250 research outputs found

    Variability between credit units dedicated to dental and clinical sciences in dental schools across the USA

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    PurposeThe Commission of Dental Accreditation (CODA) does not set minimum standards for clock hours of training in Dental and Clinical sciences. The purpose of this evaluation was to compare United States (US) dental schools for variability in clock hours. The current paper utilizes the American Dental Association’s survey of clock hours of all US dental schools which is publicly available data. Clock hours survey from 2010 to 2011 was utilized and the analysis tool, JMP, was utilized to visualize and report variability.PerspectiveThe current paper highlights the large variation in clock hours of training among core clinical subjects in accredited dental schools around the United States. For example, teaching Physical Evaluations; Oral and Maxillofacial; and Oral Diagnosis and Treatment Planning were 97.0; 126.6; and 74.4 h. Moreover, upper limit for hours of Operative Dentistry teaching was 1410 h and lower limit was 129 h. Various other fields of education do enforce strict requirements on educational clock hours. For instance, Massachusetts’ General Law states that both private and public schools must have 900 and 990 h in a school year for elementary and secondary schools, respectively. However, no such stipulation exists in the field of Dental Education. CODA’s mission is “to serve the oral health care needs of the public” and CODA must consider if the average dental patient would consider a dentist who attended the school delivering 1410 h of Operative Dentistry to be the same standard as a graduate of the school delivering 129 h.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/138359/1/jicd12229.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/138359/2/jicd12229_am.pd

    Quality of life among adolescents with sickle cell disease: Mediation of pain by internalizing symptoms and parenting stress

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    <p>Abstract</p> <p>Background</p> <p>This study aimed to clarify associations between pain, psychological adjustment, and family functioning with health-related quality of life (HRQOL) in a sample of adolescents with sickle cell disease (SCD) utilizing teen- and parent-report.</p> <p>Methods</p> <p>Forty-two adolescents (between the ages of 12 and 18) with SCD and their primary caregivers completed paper-and-pencil measures of pain, teen's psychological adjustment, and HRQOL. In addition, primary caregivers completed a measure of disease-related parenting stress. Medical file review established disease severity.</p> <p>Results</p> <p>Pearson correlations identified significant inverse associations of pain frequency with physical and psychosocial domains of HRQOL as rated by the teen and primary caregiver. Generally, internalizing symptoms (i.e. anxiety and depression) and disease-related parenting stress were also significantly correlated with lower HRQOL. Examination of possible mediator models via a series of regression analyses confirmed that disease-related parenting stress served as a mediator between pain frequency and physical and psychosocial HRQOL. Less consistent were findings for mediation models involving internalizing symptoms. For these, parent-rated teen depression and teen anxiety served as mediators of the association of pain frequency and HRQOL.</p> <p>Conclusion</p> <p>Results are consistent with extant literature that suggests the association of pain and HRQOL and identify concomitant pain variables of internalizing symptoms and family variables as mediators. Efforts to improve HRQOL should aim to address internalizing symptoms associated with pain as well as parenting stress in the context of SCD management.</p

    Vascular Health in American Football Players: Cardiovascular Risk Increased in Division III Players

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    Studies report that football players have high blood pressure (BP) and increased cardiovascular risk. There are over 70,000 NCAA football players and 450 Division III schools sponsor football programs, yet limited research exists on vascular health of athletes. This study aimed to compare vascular and cardiovascular health measures between football players and nonathlete controls. Twenty-three athletes and 19 nonathletes participated. Vascular health measures included flow-mediated dilation (FMD) and carotid artery intima-media thickness (IMT). Cardiovascular measures included clinic and 24 hr BP levels, body composition, VO2 max, and fasting glucose/cholesterol levels. Compared to controls, football players had a worse vascular and cardiovascular profile. Football players had thicker carotid artery IMT (0.49 ± 0.06 mm versus 0.46 ± 0.07 mm) and larger brachial artery diameter during FMD (4.3 ± 0.5 mm versus 3.7 ± 0.6 mm), but no difference in percent FMD. Systolic BP was significantly higher in football players at all measurements: resting (128.2 ± 6.4 mmHg versus 122.4 ± 6.8 mmHg), submaximal exercise (150.4 ± 18.8 mmHg versus 137.3 ± 9.5 mmHg), maximal exercise (211.3 ± 25.9 mmHg versus 191.4 ± 19.2 mmHg), and 24-hour BP (124.9 ± 6.3 mmHg versus 109.8 ± 3.7 mmHg). Football players also had higher fasting glucose (91.6 ± 6.5 mg/dL versus 86.6 ± 5.8 mg/dL), lower HDL (36.5±11.2 mg/dL versus 47.1±14.8 mg/dL), and higher body fat percentage (29.2±7.9% versus 23.2±7.0%). Division III collegiate football players remain an understudied population and may be at increased cardiovascular risk

