Hyperthyroidism with Periodic Paralysis

Hyperthyroidism may be associated with hypokalemic periodic paralysis. Two cases are presented demonstrating intermittent attacks of flaccid paralysis associated with clinical symptoms, signs and laboratory findings of hyperthyroidism. During an attack, one patient had a serum potassium of 2.1 mEq. per litre.Various factors such as trauma, exposure to cold, excessive carbohydrate ingestion and certain medications have been stated to precipitate an episode of paralysis. Attacks may range from mild weakness to generalized flaccid paralysis with loss of deep tendon reflexes. Several reported patients have died owing to cardiac arrest or respiratory paralysis.During attacks, the serum potassium is usually in the range of 2.2 to 3.2 mEq. per litre. It is postulated that a metabolic abnormality affecting the muscle-cell membrane can occur in the hyperthyroid state resulting in a shift of potassium to the intracellular position, thus producing a situation of hyperpolarization of the muscle-cell membrane which in turn alters the muscle contractibility.The importance of recognizing the unusual association of hypokalemic periodic paralysis with hyperthyroidism is stressed because, with successful treatment of the hyperthyroidism, the episodes of paralysis disappear.     

Psychiatric Illness in General Practice: A Detailed Study Using a New Method of Case Identification

A self-administered questionary (the General Health Questionnaire) aimed at detecting current psychiatric disturbance was given to 553 consecutive attenders to a general practitioner''s surgery. A sample of 200 of these patients was given an independent assessment of their mental state by a psychiatrist using a standardized psychiatric interview. Over 90% of the patients were correctly classified as “well” or “ill” by the questionary, and the correlation between questionary score and the clinical assessment of severity of disturbance was found to be +0·80.The “conspicuous psychiatric morbidity” of a suburban general practice assessed by a general practitioner who was himself a psychiatrist and validated against independent psychiatric assessment was found to be 20%. “Hidden psychiatric morbidity” was found to account for one-third of all disturbed patients. These patients were similar to patients with “conspicuous illnesses” in terms both of degree of disturbance and the course of their illnesses at six-month follow-up, but were distinguished by their attitude to their illness and by usually presenting a physical symptom to the general practitioner.When 87 patients who had been assessed as psychiatric cases at the index consultation were called back for follow-up six months later, two-thirds of them were functioning in the normal range. Frequency of attendance at the surgery in the six months following index consultation was found to have only a modest relationship to severity of psychiatric disturbance.It is argued that minor affective illnesses and physical complaints often accompany each other and usually have a good prognosis.     

Lipoprotein lipase mRNA in neonatal and adult mouse tissues: comparison of normal and combined lipase deficiency (cld) mice assessed by in situ hybridization

Combined lipase deficiency (cld) is a genetic abnormality in mice resulting in the production of enzymatically inactive lipoprotein lipase (LPL). After suckling, these mice have markedly elevated levels of circulating triglyceride. An alteration of LPL gene expression in cld mice may affect the amount and/or the distribution of LPL mRNA in different cell types. Therefore, we performed in situ hybridization for LPL mRNA in tissues from normal and cld pups and adult mice using an antisense 35S-labeled cRNA probe. LPL mRNA had the same pattern of distribution in both cld and normal newborn mice; the probe hybridized strongly to pyramidal neurons of the hippocampus, heart myocytes, and hepatocytes. Despite the lack of noticeable fat stores, LPL mRNA was found in the dermal layer of the skin of cld mice and normal littermates. In adult mice, the cRNA probe for LPL hybridized to the hippocampus, to the heart, and to localized areas of the kidney. We conclude that despite great variation in plasma triglyceride levels, LPL gene is similarly expressed in animals with or without LPL activity.     

Cloning and identification of bacteriophage T4 gene 2 product gp2 and action of gp2 on infecting DNA in vivo.

We sequenced bacteriophage T4 genes 2 and 3 and the putative C-terminal portion of gene 50. They were found to have appropriate open reading frames directed counterclockwise on the T4 map. Mutations in genes 2 and 64 were shown to be in the same open reading frame, which we now call gene 2. This gene codes for a protein of 27,068 daltons. The open reading frame corresponding to gene 3 codes for a protein of 20,634 daltons. Appropriate bands on polyacrylamide gels were identified at 30 and 20 kilodaltons, respectively. We found that the product of the cloned gene 2 can protect T4 DNA double-stranded ends from exonuclease V action.     

Release of endothelial cell lipoprotein lipase by plasma lipoproteins and free fatty acids

Lipoprotein lipase (LPL) bound to the lumenal surface of vascular endothelial cells is responsible for the hydrolysis of triglycerides in plasma lipoproteins. Studies were performed to investigate whether human plasma lipoproteins and/or free fatty acids would release LPL which was bound to endothelial cells. Purified bovine milk LPL was incubated with cultured porcine aortic endothelial cells resulting in the association of enzyme activity with the cells. When the cells were then incubated with media containing chylomicrons or very low density lipoproteins (VLDL), a concentration-dependent decrease in the cell-associated LPL enzymatic activity was observed. In contrast, incubation with media containing low density lipoproteins or high density lipoproteins produced a much smaller decrease in the cell-associated enzymatic activity. The addition of increasing molar ratios of oleic acid:bovine serum albumin to the media also reduced enzyme activity associated with the endothelial cells. To determine whether the decrease in LPL activity was due to release of the enzyme from the cells or inactivation of the enzyme, studies were performed utilizing radioiodinated bovine LPL. Radiolabeled LPL protein was released from endothelial cells by chylomicrons, VLDL, and by free fatty acids (i.e. oleic acid bound to bovine serum albumin). The release of radiolabeled LPL by VLDL correlated with the generation of free fatty acids from the hydrolysis of VLDL triglyceride by LPL bound to the cells. Inhibition of LPL enzymatic activity by use of a specific monoclonal antibody, reduced the extent of release of 125I-LPL from the endothelial cells by the added VLDL. These results demonstrated that LPL enzymatic activity and protein were removed from endothelial cells by triglyceride-rich lipoproteins (chylomicrons and VLDL) and oleic acid. We postulate that similar mechanisms may be important in the regulation of LPL activity at the vascular endothelium.