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Статті в журналах з теми "Hypercholesteremia"

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Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 28 лютого 2023

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1

Visavadiya, Nishant P., and A. V. R. L. Narasimhacharya. "AsparagusRoot Regulates Cholesterol Metabolism and Improves Antioxidant Status in Hypercholesteremic Rats." Evidence-Based Complementary and Alternative Medicine 6, no. 2 (2009): 219–26. http://dx.doi.org/10.1093/ecam/nem091.

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Hyperlipidemia/hypercholesteremia are major risk factors for atherosclerosis and cardiovascular diseases. Root ofAsparagus racemosus(AR) is widely used in Ayurvedic system of medicine in India and is known for its steroidal saponin content. This study was designed to investigate the hypocholesteremic and antioxidant potential of AR root in both normo- and hypercholesteremic animals. Normal and hypercholesteremic male albino rats were administered with root powder of AR (5 and 10 g% dose levels) along with normal and hypercholesteremic diets, respectively, for a duration of 4 weeks. Plasma and hepatic lipid profiles, fecal sterol, bile acid excretion and hepatic antioxidant activity were assessed. Inclusion of AR root powder in diet, resulted in a dose-dependant reduction in plasma and hepatic lipid profiles, increased fecal excretion of cholesterol, neutral sterol and bile acid along with increases in hepatic HMG-CoA reductase activity and bile acid content in hypercholesteremic rats. Further, AR root also improved the hepatic antioxidant status (catalase, SOD and ascorbic acid levels). No significant changes in lipid and antioxidant profiles occurred in the normocholesteremic rats administered with AR root powder. AR root appeared to be useful as a dietary supplement that offers a protection against hyperlipidemia/hypercholesteremia in hypercholesteremic animals. The results of the present study indicate that the potent therapeutic phyto-components present in AR root i.e. phytosterols, saponins, polyphenols, flavonoids and ascorbic acid, could be responsible for increased bile acid production, elimination of excess cholesterol and elevation of hepatic antioxidant status in hypercholesteremic conditions.

2

Kamalova, Aelita A. "Diet Therapy in Children with Hypercholesteremia." Current Pediatrics 19, no. 4 (September 19, 2020): 309–15. http://dx.doi.org/10.15690/vsp.v19i4.2140.

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3

Dietrich, Hans H. "Apolipoprotein E in Hypercholesteremia and Beyond." Stroke 38, no. 7 (July 2007): 2036. http://dx.doi.org/10.1161/strokeaha.107.489856.

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4

LEWIS, S. "P514 Hypercholesteremia induces baroreceptro reflex dysfunction." European Heart Journal 24, no. 5 (March 2003): 81. http://dx.doi.org/10.1016/s0195-668x(03)93952-2.

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5

NAKAI, TSUGUHIKO. "Familial hypercholesteremia complicated by nephrotic syndrome." Nihon Naika Gakkai Zasshi 79, no. 8 (1990): 1079–80. http://dx.doi.org/10.2169/naika.79.1079.

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6

HURLEY, D. "Hypercholesteremia induces enhanced circulating inflammatory activity." American Journal of Hypertension 17, no. 5 (May 2004): S242. http://dx.doi.org/10.1016/j.amjhyper.2004.03.648.

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7

Li, Nan F., Hong M. Wang, Jin Yang, Ling Zhou, Xiao G. Yao, and Jing Hong. "Serum uric acid is associated with metabolic risk factors for cardiovascular disease in the Uygur population." Applied Physiology, Nutrition, and Metabolism 34, no. 6 (December 2009): 1032–39. http://dx.doi.org/10.1139/h09-101.

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The prevalence of hyperuricemia is low in Uygurs, who have a high prevalence of cardiovascular risk factors such as hypertension, overweight–obesity, dyslipidemia, hyperglycemia, and insulin resistance (IR). This study sought to investigate the relationships between serum uric acid (UA) and these risk factors in this population. A cross-sectional study was conducted in Uygurs (859 males, 1268 females) aged 20 to 70 years. Demographic data, systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), and fasting and postprandial blood were obtained, and biological measurements were determined. The mean of BMI, SBP, DBP, total cholesterol, high-density lipoprotein cholesterol (HDL-c), low-density lipoprotein cholesterol (LDL-c), triglycerides, fasting blood glucose, fasting insulin, and homeostasis model assessment insulin resistance index (HOMA-IR), and the prevalence of hypertension, IR, hyperglycemia, overweight–obesity, hypercholesteremia, hyper-LDL-c, and hypertriglyceridemia increased with UA but the prevalence of hypo-HDL-c decreased (p < 0.05). Logistic regression analysis showed that the odds ratios for IR, overweight–obesity, hypercholesteremia, hyper-LDL-c, and hypertriglyceridemia against the lowest UA group increased but decreased for hypo-HDL-c (p < 0.05). The UA in the hypo-HDL-c group was lower than that of the controls; the prevalence of hypo-HDL-c in hyperuricemia subjects was lower than in those with normal UA (p < 0.05). But the opposite results were observed between overweight–obesity, hyperglycemia, IR, hypercholesteremia, hypertriglyceridemia, and hyper-LDL-c and correspondence controls, respectively (p < 0.05). In Uygur, elevated UA is associated with overweight–obesity, hypercholesteremia, hyper-LDL-c, hypertriglyceridemia, hyperglycemia, and IR. The HDL-c level significantly increases with UA, whereas the prevalence of hypo-HDL-c decreases. Further studies are needed to clarify why UA is positively correlated to HDL-c.

