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Polska spośród wszystkich krajów rozwiniętych wykazuje najwyższy wzrost umieralności na chorobę niedokrwienną serca (IHD) i choroby naczyń mózgowych. Jest to związane z rozpowszechnieniem czynników ryzyka IHD, a wśród nich podwyższonego poziomu cholesterolu w surowicy i nadwagi. Oba te czynniki zależą w istotnym stopniu od nieprawidłowego żywienia. Świadomość pilnej potrzeby podjęcia działań profilaktycznych spowodowała powołanie Narodowego Programu Profilaktyki Cholesterolowej, za którego realizację resort zdrowia uczynił odpowiedzialny Instytut Żywności i Żywienia. Na Program składają się następujące działania: 1. Popularyzacja na skalę społeczną wiedzy na temat szkodliwych następstw podwyższonego poziomu cholesterolu oraz roli racjonalnego żywienia w profilaktyce IHD. 2. Szkolenie przed- i podyplomowe lekarzy na powyższy temat. 3. Organizacyjne usprawnienie wczesnej diagnostyki podwyższonych stężeń cholesterolu. 4. Podjęcie wysiłków na rzecz nowoczesnej polityki wyżywienia w Polsce. 5. Udoskonalenie metod leczenia zaburzeń gospodarki lipidowej i ich upowszechnienie.
Food intake, body mass index (BMI), serum lipids, blood glucose, systolic and diastolic blood pressure and pulse wave velocity were measured in the population of 2559 males aged 25-59 years employed in a foundry in Cracow in 1972-1974. Abnormal dietary habits were revealed. The share of protein in total energy intake was 11.7%, fats 37.1% and carbohydrates 51.2% (sugar 11.6%). The mean BMI was 25.3 ± 3.1 BMI above 25 was found in 44% of males under study. It has been shown that serum cholesterol, total lipids, esterified fatty acids, systolic and diastolic blood pressure, and pulse wave velocity were positively correlated with BMI. It is concluded that obesity prevention and treatment should be recognized as. an important method in prevention of coronary heart disease.
To investigate the effects of feeding diets differing in the content and in the type of protein, fat and carbohydrates on feeding efficiency and serum cholesterol two experiments on male rats were carried out. In the first the animals were fed semipurified diets containing 8, 12 or 16% of energy from protein with the following ratio of energy from fats to carbohydrate (F/CHO): 1/1, 1/2 and 1/3. In the second experiment eight combined diets containing various sources of protein (casein or soybean concentrate), fat (lard of rapeseed oil) and carbohydrates (sucrose or wheat starch) were used. After 60 days of feeding it was found that feed efficiency, concentrations of serum total cholesterol (TC) and cholesterol in HDL fraction (HDL-C) significantly depended on the amount and source of protein in the diet. The ratio F/CHO and the type of consumed fat effectively modified the influence of dietary protein on serum cholesterol. Rapeseed oil produced significantly higher HDL-C concentration than lard. Dietary sucrose, compared with starch, did not influence feeding efficiency and serum cholesterol. There was a combined effect of fat source — carbohydrate source on body weight and weight/length index but not on the concentration of serum cholesterol in the rat.
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Helicobacter pylori infection in coronary artery disease

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The role of inflammation in the pathogenesis and progression of coronary artery disease (CAD) has been increasingly discussed, but still remains unclear. Inflammatory changes in the vessel wall play an important role in the pathogenesis of atherosclerosis. Systemic inflammatory reaction can be detected by showing increased plasma levels of different proinflammatory cytokines and acute-phase proteins. Infectious agents have been linked to coronary heart disease on epidemiological and pathogenetic grounds. The prevalent condition and the exact mechanism of initiation of atherosclerotic vascular disease remain unclear. Nevertheless, many similarities exist between the processes of inflammation and atherogenesis, and the evidence is growing for the role of an active inflammation in the atherosclerosis in the coronary circulation and elsewhere. Although the seroepidemiological and eradication studies have suggested a causal relationship between Helicobacter pylori (Hp) infection and coronary heart disease; the issue is still controversial. The detection of Hp specific DNA in atheromatous plaque material from coronary arteries, but more important, the reduction in restenosis of coronary vessels after Hp eradication could be interpreted as an evidence for the involvement of a Hp infection in the progression of CAD induced by a local inflammatory process.
