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Search Results: 1 - 10 of 804263 matches for " M.D.;Corrêa-Giannella "
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Mutation and genomic amplification of the PIK3CA proto-oncogene in pituitary adenomas
Murat, C.B.;Braga, P.B.S.;Fortes, M.A.H.Z.;Bronstein, M.D.;Corrêa-Giannella, M.L.C.;Giorgi, R.R.;
Brazilian Journal of Medical and Biological Research , 2012, DOI: 10.1590/S0100-879X2012007500115
Abstract: the tumorigenesis of pituitary adenomas is poorly understood. mutations of the pik3ca proto-oncogene, which encodes the p110-α catalytic subunit of pi3k, have been reported in various types of human cancers regarding the role of the gene in cell proliferation and survival through activation of the pi3k/akt signaling pathway. only one chinese study described somatic mutations and amplification of the pik3ca gene in a large series of pituitary adenomas. the aim of the present study was to determine genetic alterations of pik3ca in a second series that consisted of 33 pituitary adenomas of different subtypes diagnosed by immunohistochemistry: 6 adrenocorticotropic hormone-secreting microadenomas, 5 growth hormone-secreting macroadenomas, 7 prolactin-secreting macroadenomas, and 15 nonfunctioning macroadenomas. direct sequencing of exons 9 and 20 assessed by qpcr was employed to investigate the presence of mutations and genomic amplification defined as a copy number ≥4. previously identified pik3ca mutations (exon 20) were detected in four cases (12.1%). interestingly, the chinese study reported mutations only in invasive tumors, while we found a pik3ca mutation in one noninvasive corticotroph microadenoma. pik3ca amplification was observed in 21.2% (7/33) of the cases. this study demonstrates the presence of somatic mutations and amplifications of the pik3ca gene in a second series of pituitary adenomas, corroborating the previously described involvement of the pi3k/akt signaling pathway in the tumorigenic process of this gland.
Body weight, metabolism and clock genes
Melissa M Zanquetta, Maria Corrêa-Giannella, Maria Monteiro, Sandra MF Villares
Diabetology & Metabolic Syndrome , 2010, DOI: 10.1186/1758-5996-2-53
Abstract: The prevalence of obesity is growing rapidly, affecting all ages and social classes, despite all scientific efforts to clarify its causes. Excess body weight has become one of the biggest health issues today, and is principally due to increased food availability, high caloric diets and sedentary lifestyles. Recent studies have shown the importance of new discoveries regarding the intracellular mechanisms which can trigger obesity and other metabolic disturbances.Some studies have suggested that altered patterns of sleep/wake cycle and feeding behavior were associated to 24-hour lifestyles and changes in body weight although the mechanisms by which daily rhythms are transformed into increased adiposity remain unclear [1,2].Circadian rhythms are biological events that constantly repeat in a 24-hour period and are generated by an endogenous mechanism. This endogenous mechanism is composed of circadian clocks, including the central clock (located in the suprachiasmatic nucleus- SCN) and peripheral clocks (located in all other cells of the organism), and is defined as the intrinsic molecular mechanisms that allow the organism to adapt to changes in its environment [3]. The clocks are synchronized or adjusted to coincide with periodical environmental events such as the day/night cycle. A well-synchronized clock guarantees that all physiological and behavioral rhythms take place in a coordinated manner over the 24-hour period [4].Many researchers are investigating the function of the circadian clocks in circadian physiology regulation. Hence, the knowledge regarding the role of peripheral circadian clocks in glucose and lipids metabolism is starting to emerge. The adipocyte has an important role in endocrine system regulations, energy homeostasis, satiety signaling and in cell differentiation and proliferation. The circadian clock of the adipose cell is also probably involved in the control of many of these functions. It is reasonable to deduce that alterations in the peri
Pancreatic islet transplantation
Maria Corrêa-Giannella, Alexandre S Raposo do Amaral
Diabetology & Metabolic Syndrome , 2009, DOI: 10.1186/1758-5996-1-9