8

Nichols, E. H., and M. R. Jaff. "Hypercholesteremia, Hypertension, and Antiplatelet Therapy in PAD." MD Conference Express 13, no. 19 (December 1, 2013): 31. http://dx.doi.org/10.1177/155989771319015.

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9

Kumawat, Vinod Bihari, Surendra Kumar Sharma, Uttam Kumar Sharma, and Sudhir Sharma. "Effect of trikatu compound in hypercholesteremia- a clinical study." Environment Conservation Journal 16, no. 1&2 (June 12, 2015): 57–61. http://dx.doi.org/10.36953/ecj.2015.161209.

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10

Tokura, T. "Changes in Bruch's Membrane in Experimental Hypercholesteremia in Rats." Japanese Journal of Ophthalmology 43, no. 4 (July 8, 1999): 337–38. http://dx.doi.org/10.1016/s0021-5155(99)00055-6.

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11

BARTON, M. "Hypercholesteremia induces cardiac concentric remodeling in the guinea pig." American Journal of Hypertension 17, no. 5 (May 2004): S165—S166. http://dx.doi.org/10.1016/j.amjhyper.2004.03.434.

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12

Elbadawi, Ayman, Islam Y. Elgendy, Mohamed Omer, Mohamed Abdelazeem, Vijay Nambi, Chayakrit Krittanawong, Ravi S. Hira, Jacqueline Tamis-Holland, Christie Ballantyne, and Hani Jneid. "Outcomes of Acute Myocardial Infarction in Patients with Familial Hypercholesteremia." American Journal of Medicine 134, no. 8 (August 2021): 992–1001. http://dx.doi.org/10.1016/j.amjmed.2021.03.013.

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13

Yu, Lianlong, Qianrang Zhu, Yuqian Li, Pengkun Song, and Jian Zhang. "Dietary Branched-Chain Amino Acids (BCAAs) and Risk of Dyslipidemia in a Chinese Population." Nutrients 14, no. 9 (April 27, 2022): 1824. http://dx.doi.org/10.3390/nu14091824.

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This study aimed to explore the association between dietary BCAAs, blood lipid levels and risk of dyslipidemia. In this case–control study, a total of 9541 subjects with normal blood lipids were included as a control group, and 9792 patients with dyslipidemia were included as a case group. Dietary BCAA intake data were measured using 3-day 24 h meal recalls and household condiment weighing. All samples were from China Nutrition and Health Surveillance (2015). Generalized linear model, logistic regression, and restricted cubic spline (RCS) were used to evaluate the relationship between dietary BCAAs, blood lipids and dyslipidemia. After adjusting for confounding factors, dietary BCAAs were positively correlated with TC and LDL-C (p < 0.05). Higher dietary BCAAs were associated with higher OR for Hypercholesteremia (Q4 vs. Q1, OR = 1.29, 95% CI: 1.05–1.58, p-trend = 0.034). The ORs of Hyper-LDL-cholesterolemia showed inverted U-shaped with increasing dietary BCAAs (Q3 vs. Q1, OR = 1.20, 95% CI: 1.03–1.39; Q2 vs. Q1, OR = 1.05, 95% CI: 1.01–1.31). The relationship between dietary BCAAs and the risk of Hypercholesteremia and Hyper-LDL-cholesterolemia were both nonlinear (p nonlinearity = 0.0059, 0.0198). Our study reveals that dietary BCAAs are associated with specific types of lipids and risk of dyslipidemia, some of which may be non-linear.

14

Nagaraj, Lavanya, and Naveen Kumar Madalageri. "A comparative study of metabolic side effects of risperidone and olanzapine in the treatment of schizophrenia." International Journal of Basic & Clinical Pharmacology 8, no. 11 (October 22, 2019): 2561. http://dx.doi.org/10.18203/2319-2003.ijbcp20194803.

