Subclavian vein thrombosis: a continuing challenge

Subclavian vein thrombosis is a relatively uncommon but potentially morbid disease entity. To determine the frequency, cause, and best mode of treatment of this problem, we performed a chart review of all patients with a diagnosis of subclavian vein thrombosis at two major metropolitan hospitals during a 6-year period. A total of 40 patients were identified with subclavian vein thrombosis, which represented 3.5% of all venous thromboses detected during the 6-year period. No side or sex predilection was noted and the majority of patients were outpatients. The cause was fairly evenly divided among intravenous catheters (32%), anatomic abnormalities (45%), and carcinoma with postoperative radiation (22.5%). Despite the increasing use of the subclavian veins for pacemaker leads, hyperalimentation, and permanent intravenous access for chemotherapy, there has not been an increase in diagnosed subclavian vein thrombosis. Anatomic abnormalities with compression of the vein respond well to either heparinization or lytic therapy but require surgery if the venous abnormality persists. Treatment consisted of lytic therapy in 20%, heparinization in 55%, and elevation with removal of the central line in 25% of patients. All patients responded well to treatment, with a decrease in swelling and symptoms; no patient progressed to venous gangrene and only one (2.5%) had a documented pulmonary embolus. Medical treatment provides excellent long-term benefit in most cases unless complicated by an anatomic abnormality.     

An intervention for multiethnic obese parents and overweight children.

The purpose of this pilot study was to determine the effects of the addition of coping skills training for obese multiethnic parents whose overweight children were attending a weight management program. At 6 months, parents in the experimental group had significantly lower body mass index (BMI) and body fat percentage (BFP) and higher numbers of pedometer steps compared with those in the control group. Parents in the experimental group also demonstrated significant improvement in interpersonal relationships, behavior control, and stress management compared with those in the control group. Children in the experimental group demonstrated trends toward decreased BMI and BFP and increased pedometer steps.     

mRNAs encoding ribulose-1,5-bisphosphate carboxylase remain bound to polysomes but are not translated in amaranth seedlings transferred to darkness

When light-grown seedlings of amaranth are transferred to total darkness, synthesis of the large subunit (LS) and small subunit (SS) of ribulose-1,5-bisphosphate carboxylase [RbuP₂Case; 3-phospho-D-glycerate carboxylase (dimerizing), EC 4.1.1.39] is rapidly depressed. This reduction in RbuP₂Case synthesis occurs in the absence of any corresponding changes in levels of functional mRNA for either subunit. Four hours after light-to-dark transition little, if any, changes in the distribution of LS and SS mRNAs on polysomes could be detected. The association of these mRNAs with polysomes was authenticated by treatment with RNase A or puromycin. Furthermore, polysomes were able to synthesize LS and SS precursor in cell-free translation systems supplemented with inhibitors of initiation. Therefore, during a light-to-dark transition LS and SS mRNAs remained bound to polysomes but were not translated in vivo, suggesting that control is exercised, in part, at the translational elongation step.     

The micro gas-liquid chromatographic analysis of 4-(3',3'-dimethylallyl)-1,2-diphenylpyrazolidine-3,5-dione (feprazone) in human biosamples

A gas-liquid chromatographic method for the determination of feprazone in various biological matrixes, employing a choice of detector options, is described. After rapid, micro-scale extraction of the sample with n-butyl acetate at physiological pH, the solution was injected directly onto the chromatograph. Separation was with either an OV7 column and flame ionisation or electron capture detection, or with a carbowax high polymer column and nitrogen specific detection. When 100 mul of plasma was extracted the limit of accurate measurement was 2 mg 1(-1) for F.I.D. and N.P.D. and 0.5 mg 1(-1) with E.C. detection. Quantification was by comparison with a range of plasma calibrators carried throughout the procedure, and determination of peak height ratios against an internal standard incorporated into the extracting solvent. The CV of the assay throughout the concentration range normally encountered in patients undergoing feprazone treatment, ranged between 2.4 and 7.8% for the various detector options. The analytical method has been applied to samples collected both from patients and normal volunteers undergoing treatment with a range of feprazone maintenance doses.     

Enzymatic determination of potassium in serum

This is a kinetic assay for measuring K+ in serum, based on the activation of pyruvate kinase (EC 2.7.1.40) by K+. We eliminated interference from Na+ and NH4+ ions, which also activate this enzyme, by including Na+-binding and NH4+-consuming reagents in the reaction mixture. The assay was developed with and evaluated in the Cobas Fara centrifugal analyzer (and has been used in other kinetic analyzers). Within-run and between-run CVs were less than 1.4% and less than 1.6%, respectively. The reaction rate per millimole of K+ per liter (0.05 delta A/min) was more than double that of the reagent blank (0.02 delta A/min). Results correlated well with those by flame photometry, and interference from bilirubin, hemoglobin, lipids, heparin, and other cations was negligible. This method, in conjunction with a previous method we have reported in which beta-galactosidase is used for measuring Na+ in serum, offers a practical alternative to the use of ion-selective electrodes and flame photometry for measuring these clinically important monovalent cations in high-throughput or "stat" biochemical analyzers.     

Animal models in the investigation of anorexia

Anorexia nervosa (AN) is an eating disorder of unknown origin that most commonly occurs in women and usually has its onset in adolescence. Patients with AN invariably have a disturbed body image and an intense fear of weight gain. There is currently no definitive treatment for this disease, which carries a 20% mortality over 20 years. Development of an appropriate animal model of AN has been difficult, as the etiology of this eating disorder likely involves a complex interaction between genetic, environmental, social, and cultural factors. In this review, we focus on several possible rodent models of AN. In our laboratory, we have developed and studied three different mouse models of AN based on clinical profiles of the disease; separation stress, activity, and diet restriction (DR). In addition, we discuss the spontaneous mouse mutation anx/anx and several mouse gene knockout models, which have resulted in an anorexic phenotype. We highlight what has been learned from each of these models and possibilities for future models. It is hoped that a combination of the study of such models, together with genetic and clinical studies in patients, will lead to more rational and successful prevention/treatment of this tragic, and often fatal, disease.     

A fetus with an X;1 balanced reciprocal translocation and eye disease.

A 19 week female fetus is described with a de novo X;1 reciprocal balanced translocation, with the breakpoint on the X chromosome at Xp11.4, and eye pathology consistent with the early stages of Norrie disease. The fetus seems to be an example of a female manifesting an X linked recessive disease, and it was shown that the normal X chromosome was completely inactivated in all cells examined. Norrie disease has been mapped to Xp11.3, and fluorescence in situ hybridisation studies showed that the Norrie disease gene had not obviously been disrupted. Mutation screening by SSCP analysis showed no aberrant fragments of the coding region of the gene. Several eye disease genes map to the same region of the X chromosome, but are excluded on grounds of pathology. One possibility is that this fetus has a Norrie-like eye disease caused by the mutation of another gene located at Xp11.4. If this is so, there are implications for prenatal diagnosis.