Abstract: Human islet transplantation should be regarded as an intervention that can decrease the frequency of severe hypoglycemic episodes and improve glycemic control in selected patient for whom benefits of 4-5 years duration would be very valuable. Its limitations, however, indicate that the procedure in its current format is not suitable for all patients with type 1 diabetes.Chronic complications related to Type 1 Diabetes are closely associated to the onset and maintenance of hyperglycemia, as demonstrated by the Diabetes Control and Complication Trial (DCCT) [1] and its follow-up study (EDIC) [2]. No formulation of exogenous insulin available to date has yet been able to mimic the physiological nictemeral rhythms of this hormone. Despite all engineering advancements, the theoretical proposal of developing a mechanical replacement for pancreatic β cell, which should carry a glucose sensor attached to an insulin pump capable of performing real time interpretation of glucose variations, as well as allied and sustained automatic corrections with feedback, still has not been reached.To date, the replacement of β cells through pancreas and pancreatic islet transplantation are the only concrete alternatives for re-establishing the endogenous insulin secretion in type 1 diabetic patients. Both procedures have as a barrier the major initial obstacle to all transplants: organ scarcity [3]. The vast majority of pancreas and pancreatic islet transplantation is performed with deceased-donor organs: brain death or, more recently, following cardiac arrest [4]. The search for new sources of cells for implants, by differentiation of embryonic or somatic cells is still hindered by ethical and technical problems. Improvements in organ preservation techniques, surgical transplantation techniques, immunosuppression, rejection diagnosis and management of post-procedure complications have led to considerable progress in the overall survival of grafts and patients [5].Despite the promotion of
A predisposi??o genética para o desenvolvimento da microangiopatia no DM1
Corrêa-Giannella, Maria Lúcia;Vieira, Suzana Maria;
Arquivos Brasileiros de Endocrinologia & Metabologia , 2008, DOI: 10.1590/S0004-27302008000200026
Abstract: glycemic control and diabetes duration are believed to be the most important risk factors for the development of diabetic microangiopathy; however, the rate of progression of nephropathy, retinopathy and polyneuropathy varies considerably among patients. besides the presence of risk factors such as hypertension, dyslipidaemia and smoking, there is evidence suggesting that genetic predisposition plays a role in the susceptibility to microvascular complications. based on underlying pathogenesis, polymorphisms of several candidate genes belonging to multiple pathways have been investigated, like the genes related to mechanisms of hyperglycaemia-induced damage (such as advanced glycation end-products and reactive oxygen species increased formation, augmented activity of the aldose reductase pathway); genes related to the renin-angiotensin system; genes coding for cytokines, growth factors and its receptors, glucose transporter; among many others. this article reviews some studies that corroborate the importance of the genetic background in the development of diabetic microangiopathy.
Association of genetic variants in the promoter region of genes encoding p22phox (CYBA) and glutamate cysteine ligase catalytic subunit (GCLC) and renal disease in patients with type 1 diabetes mellitus
Suzana M Vieira, Maria B Monteiro, Tatiana Marques, Ana M Luna, Maria A Fortes, Márcia Nery, Márcia Queiroz, Sérgio A Dib, Márcio F Vendramini, Mirela J Azevedo, Luis H Canani, Maria C Parisi, Elizabeth J Pavin, Daniel Giannella-Neto, Maria L Corrêa-Giannella
BMC Medical Genetics , 2011, DOI: 10.1186/1471-2350-12-129
