Biomedical subjects

J Marín

Publications and source records attributed to J Marín.

At least 37 records · Page 2Linked to original sources

PubMed2001

Disparity for the minor histocompatibility antigen HA-1 is associated with an increased risk of acute graft-versus-host disease (GvHD) but it does not affect chronic GvHD incidence, disease-free survival or overall survival after allogeneic human leucocyte antigen-identical sibling donor transplantation.

Disparity for the minor histocompatibility antigen HA-1 between patient and donor has been associated with an increased risk of acute graft-versus-host disease (GvHD) after allogeneic human leucocyte antigen (HLA)-identical sibling donor stem cell transplantation (SCT). However, no data concerning the impact of such disparity on chronic GvHD, relapse or overall survival are available. A retrospective multicentre study was performed on 215 HLA-A2-positive patients who received an HLA-identical sibling SCT, in order to determine the differences in acute and chronic GvHD incidence on the basis of the presence or absence of the HA-1 antigen mismatch. Disease-free survival and overall survival were also analysed. We detected 34 patient-donor pairs mismatched for HA-1 antigen (15.8%). Grades II-IV acute GvHD occurred in 51.6% of the HA-1-mismatched pairs compared with 37.1% of the non-mismatched. The multivariate logistic regression model showed statistical significance (P: 0.035, OR: 2.96, 95% CI: 1.07-8.14). No differences were observed between the two groups for grades III-IV acute GvHD, chronic GvHD, disease-free survival or overall survival. These results confirmed the association between HA-1 mismatch and risk of mild acute GvHD, but HA-1 mismatch was not associated with an increased incidence of chronic GvHD and did not affect relapse or overall survival.

Acute Disease↗

PubMed2001

Relationship between airway sensitivity to adenosine 5' monophosphate and the shape of the concentration-response curve to methacholine in subjects with allergic rhinitis.

The objective of this study was to determine differences in airway sensitivity to adenosine 5'-monophosphate (AMP) between allergic rhinitis subjects with plateau and those without evidence of plateau on the concentration response curves to methacholine. A total of 51 adults (38 subjects with allergic rhinitis and 13 healthy controls) were challenged with increasing concentrations of methacholine and AMP. The methacholine challenge was terminated when there was a 40% or more decrease in forced expiratory volume in 1 sec (FEV1), whereas the AMP challenge was stopped when FEV1 had fallen by more than 20%. A plateau for methacholine was detected in all 13 healthy controls and in 27 patients with allergic rhinitis (AR-plateau group), whereas 11 subjects with allergic rhinitis did not exhibit a plateau (AR-non-plateau group). The median (range) PC20 AMP (provocative concentration required to produce a 20% fall in FEV1) value for the AR-non-plateau group was 44.0 mg ml(-1) (3.3-400.0), compared with 400.0 mgml(-1) (12.1-400.0) in the AR-plateau group (P=0.03) and 400.0 mgml(-1) in the healthy control group (P=0.007). The proportion of subjects who showed bronchoconstriction in response to AMP was higher in the AR-non-plateau group (73%) than in the AR-plateau group (30%) (P=0.03). However, three subjects with allergic rhinitis who had normal sensitivity to methacholine and plateau showed bronchoconstriction in response to AMP. We conclude that, in subjects with allergic rhinitis, the absence of plateau on the concentration response curves to methacholine is associated with a higher prevalence and degree of bronchoconstriction in response to AMP. However, the two bronchoconstrictor stimuli were not identifying the same abnormalities of the airways.

Adenosine Monophosphate↗

PubMed2001

Laryngotracheal reconstruction in subglottic stenosis: an ancient problem still present.

BACKGROUND: Subglottic stenosis is an ancient but persistent problem as a cause of airway obstruction. The etiology and the results of surgical treatment with thyrotracheal anastomosis were reviewed. METHODS: Fifty-six patients with subglottic stenosis were studied. All were subjected to laryngotracheal reconstruction by thyrotracheal anastomosis with partial resection of the cricoid. RESULTS: Of all 56 cases of subglottic stenosis, 48 (86%) had history of previous tracheal intubation, and only 8 (14%) had different non-neoplastic obstructive processes such as scleroma, direct injury, hamartoma, and amyloidosis. Immediate results were good in all cases. After 1 year follow-up, results of thyrotracheal anastomosis were successful in 44 (91%). In 4 other cases a restenosis was observed. Eight patients were lost to follow-up. CONCLUSIONS: Subglottic stenosis is still frequent after tracheal intubation, but other causes must be considered. Laryngotracheal reconstruction with thyrotracheal anastomosis with partial cricoid resection was feasible with good results in 91% of the cases with follow-up, but this procedure must be performed by a skilled surgical team.

