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             \author[1]{Kuat  Oshakbayev}

             \author[2]{Kenneth  Alibek}

             \affil[1]{  Republican Scientific Center for Emergency Medicine}

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\date{\small \em Received: 11 February 2013 Accepted: 1 March 2013 Published: 15 March 2013}

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\begin{abstract}
        


 Atherosclerosis(AS)  Atherosclerosis(AS) is one of the most common disease sleading tosevere clinical complications. Atherosclerosis forms pockets of fat and lipid deposit sunder the mucous tunic of blood vessels, which cause progressive vasoconstriction until total luminal blockage occurs. 1Many "Civilization diseases" such as coronary artery disease (CAD), arterial hypertension (AH), diabetes mellitus (DM), psoriasis, gout, and such conditions as hyper lipidemia, hyperglycemia, dyslipidemia, hyperinsulinemia, hypercortisolemia, hyperuricemia, and microalbuminuria are connected with AS development. In these regards, the problem of developing a proven clinical solution for this prevalent disease process is a socially significant one.1,2 During the last 20 years, ASmorbidity has been globally increasing.2,3 Mortality from AS complications, which account for 75-85% of general mortalityinwhole,4 is simultaneously increasing.Thus AS is one of the global problems of conventional medicine.

\end{abstract}


\keywords{atherosclerosis, fatty overweight, low-calorie, fat-free diet, weight loss therapy.}

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\let\tabcellsep& 	 	 		 \par
Background Mortality from atherosclerosis (AS) complications, which account for 75-85\% of general mortality in whole, is simultaneously increasing. Recently published studies have revealed the close correlation between AS and overweight. 
\section[{Objective}]{Objective}\par
The purposes of the current study were to study the result of a weight loss program in AS patients using a randomized clinical design. 
\section[{Design}]{Design}\par
A randomized controlled prospective clinical cross-sectional trial. Echocardiography demonstrated an increased ejection fraction from 56.3±1.1\% to 72.1±1.3\% (p<0.0001) and systolic output from 65.4±1.8 ml to 89.6±1.7 ml (p<0.0001) in weight loss AS therosclerosis(AS) is one of the most common disease sleading to severe clinical complications. Atherosclerosis forms pockets of fat and lipid deposit sunder the mucous tunic of blood vessels, which cause progressive vasoconstriction until total luminal blockage occurs. \hyperref[b0]{1} Many "Civilization diseases" such as coronary artery disease (CAD), arterial hypertension (AH), diabetes mellitus (DM), psoriasis, gout, and such conditions as hyper lipidemia, hyperglycemia, dyslipidemia, hyperinsulinemia, hypercortisolemia, hyperuricemia, and microalbuminuria are connected with AS development. In these regards, the problem of developing a proven clinical solution for this prevalent disease process is a socially significant one. \hyperref[b0]{1,}\hyperref[b2]{2} During the last 20 years, ASmorbidity has been globally increasing. \hyperref[b2]{2,}\hyperref[b3]{3} Mortality from AS complications, which account for 75-85\% of general mortality in whole, \hyperref[b4]{4} is simultaneously increasing. Thus AS is one of the global problems of conventional medicine. 