Abstract: 401 patients were sorted into two groups according to the presence (n = 104) or absence (n = 196) of overt diabetic nephropathy or according to glomerular filtration rate (GFR) estimated by Modification of Diet in Renal Disease (MDRD) equation: ≥ 60 mL (n = 265) or < 60 mL/min/1.73 m2 (n = 136) and were genotyped.No differences were found in the frequency of genotypes between diabetic and non-diabetic subjects. The frequency of GFR < 60 mL/min was significantly lower in the group of patients carrying CYBA genotypes T/A+A/A (18.7%) than in the group carrying the T/T genotype (35.3%) (P = 0.0143) and the frequency of GFR < 60 mL/min was significantly higher in the group of patients carrying GCLC genotypes C/T+T/T (47.1%) than in the group carrying the C/C genotype (31.1%) (p = 0.0082). Logistic regression analysis identified the presence of at least one A allele of the CYBA SNP as an independent protection factor against decreased GFR (OR = 0.38, CI95% 0.14-0.88, p = 0.0354) and the presence of at least one T allele of the GCLC rs17883901 SNP as an independent risk factor for decreased GFR (OR = 2.40, CI95% 1.27-4.56, p = 0.0068).The functional SNPs CYBA -675 T → A and GCLC rs17883901, probably associated with cellular redox imbalances, modulate the risk for renal disease in the studied population of type 1 diabetes patients and require validation in additional cohorts.Diabetic nephropathy (DN) represents one of the leading causes of end-stage renal disease. Unlike diabetic retinopathy, with up to 80% incidence in diabetes patients with more than 20 years' diagnoses [1], DN affects approximately one third of type 1 diabetes patients during their lifetime, at times irrespective of the glycemic control [2]. These findings taken together with results of familial studies [3], point to the existence of genetic susceptibility to the renal lesions caused by chronic hyperglycemia.Oxidative stress is currently recognized as a major pathogenic factor of cellular damage caused b
Fibronectin glycation increases IGF-I induced proliferation of human aortic smooth muscle cells
Maria Corrêa-Giannella, Maria Regina de Azevedo, Derek LeRoith, Daniel Giannella-Neto
Diabetology & Metabolic Syndrome , 2012, DOI: 10.1186/1758-5996-4-19
Abstract: Both type I and type II diabetes are powerful and independent risk factors for coronary artery disease, stroke, and peripheral arterial disease [1,2]. Prolonged exposure to hyperglycemia is recognized as the primary casual factor in the pathogenesis of diabetic complications [3,4]. Hyperglycemia induces a large number of alterations in vascular tissue that potentially promote accelerated atherosclerosis. Glycation of proteins is an important biochemical mechanism by which glucose mediates tissue damage, leading to the generation of advanced glycation endproducts (AGEs) and modifying the structure and function of several proteins, such as those which comprise extracellular matrixes [5]. It has been demonstrated that AGE formation alters some functional properties of collagen [6], vitronectin [7], laminin [8], and fibronectin (FN) [9], affecting their self-assembly and their binding to each other. AGEs can also induce synthesis and secretion of cytokines and growth factors after binding to AGE receptors (RAGE) in different cell types [7]. Monocytes exposed to AGE-modified matrix release tumor necrosis factor-α (TNF-α) [10], platelet-derived growth factor (PDGF) [11] and insulin-like growth factor-I (IGF-I) [12]. In vascular smooth muscle cells (SMC) AGE-RAGE interaction has been shown to activate cell signalling pathways linked to expression of inflammatory and prothrombotic genes, such as ERK1/ERK2 kinases and NF-kB [13].The SMC, which constitute the medial layer of arteries, are normally in a differentiated contractile phenotype, but during the development of atherosclerotic lesions, a subpopulation of SMC is converted to a synthetic phenotype that is able to migrate and proliferate. Extracellular matrix proteins actively participate in this process, affecting SMC phenotype and modulating the cellular response to growth-regulatory molecules [14]. FN, which is found in increased amounts in early atherosclerotic plaques [15,16], can interact with cell surface receptor
Apoptosis rate and transcriptional response of pancreatic islets exposed to the PPAR gamma agonist Pioglitazone
Rodrigo N Lamounier, Cassio N Coimbra, Peter White, Flavia L Costal, Leonardo S Oliveira, Daniel Giannella-Neto, Klaus H Kaestner, Maria Lúcia Corrêa-Giannella
Diabetology & Metabolic Syndrome , 2013, DOI: 10.1186/1758-5996-5-1
Abstract:
Association of C - Reactive Protein and Body Mass Index with Duration of Mechanical Ventilation in
M. Safavi, M.D,A. Honarmand, M.D
Journal of Mazandaran University of Medical Sciences , 2007,
