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Distribution of N-Acetylgalactosamine-Positive Perineuronal Nets in the Macaque Brain: Anatomy and Implications. - Neural plasticity
Perineuronal nets (PNNs) are extracellular molecules that form around neurons near the end of critical periods during development. They surround neuronal cell bodies and proximal dendrites. PNNs inhibit the formation of new connections and may concentrate around rapidly firing inhibitory interneurons. Previous work characterized the important role of perineuronal nets in plasticity in the visual system, amygdala, and spinal cord of rats. In this study, we use immunohistochemistry to survey the distribution of perineuronal nets in representative areas of the primate brain. We also document changes in PNN prevalence in these areas in animals of different ages. We found that PNNs are most prevalent in the cerebellar nuclei, surrounding >90% of the neurons there. They are much less prevalent in cerebral cortex, surrounding less than 10% of neurons in every area that we examined. The incidence of perineuronal nets around parvalbumin-positive neurons (putative fast-spiking interneurons) varies considerably between different areas in the brain. Our survey indicates that the presence of PNNs may not have a simple relationship with neural plasticity and may serve multiple functions in the central nervous system.
Device therapy for acute systolic heart failure and atrial fibrillation. - Cardiac electrophysiology clinics
Patients with newly diagnosed cardiomyopathy require careful assessment of cause and initiation of treatment before the decision is made to implant an internal cardiac defibrillator. In patients with medicine-refractory atrial fibrillation and cardiomyopathy, atrioventricular node ablation and implantation of a biventricular pacemaker is the therapy of choice when tachycardia-induced cardiomyopathy is suspected and curative therapy is not possible.Copyright Â© 2015 Elsevier Inc. All rights reserved.
Electrocardiographic patch devices and contemporary wireless cardiac monitoring. - Frontiers in physiology
Cardiac electrophysiologic derangements often coexist with disorders of the circulatory system. Capturing and diagnosing arrhythmias and conduction system disease may lead to a change in diagnosis, clinical management and patient outcomes. Standard 12-lead electrocardiogram (ECG), Holter monitors and event recorders have served as useful diagnostic tools over the last few decades. However, their shortcomings are only recently being addressed by emerging technologies. With advances in device miniaturization and wireless technologies, and changing consumer expectations, wearable "on-body" ECG patch devices have evolved to meet contemporary needs. These devices are unobtrusive and easy to use, leading to increased device wear time and diagnostic yield. While becoming the standard for detecting arrhythmias and conduction system disorders in the outpatient setting where continuous ECG monitoring in the short to medium term (days to weeks) is indicated, these cardiac devices and related digital mobile health technologies are reshaping the clinician-patient interface with important implications for future healthcare delivery.
N-acetylgalactosamine positive perineuronal nets in the saccade-related-part of the cerebellar fastigial nucleus do not maintain saccade gain. - PloS one
Perineuronal nets (PNNs) accumulate around neurons near the end of developmental critical periods. PNNs are structures of the extracellular matrix which surround synaptic contacts and contain chondroitin sulfate proteoglycans. Previous studies suggest that the chondroitin sulfate chains of PNNs inhibit synaptic plasticity and thereby help end critical periods. PNNs surround a high proportion of neurons in the cerebellar nuclei. These PNNs form during approximately the same time that movements achieve normal accuracy. It is possible that PNNs in the cerebellar nuclei inhibit plasticity to maintain the synaptic organization that produces those accurate movements. We tested whether or not PNNs in a saccade-related part of the cerebellar nuclei maintain accurate saccade size by digesting a part of them in an adult monkey performing a task that changes saccade size (long term saccade adaptation). We use the enzyme Chondroitinase ABC to digest the glycosaminoglycan side chains of proteoglycans present in the majority of PNNs. We show that this manipulation does not result in faster, larger, or more persistent adaptation. Our result indicates that intact perineuronal nets around saccade-related neurons in the cerebellar nuclei are not important for maintaining long-term saccade gain.
