Disfunción inmunológica en enfermedad de Alzheimer; proinflamatoria en etapas iniciales y regulatoria, y exhausta en etapas avanzadas / Immune dysfunction in disease Alzheimer's; proinflammatory in stages initial and regulatory, and exhaustive in advanced stages

Alzheimer disease (AD) is the main cause of dementia worldwide and a source of important population morbidity and mortality. It is estimate that its prevalence will increase dramatically in the upcoming years. The classical clinical presentation of AD is an amnesic hippocampal syndrome, and Mild Cognitive impairment (MCI) is considered the initial stage between normal cognition and dementia. The most accepted pathogenesis establishes amyloid beta (Ab) deposition in brain parenchyma as the initial mechanism, followed by the intracellular accumulation of hyperphosphorylated tau finally leading to the loss of synapses and neurons. Recently, the study of AD pathogenesis is focusing on immune mechanisms as main actors of disease development. Microglia is the macrophagic resident cell in the central nervous system (CNS), and initiates the inflammatory response and Ab phagocytosis, interacting with other glia and recruiting diverse immune cells to the CNS. The role of the adaptive immune system, and, especially T lymphocytes' role, is still controversial. We hypothesize that the pathogenesis of AD is dynamic; with a preponderant proinflammatory activity initially, but later on, the persistent presence of Ab due to the lack of its proper elimination leads to a phenomena of lymphocyte dysfunction and immunological tolerance that have a deleterious role at advanced stages of the disease. (AU)

Clinical Evaluation of Posterior Canal Benign Paroxysmal Positional Vertigo

Background: Benign paroxysmal positional vertigo (BPPV) is a mechanical peripheral vestibular disorder which may involve any of the three semicircular canals but principally the posterior. In as much as the literature has described theories to explain the mechanism of BPPV and also contains scholarly works that elucidate BPPV; its management remains an enigma to most clinicians. To this end; this work was aimed at outlining an evidence-based best practice for most common form of BPPV. Materials and Methods: A systematic review of the literature was conducted between 1948 and June 2011 in PubMed; Embase; Ovid; and Cochrane database through the online Library of the University of Cape Town. Seventy-nine worthy articles that addressed the study were selected on consensus of the two authors. Conclusion: There is consensus for the use of canalith repositioning procedures as the best form of treatment for posterior canal canalolithiasis. However; successful treatment is dependent on accurate identification of the implicated canal and the form of lithiasis. Furthermore; clinicians should note that there is no place for pharmacological treatment of BPPV; unless it is to facilitate repositioning

Monitoring the coral disease, plague type II, on coral reefs in St. John, U.S. Virgin Islands

In July 1997, conspicuous white patches of necrotic tissue and bare skeleton began to appear on scleractinian corals in several bays around St. John, US Virgin Islands. Analysis of diseased coral tissue from five different species confirmed the presence of a Sphingomonas-like bacterium, the pathogen for plague type II. To date, 14 species of hard corals have been affected by plague type II around St. John. This disease was monitored at Haulover and Tektite Reefs at depths of 7-12 meters. The study site at Tektite Reef has > 50 cover by scleractinian corals with 90 of hard corals being composed of Montastraea annularis. Monthly surveys at Tektite Reef from December 1997 to May 2001 documented new incidence of disease (bare white patches of skeleton) every month with associated loss of living coral and 90.5 of all disease patches occurred on M. annularis. The frequency of disease within transects ranged from 3 to 58, and the area of disease patches ranged from 0.25 to 9000 cm2. The average percent cover by the disease within 1 m2 ranged from 0.01 (+/- 0.04 SD) to 1.74 (+/- 9.08 SD). Photo-monitoring of 28 diseased corals of 9 species begun in September 1997 at Haulover Reef revealed no recovery of diseased portions with all necrotic tissue being overgrown rapidly by turf algae, usually within less than one month. Most coral colonies suffered partial mortality. Very limited recruitment (e.g., of Agaricia spp., Favia spp. and sponges) has been noted on the diseased areas. This coral disease has the potential to cause more loss of live coral on St. John reefs than any other stress to date because it targets the dominant reef building species, M. annularis.