Changes in intra-abdominal pressure and central venous and brain venous blood pressure in patients during extracorporeal circulation.

BACKGROUND: The aim was to analyze IAP changes and the relationships between IAP, CVP, and brain venous blood pressure, which are still unknown, in patients undergoing coronary artery bypass grafting (CABG) with extracorporeal circulation. MATERIAL/METHODS: Twenty-five male patients (aged 53-67 years) underwent CABG under general anesthesia with normovolemic hemodilution. IAPs were measured in the urinary bladder, CVP by left internal jugular vein cannulation, and brain venous blood pressure by retrograde cannulation of the right jugular vein bulb (JVP, jugular vein pressure) at seven time-points: 1) after induction of anesthesia before the operation, 2) during internal thoracic artery preparation, 3) 10 minutes after heart-lung machine disconnection, 4) after procedure completion, before sending the patient to the intensive postoperative care unit, 5) one hour after the procedure, 6) 6 hours after the procedure, and 7) 18 hours after the procedure. RESULTS: IAP increased from points 3 to 6. CVP increased from points 3, 4, and 5 and decreased at point 7. Similar changes were noted in JVP. There were significant correlations between IAP and CVP at points 1, 2, 3, 4, and 5, IAP and JVP at points 3, 4, and 5, and CVP and JVP at all points. The overall analysis showed correlations between IAP and CVP and JVP and very strong correlation between CVP and JVP. CONCLUSIONS: 1) CABG with extracorporeal circulation resulted in increases in IAP, CVP, and brain venous blood pressure. 2) The changes in CVP and brain venous blood pressure correlated with intra-abdominal pressure.     

Application of the Minnesota Code in evaluating electrocardiographic features of ischemic heart disease in patients exposed to carbon disulphide

Summary We examined 81 men exposed for a long time to carbon disulphide (CS₂) and tested the possible electrocardiographic (ECG) changes of ischemic heart disease (I.H.D.). The subjects were examined twice in two years. In order to make the ECG evaluation more objective, the Minnesota Code was applied. Two obligatory ECG examinations and only one submaximal effort test were carried out. For comparative evaluation, the control group was examined once. We proved that, in spite of the accepted opinion concerning the atheromatous action of CS₂, this compound does not cause ECG symptoms of I.H.D. in a higher percentage of exposed persons. It also does not cause any significant increase in I.H.D. symptoms in dynamic ECG observations.     

Concentration of TBA-reactive substances in type II pneumocytes exposed to oxidative stress

INTRODUCTION: Oxidative lung damage may be associated with the destruction of alveolar cells. Type II alveolar epithelial cells (AECs),as progenitors of type I cells, are indispensable for the renovation of alveolar structure after lung injury. Extensive damage to type II cells could be responsible for unfavorable outcome. However, the susceptibility of type II AECs to oxidative stress is unclear. MATERIAL/METHODS: We investigated the susceptibility of freshly isolated and cultured rat type II AECs to oxidative stress (H2O2 and Fe2+). Thiobarbituric acid reactive substances (TBARS)were measured as indices of lipid peroxidation and cytotoxicity was estimated by the MTT test. Aminotriazol (ATZ), an inhibitor of intracellular catalase, was used to estimate the protective role of catalase. RESULTS: TBARS concentration increased significantly in freshly isolated, oxidant-exposed cells (4.0 +/-1.3 vs.8.3 +/-2.2 nmol/g protein, p=0.0313)and insignificantly in cultured cells (1.7 +/-0.4 vs.4.4 +/-1.7 nmol/g protein).ATZ was toxic even to cells not exposed to oxidants. Inhibition of catalase in cells exposed to oxidants resulted in an insignificant increase in TBARs:4.5 +/-1.5 vs.16.2 +/-3.9 nmol/g protein, p=0.0625,and 4.0 +/-0.8 vs.7.6 +/-4.0 for freshly isolated and cultured cells, respectively. Oxidative stress itself did not increase cytotoxicity. CONCLUSIONS: Type II AECs are not resistant to oxidative stress. We cannot, however, explain why cells with evidence of lipid peroxidation do not show increased cytotoxicity. The toxicity of ATZ is not related to oxidative cell damage. In cells exposed to oxidants, TBARS may fur-ther increase when catalase is inhibited, which suggests an important protective role for catalase.     

Small CD4+8+TCRlow thymocytes contain precursors of mature T cells

To evaluate directly the developmental potential of cortical CD4⁺8⁺ thymocytes, highly purified populations of small, nondividing CD4⁺8⁺TCR^low and large, dividing CD4⁺8⁺TCR^high thymocytes from H-2^d mice expressing a transgenic T cell receptor restricted by H-2D^b (major histocompatibility complex class I) molecules were transferred into the thymus of normal, nonirradiated H-2^b recipient mice. The results show that both populations generate CD4^?8⁺ thymocytes under these conditions, thus providing conclusive evidence that small cortical thymocytes do not represent a “dead end” but an important intermediate stage in T cell development.     

