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71.
Maziar?Moradi-Lakeh Charbel?El Bcheraoui Marwa?Tuffaha Farah?Daoud Mohammad?Al Saeedi Mohammed?Basulaiman Ziad?A.?Memish Mohammad?A.?AlMazroa Abdullah?A.?Al Rabeeah Ali?H.?MokdadEmail author 《Journal of community health》2015,40(5):920-926
Self-rated health reflects a person’s integrated perception of health, including its biological, psychological, and social dimensions. It is a predictor of morbidity and mortality. To assess the current status of self-rated health and associated factors in the Kingdom of Saudi Arabia, we analyzed data from the Saudi Health Interview Survey. We conducted a large national survey of adults aged 15 years or older. A total of 10,735 participants completed a standardized health questionnaire. Respondents rated their health with a five-point scale. Data on socio-demographic characteristics, chronic diseases, health-related habits and behaviors, and anthropometric measurements were collected. Associated factors of self-rated health were analyzed using a backward elimination multivariate logistic regression model. More than 77 % of respondents rated their health as excellent/very good. Female sex [odds ratio (OR) 1.52, 95 % confidence interval (CI) 1.24–1.88], decades of age (OR 1.35, 95 % CI 1.25–1.46), diagnosed diabetes mellitus (OR 1.54, 95 % CI 1.22–1.93), diagnosed hypercholesterolemia (OR 1.37, 95 % CI 1.06–1.79), diagnosed hypertension (OR 1.55, 95 % CI 1.22–1.96), number of other diagnosed chronic diseases (OR 1.69, 95 % CI 1.41–2.03), limited vigorous activity (OR 3.59, 95 % CI 2.84–4.53), need for special equipment (OR 2.62, 95 % CI 1.96–3.51), and more than 3 h of daily television/computer screen time (OR 1.59, 95 % CI1.11–2.29) were positively associated with poor/fair health. Smoking, obesity, and physical inactivity were not associated with self-reported health. We found that preventable risk factors are not associated with Saudis’ self-rated health. This optimistic perception of health poses a challenge for preventive interventions in the Kingdom and calls for campaigns to educate the public about the harm of unhealthy behaviors. 相似文献
72.
Syed Ali Arsalan Naqvi Nasreen Badruddin Munsif Ali Jatoi Aamir Saeed Malik Wan Hazabbah Baharudin Abdullah 《Australasian physical & engineering sciences in medicine / supported by the Australasian College of Physical Scientists in Medicine and the Australasian Association of Physical Sciences in Medicine》2015,38(4):721-729
73.
P P Muldoon J Chen J L Harenza R A Abdullah L J Sim-Selley B F Cravatt M F Miles X Chen A H Lichtman M I Damaj 《British journal of pharmacology》2015,172(3):869-882
Background and Purpose
Abrupt discontinuation of nicotine, the main psychoactive component in tobacco, induces a withdrawal syndrome in nicotine-dependent animals, consisting of somatic and affective signs, avoidance of which contributes to drug maintenance. While blockade of fatty acid amide hydrolase, the primary catabolic enzyme of the endocannabinoid arachidonoylethanolamine (anandamide), exacerbates withdrawal responses in nicotine-dependent mice, the role of monoacylglycerol lipase (MAGL), the main hydrolytic enzyme of a second endocannabinoid 2-arachidonylglycerol (2-AG), in nicotine withdrawal remains unexplored.Experimental Approach
To evaluate the role of MAGL enzyme inhibition in nicotine withdrawal, we initially performed a genetic correlation approach using the BXD recombinant inbred mouse panel. We then assessed nicotine withdrawal intensity in the mouse after treatment with the selective MAGL inhibitor, JZL184, and after genetic deletion of the enzyme. Lastly, we assessed the association between genotypes and smoking withdrawal phenotypes in two human data sets.Key Results
BXD mice displayed significant positive correlations between basal MAGL mRNA expression and nicotine withdrawal responses, consistent with the idea that increased 2-AG brain levels may attenuate withdrawal responses. Strikingly, the MAGL inhibitor, JZL184, dose-dependently reduced somatic and aversive withdrawal signs, which was blocked by rimonabant, indicating a CB1 receptor-dependent mechanism. MAGL-knockout mice also showed attenuated nicotine withdrawal. Lastly, genetic analyses in humans revealed associations of the MAGL gene with smoking withdrawal in humans.Conclusions and Implications
Overall, our findings suggest that MAGL inhibition maybe a promising target for treatment of nicotine dependence. 相似文献74.
Kaptan Yagmur Suner Asli Taş Mehmet Nedim Oksel Fahrettin Aksu Kenan Sayiner Abdullah 《Clinical rheumatology》2021,40(9):3783-3788
Clinical Rheumatology - Although latent tuberculosis infection (LTBI) treatment is given before anti-tumor necrosis factor (TNF) treatment, tuberculosis (TB) still develops in these patients and... 相似文献
75.
Lee Michael H. Leda Mariela Buchan Tayler Malik Abdullah Rigobon Alanna Liu Helen Daza Julian F. O’Brien Kathleen Stein Madeleine Hing Nicholas Ng Fat Siemeiniuk Reed Sekercioglu Nigar Evaniew Nathan Foroutan Farid Ross Heather Alba Ana Carolina 《Heart failure reviews》2022,27(2):455-464
Heart Failure Reviews - Previous primary studies have explored the association between blood pressure (BP) and mortality in ambulatory heart failure (HF) patients reporting varying and contrasting... 相似文献
76.