\section[{Methods and}]{Methods and}\par
One of the scientific ways of working out of effective treatment strategies for AS requires the development of novel conceptions based on the accumulated scientific facts and knowledge in the field sof AS etiology and pathogenesis. For the last 20-30 years, several dozenhypotheses have been offered toexplainthe origin and progression of AS processes. However, to date, none of these has been universally recognized and proven in practice. \hyperref[b5]{5,}\hyperref[b6]{6} Recently published studies have revealed the close correlation between AS and overweight. \hyperref[b7]{7,} {\ref 8} The purposes of the current study were to study the result of a weight loss program in AS patients using a randomized clinical design.  The comparison group (control group) included 30 AS patients (aged 26-70 years, mean 47.5±1.9 years, including 14 females) who were receiving a conventional (traditional) drug therapy that included hypoglycemic (metformin 500-1500 mg per day, exenatide5-10 µg per day), lipid lowering (atorvastatin 40mg per day), antihypertensive (lisinopril 20mg per day, calcium channel blockers referring to benzodiazepines 90mg per day), anti-inflammatory (acetylsalicylate acid up to 2 g per day and/or thienopyridine class anti platelet agent 75 mg per day)treatment, and symptomatic therapy. The study was carried out between October 2009 and April 2012 at the scientific research of cardiology and internal diseases (in Almaty, the Republic of Kazakhstan) and at the republican scientific center for emergency medicine (in Astana, the Republic of Kazakhstan).\par
Inclusion criteria included: written informed consentfor participation in the study; dyslipidemia (bloodserumhigh-density lipoprotein <1.0 mmol/L, or triglycerides(TGs) ?1.7 mmol/L or cholesterol ?5.6 mmol/L); waist circumference (WCf) in men >94.0 cm or in women >80.0 cm; overweight (body fat\%>21);blood pressure (BP)>140mmHg of systolic blood pressure (SBP) and >95 mmHg of diastolic blood pressure (DBP), or ongoing treatment with antihypertensive drugs, fasting glucose >6.1 mmol/L or treatment with glucose-reducing drugs; absence of contraindications to weight loss; the possibility of treatment for 6 months and dynamic observation for 1 year. 
\section[{c) Outcome Measures}]{c) Outcome Measures}\par
The primary efficacy end point of the trial was full recovery from atherosclerotic diseases for 12 months. The secondary efficacy end point of the trial was data imaging methods (Doppler-ultrasound, computed tomography scans) and measurement of clinical presence status. Methods we diagnosed prior CAD and PICS by case history and by electrocardio graphic changes of ischemia in patient anamnesis. We diagnosed AH by blood pressure readings and from medical records. Abdominal obesity was assessed WCF using the standards for the Asian nationality by the International Diabetes Federation. 9 the weight loss intervention study period was between 2-6 months in duration, depending on the individual patient clinical course, disease severity, and disease stage. Physical activity was assessed as the number of steps taken by patients, as determined by an individual pedometer from Hoffmann-La Roche, Ltd (Basel, Switzerland). Mental status was defined by the method the test of numbers binding by Reitano.  {\ref 10} The structure of lean and fatty mass before and after the weight loss program was determined with aTanita-SC330S Body Composition Analyzer (Tanita Corp., Tokyo, Japan). We defined anthropometrical indicators including age (years), weight (kg), BMI (kg/m 2 ). We also evaluated body composition parameters, including as fat mass (in \% of total body weight and total kg), visceral fat rating (units), fat free mass (kg), total body water (in \% and kg), muscle mass (in \% and kg), bone mass (in \% and kg), metabolic age (years), basal metabolic rate (kcal per day), and bioimpedance (Ohms).General clinical study of blood and urine chemistry, liver and kidneys function tests, and imaging methods (GE Vivid 7 Ultrasound ;GE Healthcare Worldwide USA, Michigan),bone densitometry (Lunar Achilles Express Ultrasound; GE Healthcare USA, Madison), and computed tomography scans(AG Siemens Soma tom Emotion 6, Germany, Muenchen) were performed. 
