[Actinic chronic cheilitis and its relations to epitheliomas of the lower lip].
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Biomedical subjects
Publications and source records attributed to M Serra.
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Some drugs, including nonsteroidal antiinflammatory compounds, can be hemolytic in glucose-6-phosphate dehydrogenase-deficient patients. We have studied the potential hemolytic activity of feprazone, a nonsteroidal antiinflammatory compound in vitro and in vivo. Agents that may be hemolytic for glucose-6-phosphate dehydrogenase-deficient erythrocytes will stimulate the hexose monophosphate shunt in normal erythrocytes. Eleven normal subjects were treated with feprazone and their erythrocytes were incubated in their own sera (containing active feprazone metabolites) and [1-14C]-glucose. Because no statistically significant increase in 14CO2 evolution was observed, 15 pediatric male patients with glucose-6-phosphate dehydrogenase deficiency who required antiinflammatory treatment were treated with feprazone. No hemolytic crises and no statistically significant changes of hematologic tests were observed.
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CD44, the main cell surface receptor for hyaluronan (HA), is often overexpressed in tumour cells, and its presence has been related to cell proliferation and migration. Many of the functions of CD44 are mediated through its interaction with hyaluronan. This study investigated the expression of CD44 in CML-1 and CML-10c2 canine melanoma cell lines and melanoma biopsies, and the production of hyaluronan and versican by the canine melanoma cell lines. Versican is an extracellular proteoglycan that binds hyaluronan, forming a tridimensional pericellular coat surrounding the cells. Both canine melanoma cell lines expressed CD44 and produced HA, but only CML-1 produced versican. Cells expressing all three components (CD44, HA and versican) formed abundant extracellular matrices as demonstrated by a particle exclusion assay. CD44 was present within benign and malignant melanomas, but its expression was more intense in malignant melanomas (P < 0.01). In high CD44-expressing tumours, CD44 tended to be present in the periphery of malignant melanomas, whereas its expression was homogeneous in benign melanomas.
The progesterone derivative 3 alpha-hydroxy-5 alpha-pregnan-20 one (allopregnanolone/AP) and the deoxycorticosterone derivative 3 alpha-21-dihydroxy-5 alpha- pregnan-20 one (allotetra-hydrodeoxycorticosterone/THDOC) are endogenous neuroactive steroids endowed with neuromodulatory actions in the central nervous system. Their best-characterized membrane-receptor-dependent action consists in the amplification of GABA-gated chloride currents mediated by specific interactions with the GABAA receptor complex, which appears responsible for the pharmacological effects (anxiolytic, anticonvulsant, hypnotic/anaesthetic) of exogenously administered AP and THDOC. Several acute stress paradigms and different negative allosteric modulators (isoniazid and FG 7142) of GABAA receptors time dependently increase brain and plasma concentrations of AP and THDOC only in intact or sham-operated but not in adrenalectomized-orchiectomized rats. These results suggest that acute stress and inhibitors of GABAA receptors increase the brain and plasma neurosteroid concentrations via a reduction of the inhibitory action exerted by GABA on the hypothalamic-pituitary-adrenal axis. The comparison between the time course of the changes in GABAA receptor function and of their behavioral correlates (proconflict behavior) and that of the changes of endogenous neuroactive steroids are consistent with the view that AP and THDOC may play a role in restoring the GABAergic tone to prestress conditions, by limiting the duration and the extent of its stress-induced reduction. The acute stress-elicited increase of AP and THDOC is observed in adult as well as in aged rats, which show a reduced basal GABAergic transmission and a greater response to the effect of stress in terms of their brain cortical neuroactive steroid concentrations than adult rats.
