The Comparative Analysis of the Dyslexia Screening Instrument and the Dyslexia Screening Tool

STEEP is a universal screening instrument that provides effective and efficient identification of students at risk. It is hypothesized that by using the difference between the math STEEP score and the reading STEEP score that STEEP can be used to identify dyslexic children. The present research was conducted by selecting students that scored mastery/instructional in math and frustrational in reading as the sample. The current study examines the correlation between the Dyslexia Screening Instrument and the Dyslexia Screening Tool by administering those instruments to the identified population. The results were analyzed by using the Pearson correlation coefficient (r) and the Kendall’s Tau correlation coefficient (r). The results indicated a positive and significant correlation between the Dyslexia Screening Instrument and the Dyslexia Screening Tool. Recommendations were made for future research

A National Study of Health Behaviors and Health-Related Quality of Life Among Survivors of Breast, Prostate, and Colorectal Cancer Compared to Propensity Score Matched Controls, as well as, Comparisons by Cancer Type & Gender

The objectives of this study were to 1) compare the prevalence of specific measures of Health-Related Quality of Life (HRQOL) between breast, prostate, female, and male colorectal cancer survivors to propensity score matched controls, and to compare HRQOL by type of cancer and gender and 2) compare the prevalence of specific health conditions and health behaviors between breast, prostate, female, and male colorectal cancer survivors to propensity score matched controls, and to compare health behaviors by type of cancer and gender. A cross-sectional study was conducted using a sample of breast, prostate, and colorectal cancer survivors 18 years of age and older and \u3e 1 year past diagnosis were selected from the 2009 BRFSS. A greedy algorithm and matching without replacement used propensity scores to match 3 controls to every 1 case on age, gender, race/ethnicity, income, insurance status, and region of the U.S. HRQOL measures compared were life satisfaction, perceived emotional support, activity limitations, perceived general, physical and mental health, and sleep quality. Health conditions compared were arthritis, asthma, heart disease, diabetes, hypertension, high cholesterol, stroke, activity limitations, and perceived general health. Health behaviors compared were flu immunization, physical check-up, cholesterol check, BMI, physical activity, fruit and vegetable consumption, smoking, and alcohol use. Chi-square tests were used to test for covariate balance and compared prevalence of health conditions and behaviors. Binomial and multinomial logistic regression models were used to estimate the probabilities of behaviors for cancer cases compared to controls. The final study sample consisted of 6,393 breast, 3,636 prostate, 1,111 female colorectal, and 824 male colorectal cancer survivors. Compared to matched controls, cancer survivors were up to 3.67 times more likely (95%CI: 2.09, 6.47) at 1 -- 5 years since diagnosis, and up to 1.91 times more likely (95%CI: 1.30, 2.79). Breast, female, and male colorectal cancer survivors were up to 2.62 times more likely (95%CI: 1.72, 3.99) to report activity limitations compared to matched controls. Additionally, colorectal cancer survivors were more likely to report worse physical health than their matched controls. Male colorectal and prostate cancer survivors were more likely to report worse mental health, and prostate cancer survivors were more likely to report a lack of emotional support and not enough sleep compared to their matched controls. Comparisons by cancer type found that male colorectal cancer survivors were more likely to report activity limitations and perceive their general and physical health to be worse than prostate cancer survivors. Gender comparisons found that females were more likely to hold poorer perceptions of their general, physical, and mental health, report not enough sleep, and not receiving enough emotional support, but more likely to be satisfied with life. Breast and prostate cancer survivors reported a greater prevalence of chronic health conditions than matched controls. Breast cancer survivors were more likely to engage in healthier behaviors 1 -- 5 years after diagnosis, but were more likely to be obese at \u3e 5 years after diagnosis than controls. Male colorectal cancer survivors were less likely to engage in clinical preventive care at \u3e 5 years after diagnosis than controls. Female colorectal and breast cancer survivors were less likely be overweight and/or obese, former and/or current smokers, drink any alcohol, and more likely to consume ≥ 5 servings of fruits and vegetables per day, but more likely to engage in none or insufficient levels of physical activity compared to male colorectal and prostate cancer survivors, respectively. All cancer survivor groups reported more limitations and held poorer perceptions of their general health. Differences between matched controls for other HRQOL measure vary by type of cancer, although compared to similar males without cancer, male cancer survivors reported worse outcomes on measures such as mental health, sleep, and emotional support. However, when female survivors were compared to male survivors, females reported worse outcomes for all measures except life satisfaction. Breast and prostate cancer survivors have more chronic health conditions compared to matched controls than do female and male colorectal cancer survivors. Breast cancer survivors are more likely to engage in healthy behaviors than their matched controls. Female cancer survivors engage healthier lifestyle behaviors, with the exception of physical activity, compared to male cancer survivors. (Abstract shortened by UMI.)