\section[{Volume XIII Issue III Version I}]{Volume XIII Issue III Version I}\par
We employed weight loss therapy using the weight loss program was conducted by administering a caloric restriction, fat-free vegetables and salt diet and includes an increased physical activity.  {\ref [11]} {\ref [12]} {\ref [13]} {\ref [14]} Participants were asked to reduce their meals to no more than 1200-1500 kcal per day. Behavioral weight loss intervention was achieved by a request to walk no less than 10,000 steps per day. Doses of previous symptomatic conventional drugs have been decreasing from the second/third days of the treatment beginning, and up to full withdrawn from the fifth/seventh days of the treatment beginning, as clinical symptoms were improved. A combination of in-person conversations and telephone calls were conducted during the 6-month study period. Weight loss results were assessed by WCf and body mass (kg).\par
Ethics  
\section[{Results}]{Results}\par
We compared the patient and control groups with respect to metabolic age, basal metabolic rate, anthropometrical data, and body composition (Table \hyperref[tab_5]{2}).\par
As seen in Table \hyperref[tab_5]{2}, there were no significant differences between the patient group and the control group regarding passport age, weight, and height. The patient group had a significantly higher BMI on the order of an extra?3.5 kg/m 2 compared with the healthy group. Fat mass was significantly higher in the patient group compared with the healthy group, on the order of?12.1\% or?10.0 kg. Table \hyperref[tab_5]{2} makes clear the inverse relationship between fat mass percentage and muscle masspercentage: The greater the fat mass percentage, the lower the muscle mass percentage.\par
The patient group also had significantly raised visceral fat rating (3.6U), metabolic age (?6.6 years), basal metabolic rate (?240 kcal/day), and bioimpedance (?35 ohms) than did the control group. Increased body fat mass is associated with an accordingly increased impedance.\par
The healthy group displayed a significantly greater percentage of total body water on (?8\%), percentage of muscle mass (?11.5\%, and percentage of bone mass (?0.3\%) than the patient group. The regression linear analysis strongly correlated the relationships between fat mass and muscle/water/bone masses in the patients group (n=71) (Figure  {\ref 1}).\par
As seen in Figure  {\ref 1}, there are significant inverse regression correlations between fat mass in percentage and muscle mass, total body water, and bone mass (?<0.0001). This data analysis provides evidencethat fat mass could be a main risk factor for AS patients.\par
We studied the regression correlation between the levels of obesity (fat mass in \% and visceral fat level in units) and the metabolic age in the patient group (n=71) (Figure  {\ref 2}). As seen here, increased parameters of obesity (fat mass in \% and visceral fat level in units) are significantly correlated with increased metabolic age (?<0.0001).\par
We began the weight loss program with the patient group (n=31) that had been randomly assigned into this category. As a result of the treatment, average weight lost varied from6 to 18kg. Weight loss led to positive changes of the cardiovascular diseases symptoms: SBP and DBP decreased in 94.4\% of patients (p<0.001), more than 19\% from the initial state (Table \hyperref[tab_6]{3}).\par
Table \hyperref[tab_6]{3} shows that in the control group such parameters as SBP, glucose, cholesterol and triglyceride serum levels were improved significantly (p<0.001). However, the traditional treatment in AS patients did not lead to a significant improvement in DBP (p=0.289), blood hemoglobin levels (p=0.281), and bone mass density (BMD; p=0.405). It is noteworthy that in the main weight loss group we observed more significant (p<0.001) declines in SBP, DBP, glucose, cholesterol, and triglyceride levels. There was a significant increase in hemoglobin levels (p<0.001) and BMD (p<0.001).\par
Therapy by maintaining the weight loss program led to weight loss ranging between9-16 \% from the initial state (p=0.035).Importantly, the weight loss achieved in these 31 patients was due to reduction of fatty mass only (before 26.75±2.94 kg, and after15.76±2.98 kg, p=0.005; Table \hyperref[tab_7]{4}).\par
The data of Table \hyperref[tab_7]{4} show that the weight loss in AS patients was due to significant fat loss (before 29.87±2.01\%, and after 20.23±2.55\%). The percentages of water and muscle masses had tendency to increase at the study endpoint. We noted with fat mass loss does not change lean body mass. And the weight loss in the patients was due to loss from the overweight abdominal component.\par
During the first 2-3 days of the treatment, the patients noticed an intense sense of hunger, slight dizziness, weakness, lower extremity and abdominal muscle tremors, a sensation of heating or fever in the umbilical are a and/or in the solar plexus area, and psychogenic fear due to alt ered habitual food intake. All of these uncomfortable sensations disappeare don subsequent days.\par
Urine was becoming cloudier and intensely colored (dark) starting from Days 3-5 after initiating the weight loss treatment that was not present before, and persisted for several days. Microscopy of urocheras revealed that urine cloudiness was mainly been due to the organic salts such as oxalates, urates, phosphates, and carbonates of calcium and magnesium. An increase ederythrocyte sedimentation rate and elevated leukocyte count was observed between Days 4-6 after weight loss program initiation.\par
Regression of clinical AS symptoms was also gradually observed in patients; physical and mental working ability of the patients increased, and AS patients noticed a physical relief. Doppler-ultrasound imaging data revealed that blood flow in the lower extremities was restored and gastrocnemius musclemass increases were noted in four patients with Leriche's disease. The clinical picture of angina pectoris was reduced with an OR of 1.52 (95\% CI 1.24-1.81; p=0.034), exercise tolerance was improved, and objective electrocardiographyindicators of cardiovascular function were improved. Ejection fraction increased from 56.3 ±1.1\% to 72.1 ±1.3\% (p<0.0001) and the systolic output increased from 65.4 ±1.8 ml to 89.6 ±1.7 ml (p<0.0001) in CAD patients. All patients including those of with transient ischemic attack and with Alzheimer's disease noticed improvement of memory, and decreased mental fatigue with and OR of 1.47 (95\% CI 1.18-1.77; p=0.039).\par
As clinical symptoms have been improving, the doses of previous symptomatic drugs were decreased from the second/third days of the treatment beginning and were withdrawn from the fifth/seventh days of the treatment beginning. The observation period was up to1 year and there was no recurrence of clinica lAS manifestations. Shed weight was usually not regained during this time period. Appropriate clinical AS symptoms occasionally and gradually relapsed in patients that regained at fatty overweight (FOW), but the weight lossre-therapy reversed these clinical symptoms. 
