Biomedical subjects
Publications and source records attributed to M Freitas.
In children under 5 years of age, presenting to the paediatric emergency room with clinical and radiological findings of pneumonia, viridans streptococci were isolated in 10/33 positive haemocultures as the only microorganism. Viridans streptococci should therefore not be ruled out as a cause of pneumonia.
Entubulation repair of peripheral nerve injuries has a lengthy history. Several experimental and clinical studies have explored the effectiveness of many biodegradable and non-degradable tubes with or without addition of molecules and cells. The main objective of the present study was to develop an economical and also an easy way for culturing a neural cell line which is capable of growing, differentiating and producing locally nerve growth factors, that are otherwise extremely expensive, inside 90 PLA/10 PLG nerve guides. For this purpose the authors have chosen the N1E-115 cell line, a clone of cells derived from mouse neuroblastoma C-1300 with the perspective of using this differentiated cellular system to cover the inside of 90 PLA/10 PLG nerve guides placed to bridge a nerve gap of 10 mm in the rat sciatic nerve experimental model. The N1E-115 cells proliferate in normal culture medium but undergo neuronal differentiation in response to DMSO. Upon induction of differentiation, proliferation of N1E-115 cells ceases, extensive neurite outgrowth is observed and the membranes become highly excitable. While it is known that Ca2+ serves as an important intracellular signal for cellular various processes, such as growth and differentiation, be toxic to cells and be involved in the triggering of events leading to excitotoxic cell death in neurons. The [Ca2+]i in non-differentiated N1E-115 cells and after distinct periods of differentiation, have been determined by the epifluorescence technique using the Fura-2-AM probe. The results of this quantitative assessment, revealed that N1E-115 cells which undergo neuronal differentiation for 48 hours in the presence of 1.5% DMSO are best qualified to be used to cover the interior of the nerve guides since the [Ca2+]i was not found to be elevated indicating thus that the onset the cell death processes was not occurred.
Entubulation repair of peripheral nerve injuries has a lengthy history. Several experimental and clinical studies have explored the effectiveness of many biodegradable and non-degradable tubes with or without addition of molecules and cells. The main objective of the present study was to develop an economical and also an easy way for culturing a neural cell line which was capable of growing, differentiating and producing locally nerve growth factors that are otherwise extremely expensive, inside 90 PLA/10 PLG nerve guides. For this purpose the authors have chosen the N1E-115 cell line, a clone of cells derived from mouse neuroblastoma C-1300 with the perspective of using this differentiated cellular system to cover the inside of 90 PLA/10 PLG nerve guides placed to bridge a gap in the rat sciatic nerve experimental model. The N1E-115 cells proliferate in normal culture medium but undergo neuronal differentiation in response to DMSO. Upon induction of differentiation, proliferation of N1E-115 cells ceases, extensive neurite outgrowth is observed and the membranes become highly excitable. While it is known that Ca2+ serves as an important intracellular signal for various cellular processes, such as growth and differentiation. It is also known that can be toxic to cells and is involved in the triggering of events leading to excitotoxic cell death in neurons. The [Ca2+]i in non-differentiated N1E-115 cells and after distinct periods of differentiation, have been determined by the epifluorescence technique using the Fura-2-AM probe. The results of this quantitative assessment revealed that N1E-115 cells which undergo neuronal differentiation for 48 hours in the presence of 1.5% DMSO are best qualified to be used to cover the interior of the nerve guides since the [Ca2+]i was not found to be elevated indicating thus that the onset the cell death processes was not occurred.
The aim of this work was to set up and validate an in vitro model to study a molecular response of an intestinal host cell line (HT29-MTX), to a non-pathogen microflora component. We found that Bacteroides thetaiotaomicron strain VPI-5482 had the capacity to change a specific glycosylation process in HT29-MTX cells via a mechanism that involved a soluble factor. Differentiated HT29-MTX cells were grown in the presence of 20% of spent culture supernatant from the B. thetaiotaomicron during 10 days. Glycosylation processes were followed using a large panel of lectins and analysed using confocal microscopy, western blotting and flow cytometry techniques. Our results show that a B. thetaiotaomicron soluble factor modified specifically the galactosylation pattern of HT29-MTX cells, whereas other glycosylation steps remained mainly unaffected. Further characterization of this soluble factor indicates that it is a heat labile, low molecular weight compound. Reverse transcript-PCR (RT-PCR) analysis was unable to show any significant change in mRNA expression level of the main galactosyltransferases expressed in HT29-MTX cells. By contrast, galactosyltransferase activities dramatically increased in HT29-MTX cells treated by the soluble extract of B. thetaiotaomicron, suggesting a post-translational regulation of these activities. Our in vitro model allowed us to study the cross-talk between a single bacteria and intestinal cells. The galactosylation process appears to be a target of this communication, thus uncovering a new window to study the functional consequences of co-operative symbiotic bacterial-host interactions.