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ABSTRACTBackground: Schizophrenia is one of most serious chronic psychiatric disorder, which affects about 1% of population. Treatment of schizophrenia comprises of typical antipsychotics and or atypical antipsychotics. Typical antipsychotics like haloperidol have extrapyramidal side effects which limit their use in chronic cases. Atypical antipsychotics though have better treatment response, they have metabolic side effects like hypercholesteremia, hypertriglyceridemia and hyperglycaemia. As there is paucity of data in Indian population the present study has been taken up to compare the metabolic side effects of risperidone and olanzapine in the treatment of schizophrenic patients in a tertiary care hospital.Methods: It was a comparative study conducted on 60 patients of Schizophrenia for one year in a tertiary care hospital. The study subjects were randomly assigned into 2 groups of 30 patients each, where group 1 were treated with atypical antipsychotic drug risperidone and group 2 with Olanzapine and both groups received the treatment for one year. Metabolic side effects like hypercholesteremia, hypertriglyceridemia and hyperglycaemia were evaluated and compared over a period of one year.Results: Both risperidone and olanzapine were associated with comparable baseline to endpoint increase in metabolic side effects. However, risperidone treated subjects had significantly less metabolic side effects compared to olanzapine.Conclusions: Apart from total cholesterol and triglycerides, other metabolic side effects were less in risperidone treated patients than olanzapine treated patients.

15

Koo, Hui Chin, Lay Kim Tan, Geok Pei Lim, Chee Cheong Kee, and Mohd Azahadi Omar. "Obesity and Its Association with Undiagnosed Diabetes Mellitus, High Blood Pressure and Hypercholesterolemia in the Malaysian Adult Population: A National Cross-Sectional Study Using NHMS Data." International Journal of Environmental Research and Public Health 20, no. 4 (February 9, 2023): 3058. http://dx.doi.org/10.3390/ijerph20043058.

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This study aimed to report the prevalence of obesity, classified using Asian cut-off, and its relationships with undiagnosed diabetes mellitus, high blood pressure, and hypercholesteremia. We analyzed the nationally representative data from 14,025 Malaysian adults who participated in the NHMS 2015. The relationship between obesity and undiagnosed diabetes mellitus, high blood pressure, and hypercholesteremia was determined using multivariable logistic regressions, and lifestyle risk factors and sociodemographic characteristics were adjusted. The undiagnosed high blood pressure group showed the highest proportionate of overweight/obese (80.0%, 95% CI: 78.1–81.8) and central obesity (61.8%, 95% CI: 59.3–64.2). Inverse association was observed between underweight with undiagnosed high blood pressure (aOR: 0.40, 95% CI: 0.26–0.61) and hypercholesterolemia (aOR: 0.75, 95% CI: 0.59–0.95) groups. In contrast, positive relationships were shown between overweight/obese and risk of undiagnosed diabetes mellitus (aOR: 1.65, 95% CI: 1.31–2.07), high blood pressure (aOR: 3.08, 95% CI: 2.60–3.63), and hypercholesterolemia (aOR: 1.37, 95% CI: 1.22–1.53). Likewise, central obesity was positively associated with a risk of undiagnosed diabetes mellitus (aOR: 1.40, 95% CI: 1.17–1.67), high blood pressure (aOR: 2.83, 95% CI: 2.45–3.26), and hypercholesterolemia (aOR: 1.26, 95% CI: 1.12–1.42). Our findings indicated the importance of periodical health examinations to assess the risk of non-communicable diseases among the general and abdominal obese Malaysian adults.

16

Didia, S. Claudia. "PCSK9-Inhibitors: A Review of a Novel Approach in Hypercholesteremia Management." Medical Science Review 1 (2014): 1–6. http://dx.doi.org/10.12659/msrev.890836.

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17

Verma, Isha, Antonio Fernandez, and Paul Thompson. "FAMILIAL HYPERCHOLESTEREMIA: WHEN STATINS, EZETIMIBE & PCSK9 INHIBITORS ARE NOT ENOUGH." Journal of the American College of Cardiology 71, no. 11 (March 2018): A2439. http://dx.doi.org/10.1016/s0735-1097(18)32980-2.

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18

Verma, Isha, Paul D. Thompson, and Antonio B. Fernandez. "Familial Hypercholesteremia: When Statins, Ezetimibe & PCSK9 Inhibitors Are Not Enough." Journal of Clinical Lipidology 12, no. 2 (March 2018): 545. http://dx.doi.org/10.1016/j.jacl.2018.03.043.

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19

Valentine, V. G., L. Seoane, D. M. Fuchs, S. G. LaPlace, G. A. Lombard, and D. E. Taylor. "Potential benefits of treating hypercholesteremia and hypertension in lung allograft recipients." Journal of Heart and Lung Transplantation 24, no. 2 (February 2005): S170. http://dx.doi.org/10.1016/j.healun.2004.12.105.

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20

MUNDAY, J. "Hypercholesteremia-induced changes in left ventricular geometry in the guinea pig." American Journal of Hypertension 17, no. 5 (May 2004): S168. http://dx.doi.org/10.1016/j.amjhyper.2004.03.441.

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21

Fan, Jing, Caicui Ding, Weiyan Gong, Fan Yuan, Yanning Ma, Ganyu Feng, Chao Song, and Ailing Liu. "The Relationship between Leisure-Time Sedentary Behaviors and Metabolic Risks in Middle-Aged Chinese Women." International Journal of Environmental Research and Public Health 17, no. 19 (September 30, 2020): 7171. http://dx.doi.org/10.3390/ijerph17197171.