    Reelin Secreted by GABAergic Neurons Regulates Glutamate Receptor Homeostasis

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    BACKGROUND: Reelin is a large secreted protein of the extracellular matrix that has been proposed to participate to the etiology of schizophrenia. During development, reelin is crucial for the correct cytoarchitecture of laminated brain structures and is produced by a subset of neurons named Cajal-Retzius. After birth, most of these cells degenerate and reelin expression persists in postnatal and adult brain. The phenotype of neurons that bind secreted reelin and whether the continuous secretion of reelin is required for physiological functions at postnatal stages remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Combining immunocytochemical and pharmacological approaches, we first report that two distinct patterns of reelin expression are present in cultured hippocampal neurons. We show that in hippocampal cultures, reelin is secreted by GABAergic neurons displaying an intense reelin immunoreactivity (IR). We demonstrate that secreted reelin binds to receptors of the lipoprotein family on neurons with a punctate reelin IR. Secondly, using calcium imaging techniques, we examined the physiological consequences of reelin secretion blockade. Blocking protein secretion rapidly and reversibly changes the subunit composition of N-methyl-D-aspartate glutamate receptors (NMDARs) to a predominance of NR2B-containing NMDARs. Addition of recombinant or endogenously secreted reelin rescues the effects of protein secretion blockade and reverts the fraction of NR2B-containing NMDARs to control levels. Therefore, the continuous secretion of reelin is necessary to control the subunit composition of NMDARs in hippocampal neurons. CONCLUSIONS/SIGNIFICANCE: Our data show that the heterogeneity of reelin immunoreactivity correlates with distinct functional populations: neurons synthesizing and secreting reelin and/or neurons binding reelin. Furthermore, we show that continuous reelin secretion is a strict requirement to maintain the composition of NMDARs. We propose that reelin is a trans-neuronal messenger secreted by GABAergic neurons that regulates NMDARs homeostasis in postnatal hippocampus. Defects in reelin secretion could play a major role in the development of neuropsychiatric disorders, particularly those associated with deregulation of NMDARs such as schizophrenia

    Epileptiform Activity in Alcohol Dependent Patients and Possibilities of Its Indirect Measurement

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    Background: Alcohol dependence during withdrawal and also in abstinent period in many cases is related to reduced inhibitory functions and kindling that may appear in the form of psychosensory symptoms similar to temporal lobe epilepsy frequently in conditions of normal EEG and without seizures. Because temporal lobe epileptic activity tend to spread between hemispheres, it is possible to suppose that measures reflecting interhemispheric information transfer such as electrodermal activity (EDA) might be related to the psychosensory symptoms. Methods and Findings: We have performed measurement of bilateral EDA, psychosensory symptoms (LSCL-33) and alcohol craving (ACQ) in 34 alcohol dependent patients and 32 healthy controls. The results in alcohol dependent patients show that during rest conditions the psychosensory symptoms (LSCL-33) are related to EDA transinformation (PTI) between left and right EDA records (Spearman r = 0.44, p,0.01). Conclusions: The result may present potentially useful clinical finding suggesting a possibility to indirectly assess epileptiform changes in alcohol dependent patients

    Corticosteroid suppression of lipoxin A4 and leukotriene B4from alveolar macrophages in severe asthma

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    <p>Abstract</p> <p>Background</p> <p>An imbalance in the generation of pro-inflammatory leukotrienes, and counter-regulatory lipoxins is present in severe asthma. We measured leukotriene B<sub>4 </sub>(LTB<sub>4</sub>), and lipoxin A<sub>4 </sub>(LXA<sub>4</sub>) production by alveolar macrophages (AMs) and studied the impact of corticosteroids.</p> <p>Methods</p> <p>AMs obtained by fiberoptic bronchoscopy from 14 non-asthmatics, 12 non-severe and 11 severe asthmatics were stimulated with lipopolysaccharide (LPS,10 μg/ml) with or without dexamethasone (10<sup>-6</sup>M). LTB<sub>4 </sub>and LXA<sub>4 </sub>were measured by enzyme immunoassay.</p> <p>Results</p> <p>LXA<sub>4 </sub>biosynthesis was decreased from severe asthma AMs compared to non-severe (p < 0.05) and normal subjects (p < 0.001). LXA<sub>4 </sub>induced by LPS was highest in normal subjects and lowest in severe asthmatics (p < 0.01). Basal levels of LTB<sub>4 </sub>were decreased in severe asthmatics compared to normal subjects (p < 0.05), but not to non-severe asthma. LPS-induced LTB<sub>4 </sub>was increased in severe asthma compared to non-severe asthma (p < 0.05). Dexamethasone inhibited LPS-induced LTB<sub>4 </sub>and LXA<sub>4</sub>, with lesser suppression of LTB<sub>4 </sub>in severe asthma patients (p < 0.05). There was a significant correlation between LPS-induced LXA<sub>4 </sub>and FEV<sub>1 </sub>(% predicted) (r<sub>s </sub>= 0.60; p < 0.01).</p> <p>Conclusions</p> <p>Decreased LXA<sub>4 </sub>and increased LTB<sub>4 </sub>generation plus impaired corticosteroid sensitivity of LPS-induced LTB<sub>4 </sub>but not of LXA<sub>4 </sub>support a role for AMs in establishing a pro-inflammatory balance in severe asthma.</p

