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Correctional facilities, in their mission to provide security and prevent escapes, need a well-planned, comprehensive perimeter security system. The main function of a perimeter security system is to keep inmates [...]

Background. Tactical emergency medical support (TEMS) is a rapidly growing area within the field of prehospital medicine. As TEMS has grown, multiple training programs have emerged. A review of the existing programs demonstrated a lack of competency-based education. Objective. To develop educational competencies for TEMS as a first step toward enhancing accountability. Methods. As an initial attempt to establish accepted outcome-based competencies, the National Tactical Officers Association (NTOA) convened a working group of subject matter experts. Results. This working group drafted a competency-based educational matrix consisting of 18 educational domains. Each domain included competencies for four educational target audiences (operator, medic, team commander, and medical director). The matrix was presented to the American College of Emergency Physicians (ACEP) Tactical Emergency Medicine Section members. A modified Delphi technique was utilized for the NTOA and ACEP groups, which allowed for additional expert input and consensus development. Conclusion. The resultant matrix can serve as the basic educational standard around which TEMS training organizations can design programs of study for the four target audiences. [ABSTRACT FROM AUTHOR]

Redpoll (primarily Carduelis flammea) data from the New Brunswick-Nova Scotia border region were reviewed in the context of alleged biennial periodicity of irruptions south of their breeding range. Long-term records by the authors suggested a number of departures from visitation in alternate years. Three local Christmas Bird Counts (CBCs) spanning the last 41 winters supported the less-than-regular pattern shown by individual observations. CBC redpoll data from across the Atlantic Provinces revealed annual redpoll visitations across southern New Brunswick, where the largest regional counts (adjusted for observer effort) usually occurred. Visitation to Prince Edward Island, Nova Scotia, and Newfoundland was less frequent, and patterns there were often obscured by scarcity of CBCs with both long-run coverage and redpolls. Examination of those data in relation to varying food availability suggested that irregular abundance but near-annual occurrence of redpoll visitation explains observed observations better than attempts to find periodicity in their irruptions. [ABSTRACT FROM AUTHOR]

Purpose/objectives: There is a robust body of research on which factors dental schools consider when selecting students for acceptance, but there is considerably less research regarding what factors dental applicants consider when selecting a particular program. The aim of this investigation was to better understand which factors most influenced students to matriculate at a particular dental school and how the value of these factors has changed over time., Methods: To answer this research question, an online survey was utilized to determine why students chose to attend Columbia University College of Dental Medicine (CUCDM). This survey was administered to students in the Class of 2023 and was compared to the responses of an identical survey that was administered to the Class of 2013. The response rate for the classes of 2013 and 2023 were 70.0% and 42.2%, respectively. Results from the Classes of 2013 and 2023 were analyzed using independent sample T-tests., Results: The Class of 2013 ranked academic reputation, location, and admissions into specialty programs as the three most important factors in their selection of a dental school. The Class of 2023 ranked tuition cost, perceived patient pool, and financial aid as their three most important factors., Conclusion(s): For dental schools to continue to successfully attract and enroll students, they must understand what motivates a student to matriculate in a specific dental program. One way to accomplish this is through the use of a survey., (© 2022 American Dental Education Association.)

In Caenorhabditis elegans, the cha-1 gene encodes choline acetyltransferase (ChAT), the enzyme that synthesizes the neurotransmitter acetylcholine. We have analyzed a large number of cha-1 hypomorphic mutants, most of which are missense alleles. Some homozygous cha-1 mutants have approximately normal ChAT immunoreactivity; many other alleles lead to consistent reductions in synaptic immunostaining, although the residual protein appears to be stable. Regardless of protein levels, neuromuscular function of almost all mutants is temperature-sensitive, i.e., neuromuscular function is worse at 25° than at 14°. We show that the temperature effects are not related to acetylcholine release, but specifically to alterations in acetylcholine synthesis. This is not a temperature-dependent developmental phenotype, because animals raised at 20° to young adulthood and then shifted for 2 h to either 14° or 25° had swimming and pharyngeal pumping rates similar to animals grown and assayed at either 14° or 25°, respectively. We also show that the temperature-sensitive phenotypes are not limited to missense alleles; rather, they are a property of most or all severe cha-1 hypomorphs. We suggest that our data are consistent with a model of ChAT protein physically, but not covalently, associated with synaptic vesicles; and there is a temperature-dependent equilibrium between vesicle-associated and cytoplasmic (i.e., soluble) ChAT. Presumably, in severe cha-1 hypomorphs, increasing the temperature would promote dissociation of some of the mutant ChAT protein from synaptic vesicles, thus removing the site of acetylcholine synthesis (ChAT) from the site of vesicular acetylcholine transport. This, in turn, would decrease the rate and extent of vesicle-filling, thus increasing the severity of the behavioral deficits., (© The Author(s) 2021. Published by Oxford University Press on behalf of Genetics Society of America. All rights reserved. For permissions, please email: journals.permissions@oup.com.)

