Pendulum Exercises After Hip Arthroscopy: A Video Technique.

Advanced hip joint-preserving arthroscopic techniques have been shown to improve patient-reported functional outcomes with low rates of postoperative complications. Prior work has shown that formation of adhesive scar is a potential source of persistent pain and cause for revision surgery. As resources for postoperative in-studio physical therapy become scarce, a home-based strategy to avoid scar formation without adding formal therapy cost may be beneficial.

Efficacy and Safety of OM-85 in Patients with Chronic Bronchitis and/or Chronic Obstructive Pulmonary Disease.

Background: Recurrent acute exacerbations are generally associated with accelerated decline of lung function and characterized by reduced physical activity and worsening of clinical status in patients with chronic obstructive pulmonary disease (COPD). Effective practices and therapies aimed at preventing acute exacerbations are continuously under investigation by healthcare providers. This double-blind, placebo-control, randomized clinical trial sought to evaluate the preventive effect of a bacterial lysate (OM-85) on acute exacerbations in patients with COPD or chronic bronchitis in China.

Influenza-associated Hospitalizations and Deaths, Costa Rica, 2009-2012.

Data needed to guide influenza vaccine policies are lacking in tropical countries. We multiplied the number of severe acute respiratory infections by the proportion testing positive for influenza. There were ≈6,699 influenza hospitalizations and 803 deaths in Costa Rica during 2009-2012, supporting continuation of a national influenza vaccine program.

Identification of VHY/Dusp15 as a regulator of oligodendrocyte differentiation through a systematic genomics approach.

Multiple sclerosis (MS) is a neuroinflammatory disease characterized by a progressive loss of myelin and a failure of oligodendrocyte (OL)-mediated remyelination, particularly in the progressive phases of the disease. An improved understanding of the signaling mechanisms that control differentiation of OL precursors may lead to the identification of new therapeutic targets for remyelination in MS. About 100 mammalian Protein Tyrosine Phosphatases (PTPs) are known, many of which are involved in signaling both in health and disease.

Factors affecting phenological patterns of bombacaceous trees in seasonal forests in Costa Rica and Mexico.

We compared phenological patterns of tree species of the family Bombacaceae in three seasonal forests in Mexico and Costa Rica whose dry seasons vary in duration and intensity. The objectives were to (1) determine intraspecific variation in phenology between sites in different geographic locations with different precipitation regimes, (2) compare interspecific phenological patterns within sites during one year, and (3) document seasonal pollinator use of floral resources at one site in relation to the flowering phenology of these species. To determine the sequence of phenological events in trees of the family Bombacaceae across three study sites, phenology of marked individuals was recorded every 2 wk from September 2000 through August 2001 for six species.

Are beta-sheet breaker peptides dissolving the therapeutic problem of Alzheimer's disease?

Alzheimer's disease (AD) is a neurodegenerative disorder for which there is no cure or effective treatment. One of the major neuropathological signatures of AD is the deposition of amyloid plaques in the brain of affected people. Although the role of these structures in the pathogenesis of the disease is not fully understood, recent findings have provided evidence that amyloid may be a key player in the disease.

Changes in the glycosylation pattern of prion protein in murine scrapie. Implications for the mechanism of neurodegeneration in prion diseases.

In prion diseases, the normal prion protein (PrP(c)) undergoes a conformational change that results in the abnormal form, named scrapie prion protein (PrP(sc)). The visual system of rodents provides a relatively simple neuronal model in which the cell bodies of neurons are confined to the retina and the axons constitute the optic nerve. We investigated by Western blot the profile of PrP(c) in the optic nerve and retina of normal hamsters and mice.

Cyclic amplification of protein misfolding: application to prion-related disorders and beyond.

Diverse human disorders, including the majority of neurodegenerative diseases, are thought to arise from the misfolding and aggregation of protein. We have recently described a novel technology to amplify cyclically misfolded proteins in vitro. This procedure, named protein misfolding cyclic amplification (PMCA), is conceptually analogous to DNA amplification by PCR and has tremendous implications for research and diagnosis.

Reduction of amyloid load and cerebral damage in a transgenic mouse model of Alzheimer's disease by treatment with a beta-sheet breaker peptide.