\section[{IV.}]{IV.} 
\section[{Discussion}]{Discussion}\par
Cardiovascular risk due to AS depends on visceral obesity developing over time.  {\ref 16} Much attention has been paid to understanding the interactions of plasma lipoproteins (LPs), blood monocytes and the with arterial endothelium.  {\ref 17} The genetic theory of AS development cannot be the complete underlying cause of AS disease, because corresponding parameters may be changed within the same persons, including inflammatory, immunologic, endothelial, metabolic and otherdisorders.  {\ref [18]} {\ref [19]} {\ref [20]} The results of our study suggest that in the patient with AS compared with the healthy people a fat mass was significantly higher on the order of ?12.1\%. The patient group had significantly raised metabolic age (on?6.6 years), basal metabolic rate (on?240 kcal/day), and bioimpedance (on?35 ohms) than did the healthy people. The regression linear analysis strongly significant inverse correlated the relationships between fat mass in percentage and muscle/water/bone masses in the body of the patients (?<0.0001). The more a percentage of fat mass the less percentage of muscle/water/bone masses. Also increased parameters of obesity (fat mass in \% and visceral fat level in units) are significantly correlated with increased metabolic age (?<0.0001). This data analysis provides evidencethat fat mass could be a main risk factor for AS patients.\par
The concept of insulin atherogeneity supports an independent atherogenic role for hyperinsulinemia.  {\ref 21} In patients with simultaneously increased levels of very low density of LP sand TGs, high concentration of insulin were found after anoraltest for glucose tolerance.  {\ref 22} The nutriceptive-metabolic theory of AS has been developed recently. There exist substantial amounts of scientific data indicating an interrelationbetween AS and visceral obesity.  {\ref 23} Researchers 35 indicate that accumulation of visceral adiposity along with hyperinsulinemia and insulin resistance may be considered as fundamental signs of AS. One characteristic metabolic abnormality in insulin resistance is a high blood concentration of free fatty acids, both fasting and also postprandial. Permanently elevated free fatty acid concentrations in insulin resistance is a way to damage of vascular structures, endothelial function, and hinders insulin-mediated glucose metabolism.  {\ref 24} Young persons with FOW have hyperinsulinemia, insulin resistance, and impaired fat toleranceeven on the background of normal glucose tolerance.  {\ref 25} Intake of excess fats and carbohydrates leads to overload of the blood transport system and increased fatre serves. The fat deposit in organisms leads to aging of lipids.  {\ref 26,} {\ref 27} Exogenously-induced alimentary (postprandial) hyperlipidemia that develops after food intake is a suspected origin of AS.  {\ref 28} Alimentary hyperlipidemia usually develops after each food intake and lasts for 6 hours or more.  {\ref 29} A direct connection between the levels of postprandial lipidemia/hypertriglyceridemia and atherogenic changes after fatty overload manifested in angiographic coronary AS changes was revealed.  {\ref 30} Alimentary hyperlipidemia is a physiological process whose primary function is transport of nutritional lipids into storage depots. However, if the depot is in the stage of "overstock," the duration of postprandial hyperlipidemia is increased and develops into an intolerance to nutrients.  {\ref 31,} {\ref 32} A treatment program focused on weight loss therapy using the weight loss program including a very low-calorie, fat-free vegetables and salt diet with an adjustment to eating behavior and increased physical activity method by metabolizing "old lipids". 12,14 The weight loss program leads losses of 9-16 \% of the initial body mass (p=0.035). Weight loss led to positive changes of cardiovascular diseases symptoms (p<0.001), glucose/cholesterol/triglyceride levels. Also there was a significant increase in hemoglobin levels (p<0.001) and BMD (p<0.001).Our results are similar to database.  {\ref 33,} {\ref 34} Need to note, the weight loss was due to loss from the overweight abdominal component and reduction of fatty mass only whereas lean mass was not significantly changed. There also was a significant improvement of physical capability of individuals. During the first some days of the weight loss treatment in the patients noticed adverse effects connected with symptoms of endogenous metabolic intoxication. But all of these symptoms disappeared then.\par
The weight loss method lead to significant regression of clinical AS symptoms in observed patients. There was reduced an angina pectoris clinical picture (p=0.034), were improved objective electrocardiography indicators, an ejection fraction (p<0.0001), a systolic output (p<0.0001), an exercise tolerance and memory (p<0.05), decreased mental fatigue (p=0.039).\par
There was noted that with weight loss the disease clinical symptoms were improved and doses of previous symptomatic drugs were decreased from the second/third days of the treatment beginning, and up to full withdraw of its from the fifth/seventh days of the treatment beginning. If weight was not regained then clinical AS symptoms were not relapsed.\par
Growth of non-communicable diseases in the modern human is directly proportional with growth of the FOW prevalence.  {\ref 35} Due to current super-nutrient status of humans, we now accumulate more fat than we can use.  {\ref 36} The balanceis disturbed towards permanent lipid accumulation, wherein FOW become sun used by the body. But the process of fat accumulation does not occur infinitely, and fat in a storage depot may be qualitatively changed over time.  {\ref 37,} {\ref 38} The more FOW participates in an organism's metabolism, the more FOW creates the metabolic burden for proper functioning of thatorganism.  {\ref 39} Trophic feeding, excretion of metabolic products, correction of thermoregulation, provision of biologically active substances (e.g., hormones, enzymes, and mediators) are all necessary for providing the vital activity of the fatty resources. All of these mechanisms create an additional burden to the synthetic, immunological, antitoxic, and other functions of an organism's internal orgas.  {\ref 40} Obviously, the depositing function of an organism is not without limits. With increased fatty stores, the metabolic burden for transport function of and organism increases accordingly.  {\ref 41} Accumulation of FOW in an organism requires appropriate spaces for deposition. The process of fat deposition occurs by the physicochemical "in duration" (hardening) of lipids.  {\ref 42} This lipid in duration is a process that occursin AS development.  {\ref 43} The AS plaque development process is not a random phenomenon, but it is a logical result of aging of fatty stores. Lipid aging occurs because they have remained unused by the body over a long period of time. The protective homeostatic mechanisms could be body temperature, blood pressure, or insulin resistance, which increase the rate of biochemical metabolism.  {\ref 44,} {\ref 45} Consequently, the AS processes could be considered physiological, in which an organism exists in conditions of excess nutrient intake on the background of unused FOW.\par
Isolated struggles with clinical expressions of AS lesions such as CAD, AH, DM, hyperglycemia, microalbuminuria, and hyperlipidemia did not influence the risk of cardiovascular disaster and decrease mortality, though it did improve patient quality oflife.  {\ref 46} Improvement of therapeutic and diagnostic methods has not lead to definitive cures of human chronic non-communicable diseases.  {\ref 47,} {\ref 48} V. 
\section[{Conclusion Acknowledgement}]{Conclusion Acknowledgement}\par
We thank Elmira Nurakhanova for language and logistic support and for technical assistance. 
