Postsecondary Pathways and Persistence for STEM Versus Non-STEM Majors: Among College Students with an Autism Spectrum Disorder

Little is known about postsecondary pathways and persistence among college students with an autism spectrum disorder (ASD). This study analyzed data from the National Longitudinal Transition Study-2, 2001–2009, a nationally representative sample of students in special education with an ASD who progressed from high school to postsecondary education. Findings suggest that most college students with an ASD enrolled in a 2-year community college at some point in the postsecondary careers (81 %). Those in science, technology, engineering and mathematics (STEM) fields were more likely to persist in a 2-year community college and were twice as likely to transfer from a 2-year community college to a 4-year university than their peers in the non-STEM fields. College persistence rates varied by gender, race, parent education level, and college pathway and major. Educational policy implications are discussed.     

The ABC’s of Teaching Social Skills to Adolescents with Autism Spectrum Disorder in the Classroom: The UCLA PEERS ® Program

Social skills training is a common treatment method for adolescents with autism spectrum disorder (ASD), yet very few evidence-based interventions exist to improve social skills for high-functioning adolescents on the spectrum, and even fewer studies have examined the effectiveness of teaching social skills in the classroom. This study examines change in social functioning for adolescents with high-functioning ASD following the implementation of a school-based, teacher-facilitated social skills intervention known as Program for the Education and Enrichment of Relational Skills (PEERS ^® ). Seventy-three middle school students with ASD along with their parents and teachers participated in the study. Participants were assigned to the PEERS ^® treatment condition or an alternative social skills curriculum. Instruction was provided daily by classroom teachers and teacher aides for 14-weeks. Results reveal that in comparison to an active treatment control group, participants in the PEERS ^® treatment group significantly improved in social functioning in the areas of teacher-reported social responsiveness, social communication, social motivation, social awareness, and decreased autistic mannerisms, with a trend toward improved social cognition on the Social Responsiveness Scale. Adolescent self-reports indicate significant improvement in social skills knowledge and frequency of hosted and invited get-togethers with friends, and parent-reports suggest a decrease in teen social anxiety on the Social Anxiety Scale at a trend level. This research represents one of the few teacher-facilitated treatment intervention studies demonstrating effectiveness in improving the social skills of adolescents with ASD in the classroom: arguably the most natural social setting of all.     

Prevalence of cortical superficial siderosis in patients with cognitive impairment

Cortical superficial siderosis (cSS) is a magnetic resonance imaging marker of cerebral amyloid angiopathy (CAA) and can be its sole imaging sign. cSS has further been identified as a risk marker for future intracranial hemorrhage. Although uncommon in the general population, cSS may be much more prevalent in high risk populations for amyloid pathology. We aimed to determine the frequency of cSS in patients with cognitive impairment presenting to a memory clinic. We prospectively evaluated consecutive patients presenting to our memory clinic between April 2011 and April 2013. Subjects received neuropsychological testing using the Consortium to Establish a Registry for Alzheimer’s Disease battery (CERAD-NP). Two hundred and twelve patients with documented cognitive impairment further underwent a standardized 3T-MR-imaging protocol with T2*-weighted gradient-echo sequences for detection of cSS. Thirteen of 212 patients (6.1 %) displayed cSS. In seven of them (54 %) cSS was the only imaging sign of CAA. Patients with cSS did not differ from patients without cSS with regard to medical history, age or cardiovascular risk profile. Subjects with cSS performed worse in the mini-mental state examination (p = 0.001), showed more white matter hyperintensities (p = 0.005) and more often had microbleeds (p = 0.001) compared to those without cSS. cSS is common in patients with cognitive impairment. It is associated with lower cognitive scores, white matter hyperintensities and microbleeds and can be the only imaging sign for CAA in this patient group.     

Innere Arbeitsmodelle von Bindung und aversive Kindheitserfahrungen bei Psychotherapeuten in Ausbildung

In this paper first results of a study about competence development of psychotherapists in training in Germany are presented. In particular, the current mental processing of early relationship experiences and adversive childhood experiences of 90 trainees from three psychotherapies were examined at the beginning of their training. The internal working models of attachment and adversive early childhood experiences were assessed with the Adult Attachment Interview (AAI). The quantitative data analysis was supplemented by qualitative content analysis of four interviews to examine how trainees have dealt with adversive experiences and to work out if and how those are related to their decision to become psychotherapists. The AAIs analysis with respect to the attachment representation revealed by a first analysis of 50 interviews an overrepresentation of secure attachment patterns (78?%) and thus a significantly higher proportion of secure internal working models in comparison to former studies. Psychotherapists in training seem as burdened as the general population in terms of adversive childhood experiences. The qualitative analysis suggests a high degree of self-efficacy-enhancing parentification. The results are discussed in relation to previous psychotherapy experience, therapeutic school, age and sex of trainees.     