Strain variation in tumor necrosis factor induction by parasites from children with acute falciparum malaria.

A small proportion of individuals infected with Plasmodium falciparum develop cerebral malaria. Why it affects some infected individuals but not others is poorly understood. Since tumor necrosis factor (TNF) has been implicated strongly in the pathogenesis of cerebral malaria, here we have compared different parasite isolates for their ability to induce TNF production by human mononuclear cells in vitro. Wild isolates were collected from 34 Gambian children with cerebral malaria and 66 children with uncomplicated malaria fever. Cerebral malaria isolates tended to stimulate more TNF production than mild malaria isolates, but there was considerable overlap between the two groups, and the present data provide only limited support for the hypothesis that cerebral malaria is caused by strains of P. falciparum inducing high levels of TNF. However, it is notable that the amounts of TNF induced by different wild isolates from a single locality differed by over 100-fold. The biological significance of this polymorphism deserves further scrutiny in view of the central role that TNF is believed to play in host defense and in the clinical symptomatology of human malaria.     

Association of defensin beta-1 gene polymorphisms with asthma

BACKGROUND: Defensins are antimicrobial peptides that may take part in airway inflammation and hyperresponsiveness. OBJECTIVE: We characterized the genetic diversity in the defensin beta-1 (DEFB1) locus and tested for an association between common genetic variants and asthma diagnosis. METHODS: To identify single nucleotide polymorphisms (SNPs), we resequenced this gene in 23 self-defined European Americans and 24 African Americans. To test whether DEFB1 genetic variants are associated with asthma, we genotyped 4 haplotype-tag SNPs in 517 asthmatic and 519 control samples from the Nurses' Health Study (NHS) and performed a case-control association analysis. To replicate these findings, we evaluated the DEFB1 polymorphisms in a second cohort from the Childhood Asthma Management Program. RESULTS: Within the NHS, single SNP testing suggested an association between asthma diagnosis and a 5' genomic SNP (g.-1816 T>C; P = .025) and intronic SNP (IVS+692 G>A; P = .054). A significant association between haplotype (Adenine, Cytosine, Thymine, Adenine [ACTA]) and asthma ( P = .024) was also identified. Associations between asthma diagnosis and both DEFB1 polymorphisms were observed in Childhood Asthma Management Program, a second cohort: g.-1816 T>C and IVS+692 G>A demonstrated significant transmission distortion ( P = .05 and .007, respectively). Transmission distortion was not observed in male subjects. The rare alleles (-1816C and +692A) were undertransmitted to offspring with asthma, suggesting a protective effect, contrary to the findings in the NHS cohort. Similar effects were evident at the haplotype level: ACTA was undertransmitted ( P = .04) and was more prominent in female subjects ( P = .007). CONCLUSION: Variation in DEFB1 contributes to asthma diagnosis, with apparent gender-specific effects.     

Effectiveness of divergent selection for open-field activity in rabbits and correlated response for body weight and fertility

Two lines deriving from the same rabbit stock were selected for 8 generations for high (H) or low (L) locomotor activity score in the open field (OFS). The divergent selection was most effective up to the 3rd generation in the H line and up to the 4th generation in the L line. In further generations a decrease of OFS in the H line and a floor effect (OFS = 0) in the L line were observed. The mean OFS increased significantly in consecutive trials in the H line, whereas this increase was non-significant in the L line. There was a negative and very high correlation between the latency to enter the open field and the OFS (–0.95 and –0.98 for the H and L line, respectively). The realized heritability of the OFS was 0.46 and 0.23 in generations 0–3 within the L and H line, respectively, and 0.44 and –0.06 in generations 0–8. As calculated on the basis of divergent selection, the heritability was 0.31 and 0.15 for generations 0–3 and 0–8, respectively. The L rabbits were heavier shortly before (4th wk, P < 0.001) and after (8th wk, P < 0.01) weaning, than those of the H line, whereas the H rabbits grew faster (P < 0.05) between the 4th and 20th wk of age. There was a tendency for decreasing weight gains in consecutive generations. Generally, a lower percentage of H females delivered litters than those of the L line, but this was due to a very low percentage of such females in the 3rd and 6th generations. It can be assumed that H and L lines represent different, i.e., active and passive, coping strategies. These lines of rabbits offer increased possibilities for physiologically and ethologically oriented studies, e.g., on the welfare of caged animals.