Removal of potentially confounding phenotypes from a Siamese-derived feline glaucoma breeding colony. - Comparative medicine
Feline breeding colonies face genetic constraints involving founder effects. A Siamese-founded colony used to study primary congenital glaucoma displayed coat colors additional to the Siamese coat. Genes affecting pigment can exhibit pleiotropy on ocular development and function. To remove potentially confounding phenotypes from our colony, we documented the source and frequency of the Siamese allele at the gene for tyrosinase (TYR), the dilution allele at melanophilin (MLPH), and the brown allele at tyrosinase-related protein 1 (TYRP1). We used PCR-RFLP diagnostics to genotype cats in our colony for the published alleles. A commercially acquired phenotypically normal tom was the source of the dilute allele. A founding Siamese queen was the source of the brown allele. Founders also were blood-typed and screened for disease-associated alleles segregating in Siamese cats at 3 loci (ASB, GLB1, and CEP290). Siamese founders were normal at all loci except ASB, at which both animals carried the hypomorpic allele. Current stock is being managed to limit production of glaucomatous cats with brown, dilute, or Siamese phenotypes or homozygosity for the ASB hypomorphic allele. Genotyping will aid in the elimination of these alleles. The clinical effect of these phenotypes and alleles on the glaucoma phenotype is uncertain, but their elimination will remove potentially confounding effects. In conclusion, when founding a colony, stock should be selected or screened to limit potentially confounding phenotypes. When studying the immune, nervous, and visual systems, screening stock for alleles known to be associated with coat color may be warranted.Copyright 2011 by the American Association for Laboratory Animal Science
Presynaptic calcium channels and Î±3-integrins are complexed with synaptic cleft laminins, cytoskeletal elements and active zone components. - Journal of neurochemistry
At chemical synapses, synaptic cleft components interact with elements of the nerve terminal membrane to promote differentiation and regulate function. Laminins containing the Î²2 subunit are key cleft components, and they act in part by binding the pore-forming subunit of a pre-synaptic voltage-gated calcium channel (Ca(v)Î±) (Nishimune et al. 2004). In this study, we identify Ca(v)Î±-associated intracellular proteins that may couple channel-anchoring to assembly or stabilization of neurotransmitter release sites called active zones. Using Ca(v)Î±-antibodies, we isolated a protein complex from Torpedo electric organ synapses, which resemble neuromuscular junctions but are easier to isolate in bulk. We identified 10 components of the complex: six cytoskeletal proteins (Î±2/Î²2 spectrins, plectin 1, AHNAK/desmoyokin, dystrophin, and myosin 1), two active zone components (bassoon and piccolo), synaptic laminin, and a calcium channel Î² subunit. Immunocytochemistry confirmed these proteins in electric organ synapses, and PCR analysis revealed their expression by developing mammalian motor neurons. Finally, we show that synaptic laminins also interact with pre-synaptic integrins containing the Î±3 subunit. Together with our previous finding that a distinct synaptic laminin interacts with SV2 on nerve terminals (Son et al. 2000), our results identify three paths by which synaptic cleft laminins can send developmentally important signals to nerve terminals.Â© 2010 The Authors. Journal of Neurochemistry Â© 2010 International Society for Neurochemistry.
Hyperadherence of an hha mutant of Escherichia coli O157:H7 is correlated with enhanced expression of LEE-encoded adherence genes. - FEMS microbiology letters
Enterohemorrhagic Escherichia coli (EHEC) O157:H7 virulence factors, specifically those conferring intimate adherence to and formation of attaching and effacing lesions (A/E) on host cells, are encoded by a horizontally acquired locus of enterocyte effacement (LEE). Expression of several LEE-encoded genes, which are organized into operons LEE1 through LEE5, is under the positive regulation of ler, the first gene in the LEE1 operon. We have recently demonstrated that EHEC O157:H7 lacking hha exhibited greater than a 10-fold increase in ler expression and that the repression of ler results from the binding of Hha to the ler promoter. In this report, we show that an hha mutant of EHEC O157:H7 exhibited increased adherence to Hep-2 cells, had increased transcriptional activities of LEE1, LEE2, LEE3, and LEE5 as determined by reverse transcriptase-polymerase chain reaction assays, and expressed LEE5::lac transcriptional fusion at levels that were several-fold higher than that expressed by the parental hha+ strain. These results demonstrate that hha is an important regulatory component of the cascade that governs the expression of LEE operons and the resulting ability of EHEC O157:H7 to intimately adhere to host cells.
