Avaliação eletrofisiológica e histopatológica do músculo estriado esquelético em cães naturalmente acometidos pela leishmaniose visceral

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Reconstruction of molecular networks involved in citokine-induced myotubes atrophy integrating microRNA and mRNA expression

Pós-graduação em Ciências Biológicas (Genética) - IBB

Progressive recovery of a tropical deforested stream community after a flash flood

AIM: In this study, we evaluated and compared community attributes from a tropical deforested stream, located in a pasture area, in a period before (PRED I) and three times after (POSD I, II, and III) a flash flood, in order to investigate the existence of temporal modifications in community structure that suggests return to conditions previous to the flash flood. METHODS: Biota samples included algae, macrophytes, macroinvertebrates, and fish assemblages. Changes in stream physical structure we also evaluated. Similarity of the aquatic biota between pre and post-disturbance periods was examined by exploratory ordination, known as Non-Metric Multidimensional Scaling associated with Cluster Analysis, using quantitative and presence/absence Bray-Curtis similarity coefficients. Presence and absence data were used for multivariate correlation analysis (Relate Analysis) in order to investigate taxonomic composition similarity of biota between pre and post-disturbance periods. RESULTS: Our results evidenced channel simplification and an expressive decrease in richness and abundance of all taxa right after the flood, followed by subsequent increases of these parameters in the next three samples, indicating trends towards stream community recovery. Bray-Curtis similarity coefficients evidenced a greater community structure disparity among the period right after the flood and the subsequent ones. Multivariate correlation analysis evidenced a greater correlation between macroinvertebrates and algae/macrophytes, demonstrating the narrow relation between their recolonization dynamics. CONCLUSIONS: Despite overall community structure tended to return to previous conditions, recolonization after the flood was much slower than that reported in literature. Finally, the remarkably high flood impact along with the slow recolonization could be a result of the historical presence of anthropic impacts in the region, such as siltation, riparian forest complete depletion, and habitat simplification, which magnified the effects of a natural disturbance.

Recurrent genomic alterations in sequential progressive leukoplakia and oral cancer: drivers of oral tumorigenesis?

A significant proportion (up to 62) of oral squamous cell carcinomas (OSCCs) may arise from oral potential malignant lesions (OPMLs), such as leukoplakia. Patient outcomes may thus be improved through detection of lesions at a risk for malignant transformation, by identifying and categorizing genetic changes in sequential, progressive OPMLs. We conducted array comparative genomic hybridization analysis of 25 sequential, progressive OPMLs and same-site OSCCs from five patients. Recurrent DNA copy number gains were identified on 1p in 20/25 cases (80) with minimal, high-level amplification regions on 1p35 and 1p36. Other regions of gains were frequently observed: 11q13.4 (68), 9q34.13 (64), 21q22.3 (60), 6p21 and 6q25 (56) and 10q24, 19q13.2, 22q12, 5q31.2, 7p13, 10q24 and 14q22 (48). DNA losses were observed in 20 of samples and mainly detected on 5q31.2 (35), 16p13.2 (30), 9q33.1 and 9q33.29 (25) and 17q11.2, 3p26.2, 18q21.1, 4q34.1 and 8p23.2 (20). Such copy number alterations (CNAs) were mapped in all grades of dysplasia that progressed, and their corresponding OSCCs, in 70 of patients, indicating that these CNAs may be associated with disease progression. Amplified genes mapping within recurrent CNAs (KHDRBS1, PARP1, RAB1A, HBEGF, PAIP2, BTBD7) were selected for validation, by quantitative real-time PCR, in an independent set of 32 progressive leukoplakia, 32 OSSCs and 21 non-progressive leukoplakia samples. Amplification of BTBD7, KHDRBS1, PARP1 and RAB1A was exclusively detected in progressive leukoplakia and corresponding OSCC. BTBD7, KHDRBS1, PARP1 and RAB1A may be associated with OSCC progression. Proteinprotein interaction networks were created to identify possible pathways associated with OSCC progression.