Genetic, neuropathological, and biochemical studies have provided strong evidence for a central role of amyloid in the pathogenesis of Alzheimer's disease (AD). We have proposed previously that peptides designed as beta-sheet breakers may be useful in preventing the formation of amyloid plaques. In this study, we describe a modified beta-sheet breaker peptide with improved pharmacological properties, a high rate of penetration across the blood-brain barrier, and the ability to induce a dramatic reduction in amyloid deposition in two different transgenic AD models.

Biochemical and structural studies of the prion protein polymorphism.

A hallmark event in transmissible spongiform encephalopathies is the conversion of the physiological prion protein into the disease-associated isoform. A natural polymorphism at codon 129 of the human prion gene, resulting in either methionine or valine, has profound influence on susceptibility and phenotypic expression of the disease in humans. In this study, we investigated the local propensity of synthetic peptides, corresponding to the region of the polymorphism and containing either methionine or valine, to adopt a beta-sheet-rich structure similar to the pathological protein.

Infected splenic dendritic cells are sufficient for prion transmission to the CNS in mouse scrapie.

Transmissible spongiform encephalopathies display long incubation periods at the beginning of which the titer of infectious agents (prions) increases in peripheral lymphoid organs. This "replication" leads to a progressive invasion of the CNS. Follicular dendritic cells appear to support prion replication in lymphoid follicles.

Sensitive detection of pathological prion protein by cyclic amplification of protein misfolding.

Prions are the infectious agents responsible for transmissible spongiform encephalopathies. The principal component of prions is the glycoprotein PrP(Sc), which is a conformationally modified isoform of a normal cell-surface protein called PrP(C) (ref. 1).

Prions: disease propagation and disease therapy by conformational transmission.

Transmissible spongiform encephalopathies - also known as prion-related diseases - are a group of fatal neurodegenerative disorders associated with the misfolding of prion protein. Several unprecedented scientific findings, which have directly confronted popular dogmas in biology, have put prion research in the spotlight. The experimental evidence supports an entirely novel disease mechanism, involving disease transmission by replication of protein conformation.

Inhibiting the conversion of soluble amyloid-beta peptide into abnormally folded amyloidogenic intermediates: relevance for Alzheimer's disease therapy.

Alzheimer's disease is a degenerative disorder of the brain for which there is no cure or effective treatment. Recent studies suggest that cerebral amyloid plaques are central to the disease process. However, it is not clear which of the species going from the normal soluble amyloid-beta peptide to the mature amyloid plaque is the toxic agent in the brain.

Reversion of prion protein conformational changes by synthetic beta-sheet breaker peptides.

Background: Transmissible spongiform encephalopathies are associated with a structural transition in the prion protein that results in the conversion of the physiological PrPc to pathological PrP(Sc). We investigated whether this conformational transition can be inhibited and reversed by peptides homologous to the PrP fragments implicated in the abnormal folding, which contain specific residues acting as beta-sheet blockers (beta-sheet breaker peptides).

Methods: We studied the effect of a 13-residue beta-sheet breaker peptide (iPrP13) on the reversion of the abnormal structure and properties of PrP(Sc) purified from the brains of mice with experimental scrapie and from human beings affected by sporadic and variant Creutzfeldt-Jakob disease.

Cell-lysate conversion of prion protein into its protease-resistant isoform suggests the participation of a cellular chaperone.

A conformational transition between the normal cellular prion protein (PrPC) and the beta-sheet-rich pathological isoform (PrPSc) is a central event in the pathogenesis of spongiform encephalopathies. The prion infectious agent seems to contain mainly, if not exclusively, PrPSc, which has the ability to propagate its abnormal conformation by transforming the host PrPC into the pathological isoform. We have developed an in vitro system to induce the PrPC --> PrPSc conversion by incubating a cell-lysate containing mouse PrPC with partially purified mouse PrPSc.

[Simultaneous repair of type IV rectovaginal fistula (cloaca) and "ectopic anus" deformity. Presentation of a case and review of the literature].

A 40-year-old woman presented with a 7-year-old type IV rectovaginal fistula (cloaca) and an associated "ectopic anus" deformity. The initial step of the operation was the creation of two v-shaped full-thickness skin flaps. Subsequently, a longitudinal repair was performed.