著升高(P0.0001),且治疗后治疗组α1抗胰蛋白酶水平在显著高于对照组(P0.0001),MDA的水平显著低于对照组(P0.0001)。相关性的分析结果显示,MDA水平与NE的水平呈明显正相关(r=0.9863,P=0.0003),MDA水平与α1抗胰蛋白酶呈显著负相关(r=-0.9670,P=0.0016)。结论水陆二仙丹可能通过增加精液中NE抑制剂(α1抗胰蛋白酶)含量抑制精子氧化损伤的发生。     

儿童支气管哮喘患者血清NETs和IL-4水平表达与发作期中医证型的相关性分析

目的　探究支气管哮喘发作期患儿血清中性粒细胞胞外诱捕网（NETs）、白介素-4（IL-4）表达水平及其与中医证型的相关性。方法　选取2017年1月~2020年1月湖南中医药高等专科学校附属第一医院收治的支气管哮喘急性发作期患儿98例作为观察组,其中热喘证37例（热喘证组）、寒喘证28例（寒喘证组）、虚喘证33例（虚喘证组）。另选取同期在该院体检的25例健康儿童作为健康对照组。使用PicoGreen荧光染料及单管型多功能检测仪检测血清游离DNA（cf-DNA）/NETs水平,采用酶联免疫吸附法（ELISA）检测血清IL-4表达水平,采用Pearson法分析支气管哮喘发作期患儿血清cf-DNA/NETs和IL-4水平与中性粒细胞、淋巴细胞、单核细胞及肺功能指标第1秒用力呼气量（FEV1）占预计值百分比（FEV1%）、FEV1/用力肺活量（FVC）水平相关性。结果　健康对照组、虚喘证组、寒喘证组、热喘证组患儿血清cf-DNA/NETs和IL-4水平及外周血中性粒细胞、单核细胞水平依次升高,差异均有统计学意义（F=895.500,69.590,63.250和50.590,均P＜0.05）,淋巴细胞水平及肺功能指标FEV1%,FEV1/FVC水平均依次降低,差异具有统计学意义（F=71.410,75.790,均P＜0.05）。支气管哮喘发作期患儿血清cf-DNA/NETs与IL-4水平呈正相关（r=0.431,P=0.000）;血清cf-DNA/NETs水平与中性粒细胞、单核细胞水平呈正相关（r=0.541,0.401,均P＜0.05）,与淋巴细胞、FEV1%和FEV1/FVC水平呈负相关（r=-0.456,-0.462和-0.503,均P＜0.05）;血清IL-4水平与中性粒细胞、单核细胞水平呈正相关（r=0.461,0.405,均P＜0.05）,与淋巴细胞、FEV1%和FEV1/FVC水平呈负相关（r=-0.438,-0.479和-0.534,均P＜0.05）。结论　 支气管哮喘发作期患儿血清cf-DNA/NETs,IL-4水平明显升高,且热喘证患儿血清中二者水平最高,其次为寒喘证和虚喘证,二者水平变化可能与不同中医证型存在一定相关性。     

Evidence of impaired microvascular function in pre-eclampsia: a non-invasive study

The clinical presentation of pre-eclampsia suggests that microvascular dysfunction may play a role in the maternal manifestations of the disease. Isovolumetric venous pressure ( P V(i)) is an index of microvascular function, reflecting local plasma colloid osmotic (oncotic) pressure, and is abnormal in clinical conditions with microvascular dysfunction. We hypothesized that, in pre-eclampsia, post-capillary margination of neutrophils would increase post-capillary resistance, and therefore P V(i). A small cumulative step strain-gauge plethysmography protocol was used to compare P V(i) in 18 women with pre-eclampsia, 16 normal pregnant women and 17 non-pregnant controls. Circulating levels of vascular cell-adhesion molecule-1 (VCAM-1), intercellular cell-adhesion molecule-1 (ICAM-1) and E-selectin, and neutrophil elastase, were measured to assess endothelial and neutrophil activation respectively. P V(i) was significantly greater in the pre-eclampsia group, relative to the normal pregnant and non-pregnant controls ( P <0.001, ANOVA, for both comparisons). P V(i) was significantly lower during normal pregnancy compared with the non-pregnant controls ( P =0.001). Plasma levels of neutrophil elastase, VCAM-1, ICAM-1 and E-selectin ( P =0.001) were significantly greater in the pre-eclamptics than the controls. Significant positive correlations were observed between P V(i) and neutrophil elastase ( r =0.71, P =0.001), VCAM-1 ( r =0.52, P =0.03), ICAM-1 ( r =0.67, P =0.002), E-selectin ( r =0.69, P =0.001), uric acid levels ( r =0.54, P =0.02) and haematocrit ( r =0.64, P =0.004) in pre-eclampsia. The relationship with the platelet count was negative ( r =-0.65, P =0.003). No significant correlations were observed between P V(i) and maternal age, gestational age, total protein, albumin, diastolic blood pressures, age, body mass index and infant birth mass in the normal pregnant and non-pregnant controls. These data suggest that microvascular dysfunction occurs in pre-eclampsia, and that it is related to alterations in endothelial cell and neutrophil activation.     