Adult↗

PubMed2001

Bronchoconstriction induced by inhaled adenosine 5'-monophosphate in subjects with allergic rhinitis.

Adenosine and its related nucleotide, adenosine 5'-monophosphate (AMP) induce bronchoconstriction in asthmatics, probably caused by histamine release from airway mast cells. The objective of this study was to determine the effect of inhaled AMP on lung function in subjects with allergic rhinitis. A total of 52 adults (28 subjects with allergic rhinitis, 14 asthmatics and 10 healthy subjects) were challenged with increasing concentrations of AMP and methacholine. Airflow was assessed after each concentration and the response to each bronchoconstrictor agent was measured by the provocative concentration required to produce a 20% fall (PC20) in forced expired volume in one second (FEV1). All 14 asthmatics, 10 subjects with allergic rhinitis and none of the healthy controls were hyperresponsive to AMP. Subjects with allergic rhinitis had higher prevalence of hyperresponsiveness to AMP than healthy controls (p=0.038). Although the prevalence of hyperresponsiveness for methacholine and for AMP in subjects with allergic rhinitis was similar (39% and 36%, respectively), four subjects had hyperresponsiveness to methacholine but not to AMP, whereas three subjects had hyperresponsiveness to AMP but not to methacholine. To conclude, inhaled adenosine 5'-monophosphate causes airway narrowing in a significantly higher proportion of subjects with allergic rhinitis than healthy volunteers. Furthermore, methacholine and adenosine 5'-monophosphate hyperresponsiveness are not detected in the same individuals with allergic rhinitis, thus suggesting that responsiveness to the two bronchoconstrictor stimuli is not reflecting the same abnormalities of the airways.

Adenosine Monophosphate↗

PubMed2001

Magnetic resonance imaging of the pharynx in OSA patients and healthy subjects.

Obstructive sleep apnoea (OSA) occurs because of recurrent narrowing and occlusion of the velopharynx (VP) during sleep. The specific cause of OSA is unknown. Cephalometric radiography, fibreoptic nasopharyngoscopy, acoustic reflection techniques, and computerized tomography have limitations (dynamic and tridimensional evaluation) in the mechanism of occlusion investigation. Static and dynamic examination of the soft tissue structures surrounding the upper airway during the respiratory cycle in wakefulness and sleep, can lead to a better understanding of the process. Ultrafast magnetic resonance imaging (one image per 0.8 s) was used to study the upper airway and surrounding soft tissue in 17 patients with OSA during wakefulness and sleep, and in eight healthy subjects whilst awake. The major findings of this investigation in the 25 subjects were as follows: 1) the VP was smaller in apnoeic patients, only during part of the respiratory cycle; 2) the variation in VP area during the respiratory cycle was greater in apnoeic patients than in controls, particularly during sleep, suggesting an increased compliance of the VP in these patients; 3) VP narrowing was similar in the lateral and anterior-posterior dimensions, both in controls and apnoeic patients while awake; apnoeic patients during sleep have a more circular VP upon reaching the minimum area; 4) there was an inverse relationship between dimensions of the lateral pharyngeal walls and airway area, probably indicating that lateral walls are passively compressed or stretched as a result of changes in the airway calibre; and 5) soft palate and parapharyngeal fatpads were larger in apnoeic patients, although their role in the genesis of OSA is uncertain. It was concluded that changes in the velopharynx area and diameter during the respiratory cycle are greater in apnoeic patients than in normal subjects, particularly during sleep. This suggests that apnoeic patients have a more collapsible velopharynx, this being the main mechanism of obstruction.

Adult↗

PubMed2001

[Adrenocortical macronodular hyperplasia with massive enlargement of the gland. A rare variant of autonomous hypercortisolism].

