Search PubMed⌕ Search

Biomedical subjects

C Roussos

Publications and source records attributed to C Roussos.

At least 37 records · Page 2Linked to original sources
PubMed2004

The immune response to resistive breathing.

Resistive breathing is an "immune challenge" for the body, initiating an inflammatory response consisting of an elevation of plasma cytokines, and the recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes, but are, instead, produced within the diaphragm, secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction, secondary to resistive breathing. The production of cytokines within the diaphragm may be mediating the diaphragm muscle fibre injury that occurs with strenuous contractions, or contributing towards the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute towards the development of muscle cachexia. They may also have systemic effects, mobilising glucose from the liver and free fatty acid from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to production of adrenocorticotropin and beta-endorphins. The adrenocorticotropin response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles via the production of glucocorticoids and the induction of the acute phase-response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles.

Airway Resistance↗
PubMed2003

Protein S-100b serum levels in trauma-induced brain death.

OBJECTIVE: To analyze the time course of serum protein S-100b in patients with traumatic brain injury deteriorating to brain death and to investigate the predictive value of initial S-100b levels in relation to clinical and radiologic measures of injury severity with regard to brain death. METHODS: Forty-seven patients who sustained severe head injury were studied. Blood samples for measurement of S-100b were drawn on admission in the intensive care unit and every 24 hours thereafter for a maximum of 6 consecutive days or until brain death occurred. Variables related to outcome were recorded, including age, sex, Glasgow Coma Scale (GCS), and brain CT findings on admission. Outcome was defined as deterioration to brain death or not. RESULTS: Of the 47 patients studied, 17 deteriorated to brain death and 30 did not. On admission, patients who became brain dead had higher median serum S-100b levels compared with those who did not (2.32 microg/L vs 1.04 micro g/L, p = 0.0028). Logistic regression analysis showed that initial S-100b was an independent predictor of brain death (p = 0.041), in the presence of advanced age (p = 0.043) and low GCS score (p = 0.013). The odds ratio of 2.09 (95% CI, 1.03 to 4.25) indicates a more than doubling of the probability of deteriorating to brain death per 1- micro g/L increase in S-100b on admission. At clinical brain death, median S-100b was higher in patients with brain death compared with the peak S-100b value obtained over a 6-day period in those who did not become brain dead (6.58 microg/L vs 1.49 microg/L, p < 0.0001). CONCLUSIONS: Prediction of brain death after severe head injury can be improved by combining clinical and S-100b data; thus, serum S-100b determination deserves to be included in the neuromonitoring of patients with severe traumatic brain injury.

Adolescent↗
PubMed2003

Mediastinal mass with Dysphagia in an elderly patient.

We report the use of endoscopic techniques for successful diagnosis in a case of atypical esophageal tuberculosis. Tuberculosis of the esophagus is an unusual presentation of this disease, having been estimated to occur in 0.15% of the people who die of tuberculosis. A few cases of possible primary tuberculous esophagitis have been described. This report describes a patient with dysphagia who appeared to have esophageal tuberculosis without HIV and in the absence of other signs of tuberculosis. The patient responded promptly to treatment with tuberculostatics.

Aged↗
PubMed2003

Detection of enterococcal surface protein gene (esp) and amplified fragment length polymorphism typing of glycopeptide-resistant Enterococcus faecium during its emergence in a Greek intensive care unit.

The emergence of glycopeptide-resistant Enterococcus faecium (GREF) in a Greek intensive care unit was studied by amplified fragment length polymorphism analysis and esp gene detection. Three GREF clones harboring the esp gene were recovered from 17 out of 21 patients, indicating the dissemination of genetically homogenous and virulent strains of GREF.

Adolescent↗
PubMed2003

Respiratory failure.

Respiratory failure occurs due mainly either to lung failure resulting in hypoxaemia or pump failure resulting in alveolar hypoventilation and hypercapnia. Hypercapnic respiratory failure may be the result of mechanical defects, central nervous system depression, imbalance of energy demands and supplies and/or adaptation of central controllers. Hypercapnic respiratory failure may occur either acutely, insidiously or acutely upon chronic carbon dioxide retention. In all these conditions, pathophysiologically, the common denominator is reduced alveolar ventilation for a given carbon dioxide production. Acute hypercapnic respiratory failure is usually caused by defects in the central nervous system, impairment of neuromuscular transmission, mechanical defect of the ribcage and fatigue of the respiratory muscles. The pathophysiological mechanisms responsible for chronic carbon dioxide retention are not yet clear. The most attractive hypothesis for this disorder is the theory of "natural wisdom". Patients facing a load have two options, either to push hard in order to maintain normal arterial carbon dioxide and oxygen tensions at the cost of eventually becoming fatigued and exhausted or to breathe at a lower minute ventilation, avoiding dyspnoea, fatigue and exhaustion but at the expense of reduced alveolar ventilation. Based on most recent work, the favoured hypothesis is that a threshold inspiratory load may exist, which, when exceeded, results in injury to the muscles and, consequently, an adaptive response is elicited to prevent and/or reduce this damage. This consists of cytokine production, which, in turn, modulates the respiratory controllers, either directly through the blood or probably the small afferents or via the hypothalamic-pituitary-adrenal axis. Modulation of the pattern of breathing, however, ultimately results in alveolar hypoventilation and carbon dioxide retention.