慢性阻塞性肺疾病患者血清S100A8/A9和sRAGE水平变化及临床意义

目的分析慢性阻塞性肺疾病患者血清钙结合蛋白S100A8/A9和可溶性糖基化终末产物受体(sRAGE)水平的变化及临床意义。方法病例对照研究。选取2018年4月至2019年1月湖北中医药大学附属中西医结合医院呼吸科慢性阻塞性肺疾病(COPD)患者203例,其中男166例,女37例,年龄52~92岁,平均(69.72±9.08)岁。收集体检中心吸烟老年非COPD且相对健康体检者41例为吸烟对照组,其中男35例,女6例,年龄55~89岁,平均(68.66±8.74)岁。收集不吸烟老年健康体检者167名为不吸烟对照组,其中男132名,女35名,年龄57~92岁,平均(69.13±7.21)岁。采用酶联免疫吸附测定(ELISA)方法检测不同分期COPD患者和两组对照组血清中S100A8/A9和sRAGE的水平,将其与COPD患者的各临床指标:第一秒用力呼气容积FEVl占预计值%、FEV1/FVC(用力肺活量)、中性粒细胞比率(NEU%)、吸烟量:每日吸烟包数乘吸烟年数(pack-year)做相关性分析。利用受试者工作特征(ROC)曲线分析S100A8/A9,sRAGE以及二者联合检测对于COPD的诊断价值。结果COPD患者血清S100A8/A9水平[(2.70±1.11)μg/ml]与吸烟对照组[(1.65±0.63)μg/ml]和不吸烟对照组[(0.99±0.48)μg/ml]相比均明显上升(t=5.807,P<0.0001;t=18.45,P<0.0001);COPD患者GOLDⅠ、Ⅱ、Ⅲ、Ⅳ期血清S100A8/A9水平[(2.08±1.08)μg/ml,(2.58±1.06)μg/ml,(2.69±1.12)μg/ml,(2.95±1.10)μg/ml]与不吸烟对照组[(0.99±0.48)μg/ml]相比明显上升,差异均有统计学意义(t=6.616,P<0.0001;t=14.56,P<0.0001;t=17.10,P<0.0001;t=18.09,P<0.0001)。COPD患者血清sRAGE水平[(0.29±0.25)ng/ml]与吸烟对照组[(0.60±0.24)ng/ml]和不吸烟对照组[(0.85±0.35)ng/ml]相比均明显下降(t=7.367,P<0.0001;t=18.14,P<0.0001);COPD患者GOLDⅠ、Ⅱ、Ⅲ、Ⅳ期血清sRAGE水平[(0.46±0.40)、(0.28±0.25)、(0.29±0.25)和(0.25±0.19)ng/ml]与不吸烟对照组[(0.85±0.35)ng/ml]相比明显下降,差异均有统计学意义(t=3.459,P=0.0005;t=10.23,P<0.0001;t=13.95,P<0.0001;t=11.70,P<0.0001)。血清S100A8/A9水平与患者吸烟量、NEU%均呈正相关(r=0.4585,P<0.0001;r=0.2283,P=0.0011),与FEV1/FVC、FEV1占预计值百分比、sRAGE均呈负相关(r=-0.1906,P=0.0064;r=-0.1863,P=0.0078;r=-0.2017,P=0.0039)。sRAGE与NEU%呈负相关(r=-0.1559,P=0.0264)。ROC曲线中S100A8/A9,sRAGE以及二者联合检测的曲线下面积分别为0.922[95%CI(0.897~0.947)],0.926[95%CI(0.899~0.952)],0.966[95%CI(0.950~0.983)]。结论S100A8/A9和sRAGE水平与气流受限严重程度和血清炎症介质水平相关,有望作为COPD的潜在的生物标志物。     

Protein and energy metabolism in chronic bacterial infection: studies in melioidosis

Chronic infection is often accompanied by a wasting process, the metabolic basis of which is not fully understood. The aims of the present study were to measure protein and energy metabolism in patients with melioidosis (a serious and antibiotic-refractory Gram-negative bacterial infection which is endemic in South-East Asia) in order to define the metabolic abnormalities that might contribute to wasting. Whole-body protein turnover was measured using the [(13)C]leucine technique, both in the fasted state and while consuming a high-energy meal. Resting energy expenditure was measured by indirect calorimetry, and total energy expenditure by the bicarbonate/urea method. Results were normalized for fat-free mass, as estimated from skinfold thickness. Protein turnover was increased in melioidosis patients compared with healthy controls during fasting (170.9 compared with 124.1 micromol x kg(-1) x h(-1); P=0.04), but the net rate of catabolism (22.2 compared with 20.5 micromol x kg(-1) x h(-1); P=0.77) and the anabolic response to feeding were similar in the two groups. Resting energy expenditure was higher in melioidosis patients compared with controls (191.4 and 157.3 kJ x kg(-1) x day(-1) respectively; P=0.04), but total energy expenditure (measured in a separate group of eight patients with melioidosis) was low (192.1 kJ x kg(-1) x day(-1)). In conclusion, this study found no evidence of metabolic causative factors, such as accelerated net protein catabolism during fasting, a blunted anabolic response to feeding or increased daily energy expenditure, and therefore suggests that reduced energy intake is the prime cause of wasting. The observed normal response to feeding should encourage nutritional approaches to prevent wasting.