C-Jun N-terminal kinase 2 promotes liver injury via the mitochondrial permeability transition after hemorrhage and resuscitation

Hemorrhagic shock leads to hepatic hypoperfusion and activation of mitogen-activated stress kinases (MAPK) like c-Jun N-terminal kinase (JNK) 1 and 2. Our aim was to determine whether mitochondrial dysfunction leading to hepatic necrosis and apoptosis after hemorrhage/resuscitation (H/R) was dependent on JNK2. Under pentobarbital anesthesia, wildtype (WT) and JNK2 deficient (KO) mice were hemorrhaged to 30 mm Hg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer's solution. Serum alanine aminotransferase (ALT), necrosis, apoptosis and oxidative stress were assessed 6 h after resuscitation. Mitochondrial polarization was assessed by intravital microscopy. After H/R, ALT in WT-mice increased from 130 U/L to 4800 U/L. In KO-mice, ALT after H/R was blunted to 1800 U/l (P < 0.05). Necrosis, caspase-3 activity and ROS were all substantially decreased in KO compared to WT mice after H/R. After sham operation, intravital microscopy revealed punctate mitochondrial staining by rhodamine 123 (Rh123), indicating normal mitochondrial polarization. At 4 h after H/R, Rh123 staining became dim and diffuse in 58% of hepatocytes, indicating depolarization and onset of the mitochondrial permeability transition (MPT). By contrast, KO mice displayed less depolarization after H/R (23%, P < 0.05). In conclusion, JNK2 contributes to MPT-mediated liver injury after H/R

Dying a Thousand Deaths: Redundant Pathways From Different Organelles to Apoptosis and Necrosis

Cell death is an essential event in normal life and development, as well as in the pathophysiological processes that lead to disease. Although the literature on cell death has grown enormously in size and complexity, a pattern has emerged that each of several distinct organelles (plasma membrane, mitochondrion, nucleus, endoplasmic reticulum, lysosome) gives rise to signals that induce cell death. Most often these signals converge on mitochondria to initiate a common pathway to either caspase-dependent apoptosis or ATP depletion-dependent necrosis. This brief overview emphasizes the multiple and often redundant pathways between different organelles that lead ultimately to a cell's demise

Survival and recovery modeling of acute kidney injury in critically ill adults

Objectives: Acute kidney injury is common among the critically ill. However, the incidence, medication use, and outcomes of acute kidney injury have been variably described. We conducted a single-center, retrospective cohort study to examine the risk factors and correlates associated with acute kidney injury in critically ill adults with a particular focus on medication class usage. Methods: We reviewed the electronic medical records of all adult patients admitted to an intensive care unit between 1 February and 30 August 2020. Acute kidney injury was defined by the 2012 Kidney Disease: Improving Global Outcomes guidelines. Data included were demographics, comorbidities, symptoms, laboratory parameters, interventions, and outcomes. The primary outcome was acute kidney injury incidence. A Least Absolute Shrinkage and Selection Operator regression model was used to determine risk factors associated with acute kidney injury. Secondary outcomes including acute kidney injury recovery and intensive care unit mortality were analyzed using a Cox regression model. Results: Among 226 admitted patients, 108 (47.8%) experienced acute kidney injury. 37 (34.3%), 39 (36.1%), and 32 patients (29.6%) were classified as acute kidney injury stages I–III, respectively. Among the recovery and mortality cohorts, analgesics/sedatives, anti-infectives, and intravenous fluids were significant (p-value \u3c 0.05). The medication classes IV-fluid electrolytes nutrition (96.7%), gastrointestinal (90.2%), and anti-infectives (81.5%) were associated with an increased odds of developing acute kidney injury, odd ratios: 1.27, 1.71, and 1.70, respectively. Cox regression analyses revealed a significantly increased time-varying mortality risk for acute kidney injury-stage III, hazard ratio: 4.72 (95% confidence interval: 1–22.33). In the recovery cohort, time to acute kidney injury recovery was significantly faster in stage I, hazard ratio: 9.14 (95% confidence interval: 2.14–39.06) cohort when compared to the stage III cohort. Conclusion: Evaluation of vital signs, laboratory, and medication use data may be useful to determine acute kidney injury risk stratification. The influence of particular medication classes further impacts the risk of developing acute kidney injury, necessitating the importance of examining pharmacotherapeutic regimens for early recognition of renal impairment and prevention