Purpose of Review: Late diagnosis of glaucoma is a leading factor in vision loss associated with this disease. Screening programs seek to diagnose glaucoma at an earlier, more treatable stage. Our purpose was to review the influence of screening location and testing strategies in glaucoma screening., Recent Findings: Screening high-risk groups appears effective, although general population-based screening programs have not been cost effective. Community-based screening programs have achieved limited success due to lack of follow-up of screened patients. High-risk patients often do not present for office-based screening programs. Screening strategies that employ a single test or few tests are generally more effective compared with strategies using multiple tests, due to avoidance of false positives. Compared with currently available screening tests, frequency-doubling technology (FDT) perimetry has shown higher sensitivity and specificity. Recent evidence suggests that automated assessment of the optic nerve and retinal nerve fiber layer may be superior to FDT perimetry, but the techniques remain unproven in screening settings., Summary: Community-based screening of high-risk groups with functional testing using FDT perimetry can be effective, but newer automated structural measurements of the optic nerve and retinal nerve fiber layer may allow improved glaucoma screening sensitivity and specificity in the future.

The recycling of synaptic vesicles requires the recovery of vesicle proteins and membrane. Members of the stonin protein family (Drosophila Stoned B, mammalian stonin 2) have been shown to link the synaptic vesicle protein synaptotagmin to the endocytic machinery. Here we characterize the unc-41 gene, which encodes the stonin ortholog in the nematode Caenorhabditis elegans. Transgenic expression of Drosophila stonedB rescues unc-41 mutant phenotypes, demonstrating that UNC-41 is a bona fide member of the stonin family. In unc-41 mutants, synaptotagmin is present in axons, but is mislocalized and diffuse. In contrast, UNC-41 is localized normally in synaptotagmin mutants, demonstrating a unidirectional relationship for localization. The phenotype of snt-1 unc-41 double mutants is stronger than snt-1 mutants, suggesting that UNC-41 may have additional, synaptotagmin-independent functions. We also show that unc-41 mutants have defects in synaptic vesicle membrane endocytosis, including a ∼50% reduction of vesicles in both acetylcholine and GABA motor neurons. These endocytic defects are similar to those observed in apm-2 mutants, which lack the µ2 subunit of the AP2 adaptor complex. However, no further reduction in synaptic vesicles was observed in unc-41 apm-2 double mutants, suggesting that UNC-41 acts in the same endocytic pathway as µ2 adaptin.

This study evaluated daily cleaning with germicidal bleach wipes on wards with a high incidence of hospital-acquired Clostridium difficile infection (CDI). The intervention reduced hospital-acquired CDI incidence by 85%, from 24.2 to 3.6 cases per 10,000 patient-days, and prolonged the median time between hospital-acquired CDI cases from 8 to 80 days.

Neuroligins are postsynaptic cell adhesion proteins that bind specifically to presynaptic membrane proteins called neurexins. Mutations in human neuroligin genes are associated with autism spectrum disorders in some families. The nematode Caenorhabditis elegans has a single neuroligin gene (nlg-1), and approximately a sixth of C. elegans neurons, including some sensory neurons, interneurons and a subset of cholinergic motor neurons, express a neuroligin transcriptional reporter. Neuroligin-deficient mutants of C. elegans are viable, and they do not appear deficient in any major motor functions. However, neuroligin mutants are defective in a subset of sensory behaviors and sensory processing, and are hypersensitive to oxidative stress and mercury compounds; the behavioral deficits are strikingly similar to traits frequently associated with autism spectrum disorders. Our results suggest a possible link between genetic defects in synapse formation or function, and sensitivity to environmental factors in the development of autism spectrum disorders.

Objective: Several topical therapies have been proposed to treat acute pain from exposure to oleoresin capsaicin (OC). The purpose of this study was to determine the most beneficial topical treatment for relieving contact dermatitis pain caused by OC exposure., Methods: We performed a single-blind, randomized human experiment evaluating the effectiveness of five different regimens for the treatment of topical facial OC exposure. Forty-nine volunteer, adult law enforcement trainees were exposed to OC during a routine training exercise and were randomized to one of five treatment groups (aluminum hydroxide-magnesium hydroxide [Maalox], 2% lidocaine gel, baby shampoo, milk, or water). After initial self-decontamination with water, subjects rated their pain using a 10-cm visual analog scale (VAS) and then every 10 minutes, for a total of 60 minutes. Subjects were blinded to previous VAS recordings. A two-factor analysis of variance (ANOVA) (treatment, time) with repeated measures on one factor (time) was performed using a 1.3-cm difference as clinically significant., Results: Forty-four men and five women, with an average age of 24 years, participated in the study. There was a significant difference in pain with respect to time (p < 0.001), but no significant interaction between time and treatment (p > 0.05). There was no significant difference in pain between treatment groups (p > 0.05)., Conclusion: In this study, there was no significant difference in pain relief provided by five different treatment regimens. Time after exposure appeared to be the best predictor for decrease in pain.