Abstract: Background and purpose: The aim of this study was to determine the incidence and presence of a relationship between predictors of body mass index (BMI) or C-reactive protein (CRP) and duration of mechanical ventilation, in trauma patients who were admitted to the intensive care unite (ICU). Furthermore, we compared their prognostic significance, with known indicators such as, the Sequential Organ Failure Assessment (SOFA) score.Materials and Methods: This prospective observational study was preformed on 72 admitted critically ill trauma patients in a general ICU setting, in Alzahra Medical Center of Isfahan University. Patients were categorized by duration of mechanical ventilation to the group A (≤ 7 days) and group B (> 7 days). The severity of illness was assessed by the Revised Trauma Score (RTS) calculated on the first admission to the ICU unit. The biological status of the patients was assessed by the serial measurement of CRP on admission to ICU (T1), at 48, 72 hours subsequently, and on the beginning day (T2) or discontinuation (T3) from mechanical ventilation. Data on BMI, serum albumin, and the SOFA score, were also collected on T2 and T3.Results: There was no significant difference between two groups in demographic characteristic or RTS. On T3, the SOFA score, BMI, albumin, and CRP were significantly higher within group B patients, as compared with group A (P < 0.01). The incidence of low BMI (≤ 20 kg/m2) or high CRP (> 10 mg/L) on T2 was 72.2% (52/72) and 81.9% (59/72) respectively. The incidences of low BMI or high CRP in group B patients were significantly higher on T2 or T3, as compared with group A (P < 0.05). CRP or BMI on T3 had high specificity for predicting more than seven days of MV. On T3, the SOFA score, serum albumin, CRP, and BMI provided significantly good discrimination (area under curve > 0.5) in descending order. Mean serum CRP level within 72 hours after admission to the ICU or on T3 was significantly more in group B patients, as compared with group A (P < 0.01). The most significant predictor more than seven days of mechanical ventilation was CRP followed by BMI on T3. Conclusion: Both the BMI and CRP comparables with the SOFA score can be used in estimating the risk of prolonged mechanical ventilation. It is also concluded that maintaining the level of BMI or CRP in normal range, could shorten the duration of mechanical ventilation.
A survey of Obsessive-Compulsive Disorder prevalence among High school girl students in Sari
A. Massoudzadeh, M.D.
Journal of Mazandaran University of Medical Sciences , 2007,
Abstract: Background and purpose: Obsessive-Compulsive Disorder (OCD) is a disease that appears to be under-diagnosed and under-treated despite the evidence for effective treatments. There are variable estimates of OCD prevalence (many studies reported that its prevalence is betwent 2% and 3% in general population). It is dependented to age, sex, marital status, socio-economic & educational state, in population.Materials and Methods: This method was a cross sectional descriptive study on high school girl students in Sari city. 3104 girls were selected and interviewed through randomized systematic & cluster sampling method from all high school girl students. The assessment was done by Muadsley obsession compulsive inventory & demographic inventory. After the data were analized by descriptive and qualitative methods.Results: 108 students were excluded then 2996 girls were entered in this study, 31.2% (936 individuals) had OCD and mean of their age was 16.22 ± 3.4. 30.7% of girls was first child, 35.1% of mothers & 34.7% of fathers had low educational class and low socio economic state.Conclusion: Prevalence of OCD in high school girl students was significant in sari city, and it was related to number of birth, family size, and low socio-economic and educational level.
Yellow Nail Syndrome, A Case Report
A. Soltani, M.D.,A. Arjmand, M.D.,F. Aghabarari, M.D,A. Kazemi, M.D
Journal of Mazandaran University of Medical Sciences , 2007,
Abstract: Yellow nail syndrome (YNS) is a rare disorder characterized by a triad of yellow discoloration and destructive changes of nails, lymph edema and a variety of pathologies in the respiratory system.This disorder can be associated with and herald the presence of internal diseases. An increased awareness of these conditions may help with the early diagnosis and therapy of the associated disorders.We report a 24 years old whom with yellow nail syndrome whom was admitted at hospital. She also had fever, lymph edema and pulmonary manifestations.
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