Computing performability for wireless sensor networks

The performability of a wireless sensor network (WSN) can be measured using a range of metrics, including reliability (REL) and expected hop count (EHC). EHC assumes each link has a delay value of 1 and devices have no delay or vice versa, which is not necessarily appropriate for WSNs. This paper generalizes the EHC metric into an expected message delay (EMD) that permits arbitrary delay values for both links and devices. Further, it proposes a method based on Augmented Ordered Multivariate Decision Diagram (OMDD-A) that can be used to compute REL, EHC and EMD for WSN with both device and link failures. Simulation results on various networks show the benefits of the OMDD-A approach

Blunted angiogenesis and hypertrophy are associated with increased fatigue resistance and unchanged aerobic capacity in old overloaded mouse muscle.

We hypothesize that the attenuated hypertrophic response in old mouse muscle is (1) partly due to a reduced capillarization and angiogenesis, which is (2) accompanied by a reduced oxidative capacity and fatigue resistance in old control and overloaded muscles, that (3) can be rescued by the antioxidant resveratrol. To investigate this, the hypertrophic response, capillarization, oxidative capacity, and fatigue resistance of m. plantaris were compared in 9- and 25-month-old non-treated and 25-month-old resveratrol-treated mice. Overload increased the local capillary-to-fiber ratio less in old (15 %) than in adult (59 %) muscle (P < 0.05). Although muscles of old mice had a higher succinate dehydrogenase (SDH) activity (P < 0.05) and a slower fiber type profile (P < 0.05), the isometric fatigue resistance was similar in 9- and 25-month-old mice. In both age groups, the fatigue resistance was increased to the same extent after overload (P < 0.01), without a significant change in SDH activity, but an increased capillary density (P < 0.05). Attenuated angiogenesis during overload may contribute to the attenuated hypertrophic response in old age. Neither was rescued by resveratrol supplementation. Changes in fatigue resistance with overload and aging were dissociated from changes in SDH activity, but paralleled those in capillarization. This suggests that capillarization plays a more important role in fatigue resistance than oxidative capacity

Improved skeletal muscle oxidative enzyme activity and restoration of PGC-1α and PPARß/δ gene expression upon rosiglitazone treatment in obese patients with type 2 diabetes mellitus

Objective: To examine whether rosiglitazone alters gene expression of some key genes involved in mitochondrial biogenesis and oxidative capacity in skeletal muscle of type 2 diabetic patients, and whether this is associated with alterations in skeletal muscle oxidative capacity and lipid content.Design: Skeletal muscle gene expression, mitochondrial protein content, oxidative capacity and lipid accumulation were measured in muscle biopsies obtained from diabetic patients, before and after 8 weeks of rosiglitazone treatment, and matched controls. Furthermore, whole-body insulin sensitivity and substrate utilization were assessed.Subjects: Ten obese type 2 diabetic patients and 10 obese normoglycemic controls matched for age and BMI.Methods: Gene expression and mitochondrial protein content of complexes I&ndash;V of the respiratory chain were measured by quantitative polymerase chain reaction and Western blotting, respectively. Histochemical staining was used to quantify lipid accumulation and complex II succinate dehydrogenase (SDH) activity. Insulin sensitivity and substrate utilization were measured during a hyperinsulinemic&ndash;euglycemic clamp with indirect calorimetry.Results: Skeletal-muscle mRNA of PGC-1a and PPARb/d &ndash; but not of other genes involved in glucose, fat and oxidative metabolism &ndash; was significantly lower in diabetic patients (Po0.01). Rosiglitazone significantly increased PGC-1a (B2.2-fold, Po0.01) and PPARb/d (B2.6-fold, Po0.01), in parallel with an increase in insulin sensitivity, SDH activity and metabolic flexibility (Po0.01). Surprisingly, none of the measured mitochondrial proteins was reduced in type 2 diabetic patients, nor affected by rosiglitazone treatment. No alterations were seen in muscular fat accumulation upon treatment. Conclusion: These results suggest that the insulin-sensitizing effect of rosiglitazone may involve an effect on muscular oxidative capacity, via PGC-1a and PPARb/d, independent of mitochondrial protein content and/or changes in intramyocellular lipid.<br /

Age-related change in duration of afterhyperpolarization of human motoneurones

Motor unit (MU) potentials were recorded from brachial biceps of healthy subjects aged 5.5–79 years. The subjects were subdivided into young (5.5–19 year) and adult (37.5–79 year) groups, between which single MU discharge characteristics were compared. Firing rates were in the ranges of 8.3–21.7 s−1 (mean 12.87 s−1) and 5.9–18.7 s−1 (mean 11.08 s−1) for young and adult groups, respectively. Standard deviations (s.d.) of interspike intervals (ISIs) were in the range 4.84–11.57 ms (mean 8.39 ms) for the young group and 4.26–12.23 ms (mean 7.76 ms) for the adult group. Both differences were statistically significant (P < 0.001). Special attention was paid to the previously developed method of ISI variability analysis, which enabled the comparison of MUs with respect to afterhyperpolarization (AHP) duration of their motoneurones (MNs). The results show that AHP duration increases gradually with increasing age, which is in line with the transformation of muscle properties towards a slower phenotype. This transformation seems to be a continuous process, covering the entire lifespan of a human being, from childhood to senescence. The results presented here are significant for their insight into the ageing process of the neuromuscular system. The age-related change in AHP duration has not been investigated previously in human studies and has been met with ambiguous results in animal studies

Eletroestimulação muscular: alternativa de tratamento coadjuvante para pacientes com doença arterial obstrutiva periférica Muscle electrostimulation: alternative adjuvant treatment to patients with peripheral arterial obstructive disease

A doença arterial periférica faz parte de um grupo de patologias vasculares que evolui de forma lenta e progressiva. A proposta deste artigo foi avaliar, por meio de revisão bibliográfica, os possíveis benefícios da eletroestimulação crônica como tratamento coadjuvante para pacientes arteriopatas. De acordo com a literatura analisada, concluímos que a eletroestimulação é capaz de provocar alterações importantes no perfil metabólico das fibras musculares, convertendo-as do tipo II para o tipo I, o que induz o crescimento capilar, a densidade capilar e o suprimento de oxigênio. Desta forma, este recurso terapêutico aumenta a capacidade aeróbica oxidativa e a resistência à fadiga dos músculos isquêmicos. Assim, a eletroestimulação é mais um recurso terapêutico capaz de melhorar a habilidade para caminhar destes pacientes, diminuindo gastos com cirurgias de revascularização e complicações maiores.<br>Peripheral arterial disease is included in a group of vascular diseases whose evolution is slow and progressive. This article aimed at performing a literature review to evaluate the benefits of chronic electrostimulation as adjuvant treatment for arteriopathic patients. Based on the literature, we concluded that electrostimulation can generate important changes in the metabolic profile of muscle fibers, switching them from type II to type I, which leads to capillary increase, capillary density and suppression of oxygen. Therefore, this therapeutic resource increases aerobic oxidative capacity and ischemic muscle resistance to fatigue. Thus, electrostimulation is another therapeutic option able to improve these patients' walking ability, reducing expenses related to revascularization surgeries and major complications