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Lucas Long
Lucas Long

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The unembryonated eggs are passed with the stool . In the soil, the eggs develop into a 2-cell stage , an advanced cleavage stage , and then they embryonate ; eggs become infective in 15 to 30 days. After ingestion (soil-contaminated hands or food), the eggs hatch in the small intestine, and release larvae that mature and establish themselves as adults in the colon . The adult worms (approximately 4 cm in length) live in the cecum and ascending colon. The adult worms are fixed in that location, with the anterior portions threaded into the mucosa. The females begin to oviposit 60 to 70 days after infection. Female worms in the cecum shed between 3,000 and 20,000 eggs per day. The life span of the adults is about 1 year.

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Introduction: During human myogenesis and synaptogenesis, the first contact between multiaxonal nerve terminals and the primary myotube occurs at an early stage of gestation, then monoaxonal nerve terminals form and postsynaptic clusters of acetylcholine-receptor are modified and redistributed to the site of muscle-nerve contact. The aim of this study is to present the ultrastructural features of muscle and motor-junction immaturity severe enough to lead to death in the first months of life.

Material and methods: Ultrastructural-level analysis was carried out on the quadriceps femoris muscle of an infant born at full term with severe respiratory distress but with normal SMN1 and IGHMBP2 genes.

Results: Arrested muscle maturation was manifested in the presence of primary and mature myotubes, prepatterned acetylcholine-receptor clusters devoid of terminal axons, lack of synapses and multiaxonal unmyelinated intramuscular nerves.

Background: Several studies have demonstrated increased numbers of angiographically detectable collaterals after vascular endothelial growth factor (VEGF) gene transfer. However, VEGF appears to be insufficient for stimulating the growth of mature blood vessels. Therefore, we decided to reinvestigate in what way the VEGF gene transfer to rabbit ischaemic muscle can restore blood flow impaired by femoral artery excision.

Results: Human VEGF165 mRNA was detected in the ischaemic muscle injected with pSG5-VEGF165, and human VEGF protein was present in the blood plasma of the same animals but not in rabbits treated with control plasmid. However, rabbit VEGF synthesis was also enhanced in ischaemic legs of both β-gal and VEGF-treated animals. In spite of the augmented generation of endogenous VEGF, the local blood flow decreased to 7513.9 % (of flow before excision) after 28 days in pSVβgal injected animals, whereas it was preserved (97.315 %) in pSG5-VEGF165 treated rabbits (P

A sizable amount of effort is devoted to the comparative biology of aging, and in particular mapping the noteworthy differences between naked mole-rats and other similar-sized rodent species. Naked mole-rats live nearly ten times longer than mice and are near immune to cancer. It is possible that a sufficiently comprehensive understanding of why this is the case could result in therapies for humans, though I believe the odds of this coming to pass in the near future of the next couple of decades are much larger for cancer than aging. Research into calorie restriction mimetic drugs has demonstrated that safely inducing even small shifts in the operation of metabolism, even when aiming to mimic states that occur naturally and are very well studied, is very expensive and very slow work. While naked mole-rat resistance to cancer may boil down to just a couple of mechanisms, any one of which might be exploited alone, their longevity most likely has many contributing factors, and will be much harder to map and understand.

The open access papers noted here report on what are fairly standard fishing expeditions into the cellular biochemistry of the naked mole-rat, comparing it with that of the guinea pig. This sort of work takes place throughout the research community, and in many contexts. Researchers pick likely tissues and processes to examine, and then compare as much genetic, epigenetic, and proteomic data as they have the capacity to produce and process. Differences are pulled up from the depths for examination, and theories advanced based on what is presently known. Of the findings in these papers, some reinforce earlier theories on the damage resistance of specific cellular components in naked mole-rats, particularly mitochondria, while the most interesting item is the presence of raised levels of enzymes that are protective against oxidative damage. Past research has shown that older naked mole-rats appear to have all the signs of high levels of oxidative stress, but are largely unaffected by it.

Sarcopenia is the name given to loss of muscle mass and strength that occurs with age. When it comes to assembling evidence for causes of the condition, this is one of the better examples of the present state of understanding in aging. A sizable number of potential causes have convincing evidence, all may be relevant, but the degree to which they are important relative to one another is hard to discern. Further, the layering of the causative mechanisms, how they interact, and whether and to what degree some are secondary to others, is also hard to discern. The only truly reliable method of answering such questions is to fix just one contributing cause, and observe the results. The field of biotechnology is on the verge of being able to achieve that goal for sarcopenia and a number of other age-related conditions, but not quite there yet.

Among the candidates for contributing causes of sarcopenia are chronic inflammation, loss of stem cell activity, dysregulation of dietary protein processing necessary for tissue growth, decline of nerve-muscle junctions, and reduced density of capillary networks and thus a reduction in nutrient supply to tissues. There are others. The paper here looks at rising levels of oxidative stress, increased amounts of reactive oxidizing molecules generated by cells and roaming throughout tissues; these molecules cause damage that must be repaired, but more importantly trigger all sorts of cellular reactions that, collectively, don't help the situation. This is an aspect of aging that goes hand in hand with chronic inflammation, and is secondary to deeper causes that include mitochondrial dysfunction and cellular senescence. 041b061a72


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