Effects of microcin 24-producing Escherichia coli on shedding and multiple-antimicrobial resistance of Salmonella enterica serotype typhimurium in pigs. - American journal of veterinary research
To investigate the effect of an Escherichia that produced microcin 24 (Mcc24) on shedding of of Salmonella enterica serotypeTyphimurium in swine and evaluate evidence of in vivo activation of the Mcc24-mediated, multiple-antibiotic resistance (mar) operon.36 crossbred weaned pigs.24 pigs were allocated to 2 groups (12 pigs/group). Pigs in 1 group received daily oral administration of an Mcc24-producing E coli, whereas the other group received a non-Mcc24-producing E coli. All pigs were challenge exposed with Salmonella Typhimurium chi4232. A third group of 6 pigs received Mcc24-producing E coli and was challenge exposed with an Mcc24-sensitive, marA-deleted strain of Salmonella Typhimurium 4232. After challenge exposure, fecal samples from all pigs were cultured to detect shedding of Salmonella Typhimurium and Salmonella Typhimurium isolates were screened for resistance to ciprofloxacin. Fecal samples were collected throughout the study, and tissue samples were collected during necropsy.Differences in shedding of Salmonella Typhimurium were not detected between groups receiving Mcc24-producing or non-Mcc24-producing E coli. No significant differences were found in quantitative analysis between groups receiving Mcc24-producing and non-Mcc24-producing E coli. Evidence of mar activation was not detected.Microcin-producing E coli did not exert an effect on shedding of SalmonellaTyphimurium or mar activation in pigs. It may be difficult or impractical to create the conditions required for Mcc24 to be an effective part of a food safety intervention to reduce shedding of Salmonella Typhimurium.
A synaptic laminin-calcium channel interaction organizes active zones in motor nerve terminals. - Nature
Synapse formation requires the differentiation of a functional nerve terminal opposite a specialized postsynaptic membrane. Here, we show that laminin beta2, a component of the synaptic cleft at the neuromuscular junction, binds directly to calcium channels that are required for neurotransmitter release from motor nerve terminals. This interaction leads to clustering of channels, which in turn recruit other presynaptic components. Perturbation of this interaction in vivo results in disassembly of neurotransmitter release sites, resembling defects previously observed in an autoimmune neuromuscular disorder, Lambert-Eaton myasthenic syndrome. These results identify an extracellular ligand of the voltage-gated calcium channel as well as a new laminin receptor. They also suggest a model for the development of nerve terminals, and provide clues to the pathogenesis of a synaptic disease.
Serum lactoferrin concentrations in colostrum-fed calves. - American journal of veterinary research
To determine serum lactoferrin concentrations (SLFC) in neonatal calves before and after ingestion of colostrum and to develop models that predict SLFC as a function of colostral lactoferrin concentrations (CLFC) in calves.13 Holstein calves.Calves were fed 4 L of colostrum via oroesophageal feeder within 3 hours after birth. Serum samples were collected before ingestion of colostrum (day 0) and 2, 4, 6, and 7 days after birth. Colostrum and serum IgG concentrations were measured by use of radial immunodiffusion. The CLFC and SLFC were determined by use of an ELISA.Mean +/- SD SLFC on days 0, 2, 4, 6, and 7 were 2.5+/-1.6 (range 0.47 to 71), 6.0+/-3.0 (range 2.0 to 16.6), 12.0+/-12.4 (range 0.0 to 43.5), 171+/-13.6 (range 2.2 to 39.4), and 13.6+/-16.4 (range 0.0 to 43.8) mg/ml, respectively. The SLFC on days 6 and 7 differed significantly from SLFC on day 0. The model that best estimated SLFC on day 6 predicted that (SLFC)2 was a function of the logarithm of relative efficiency of passive transfer (REPT) and ([CLFC]2 x [REPT]2), where R2 = 0.4. The model for SLFC on day 7 predicted that (SLFC)2 was a function of log(REPT), where R2 = 0.44.Definitive evidence for passive transfer of lactoferrin via colostrum is lacking, because SLFC on day 2 or 4 were not significantly different than day 0. Relative efficiency of lactoferrin absorption was directly related to SLFC on day 6 but inversely related to SLFC on day 7.
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