Relationship of the blood pressure's level and skinfold thickness]

OBJECTIVE: Hypertension is an important problem of the public health. Insufficient education of the people along with insufficient physical examination also plays a role in the poor success of the diagnosis and treatment of the hypertension. We investigated whether the skinfold thickness has an importance in the prediction of blood pressure or not. METHODS: In Aydin City area 110 women and 100 men selected by randomized sampling method were included into our study. Body mass index, blood pressure and skinfold thickness were measured according to the international guidelines. RESULTS: There was a moderate correlation between the skinfold and body mass index (r= 0.494, p=0.000) and there was a mild correlation between the body mass index and systolic and diastolic blood pressures (r=0.225, p=0.000 and r=0.300, p=0.000, respectively). There was no correlation between the skinfold thickness and systolic and diastolic blood pressures (r=0.058, p=0.400 and r=0.090, p=0.194, respectively). CONCLUSION: It is concluded that body mass index, not skinfold thickness, can be used for the prediction of the blood pressure. Some other factors independent from the body mass index might be the determinants of the skinfold thickness.     

Positive sign of the stenocardia syndrome as a criterion of myocardial ischemia during the treadmill test

Diagnostic validity of the criteria of myocardial ischemia in coronary patients exposed to the treadmill test is assessed. The risk of a false diagnosis of coronary insufficiency on the basis of the pain syndrome was 5 times as high as that of diagnosis based on ischemic electrocardiographic ST depression. In subjective assessment of walking tolerance, patients with severe angina were particularly prone to mistakes. Limitations of angina classifications by severity, based on subjective sensations of coronary patients, are considered.     

Near-infrared spectrophotometric monitoring of oxygen distribution to intact brain and skeletal muscle tissues

During continuous near-infrared optical monitoring of brain cortex and hindlimb skeletal muscles, anesthetized, ventilated cats were exposed either to progressive alveolar hypoxia, or to acute hemorrhage followed in some cases by resuscitation. Hypoxia decreased cytochrome a,a3 oxidation state in muscle more than in brain, while tissue blood volume increased in brain and decreased in muscle. At a PaO2 of 25 torr, cytochrome a,a3 oxidation level in the brain was sufficient to support EEG activity, but the cytochrome a,a,3 oxidation state in resting, innervated hindlimb muscle was near zero. Hemorrhagic hypotension invariably decreased cytochrome a,a3 oxidation state and tissue blood volume more in muscle than in brain, and muscle cytochrome a,a3 was completely reduced at about a 25-ml/kg blood loss. These observations, supported by noninvasively measured changes in near-infrared absorption in the tissues during serial intravascular injections of indocyanine green dye, indicate that different cytochrome responses to hypoxia and oligemia in muscle vs. brain tissue are attributable to different regional circulatory adjustments.     

In vivo effect of prothymosin-alpha 1 on humoral and cell-mediated immune responses in the young rat.

There is a large body of evidence for the role of thymosin peptides in immunogenesis and immunity. In this paper we report on the influence of prothymosin alpha 1 (ProT-alpha 1), a hormone-like peptide derived from the calf thymus, on humoral and cellular immune reactions in the rat. Young adults received intraperitoneal injections of ProT-alpha 1 in the periods before and after immunization with cellular and soluble antigens. ProT-alpha-treatment produced a dose-dependent increase of both humoral and cell-mediated immune responses. The thymus weight increased but not that of spleen. Treatment of nonimmunized rats with this polypeptide significantly elevated the number of CD4+ and decreased the number of CD8+ cells in the peripheral blood. The results suggest a potent immunostimulatory activity of ProT-alpha 1 and imply direct action of this polypeptide on T lymphocytes.     

Activation of human blood monocytes by oxidized polyunsaturated fatty acids: a possible mechanism for the generation of lipid peroxides in the circulation.