\section[{Authors' Contributions}]{Authors' Contributions}\par
Kuat P. Oshakbayev: design and performance, scientific executor, collect of the clinical material, treatment and diagnosis of the patients, invention patent fulfillment, bibliography review, scientific analysis, statistical advancing, writing the paper.\par
Kenneth Alibek: design and performance, scientific executor, invention patent fulfillment, paper review, writing the paper.\par
Igor O. Ponomarev:design and performance, scientific executor, treatment and diagnosis of the patients, invention patent fulfillment, scientific analysis.\par
Meruyert A. Gazaliyeva:preparation e-version statistical data in Excel, collect of the clinical material, bibliography search and review, scientific analysis, statistical advancing, writing the paper.\par
Bibazhar A. Dukenbayeva: collect of the clinical material, preparation e-version statistical data in Excel, diagnosis of the patients, invention patent fulfillment, bibliography search and review, paper print.\par
PernekulOshakbayev: design, bibliography search and review, scientific analysis.\par
Baglan K. Zhumabekova: collect of the clinical material, bibliography search and review, scientific analysis, statistical advancing, writing the paper.\par
SholpanKaliyeva: collect of the clinical material, bibliography search.\par
KairatShakeyev: collect of the clinical material, paper print.\par
We observed that the more fat mass is stored in organism the less a muscle, bone and water masses are present. Increased fat mass in an organism is an impedance indicator, and impedance and metabolic age are significantly increased, accordingly.\par
Weight loss therapy using the weight loss program including a caloric restriction, fat-free vegetables and salt diet with an increased physical activity is a performance method of curing the clinical manifestations of AS. The weight loss treatment led to positive changes of diseases symptoms, improve in laboratory and instrumental parameters in patients with AS. The weight loss programs lead to loss of adipose tissue only. If the "old" lipids are used during weight loss-mediated FOW reduction it will be possible to influence AS processes, as desired.\par
Study limitation. Published studies into the possible role of fatty overweight in AS etiology are limited in scope and number. We acknowledge that the current randomized clinical trial had a small sample size, and that future studies into the exact relationship between fatty overweight and AS development should be carried out on a larger scale. \begin{figure}[htbp]
\noindent\textbf{}\includegraphics[]{image-2.png}
\caption{\label{fig_0}}\end{figure}
  \begin{figure}[htbp]
\noindent\textbf{} \par 
\begin{longtable}{}
\end{longtable} \par
 
\caption{\label{tab_1}A}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{} \par 
\begin{longtable}{P{0.85\textwidth}}
.Ethical Committee of Scientific research\\
institute of cardiology and internal diseases approved\\
the study. Approval Number is the Protocol \#9 from\\
06.02.2009.Board Affiliation: Health Ministry of the\\
Republic of Kazakhstan Statistics. The two-sample\\
Student's t-test and odds ratios (ORs) with 95\%\\
confidence intervals (CIs) were used. The study data are\\
presented in\end{longtable} \par
  {\small\itshape [Note: 15III.]} 
\caption{\label{tab_3}}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{1} \par 
