An Investigation of School Counselor Understanding and Response to Help Seeking among Second Generation Asian American Students in the Us Public School System

Asian Americans are a rapidly growing population in the US and have high levels of psychological distress. However, Asian Americans tend not to ask for help from mental health professionals in regards to social/emotional issues, including school counselors. Asian American students are typical in terms of their presence within the US mainstream public school system, yet they are atypical in experiencing a variety of stressors and issues such as academic pressures, language and communication difficulties with parents/guardians, acculturative stress, and many more (Chang & Smith, 2015; Mouw & Xie, 1999; Berry, 2005). Despite mental health needs and the growing relevance of this population, research on the Asian American population is limited (Cho & Haslam, 2010). Thus, the purpose of this research study was to gain an understanding of participants’ experiences with Asian American students through the lens of the help-seeking model (Cauce et al., 2002). Two high schools and one middle school in a suburban area within the Southeast region of the US were purposefully selected for this study, and from these schools, eight high school counselors and two middle school counselors were interviewed. Participants were specifically asked about interactions, observations, and accommodations pertaining to the help-seeking needs of Asian American students. Data was collected through semi-structured individual interviews, which were then transcribed and analyzed for themes and conclusions. Four main themes (acculturative stress, school based expectations, lack of mental health counseling, and counselor involvement) with 10 subthemes were extrapolated from the data and confirmed the current literature on the help-seeking needs and processes of Asian American students. The study brought new insights to this topic and provided implications for future practice and research

The Relationship of the Clinical Disc Margin and Bruch's Membrane Opening in Normal and Glaucoma Subjects.

PurposeWe tested the hypotheses that the mismatch between the clinical disc margin (CDM) and Bruch's membrane opening (BMO) is a function of BMO area (BMOA) and is affected by the presence of glaucoma.MethodsA total of 45 normal eyes (45 subjects) and 53 glaucomatous eyes (53 patients) were enrolled and underwent radial optic nerve head (ONH) imaging with spectral domain optical coherence tomography. The inner tip of the Bruch's membrane (BM) and the clinical disc margin were marked on radial scans and optic disc photographs, and were coregistered with custom software. The main outcome measure was the difference between the clinical disc area (CDA) and BMOA, or CDA-BMOA mismatch, as a function of BMOA and diagnosis. Multivariate regression analyses were used to explore the influence of glaucoma and BMOA on the mismatch.ResultsGlobal CDA was larger than BMOA in both groups but the difference was statistically significant only in the normal group (1.98 ± 0.37 vs. 1.85 ± 0.45 mm2, P = 0.02 in the normal group; 1.96 ± 0.38 vs. 1.89 ± 0.56 mm2, P = 0.08 in the glaucoma group). The sectoral CDA-BMOA mismatch was smaller in superotemporal (P = 0.04) and superonasal (P = 0.05) sectors in the glaucoma group. The normalized CDA-BMOA difference decreased with increasing BMOA in both groups (P < 0.001). Presence or severity of glaucoma did not affect the CDA-BMOA difference (P > 0.14).ConclusionsClinical disc area was larger than BMOA in normal and glaucoma eyes but reached statistical significance only in the former group. The CDA-BMOA mismatch diminished with increasing BMOA but was not affected by presence of glaucoma. These findings have important clinical implications regarding clinical evaluation of the ONH

Whole exome and targeted deep sequencing identify genome-wide allelic loss and frequent SETDB1 mutations in malignant pleural mesotheliomas.

Malignant pleural mesothelioma (MPM), a rare malignancy with a poor prognosis, is mainly caused by exposure to asbestos or other organic fibers, but the underlying genetic mechanism is not fully understood. Genetic alterations and causes for multiple primary cancer development including MPM are unknown. We used whole exome sequencing to identify somatic mutations in a patient with MPM and two additional primary cancers who had no evidence of venous, arterial, lymphovascular, or perineural invasion indicating dissemination of a primary lung cancer to the pleura. We found that the MPM had R282W, a key TP53 mutation, and genome-wide allelic loss or loss of heterozygosity, a distinct genomic alteration not previously described in MPM. We identified frequent inactivating SETDB1 mutations in this patient and in 68 additional MPM patients (mutation frequency: 10%, 7/69) by targeted deep sequencing. Our observations suggest the possibility of a new genetic mechanism in the development of either MPM or multiple primary cancers. The frequent SETDB1 inactivating mutations suggest there could be new diagnostic or therapeutic options for MPM

The lift industry in Hong Kong : regulatory action and capacity building

published_or_final_versionPolitics and Public AdministrationMasterMaster of Public Administratio

Development and Implementation of a Pharmacist-managed Outpatient Parenteral Antimicrobial Therapy Program

Purpose The development and implementation of a pharmacist-managed outpatient parenteral antimicrobial therapy (OPAT) program in a county teaching hospital are described. Summary A pharmacist-managed OPAT program was developed and implemented at a county teaching hospital to provide consistent evaluation, approval, and monitoring of patients requiring OPAT for the treatment of infection. The developmental and implementation stages of the OPAT program included (1) a needs assessment, (2) the identification of resources necessary for program operation, (3) delineation of general OPAT program operations and activities of individual OPAT clinicians, (4) the development of patient selection criteria, including a plan of care algorithm, and (5) acquisition of administrative support to approve the program. In this program, the OPAT pharmacist plays an integral role in the management and oversight of OPAT patients, working under a collaborative agreement with infectious diseases physicians. The OPAT pharmacist assists with appropriate patient and regimen selection, confirmation of orders on discharge, assuring that laboratory tests for safety surveillance are performed and evaluated, performing routine monitoring for adverse events and line complications, and assuring the removal of the vascular access device upon the completion of OPAT. Conclusion: The OPAT program provides structured monitoring, patient follow-up, and led to improvements in patient outcome with minimization of treatment and line-related adverse events

Charles W. Bolen Faculty Recital Series: String Faculty Showcase, November 4, 2021

Center for the Performing Arts November 4, 2021 Thursday Evening 8:00 p.m

Faculty String Quartet: Sarah Gentry, Violin; Rebecca Cutler, Violin; Katherine Lewis, Viola; Adriana La Rossa Ransom, Cello; Sharon Chung, Viola; April 5, 2009

Kemp Recital HallApril 5, 2009Monday Evening7:30 p.m

Restoring mitofusin balance prevents axonal degeneration in a Charcot-Marie-Tooth type 2A model

Mitofusin-2 (MFN2) is a mitochondrial outer-membrane protein that plays a pivotal role in mitochondrial dynamics in most tissues, yet mutations in MFN2, which cause Charcot-Marie-Tooth disease type 2A (CMT2A), primarily affect the nervous system. We generated a transgenic mouse model of CMT2A that developed severe early onset vision loss and neurological deficits, axonal degeneration without cell body loss, and cytoplasmic and axonal accumulations of fragmented mitochondria. While mitochondrial aggregates were labeled for mitophagy, mutant MFN2 did not inhibit Parkin-mediated degradation, but instead had a dominant negative effect on mitochondrial fusion only when MFN1 was at low levels, as occurs in neurons. Finally, using a transgenic approach, we found that augmenting the level of MFN1 in the nervous system in vivo rescued all phenotypes in mutant MFN2R94Q-expressing mice. These data demonstrate that the MFN1/MFN2 ratio is a key determinant of tissue specificity in CMT2A and indicate that augmentation of MFN1 in the nervous system is a viable therapeutic strategy for the disease