Fiebre chikungunya en México: caso confirmado y apuntes para la respuesta epidemiológica / Chikungunya fever in Mexico: confirmed case and notes on the epidemiologic response

La fiebre chikungunya (CHIK) es una enfermedad viral transmitida al ser humano por el mismo vector del dengue, el mosquito Aedes. Además de fiebre y fuertes dolores articulares, produce otros síntomas como mialgias, cefalea, náuseas, cansancio y exantema. No tiene tratamiento específico; el manejo terapéutico de los pacientes se enfoca en el alivio de los síntomas. Históricamente se han reportado brotes de grandes proporciones; incluso desde 2010 se llegó a considerar como una potencial epidemia emergente. En 2013 se introdujo a las islas del Caribe y recientemente se ha reportado en el continente americano. En este trabajo se describe el primer caso confirmado de chikungunya en México, en el municipio de Tlajomulco de Zúñiga, Jalisco, en mayo de 2014, importado de la isla Antigua y Barbuda, en el Caribe, por una mujer de 39 años de edad.

Chikungunya fever (CHIK) is a viral disease transmitted to human beings by the same vector as dengue -the Aedes mosquito. Besides fever and severe pain in the joints, it produces other symptoms such as myalgias, headache, nausea, fatigue and exanthema. There is no specific treatment for it; the therapeutic management of patients focuses on symptom relief. Historically, outbreaks of large proportions have been reported; even since 2010 it was considered to be a potential emerging epidemic. In 2013 it was introduced into the islands of the Caribbean, and it has recently been reported in the American continent. This paper describes the first confirmed case of chikungunya in Mexico -in the municipality of Tlajomulco de Zúñiga, Jalisco, in May, 2014-, which was imported from the Caribbean island of Antigua and Barbuda by a 39 year-old woman.

Effect of eccentric training on mitochondrial function and oxidative stress in the skeletal muscle of rats

The objective of the present study was to investigate the effects of eccentric training on the activity of mitochondrial respiratory chain enzymes, oxidative stress, muscle damage, and inflammation of skeletal muscle. Eighteen male mice (CF1) weighing 30-35 g were randomly divided into 3 groups (N = 6): untrained, trained eccentric running (16°; TER), and trained running (0°) (TR), and were submitted to an 8-week training program. TER increased muscle oxidative capacity (succinate dehydrogenase and complexes I and II) in a manner similar to TR, and TER did not decrease oxidative damage (xylenol and creatine phosphate) but increased antioxidant enzyme activity (superoxide dismutase and catalase) similar to TR. Muscle damage (creatine kinase) and inflammation (myeloperoxidase) were not reduced by TER. In conclusion, we suggest that TER improves mitochondrial function but does not reduce oxidative stress, muscle damage, or inflammation induced by eccentric contractions.

Ginseng administration protects skeletal muscle from oxidative stress induced by acute exercise in rats

Enzymatic activity was analyzed in the soleus, gastrocnemius (red and white) and plantaris muscles of acutely exercised rats after long-term administration of Panax ginseng extract in order to evaluate the protective role of ginseng against skeletal muscle oxidation. Ginseng extract (3, 10, 100, or 500 mg/kg) was administered orally for three months to male Wistar rats weighing 200 ± 50 g before exercise and to non-exercised rats (N = 8/group). The results showed a membrane stabilizing capacity of the extract since mitochondrial function measured on the basis of citrate synthase and 3-hydroxyacyl-CoA dehydrogenase activities was reduced, on average, by 20 percent (P < 0.05) after exercise but the activities remained unchanged in animals treated with a ginseng dose of 100 mg/kg. Glutathione status did not show significant changes after exercise or treatment. Lipid peroxidation, measured on the basis of malondialdehyde levels, was significantly higher in all muscles after exercise, and again was reduced by about 74 percent (P < 0.05) by the use of ginseng extract. The administration of ginseng extract was able to protect muscle from exercise-induced oxidative stress irrespective of fiber type.