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The prevalence of metabolic diseases has increased over the past few decades, and epidemiological studies suggest that metabolic diseases may be associated with lifestyle. The purpose of the present study was to investigate the relationship between leisure-time sedentary behaviors (LTSBs) and metabolic risks in middle-aged women in China. Data came from the China National Nutrition and Health Surveillance (CNNHS) in 2010–2012. A total of 2643 women aged 46 to 53 years were involved. Multiple linear regression was used to examine the association of leisure-time sedentary duration (LTSD) with total cholesterol (TC), triglyceride (TG), waist circumference (WC), and body mass index (BMI). Restrictive cubic splines (RCS) were used to plot the curves between LTSD and the risk of metabolic diseases. Region, education, income, alcohol consumption, exercise, daily energy intake, and fat energy ratio were adjusted for all models. After adjusting for potential influencing factors, the results of multiple linear regression showed that for each additional hour increase in LTSD, TC and TG increased by 0.03 mmol/L and 0.04 mmol/L, respectively. The results of RCS curves showed that the risks of MetS (p for trend = 0.0276), obesity (p for trend = 0.0369), hypertension (p for trend = 0.0062), and hypercholesteremia (p for trend = 0.0033) increased with the increase in LTSD. LTSB was associated with the risks of MetS, obesity, hypertension, and hypercholesteremia in middle-aged women. Reducing LTSD may be an effective way of preventing metabolic diseases in middle-aged women.

22

Zhang, Haoqiang, Rong Huang, Sai Tian, Ke An, Wenwen Zhu, Jijing Shi, Wuyou Cao, and Shaohua Wang. "The CC Genotype of Insulin-Induced Gene 2 rs7566605 Is a Protective Factor of Hypercholesteremia Susceptible to Mild Cognitive Impairment, Especially to the Executive Function of Patients with Type 2 Diabetes Mellitus." BioMed Research International 2020 (June 10, 2020): 1–7. http://dx.doi.org/10.1155/2020/4935831.

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Backgrounds and Aims. Insulin-induced gene 2 (INSIG-2) is closely related to hypercholesteremia, which is a well-recognized risk factor of mild cognitive impairment (MCI) in type 2 diabetes mellitus (T2DM). We aim to investigate the association between promoter of the INSIG-2 rs7566605 single-nucleotide polymorphism (SNP) and T2DM with MCI. Methods. 233 T2DM patients with MCI or without MCI were recruited. Baseline data and genotype frequency were compared between MCI and non-MCI groups. Demographic parameters and neuropsychological tests results were analyzed among patients with different genotypes. Further correlation and regression analysis were conducted to find the association between cognition and cholesterol. Results. Despite no significant statistical difference was detected, we observed higher levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) in patients with MCI than those without MCI. In addition, we observed higher TC and LDL levels in patients with GG or GC genotypes than those with CC genotype (P<0.001, P=0.004, or P<0.001, P=0.002). Interestingly, increased MoCA and decreased TMTB scores were found in patients with CC genotype, compared to those with GG or CG genotype (P=0.009, P=0.024, or P=0.005, P=0.109). Moreover, partial correlation (P=0.030 and P=0.004, respectively) and multiple linear regression (P=0.030 and P=0.005, respectively) showed that TC and LDL levels are associated with the TMTB score, indicating the executive function. Conclusions. CC genotype of INSIG-2 rs7566605 may be a protective factor of hypercholesteremia susceptible to MCI, especially to the executive function of T2DM. This trial is registered with ChiCTROCC15006060.

23

Jha, Niharika, and Vanya Narayan. "Multiple giant tuberous xanthomas with type IIa hypercholesteremia in a young male." Indian Journal of Dermatopathology and Diagnostic Dermatology 7, no. 1 (2020): 38. http://dx.doi.org/10.4103/ijdpdd.ijdpdd_40_20.

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24

Miyayama, Takeshi, Shin-ichiro Miura, Tomo Komaki, Takashi Kuwano, Joji Morii, Hiroaki Nishikawa, and Keijiro Saku. "Acute Myocardial Infarction in a 26-Year-Old Patient With Familial Hypercholesteremia." Journal of Clinical Medicine Research 8, no. 7 (2016): 562–65. http://dx.doi.org/10.14740/jocmr2596w.

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25

Yakimenko, O., and Ie Maznichenko. "COMPLEX HYPOLIPIDEMIC THERAPY OF PATIENTS WITH NON-ALCOHOLIC STEATOHEPATITIS AND FAMILIAL HYPERCHOLESTEREMIA." Bulletin of Problems Biology and Medicine 1, no. 2 (2019): 207. http://dx.doi.org/10.29254/2077-4214-2019-1-2-149-207-211.

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26

Hyvärinen, Lea. "FLUORESCENCE CINEANGIOGRAPHIC AND HISTOLOGICAL STUDIES ON THE RABBIT EYE DURING EXPERIMENTAL HYPERCHOLESTEREMIA." Acta Ophthalmologica 46, no. 1 (May 27, 2009): 57–70. http://dx.doi.org/10.1111/j.1755-3768.1968.tb02495.x.