Electrical impedance myography for the in vivo and ex vivo assessment of muscular dystrophy (mdx) mouse muscle

Introduction: Sensitive, non‐invasive techniques are needed that can provide biomarkers of disease status and the effects of therapy in muscular dystrophy. Methods: We evaluated electrical impedance myography (EIM) to serve in this role by studying 2‐month‐old and 18‐month‐old mdx and wild‐type (WT) animals (10 animals in each of 4 groups). Results: Marked differences were observed in EIM values between mdx and WT animals; the differences were more pronounced between the older age groups (e.g., reactance of 92.6 ±4.3 Ω for mdx animals vs. 130 ± 4.1 Ω for WT animals, P < 0.001). In addition, in vivo EIM parameters correlated significantly with the extent of connective tissue deposition in the mdx animals. Conclusions: EIM has the potential to serve as a valuable non‐invasive method for evaluating muscular dystrophy. It can be a useful biomarker to assist with therapeutic testing in both pre‐clinical and clinical studies. Muscle Nerve 49 : 829–835, 2014     

Elevated alkaline phosphatase velocity strongly predicts overall survival and the risk of bone metastases in castrate-resistant prostate cancer

ObjectivesIn patients with a rising prostate-specific antigen (PSA) level during treatment with androgen deprivation therapy, identification of men who progress to bone metastasis and death remains problematic. Accurate risk stratification models are needed to better predict risk for bone metastasis and death among patients with castration-resistant prostate cancer (CRPC). This study evaluates whether alkaline phosphatase (AP) kinetics predicts bone metastasis and death in patients with CRPC.Methods and materialsA retrospective cohort study of 9,547 patients who underwent treatment for prostate cancer was conducted using the Center for Prostate Disease Research Multi-center National Database. From the entire cohort, 347 were found to have CRPC and, of those, 165 had 2 or more AP measurements during follow-up. To determine the AP velocity (APV), the slope of the linear regression line of all AP values was plotted over time. Rapid APV was defined as the uppermost quartile of APV values, which was found to be ≥6.3 IU/l/y. CRPC was defined as 2 consecutive rising PSA values after achieving a PSA nadir<4 ng/ml and documented testosterone values less than 50 ng/dl. The primary study outcomes included bone metastasis–free survival (BMFS) and overall survival (OS).ResultsRapid APV and PSA doubling time (PSADT) less than 10 months were strong predictors of both BMFS and OS in a multivariable analysis. Faster PSADT was a stronger predictor for BMFS (odds ratio [OR] = 12.1, P<0.0001 vs. OR = 2.7, P = 0.011), whereas rapid APV was a stronger predictor of poorer OS (OR = 5.11, P = 0.0001 vs. OR = 3.98, P = 0.0034). In those with both a rapid APV and a faster PSADT, the odds of developing bone metastasis and death exceeded 50%.ConclusionAPV is an independent predictor of OS and BMFS in patients with CRPC. APV, in conjunction with PSA-based clinical parameters, may be used to better identify patients with CRPC who are at the highest risk of metastasis and death. These findings need validation in prospective studies.     

Cultural diversity at the end of life: issues and guidelines for family physicians

Ethnic minorities currently compose approximately one third of the population of the United States. The U.S. model of health care, which values autonomy in medical decision making, is not easily applied to members of some racial or ethnic groups. Cultural factors strongly influence patients' reactions to serious illness and decisions about end-of-life care. Research has identified three basic dimensions in end-of-life treatment that vary culturally: communication of "bad news"; locus of decision making; and attitudes toward advance directives and end-of-life care. In contrast to the emphasis on "truth telling" in the United States, it is not uncommon for health care professionals outside the United States to conceal serious diagnoses from patients, because disclosure of serious illness may be viewed as disrespectful, impolite, or even harmful to the patient. Similarly, with regard to decision making, the U.S. emphasis on patient autonomy may contrast with preferences for more family-based, physician-based, or shared physician- and family-based decision making among some cultures. Finally, survey data suggest lower rates of advance directive completion among patients of specific ethnic backgrounds, which may reflect distrust of the U.S. health care system, current health care disparities, cultural perspectives on death and suffering, and family dynamics. By paying attention to the patient's values, spirituality, and relationship dynamics, the family physician can elicit and follow cultural preferences.     

The selective poly(ADP-ribose) polymerase-1(2) inhibitor, CEP-8983, increases the sensitivity of chemoresistant tumor cells to temozolomide and irinotecan but does not potentiate myelotoxicity