OBJECTIVE: To present a case of Cushing's syndrome due to massive adrenocortical macronodular hyperplasia that gave the gland the appearance of a pseudotumor. METHODS: In a review of the surgical pathology of the adrenal gland recently performed in our hospital, 82 adrenalectomy specimens obtained from 1978-1998 were found. Of these 82 surgical specimens, 44 (53.6%) were cortical pathologies and 10 of these (12.1%) were hyperplasia. There was only one with massive adrenocortical macronodular hyperplasia. A 53-year-old male, chronic alcoholic with cushingoid obesity and hypercortisolism is described. RESULTS: Ultrasound and CT assessment showed enlarged, asymmetrical adrenal glands and macronodules. The analytical and MRI study of the sella turcica showed primary adrenal hypercortisolism. Adrenalectomy of the dominant gland (the left adrenal whose activity was demonstrated on the 131Iodine scintiscan) was performed. The postoperative cortisol levels returned to normal and remain normal up to the present time, 18 months after surgery. The surgical specimen weighed 104 gms and was completely macronodular. CONCLUSIONS: Massive adrenocortical macronodular hyperplasia is a rare cause of pituitary-independent autonomous primary adrenal hypercortisolism. It is always bilateral. Adrenal weight is significantly increased (total weight of both adrenals 60-180 gms) and present yellow or golden, non-encapsulated nodules of a few millimeters to up to 4 cms, comprised of cells with scanty activity, therefore massive enlargement of the glands is necessary to produce Cushing's syndrome. The clinical, biochemical and surgical aspects can cause confusion and can be suggestive of an adrenocortical neoplasm. Treatment is by adrenalectomy.

Adrenal Cortex↗

PubMed2001

Serological response (Western blot) to fractions of Mycobacterium tuberculosis sonicate antigen in tuberculosis patients and contacts.

OBJECTIVE: To assess the serological response to fractions of Mycobacterium tuberculosis sonicate antigen by Western blot analysis in patients with tuberculosis and contacts. METHODS: We studied 71 individuals including 43 patients with active tuberculosis, 16 contacts and 12 healthy blood donors. For Western blot analysis, M. tuberculosis (H37Rv strain) sonicate antigen extract was fractionated by electrophoresis on polyacrylamide gel (SDS-PAGE). RESULTS: We obtained antibody responses directed against four antigenic fractions with molecular weights of 71, 65, 26-38 and 19 kDa. Sixty per cent of pleural tuberculosis and 52.4% of smear-positive pulmonary tuberculosis had whole responses against all four fractions; there were no partial responses in these groups. For patients with smear-negative pulmonary tuberculosis whole responses were 17.6% and partial responses 41.2%. All contacts whose tuberculin tests converted from negative to positive (three cases) reacted exclusively against the 19 kDa fraction. CONCLUSIONS: Western blot-positive results in patients with pleural and smear-positive pulmonary tuberculosis were characterised by a whole pattern against all four antigenic fractions, whereas patients with smear-negative pulmonary tuberculosis showed heterogeneous results. The exclusive response against the 19 kDa fraction observed in contacts with tuberculin conversion could help to identify candidates for preventive therapy.

Adult↗

PubMed2000

Hypothermic storage of coronary endothelial cells reduces nitric oxide synthase activity and expression.

Preservation with University of Wisconsin (UW) solution has been implicated in coronary artery endothelial damage and loss of endothelium-dependent vasodilatation. Therefore, the objective of this study was to investigate the effect of this solution on basal nitric oxide (NO) release from porcine coronary endothelial cells (CEC). Cultures were exposed to cold (4 degrees C) storage in UW solution for 6, 8 and 12 h. Parallel cultures were incubated with control medium at 37 degrees C. After treatment, NO release was evaluated by nitrite production, a stable metabolite of NO. Activity of the constitutive endothelial nitric oxide synthase (eNOS) was measured by the conversion [3H]-l-arginine to [3H]-l-citrulline and eNOS protein expression by Western blotting. Nitrite production by control cells was augmented with increasing times of incubation, whereas no change was observed in those cultures preserved with UW solution. Activity of eNOS was significantly decreased compared to the respective control group by cold storage of cells for longer periods than 6 h. Such decrease was correlated with a diminished eNOS protein expression in CEC preserved with UW solution after 8- and 12-h storage. These results suggest that prolonged hypothermic storage of CEC with UW solution does not preserve basal NO release because of a certain loss of eNOS protein, which may contribute to the reported injury of heart transplants after long-term preservation.

