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Results for “VACATIONS”

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At least 73 records · Page 4Linked to original sources
PubMed1999

[Cutaneous myiasis--a vacation souvenir].

Cutaneous myiasis is a temporary infestation of the skin with fly larvae. Travelling to subtropical areas accounts for a higher risk and increasing incidence in Europeans. In Middle- and South American myiasis is mainly caused by the botfly (Dermatobia hominis). Blood-suckling arthropods, usually mosquitoes, transmit the larvae of the botfly via phoresis, a unique mechanism of egg deposition. In Africa cutaneous myiasis is mostly due to the tumbu fly (Cordylobia anthropophaga). Infection with the tumbu fly larvae occurs after direct contact with the eggs that are often deposited in clothes and towels. Clinically an abscess-like lesion develops. Creeping sensations of movement under the skin are occasionally described. Following hatching, spontaneous healing can normally be expected, although extraction of the larvae is recommended to prevent abscess formation and superinfection.

Adult↗
PubMed2005

Annoying vacation souvenir: Fish tapeworm (Diphyllobothrium sp.) infestation in an Austrian fisherman.

Diphyllobothriosis is infestation with the fish tapeworm. Although the worldwide incidence has decreased in recent decades, increased travel and the new popularity of dishes involving raw fish (e.g. sushi) may provide a higher risk of infestation in formerly low-risk areas. We report an Austrian fisherman who passed a 75 cm tapeworm segment in his stool. Infestation presumably occurred 14 months earlier during a fishing tour in Alaska. At presentation, the patient was asymptomatic, reported no weight loss and showed neither anaemia nor eosinophilia. He was cured with a single dose of 10 mg/kg body weight praziquantel.

Alaska↗
PubMed2003

Sprouting of mossy fibers and the vacating of postsynaptic targets in the inner molecular layer of the dentate gyrus.

Aberrant mossy fiber sprouting, which presumably results from hilar mossy cell death after status epilepticus (SE), is a frequently studied feature of temporal lobe epilepsy. Although mossy fiber sprouting can be suppressed by the protein synthesis inhibitor cycloheximide, spontaneous seizures remain unaltered. We have investigated the mechanisms underlying the ability of cycloheximide to block SE-induced mossy fiber sprouting in the inner molecular layer of dentate gyrus (IML). Pilocarpine-induced SE in the presence of cycloheximide resulted in a reduced number of injured hilar cells compared to rats not pretreated with cycloheximide. Presumed mossy cells, identified by calcitonin gene related peptide (CGRP) immunohistochemistry, were not significantly reduced in either group 60 days after SE. Whereas controls had a strong band of CGRP-positive fibers (putative mossy cell axons) and no neo-Timm stained fibers in the IML, pilocarpine-treated rats had no CGRP fibers and strong neo-Timm staining. Cycloheximide-pilocarpine-treated animals, in contrast, had CGRP and neo-Timm staining similar to controls. Cycloheximide might protect hilar CGRP-positive cells during SE and, by allowing those cells to retain their normal axonal projection, prevent mossy fiber sprouting. The recently suggested "irritable" mossy cell hypothesis relies on the survival of mossy cells for network hyperexcitability. We hypothesized that CGRP may be a marker for a subpopulation of relatively resistant mossy cells in rats, which, if they survive injury, may become irritable and contribute to hyperexcitability. We suggest that cycloheximide prevents SE-induced mossy fiber sprouting by preventing the loss of hilar CGRP-positive cells (putative mossy cells).

Animals↗
PubMedDate not supplied

A summer vacation.

Explore the source record for details and available documents.

Education, Nursing, Continuing↗
PubMed2007

Our FABulous VACation: a decade of phosphatidylinositol 3,5-bisphosphate.

PtdIns(3,5)P2 was discovered about a decade ago and much of the machinery that makes, degrades and senses it has been uncovered. Despite this, we still lack a complete understanding of how the pieces fit together but some patterns are beginning to emerge. Molecular functions for PtdIns(3,5)P2 are also elusive, but the identification of effectors offers a way into some of these processes. An examination of the defects associated with loss of synthesis of PtdIns(3,5)P2 in lower and higher eukaryotes begins to suggest a unifying theme; this lipid regulates membrane retrieval via retrograde trafficking from distal compartments to organelles that are more proximal in the endocytic/lysosomal system. Another unifying theme is stress signalling to organelles, possibly both to change their morphology in response to external insults and to maintain the lumenal pH or membrane potential of organelles. The next few years seem likely to uncover details of the molecular mechanisms underlying the biology of this fascinating lipid. This review also highlights some areas where further research is needed.

Animals↗