kinematic and neurophysiological models future applications in neurorehabilitation

This paper emphasizes the importance of developing kinematic and neurophysiological methods for evaluating motor and functional recovery in the field of neurorehabilitation. From a review of the literature, it is concluded that optoelectronic motion analysis and neurophysiological techniques, such as the study of nociceptive withdrawal reflex, might constitute useful applications for future research

Clinical consequences of asbestos-related diffuse pleural thickening: A review

Asbestos-related diffuse pleural thickening (DPT), or extensive fibrosis of the visceral pleura secondary to asbestos exposure, is increasingly common due to the large number of workers previously exposed to asbestos. It may coexist with asbestos related pleural plaques but has a distinctly different pathology. The pathogenesis of this condition as distinct from pleural plaques is gradually becoming understood. Generation of reactive oxygen and nitrogen species, profibrotic cytokines and growth factors in response to asbestos is likely to play a role in the formation of a fibrinous intrapleural matrix. Benign asbestos related pleural effusions commonly antedate the development of diffuse pleural thickening. Environmental as well as occupational exposure to asbestos may also result in pleural fibrosis, particularly in geographic areas with naturally occurring asbestiform soil minerals. Pleural disorders may also occur after household exposure. High resolution computed tomography (CT) is more sensitive and specific than chest radiography for the diagnosis of diffuse pleural thickening, and several classification systems for asbestos-related disorders have been devised. Magnetic resonance imaging and fluorodeoxyglucose positron emission tomography (PET) scanning may be useful in distinguishing between DPT and malignant mesothelioma. DPT may be associated with symptoms such as dyspnoea and chest pain. It causes a restrictive defect on lung function and may rarely result in respiratory failure and death. Treatment is primarily supportive

Zoneamento para a fruticultura em Mato Grosso do Sul.

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Avaliação da qualidade física e da matéria orgânica de um argissolo vermelho derivado de arenito da fronteira Oeste do Rio Grande do Sul.

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Sensitisation of spinal cord pain processing in medication overuse headache involves supraspinal pain control.

Medication overuse could interfere with the activity of critical brain regions involved in the supraspinal control of pain signals at the trigeminal and spinal level, leading to a sensitisation phenomenon responsible for chronic pain. We hypothesised that medication-overuse headache ( MOH) patients might display abnormal processing of pain stimuli at the spinal level and defective functioning of the diffuse noxious inhibitory controls. We tested 31 MOH patients before (bWT) and after (aWT) standard inpatient withdrawal treatment, 28 episodic migraine ( EM) patients and 23 healthy control subjects. We measured the threshold, the area and the temporal summation threshold (TST) of the nociceptive withdrawal reflex before, during and after activation of the diffuse noxious inhibitory controls by means of the cold pressor test. A significantly lower TST was found in both the MOH (bWT and aWT) and the EM patients compared with the controls, and in the MOH patients bWT compared with both the MOH patients aWT and the EM patients. In the MOH bWT patients the cold pressor test induced a TST increase significantly lower than that found in the MOH aWT, EM and control groups. Abnormal spinal cord pain processing and a decrease of the antinociceptive activity of the supraspinal structures in MOH patients can be hypothesised. These abnormalities could, in part, be related to the medication overuse, given that the withdrawal treatment was related to an improvement in the neurophysiological findings

Colorectal neuroendocrine carcinomas and adenocarcinomas share oncogenic pathways. A clinico-pathologic study of 12 cases

OBJECTIVE: Neuroendocrine carcinomas (NECs) are rare neoplasms with an increasing incidence. Oncogenetic pathways of colorectal NEC are still poorly understood, and no treatment standards are available for these rare tumors. METHODS: We analyzed retrospectively the clinical records and histology of 12 patients with colorectal NEC. KRAS and BRAF mutations were investigated after the dissection of exoendocrine and neuroendocrine components. ALK alterations and EML4-ALK transcripts were detected by in-situ hybridization and determination of fusion transcripts, respectively. RESULTS: At the time of diagnosis, the mean age of the patients was 60 years (40-79) and 10 patients had synchronous metastases. A transient response occurred in two patients and one patient treated with cisplatin-etoposide or fluoropyrimidine-oxaliplatin, respectively. Tumor progression-related death occurred in 11 of 12 patients. Ten tumors contained an exocrine component, accounting for 5-70% of the tumor, and the other two contained an amphicrine component. BRAF/KRAS mutations were found in six of 10 tumors, corresponding to BRAF(V600E) (n=2) or KRAS(G12D) (n=2), KRAS(G12V) or KRAS(G13D). DNA was obtained from both exocrine and endocrine components in seven cases, and the BRAF/KRAS status was identical in all cases. Split of the ALK locus was detected in a minority of tumor cells in two of eight cases, but EML4-ALK transcripts were absent. CONCLUSION: The association of an exocrine component in all cases and the similar profile of BRAF/KRAS mutations indicate that colorectal NEC may correspond to a high-grade transformation of colorectal carcinoma. New chemotherapy regimens using targeted therapies should be assessed in these tumors