Adenosine↗

PubMed2000

Initial pleural pressure measurement in spontaneous pneumothorax.

To assess whether pleural pressure (PP) measurement is helpful in evaluating the evolution of spontaneous pneumothorax (SP). To measure the inspiratory and expiratory PP at tidal volume in the SP in 85 cases. Ninety-one percent were cured with medical treatment, whereas the remaining 9% required surgery. In the cases medically resolved, the inspiratory pleural pressure (IPP) was -9 +/- 5 mbar, and the expiratory pleural pressure (EPP) was -3 +/- 6 mbar, whereas in the surgical cases, IPP was -7 +/- 2 mbar (p = not significant), and EPP was 1 +/- 3 mbar (p < 0.01). In the SP cases, which resolved in less than 7 days of drainage, IPP was -10 +/- 5 mbar, and EPP was -3 +/- 5 mbar, whereas IPP was -8 +/- 3 mbar (p < 0.01), and EPP was 0 +/- 4 mbar (p < 0.001) in those cases in which SP resolution required more than 7 days. The sensitivity to predict the need for surgery with an EPP > or = 2 mbar was 100%, with a specificity of 49%. The cutoff of the curve was > or = 1 mbar, with a sensitivity of 65% and specificity of 70%. The values of PP at the end of an expiration to tidal volume were negative in the SP cases, which were resolved by medical treatment, whereas they were atmospheric in those cases that required surgery. The static inspiratory and expiratory PP in the SP cases requiring thoracic drainage during < 7 days showed more negative PP than those that resolved in a period longer than 7 days.

Adolescent↗

PubMed2000

Diabetes alters neuronal nitric oxide release from rat mesenteric arteries. Role of protein kinase C.

The objective of the present study was to assess the influence of diabetes in the neuronal nitric oxide (NO) release elicited by electrical field stimulation (EFS, 200 mA, 0.3 ms, 1-16 Hz, for 30 s, at 1 min interval) in endothelium-denuded mesenteric artery segments from control and streptozotocin-induced diabetic rats, assessing the influence of protein kinase C (PKC) in this release. N(G)-nitro-L-arginine-methyl ester (L-NAME, 10 microM, a NO synthase inhibitor) enhanced EFS-elicited contractions in control, and specially in diabetic rats, whereas they were unaltered by AMT (5 nM, an inducible NO synthase inhibitor) and capsaicin (0.5 microM, a sensory neurone toxin). Calphostin C (0.1 microM, a PKC inhibitor) increased the contraction elicited by EFS in both types of arteries. This increase was further enhanced by calphostin C + L-NAME in diabetic rats. Phorbol 12,13-dibutyrate (PDBu, 1 microM) reduced and unaltered EFS-induced contractions in control and diabetic rats, respectively. The further addition of L-NAME reversed the reduction obtained in control rats, and enhanced the response observed in diabetic rats. These results suggest that the EFS-induced NO release from perivascular nitrergic nerves, that negatively modulates the contraction, which is synthesized by neuronal constitutive NO synthase. The NO synthesis is positively stimulated by PKC. This NO release is increased in diabetes, likely due to an increase in the activity of this enzyme. The sensory nerves of these arteries do not seem to be involved in the contractile response.

Animals↗

PubMed2000

Mechanisms involved in the hemodynamic alterations in congestive heart failure as a basis for a rational pharmacological treatment.

Congestive heart failure is a complex syndrome and one of the major cardiological problems of our time. It is characterized by an important neurohumoral activation to compensate for the reduction of cardiac output and blood pressure, that worsens the prognosis with time. The aim of the treatment is focused on how to improve the quality of life and how to prolong survival. Usually, treatment, either symptomatic or directed to control the neuroendocrine compensatory changes, is necessary. The drugs currently used are angiotensin-converting enzyme inhibitors, diuretics, digoxin, and beta-adrenoceptor agonists. In addition, new drugs, such as angiotensin II receptor antagonists, beta-adrenoceptor antagonists, ibopamine, Ca(2+) antagonists, neutral endopeptidase inhibitors, vasopressin antagonists, Ca(2+)-sensitizers with cyclic AMP-dependent or -independent mechanisms, and endothelin antagonists, are also being used.