The insulin-like growth factor receptor I (IGF-I)-mediated circuit is a major autocrine loop for Ewing's sarcoma (ES) cells, and plays a role the pathogenesis and malignancy of this tumor. IGF-I receptor (IGF-IR) has emerged as a good therapeutic site for ES patients. In this study, we analyzed the impact of strategies targeting the IGF-IR on the regulation of VEGFs, which are of fundamental importance in angiogenesis, and TGFbeta, CTGF and Cyr61, which are factors primarily involved in skeletal growth control and angiogenesis. IGF-I increases expression of VEGF-A, TGFbeta, CTGF and Cyr61 mRNA. However, only the modulation of VEGF-A expression appears to be mediated by IGF-IR. Functional assays on endothelial cells indicate a strict correlation between survival and proliferation of HUVECs and VEGF-A levels, confirming a major role for this factor in angiogenesis. Blockage of IGF-IR functions by neutralizing antibody or antisense strategies significantly reduced the expression and secretion of VEGF-A by ES cells, and supernatants of treated cells were unable to sustain the survival and proliferation of HUVECs. Analysis of the signaling mechanisms involved in constitutive or IGF-induced expression and secretion of VEGF-A indicated that PI3-K and MAPK signaling pathways are both required for VEGF expression and production in ES cells. Selective inhibitors LY294002 or PD98059 were highly effective in reducing the ability of ES cells to produce VEGF-A and stimulate survival and proliferation of HUVECs. Taken together, these findings add a new activity to the IGF-I repertoire in ES and highlight how disruption of IGF-IR functions may constitute an effective tool for the control of neovascularization in this tumor.
OBJECTIVE: To identify a correlation between dialysis treatment duration and severity of acquired cystic disease of the end-stage kidney measured by cyst sizes; and assess its effect on spontaneous improvement of anemia. MATERIALS AND METHODS: Ten patients, 6 males and 4 females were selected, who have been on hemodialytic treatment for more than 5 years. There was no patient selected with autosomal dominant polycystic kidney disease. The renal evaluation has been made through ultrasonographic studies. Acquired cystic disease of the end-stage kidney was characterized by finding four or more cysts in both kidneys. The largest cysts were measured for correlation effect. The diagnosis of anemia was established by hematocrit and hemoglobin serum values. It has also been analyzed serum urea, creatinine, albumin, iron, total iron-binding capacity and the per cent saturation of serum transferrin were tested. RESULTS: The patients were properly dialysed (serum urea and creatinine = 98.7 +/- 35 mg/dL e 9.7 +/- 2.7 mg/dL, respectively). There were in good nutritional shape (serum albumin = 4.5 +/- 0.5 g/dL) and had normal serum iron level (serum iron = 80 +/- 34 mg/dL). The prevalence of acquired renal cystic disease was 80%. No finding of malignancy has been detected in these cysts. There was a significant correlation between time on dialysis treatment and hematocrit values (R = 0.70; p < 0.05). Cyst sizes had a direct and significant correlation with hematocrit levels (R = 0.74; p < 0.05). CONCLUSION: These results show that spontaneous improvement on anemia seen in patients on chronic dialysis has a significant correlation with the severity of acquired cystic disease of the end-stage kidney. Our data suggest a functional role of acquired kidney cysts on endogenous erythropoietin production.
Castleman's disease is an enigmatic lymphoid disease of unknown etiology and has different clinical manifestations. The authors present a case of a young woman with cervical localization of Castleman disease, asymptomatic. The disease was misdiagnosed and was treated for five years as thyroiditis, diagnosis confirmed by ultrasonography, scintigraphy and cytology. The particular size of the neoformation and its constant growth leaded the authors to the surgical treatment. The thyroid was normal both macroscopically and with biopsy. The neoformation was 10 cm of diameter and covered the left side of the thyroid.
INTRODUCTION: 40 to 50% of elderly with hip fracture present delirium. The morbimortality increase in patients whose presented delirium. OBJECTIVE: To study the use of citicoline (CDP choline) in the prevention of delirium in elderly under hip fracture surgery. PATIENTS AND METHODS: A randomized control trial. The patients with hip fracture without dementia or an other organic brain illness. The medication were administered 24 hours before and during 4 days after surgery. The doses was 1.2 g/day. The primary outcome measure was percentage of patients with delirium measured with Abbreviated Mental Test (AMT) and Confusion Assessment Method (CAM). The Mini Mental State (MMS) was used before and 4 days after surgery. All treatment comparation was considered statistically significant at p< 0.05 calculating chi square and Wilcoxon test. RESULTS: The sample size was 81 patients (46 placebo and 35 citicoline). The mean age was 79.45 for tested group and 79.97 for placebo. There was no statistically significant difference between groups with respect to ASA class of anesthesia. The incidence of delirium was 17.39% in placebo and 11.76% in citicoline group (p= 0.6). CAM and AMT at 1, 2, 3, 4 days post surgery was not significant in placebo and citicoline group (p= 0.8 and p= 0.34). CONCLUSION: In the present study the citicoline did not prevent or reduce the incidence of delirium in hip fracture surgery in elderly.
