Microstructures and Corrosion Properties of Wire Arc Additive Manufactured Copper-Nickel Alloys.

The 70/30 copper-nickel alloy is used mainly in critical parts with more demanding conditions in marine settings. There is a need for innovative methods that offer fast production and cost-effectiveness in order to supplement current copper-nickel alloy manufacturing processes. In this study, we employ wire arc additive manufacturing (WAAM) to fabricate the 70/30 copper-nickel alloy. The as-built microstructure is characterized by columnar grains with prominent dendrites and chemical segregation in the inter-dendritic area. The aspect ratio of the columnar grain increases with increasing travel speed (TS) at the same wire feed speed (WFS). This is in contrast with the equiaxed grain structure, with a more random orientation, of the conventional sample. The sample built with a WFS of 8 m/min, TS of 1000 mm/min, and a track distance of 3.85 mm exhibits superior corrosion properties in the 3.5 wt% NaCl solution when compared with the conventional sample, as evidenced by a higher film resistance and breakdown potential, along with a lower passive current density of the WAAM sample. The corrosion morphology reveals the critical roles played by the nickel element that is unevenly distributed between the dendrite core and inter-dendritic area.

Acute movement disorders in the medical setting.

Objective Psychosomatic medicine psychiatrists are often tasked with the evaluation and treatment of complex neuropsychiatric states which may be motoric in phenotype. Little energy has been dedicated to understanding acute movement disorders in the hospital environment. Method Recognizing the importance of frontal-subcortical (corticostriatothalamocortical) circuitry and basal ganglia structures, we present a case series of acute movement disorder phenotypes resulting from underlying medical conditions, commonly-administered medications, or the interaction of both. We organize these scenarios into neurodegenerative disorders, primary psychiatric disorders, neuroinflammation, and polypharmacy, demonstrating a clinical example of each followed by background references on a variety of clinical states and medications contributing to acute movement disorders. In addition, we offer visual illustration of implicated neurocircuitry as well as proposed neurotransmitter imbalances involving glutamate, gamma aminobutyric acid, and dopamine. Furthermore, we review the various clinical syndromes and medications involved in the development of acute movement disorders. Results Acute movement disorder's involve complex interactions between frontal-subcortical circuits and acute events. Given the complexity of interactions, psychopharmacological considerations become critical, as some treatments may alleviate acute movement disorders while others will exacerbate them. Conclusion Integrating underlying medical conditions and acutely administered (or discontinued) pharmacological agents offers an interactional, neuromedical approach to acute movement disorders that is critical to the work of psychosomatic medicine.

Teaching a neuromedical-contextual approach to psychosomatic medicine.

The practice of psychosomatic medicine in the general hospital setting can be challenging, particularly for the inexperienced trainee. Guidance for how to approach a psychiatric consultation can be nonspecific or lacking altogether. In response, we offer a pedagogical model that emphasizes patient-specific neurological, medical, and contextual variables. A stepwise, "ABC" approach to psychiatric consultation is elaborated, beginning with collection of critical history ("Admission, Background, Consultation Question"), followed by both patient encounter ("Appearance, Behavior, Context") and actual patient examination ("Arousal, Brain/Body, Cognitive Assessment"), ultimately informing any given case formulation. Multiple clinical vignettes illustrate this approach and are offered for educational purposes in dissemination to trainees.

[(11)C]-DASB microPET imaging in the aged rat: frontal and meso-thalamic increases in serotonin transporter binding.

Whereas molecular imaging studies in the aging human brain have predominantly demonstrated reductions in serotonin transporter (5-HTT) availability, the majority of the rodent studies, using autoradiographic methods, report increases in neural 5-HTT levels with age. To our knowledge, however, no previous rodent studies have assessed this topic in vivo, and therefore it remains unclear whether this discrepancy arises from methodological or inter-species differences. We performed an [(11)C]-DASB microPET study to evaluate the effects of aging on 5-HTT availability in the rat brain. To generate binding potential estimates, quantitative tracer kinetic modeling was applied using the simplified reference tissue model. A global increase in whole-brain [(11)C]-DASB binding potential was observed in the aged rats in comparison to the control group. More specifically, regional analyses revealed a highly significant increase in 5-HTT binding in the medial frontal cortex, and more modest increments in the midbrain/thalamus. Our results suggest that the frontal cortex represents a site of robust age-related alterations in the rat serotonergic system, and stress the need for further research assessing this topic in the human frontal cortex. Moreover, these findings suggest that the reported discrepancies between rodent and human data may reflect a divergence in the aging processes affecting human and rat serotonergic terminals.