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Nerve biopsy specimens from 53 patients with leprosy and neuropathy were taken from the sural, the dorsal branch of the ulnar, or the superficial radial nerves and processed for light and electron microscopy. There was inflammation in 40 cases (75%), 7 with a granulomatous reaction, various stages of fibrosis in 35 (66%), and endoneurial vascular neoformation in 7. In two cases, small focal infarcts were associated with marked endoneurial inflammation compressing the vessels, in addition to endoneurial lymphocytic vasculitis. Most had an axonal neuropathy of varying degree, some with total fibre loss, others with predominant small myelinated and unmyelinated fibre loss. Signs of demyelination and remyelination were the main findings in 9 cases (17%). Bacilli were present in endothelial, perineurial, Schwann cells and in macrophages. On two occasions, they lost their alcohol acid resistance, were suspected in semithin sections, and confirmed ultrastructurally. The biopsy was decisive for the diagnosis of leprosy in 15 cases (28%), most without skin lesions. We evaluated the effectiveness of the treatment in 20 (37.7%), 12 without and 8 with bacilli, despite negativity in the skin. The diagnosis of leprosy based on skin lesions was confirmed with the nerve biopsy in 9 cases, 6 had an inflammatory neuropathy suggestive of leprosy in the absence of bacilli, and 3 had nonspecific changes in the sural nerve since the neuropathy was in the upper limbs. We conclude that nerve biopsy is indicated for the diagnosis of leprosy in cases without clinically visible skin lesions and to evaluate the effectiveness of the treatment. In these cases the ultrastructural studies are important for recognition of the bacilli. Vascular lesions may play an important role in the progression of the nerve damage, including the occurrence of focal nerve infarcts which, to our knowledge, have not been previously reported in association with leprosy.
With regard to the concept of reperfusion injury, there is no doubt that the benefit of reperfusion can cause serious arrhythmias, mechanical stunning, myovascular damage, new necrosis, or as some people consider more likely, apotosis. Advances in cell biology of cardiomyocytes have been remarkable in recent years. However, it is still impossible to monitor all the events that occur in these cells, especially in relation to their function and dysfunction. Our understanding of cellular dysfunction would be enhanced if different types of morphological changes could be related to specific metabolic and functional disorders of the cells. The most important of these changes are those leading to cell necrosis. In terms of therapy, it is essential to identify and prevent the progression of these lethal processes. The concepts of modern interventional cardiology have shown that steps such as thrombolysis, primary angioplasty, relief of coronary spasm-calcium antagonists and drugs such as trimetazidine (myocardial protection) are all important to promote coronary flow and to improve tissue metabolism. The pre-treatment and treatment with trimetazidine during the experimental period is almost totally able to prevent ischemic contracture. The mode of action is metabolic. The site of action is not clear. There is a very interesting trial called EMIP, presently under way in Europe, on the use of trimetazine in early thrombolysis that may help to show that this drug could prevent reperfusion injury. The results have not yet been disclosed.
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PURPOSE: To compare two groups of 80 patients undergoing to myocardial revascularization with the use of antifibrinolytic drug tranexamic acid and its efficacy in reduce bleeding and blood transfusion. METHODS: Prospective analysis of two groups of 80 patients. Group A-no antifibrinolytic therapy (dec 91-may 92) and group B-fibrinolytic therapy-tranexamic acid-10g EV (jun-dec/92). Quantification of mediastinal drainage over 12h as well as the blood or derivatives received at the same time. RESULTS: Hospital mortality: group A-3.8%, group B-2.5%. Drainage (12h): group A-602 +/- 547 ml and group B-260 +/- 260 ml (p < 0.001). Blood transfusion (12h): group A-1,782 +/- 1,163 ml and group B-1,105 +/- 839 ml (p < 0.001). COMPLICATIONS: group A-two cases of intraoperative myocardial infarction, one episode of jaundice; group B-one case of intraoperative MI, one reoperation for bleeding control, one episode of jaundice, one of renal insufficiency, two mediastinitis and one seizure. The mean hospitalization time was ten days in both groups. CONCLUSION: Tranexamic acid was an effective drug in bleeding control and in reducing blood transfusion in the postoperative of patients submitted to myocardial revascularization.
