scholarly journals Mechanisms of Change in Psychotherapy for People Diagnosed with Schizophrenia: The Role of Narrative Reflexivity in Promoting Recovery

2014 ◽  
Vol 20 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Melissa Greben ◽  
Robert D Schweitzer ◽  
Rebecca Bargenquast
Keyword(s):  
Therapeutic Change ◽  
Mechanisms Of Change ◽  
Coding System ◽  
Potential Mechanism ◽  
Limited Sample ◽  
Limited Sample Size ◽  
Dsm Iv ◽  
Recovery Assessment ◽  
Preliminary Support

Narrative reflexivity was investigated as a potential mechanism of therapeutic change during a 12–18 month trial of Metacognitive Narrative Psychotherapy for people diagnosed with schizophrenia. Participants were nine adult clients (8 male, 1 female) aged between 25–65 years (M = 44, SD = 12.76) with a diagnosis of schizophrenia consistent with DSM-IV criteria and seven female provisional psychologists aged between 25–29 years (M = 26.8 years, SD = 1.47 years). Recovery and narrative reflexivity were measured at three time points using the Recovery Assessment Scale (RAS) and the Narrative Processes Coding System (NPCS). Results were reported descriptively due to limited sample size (n = 9). The majority of clients (n = 7) reported an increase in recovery over the course of treatment. For six clients, an overall increase in recovery was associated with an increase in narrative reflexivity. This study provides preliminary support for narrative reflexivity as a potential mechanism of therapeutic change in the psychotherapy of people diagnosed with schizophrenia.

scholarly journals Contribution of Four Polymorphisms in Renin-Angiotensin-Aldosterone-Related Genes to Hypertension in a Thai Population

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Pimphen Charoen ◽  
Jakris Eu-ahsunthornwattana ◽  
Nisakron Thongmung ◽  
Pedro A. Jose ◽  
Piyamitr Sritara ◽  
...  
Keyword(s):  
Statistical Power ◽  
Angiotensin Ii Receptor ◽  
Multivariate Logistic Regression ◽  
Limited Sample ◽  
Thai Population ◽  
Limited Sample Size ◽  
Renin Angiotensin ◽  
Entire Distribution

Introduction. The roles of genes in the renin-angiotensin-aldosterone system (RAAS) in hypertension, including angiotensin-converting enzyme (ACE), angiotensinogen (AGT), angiotensin II receptor type 1 (AGTR1), and aldosterone synthase (CYP11B2), have been widely studied across different ethnicities, but there has been no such investigation in Thai population. Materials and Methods. Using 4,150 Thais recorded in the Electricity Generating Authority of Thailand (EGAT) study, we examined the association of rs1799752, rs699, rs5186, and rs1799998 located in or near ACE, AGT, AGTR1, and CYP11B2 genes in hypertension. We investigated their roles in hypertension using multivariate logistic regression and further examined their roles in blood pressure (BP) using quantile regression. Sex, age, and BMI were adjusted as potential confounders. Results. We did not observe associations between hypertension and rs1799752 (P=0.422), rs699 (P=0.36), rs5186 (P=0.49), and rs1799998 (P=0.71). No evidence of association between these SNPs and BP was found across an entire distribution. A nonlinear relationship between age and BP was observed. Conclusion. In Thai population, our study showed no evidence of association between RAAS-related genes and hypertension. While our study is the first and largest study to investigate the role of RAAS-related genes in hypertension in Thai population, restricted statistical power due to limited sample size is a limitation.

scholarly journals Acupuncture for Primary Dysmenorrhea: A Potential Mechanism from an Anti-Inflammatory Perspective

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Wen-Yan Yu ◽  
Liang-Xiao Ma ◽  
Zhou Zhang ◽  
Jie-Dan Mu ◽  
Tian-Yi Sun ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Animal Studies ◽  
Visceral Pain ◽  
Self Healing ◽  
Primary Dysmenorrhea ◽  
Potential Mechanism ◽  
Future Studies ◽  
Anti Inflammatory ◽  
Proinflammatory Factors

The low adverse effects of acupuncture for primary dysmenorrhea (PD), known as one of the most commonly reported gynecological debilitating conditions affecting women’s overall health, have been thus far confirmed. Moreover, it has been increasingly recognized that inflammation is involved in such menstrual cramps, and recent studies have further shown that the anti-inflammatory effects of acupuncture are helpful in its control. This review portrays the role of inflammation in PD pathophysiology, provides evidence from clinical and animal studies on acupuncture for inflammation-induced visceral pain, and reflects on acupuncture-related therapies for dysmenorrhea with regard to their anti-inflammatory characteristics. Further research accordingly needs to be carried out to clarify the effects of acupuncture on proinflammatory factors in PD, particularly chemokines and leukocytes. Future studies on this condition from an anti-inflammatory perspective should be also performed in line with the notion of emphasizing stimulation modes to optimize the clinical modalities of acupuncture. Additionally, the effects and mechanism of more convenient self-healing approaches such as TENS/TEAS for PD should be investigated.