Dysregulation of Anti-Inflammatory Annexin A1 Expression in Progressive Crohns Disease

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

A phylogenetic analysis of Pseudopaludicola (Anura) providing evidence of progressive chromosome reduction

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Low-intensity resistance training attenuates dexamethasone-induced atrophy in the flexor hallucis longus muscle

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Aerobic Exercise Training Prevents Heart Failure-Induced Skeletal Muscle Atrophy by Anti-Catabolic, but Not Anabolic Actions

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Using Threads to Overcome Synchronization Delays in Parallel Multiple Progressive Alignment Algorithms

Sao Paulo State Research Foundation-FAPESP

Effects of lithium on the proliferation and migration of neuroblasts in the rostral migratory stream in adult mice

The discovery of neurogenesis in adult brains opened the possibility of cellular therapy strategies for the treatment of neurodegenerative diseases, such as Alzheimer’s disease. Neurogenesis in the adult brain occurs in two areas: subgranular zone of the hippocampus and subventricular zone (SVZ) of the lateral ventricles. Neurons that originate from the SVZ migrate to the olfactory bulb (OB) through the rostral migratory stream (RMS). In Alzheimer’s disease, there is a progressive neuronal dysfunction and degeneration, resulting in brain atrophy and cognitive impairments including olfactory dysfunction. Several studies have demonstrated that pharmacological treatment with lithium exerts positive effects on adult neurogenesis, and one pathway seems to be the modulation of factors that regulate the migration of neuroblasts. The objective of this study was to investigate whether treatment with lithium promotes the increase of migratory neuroblasts using as parameter the RMS. Adult male C57BL/6 mice were divided into control and lithium-treated groups. The animals were treated for 6 weeks and, at four different time points, i.e., 10 days, 7 days, 3 days and 1 day before the end of treatments, they received an injection of BrdU (cell proliferation marker). The animals were sacrificed by perfusion fixation and the brains were immunohistochemically labeled for BrdU for analysis of migrating neuroblasts in the RMS. The results showed that the number of BrdU+ cells in the RMS was not significantly different between the two groups, suggesting that lithium, alone, is not capable of increasing the number of neuroblasts migrating from the SVZ to the OB

Growth hormone influences atrophy pathways in skeletal muscle of heart failure rats

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Myosin heavy chain expression and atrophy in rat skeletal muscle during transition from cardiac hypertrophy to heart failure

The purpose of this investigation was to determine whether changes in myosin heavy chain (MHC) expression and atrophy in rat skeletal muscle are observed during transition from cardiac hypertrophy to chronic heart failure (CHF) induced by aortic stenosis (AS). AS and control animals were studied 12 and 18 weeks after surgery and when overt CHF had developed in AS animals, 28 weeks after the surgery. The following parameters were studied in the soleus muscle: muscle atrophy index (soleus weight/body weight), muscle fibre diameter and frequency and MHC expression. AS animals presented decreases in both MHC1 and type I fibres and increases in both MHC2a and type IIa fibres during late cardiac hypertrophy and CHF. Type IIa fibre atrophy occurred during CHF. In conclusion, our data demonstrate that skeletal muscle phenotype changes occur in both late cardiac hypertrophy and heart failure; this suggests that attention should be given to the fact that skeletal muscle phenotype changes occur prior to overt heart failure symptoms.

Diabetes triggers the loss of tooth structure associated to radiographical and histological dental changes and its evolution to progressive pulp and periapical lesions in rats

The aim of this study was to evaluate the putative influence of diabetes without metabolic control in the loss of tooth structure as well as histological changes in dentin and pulp tissue in rats. Diabetes was induced in Wistar rats (n=25) by intravenous administration of alloxan (42mg/kg). Diabetic and non-diabetic control rats were evaluated at 1, 3, 6, 9 and 12 months of follow-up. In order to evaluate the presence and progression of dental caries and periapical lesions, hemimandibles were removed and submitted to radiographical, histological, and morphometrical procedures. Dental caries were detected after radiographical and histological evaluations in diabetic group from the third month of diabetes onset, increasing gradually in frequency and severity in periods. Diabetic rats dental pulps also presented significant reduction in volume density of collagen fibers and fibroblasts at third month, parallel with a trend towards the increase in inflammatory cells volume density. Diabetic rats presented a generalized pulp tissue necrosis after 6 months of diabetes induction. Moreover, periapical lesions were not detected in control group, while these lesions were observed in all rats after 3, 6, 9, and 12 months of diabetes induction. Uncontrolled diabetes seems to trigger the loss of tooth structure, associated to histological dental changes and mediates its evolution to progressive severe pulp and periapical lesions in rats. Therefore, diabetes may be considered a very important risk factor regarding alterations in dental pulp, development of dental caries, and periapical lesions.

Aging voice and the laryngeal muscle atrophy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Cimetidine-induced Leydig cell apoptosis and reduced EG-VEGF (PK-1) immunoexpression in rats: evidence for the testicular vasculature atrophy

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)