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PurposeTwo stuttering measurement training programs currently used for training clinicians were evaluated for their efficacy in improving the accuracy of total stuttering event counting.MethodFour groups, each with 12 randomly allocated participants, completed a pretest-posttest design training study. They were evaluated by their counts of stuttering events on eight 3-min audiovisual speech samples from adults and children who stutter. Stuttering judgment training involved use of either the Stuttering Measurement System (SMS), Stuttering Measurement Assessment and Training (SMAAT) programs, or no training. To test for the reliability of any training effect, SMS training was repeated with the 4th group.ResultsBoth SMS-trained groups produced approximately 34% improvement, significantly better than no training or the SMAAT program. The SMAAT program produced a mixed result.ConclusionsThe SMS program was shown to produce a "medium" effect size improvement in the accuracy of stuttering event counts, and this improvement was almost perfectly replicated in a 2nd group. Half of the SMAAT judges produced a 36% improvement in accuracy, but the other half showed no improvement. Additional studies are needed to demonstrate the durability of the reported improvements, but these positive effects justify the importance of stuttering measurement training.

Introduction: Cardiovascular morbidity and mortality are high in people with serious mental illness (SMI). This problem is mediated, at least in part, by metabolic side effects of second-generation antipsychotics (SGAs) and by unhealthy lifestyle behaviors. We asked whether oral glucose tolerance testing (oGTT) or hemoglobin A1c (HbA1c) is superior in identifying people with SMI at high cardiometabolic risk and whether this risk is shaped by mood, cognition, or lifestyle habits. Methods: We evaluated 40 patients with schizophrenia, schizoaffective, or bipolar disorder receiving SGAs by oGTT, HbA1c, comprehensive metabolic and lipid panels, and CRP. Mood was assessed using the Patient Health Questionnaire (PHQ-9), and cognition was assessed using the Saint Louis University Mental Status examination. Diet was assessed using the UK Diabetes and Diet Questionnaire (UKDDQ), and physical activity was assessed using daily step counts. Results: Most patients had prediabetes (preDM) or diabetes mellitus (DM), 72.5% by oGTT, and 52.5% by HbA1c criteria. Pulse rates and insulin resistance indices (Homeostatic Model Assessment of Insulin Resistance, HOMA IR; Matsuda) were significantly different between patients classified as normal or with preDM/DM, using either oGTT or HbA1c criteria. Patients with preDM/DM by HbA1c but not oGTT criteria also had higher waist/hip ratios, triglyceride, and CRP levels (p<0.05). A strong negative correlation was found between average daily step counts and CRP levels (rho = -0.62, p<0.001). Higher UKDDQ scores, or unhealthier diet habits, were associated with higher fasting plasma glucose (rho = 0.28, p = 0.08), triglyceride levels (rho = 0.31, p = 0.05), and insulin resistance (HOMA IR: rho = 0.31, p = 0.06). Higher PHQ-9 scores correlated with lower 2h-oGTT glucose levels (rho = -0.37, p<0.05). Conclusions: OGTT screening is superior to HbA1c screening in detecting preDM and DM early. Patients identified with preDM/DM by oGTT or HbA1c screening are insulin-resistant and have higher pulse rates. Abdominal obesity, unfavorable lipid profiles, and higher CRP levels were noted in patients screened by HbA1c, but not by oGTT. Low physical activity, low depression scores, and unhealthy diet habits were associated with higher CRP and higher glucose and triglyceride levels, respectively. Future studies should assess the impact of specifically tailored individual lifestyle counseling and medical management interventions in this high-risk population. [ABSTRACT FROM AUTHOR]

R2833 --> Renal GLUT2 is increased in diabetes causing enhanced glucose reabsorption and therefore, aggravating hyperglycemia. We recently reported that reduced levels of GLUT2 in the kidneys protect melanocortin 4 receptor‐deficient mice from diabetes, even in the presence of insulin resistance and obesity, by elevating their glycosuria. Based on these findings, we hypothesized that loss of function of kidney‐specific GLUT2 would blunt hyperglycemia in diabetes by elevating glycosuria. To test our hypothesis, we generated kidney‐specific inducible Glut2 knockout (KO) mice [Glut2LoxP/LoxP x KspCadCreERT2 (inducible by tamoxifen)]. To investigate the therapeutic potential of kidney‐specific GLUT2 inhibition in treating diabetes, we administered the diabetogenic agent streptozocin (STZ, 50mg/kg i.p. for 5 consecutive days) in kidney‐specific Glut2 KO mice as well as their control littermates (Ctrl) and measured their fasting blood glucose levels. Three weeks after the STZ administration, the Glut2 KO mice exhibited significantly lower blood glucose levels (183 ±23 vs. 359 ±30 mg/dL) compared to the Ctrl mice that demonstrated overt diabetes. Moreover, the Glut2 KO mice had elevated glycosuria compared to the Ctrl mice (urine glucose: 1,897 ±184 vs. 1,190 ±111 mg/24h), indicating that excess loss of glucose in urine in the KO mice contributed toward improving the glycemia. To determine whether SGLT2 inhibition can further improve glycemia in kidney‐specific Glut2 KO mice, we administered the SGLT2 inhibitor dapagliflozin (DAPA) in these mice and evaluated glucose homeostasis. Indeed, DAPA (5 mg/Kg, i.p.) enhanced glucose tolerance in the Glut2 KO mice compared to that injected with saline (AUC of OGTT, 32,010 ±1,868 vs. 35,850 ±913 mg/dL.min). Moreover, the DAPA treatment further elevated glycosuria in the GLUT2 deficient mice compared to the mice injected with saline (urine glucose: 427 ±32 vs. 249 ±24 mg/24h). Altogether, using a new mouse model – in which we induced kidney‐specific GLUT2 deficiency in adult mice – we show that loss of function of kidney‐specific GLUT2 blunts hyperglycemia in STZ‐mediated diabetes, and SGLT2 inhibition further improves glucose tolerance as well as increases glycosuria in the GLUT2 KO mice. Therefore, we conclude that inhibiting kidney‐specific GLUT2 is a promising approach to treat diabetes and may yield optimal glucose control when combined with current SGLT2 inhibitors. [ABSTRACT FROM AUTHOR]