scholarly journals A Triple Threat? The Role of Diet, Nutrition, and the Microbiota in T1D Pathogenesis

2021 ◽  
Vol 8 ◽  
Author(s):  
Emma E. Hamilton-Williams ◽  
Graciela L. Lorca ◽  
Jill M. Norris ◽  
Jessica L. Dunne
Keyword(s):  
Beta Cell ◽  
Intestinal Microbiota ◽  
Beta Cell Function ◽  
Cell Function ◽  
The Body ◽  
Islet Autoimmunity ◽  
Potential Mechanism ◽  
Modifiable Factors ◽  
And Function

In recent years the role of the intestinal microbiota in health and disease has come to the forefront of medical research. Alterations in the intestinal microbiota and several of its features have been linked to numerous diseases, including type 1 diabetes (T1D). To date, studies in animal models of T1D, as well as studies in human subjects, have linked several intestinal microbiota alterations with T1D pathogenesis. Features that are most often linked with T1D pathogenesis include decreased microbial diversity, the relative abundance of specific strains of individual microbes, and altered metabolite production. Alterations in these features as well as others have provided insight into T1D pathogenesis and shed light on the potential mechanism by which the microbiota plays a role in T1D pathogenesis, yet the underlying factors leading to these alterations remains unknown. One potential mechanism for alteration of the microbiota is through diet and nutrition. Previous studies have shown associations of diet with islet autoimmunity, but a direct contributing factor has yet to be identified. Diet, through introduction of antigens and alteration of the composition and function of the microbiota, may elicit the immune system to produce autoreactive responses that result in the destruction of the beta cells. Here, we review the evidence associating diet induced changes in the intestinal microbiota and their contribution to T1D pathogenesis. We further provide a roadmap for determining the effect of diet and other modifiable factors on the entire microbiota ecosystem, including its impact on both immune and beta cell function, as it relates to T1D. A greater understanding of the complex interactions between the intestinal microbiota and several interacting systems in the body (immune, intestinal integrity and function, metabolism, beta cell function, etc.) may provide scientifically rational approaches to prevent development of T1D and other childhood immune and allergic diseases and biomarkers to evaluate the efficacy of interventions.

Schizoaffective disorder and life events

2017 ◽  
Vol 41 (S1) ◽  
pp. s845-s845
Author(s):  
B. walid ◽  
I. Marrag ◽  
F. Ellouze ◽  
A. Dekhil ◽  
M. Nasr
Keyword(s):  
Life Events ◽  
Schizoaffective Disorder ◽  
Age At Onset ◽  
Dsm Iv ◽  
The Mean ◽  
Competing Interest ◽  
New Perspective ◽  
Emotional Events ◽  
Psychiatric Department

IntroductionThe schizoaffective disorder is multifactorial. Several factors almost unquestioned, even indisputable, participate in the episodes’ decompensation and affect various fields: biological, pharmacological or neurobiochemical.ObjectivesDraw up the sociodemographic and clinical profile of patients treated for schizoaffective disorder and determine the role of life events in the onset of the disorder.MethodsThis is a retrospective study of 52 patients hospitalized in the psychiatric department of Mahdia diagnosed with schizoaffective disorder according to DSM-IV-TR during the period from January 2014 until June 2014. The information was collected using a preset sheet with 35 items.ResultsA total of 52 records was gathered. The average age was 38 years. The sample was predominantly male, of rural origin in 61.5% of cases. The level of education was low in 59.6% of cases. More than half were without profession and single in 46.2% of cases. The mean age at onset of the disorder was 25.2 years. The presence of life events preceding the onset of the disorder was noted in 22 patients, that to say, 42.3% of the sample. Family and emotional events were most frequently encountered with respective rates of 48.2 and 24.7%, followed by the professional events (20%) and social ones (6%).ConclusionLife events are due to chance but also to the environment. The complexity of the “event” concept was again underlined in a new perspective, breaking social rhythms.Disclosure of interestThe authors have not supplied their declaration of competing interest.