    Population health diagnosis with an ecohealth approach

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    OBJECTIVE To analyze the characteristics of health diagnosis according to the ecohealth approach in rural and urban communities in Mexico.METHODS Health diagnosis were conducted in La Nopalera, from December 2007 to October 2008, and in Atlihuayan, from December 2010 to October 2011. The research was based on three principles of the ecohealth approach: transdisciplinarity, community participation, gender and equity. To collect information, a joint methodology and several techniques were used to stimulate the participation of inhabitants. The diagnostic exercise was carried out in five phases that went from collecting information to prioritization of problems.RESULTS The constitution of the transdisciplinary team, as well as the participation of the population and the principle of gender/equity were differentials between the communities. In the rural community, the active participation of inhabitants and authorities was achieved and the principles of transdisciplinarity and gender/equity were incorporated.CONCLUSIONS With all the difficulties that entails the boost in participation, the incorporation of gender/equity and transdisciplinarity in health diagnosis allowed a holistic public health approach closer to the needs of the population

    Direction-Selective Circuitry in Rat Retina Develops Independently of GABAergic, Cholinergic and Action Potential Activity

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    The ON-OFF direction selective ganglion cells (DSGCs) in the mammalian retina code image motion by responding much more strongly to movement in one direction. They do so by receiving inhibitory inputs selectively from a particular sector of processes of the overlapping starburst amacrine cells, a type of retinal interneuron. The mechanisms of establishment and regulation of this selective connection are unknown. Here, we report that in the rat retina, the morphology, physiology of the ON-OFF DSGCs and the circuitry for coding motion directions develop normally with pharmacological blockade of GABAergic, cholinergic activity and/or action potentials for over two weeks from birth. With recent results demonstrating light independent formation of the retinal DS circuitry, our results strongly suggest the formation of the circuitry, i.e., the connections between the second and third order neurons in the visual system, can be genetically programmed, although emergence of direction selectivity in the visual cortex appears to require visual experience

    The Effects of NR2 Subunit-Dependent NMDA Receptor Kinetics on Synaptic Transmission and CaMKII Activation

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    N-Methyl-d-aspartic acid (NMDA) receptors are widely expressed in the brain and are critical for many forms of synaptic plasticity. Subtypes of the NMDA receptor NR2 subunit are differentially expressed during development; in the forebrain, the NR2B receptor is dominant early in development, and later both NR2A and NR2B are expressed. In heterologous expression systems, NR2A-containing receptors open more reliably and show much faster opening and closing kinetics than do NR2B-containing receptors. However, conflicting data, showing similar open probabilities, exist for receptors expressed in neurons. Similarly, studies of synaptic plasticity have produced divergent results, with some showing that only NR2A-containing receptors can drive long-term potentiation and others showing that either subtype is capable of driving potentiation. In order to address these conflicting results as well as open questions about the number and location of functional receptors in the synapse, we constructed a Monte Carlo model of glutamate release, diffusion, and binding to NMDA receptors and of receptor opening and closing as well as a model of the activation of calcium-calmodulin kinase II, an enzyme critical for induction of synaptic plasticity, by NMDA receptor-mediated calcium influx. Our results suggest that the conflicting data concerning receptor open probabilities can be resolved, with NR2A- and NR2B-containing receptors having very different opening probabilities. They also support the conclusion that receptors containing either subtype can drive long-term potentiation. We also are able to estimate the number of functional receptors at a synapse from experimental data. Finally, in our models, the opening of NR2B-containing receptors is highly dependent on the location of the receptor relative to the site of glutamate release whereas the opening of NR2A-containing receptors is not. These results help to clarify the previous findings and suggest future experiments to address open questions concerning NMDA receptor function
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