Search

The aim of this study is to determine the feasibility of using reduced scan range CT pulmonary angiography technique in pregnancy for pulmonary embolism (PE) and to quantify resulting dose reduction. This was a retrospective study. Eighty-four CTPA exams performed on pregnant women during 2004-2012. The scans were modified to create reduced anatomic coverage scans extending from aortic arch to base of heart. These were separately evaluated by two radiologists for PE and non-PE abnormalities. The results were then compared by the third radiologist with original radiology report and scans. Radiation dose reduction was evaluated prospectively in 36 patients as part of a quality control project. Two patients had PE and were successfully identified on reduced z-axis scans. Thirty-two exams were normal; rest had 60 pertinent and 16 had incidental findings. There were four incidental findings which included three benign thyroid nodules and one benign small lung nodule which were missed. None of these affected clinical outcome or management. There was 71 % radiation dose reduction. No PE or any important diagnoses are missed using reduced z-axis CTPA in pregnancy. There is a substantial radiation dose reduction. Hence, this technique is highly recommended in pregnancy.

As can be seen from this review, protein phosphorylation appears involved in both positive and negative regulation of platelets. To date, good evidence has been presented for the involvement of protein phosphorylation in the regulation of granule centralization (i.e. myosin light chain phosphorylation). It is probable that protein phosphorylation may also be involved in granule labilization, pseudopod formation and ATP synthesis. Protein phosphorylation in association with platelet activation appears mediated through calcium flux, in the case of myosin light chain phosphorylation, and through diglyceride or other substances in the case of 47P phosphorylation. A summary scheme is shown in Figure 1.

Transfer RNA's were isolated from Euglena gracilis. Chloroplast cistrons for tRNA were quantitated by hybridizing tRNA to ct DNA. Species of tRNA hybridizing to ct DNA were partially purified by hybridization-chromatography. The tRNA's hybridizing to ct DNA and nuclear DNA appear to be different. Total cellular tRNA was hybridized to ct DNA to an equivalent of approximately 25 cistrons. The total cellular tRNA was also separated into 2 fractions by chromatography on dihydroxyboryl substituted amino ethyl cellulose. Fraction I hybridized to both nuclear and ct DNA. Hybridizations to ct DNA indicated approximately 18 cistrons. Fraction II-tRNA hybridized only to ct DNA, saturating at a level of approximately 7 cistrons. The tRNA from isolated chloroplasts hybridized to both chloroplast and nuclear DNA. The level of hybridization to ct DNA indicated approximately 18 cistrons. Fraction II-type tRNA could not be detected in the isolated chloroplasts.

Platelet responses to halothane in normal individuals and in patients susceptible to malignant hyperthermia were evaluated. Platelets in platelet-rich plasma from both normal controls and patients underwent aggregation in response to halothane. There was no significant difference in the degree of aggregation between normal subjects and patients. Aggregation by halothane was associated with a change in platelet shape, centralization of platelet granules, and phosphorylation of platelet actin binding protein, myosin light chain, and a 40 000-dalton protein. Aggregation induced by halothane could be inhibited by EGTA, PGE1, adenosine and verapamil, but not by aspirin. Aggregation induced by halothane could be potentiated by small doses of adrenaline or ADP and in some individuals by caffeine. However, previous exposure of platelets to halothane made them subsequently less aggregable to ADP. The results of these studies do not support a use of halothane-induced aggregation of platelets to detect an abnormality in individuals susceptible to malignant hyperthermia, but do provide new evidence of the effects of halothane on cellular function.

Addition of thrombin to human platelets results in production of lysophosphatidic acid. Such synthesis of lysophosphatidic acid can be inhibited by mepacrine, an inhibitor of the phospholipase A2 which attacks phosphatidic acid to give lysophosphatidic acid. In the present study, mepacrine was used at a concentration of 2.5-20 microM, sufficient to block aggregation and lysophosphatidic acid formation induced by 0.1 U/ml thrombin. Mepacrine, at this concentration, also blocked thrombin-induced phosphorylation of platelet myosin light chain and a 47 kDa protein, thrombin-induced secretion and thrombin-induced release of arachidonic acid from platelet phospholipids. However, mepacrine also partly inhibited the formation of phosphatidic acid in response to thrombin, consistent with some simultaneous inhibition of phospholipase C. Lysophosphatidic acid (2.5-22 microM) overcame the mepacrine block in thrombin-stimulated aggregation, protein phosphorylation and secretion without stimulating the release of arachidonic acid from platelet phospholipids or the formation of lysophosphatidic acid, and only slightly increasing phosphatidic acid formation. The results suggest that lysophosphatidic acid primarily acts distal to mepacrine inhibition of phospholipase A2 and phospholipase C and are consistent with the possibility that lysophosphatidic acid might be a mediator of part of the effects of low-dose thrombin on human platelets.