RESUMO
CLINICAL RELEVANCE: Surface alterations of dental restorations can result in increased plaque biofilm. This leads to increased risk of premature restoration failure. Smokeless tobacco, in common use by some US military personnel, represents a potential source for surface alteration. If smokeless tobacco causes an untoward effect, selection of a more resistant restorative material could increase restoration longevity, thus minimizing lost work time and costs associated with replacement of failed restorations. PURPOSE: Comparatively assess the effect of smokeless tobacco/salivary substitute mixture on altering surface roughness of amalgam, composite resin, and resin modified glass ionomer (RMGI) restorations. MATERIALS AND METHODS: Sixty cubic restorations (3 groups of 20) were fabricated using a 4 mm by 3 mm Teflon mold. One examiner assessed the restorations at time points representing zero days, one day, one week, 2 weeks, one month, and 3 months. The data obtained were collected using a surface profilometer, measured in micrometers. Data were statistically analyzed using 2-way analysis of variance (ANOVA) test. A difference was significant if P< .05. RESULTS: Confidence levels with a 95% overall rating received a clinically acceptable classification. The 2-way ANOVA test detected significant differences between baseline, one day, one week, 2 weeks, one month, and 3-month data for surface roughness (P<.05). With respect to time and restoration type, results proved statistically significant with P<.0001. All restorations were statistically significant with respect to change in surface roughness with RMGIs showing the greatest surface roughness alteration. CONCLUSION: Smokeless tobacco mixed with a salivary substitute altered restoration surface roughness over time. Resin-modified glass isonomer restorations demonstrate the greatest alteration of surface roughness, with amalgam restorations showing the least. Amalgam remains the preferential restorative material in patients who use smokeless tobacco.
Assuntos
Resinas Acrílicas/análise , Resinas Compostas/análise , Amálgama Dentário/análise , Dióxido de Silício/análise , Tabaco sem Fumaça/efeitos adversos , Humanos , MilitaresRESUMO
Numerous national reports have called for reforming laboratory courses so that all students experience the research process. In response, many course-based research experiences (CREs) have been developed and implemented. Research on the impact of these CREs suggests that student benefits can be similar to those of traditional apprentice-model research experiences. However, most assessments of CREs have been in individual courses at individual institutions or across institutions using the same CRE model. Furthermore, which structures and components of CREs result in the greatest student gains is unknown. We explored the impact of different CRE models in different contexts on student self-reported gains in understanding, skills, and professional development using the Classroom Undergraduate Research Experience (CURE) survey. Our analysis included 49 courses developed and taught at seven diverse institutions. Overall, students reported greater gains for all benefits when compared with the reported national means for the Survey of Undergraduate Research Experiences (SURE). Two aspects of these CREs were associated with greater student gains: 1) CREs that were the focus of the entire course or that more fully integrated modules within a traditional laboratory and 2) CREs that had a higher degree of student input and results that were unknown to both students and faculty.
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This review focuses on post-traumatic stress disorder (PTSD). Several sequelae of PTSD are partially attributed to glucocorticoid-induced neuronal loss in the hippocampus and amygdala. Glucocorticoids and adrenergic agents cause both immediate and late sequelae and are considered from the perspective of their actions on the expression of cytokines as well as some of their physiological and psychological effects. A shift in immune system balance from Th1 to Th2 dominance is thought to result from the actions of both molecular groups. The secretion of glucocorticoids and adrenergic agents is commonly induced by trauma or stress, and synergy between these two parallel but separate pathways can produce long- and short-term sequelae in individuals with PTSD. Potential therapies are suggested, and older therapies that involve the early effects of adrenergics or glucocorticoids are reviewed for their control of acute symptoms. These therapies may also be useful for acute flashback therapy. Timely and more precise glucocorticoid and adrenergic control is recommended for maintaining these molecular groups within acceptable homeostatic limits and thus managing immune and brain sequelae. Psychotherapy should supplement the above therapeutic measures; however, psychotherapy is not the focus of this paper. Instead, this review focuses on the probable molecular basis of PTSD. Integrating historical findings regarding glucocorticoids and adrenergic agents into current research and clinical applications returns the focus to potentially life-changing treatments. Autologous adoptive immune therapy may also offer utility. This paper reports clinical and translational research that connects and challenges separate fields of study, current and classical, in an attempt to better understand and ameliorate the effects of PTSD.
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Alzheimer's disease is a chronic neurodegenerative disorder characterized by a progressive loss of cognitive and behavioral abilities. Extracellular senile plaques and intracellular neurofibrillary tangles are hallmarks of AD. Researchers aim to analyze the molecular mechanisms underlying AD pathogenesis; however, the therapeutic options available to treat this disease are inadequate. In the past few years, several studies have reported interesting insights about the neuroprotective properties of the polyphenolic compound resveratrol (3, 5, 4'-trihydroxy-trans-stilbene) when used with in vitro and in vivo models of AD. The aim of this review is to focus on the neuroprotective and antioxidant effects of resveratrol on AD and its multiple potential mechanisms of action. In addition, because the naturally occurring forms of resveratrol have a very limited half-life in plasma, a description of potential analogs aimed at increasing the bioavailability in plasma is also discussed.