\begin{longtable}{P{0.42976030465949816\textwidth}P{0.003998655913978495\textwidth}P{0.0034274193548387093\textwidth}P{0.00228494623655914\textwidth}P{0.0020945340501792114\textwidth}P{0.003808243727598566\textwidth}P{0.08968413978494624\textwidth}P{0.29723342293906807\textwidth}P{0.00799731182795699\textwidth}P{0.006093189964157706\textwidth}P{0.0020945340501792114\textwidth}P{0.0015232974910394264\textwidth}}
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\multicolumn{7}{l}{property of the Republic of Kazakhstan, \#206 from}\tabcellsep and atherosclerotic lesion development in Ldlr-\\
\multicolumn{3}{l}{21.06.2006; IP 01875.}\tabcellsep \tabcellsep \tabcellsep \tabcellsep deficient mice on a long-term high-fat diet. PLoS\\
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Authors:\tabcellsep \multicolumn{2}{l}{Oshakbayev}\tabcellsep KP,\tabcellsep \multicolumn{2}{l}{Izatullayev}\tabcellsep EA,\tabcellsep with carotidatherosclerosisin theyoungNorth Indian\\
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\multicolumn{7}{l}{Theriault G, et al. Age differences in cardiovascular}\tabcellsep Dukenbayeva BA. The conception of atherosclerosis\\
\multicolumn{7}{l}{disease risk factors explained by the level of visceral}\tabcellsep evolution development in ontogenesis. Certificate of\\
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115-20.\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep Postprandial\tabcellsep dyslipidaemia\tabcellsep and\tabcellsep diabetes:\\
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409.\tabcellsep \tabcellsep \tabcellsep \tabcellsep \tabcellsep \\
\multicolumn{7}{l}{20. Hoi Y, Zhou YQ, Zhang X, Henkelman RM, Steinman}\\
\multicolumn{7}{l}{DA. Correlation between local hemo dynamics and}\end{longtable} \par
 
\caption{\label{tab_4}Table 1 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{2} \par 
\begin{longtable}{P{0.30691676436107856\textwidth}P{0.10463071512309495\textwidth}P{0.0727432590855803\textwidth}P{0.10463071512309495\textwidth}P{0.07174677608440796\textwidth}P{0.0906799531066823\textwidth}P{0.09865181711606096\textwidth}}
Parameters\tabcellsep \multicolumn{2}{l}{Patientgroup(n=71)}\tabcellsep \multicolumn{2}{l}{Healthy group(n=26)}\tabcellsep t-test\tabcellsep P-value\\
\tabcellsep ?\tabcellsep SEM\tabcellsep ?\tabcellsep SEM\tabcellsep \tabcellsep \\
Passport age (years)\tabcellsep 46.45\tabcellsep 2.29\tabcellsep 48.55\tabcellsep 3.69\tabcellsep 0.484\tabcellsep 0.315\\
Weight (kg)\tabcellsep 83.90\tabcellsep 2.70\tabcellsep 75.61\tabcellsep 4.45\tabcellsep 1.687\tabcellsep 0.057\\
Height (cm)\tabcellsep 167.93\tabcellsep 1.12\tabcellsep 169.27\tabcellsep 1.99\tabcellsep 0.587\tabcellsep 0.279\\
BMI (kg/m 2 )\tabcellsep 29.75\tabcellsep 0.78\tabcellsep 26.22\tabcellsep 1.37\tabcellsep 2.239\tabcellsep 0.014\\
Fat mass (\%)\tabcellsep 32.40\tabcellsep 1.28\tabcellsep 20.27\tabcellsep 2.67\tabcellsep 4.097\tabcellsep 0.00004\\
Fat mass (kg)\tabcellsep 28.34\tabcellsep 1.61\tabcellsep 17.64\tabcellsep 3.18\tabcellsep 3.002\tabcellsep 0.0017\\
Visceral fat rating (Unit)\tabcellsep 10.04\tabcellsep 0.73\tabcellsep 6.40\tabcellsep 0.70\tabcellsep 3.599\tabcellsep 0.0003\\
Fat free mass (kg)\tabcellsep 54.80\tabcellsep 1.53\tabcellsep 58.37\tabcellsep 2.04\tabcellsep 1.400\tabcellsep 0.08\\
Total body water (kg)\tabcellsep 40.91\tabcellsep 1.16\tabcellsep 41.22\tabcellsep 1.63\tabcellsep 0.155\tabcellsep 0.44\\
Total body water (\%)\tabcellsep 48.70\tabcellsep 0.80\tabcellsep 56.18\tabcellsep 2.01\tabcellsep 3.458\tabcellsep 0.0004\\