Animals↗

PubMed2000

Differences in airway responsiveness to acetaldehyde and methacholine in asthma and chronic bronchitis.

Inhaled acetaldehyde may induce bronchoconstriction in asthmatic subjects and provides a new method to investigate airway responsiveness. The objective of the study was to determine whether acetaldehyde was a more specific stimulus than methacholine in differentiating asthma from chronic bronchitis with or without airflow limitation. Bronchial provocation challenges with methacholine and acetaldehyde were performed in 62 asthmatics and in 59 smokers with chronic bronchitis (32 with chronic bronchitis alone and 27 with chronic bronchitis and coexisting chronic obstructive pulmonary disease (COPD)). The response to both bronchoconstrictor agents was measured by the provocative concentration required to produce a 20% fall in forced expiratory volume in one second (FEV1; PC20). The two types of challenge yielded a similarly high level of sensitivity (100% for methacholine and 92% for acetaldehyde) in revealing airway hyperresponsiveness in asthma. However, bronchoprovocation with acetaldehyde yielded considerably greater specificity (95%) than bronchoprovocation with methacholine (24%) in separating asthma from chronic bronchitis. In subjects with asthma, methacholine and acetaldehyde responsiveness were weakly but significantly correlated (r=0.42, p=0.001) but no correlation was found between airway responsiveness to acetaldehyde and baseline FEV1 (r=0.13, p=0.33). These findings suggest that the demonstration of bronchoconstriction in response to acetaldehyde may be a more specific test than methacholine in the differentiation of asthma from chronic bronchitis. Furthermore, methacholine and acetaldehyde hyperresponsiveness are not reflecting the same pathophysiological process in the airways.

Acetaldehyde↗

PubMed2000

Influence of hypertension on nitric oxide synthase expression and vascular effects of lipopolysaccharide in rat mesenteric arteries.

1. Experiments were designed to investigate the effects of the inducible nitric oxide synthase (iNOS) stimulator, lipopolysaccharide (LPS), on noradrenaline (NA) responses and on NOS activity and its expression in intact mesenteric resistance arteries (MRAs) from Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. 2. In MRAs from WKY, LPS (10 microg ml(-1); 1-5 h) reduced the vasoconstrictor responses to NA (0.1 - 30 microM) in the presence, but not in the absence of L-arginine (L-Arg, 10 microM). However, in SHR arteries, LPS induced an incubation-time dependent reduction of NA responses in the absence, as well as the presence, of L-Arg. The LPS inhibitory effect was reduced by the non-specific NOS inhibitor L-N(G)-nitroarginine methyl ester (L-NAME, 100 microM) and the selective iNOS inhibitor, aminoguanidine (100 microM). 3. L-NAME alone similarly shifted the concentration-response curve to NA leftward in arteries from both strains, while aminoguanidine had no effect. L-Arg shifted the curve to NA rightward only in SHR MRAs. 4. Basal activity of both iNOS and constitutive NOS (conversion of [(3)H]-L-Arg to [(3)H]-L-citrulline) was similar in arteries from both strains. After 5 h incubation with LPS, only iNOS activity in arteries from SHR was increased. 5. Basal iNOS protein expression was undetectable; basal endothelial (eNOS) protein expression was similar in arteries from both strains, while neuronal (nNOS) was greater in arteries from SHR. LPS induced iNOS protein expression, that was higher in arteries from SHR than in those from WKY. 6. These results indicate that NO production, via iNOS induction, is greater than in those from MRAs from SHR to WKY.

Animals↗

PubMed2000

Conditioning regimens in autologous stem cell transplantation for multiple myeloma: a comparative study of efficacy and toxicity from the Spanish Registry for Transplantation in Multiple Myeloma.