Synaptotagmin 1, encoded by the snt-1 gene in Caenorhabditis elegans, is a major synaptic vesicle protein containing two Ca(2+)-binding (C2) domains. Alternative splicing gives rise to two synaptotagmin 1 isoforms, designated SNT-1A and SNT-1B, which differ in amino acid sequence in the third, fourth, and fifth beta-strands of the second C2 domain (C2B). We report here that expression of either SNT-1 isoform under control of a strong pan-neural promoter fully rescues the snt-1 null phenotype. Furthermore, C-terminal fusions of either isoform with GFP are trafficked properly to synapses and are fully functional, unlike synaptotagmin 1Colon, two colonsGFP fusions in mice. Analysis of isoform expression with genomic GFP reporter constructs revealed that the SNT-1A and-1B isoforms are differentially expressed and localized in the C. elegans nervous system. We also report molecular, behavioral, and immunocytochemical analyses of twenty snt-1 mutations. One of these mutations, md259, specifically disrupts expression of the SNT-1A isoform and has defects in a subset of synaptotagmin 1-mediated behaviors. A second mutation, md220, is an in-frame 9-bp deletion that removes a conserved tri-peptide sequence (VIL) in the second beta-strand of the C2B domain and disrupts the proper intracellular trafficking of synaptotagmin. Site-directed mutagenesis of a functional SNT-1Colon, two colonsGFP fusion protein was used to examine the potential role of the VIL sequence in synaptotagmin trafficking. Although our results suggest the VIL sequence is most likely not a specific targeting motif, the use of SNT-1Colon, two colonsGFP fusions has great potential for investigating synaptotagmin trafficking and localization.

Sodium-dependent neurotransmitter transporters participate in the clearance and/or recycling of neurotransmitters from synaptic clefts. The snf-11 gene in Caenorhabditis elegans encodes a protein of high similarity to mammalian GABA transporters (GATs). We show here that snf-11 encodes a functional GABA transporter; SNF-11-mediated GABA transport is Na+ and Cl- dependent, has an EC50 value of 168 microM, and is blocked by the GAT1 inhibitor SKF89976A. The SNF-11 protein is expressed in seven GABAergic neurons, several additional neurons in the head and retrovesicular ganglion, and three groups of muscle cells. Therefore, all GABAergic synapses are associated with either presynaptic or postsynaptic (or both) expression of SNF-11. Although a snf-11 null mutation has no obvious effects on GABAergic behaviors, it leads to resistance to inhibitors of acetylcholinesterase. In vivo, a snf-11 null mutation blocks GABA uptake in at least a subset of GABAergic cells; in a cell culture system, all GABA uptake is abolished by the snf-11 mutation. We conclude that GABA transport activity is not essential for normal GABAergic function in C. elegans and that the localization of SNF-11 is consistent with a GABA clearance function rather than recycling.

Pain measurement and relief is complex and should be a priority for prehospital providers and supervisors. The literature continues to prove that we are poor pain relievers, despite the high prevalence of pain in the out-of-hospital patient population. Lack of education and research, along with agent availability, controlled substance regulation, and many myths given credence by health care providers, hinder our ability to achieve adequate pain assessment and treatment in the prehospital setting. Protocols must be established to help guide providers through proper acknowledgment, measurement, and treatment for prehospital pain. Nonpharmacologic therapies must also be taught and reinforced as important adjuncts to pain management. Finally, formation of quality improvement pain programs that evaluate patient outcomes and provider practice patterns will help EMS systems understand the pain management process and outline areas for improvement. Only through emphasis on pain education, research, protocol and program monitoring development will the quality of pain assessment and management in the prehospital setting improve.

Over the past 25 years, pediatric emergency medicine research and literature have progressively augmented our knowledge of safe and effective pediatric pain management strategies. Yet there is still much more we need to do to understand the painful experiences of children, and to develop optimal safe ways of addressing their needs within the context of a busy pediatric emergency department (ED). In this article, the authors review the history of ED pediatric pain management and sedation, discuss special considerations in pediatric pain assessment and management, review various pharmacologic and nonpharmacologic methods of alleviating pain and anxiety, and present ideas to improve the culture of the pediatric ED, so that it can achieve the goal of becoming pain-free.