Fenretinide treatment accelerates atherosclerosis development in apoE-deficient mice in spite of beneficial metabolic effects

Background and Purpose Fenretinide, a synthetic retinoid derivative first investigated for cancer prevention and treatment, has been shown to ameliorate glucose tolerance, improve plasma lipid profile and reduce body fat mass. These effects, together with its ability to inhibit ceramide synthesis, suggest that fenretinide may have an anti-atherosclerotic action. Experimental Approach To this aim, nine-week-old apoE-knockout (EKO) female mice were fed for twelve weeks a Western diet, without (control) or with (0.1% w/w) fenretinide. As a reference, wild-type (WT) mice were treated similarly. Growth and metabolic parameters were monitored throughout the study. Atherosclerosis development was evaluated in the aorta and at the aortic sinus. Blood and lymphoid organs were further characterized with thorough cytological/histological and immunocytofluorimetric analyses. Key Results Fenretinide treatment significantly lowered body weight, glucose levels and plasma levels of total cholesterol, triglycerides, and phospholipids. In the liver, fenretinide remarkably reduced hepatic glycogenosis and steatosis driven by the Western diet. Treated spleens were abnormally enlarged, with severe follicular atrophy and massive extramedullary haematopoiesis. Severe renal hemosiderin deposition was observed in treated EKO mice. Treatment resulted in a threefold increase of total leukocytes (WT and EKO) and raised the activated/resting monocyte ratio in EKO mice. Finally, atherosclerosis development was markedly increased at the aortic arch, thoracic and abdominal aorta of fenretinide-treated mice. Conclusions and Implications We provide the first evidence that, despite beneficial metabolic effects, fenretinide treatment may enhance the development of atherosclerosis

Fenretinide treatment accelerates atherosclerosis development in apolipoprotein e-deficient mice in spite of beneficial metabolic effects

Aim. Fenretinide, a synthetic retinoid derivative first investigated for cancer prevention and treatment, has been shown to ameliorate glucose tolerance and the plasma lipid profile, and to reduce body fat mass. These effects, together with its ability to inhibit ceramide synthesis, have suggested that fenretinide may display anti-atherosclerotic effects. Methods. To this aim, 9-weeks-old apoE-knockout (EKO) female mice were fed for 12 weeks a Western diet, without (EKO-Ctrl) or with (0.1% w/w) fenretinide (EKO-Fen). As a reference, wild-type (WT) mice were likewise treated. Growth and metabolic parameters were monitored throughout the study. Atherosclerosis development was evaluated in the aorta and at the aortic sinus. Blood and lymphoid organs were further characterized with thorough cytological/histological and immunocytofluorimetric analyses. Results. Fenretinide treatment significantly lowered body weight, glucose levels and plasma levels of total cholesterol, triglycerides and phospholipids. In the liver, fenretinide remarkably reduced hepatic glycogenosis and steatosis driven by the Western diet. Treated spleens were abnormally enlarged, with severe follicular atrophy and massive extramedullary hematopoiesis. Severe renal hemosiderin deposition was observed in EKO-Fen. Treatment resulted in a threefold increase of total leukocytes (WT and EKO) and raised the activated/resting monocyte ratio in EKO-Fen. Finally, atherosclerosis development was markedly increased at the aortic arch (34.4\uc5}7.3% vs 26.1\uc5}5.8%, +32%), thoracic (14.3\uc5}4.9% vs 4.9\uc5}2.1%, +191%) and abdominal aorta (7.6\uc5}3.3% vs 3.3\uc5}1.8%,+130%) of fenretinide-treated mice. Plaque extent was further quantified at the aortic sinus and provided similar results (810.000 \u3bcm2 vs. 540.000 \u3bcm2, +50% in EKO-Fen). Plaques of treated mice were characterized by an increased collagen content and a larger necrotic core, whereas the area occupied by macrophages, foam cells and neutral lipids was comparable between EKO-Fen and EKO-Ctrl. Conclusion. We provide the first evidence that, despite beneficial metabolic effects, fenretinide treatment may prove detrimental for atherosclerosis development

Why do GPs with a special interest in headache investigate headache presentations with neuroradiology and what do they find?

The general practitioner with a special interest in headache offers an important contribution to the management of headache in primary care where the majority of presentations take place. A number of guidelines have been developed for neuroradiological investigation of headache, but their clinical utility and relevance is not known. Fourteen general practitioners with a special interest in headache recorded consecutive headache consultations over a 3-month period, whether patients were investigated with neuroradiology and if so the reason for investigation and outcome. Reason for investigation was compared to the guidelines published for the use in primary care. 895 patients were seen, of whom 270 (30.1%) were investigated. 47% of indications were outside the guidance framework used, the most common reason for investigation being reassurance. Of those investigated, 5.6% showed positive findings but only 1.9% of findings were felt to be of clinical significance. General practitioners with a special interest investigated with neuroradiology a greater level than general practitioners, but less than neurologists. However, yields of significant findings are broadly comparative across all groups. This report confirms other studies that suggest that even when there is a high level of clinical suspicion, yields of significant findings are very low