Diets rich in n-9, n-6 and n-3 fatty acids differentially affect the generation of inositol phosphates and of thromboxane by stimulated platelets, in the rabbit

We have studied the effects of semi-synthetic diets rich in either n-9 (olive oil, OO) or n-6 (corn oil, CO), or n-3 (fish oil, FO, as MaxEPA) fatty acids on the levels of major PUFA in platelet lipids, on the generation of inositol phosphates by [3H]inositol labelled platelets after stimulation with thrombin and of thromboxane B2 (TxB2) by platelet rich plasma (PRP) after stimulation with collagen. The predicted elevations of oleic (OA), linoleic (LA) and eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids were observed in platelet lipids of each animal group, but in the MaxEPA fed group accumulation of EPA was associated with depletion of linoleic acid (LA) rather than of arachidonic acid (AA). Basal levels of inositol-tris-phosphate (IP3) in platelets were lowest in the OO group and highest in the CO group, whereas the increment after thrombin stimulation (1 unit/ml NIH) was maximal in the OO group and minimal in the FO group. Instead, when generation of TxB2 by stimulated platelets was evaluated, no appreciable difference among the various groups could be detected, in accordance with the limited modifications of platelet AA content induced by the diets. The overall data indicate that dietary fatty acids modulate the pathway of inositol phosphate generation in rabbit platelets, independently of modifications of TxB2 production.     

Giant hydronephrosis presenting as unilateral iliofemoral vein thrombosis

We report a case of left iliofemoral vein thrombosis with extension to the inferior vena cava associated with giant right hydronephrosis secondary to ureteropelvic junction obstruction. Surgery revealed marked infrarenal vena caval compression and deviation to the left side caused by the dilated right renal pelvis, with resultant kinking of the origin of the left iliac vein. It is postulated that the reduction in blood flow caused by this compression and distortion predisposed this patient to venous thrombosis.     

Differences in the kinetic properties and sensitivity to inhibitors of human placental, erythrocyte, and major hepatic aldehyde dehydrogenase isoenzymes

(i) The characteristics of the major human hepatic isoenzymes of aldehyde dehydrogenase (ALDH), ALDH I and ALDH II, were compared with the ALDH activities found in human placenta and erythrocytes, (ii) In human liver biopsies, the Km of ALDH I was approximately 7 mumol/L whereas it was 32 mumol/L for ALDH II. The Vmax for ALDH I was 2-3 times greater than the ALDH II Vmax. Human liver ALDH I and II also differed in their sensitivity in inhibitors. Namely, ALDH I was less sensitive to disulfiram than the ALDH II isoenzyme. (iii) ALDH activity in human placenta and erythrocytes was much lower than in liver tissue. Kinetic data showed that placental ALDH isoenzyme had a high Km (in the millimolar range) and increased its activity raising the pH from 7.4 to 8.8, more than the hepatic ALDH I and ALDH II isoenzymes did. Erythrocyte ALDH activity presented a dual component; the smaller one was characterized by a low Km (micromolar range), whereas most of the ALDH activity showed a high Km (millimolar range). (iv) Placental ALDH was resistant to nitrefazole inhibition and was inhibited by disulfiram in a manner similar to the hepatic ALDH I isoenzyme; erythrocyte ALDH was more sensitive to the inhibitory action of disulfiram and nitrefazole. (v) It is concluded that erythrocyte and placental ALDH isoenzymes are different from the hepatic ALDH I and ALDH II forms. It is also suggested that placental and erythrocyte ALDH isoenzymes are different high-Km isoenzymes.     

Corneal endothelial cell loss following trephination

The amount of endothelial cell loss that occurs to the donor cornea during the trephination process was evaluated in 40 porcine eyes. A vital staining technique (alizarin red S and acid violet 19) was used to quantify the extent of endothelial damage and removal. Two types of corneal punches (Weck and H&I0 were used for trephination. The average amount of endothelial loss from the peripheral cornea was 7.9%, accounting for only a 3% loss of endothelial cells over the total surface area of the corneal button. a comparison of the Weck and H&I corneal punches showed no significant difference (P greater than 0.1) by Student's test for both endothelial cell damage and removal.     

The acting or interim leadership position: expectations, perceptions, realities

The acting or interim leadership position has been neglected in terms of selection, role identification, and status. Individuals, programs, and organizations are paying a price for this inattention.     

ACETALDEHYDE ADDUCTS WITH HAEMOGLOBIN: DETERMINATION OF ACETALDEHYDE RELEASED FROM HAEMOGLOBIN BY ACID HYDROLYSIS

Acetaldehyde, the first metabolite of ethanol, reacts with haemoglobinin vitro to produce acetaldehyde—haemoglobin adducts.Some clinical studies on the minor haemoglobins have suggestedthat these adducts may be formed in people abusing alcohol.Under hydrolysis of haemoglobin, with oxalic acid at 100°Cin sealed vials, some acetaldehyde was released and then specificallydetermined by HPLC. The kinetics of hydrolysis were studiedusing haemoglobin previously labelled with ¹⁴[C] acetaldehyde.The maximum liberation of ¹⁴[C] acetaldehyde was obtained after3 hr 30 min hydrolysis and this time factor was then utilizedin the analysis of alcoholic and control haemoglobin. Thus,we have confirmed the formation of acetaldehyde haemoglobinadducts in vivo. It must be noted that the released acetaldehydecorresponds only to an index of the stable adducts. The levelswere higher in alcoholics than in controls (1.417±0.171and 1.295±0.139 nmol/mg Hb, respectively, P<0.001).In conclusion, this marker is not a convenient tool for themonitoring of alcohol exposure levels because of the low differencesbetween alcoholic and control haemoglobins.     

The effect of psychosocial factors on lung cancer mortality at one year

In this study newly diagnosed male and female lung cancer patients admitted to two Ontario Cancer Foundation treatment clinics were interviewed. Information was obtained on demographic variables, presence of other chronic illness and the following psychosocial attributes: locus of control, social support and personality traits. From the clinic charts, information on stage of disease and pathological diagnosis was obtained. After controlling for the effects of stage and pathological diagnosis, the following psychological variables were found to increase the odds of death from lung cancer among males and females combined at one year after diagnosis: a high need for one aspect of social support, a reserved personality and the extremes of the personality trait soberness vs enthusiasm.