In summary adolescence is a crucial period in the chronology of health. Most lifelong health choices are decided at this stage and clinicians can help adolescents make healthy choices to ensure a safe, secure future. They also develop skills for the rest of their lives to cope with stress, take care of their bodies, and decide whom to spend time with in meaningful relationships. Preventive health for adolescence stems from the relationship the provider cultivates with the patient and the power that comes from that dynamic relationship to respond to patient needs and promote health throughout the life cycle.

Cholinergic neurotransmission depends upon the regulated release of acetylcholine. This requires the loading of acetylcholine into synaptic vesicles by the vesicular acetylcholine transporter (VAChT). Here, we identify point mutants in Caenorhabditis elegans that map to highly conserved regions of the VAChT gene of Caenorhabditis elegans (CeVAChT) (unc-17) and exhibit behavioral phenotypes consistent with a reduction in vesicular transport activity and neurosecretion. Several of these mutants express normal amounts of VAChT protein and exhibit appropriate targeting of VAChT to synaptic vesicles. By site-directed mutagenesis, we have replaced the conserved amino acid residues found in human VAChT with the mutated residue in CeVAChT and stably expressed these cDNAs in PC-12 cells. These mutants display selective defects in initial acetylcholine transport velocity (K(m)), with values ranging from 2- to 8-fold lower than that of the wild-type. One of these mutants has lost its specific interaction with vesamicol, a selective inhibitor of VAChT, and displays vesamicol-insensitive uptake of acetylcholine. The relative order of behavioral severity of the CeVAChT point mutants is identical to the order of reduced affinity of VAChT for acetylcholine in vitro. This indicates that specific structural changes in VAChT translate into specific alterations in the intrinsic parameters of transport and in the storage and synaptic release of acetylcholine in vivo.

The Caenorhabditis elegans UNC-13 protein and its mammalian homologues are important for normal neurotransmitter release. We have identified a set of transcripts from the unc-13 locus in C. elegans resulting from alternative splicing and apparent alternative promoters. These transcripts encode proteins that are identical in their C-terminal regions but that vary in their N-terminal regions. The most abundant protein form is localized to most or all synapses. We have analyzed the sequence alterations, immunostaining patterns, and behavioral phenotypes of 31 independent unc-13 alleles. Many of these mutations are transcript-specific; their phenotypes suggest that the different UNC-13 forms have different cellular functions. We have also isolated a deletion allele that is predicted to disrupt all UNC-13 protein products; animals homozygous for this null allele are able to complete embryogenesis and hatch, but they die as paralyzed first-stage larvae. Transgenic expression of the entire gene rescues the behavior of mutants fully; transgenic overexpression of one of the transcripts can partially compensate for the genetic loss of another. This finding suggests some degree of functional overlap of the different protein products.

Recent studies describe a network of signaling proteins centered around G(o)alpha and G(q)alpha that regulates neurotransmitter secretion in C. elegans by controlling the production and consumption of diacylglycerol (DAG). We sought other components of the Goalpha-G(q)alpha signaling network by screening for aldicarb-resistant mutants with phenotypes similar to egl-30 (G(q)alpha) mutants. In so doing, we identified ric-8, which encodes a novel protein named RIC-8 (synembryn). Through cDNA analysis, we show that RIC-8 is conserved in vertebrates. Through immunostaining, we show that RIC-8 is concentrated in the cytoplasm of neurons. Exogenous application of phorbol esters or loss of DGK-1 (diacylglycerol kinase) rescues ric-8 mutant phenotypes. A genetic analysis suggests that RIC-8 functions upstream of, or in conjunction with, EGL-30 (G(q)alpha).

The cha-1 gene of Caenorhabditis elegans encodes choline acetyl-transferase (the acetylcholine synthetic enzyme). The C. elegans unc-17 gene encodes a synaptic vesicle-associated acetylcholine transporter. The two genes thus define sequential biochemical steps in the metabolism of the neurotransmitter acetylcholine. Cloning, sequencing, and molecular analysis of the unc-17 region indicate that cha-1 and unc-17 transcripts share a 5' untranslated exon, and the rest of the unc-17 transcript is nested within the long first intron of cha-1. Thus, two proteins with related functions but with no sequences in common are produced as a result of alternative splicing of a common mRNA precursor. The structure of this transcription unit suggests a novel type of coordinate gene expression, and a temporal processing model is proposed for the regulation of cha-1 and unc-17 expression.

A case of a young man with an extensive total-body-surface burn complicated by wound infection is presented. One of the fungal organisms in the cutaneous burn wound had morphologically characteristic and diagnostic features by development of conidiophores ("fruiting bodies") pathognomonic of Aspergillus spp.