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Central oxytocin (OT) modulates many social behaviors, including female rat sexual receptivity, quantified as the copulatory stance known as lordosis. The expression of the lordosis response is modulated by OT action in the ventromedial nucleus of the hypothalamus (VMH), as demonstrated by behavioral pharmacology experiments. However, the subcellular localization of OT in this brain region has been unclear. We tested the hypothesis that ovarian hormones reorganize OT-labeled pre- or postsynaptic elements in the fiber complex lateral to the VMH by using immunoelectron microscopy. OT immunolabeling occurred in axonal boutons identified by the presence of small, clear synaptic vesicles and double labeling with the presynaptic markers synaptophysin and vesicular glutamate transporter 2. OT immunoreactivity also was observed in dendritic profiles, verified with double labeling for the dendrite-specific marker microtubule-associated protein 2. Ovarian hormones did not alter the density of axonal boutons; however, estradiol treatment reduced the density of dendritic profiles by 34%. This effect was reversed when progesterone was given subsequent to estradiol. The effect of estradiol treatment was specific to dendrites that lacked OT immunostaining; the density of OT-labeled dendritic profiles remained constant during estradiol treatment. With the estradiol-induced exit of non-OT-labeled dendritic profiles, the remaining OT-labeled dendritic profiles experienced an increase in their number of synaptic contacts. Thus, hormone treatments that mimic the 4-day rat estrous cycle provoke a chemically coded reorganization of dendrite innervation in the fiber plexus lateral to the VMH that may underlie the hormone-specific effect of OT on reproductive behavior.
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Dendritos/efeitos dos fármacos , Hormônios/farmacologia , Neurônios/citologia , Ocitocina/metabolismo , Sinapses/efeitos dos fármacos , Núcleo Hipotalâmico Ventromedial/citologia , Animais , Dendritos/metabolismo , Dendritos/ultraestrutura , Estradiol/análogos & derivados , Estradiol/farmacologia , Feminino , Microscopia Imunoeletrônica/métodos , Proteínas Associadas aos Microtúbulos/metabolismo , Ovariectomia/métodos , Progesterona/farmacologia , Progestinas/farmacologia , Ratos , Ratos Sprague-Dawley , Sinapses/metabolismo , Sinapses/ultraestrutura , Sinaptofisina/metabolismo , Núcleo Hipotalâmico Ventromedial/efeitos dos fármacos , Proteína Vesicular 2 de Transporte de Glutamato/metabolismoRESUMO
The hypothalamic ventromedial nucleus (VMH) displays sexual dichotomies in its overall size, neurochemistry, and neuronal morphology. These differences may underlie the sex differences observed in functions mediated by the VMH, such as reproductive behaviors and energy balance. A previous Golgi impregnation analysis of VMH dendrites reported sex differences in total dendrite length in the ventrolateral region of the VMH. The present study tested the hypothesis that this sex difference is localized to a specific dendrite type. VMH neurons were visualized with Golgi impregnation. Overall, male rats displayed significantly longer dendrites than females for VMH neurons. This sex difference was apparent in both the dorsomedial and the ventrolateral subdivisions of the VMH. When dendrites were classified based on dendrite type, namely long primary, short primary and secondary dendrites, the increased length for males was observed for all dendrite types. Furthermore, when long primary dendrites were categorized according to whether they extended in the dorsomedial, ventrolateral, ventromedial or dorsolateral direction, the sex difference in length occurred for all directions. These results indicate that the previously identified dendrite categories for VMH neurons are integral to VMH circuitry for both males and females. Given that the sex difference in dendrite length applied to all dendrite types, the elongated male VMH dendrites may provide additional sites to process input from both local interneurons and extranuclear afferents.
Assuntos
Dendritos/fisiologia , Neurônios/citologia , Caracteres Sexuais , Núcleo Hipotalâmico Ventromedial/citologia , Animais , Dendritos/efeitos dos fármacos , Dendritos/ultraestrutura , Estradiol/análogos & derivados , Estradiol/farmacologia , Feminino , Masculino , Ovariectomia/métodos , Progesterona/farmacologia , Ratos , Ratos Sprague-Dawley , Coloração pela Prata/métodosRESUMO
The ventromedial nucleus of the hypothalamus (VMH), with its major subdivisions, the dorsomedial and ventrolateral VMH (dmVMH and vlVMH, respectively), has been studied extensively for its role in female sexual behavior. This behavior is controlled by the vlVMH through the cellular actions of estradiol combined with progesterone. Although the effects of treatment with estradiol alone on neuronal morphology in the vlVMH have been examined, much less is known about the combined effects of estradiol and progesterone on neuronal structure. The present study employed Golgi impregnation to investigate the effects of estradiol treatment alone vs. estradiol combined with progesterone treatment on dendritic arbor of VMH neurons. The dendritic arbor of VMH neurons was somewhat different in the vlVMH vs. the dmVMH, with longer and more dendrites in the vlVMH. Estradiol treatment alone caused a marked reduction in the length of long primary dendrites in the vlVMH, but not in the dmVMH. The estradiol-induced retraction of long primary dendrites in the vlVMH was reversed within 4 hours of progesterone treatment. The differences in the dendritic arbors of dmVMH and vlVMH provide further support for the notion that these two regions have different patterns of neural connectivity. In addition, this study is the first to report opposing effects of estradiol alone vs. estradiol plus progesterone on the dendritic arbor of neurons in the vlVMH. These results suggest a structural mechanism for estradiol alone to have a modest effect on mating behavior while setting the stage for its ample expression.