Background. Coronary arteriosclerosis risk factors increase the probability of the coronary heart disease and accompanying complications to a significant extent, acting independently from other circumstances. Material and methods. The study was conducted in a group of 250 students of the 1st-year medical studies, using an independently prepared questionnaire relating to the risk factors and particular lifestyles. Results. 1. Level of knowledge of the examined students on coronary arteriosclerosis risk factors: obesity - 250(100%); reduced physical activity - 240(96%); smoking - 230(92%); unhealthy diet - 223(89%); elevated LDL cholesterol concentration - 218(87%); arterial hypertension - 210(84%). 2. Incidence of coronary arteriosclerosis risk factors in students: strong family history - 75(30%); excessive stress - 50(20%); reduced physical activity - 190(76%); smoking - 55(22%), alcohol abuse - 95(38%). 3. Lifestyle of the examined group of students: eating fast-food – 180 (72%); drinking energetic beverages – 82(33%); “trying” and using drugs – 88(35%); insufficient amount of sleep – 190(76%). Conclusions. 1. Level of the examined students’ knowledge on coronary arteriosclerosis risk factors is satisfactory. 2. Despite the satisfactory level of knowledge on risk factors, their incidence in the tested group is significant. 3. Majority of the examined students live a healthy lifestyle.
Zaburzenia w zapisie Ekg charakterystyczne dla niedokrwiennej choroby serca były częstsze (15%) u pacjentów z otyłością typu brzusznego niż u osób z otyłością pośladkowo-udową (3%). Wykazano, że podwyższone ciśnienie skurczowe i rozkurczowe oraz poziom cholesterolu i trójglicerydów w surowicy są częstsze w otyłości brzusznej (AO) niż w otyłości pośladkowo-udowej (GO).
Long-term changes in the national diet and in the CHD mortality rate in Poland were examined. The level and the composition of the national diet was assessed on the basis of the food balance sheets data. Statistics of the Central Statistical Office were used to study the trends in he CHD mortality rate. The period covering 1960—1989 was considered. It was shown that the CHD mortality rate rose fivefold between 1960 and 1989 while the total morality rate increased by some 40 per cent. It was revealed that Polish national diet was shifting towards more affluent one over this period. Alcohol consumption and tobacco use were subject to considerable increase too in the last three decades. It was demonstrated that there was a temporary decrease in the CHD mortality rate covering the period of 1979—1982. This decrease coincided with severe economic crisis which contributed to transitory reverse in the former long-term upward trend in the consumption of atherogenic foods, alcohol and tobacco.
W okresie powojennym nastąpiła w Polsce gruntowna zmiana w strukturze zachorowalności i umieralności. Choroby zakaźne, stanowiące niegdyś główną przyczynę zgonów, ustąpiły miejsca chorobom układu krążenia i nowotworom złośliwym. W roku 1985 choroby układu krążenia i nowotwory przyczyniły się łącznie do prawie 70% wszystkich zgonów. Przyczyną tych zmian były liczne czynniki, a wśród nich niewłaściwy model żywienia się populacji. W grupie chorób układu krążenia szczególnie szybko zwiększała się umieralność na niedokrwienną chorobę serca. W roku 1985 wskaźnik zgonów z powodu tej choroby był czterokrotnie wyższy niż w roku 1960, przy czym wykazał on przejściowe obniżenie w latach 1979—1983. Wskazano na zbieżność między kształtowaniem się tego wskaźnika w latach 1960—1985 a zmianami w modelu żywienia, konsumpcji alkoholu i palenia tytoniu.
Twenty-four growing male rats of Wistar strain, weighing initially 120±3.5 g were randomly divided into four groups of six animals each and fed four different diets for 14 days: I - control diet (AIN-93G with soybean oil as a source of fat: 7 g/100 g), II - high-cholesterol diet (AIN-93G with soybean oil as a source of fat: 7 g/100 g + 1 g/100 g cholesterol), III - high-cholesterol diet (AIN-93G with lard as a source of fat: 7 g/100 g + + 1 g/100 g cholesterol), and IV - high-cholesterol diet (AIN-93G with lard as a source of fat: 7 g/100 g lard + 1 g/100 g cholesterol + 0.5 g/100 g cholic acid). On the day 14, the rats were anaesthetized and killed by withdrawing blood from the heart to obtain serum samples. The most striking increases (PcO.Ol) in the serum total and LDL+VLDL cholesterol were induced by the diet containing lard and supplemented with cholesterol + cholic acid (Group IV). Conversely, feeding the above diet to rats produced minimum (P<0.01) concentrations of the serum HDL cholesterol. It is concluded that the present animal model may be useful for evaluating the role of dietary factors in the development or regression of hypercholesterolemia.
