Evaluation of asymptomatic subjects with low forced expiratory ratios (FEV1/VC).

BACKGROUND--Heightened bronchial hyperreactivity is frequently associated with airflow limitation, atopy, or cigarette smoking. The purpose of this study was to evaluate healthy subjects with significantly low values of forced expiratory volume in one second/vital capacity % (FEV1/VC%) by measuring their airway response to exercise and methacholine challenge, compared with a control group with normal spirometric values. METHODS--Eighty four healthy subjects with significantly low flow rates (group A, FEV1/VC% < 2 SD% predicted) were evaluated and compared with 37 subjects with normal flow rates (group B). Static lung volumes, spirometric tests, exercise, and methacholine challenges were performed. RESULTS--Lung volumes were normal for both groups. Mean FEV1/VC% was 69% for group A and 82% for the control group. Salbutamol improved baseline FEV1 in eight subjects in group A (mean 15%), while methacholine induced a drop in FEV1 in 12 subjects. The dose-response curve to methacholine reached a plateau in all the responders. None of the subjects in the control group improved their baseline FEV1/VC% to salbutamol, but three showed bronchial hyperreactivity similar to those in group A. CONCLUSIONS--Bronchial hyperreactivity does not occur more often in asymptomatic subjects with mildly low FEV1/VC% so these subjects do not require special investigations for airway disease.     

Neuromuscular disease, respiratory failure and cor pulmonale.

Respiratory muscle weakness is an uncommon cause of chronic respiratory failure and a rare cause of cor pulmonale. The problem may not be apparent unless specific physical signs are sought or appropriate investigations performed. We present three patients who presented diagnostic difficulty for prolonged periods until the presence of respiratory muscle weakness was considered. Once the diagnosis was established treatment with nocturnal nasal intermittent positive pressure ventilation produced a dramatic improvement in symptoms and allowed a return to a near normal lifestyle.     

Evaluation of topical ibuprofen cream in the treatment of acute ankle sprains.

One hundred patients who presented to the accident and emergency (A&E) department with an acute ankle sprain were entered into a study to determine the efficacy of topical ibuprofen cream by using a double-blind placebo controlled design in a single type of soft-tissue injury. The subjects were given either topical ibuprofen cream or a placebo cream in addition to the standard management of the department. Patients kept diaries recording walking ability and pain visual analogue scales for resting, standing and walking. A total of 51 patients returned diaries that were suitable for analysis. Patients using the topical ibuprofen cream had significant reduction in pain scores over the first 48 h of treatment.     

Atrial natriuretic peptide inhibits sympathetic outflow in NaCl-sensitive spontaneously hypertensive rats.

The current study tested the hypothesis that circulating atrial natriuretic peptide (ANP) inhibits sympathetic outflow, as reflected in lumbar sympathetic nerve activity (LSNA), in NaCl-sensitive spontaneously hypertensive rats (SHR-S) and that this effect is exaggerated by high NaCl feeding. NaCl-resistant SHR (SHR-R) and Wistar-Kyoto (WKY) rats maintained on basal and high-NaCl diets were used as controls. Intravenous administration of ANP to conscious, freely moving rats with intact baroreflexes decreased blood pressure and LSNA in SHR-S, SHR-R and WKY rats maintained on basal or high-NaCl diets for 2-3 weeks. The depressor response to intravenous ANP was greater in 8% NaCl-fed SHR-S than in any other group; the LSNA response was greater in SHR-S on either diet than in any other group. Intracerebroventricular administration of ANP evoked small, transient sympatholytic responses in SHR-S on both diets and minimal responses in SHR-R and WKY rats; these responses could not be attributed to leakage of ANP into the peripheral circulation. Thus, circulating ANP has a sympatholytic effect in SHR-S that is not amplified by high-NaCl feeding and can be only partially accounted for by a central action.     

美国医院的集团化运作

自1923年以来的这段时间,是医院发展史上最具探索性的时期.许多医院因为严峻的经济大环境而艰难度日,住院率低下,公益负担日增,融资渠道日益萎缩,私立机构的状况更是让人揪心,前景看起来一片黯淡.然而所幸的是,每次经济危机也带来了新的观念和方法.医院在逆境中反思,逐渐改变旧有的行为方式,引入商业运营模式,学会当家理财.     

Binding of lysozyme to lipopolysaccharide suppresses tumor necrosis factor production in vivo.

Endotoxin (lipopolysaccharide [LPS]) released during gram-negative bacterial infection induces varieties of cytokines which directly and/or indirectly cause shock, disseminated intravascular coagulation, and death. We previously showed that lysozyme (LZM) was an LPS-binding protein and inhibited various immunomodulating activities of LPS. In this study, we examined the effect of LZM on the LPS-triggered septic shock model induced by carrageenan treatment and assessed by tumor necrosis factor production. The data presented in this report strongly suggest that LZM-LPS complex formation completely abrogates tumor necrosis factor production and the mortality caused by LPS and that LZM may be useful for the treatment of endotoxin shock.     

Rapid induction of apoptosis in rat liver by cycloheximide.

A single administration of the inhibitor of protein synthesis cycloheximide results in the occurrence of apoptosis in rat liver. The presence of intracellular apoptotic bodies was detected as early as 2 hours after treatment. No evidence of cell necrosis could be observed by histologic and biochemical analysis. Apoptosis was followed by an increased expression of testosterone-repressed prostate message-2 RNA, a gene whose activity has been associated to apoptotic cell death in involuting rat prostate. The finding of in vivo induction of apoptosis in nonproliferating cells by an inhibitor of protein synthesis, together with the rapidity and synchrony in the occurrence of cell death make this model potentially useful for the analysis of the kinetics of the apoptotic cycle and in exploring some of the mechanisms of regulation of genes possibly involved in this type of cell death.