High-dose chemoradiotherapy conditioning regimens for autologous stem cell transplantation (ASCT) are generally held to give similar results in multiple myeloma (MM), but no specific comparative study has been published. We addressed this issue by comparing the main high-dose chemoradiotherapy regimens used in the Spanish Registry. Patient cohorts included 315 cases treated with 200 mg/m2 melphalan (MEL200), 127 patients with 140 mg/m2 melphalan plus total body irradiation (MEL140 + TBI) and 121 cases with 12 mg/kg busulphan plus 140 mg/m2 melphalan (BUMEL). After ASCT, granulocyte and platelet recovery time was similar in all conditioning groups. There were no differences in transplant-related mortality. All regimens yielded a similar response in reference to pre-ASCT MM status, although BUMEL produced a slightly better overall response when compared with the other regimens (97% vs. 89% and 92%, P = 0.003). The 5-year overall survival (OS) with BUMEL was 47% [95% confidence interval (CI) 26-68] compared with 43% (CI 31-54) for MEL140 + TBI and 37% (CI: 18-56) for MEL200. The median survival for the BUMEL group was 64 months compared with 45 and 37 months for the MEL200 and MEL140 + TBI groups respectively. These differences were non-significant (P = 0.2). The median event-free survival (EFS) was better for BUMEL (32 months) than for MEL200 (22 months) or for MEL140 + TBI (20 months). The differences in EFS between BUMEL and the other conditioning regimens reached statistical significance (P = 0.01). Nevertheless, the adjusted multivariate analysis for OS and EFS revealed that the conditioning regimens had no independent prognostic value. We concluded that three different conditioning regimens, commonly used for ASCT in MM, have a similar antimyeloma effect. However, the trend for better results observed in our series with BUMEL requires a prospective trial.

Busulfan↗

PubMed2000

Different sensitivity of isoprenaline-induced responses in ventricular muscle to sodium nitroprusside in normotensive and spontaneously hypertensive rats.

1. The aim of the present work was to study the possible modulatory role of nitric oxide (NO) on the positive inotropic effect induced by the beta-adrenoceptor agonist isoprenaline in myocardial contractility, and whether this modulation is altered by hypertension. 2. The study was performed using right ventricular strips from the hearts of 6-month-old male Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The contractile force of electrically-stimulated ventricular strips was measured by a force-displacement transducer. 3. Isoprenaline (from 10 nmol l(-1) to 10 micromol l(-1)) induced a concentration-dependent increase in cardiac contractility in strips from both rat strains. This positive inotropic effect to isoprenaline was reduced by the NO donor sodium nitroprusside (SNP, 0.1 mmol l(-1)) in muscles from WKY rats and slightly increased in those from SHR. The SNP-induced increase in strips from SHR was abolished by superoxide dismutase (100 U ml(-1)). 4. N(G)-nitro-arginine-methyl ester (L-NAME, 0.1 mmol l(-1)) and 1H-[1,2,4]oxadiazolo[4,3]-quinoxalin-1-one (ODQ, 10 micromol l(-1)), respective inhibitors of NO synthase and guanylate cyclase, increased the response to isoprenaline in muscles from WKY rats, whereas it was unaltered in strips from SHR. 5. In strips from WKY rats, the combination of ODQ and SNP produced an increase in the response elicited by isoprenaline, which was similar to that observed with ODQ or L-NAME. 8-Br-cyclicGMP (8-Br-cGMP, 0.1 mmol l(-1)), a permeable and structural cGMP analogue, decreased the effect induced by isoprenaline only in muscles from WKY rats. 6. These results suggest that the positive inotropic response to isoprenaline in ventricular strips from WKY rats is negatively modulated by NO, and positively by superoxide anions in those from SHR. The lack of a modulatory response to NO in ventricular strips from SHR is probably a result of an alteration of mechanisms in NO-signalling pathway downstream of cGMP formation in SHR hearts.

Adrenergic beta-Agonists↗

PubMed2000

Psychological and occupational predictive factors for back pain among employees of a university hospital in southern Spain.