OBJECTIVE: Several studies suggest that anaesthetic drugs influence the haemodynamic effects of the antiarrhythmic drugs. The aim of this study was to compare the haemodynamic effects of a standard dose of propafenone (1.5 mg/kg) on dogs anaesthetized with halothane or with isoflurane. DESIGN: Randomized laboratory animal study. MATERIAL AND METHODS: Six dogs were anaesthetized with 1% of halothane-Group I, and six dogs with an equianaesthetic dosage of isoflurane (1.5%)-Group II. Dogs breathed in spontaneous ventilation. Haemodynamic monitoring was performed with a femural arterial catheter and a flow-directed pulmonary artery catheter and cardiac output was measured by thermodilution. After a haemodynamic assessment considered as initial a bolus of 1.5 mg/kg of propafenone was given during a period of 30 seconds and similar assessments were made 5, 15, 30 and 60 minutes after. RESULTS: Before propafenone, heart rate was significantly higher in Group II-isoflurane (p < 0.05). After propafenone we found: In both Groups, a decrease in the cardiac output (p < 0.05) with the mean arterial pressure maintained; in Group I (halothane) a decrease in the stroke volume (p < 0.05) which was not found in Group II (p = ns); In Group II (isoflurane) a decrease in heart rate (p < 0.05) not found in Group I (p = ns). All the changes were higher at the 5th minute values. 30th minute and 60th minute values were not significantly different from initial values. CONCLUSION: In dogs anaesthetized with halothane 1.2 MAC a reduction in the stroke volume, resulting in a cardiac output decrease, was observed, suggesting that propafenone increases the negative inotropic action of halothane. In dogs anaesthetized with isoflurane 1.2 MAC the decrease in cardiac output was similar to the decrease in heart rate, and therefore no reduction in the stroke volume was observed. The decrease in the heart rate found in this group but not in the halothane group was probably related with the beta-blocker action of the propafenone. Looking to the systemic vascular resistances, our study suggested that propafenone didn't have any vasodilator effect during halogenated anaesthesia.
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Significant advances are emerging in what concerns the newer inotropic agents. Despite the ideal agent, whose sole action is to increase the sensitivity of contractile proteins to calcium is yet to be found, the identification of specific receptors of dopamine in the CNS and peripheral circulation, had stimulated the pharmacological research of dopaminergic receptors agonists, selective for the subtypes DA1 and DA2, selective DA1 and DA2 antagonists and the dopamine beta-hidroxilase inhibitors and represent an unequivocal value. Beta-adrenergic agonists have been extensively evaluated as positive inotropic agents in the patients with congestive heart failure. Although norepinephrine, epinephrine and isoproterenol are potent stimulators of myocardial beta-adrenergic receptors, the clinical use of these agents has been limited by their positive chronotropic actions and their tendency to exacerbate cardiac arrhythmias (epinephrine and isoproterenol); their potent effects on vascular alpha 1-adrenergic receptors, which cause vasoconstriction (norepinephrine); and their effects on vascular beta 2 receptors, which cause vasodilation (isoproterenol). Dopamine, endogenous precursor of norepinephrine, is a sympathomimetic amine that has been widely used clinically as a cardiac stimulant. The effects of this drug are due to a combination of its actions on alpha, beta, and dopaminergic receptors, as well as a tyramine-like effect that causes the release of endogenous norepinephrine. Dopamine's positive inotropic effects are due principally to stimulation of cardiac beta-adrenergic receptors. At low doses it also stimulates renal dopaminergic receptors, thereby increasing renal cortical blood flow and promotion diuresis; higher doses causes stimulation of alpha 1-adrenergic receptors, resulting in increasing systemic arterial and venous pressures and, potentially, decrease renal blood flow. This vasoconstrictor action is frequently undesirable in patients with severe heart failure, and limits the drug's usefulness as a positive inotropic agent. Despite this risk, the use of synthetically derived catecholamines, i.e. dobutamine, has gained wide acceptance for the treatment of low output state associated with systemic hypotension. Despite the well reported down regulation of beta 1-adrenergic receptors in patients with chronic congestive heart failure, dobutamine consistently exerts hemodynamic benefits in this clinical situation. An attenuation of these benefits may be observed at times, although new tachyphylaxis very rarely occurs. Since dobutamine does not preferentially dilate the renal vasculature, concomitant administration of dopamine, at a dose which only stimulates the dopaminergic receptors in the renal artery, had the advantage of increasing renal perfusion and improving renal function. Administration of dopamine is often prolonged after that of dobutamine, and may help the wearing off of dobutamine.(ABSTRACT TRUNCATED AT 400 WORDS)
