EFFECT OF DIFFERENT LOW BACK TRAINING PROGRAMS ON LUMBAR SPINE KINESTHESIA

Reduced kinesthetic perceptions can impair lower back sensorimotor functions and result in increased injury risk. The effect of low back training programs on lumbar spine kinesthetic sensibility is undetermined. There was a back strengthening exercise group (with low back pain; training 4.4 h/wk), a “classical” back training program group (with low back pain; training 4.9 h/wk) and a control group (training 5.4 h/wk). During an active reproduction test, subjects performed trunk positions in random order: flexion [A(0°-20°), B(20°-40°)], lateral flexion [C(0°-30°)], Using a 3D-ultrasound motion analysis system the repositioning error was calculated from the given target position to the subject perceived target position, before and after a 5 week training period. Results show decreased repositioning error after the training for both training groups

Src Dependent Pancreatic Acinar Injury Can Be Initiated Independent of an Increase in Cytosolic Calcium

Several deleterious intra-acinar phenomena are simultaneously triggered on initiating acute pancreatitis. These culminate in acinar injury or inflammatory mediator generation in vitro and parenchymal damage in vivo. Supraphysiologic caerulein is one such initiator which simultaneously activates numerous signaling pathways including non-receptor tyrosine kinases such as of the Src family. It also causes a sustained increase in cytosolic calcium- a player thought to be crucial in regulating deleterious phenomena. We have shown Src to be involved in caerulein induced actin remodeling, and caerulein induced changes in the Golgi and post-Golgi trafficking to be involved in trypsinogen activation, which initiates acinar cell injury. However, it remains unclear whether an increase in cytosolic calcium is necessary to initiate acinar injury or if injury can be initiated at basal cytosolic calcium levels by an alternate pathway. To study the interplay between tyrosine kinase signaling and calcium, we treated mouse pancreatic acinar cells with the tyrosine phosphatase inhibitor pervanadate. We studied the effect of the clinically used Src inhibitor Dasatinib (BMS-354825) on pervanadate or caerulein induced changes in Src activation, trypsinogen activation, cell injury, upstream cytosolic calcium, actin and Golgi morphology. Pervanadate, like supraphysiologic caerulein, induced Src activation, redistribution of the F-actin from its normal location in the sub-apical area to the basolateral areas, and caused antegrade fragmentation of the Golgi. These changes, like those induced by supraphysiologic caerulein, were associated with trypsinogen activation and acinar injury, all of which were prevented by Dasatinib. Interestingly, however, pervanadate did not cause an increase in cytosolic calcium, and the caerulein induced increase in cytosolic calcium was not affected by Dasatinib. These findings suggest that intra-acinar deleterious phenomena may be initiated independent of an increase in cytosolic calcium. Other players resulting in acinar injury along with the Src family of tyrosine kinases remain to be explored. © 2013 Mishra et al

The Bosnian version of the international self-report measure of posttraumatic stress disorder, the Posttraumatic Stress Diagnostic Scale, is reliable and valid in a variety of different adult samples affected by war

BACKGROUND: The aim of the present study was to assess the internal consistency and discriminant and convergent validity of the Bosnian version of a self-report measure of posttraumatic stress disorder (PTSD), the Posttraumatic Stress Diagnostic Scale (PTDS). The PTDS yields both a PTSD diagnosis according to the Diagnostic and Statistical Manual of Mental Disorders 4(th )edition (DSM-IV) and a measure of symptom severity. METHODS: 812 people living in Sarajevo or in Banja Luka in Bosnia-Herzegovina, of whom the majority had experienced a high number of traumatic war events, were administered the PTDS and other measures of trauma-related psychopathology. The psychometric properties of the instrument were assessed using Cronbach's alpha and principal components analysis, and its construct validity was assessed via Spearman correlation coefficients with the other instruments. RESULTS: The PTDS and its subscales demonstrated high internal consistency. The principal components revealed by an exploratory analysis are broadly consistent with the DSM-IV subscales except that they reproduce some previously reported difficulties with the "numbing" items from the avoidance subscale. The construct validity of the PTDS was supported by appropriate correlations with other relevant measures of trauma related psychopathology. CONCLUSION: The Bosnian version of the PTDS thus appears to be a time-economic and psychometrically sound measure for screening and assessing current PTSD. This self-report measure awaits further validation by interview methods

The effect on mental health of a large scale psychosocial intervention for survivors of mass violence: A quasi-experimental study in Rwanda

Background: War has serious and prolonged mental health consequences. It is argued that post-emergency mental health interventions should not only focus on psychological factors but also address the social environment. No controlled trials of such interventions exist. We studied the effect on mental health of a large scale p

Cognitive Behavioral Therapy versus Short Psychodynamic Supportive Psychotherapy in the outpatient treatment of depression: a randomized controlled trial

