Biomedical subjects
Publications and source records attributed to A Rubinstein.
An elderly patient presenting with severe tetany secondary to hypocalcaemia causing bilateral fractures of the femoral necks, was proved to have coeliac disease. Severe muscle pains, an organic mental syndrome and personality changes are rare complications of coeliac disease and are reversible with treatment.
We have identified seven adenine nucleosides in urines of untreated adenosine deaminase (ADA) deficient patients, four of which (adenosine, 2'-deoxyadenosine, 1-methyladenosine and N6-methyladenosine) have been previously identified in urines of normals and/or ADA deficient patients. We confirm that ADA deficient patients excrete markedly increased amounts of 2'-deoxyadenosine (582 +/- 363 versus normal of less than 0.1 nmoles/mg creatinine) and increased amounts of adenosine (29.4 +/- 5.7 versus normal of 4.12 +/- 1.0 nmoles/mg creatinine). We have found three modified adenine nucleosides previously undetected in human urine. These three compounds are 2'-O-methyladenosine, N6, 2'-O-dimethyladenosine and an as yet incompletely characterized modified adenine nucleoside, R-adenosine. Only ADA deficient patients excrete detectable amounts of 2'-O-methyladenosine (2.1 +/- 1.1 versus normal of less than 0.1 nmoles/ mg creatinine), whereas both normals and ADA deficient children excrete N6, 2'-O-dimethyladenosine and R-adenosine. However, ADA deficient patients do excrete increased amounts of R-adenosine (5.5 +/- 1.0 versus normal of 1.4 +/- 0.4 nmoles/mg creatinine).
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A patient with acquired agammaglobulinemia was treated with plasmapheresis. The rationale for this procedure was based on the presence of a cytotoxic autoantibody with specificity for helper (TH2-) T lymphocytes. Plasmapheresis reduced the autoantibody concentration to undetectable levels, which resulted in an increase number of helper T cells. These T cells provided normal in vitro helper activity. Plasmapheresis did not correct a concomitant suppressor T-cell defect, and the clinical remission ended during the fifth month of exchange therapy.
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Coculture experiments between lymphocytes of a 17-year-old immunodeficient male, DL, and a group of normal subjects, assaying pokeweed mitogen (PWM)-stimulated Ig secretion as a measure of B-cell function, revealed immunoregulatory abnormalities. Initial studies disclosed that DL had corticosteroid-sensitive T suppressor (Ts) cells capable of blocking Ig secretion by both HLA-identical and HLA-nonidentical cells in coculture. Cocultures of DL's peripheral blood mononuclear cells could be induced to secrete Ig in large amounts after certain maneuvers--the most informative of which involved mixing prednisolone-treated DL mononuclear cells with any normal T lymphocytes except those from DL himself. When these same experimental manipulations were performed individually, i.e., prednisolone treatment of cultured DL cells to remove Ts activity, or mixing equal numbers of normal T cells with untreated DL mononuclear cells, Ig was not produced. The data indicated that the T-cell abnormalities in DL included an excess of Ts cells and a deficiency to T helper (Th) cells. When repeat studies were performed later in the clinical course, during which interval a number of clinical interventions were attempted, it was found that the patient's cells were no longer corticosteroid sensitive and, further, they suppressed only HLA-identical cells.
Serum lipids and lipoproteins were investigated in 10 young quadriplegic patients. All received intermittently a liquid formula diet via a naso-gastric tube, consisting of 2900 calories/day. The polyunsaturated/saturated fatty acids ratio was 1.1 : 1. Their mean body weight was 70% of the ideal body weight. The results were compared to a control group receiving a diet containing 2600 calories per day, and the polyunsaturated/saturated fatty acids ratio was 0.9 : 1. Their mean body weight was 95% of the ideal body weight. In the quadriplegic group the serum HDL-cholesterol levels and linoleic acid content of cholesterol ester were reduced. Similar findings have been observed in patients with coronary disease.
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This study was concerned with the effect of Cetomacrogol (polyethylene glycol 1000 monocetyl ether), a nonionic surfactant, on the absorption of gentamicin and amikacin from the gastrointestinal tract of rats. A 200-mg dose of Cetomacrogol coadministered orally with 10 mg of gentamicin resulted in a mean peak gentamicin blood concentration of 14.1 microgram/ml, compared with 67.8 microgram/mg when the same gentamicin dose was administered intramuscularly. The area under the curve after administration of the oral mixture was 23% of that after the intramuscular dose. The rectal administration of the mixture resulted in a mean peak gentamicin blood level of 8.2 micrograms/ml, compares to 16.5 microgram/ml when the mixture was administered orally. A 50-mg dose of amikacin coadministered orally with 200 mg of Cetomacrogol resulted in a mean peak amikacin blood level of 13.3 microgram/ml, compared to 310 microgram/ml when this amikacin dose was administered intramuscularly. Cetomacrogol augments the intestinal absorption of gentamicin and amikacin in rats. If the toxicity of the combination in humans is limited, the combination may be potentially clinically useful.
A patient with acquired agammaglobulinemia had an antihelper T cell factor that was identified as an immunoglobulin of the IgG class. The factor specifically bound to the TH2- T cell subset and, in the presence of complement, abolished the helper effect of normal T cells. The antihelper T cell antibody preceded by several years the appearance of suppressor TH2+Ia+ T cells, at which time the clinical course rapidly deteriorated. Plasmapheresis resulted in lymphocytosis and reappearance of a functionally intact helper T cell population. It did not affect the suppressor cells. Conversely, total thymectomy resulted in a temporary disappearance of the TH2+Ia+ suppressor cells, but did not decrease the levels of the autoantibody to helper T cells. Neither of these treatments reversed the state of agammaglobulinemia.
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The concentrations of serum lipids and lipoprotein cholesterol were measured serially during the acute phase (14 days) following myocardial infarction (MI) in 13 male survivors. All patients were re-examined at least two months after discharge from hospital. A significant increase in serum triglyceride (TG) concentration occurred during the acute phase, with values returning to baseline two months after recovery. No changes in the concentrations of the other lipids or lipoprotein cholesterol were observed.
Insulin injected intra-jejunally together with the non-ionic surfactant cetomacrogol was effective in streptozocin-induced diabetes in the rat, as measured by the hypoglycaemic effect. The reduction in blood sugar was maximal at about 2 h after administration but continued at a high level for the 4 h of the experiment. No hypoglycaemic effect was observed in controls injected with insulin or saline alone. Intestinal absorption of insulin has thus been effected by the addition of cetomacrogol, which appears to enhance membrane-permeability to insulin rather than to function as a protective agent preventing insulin degradation, as in liposome-encapsulation. In support of this, a significant hypoglycaemic action was still obtained when the insulin injection was given half-hour after that of the cetomacrogol, both intra-jejunally. Furthermore, oral administration of the surfactant followed by intra-jejunal injection of the insulin also gave a hypoglycaemic effect. The use of this agent to enhance insulin absorption offers the possibility of a new approach to oral insulin therapy.