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Most of the knowledge of racial/ethnic disparities in mental health treatment utilization comes from studies examining outpatient services, and less is known about these disparities in inpatient services. This empirical gap may limit our understanding of these disparities since inpatient treatment is the most intensive form of specialty mental health care for patients with psychological disorders. We conducted a systematic chart review of 129 Asian American and 198 White American psychiatric inpatients to examine patterns of inpatient psychiatric treatment utilization. Demographic and clinical data were extracted from admission and discharge records during a two-year timeframe. Patterns of diagnoses revealed that Asian American patients utilized inpatient services for more severe psychiatric diagnoses compared to White American patients. Despite this, there were no racial/ethnic differences in levels of functional impairment at admission, and there were no racial/ethnic differences in length of treatment stay. For Asian American patients, level of psychosocial functioning at admission predicted length of stay. A better understanding of patterns of inpatient treatment use is needed to meet the clinical needs of Asian Americans with psychiatric disorders.

Reading provides a unique window into the history and nature of science and the norms of scientific communication and supports students in developing critical-reading skills in engaging ways. Effective use of reading promotes a spirit of inquiry and an understanding of science concepts while also addressing expectations of the Common Core State Standards for literacy in science. This article demonstrates how teachers can blend close reading of challenging text with traditional science instruction to achieve these goals. Close reading is the practice of investigating a short piece of high-quality text. The authors share a lesson plan and strategies that they used to implement close reading in a physical science class.

Abstract "Experts" appear in the modern American courtroom on the jury as well as in the witness box, posing a dilemma for the legal system by offering a potentially valuable [...]

The mechanisms by which glucose regulates the activity of glucose-inhibited (GI) neurons in the ventromedial hypothalamus (VMH) are largely unknown. We have previously shown that AMP-activated protein kinase (AMPK) increases nitric oxide (NO) production in VMH GI neurons. We hypothesized that AMPK-mediated NO signaling is required for depolarization of VMH GI neurons in response to decreased glucose. In support of our hypothesis, inhibition of neuronal nitric oxide synthase (nNOS) or the NO receptor soluble guanylyl cyclase (sGC) blocked depolarization of GI neurons to decreased glucose from 2.5 to 0.7 mM or to AMPK activation. Conversely, activation of sGC or the cell-permeable analog of cGMP, 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP), enhanced the response of GI neurons to decreased glucose, suggesting that stimulation of NO-sGC-cGMP signaling by AMPK is required for glucose sensing in GI neurons. Interestingly, the AMPK inhibitor compound C completely blocked the effect of sGC activation or 8-Br-cGMP, and 8-Br-cGMP increased VMH AMPK[alpha]2 phosphorylation. These data suggest that NO, in turn, amplifies AMPK activation in GI neurons. Finally, inhibition of the cystic fibrosis transmembrane regulator (CFTR) [Cl.sup.-] conductance blocked depolarization of GI neurons to decreased glucose or AMPK activation, whereas decreased glucose, AMPK activation, and 8-BrcGMP increased VMH CFTR phosphorylation. We conclude that decreased glucose triggers the following sequence of events leading to depolarization in VMH GI neurons: AMPK activation, nNOS phosphorylation, NO production, and stimulation of sGC-cGMP signaling, which amplifies AMPK activation and leads to closure of the CFTR. soluble guanylyl cyclase; guanosine 3',5'-cyclic monophosphate; cystic fibrosis transmembrane regulator; glucose-sensing neurons; membrane potential sensitive dye

Fasting increases neuropeptide Y (NPY) expression, peptide levels, and the excitability of NPY-expressing neurons in the hypothalamic arcuate (ARC) nucleus. A subpopulation of ARC-NPY neurons (~40%) are glucose-inhibited (GI)-type glucose-sensing neurons. Hence, they depolarize in response to decreased glucose. Because fasting enhances NPY neurotransmission, we propose that during fasting, GI neurons depolarize in response to smaller decreases in glucose. This increased excitation in response to glucose decreases would increase NPY-GI neuronal excitability and enhance NPY neurotransmission. Using an in vitro hypothalamic explant system, we show that fasting enhances NPY release in response to decreased glucose concentration. By measuring relative changes in membrane potential using a membrane potential-sensitive dye, we demonstrate that during fasting, a smaller decrease in glucose depolarizes NPY-GI neurons. Furthermore, incubation in low (0.7 mM) glucose enhanced while leptin (10 nM) blocked depolarization of GI neurons in response to decreased glucose. Fasting, leptin, and glucose-induced changes in NPY-GI neuron glucose sensing were mediated by 5'-AMP-activated protein kinase (AMPK). We conclude that during energy sufficiency, leptin reduces the ability of NPY-GI neurons to sense decreased glucose. However, after a fast, decreased leptin and glucose activate AMPK in NPY-GI neurons. As a result, NPY-GI neurons become depolarized in response to smaller glucose fluctuations. Increased excitation of NPY-GI neurons enhances NPY release. NPY, in turn, shifts energy homeostasis toward increased food intake and decreased energy expenditure to restore energy balance. arcuate nucleus; glucose-inhibited neuron; adenosine 5'-monophosphate kinase; leptin; fasting

The transmission of pain signals after injury or inflammation depends in part on increased excitability of primary sensory neurons. Nociceptive neurons express multiple subtypes of voltage-gated sodium channels ([Na.sub.v]1s), each of which possesses unique features that may influence primary afferent excitability. Here, we examined the contribution of [Na.sub.v]1.9. to nociceptive signaling by studying the electrophysiological and behavioral phenotypes of mice with a disruption of the SCN11A gene, which encodes [Na.sub.v]1.9. Our results confirm that [Na.sub.v]1.9. underlies the persistent tetrodotoxin-resistant current in small-diameter dorsal root ganglion neurons but suggest that this current contributes little to mechanical thermal responsiveness in the absence of injury or to mechanical hypersensitivity after nerve injury or inflammation. However, the expression of [Na.sub.v]1.9. contributes to the persistent thermal hypersensitivity and spontaneous pain behavior after peripheral inflammation. These results suggest that inflammatory mediators modify the function of [Na.sub.v]1.9. to maintain inflammation-induced hyperalgesia. hyperalgesia | pain | mouse | inflammation | C-fibers

Author(s): Andrew D. Howard [1, 2]; Ruiping Wang [3, 2]; Sheng-Shung Pong [1]; Theodore N. Mellin [4]; Alison Strack [4]; Xiao-Ming Guan [1]; Zhizhen Zeng [3]; David L. Williams, Jr [...]