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27

Harper, Claudia, Radhika Seimon, Brendon Yee, Amanda Sainsbury, and Elizabeth Cayanan. "Translating Evidence into Practice: A Case Study of Extended Use of a Very Low Energy Diet for Treatment of Co-Morbid Obesity and Chronic Disease." Recent Progress in Nutrition 2, no. 2 (February 21, 2022): 1. http://dx.doi.org/10.21926/rpn.2202015.

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We report the case of a 30-year-old male with significant obesity (body mass index 47 kg/m2) with co-existing moderate obstructive sleep apnoea, hypertension, hypercholesteremia and hypogonadotropic hypogonadism, who was treated with a very-low-energy diet (VLED) and lifestyle modification programme for 12 months. The patient lost weight throughout the entire treatment period (average weight loss was 2.1 kg/week, for a total of 42.7 kg), and showed marked improvement in co-morbidities and no adverse effects. This case demonstrates that prolonged (5-month) use of a VLED, under close medical supervision, is safe and effective in certain patients with obesity.

28

Barrios, Vivencio, and Carlos Escobar. "Fixed-dose combination of rosuvastatin and ezetimibe: treating hypercholesteremia according to cardiovascular risk." Expert Review of Clinical Pharmacology 14, no. 7 (May 24, 2021): 793–806. http://dx.doi.org/10.1080/17512433.2021.1925539.

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29

Godal, H. C., J. C. Lund, and E. Sivertssen. "LIPIDS AND LIPOPROTEINS IN SERUM IN CASES OF FAMILIAL ESSENTIAL HYPERCHOLESTEREMIA AND XANTHOMATOSIS." Acta Medica Scandinavica 156, S319 (April 24, 2009): 125–34. http://dx.doi.org/10.1111/j.0954-6820.1956.tb06306.x.

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30

Li, Zhi-Zhao, Qiong Huang, Xiao-li Yang, Jieqiong Zeng, QI-Hui Wang, Hai-Ming Tang, Zhen-qiu Yu, Yu-Qing Song, and Yang Liu. "Cholesterol Metabolic Markers for Differential Evaluation of Patients with Hyperlipidemia and Familial Hypercholesterolemia." Disease Markers 2022 (April 21, 2022): 1–9. http://dx.doi.org/10.1155/2022/2008556.

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The cholesterol metabolism in humans can be indirectly reflected by measuring cholesterol metabolism marker levels. We aimed to investigate the association of cholesterol homeostasis markers on standard lipid profiling components in familial hypercholesteremia and hyperlipidemia patients. A total of 69 hyperlipidemia patients, 25 familial hypercholesteremia (FHC) patients, and 64 healthy controls were enrolled in this study. We performed routine testing of blood lipid water. Gas chromatography was used to determine the changes in the concentration of cholesterol synthesis (squalene, desmosterol, and lathosterol) and absorption markers (campesterol, sitosterol, and stigmasterol) in the blood. Baseline hyperlipidemia patients displayed significantly higher total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) levels in comparison to the control group, which was reflected in the increased levels of squalene, desmosterol, campesterol, and sitosterol observed ( P < 0.05 ) in the hyperlipidemia patients. The desmosterol, lathosterol, campesterol, stigmasterol, and sitosterol were statistically different in the FHC group than the hyperlipidemic group ( P < 0.05 ). The proportions of squalene/cholesterol, lathosterol/cholesterol, stigmasterol/cholesterol, and sitosterol/cholesterol in the FHC group were lower than those in the hyperlipidemic group; only desmosterol/cholesterol was higher than that in the hyperlipidemic group. Correlation studies between lipid metabolic factors showed that the proportion of moderate and strong correlations was much higher in the FHC group than in the other two groups (76.92% vs. 32.50% and 31.25%). Logistic regression analysis showed that the concentrations of glucose, LDL-C, lactosterol, and sitosterol were all independent risk factors for developing hyperlipidemia. This result was further confirmed by the ROC curve. These results indicated that the study of cholesterol synthesis and decomposition markers can serve as a reference index for related diseases caused by changes in its concentration.

31

RANA, MOHAMMAD MOHSIN, BADAR BASHIR, MUHAMMAD SAEED AKHTAR, and Abaid Ur-Rehman. "TYPE 2 DIABETICS." Professional Medical Journal 14, no. 02 (September 6, 2007): 337–43. http://dx.doi.org/10.29309/tpmj/2007.14.02.4900.

