Search

Autologus augmentation of wound remodeling with platelet concentrate is a burgeoning field with promising results. We hypothesized that the addition of filtered platelet concentrate (fPC) to an acellular biologic graft would improve crural healing and tissue integrity in hiatal hernia repair. Sixteen healthy Yorkshire female pigs were divided into three groups: hiatus repair (HR) (n = 7), HR with biologic graft (HRM; n = 8, and HR with biologic graft and fPC (fPC; n = 9). Surgeries were performed by a single surgeon. Animals were euthanized at 8 weeks, and the distal esophagus with hiatus was harvested en-block. Tissue was graded by a histopathologist on collagen deposition, vascularization, and inflammation at the graft–hiatal interface. Tensile strength testing was performed using the Teststar IIs (MTS), coupled with a strain extensometer (Epsilon). Samples of equal dimensions were preloaded to 1 N and deformed at a constant rate of 0.2 mm/s. Statistical analysis was performed via Kruskal–Wallis one-way analysis of variance. Aspirate analysis revealed a mean platelet count of 3 million platelets/1 mL of aspirate. Animals in the fPC group had significantly increased mean chronic inflammation (3.1 ± 1.1 vs. 1.8 ± 1.6, 1.2 ± 1.2, p = 0.04) compared to HR alone and HR + biologic graft. Vascular deposition did not differ between groups (p = 0.8). A trend toward increased collagen deposition was demonstrated for the fPC group (1.4 ± 1.1 vs. 2.0 ± 0.6 in HR group and 3.0 ± 1.2 in HRM group, p = 0.06). There was a statistically significant increase in tensile strength, yield force, and Young’s modulus in the fPC group compared with HR and HR + biologic mesh (p

Multiple sclerosis (MS) is a neurodegenerative disease characterized by demyelination and inflammation. Dysregulated lipid metabolism and mitochondrial dysfunction are hypothesized to play a key role in MS. Carnitine Palmitoyl Transferase 1 (CPT1) is a rate-limiting enzyme for beta-oxidation of fatty acids in mitochondria. The therapeutic effect of pharmacological CPT1 inhibition with etomoxir was investigated in rodent models of myelin oligodendrocyte glycoprotein- and myelin basic protein-induced experimental autoimmune encephalitis (EAE). Mice receiving etomoxir showed lower clinical score compared to placebo, however this was not significant. Rats receiving etomoxir revealed significantly lower clinical score and lower body weight compared to placebo group. When comparing etomoxir with interferon-β (IFN-β), IFN-β had no significant therapeutic effects, whereas etomoxir treatment starting at day 1 and 5 significantly improved the clinical scores compared to the IFN-β and the placebo group. Immunohistochemistry and image assessments of brain sections from rats with EAE showed higher myelination intensity and decreased expression of CPT1A in etomoxir-treated rats compared to placebo group. Moreover, etomoxir mediated increased interleukin-4 production and decreased interleukin-17α production in activated T cells. In conclusion, CPT1 is a key protein in the pathogenesis of EAE and MS and a crucial therapeutic target for the treatment.

With the advent of the so-called genomic revolution and improved techniques of DNA analysis, combined with a rapidly vanishing biodiversity, the systematic community has been facing a remarkable—and often neglected—challenge for the past 50 years: to preserve genetic resources issued from research. The preservation and long-term storage of biological specimens’ derived materials (e.g., DNA extracts) and associated data are essential to ensure comparability and reproducibility in all areas of biological research. Natural history museums and herbaria around the world are now in a position to face the exciting and challenging task of preserving the genetic library of life for generations to come. However, the lack and/or poor condition of preservation of molecular vouchers generated from often fragile and rare specimens have been problems too often underestimated or unable to be addressed due to lack of funding or, more pointedly, lack of interest in preservation of these important research materials. The present article does not seek to reiterate the plea for genetic resource collections introduce by Dessauer et al. in 1984 (and more recently by Sheldon, 2001, and Savolainen and Reeves, 2004). It seeks to bring these collections, and the issues of preservation of genetic resources, to the awareness of the systematic biology community through the case study of the American Museum of Natural History new cryogenic repository, the Ambrose Monell Collection for Molecular and Microbial Research (AMCC; website: http://research.amnh.org/ amcc/).

With the advent of the “genomic revolution” and the rapid refinement of techniques of molecular biology, academic institutions, such as museums and university collections, are at the forefront of specimen analysis. However, the lack and/or poor condition of preservation of molecular voucher generated from often fragile and rare specimens is a problem rarely addressed. To remedy this problem, the AMNH launched a frozen tissue collection, the Ambrose Monell Cryocollection (AM-CC) in May 2001. The AM-CC maintains specimens below -150 o Celsius and supports ongoing genetic research across taxa, from ancient to modern samples, by insuring that all research materials are vouchered (i.e. they point back to a specimen in a curated collection), a much-needed service that the Museum extends to the entire scientific community. Scientists using the Monell Collection have access to legally collected, authoritatively identified and properly documented specimens for use in their research, complete with Museum catalog numbers to reference in their scholarly publications. Researcher are also offered the possibility of vouchering their research by depositing the DNA or tissue samples gathered for their studies