The ability of native and oxidized lipids and lipoproteins to stimulate production of reactive oxygen species (ROS; superoxide and hydrogen peroxide) by human blood monocytes has been studied in vitro. Neither native human low density lipoprotein (LDL), ''altered'' LDL (oxidized either by lipoxygenase, activated human monocytes or air) nor oxidized cholesterol had any significant effect on ROS production of monocytes. However, different oxidation products of a lipid emulsion (Lipofundin; largely consisting of linoleic acid oxidized either by lipoxygenase, Fe3+ or ultraviolet irradiation) greatly enhanced ROS production of monocytes. A hypothesis that activation of circulating leucocytes by oxidized fatty acids may generate oxidized plasma LDL, was tested in rabbits. Characteristics of LDL, separated from rabbit plasma 6 h after intravenous injection of an oxidized lipid emulsion, was compared to that of LDL isolated before the lipid treatment. Post-treatment LDL-fraction of plasma had increased lipid peroxide content and compared to the pretreatment LDL, caused a threefold increase in the incorporation of cholesterol into cultured (rat aortic) endothelial cells. The observed intense and lasting stimulation of monocytes by oxidized polyunsaturated fatty acids in vitro, and the generation of ''altered'' LDL by these oxidized lipids in vivo suggests a mechanism by which atherogenic oxidized LDL could form in the circulation.     

A selective LC/RIA for dexamethasone and its prodrug dexamethasone-21-isonicotinate in biological fluids.

A combined LC/RIA procedure is described for the selective determination of dexamethasone (DEX) and its prodrug dexamethasone-21-isonicotinate (DIN) in plasma. The low affinity of the employed dexamethasone antiserum for DIN (cross-reactivity less than 0.5%) allowed the direct determination of DEX in plasma extracts. For the determination of DIN, both substances of interest were separated by LC, the DIN containing fraction was collected, hydrolysed and the generated DEX was consequently assayed by radioimmunoassay. The assay detection limits were 0.1 ng ml-1 for DEX and 0.75 ng ml-1 for DIN. For both substances, inter- and intra-day variabilities (RSDs) were 6 and 12%, respectively.     

Molecular determinants of cetuximab efficacy.

PURPOSE: To investigate whether mRNA expression levels of cyclin D1 (CCND1), cyclooxygenase 2 (Cox-2), epidermal growth factor receptor (EGFR), interleukin 8 (IL-8), and vascular endothelial growth factor (VEGF), all members of the EGFR signaling pathway, are associated with clinical outcome in patients with EGFR-expressing metastatic colorectal cancer (CRC) treated with cetuximab. PATIENTS AND METHODS: Thirty-nine patients with metastatic CRC, refractory to both irinotecan and oxaliplatin, were enrolled on IMCL-0144 and treated with single-agent cetuximab. The intratumoral mRNA levels of CCND1, Cox-2, EGFR, IL-8, and VEGF were assessed from paraffin-embedded tissue samples using laser-capture microdissection and quantitative real-time polymerase chain reaction. RESULTS: There were 21 women and 18 men with a median age of 64 years (range, 35 to 83 years). Higher gene expression levels of VEGF were associated with resistance to cetuximab (P = .038; Kruskal-Wallis test). The combination of low gene expression levels of Cox-2, EGFR, and IL-8 was significantly associated with overall survival (13.5 v 2.3 months; P = .028; log-rank test). Both findings were independent of skin toxicity that was itself significantly correlated to survival. Patients with a lower mRNA amount of EGFR had a longer overall survival compared with patients that had a higher mRNA amount (7.3 v 2.2 months; P = .09; log-rank test). Patients with lower expression of Cox-2 had a significantly higher rate of grade 2 to 3 skin reactions under cetuximab treatment. CONCLUSION: This pilot study suggests that gene expression levels of Cox-2, EGFR, IL-8, and VEGF in patients with metastatic CRC may be useful markers of clinical outcome in single-agent cetuximab treatment.