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Amiodarone is one of the most common anti-arrhythmic drugs used in the Emergency Department. Recent guidelines on cardiac arrest with shockable rhythm [refractory ventricular fibrillation (VF)/pulseless ventricular tachycardia (VT)] recommend amiodarone as anti-arrhythmic of first choice. Amiodarone is also first choice drug in the treatment of various ventricular and supra-ventricular tachyarrhythmias. This paper deals with the main therapeutical indications of amiodarone in emergency medicine: dosage, side effects, contraindications and pharmacological interactions are reviewed. Amiodarone is effective for control of hemodynamically stable VT, polymorphic VT and wide-complex tachycardia of uncertain origin. It is also helpful for ventricular rate control of rapid atrial arrhythmias in patients with severely impaired left ventricular (LV) function, when digitalis has been ineffective, and is an adjunct to electrical cardioversion. The major side effects of amiodarone are hypotension, bradycardia and peripheral phlebitis. Major contraindications to the intravenous (i.v.) injection of amiodarone are bradycardia, senoatrial block, severe disturbs of conduction, second or third degree atrio-ventricular blocks. Other contraindications are hypotension, severe respiratory failure, hepatocellular failure and hyperthyroidism. Pharmacological interactions are reported with HMG-CoA reductase inhibitors, class I antiarrhythmic agents and other drugs which contribute to prolong QT interval, digoxin, oral anticoagulants and general anaesthesia.
In this study we have evaluated the ability of interferons (IFNs) alpha, beta, gamma and Tumor Necrosis Factor (TNF) alpha to modulate the expression of the Major Histocompatibility Complex (MHC) antigens in human osteosarcoma cells. The osteosarcoma cell lines Saos-2 and U-2 OS, treated in vitro with IFNs and TNF alpha, showed an increased expression of class I HLA antigens. However, only IFN gamma and, to a lower extent, IFN beta induced the expression of class II HLA antigens. These effects were dose and time-dependent. Simultaneous treatment with IFN gamma and IFN beta or TNF alpha, which by itself was unable to induce the expression of class II HLA antigens, produced different effects on the two osteosarcoma cell lines: in Saos-2 IFN beta and TNF alpha amplified the effects obtained with IFN gamma alone; in U-2 OS, TNF alpha increased the expression induced by IFN gamma on class II HLA antigens, whereas IFN beta antagonized the effects of IFN gamma. IFN alpha did not influence the induction of class II HLA antigens by IFN gamma in the two osteosarcoma cell lines. IFNs have been introduced in some clinical protocols for the treatment of osteosarcoma, based on their antiproliferative activity. Our findings may contribute to a better knowledge of the effects of IFNs and TNF alpha in osteosarcoma by showing the existence of more complex interactions.
Sweet's syndrome (acute febrile neutrophilic dermatosis) is a disease characterized by the abrupt onset of red, tender, cutaneous plaques on the face, extremities and upper trunk accompanied by fever, arthralgia or arthritis and neutrophilic leukocytosis. Histologically, there are distinctive, dense, dermal infiltrates of neutrophils. This case report describes a case of Sweet's syndrome characterized by rheumatic onset, microhematuria and subcutaneous nodular lesions on the legs resembling erythema nodosum. The etiopathogenesis and relationship between Sweet's syndrome and infectious and non infectious diseases is discussed. The overlap between this peculiar syndrome and some aspects of inflammatory rheumatic diseases, namely seronegative spondyloarthritides, is suggested.
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