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Objective: To find the relationship between the serum cholesterol andtriglyceroid in type 2 diabetics with different parameters of obesity. Design: Descriptive study. Setting: Al-ShifaMetabolic Center Faisalabad. Period: From January 2003 to June 2005. Material and methods: A total of 2034patients, who fulfill the inclusion criteria were included in this study. Out of these patients 1188 females and 846 males,patients presented to the metabolic center for lipids screening. Body parameters i.e. weight, height, waist and hipcircumference and blood pressure. BMI and WHR were calculated as per standard. Fasting serum cholesterol andtriglyceroid were tested on capillary blood by GCT meter. Results: There is a sharp and definite increase in the % ofpatients having > 200 mg/dl total cholesterol after 10 years of DM, from 34-36% to 59%. More patients in above 50 agegroup had higher than 200-mg/dl-cholesterol i.e.38%, 50% and 36% than below 50 years i.e. 30% and 24%. Serumtriglyceroid levels in the middle range of 150-300 had a definite ascending relationship with increasing BMI, 17%, 47%and 71% respectively. High WHR in both sexes had the strongest relation with high serum cholesterol both in 150-200and >200 mg/dl range, 37% and 41% and 40 and 41% respectively. Serum triglyceroid was definitely higher in patientswith high WHR in both sexes in 150-300 ranges. Conclusions: It is clearly evident that the duration of hyperglycemia,age at onset of DM and the central obesity, all increases the chances of having hypercholesteremia. It is again evidentthat so many other factors influence the incidence of hypercholesteremia; screening is the only way to pick thesepatients. Every patient with any component of the Metabolic Syndrome must be screened for other components foroptimal stratification of the coronary risk factors.

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Yuefeng, Yu, Lin Zhiqi, Chen Yi, Zhu Keyu, Wan Heng, Wang Yuying, Wang Ningjian, et al. "Testosterone Deficiency Promotes Hypercholesteremia and Attenuates Cholesterol Liver Uptake via AR/PCSK9/LDLR Pathways." International Journal of Endocrinology 2022 (May 13, 2022): 1–10. http://dx.doi.org/10.1155/2022/7989751.

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Background. Testosterone deficiency is reportedly correlated with an elevation of cholesterol in plasma, but the mechanism remains unclear. Our objective was to investigate the effects of testosterone deficiency on cholesterol metabolism and the corresponding molecular changes in vivo and in vitro. Methods. SD rats were randomized into three groups: sham-operated (SHAM), subtotal orchiectomized (SO), and orchiectomized (ORX) and fed for 8 weeks. HepG2 cells were cultured with medium containing testosterone with the final concentrations of 0, 10, 30, and 300 nM. Method of isotope tracing and fluorescence labelling was adopted to investigate cholesterol metabolism. Several key molecules of cholesterol metabolism were also analyzed. Results. SO and ORX rats displayed dysfunctional liver uptake of cholesterol. HepG2 cells incubated with testosterone of lower and excessive level exhibited reduced capacity of cholesterol uptake. Further investigation revealed that lack of testosterone induced increased proprotein convertase subtilisin/kexin type 9 (PCSK9) and decreased low-density lipoprotein receptor (LDLR) both in vivo and in vitro. Moreover, the androgen receptor (AR) antagonist flutamide mimicked the effects of testosterone deficiency on PCSK9 and LDLR indicating the role of AR as a mediator in triggering attenuating liver cholesterol uptake in which testosterone instead of dihydrotestosterone (DHT) is the major functional form of androgen. Conclusion. Testosterone deficiency attenuated cholesterol liver uptake mediated by the PCSK9-LDLR pathway, in which AR and testosterone without transforming to DHT play important roles.

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Drew-Nord, Dana C., OiSaeng Hong, Erika S. Froelicher, Phyllis Berryman, and Eileen Lukes. "Cardiovascular Risk Factors among Career Firefighters." AAOHN Journal 57, no. 10 (October 2009): 415–24. http://dx.doi.org/10.1177/216507990905701004.

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Sudden cardiac death is the leading cause of on-duty death among firefighters. Determining firefighters' risk of cardiovascular death or all-cause mortality, cardiovascular risk factor profiles, and energy demands while firefighting may aid in understanding why this occupational group is at risk for on-duty sudden cardiac death. A literature review conducted between 2006 and 2009 did not demonstrate that firefighters are at increased risk of all-cause death compared to the general population. In addition, cardiovascular risk profiles of firefighters are similar to those of the general population. Firefighters may be part of the national obesity epidemic; their hypertension and hypercholesteremia often are not diagnosed or are undertreated. The combination of personal cardiovascular risk factors and extreme physical work demands may contribute to sudden cardiac death in this population.

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Bardia, A., and G. Garg. "Mipomersen For Treatment Of Hypercholesteremia: Evidence Review And Meta Analytic Evaluation Of Randomized Controlled Trials." Value in Health 18, no. 3 (May 2015): A132. http://dx.doi.org/10.1016/j.jval.2015.03.771.

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Naik, Aleš Belič Adviti. "Analysis of the Cholesterol Biosynthesis Feedback Control and its Consequences for the Hypercholesteremia Treatment Strategies." IFAC Proceedings Volumes 45, no. 2 (2012): 624–28. http://dx.doi.org/10.3182/20120215-3-at-3016.00111.