<p>Abstract</p> <p>Background</p> <p>Previous research has shown that Short Psychodynamic Supportive Psychotherapy (SPSP) is an effective alternative to pharmacotherapy and combined treatment (SPSP and pharmacotherapy) in the treatment of depressed outpatients. The question remains, however, how Short Psychodynamic Supportive Psychotherapy compares with other established psychotherapy methods. The present study compares Short Psychodynamic Supportive Psychotherapy to the evidence-based Cognitive Behavioral Therapy in terms of acceptability, feasibility, and efficacy in the outpatient treatment of depression. Moreover, this study aims to identify clinical predictors that can distinguish patients who may benefit from either of these treatments in particular. This article outlines the study protocol. The results of the study, which is being currently carried out, will be presented as soon as they are available.</p> <p>Methods/Design</p> <p>Adult outpatients with a main diagnosis of major depressive disorder or depressive disorder not otherwise specified according to DSM-IV criteria and mild to severe depressive symptoms (<it>Hamilton Depression Rating Scale </it>score ≥ 14) are randomly allocated to Short Psychodynamic Supportive Psychotherapy or Cognitive Behavioral Therapy. Both treatments are individual psychotherapies consisting of 16 sessions within 22 weeks. Assessments take place at baseline (week 0), during the treatment period (week 5 and 10) and at treatment termination (week 22). In addition, a follow-up assessment takes place one year after treatment start (week 52). Primary outcome measures are the number of patients refusing treatment (acceptability); the number of patients terminating treatment prematurely (feasibility); and the severity of depressive symptoms (efficacy) according to an independent rater, the clinician and the patient. Secondary outcome measures include general psychopathology, general psychotherapy outcome, pain, health-related quality of life, and cost-effectiveness. Clinical predictors of treatment outcome include demographic variables, psychiatric symptoms, cognitive and psychological patient characteristics and the quality of the therapeutic relationship.</p> <p>Discussion</p> <p>This study evaluates Short Psychodynamic Supportive Psychotherapy as a treatment for depressed outpatients by comparing it to the established evidence-based treatment Cognitive Behavioral Therapy. Specific strengths of this study include its strong external validity and the clinical relevance of its research aims. Limitations of the study are discussed.</p> <p>Trial registration</p> <p>Current Controlled Trails ISRCTN31263312</p

Control of actin polymerization via the coincidence of phosphoinositides and high membrane curvature

The conditional use of actin during clathrin-mediated endocytosis in mammalian cells suggests that the cell controls whether and how actin is used. Using a combination of biochemical reconstitution and mammalian cell culture, we elucidate a mechanism by which the coincidence of PI(4,5)P2 and PI(3)P in a curved vesicle triggers actin polymerization. At clathrin-coated pits, PI(3)P is produced by the INPP4A hydrolysis of PI(3,4)P2, and this is necessary for actin-driven endocytosis. Both Cdc42⋅guanosine triphosphate and SNX9 activate N-WASP–WIP- and Arp2/3-mediated actin nucleation. Membrane curvature, PI(4,5)P2, and PI(3)P signals are needed for SNX9 assembly via its PX–BAR domain, whereas signaling through Cdc42 is activated by PI(4,5)P2 alone. INPP4A activity is stimulated by high membrane curvature and synergizes with SNX9 BAR domain binding in a process we call curvature cascade amplification. We show that the SNX9-driven actin comets that arise on human disease–associated oculocerebrorenal syndrome of Lowe (OCRL) deficiencies are reduced by inhibiting PI(3)P production, suggesting PI(3)P kinase inhibitors as a therapeutic strategy in Lowe syndrome.J.L. Gallop is supported by a Wellcome Trust Research Career Development Fellowship (grant WT095829AIA). F.  Daste, A.  Walrant, J.R. Gadsby, and J. Mason are supported by an H2020 European Research Council Starting Grant (281971) awarded to J.L. Gallop. Gurdon Institute funding is provided by the Wellcome Trust (grant 092096) and Cancer Research UK (grant C6946/A14492). The Swedish Medical Research Council and the Swedish Foundation for Strategic Research supported the work of M.R. Holst and R. Lundmark. S.F. Lee is funded by a Royal Society University Research Fellowship (grant UF120277). M. Mettlen is funded by grant MH73125 to Sandra L. Schmid (University of Texas Southwestern Medical Center)

The Influence of Education and Socialization on Radicalization: An Exploration of Theoretical Presumptions and Empirical Research

Background and Objective: Research into radicalization does not pay much attention to education. This is remarkable and possibly misses an important influence on the process of radicalization. Therefore this article sets out to explore the relation between education on the one hand and the onset or prevention of radicalization on the other hand. Method: This article is a theoretical literature review. It has analyzed empirical studies-mainly from European countries-about the educational aims, content and style of Muslim parents and parents with (extreme) right-wing sympathies. Results: Research examining similarity in right-wing sympathies between parents and children yields mixed results, but studies among adolescents point to a significant concordance. Research also showed that authoritarian parenting may play a significant role. Similar research among Muslim families was not found. While raising children with distrust and an authoritarian style are prevalent, the impact on adolescents has not been investigated. The empirical literature we reviewed does not give sufficient evidence to conclude that democratic ideal in and an authoritative style of education are conducive to the development of a democratic attitude. Conclusion: There is a knowledge gap with regard to the influence of education on the onset or the prevention of radicalization. Schools and families are underappreciated sources of informal social control and social capital and therefore the gap should be closed. If there is a better understanding of the effect of education, policy as well as interventions can be developed to assist parents and teachers in preventing radicalization. © 2011 The Author(s)

SARS-CoV-2 infects the human kidney and drives fibrosis in kidney organoids

Kidney failure is frequently observed during and after COVID-19, but it remains elusive whether this is a direct effect of the virus. Here, we report that SARS-CoV-2 directly infects kidney cells and is associated with increased tubule-interstitial kidney fibrosis in patient autopsy samples. To study direct effects of the virus on the kidney independent of systemic effects of COVID-19, we infected human induced pluripotent stem cell-derived kidney organoids with SARS-CoV-2. Single cell RNA-sequencing indicated injury and dedifferentiation of infected cells with activation of pro-fibrotic signaling pathways. Importantly, SARS-CoV-2 infection also led to increased collagen 1 protein expression in organoids. A SARS-CoV-2 protease inhibitor was able to ameliorate the infection of kidney cells by SARS-CoV-2. Our results suggest that SARS-CoV-2 can directly infect kidney cells and induce cell injury with subsequent fibrosis. These data could explain both acute kidney injury in COVID-19 patients and the development of chronic kidney disease in Long-COVID