AIM OF THE STUDY: The aim of the present study was to analyze the angiographic findings of patients with residual ischemia after acute myocardial infarction (spontaneous angina versus ischemia stress induced), testing the following theoretical hypothesis: those patients with early spontaneous angina after acute myocardial infarction have singular angiographic characteristics that justify their clinical instability. PATIENTS: A consecutive group of 60 patients admitted in the Coronary Care Unit with acute myocardial infarction, all of them presenting signs or symptoms of residual ischemia, was divided into two subgroups: A--25 patients with spontaneous angina before discharge; B--35 patients with myocardial ischemia (symptomatic or not) during exercise test performed before discharge. METHODS: The angiographic studies were analyzed according to following parameters: number of vessels with significant stenosis (more than 70%), involvement of the left anterior descending artery: "TIMI" score, presence of thrombi and morphology of the culprit lesion, presence of collaterals. RESULTS: We did not find any significant differences between the analyzed parameters. CONCLUSIONS: The present study does not disclose any significant differences related with coronary anatomy in patients with residual ischemia after acute myocardial infarction when we considered the two most frequent kinds of presentation: spontaneous angina or stress induced ischemia before discharge. Therefore the previous postulated hypothesis had not been confirmed.
The authors make a short revision about Lipoprotein(a) [Lp(a)], which has been referred as an independent risk factor for coronary disease. To confirm this results in a portuguese population, we studied serum Apo(a) [method IRMA.Kit Pharmacia.1 U/L Apo(a) = 1 mg/L Lp(a)], Apo A, Apo B, total cholesterol, HDL-cholesterol, triglycerides, calcium, uric acid, glucose, fibrinogen and ESR in 37 patients who were submitted to postmyocardial infarction coronarography (Judkins technic--Seldinger. Classic incidences. Significative lesions: greater than or equal to 75% in coronary vessels or greater than or equal to 50% in common main nk). The purpose was to search for changes on the plasmatic levels according to the results of the coronarography. The only change observed was in the Lp(a) levels, with important variations (p less than 0.05) between the defined groups: patients without significant coronary disease or disease on just one vessel [media (mean) = 30.1 mg/dl. Standard error (SE) = 7.9 mg/dl.n = 11] and another group of patients with coronary disease of two or three vessels [mean = 50.5 mg/dl.SE = 7.0 mg/dl.n = 26]; among the patients with two vessels disease were found significant changes (p less than 0.02) on Lp(a) levels according to the descending anterior coronary being [mean = 79.5 mg/dl.SE = 4.3 mg/dl.n = 8] or not [mean = 38.5 mg/dl.SE = 14.3 mg/dl.n = 7] implicated. These observations make the suggestion of Lp(a) as a risk factor for coronary disease, and a predictor for the gravity of the coronary disease in myocardial infarction.
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Lymphocyte dependent-antibody cytotoxicity (LDAC) was studied in 29 patients with rheumatoid arthritis (RA) and 22 controls. A significant increase of cytotoxic index has been noted in RA patients (p less than 0.0001) whatever the ratio effector-target cells could be. There is a correlation between cytotoxic activity and so called "rheumatoid rosettes" (RR) level. This cytotoxic activity is linked to EA rosette forming cells without T cell markers or surface immunoglobulins, as shown by fractionation experiments. EA rosette forming cell depletion is followed by the disappearance of RR and a very important decrease of cytotoxic index. Cytotoxic activity is abolished after RR forming cell depletion while EA rosette level is nearly unmodified. RR forming cells belong to Fc receptor bearing lymphoïd population. They take place in EA rosette forming cell population. Increase of cytotoxicity in RA seems to be directly linked to these so called RR forming cells.
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