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Huige, M. C., J. J. R. M. Bonnier, H. J. Rila, L. J. Jansen, K. te VElde, A. J. te Rijdt, P. de Weerd, and P. A. Leijten. "Efficacy and safety of pravastatin in Dutch patients with hypercholesteremia and additional coronary risk factors." Atherosclerosis 115 (June 1995): S128. http://dx.doi.org/10.1016/0021-9150(95)96739-f.

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Cheung, Brian, Jay Hwang, Ania Stolarczyk, Elliot Mahlof, and Robert Block. "Case Study of Hypertriglyceridemia from COVID-19 Pfizer-BioNTech Vaccination in a Patient with Familial Hypercholesteremia." Journal of Clinical Lipidology 16, no. 1 (January 2022): e13-e14. http://dx.doi.org/10.1016/j.jacl.2021.09.019.

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Kirkorowicz, JM, P. Sapukotana, PV De Silva, M. Noda, JS De Oliveira, and T. Østbye. "Work-Related Stress and Substance Use as Risk Factors for Chronic Disease Among Three-Wheel Drivers in Galle, Sri Lanka: A Qualitative Study." International Journal of Occupational Safety and Health 3, no. 2 (February 10, 2014): 21–24. http://dx.doi.org/10.3126/ijosh.v3i2.7662.

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Background: Motor three-wheel drivers provide an important means of transportation in Sri Lanka, comprising 15% of motorized road vehicles. Although three-wheel driving is a widespread occupation for Sri Lankan men, little is known about their general health or risk factors.Objectives: This paper investigates chronic illnesses and risk factors for such illnesses in a sample of 33 three-wheel drivers in Galle, Sri Lanka.Methods: A qualitative investigation was conducted between June and August 2012. 20 three-wheel drivers participated in 60-minute semi-structured interviews, and 13 participated in semi- structured focus groups related to their work-related health concerns.Results: Illness reported included musculoskeletal pain, hypercholesteremia, hypertension, and diabetes. Participants identified work-related stress and substance abuse as risk factors.Conclusions: Participants described a cycle of work related stress, substance use, and chronic illness. Community-based education on the risks of substance use and alternative means of coping may be an effective intervention for these workers. DOI: http://dx.doi.org/10.3126/ijosh.v3i2.7662

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Ezratty, Ellen J., Claire Bertaux, Eugene E. Marcantonio, and Gregg G. Gundersen. "Clathrin mediates integrin endocytosis for focal adhesion disassembly in migrating cells." Journal of Cell Biology 187, no. 5 (November 30, 2009): 733–47. http://dx.doi.org/10.1083/jcb.200904054.

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Focal adhesion disassembly is regulated by microtubules (MTs) through an unknown mechanism that involves dynamin. To test whether endocytosis may be involved, we interfered with the function of clathrin or its adaptors autosomal recessive hypercholesteremia (ARH) and Dab2 (Disabled-2) and found that both treatments prevented MT-induced focal adhesion disassembly. Surface labeling experiments showed that integrin was endocytosed in an extracellular matrix–, clathrin-, and ARH- and Dab2-dependent manner before entering Rab5 endosomes. Clathrin colocalized with a subset of focal adhesions in an ARH- and Dab2-dependent fashion. Direct imaging showed that clathrin rapidly accumulated on focal adhesions during MT-stimulated disassembly and departed from focal adhesions with integrin upon their disassembly. In migrating cells, depletion of clathrin or Dab2 and ARH inhibited focal adhesion disassembly and decreased the rate of migration. These results show that focal adhesion disassembly occurs through a targeted mechanism involving MTs, clathrin, and specific clathrin adaptors and that direct endocytosis of integrins from focal adhesions mediates their disassembly in migrating cells.

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CHISAKA, TAKESHI, HISASHI MATSUDA, YASUSHI KUBOMURA, MICHIHIKO MOCHIZUKI, JOHJI YAMAHARA, and HAJIME FUJIMURA. "The effect of crude drugs on experimental hypercholesteremia: Mode of action of (-)-epigallocatechin gallate in tea leaves." CHEMICAL & PHARMACEUTICAL BULLETIN 36, no. 1 (1988): 227–33. http://dx.doi.org/10.1248/cpb.36.227.

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Weng, Pei-Hsuan, Jen-Hau Chen, Ta-Fu Chen, Yu Sun, Li-Li Wen, Ping-Keung Yip, Yi-Min Chu та Yen-Ching Chen. "P3-253: Interactions between ApoE ε4 status and hypercholesteremia on response to acetylcholinesterase inhibitor in Alzheimer's disease". Alzheimer's & Dementia 11, № 7S_Part_16 (липень 2015): P728. http://dx.doi.org/10.1016/j.jalz.2015.06.1626.

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MIYAMURA, Mitsuhiko, Hironori MORIYAMA, Shuuzo MURATA, Junko YOKOTA, Saburo YOSHIOKA, Daisuke TAKUMA, Atsuhide HAMADA, and Yutaka NISHIOKA. "Inhibitory Effects of “Goishi-tea” as a Post-Fermented-tea on Dietary-Induced Hypercholesteremia and Atherosclerosis in Rabbits." YAKUGAKU ZASSHI 128, no. 7 (July 1, 2008): 1037–44. http://dx.doi.org/10.1248/yakushi.128.1037.