Heat Shock Suppresses the Permeability Transition in Rat Liver Mitochondria

Heat shock proteins inhibit apoptotic and necrotic cell death in various cell types. However, the specific mechanism underlying protection by heat shock proteins remains unclear. To test the hypothesis that heat shock proteins inhibit cell death by blocking opening of mitochondrial permeability transition (MPT) pores, mitochondria from heat-preconditioned rat livers were isolated by differential centrifugation. Heat shock inhibited MPT pore opening induced by 50 microm CaCl(2) plus 5 microm HgCl(2) or 1 microm mastoparan and by 200 microm CaCl(2) alone. Half-maximal swelling was delayed 15 min or more after heat shock compared with control. Heat shock also increased the threshold of unregulated (Ca(2+)-independent and cyclosporin A-insensitive) MPT pore opening induced by higher doses of HgCl(2) and mastoparan. Heat shock treatment decreased mitochondrial reactive oxygen species formation by 27% but did not change mitochondrial respiration, membrane potential, Ca(2+) uptake, or total glutathione in mitochondrial and cytosolic extracts of liver. Western blot analysis showed that mitochondrial Hsp25 increased, whereas Hsp10, Hsp60, Hsp70, Hsp75, cyclophilin D, and voltage-dependent anion channel did not change after heat shock. These results indicate that heat shock causes resistance to opening of MPT pores, which may contribute to heat shock protection against cellular injury

Small-for-Size Liver Transplantation Increases Pulmonary Injury in Rats: Prevention by NIM811

Pulmonary complications after liver transplantation (LT) often cause mortality. This study investigated whether small-for-size LT increases acute pulmonary injury and whether NIM811 which improves small-for-size liver graft survival attenuates LT-associated lung injury. Rat livers were reduced to 50% of original size, stored in UW-solution with and without NIM811 (5 μM) for 6 h, and implanted into recipients of the same or about twice the donor weight, resulting in half-size (HSG) and quarter-size grafts (QSG), respectively. Liver injury increased and regeneration was suppressed after QSG transplantation as expected. NIM811 blunted these alterations >75%. Pulmonary histological alterations were minimal at 5–18 h after LT. At 38 h, neutrophils and monocytes/macrophage infiltration, alveolar space exudation, alveolar septal thickening, oxidative/nitrosative protein adduct formation, and alveolar epithelial cell/capillary endothelial apoptosis became overt in the lungs of QSG recipients, but these alterations were mild in full-size and HSG recipients. Liver pretreatment with NIM811 markedly decreased pulmonary injury in QSG recipients. Hepatic TNFα and IL-1β mRNAs and pulmonary ICAM-1 expression were markedly higher after QSG transplantation, which were all decreased by NIM811. Together, dysfunctional small-for-size grafts produce toxic cytokines, leading to lung inflammation and injury. NIM811 decreased toxic cytokine formation, thus attenuating pulmonary injury after small-for-size LT

Ethanol exposure decreases mitochondrial outer membrane permeability in cultured rat hepatocytes

Mitochondrial metabolism depends on movement of hydrophilic metabolites through the mitochondrial outer membrane via the voltage-dependent anion channel (VDAC). Here we assessed VDAC permeability of intracellular mitochondria in cultured hepatocytes after plasma membrane permeabilization with 8 μM digitonin. Blockade of VDAC with Koenig's polyanion inhibited uncoupled and ADP-stimulated respiration of permeabilized hepatocytes by 33% and 41%, respectively. Tenfold greater digitonin (80 μM) relieved KPA-induced inhibition and also released cytochrome c, signifying mitochondrial outer membrane permeabilization. Acute ethanol exposure also decreased respiration and accessibility of mitochondrial adenylate kinase (AK) of permeabilized hepatocytes membranes by 40% and 32%, respectively. This inhibition was reversed by high digitonin. Outer membrane permeability was independently assessed by confocal microscopy from entrapment of 3 kDa tetramethylrhodamine-conjugated dextran (RhoDex) in mitochondria of mechanically permeabilized hepatocytes. Ethanol decreased RhoDex entrapment in mitochondria by 35% of that observed in control cells. Overall, these results demonstrate that acute ethanol exposure decreases mitochondrial outer membrane permeability most likely by inhibition of VDAC