OBJECTIVES: To identify the individual and occupational factors that are predictors for low back pain among the employees of a university hospital in southern Spain. METHODS: A transverse study was conducted in which the population used was the hospital employees who volunteered to participate. The information was obtained by using a questionnaire, which included demographic and anthropometric variables, habits, characteristics of the work done, and of any pain experienced. The mental health condition of subjects was measured using the GHQ-28, using a score of > or = 6 as the cut-off point. To study the variables associated with pain, crude odds ratios (ORs) were calculated (+/- 95% CI) and adjusted according to a logistic regression model. RESULTS: One thousand one hundred and four subjects participated in the study but only 890 of these completed the questionnaire in full (rate of response, 35.7% of total employees). The population studied was notable for the high proportion of women, for subjects > 41 years of age, and subjects who undertook little or no physical exercise. In addition, according to the GHQ-28 test, 29.9% of the total were 'probable psychiatric cases'. The crude ORs were high in all the occupational categories in comparison with the doctors, with the exception of the maintenance, cleaning, and catering group. They were also higher among women, among subjects with poor mental health, and among women with one or more children. The adjusted ORs showed that having a GHQ-28 score of > or = 6, and belonging to the auxiliary technician category, were independent risk factors for suffering low back pain. Being older than 41 years and in temporary employment were protective variables. CONCLUSIONS: The presence of probable mental illness is the variable most strongly associated with the presence of low back pain in the population studied. Its diagnostic confirmation and appropriate treatment could contribute to reducing the prevalence of vertebral pains in this occupational group.

Adult↗

PubMed2000

Nitric oxide synthase induction by ouabain in vascular smooth muscle cells from normotensive and hypertensive rats.

OBJECTIVE: To investigate the effect of ouabain on inducible nitric oxide synthase (iNOS) activity and expression in cytokine-stimulated vascular smooth muscle cells (VSMC) from normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: VSMC were treated for 24 h and afterwards, nitric oxide (NO) release was determined by the production of nitrite, a stable metabolite of NO. Activity of iNOS was measured by the conversion of [3H]-L-arginine to [3H]-L-citrulline and iNOS protein expression by Western blotting. RESULTS: Ouabain (0.01-1 mmol/l) further enhanced interleukin-1beta (II-1beta)-induced nitrite production by WKY and SHR VSMC, although a more pronounced effect was observed in SHR cells (maximum response 52.1 +/- 5.2 and 71.2 +/- 6.4% of 11-1beta effect in WKY and SHR cells, respectively). Such response on NO release was mimicked by the calcium ionophore A 23187 (0.01-1 micromol/l) and abolished by the voltage-operated calcium channels (VOCC) nifedipine (0.1 micromol/l). Expression of iNOS showed that ouabain increased the synthesis of the enzyme in WKY and SHR VSMC stimulated with II-1beta, and this effect was higher in SHR cells. The increased iNOS expression was significantly reduced by nifedipine. CONCLUSIONS: Ouabain stimulation of iNOS expression and activity in II-1beta-stimulated VSMCs from WKY rats and SHR seems to be related to increased intracellular calcium influx through VOCC. The more pronounced effect observed in SHR VSMC could be explained by an altered calcium entry in the hypertensive strain.

Animals↗

PubMed2000

Increase in neurogenic nitric oxide metabolism by endothelin-1 in mesenteric arteries from hypertensive rats.

We investigated, in mesenteric arteries from hypertensive rats (SHRs), the possible changes in neurogenic nitric oxide (NO) release produced by endothelin-1 (ET-1), and the mechanisms involved in this process. The contractile response induced by electrical field stimulation (EFS; 200 mA, 0.3 ms, 1-16 Hz, for 30 s) in deendotheliumized mesenteric segments was abolished by tetrodotoxin and phentolamine. The NO synthase inhibitor N(G)-nitro-L-arginine (L-NAME, 10 microM) increased the contractions caused by EFS. ET-1 enhanced the contraction induced by EFS, which was unaltered by the subsequent addition of L-NAME. The ETA antagonist-receptor BQ-123 (1 microM) inhibited the effect of ET-1 on EFS response, whereas the ETB antagonist-receptor BQ-788 (3 microM) partially blocked it, and the subsequent addition of L-NAME restored the contractile response in both cases. SOD (25 unit/ml) decreased the response to EFS, and the subsequent addition of L-NAME increased this response. ET-1 did not modify the decrease in EFS response induced by SOD, and the addition of L-NAME increased the response. None of these drugs altered the response to exogenous noradrenaline (NA) or basal tone except SOD, which increased the basal tone, an effect blocked by phentolamine (1 microM). In arteries preincubated with [3H]NA, ET-1 did not modify the tritium efflux evoked by EFS, which was diminished by SOD. ET-1 did not alter basal tritium efflux, whereas SOD significantly increased the efflux. These results suggest that EFS of SHR mesenteric arteries releases neurogenic NO, the metabolism of which is increased in the presence of ET-1 by the generation of superoxide anions.

Analysis of Variance↗