Muscle mass (kg)\tabcellsep 52.05\tabcellsep 1.46\tabcellsep 55.39\tabcellsep 1.96\tabcellsep 1.367\tabcellsep 0.087\\
Muscle mass (\%)\tabcellsep 64.19\tabcellsep 1.21\tabcellsep 75.74\tabcellsep 2.56\tabcellsep 4.079\tabcellsep 0.00005\\
Bone mass (kg)\tabcellsep 3.16\tabcellsep 0.07\tabcellsep 3.01\tabcellsep 0.10\tabcellsep 1.229\tabcellsep 0.111\\
Bone mass (\%)\tabcellsep 3.77\tabcellsep 0.09\tabcellsep 4.01\tabcellsep 0.10\tabcellsep 1.784\tabcellsep 0.039\\
Metabolic age (years)\tabcellsep 49.00\tabcellsep 1.73\tabcellsep 42.35\tabcellsep 2.60\tabcellsep 2.129\tabcellsep 0.018\\
Basal metabolic rate (kcal/day)\tabcellsep 1661.6\tabcellsep 46.45\tabcellsep 1419.8\tabcellsep 52.77\tabcellsep 3.439\tabcellsep 0.0004\\
Bioimpedance (ohms)\tabcellsep 502.10\tabcellsep 10.30\tabcellsep 467.42\tabcellsep 9.11\tabcellsep 2.522\tabcellsep 0.0067\end{longtable} \par
  {\small\itshape [Note: Abbreviations: BMI, body mass index; M, mean; SEM, standard error of the mean]} 
\caption{\label{tab_5}Table 2 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{3} \par 
\begin{longtable}{}
\end{longtable} \par
 
\caption{\label{tab_6}Table 3 :}\end{figure}
 \begin{figure}[htbp]
\noindent\textbf{4} \par 
\begin{longtable}{P{0.29013722126929675\textwidth}P{0.13413379073756432\textwidth}P{0.06852487135506004\textwidth}P{0.12538593481989707\textwidth}P{0.06415094339622641\textwidth}P{0.08310463121783876\textwidth}P{0.08456260720411664\textwidth}}
\tabcellsep \multicolumn{2}{l}{Before the weight loss therapy}\tabcellsep \multicolumn{2}{l}{After the weight loss therapy}\tabcellsep \tabcellsep \\
Parameters\tabcellsep (n=31)\tabcellsep \tabcellsep (n=31)\tabcellsep \tabcellsep t-test\tabcellsep P-value\\
\tabcellsep M\tabcellsep SEM\tabcellsep M\tabcellsep SEM\tabcellsep \tabcellsep \\
Passport age (years)\tabcellsep 48.11\tabcellsep 2.10\tabcellsep -\tabcellsep -\tabcellsep -\tabcellsep -\\
Weight (kg)\tabcellsep 89.56\tabcellsep 4.59\tabcellsep 77.91\tabcellsep 4.39\tabcellsep 1.834\tabcellsep 0.035\\
BMI (kg/m 2 )\tabcellsep 30.15\tabcellsep 1.38\tabcellsep 26.23\tabcellsep 1.30\tabcellsep 2.068\tabcellsep 0.021\\
Fat mass (\%)\tabcellsep 29.87\tabcellsep 2.01\tabcellsep 20.23\tabcellsep 2.55\tabcellsep 2.969\tabcellsep 0.0019\\
Fat mass (kg)\tabcellsep 26.75\tabcellsep 2.94\tabcellsep 15.76\tabcellsep 2.98\tabcellsep 2.625\tabcellsep 0.005\\
Visceral fat rating (units)\tabcellsep 11.73\tabcellsep 1.26\tabcellsep 8.02\tabcellsep 1.64\tabcellsep 1.794\tabcellsep 0.038\\
Fat free mass (kg)\tabcellsep 62.81\tabcellsep 2.18\tabcellsep 60.82\tabcellsep 2.01\tabcellsep 0.671\tabcellsep 0.25\\
Total body water (kg)\tabcellsep 43.98\tabcellsep 1.69\tabcellsep 43.11\tabcellsep 1.58\tabcellsep 0.376\tabcellsep 0.35\\
Total body water (\%)\tabcellsep 49.11\tabcellsep 1.41\tabcellsep 55.33\tabcellsep 1.99\tabcellsep 2.553\tabcellsep 0.0061\\
Muscle mass (kg)\tabcellsep 58.56\tabcellsep 2.11\tabcellsep 57.55\tabcellsep 1.91\tabcellsep 0.355\tabcellsep 0.36\\
Muscle mass (\%)\tabcellsep 65.39\tabcellsep 1.87\tabcellsep 73.87\tabcellsep 2.49\tabcellsep 2.723\tabcellsep 0.0038\end{longtable} \par
 
\caption{\label{tab_7}Table 4 :}\end{figure}
 			\footnote{© 2013 Global Journals Inc. (US)} 			\footnote{( ) F Weight Loss Programin Patients with Atherosclerosis: Arandomised Controlled Clinical Trial} 		 		\backmatter  			 \par
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\end{document}