We studied the effect of ischemia and reperfusion on the total antioxidant capacity (TAC) of blood plasma during cardiopulmonary bypass surgery employing the modified St. Thomas Hospital cardioplegic solution. TAC was determined using the FRAP method. TAC decreased during surgery, but no further decrease in TAC was observed during reperfusion, indicating that it is a relatively stable parameter of the antioxidative barrier of the body.
In this study we asked a question whether H. pylori LPS with or without LewisXY (Le) determinants as well as LBP (lipopolysaccharide binding protein) and sCD14 molecules recognizing bacterial LPS may be involved in atherogenesis. Sera from 57 patients with coronary heart disease (CHD), 27 H. pylori infected dyspeptic patients-H.p.(+) and 49 healthy controls (HC) were tested for IgM and IgG to H. pylori LPS expressing LeX (LPS LeX) or LeXY (LPS LeXY) determinants and to a glycine acid extract (GE). Immune complexes (ICs) of Lewis antigens and specific IgM or IgG were also determined. The prevalence of anti-GE IgG and IgA was significantly higher in CHD as compared to HC and the same as in the H.p.(+) group. The highest levels of anti-GE IgG were detected only for CHD group. CHD patients showed upregulation of IgG to LPS LeX and LeXY. In contrast, an upregulation of IgM to such LPSs was found for healthy subjects. The levels of LeY-anti-LeY IgG ICs were higher in CHD patients than in healthy controls similarly to the levels of LBP. There was no difference in sCD14 concentration between CHD and HC groups. The results obtained in this study indicate that H. pylori infections may be the risk factors of atherosclerosis due to: 1) an enhanced humoral response to H. pylori surface antigens, 2) a host predisposition to respond to Lewis determinants present in H. pylori LPS by IgG, 3) increased levels of serum LBP.
 To develop a more potent antithrombin agent with thrombolytic and antiplatelet properties, a new staphylokinase (SAK) variant was constructed. The kringle 2 domain (K2) of tissue type-plasminogen activator (t-PA) containing a fibrin-specific binding site (i), the RGD sequence (Arg-Gly-Asp) for the prevention of platelet aggregation (ii) and the antithrombotic agent - hirulog (iii) was assembled to the C-terminal part of recombinant staphylokinase (r-SAK). cDNA for the hybrid protein SAK-RGD-K2-Hirul was cloned into Pichia pastoris pPIC9K yeast expression vector. The introduction of K2 t-PA, the RGD sequence and hirulog into the C-terminus of r-SAK did not alter the staphylokinase activity. We observed a higher clot lysis potency of SAK-RGD-K2-Hirul as evidenced by a faster and more profound lysis of 125I-labeled human fibrin clots. The potency of thrombin inhibition by the hirulog C-terminal part of the recombinant fusion protein was almost identical to that of r-Hir alone. These results suggest that the SAK-RGD-K2-Hirul construct can be a more potent and faster-acting thrombolytic agent with better antithrombin and antiplatelet properties compared to r-SAK and SAK-RGD-K2-Hir.
The aim of this study was to evaluate the effect of carvedilol on the enzymatic antioxidative defence and plasma antioxidative activity in patients with stable angina. The study comprised 30 patients, aged 37–49 years with stable angina. Patients received carvedilol in escalating doses of 12.5 mg/24 h, 25 mg/24 h, and 50 mg/24 h for 4 weeks each. The control group was matched for age and gender, and consisted of 12 healthy volunteers, aged 39-49 years. Blood samples were collected from the cubital vein before and 4, 8 and 12 weeks after the therapy from the patients and once from the control group. For all the subjects, the superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px), catalase (CAT) activities in the erythrocytes and the antioxidant activity of the blood plasma were determined. The enzymatic antioxidative defence was significantly decreased in patients with stable angina in comparison to the healthy subjects. During the carvedilol therapy, an increase in the SOD-1, GSH-Px and CAT activities was observed. Moreover, 8 and 12 weeks after carvedilol therapy, the GSH-Px activity did not differ significantly from that observed in the group of healthy subjects. Carvedilol also increased the plasma antioxidative activity in patients with stable angina, but its level remained significantly lower than in the control group. In conclusion, carvedilol enhances antioxidant defense mechanisms in patients with chronic stable angina pectoris.
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