The role of oxidative stress in the cardiovascular actions of particulate air pollution

2014 ◽  
Vol 42 (4) ◽  
pp. 1006-1011 ◽  
Author(s):  
Mark R. Miller
Keyword(s):  
Oxidative Stress ◽  
Air Pollution ◽  
Diesel Exhaust ◽  
Vascular Function ◽  
Cardiovascular Effects ◽  
Increase Blood Pressure ◽  
Potential Mechanism ◽  
Particulate Air Pollution ◽  
Cardiovascular Actions

Air pollution has been estimated to be responsible for several millions of deaths worldwide per year, the majority of which have been attributed to cardiovascular causes. The particulate matter in air pollution has been shown impair vascular function, increase blood pressure, promote thrombosis and impair fibrinolysis, accelerate the development of atherosclerosis, increase the extent of myocardial ischaemia, and increase susceptibility to myocardial infarction. The pathways underlying these effects are complex and poorly understood; however, particulate-induced oxidative stress repeatedly emerges as a potential mechanism in all of these detrimental cardiovascular actions. The present mini-review will use diesel exhaust as an example of a pollutant rich in combustion-derived nanoparticles, to describe the potential by which oxidative stress could drive the cardiovascular effects of air pollution.

scholarly journals AP-1 elements and TCL1 protein regulate expression of the gene encoding protein tyrosine phosphatase PTPROt in leukemia

Blood ◽  
2011 ◽  
Vol 118 (23) ◽  
pp. 6132-6140 ◽  
Author(s):  
Tasneem Motiwala ◽  
Nicola Zanesi ◽  
Jharna Datta ◽  
Satavisha Roy ◽  
Huban Kutay ◽  
...  
Keyword(s):  
Protein Tyrosine Phosphatase ◽  
Tyrosine Phosphatase ◽  
Lymphocytic Leukemia ◽  
Potential Mechanism ◽  
Wild Type ◽  
Truncated Form ◽  
Gene Encoding ◽  
Protein Tyrosine ◽  
Encoding Protein

Abstract We previously demonstrated that the gene encoding PTPROt, the truncated form of protein tyrosine phosphatase receptor type O expressed predominantly in hematopoietic cells, is a candidate tumor suppressor and is down-regulated in chronic lymphocytic leukemia (CLL). Here, we show that PTPROt expression is significantly reduced in CD19+ spleen B cells from Eμ-T cell leukemia 1 (TCL1) transgenic mice relative to the wild-type mice. Strikingly, as much as a 60% decrease in PTPROt expression occurs at 7 weeks independently of promoter methylation. To elucidate the potential mechanism for this early suppression of PTPROt in these mice, we explored the role of activating protein-1 (AP-1) in its expression. We first demonstrate that AP-1 activation by 12-O-tetradecanoylphorbol-13-acetate induces PTPROt expression with concurrent recruitment of c-fos and c-jun to its promoter. The PTPROt promoter is also responsive to over- and underexpression of AP-1, confirming the role of AP-1 in PTPROt expression. Next, we demonstrate that TCL1 can repress the PTPROt promoter by altering c-fos expression and c-jun activation state. Finally, using primary CLL cells we have shown an inverse relationship between TCL1 and PTPROt expression. These findings further substantiate the role of TCL1 in PTPROt suppression and its importance in the pathogenesis of CLL.

scholarly journals Garcinoic Acid Improves Cardiac Function and Enhances Angiogenesis Following Myocardial Infarction

2021 ◽  
Author(s):  
Hongyao Hu ◽  
Wei Li ◽  
Yanzhao Wei ◽  
Hui Zhao ◽  
Zhenzhong Wu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Function ◽  
Ventricular Remodeling ◽  
Vehicle Group ◽  
Potential Mechanism ◽  
Garcinia Kola ◽  
Angiogenic Proteins

Abstract Cardiac ischemia impairs angiogenesis in response to hypoxia, resulting in ventricular remodeling. Garcinoic acid (GA), the extraction from the plant garcinia kola, is validated to attenuate inflammatory response. However, the role of GA in heart failure (HF) and neovascularization after myocardial infarction (MI) is incompletely understood. The present study is striving to explore the role of GA and the potential mechanism of which in cardiac function after MI. SD rats were randomized into sham group, MI+vehicle group, and MI+GA group in vivo. Human umbilical endothelial cells (HUVECs) were cultured in vehicle or GA, and then additionally exposed to 2% hypoxia environment in vitro. MI rats displayed a dramatically reduced myocardial injury, cardiac function and vessel density in the peri-infarcted areas. GA delivery markedly improved cardiac performance and promoted angiogenesis. In addition, GA significantly enhanced tube formation in HUVECs under hypoxia condition. Furthermore, the expressions of pro-angiogenic factors HIF-1α, VEGF-A and bFGF, and pro-angiogenic proteins phospho-VEGFR2Tyr1175 and VEGFR2, as well as phosphorylation levels of Akt and eNOS were increased by GA treatment. In conclusion, GA preserved cardiac function after MI probably via promoting neovascularization. And the potential mechanism may be partially through upregulating the expressions of HIF-1α, VEGF-A, bFGF, phospho-VEGFR2Tyr1175 and VEGFR2 and activating the phosphorylations of Akt and eNOS.

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