Intramitochondrial calcium and magnesium levels in skeletal muscle submitted to total or partial limb ischemia

Sekeletal muscle temperature and mitochondrial content of Ca2 and Mg2+ were measured after 3 h of total or partial limb ischemia in male Wistar rats (250-350g). The decreases in biceps muscle temperature, measured with a needle thermistor (4.4 ñ 0.26-C (31 rats) in partial ischemia (PI, aorta clamp) and total ischemia (TI, hind leg tourniquet), respectively) were consistent with the expected extente of blood flow reduction for the two ischemic conditions. Mitochondrial calcium levels increased after partial ischemia from 2.67 ñ 0.13 (46 rats) to 4.65 ñ 0.38 (12 rats) nmol/mg protein and increased to 7.87 ñ 0.68 (14 rats) after total ischemia (P<0.05). In contrast, mitochondrial magnesium decreased after partial ischemia from 10.14 ñ 0.35 to 8.22 ñ0.28 (13 rats) but increased in the mitochondria of muscle submitted to total ischemia to 12.0 ñ 0.80 (14 rats; P < 0.05). No changes were observed in the number of binding sites for safranine which competes for calcium binding sites on the inner mitochondrial membrane (25.46 ñ 0.38 nmol/mg protein for sham (20 rats) and 25 ñ 0.68 (7 rats) for PI and 25 ñ 0.31 (5 rats) for TI). The data suggest that the greater resistance of rats muscle to total than to partial ischemia may be due at least in part to the increased mitochondrial Mg2+ content

Mitochondrial myopathy and myoclonic epilepsy

Os autores descrevem uma família de raça negra (mäe e três filhos) com miopatia mitocondrial. Duas irmäs tinham acidose láctica concomitante e epilepsia mioclônica. Outros achados observados nos membros mais afetados foram demência, ataxia, fraqueza muscular e neuropatia sensitiva. A mäe era assintomática. Um filho sofreu acidente vascular cerebral isquêmico envolvendo a regiäo temporal direita. Todos os membros da família estudados eram hipertensos. EEG mostrou resposta fotomioclônica na paciente probanda. Biópsia muscular mostrou fibers e mitocôndrias anormais ao estudo de microscopia eletrônica. Análise bioquímica mostrou um defeito no citocromo C oxidase nas mitocôndrias extraídas do músculo esquelético de uma paciente afetada. Aspectos clínicos e genéticos sobre as encefalomiopatias mitocondriais säo discutidos

Encefalopatia mitocondrial / Mitochondrial encephapathy

Os autores relatam o caso de um paciente de 13 anos com sinais de comprometimento do sistema extrapiramidal e da musculatura estriada. O exame histopatológico muscular com histoquímica (DHS) e a microscopia eletrônica comprovaram a existência de alteraçöes mitocondrias quantitativas e qualitativas

Neuromiopatias / Neuromyopathies

O trabalho visa dar a experiência do autor após 20 anos de funcionamento do ambulatório de miopatias que seria melhor denominado de ambulatório de moléstias da unidade motora. Após mostrarem a atual classificaçäo que usa com 13 itens e 95 afecçöes, o autor refere apenas aquilo no qual tem experiência e sobre o que exista ou näo concordância com a literatura. É chamada atençäo sobretudo para o valor da eletromiografia e da biópsia muscular, exames estes que isoladamente pouco concorrem para o diagnóstico. Näo existe intençäo de descrever o quadro clínico das várias afecçöes mas, apenas colaborar com sua experiência para que especialistas em neurologia possam aproveitar de dados práticos verificados em cerca de 2000 pacientes

Muscular training through localized in vivo electrical stimulations.

In vivo electrical stimulations were applied to the gastrocnemius muscles of intact frogs for prolonged periods which lead to improved muscular efficiency and delayed onset of fatigue. The muscular strength improvement was correlated to increased tissue contractile proteins and decreased collagen content. Elevated levels of muscular fuels, mitochondrial content, oxidative metabolism in the stimulated muscles were suggested to be responsible for the delayed onset of fatigue. In view in these characteristics regarding the improvement at physical and metabolic levels, the muscles exposed to chronic electrical stimulations were termed as trained muscles. The applicability of electrical stimulations to induce the training effects into the muscles in atrophic and dystrophic conditions to avert the muscle wastings was suggested.