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Ahualli, L., A. Stewart-Harris, G. Bastianelli, D. Radlovachki, A. Bartolomé, P. L. Trigo, N. Cejas, et al. "Combined Cardiohepatic Transplantation Due to Severe Heterozygous Familiar Hypercholesteremia Type II: First Case in Argentina—A Case Report." Transplantation Proceedings 39, no. 7 (September 2007): 2449–53. http://dx.doi.org/10.1016/j.transproceed.2007.07.068.

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Matlock, John P., and J. E. Nixon. "Impaired clearance, elimination, and metabolism of plasma cholesterol esters associated with hypercholesteremia in mice fed cyclopropenoid fatty acids." Toxicology and Applied Pharmacology 84, no. 1 (June 1986): 3–11. http://dx.doi.org/10.1016/0041-008x(86)90411-4.

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Kamal, Shymaa, Ragaa A. Hamouda, Hoda Mahrous, Mohammed Labib Salem, Hanafy A. Hamza, and Ekbal Abd Elhafez. "In vitro Treatment with Intact Cells or Cell Lysates of Lactobacillus and Spirulina Induced Lowering Effects on Induced Hypercholesteremia." International Journal of Pharmacology 11, no. 6 (August 1, 2015): 638–43. http://dx.doi.org/10.3923/ijp.2015.638.643.

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Kim, Beob-Jin, Yeon-Kye Kim, Won-Hwan Park, Jeong-Heon Ko, Young-Choon Lee, and Cheorl-Ho Kim. "A water-extract of the Korean traditional formulation Geiji–Bokryung–Hwan reduces atherosclerosis and hypercholesteremia in cholesterol-fed rabbits." International Immunopharmacology 3, no. 5 (May 2003): 723–34. http://dx.doi.org/10.1016/s1567-5769(03)00073-0.

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Gopinathanpillai, Kalavarasariel, Eluri Kalpana, Balasubramaniam Dineshkumar, Elumalai Monogaran, Govindharajalu Geetha, and Ramasamy Venkatanarayanan. "Tetrahydrocurcumin: Beneficial Effects on HMG-CoA Reductase enzyme and Lipoprotein Lipase Enzymes in High-fat diet-induced Hypercholesteremia Rabbits." Pharmacognosy Communications 2, no. 2 (April 19, 2012): 50–60. http://dx.doi.org/10.5530/pc.2012.2.8.

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Li, Yun-Xi, Chao-Qun Lin, Da-Yu Shi, Shu-Ying Zeng, and Wen-Sheng Li. "Upregulated expression of human alpha-defensins 1, 2 and 3 in hypercholesteremia and its relationship with serum lipid levels." Human Immunology 75, no. 11 (November 2014): 1104–9. http://dx.doi.org/10.1016/j.humimm.2014.09.014.

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Weintraub, Spencer, Jessica A. Schillow, Bani Azari, and Benjamin Hirsh. "IMPLEMENTATION TIMELINE OF NOVEL LIPID LOWERING THERAPIES IN A REFRACTORY COMPOUND HETEROZYGOUS FAMILIAL HYPERCHOLESTEREMIA PATIENT WITH SEVERE ATHEROSCLEROTIC CARDIOVASCULAR DISEASE." Journal of the American College of Cardiology 79, no. 9 (March 2022): 3186. http://dx.doi.org/10.1016/s0735-1097(22)04177-8.

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Rani, Pratibha, Kamaldeep Singh, Anania Arjuna, and Savita Devi. "GENETIC DISORDER ALZHEIMER." Asian Journal of Pharmaceutical and Clinical Research 10, no. 12 (December 1, 2017): 36. http://dx.doi.org/10.22159/ajpcr.2017.v10i12.18684.

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Alzheimer’s disease (AD), slowly continuous neurological disorder, mostly appears in older >65 age that deals with the memory loss due to death or damage of brain cells and cognitive functions (thinking, reasoning, and behavior abnormalities) due to the accumulation of the specific protein (beta-amyloid protein) which form plaque and fibers (tau tangles) in the brain. Not only the genetic factors are responsible but also most of the non-genetic factors are responsible for AD. Several mutations in the gene (APP, APOE, PENS1, PENS2 on chromosome no. 21, 19, 14, 1) are responsible for causing four types of AD. Memory loss is most common sign of AD. Predisposing factors of AD are hereditary, severe brain injury or traumatic, and metabolic diseases such as diabetes mellitus, hypercholesteremia, and obesity. Although treatment can manage some symptoms in few people, but there is no current mechanism to cure AD or stop its progression. Beta-secretase inhibitor molecule prevents the first step in a chain accumulation which leads to the formation of amyloid plaque in the brain. However, the scientist or researchers have established a compound NIC5-15 they have been found NIC5-15 has safe and effectual treatment which has been used to stabilize cognitive performance in patients with mild to moderate AD.