Lipid abnormalities and renal disease: is dyslipidemia a predictor of progression of renal disease? 总被引:2,自引:0,他引:2
Crook ED Thallapureddy A Migdal S Flack JM Greene EL Salahudeen A Tucker JK Taylor HA 《The American journal of the medical sciences》2003,325(6):340-348
Dyslipidemia is a cardiovascular disease (CVD) risk factor that is associated with enhanced atherosclerosis and plaque instability. Renal insufficiency is associated with abnormalities in lipoprotein metabolism in both the early and the advanced stages of chronic renal failure. These include alterations in apolipoprotein A (apo A)- and B- containing lipoproteins, high-density lipoproteins, and triglycerides. In animal models, these alterations in lipid metabolism and action lead to macrophage activation and infiltration in the kidney with resultant tubulointerstitial and endothelial cell injury. Limited data in humans suggest that, in addition to contributing to CVD, dyslipidemia may be a risk factor for the progression of renal disease. The effects of dyslipidemia on the kidney are mainly observed in those with other risk factors for renal disease progression such as hypertension, diabetes, and proteinuria. Renal disease is a strong risk factor for CVD and African Americans have high rates of renal disease. Therefore, examining the effects of dyslipidemia on the development or progression or renal disease will be an important question for the Jackson Heart Study and is the topic of this review. 相似文献
77.
Infarction of prolactin-secreting or growth hormone-secreting pituitary adenomas is not unusual. However, Infarction of ACTH-secreting
adenomas has rarely been reported. Cyclical course of Cushing's syndrome alternating with adrenal insufficiency due to recurrent
infarction of an ACTH-secreting pituitary adenoma has not been reported. We report here a 20-year-old lady who presented with
florid signs of Cushing's syndrome but was found to have adrenal insufficiency on biochemical evaluation. Magnetic resonance
imaging (MRI) of the pituitary gland showed that she had infarction of an ACTH-secreting macroadenoma. Over the next 6 years,
her disease ran a cyclical course characterized by periods of hypercortisolism alternating with adrenal insufficiency due
to repeated episodes of infarctions of the ACTH-secreting pituitary macroadenoma with corresponding changes in the pituitary
adenoma on serial MRIs. The case alerts clinicians to this possibility when a patient presents with clinical picture of Cushing's
syndrome but has adrenal insufficiency on biochemical testing. It also suggests that silent or subclinical infarction of pituitary
adenomas is not uncommon and is probably under diagnosed. 相似文献
78.
激素敏感脂酶基因高度表达对泡沫细胞形成的作用 总被引:3,自引:0,他引:3
中国仓鼠卵细胞在给予β-VLDL后,细胞内蓄积胆固醇酯,形成泡沫样细胞。以腺病毒基因转移方法书激素敏感脂酶基因转染到中国仓鼠卵细胞中,得到了来自激素敏感脂酶的胆固醇酯水解活性高度表达,此时,β-VLDL导致的胆固醇酯蓄积作用被阻断,提示增加胆固醇酯水解可以防止泡沫细胞形成。 相似文献
79.
Adem Aydin Yavuz Selvi Lutfullah Besiroglu Murat Boysan Abdullah Atli Osman Ozdemir Sultan Kilic Ragıp Balaharoglu 《Journal of affective disorders》2013
It has been commonly recognized that circadian rhythm and sleep/wake cycle are causally involved in bipolar disorder. There has been a paucity of systematic research considering the relations between sleep and mood states in bipolar disorder. The current study examines the possible influences of sleep deprivation on mood states and endocrine functions among first-degree relatives of patients with bipolar disorder and healthy controls. Blood samples were taken at two time points in the consecutive mornings at predeprivation and postdeprivation periods. Participants simultaneously completed the Profiles of Mood States at two time points after giving blood samples. Plasma T3 and TSH levels increased after total sleep deprivation in both groups. Sleep deprivation induced TSH levels were reversely associated with depression–dejection among healthy controls. A paradoxical effect was detected for only the first-degree relatives of the patients that changes in plasma cortisol levels negatively linked to depression–dejection and anger–hostility scores after total sleep deprivation. Plasma DHEA levels became correlated with vigor-activity scores after sleep deprivation among first-degree relatives of bipolar patients. On the contrary, significant associations of depression–dejection, anger–hostility, and confusion–bewilderment with the baseline plasma DHEA levels became statistically trivial in the postdeprivation period. Findings suggested that first-degree relatives of patients with bipolar disorder had completely distinct characteristics with respect to sleep deprivation induced responses in terms of associations between endocrine functions and mood states as compared to individuals whose relatives had no psychiatric problems. Considering the relationships between endocrine functions and mood states among relatives of the patients, it appears like sleep deprivation changes the receptor sensitivity which probably plays a pivotal role on mood outcomes among the first-degree relatives of patients with bipolar disorder. 相似文献
80.
Kyu-Sun Lee Zhihao Wu Yan Song Siddhartha S. Mitra Abdullah H. Feroze Samuel H. Cheshier Bingwei Lu 《Genes & development》2013,27(24):2642-2647
The self-renewal versus differentiation choice of Drosophila and mammalian neural stem cells (NSCs) requires Notch (N) signaling. How N regulates NSC behavior is not well understood. Here we show that canonical N signaling cooperates with a noncanonical N signaling pathway to mediate N-directed NSC regulation. In the noncanonical pathway, N interacts with PTEN-induced kinase 1 (PINK1) to influence mitochondrial function, activating mechanistic target of rapamycin complex 2 (mTORC2)/AKT signaling. Importantly, attenuating noncanonical N signaling preferentially impaired the maintenance of Drosophila and human cancer stem cell-like tumor-forming cells. Our results emphasize the importance of mitochondria to N and NSC biology, with important implications for diseases associated with aberrant N signaling. 相似文献