The effect of the potent and selective poly(ADP-ribose) (PAR) polymerase-1 [and PAR polymerase-2] inhibitor CEP-8983 on the ability to sensitize chemoresistant glioblastoma (RG2), rhabdomyosarcoma (RH18), neuroblastoma (NB1691), and colon carcinoma (HT29) tumor cells to temozolomide- and camptothecin-induced cytotoxicity, DNA damage, and G(2)-M arrest and on the potentiation of chemotherapy-induced myelotoxicity was evaluated using in vitro assays. In addition, the effect of the prodrug CEP-9722 in combination with temozolomide and/or irinotecan on PAR accumulation and tumor growth was also determined using glioblastoma and/or colon carcinoma xenografts relative to chemotherapy alone. CEP-8983 sensitized carcinoma cells to the growth-inhibitory effects of temozolomide and/or SN38 increased the fraction of and/or lengthened duration of time tumor cells accumulated in chemotherapy-induced G(2)-M arrest and sensitized tumor cells to chemotherapy-induced DNA damage and apoptosis. A granulocyte-macrophage colony-forming unit colony formation assay showed that coincubation of CEP-8983 with temozolomide or topotecan did not potentiate chemotherapy-associated myelotoxicity. CEP-9722 (136 mg/kg) administered with temozolomide (68 mg/kg for 5 days) or irinotecan (10 mg/kg for 5 days) inhibited significantly the growth of RG2 tumors (60%) or HT29 tumors (80%) compared with temozolomide or irinotecan monotherapy, respectively. In addition, CEP-9722 showed "stand alone" antitumor efficacy in these preclinical xenografts. In vivo biochemical efficacy studies showed that CEP-9722 attenuated PAR accumulation in glioma xenografts in a dose- and time-related manner. These data indicate that CEP-8983 and its prodrug are effective chemosensitizing agents when administered in combination with select chemotherapeutic agents against chemoresistant tumors.     

Genetics of New-Onset Diabetes after Transplantation

New-onset diabetes after transplantation is a common complication that reduces recipient survival. Research in renal transplant recipients has suggested that pancreatic β-cell dysfunction, as opposed to insulin resistance, may be the key pathologic process. In this study, clinical and genetic factors associated with new-onset diabetes after transplantation were identified in a white population. A joint analysis approach, with an initial genome-wide association study in a subset of cases followed by de novo genotyping in the complete case cohort, was implemented to identify single-nucleotide polymorphisms (SNPs) associated with the development of new-onset diabetes after transplantation. Clinical variables associated with the development of diabetes after renal transplantation included older recipient age, female sex, and percentage weight gain within 12 months of transplantation. The genome-wide association study identified 26 SNPs associated with new-onset diabetes after transplantation; this association was validated for eight SNPs (rs10484821, rs7533125, rs2861484, rs11580170, rs2020902, rs1836882, rs198372, and rs4394754) by de novo genotyping. These associations remained significant after multivariate adjustment for clinical variables. Seven of these SNPs are associated with genes implicated in β-cell apoptosis. These results corroborate recent clinical evidence implicating β-cell dysfunction in the pathophysiology of new-onset diabetes after transplantation and support the pursuit of therapeutic strategies to protect β cells in the post-transplant period.One-year graft survival after renal transplantation is now excellent, exceeding 93% for organs donated after brain death and 96% for those from living donors.^1–3 Technical advancements in surgery, improved understanding of immunology, and innovative developments in pharmacology have altered the landscape of renal transplantation. The goal of preventing early graft loss has largely been achieved and arguably the greatest challenge now is the avoidance of late graft failure. Although there has been a considerable improvement in 1-year renal transplant survival, the rate of graft attrition after the first year remains frustratingly constant.^2,4New-onset diabetes after transplantation (NODAT) is a common and serious disorder that curtails recipient survival.^5–7 NODAT is associated with cardiovascular complications^8–11 and develops in 2%–50%¹² of renal transplant recipients. Approximately 50% of recipients with NODAT require insulin therapy.^{6–8,13–15} A number of clinical variables have been associated with NODAT, including black ethnicity, older recipient age, female sex, obesity, immunosuppression, and viral infections.^{5,6,8,13,16,17}Until recently, the pathophysiology of NODAT was considered to be analogous to type 2 diabetes mellitus. Renal transplant recipients have increased insulin resistance compared with transplant-naïve persons with normal renal function.¹⁸ In a nondiabetic renal transplant population, the main determinants of insulin resistance are obesity and corticosteroid therapy.¹⁹ Insulin resistance improves in renal transplant recipients after successful transplantation^20,21 and recipients have enhanced insulin sensitivity compared with dialysis patients.²² At 1 year, there is no significant difference in insulin resistance between renal transplant recipients with NODAT and those with normal glucose tolerance.^18,23 Furthermore, insulin resistance indices before transplantation and in the early post-transplant period do not predict NODAT development.¹¹Pancreatic β-cell dysfunction may prove to be the main pathologic contributor to NODAT. In glucose clamp studies, a deficit in insulin secretion was common to renal transplant recipients with NODAT.^18,20,21,24 There are a number of possible mechanisms for β-cell toxicity in renal transplantation, including hyperglycemia,²⁵ elevated free fatty acids,²⁶ and the effect of immunosuppressive medication.²⁷ A recent proof-of-concept clinical trial demonstrated that aggressive management of post-transplant hyperglycemia with insulin significantly reduced the 1-year incidence of NODAT.²⁸ This provides further evidence that post-transplant hyperglycemia plays a key role in NODAT development.This study investigates clinical and genetic factors associated with NODAT in a relatively large, white renal transplant population. Clinical variables were identified in a carefully phenotyped, ethnically homogeneous cohort. Initial exploratory analysis was conducted via a genome-wide association study (GWAS) in a subgroup of NODAT cases patients and controls to identify genetic variants associated with NODAT. De novo genotyping was then performed in a larger cohort of NODAT patients and controls to validate the findings.