Acute Disease↗
PubMed2002

Interval training as an alternative modality to continuous exercise in patients with COPD.

Understanding of what constitutes a training load adequate to induce training effects in patients with chronic obstructive pulmonary disease (COPD) is still evolving. The present study investigated whether interval training (IT) is effective in terms of inducing measurable improvements in physiological response and compared its effects on exercise tolerance (ET) and quality of life to those of continuous training (CT). Thirty-six COPD patients, with a forced expiratory volume in one second of 45+/-4% of the predicted value (mean+/-SEM), were randomly assigned to CT (exercise at 50% of baseline peak work-rate) or IT (work for 30 s at 100% of peak work-rate alternating with 30-s rest intervals) groups that cycled 40 min x day(-1) and 2 days x week(-1) for 12 weeks. After training, both groups showed significantly improved ET (IT, 57+/-6 to 71+/-8 W; CT, 57+/-5 to 70+/-6 W) and total quality-of-life score of the Chronic Respiratory Disease Questionnaire (IT, 77+/-3 to 88+/-2; CT, 78+/-3 to 93+/-2). At identical levels of exercise, minute ventilation was significantly reduced (IT, 35.8+/-2.5 to 31.7+/-2.5 L x min(-1); CT, 36.4+/-2.7 to 32.5+/-2.7 L x min(-1)). The magnitude of improvement in these variables was not significantly different among groups. The present data expand on the principles of exercise prescription for chronic obstructive pulmonary disease patients by demonstrating that interval training elicits substantial training effects, which are similar in magnitude to those produced by continuous training at half the exercise intensity but double the exercise time.

Aged↗
PubMed2001

Pulmonary capillary endothelial dysfunction in early systemic sclerosis.

OBJECTIVE: Pulmonary capillary endothelium-bound angiotensin-converting enzyme (PCEB-ACE) activity is a sensitive and quantifiable index of endothelial function in vivo. Systemic sclerosis (SSc) is characterized by endothelial damage and excess collagen formation, causing mainly pulmonary hypertension (PH) in the limited cutaneous SSc (lcSSc) subset and interstitial lung disease with pulmonary interstitial fibrosis (PIF) in the diffuse cutaneous SSc (dcSSc) subset. This study was undertaken to investigate the hypothesis that PCEB-ACE activity is reduced early in SSc, in the absence of PH or PIF. METHODS: Applying indicator-dilution techniques, we measured single-pass transpulmonary hydrolysis and percent metabolism (%M) of a synthetic ACE substrate and calculated functional capillary surface area (FCSA) in 25 SSc patients and 11 controls. Substrate hydrolysis and %M reflect ACE activity per capillary; FCSA reflects ACE activity per vascular bed. RESULTS: PCEB-ACE activity was decreased in both SSc subsets. Among patients without PH, substrate hydrolysis and %M were decreased in patients with lcSSc and more profoundly in those with dcSSc; loss of FCSA normalized to body surface area (FCSA/BSA) was observed in dcSSc, but not in lcSSc. High-resolution computed tomography of the lung, performed in all SSc patients, revealed no correlation between substrate %M, hydrolysis, or FCSA/BSA and the degree of PIF; 5 dcSSc and 5 lcSSc patients with no detectable PIF exhibited decreases in hydrolysis and %M, while FCSA/BSA was decreased only in dcSSc. CONCLUSION: Depression of PCEB-ACE activity, indicating pulmonary endothelial dysfunction, occurs early in SSc, in the absence of PH or PIF, and is more pronounced, at this early pulmonary disease stage, in dcSSc than in lcSSc.

Adult↗
PubMed2001

The effect of hypoxemic reperfusion on cerebral protection after a severe global ischemic brain insult.

BACKGROUND AND PURPOSE: Reactive oxygen species contribute to membrane lipid peroxidation and neuronal death and have been implicated in anoxic encephalopathy. We tested whether hypoxemic reperfusion (HR) after global cerebral ischemia would improve neurological recovery. METHODS: Two groups of pigs (n = 11 in each group) were subjected to a model of a 10-min global cerebral and systemic ischemia to compare the effect of hypoxemic reperfusion (group HR) with the classical hyperoxemic control (group C). A third group not subjected to ischemia served as control to the control group (n = 6, group CC), but received hyperoxygenation at the respective period of reperfusion. The outcome was evaluated by means of neurological assessment and the extent of lipid peroxidation measuring the plasma malonaldehyde (MDA) together with hydroxyalkenals (HALK). RESULTS: Animals of group HR exhibited a significantly superior neurological outcome compared with those of group C at all three consecutive assessments after reperfusion (post-resuscitation P = 0.006, at 8 h P = 0.003, and at 24 h P = 0.007). The levels of MDA and HALK are lower in the HR group than in group C (P = 0.029). Additionally, in the CC group these molecules increased significantly early at hyperoxygenation (P = 0.02). A faster lactate metabolism in the HR group was observed during reperfusion, though non-significant. CONCLUSIONS: Hypoxemic reperfusion during resuscitation from a severe global ischemic cerebral insult improves the neurological outcome compared with classic hyperoxemic reperfusion. This is additionally confirmed by the decreased production of the molecules of lipid peroxidation. In the absence of preceding ischemia, these molecules may increase by simple over-oxygenation.

Aldehydes↗