Hyperfunctioning thyroid adenomas are benign tumors characterized by their autonomous growth and functional activity, which frequently cause clinical hyperthyroidism and show a predominant radioactive iodine uptake in the nodule. Activating mutations in the gene encoding the alpha subunit of the stimulatory G protein (Gs alpha), as well as activating mutations in the gene encoding thyrotropin receptor in hyperfunctioning thyroid adenomas, have been reported. The mutations in Gs alpha involved the replacement of either arginine 201 with cysteine or histidine, or glutamine 227 with arginine or leucine. These residues are involved in GDP/GTP binding of Gs alpha and these mutations inhibit intrinsic GTPase activity that results in constitutive activation of adenylyl cyclase. The pathophysiological roles of these mutations in the formation of hyperfunctioning thyroid adenoma have been suggested.

Adenoma↗

PubMedDate not supplied

Alignment of x-ray tube focal spots for spectral measurement.

A general method to align a diagnostic x-ray machine for x-ray spectrum measurement purpose was theoretically and experimentally investigated by means of the optical alignment of focal pinhole images. Focal pinhole images were obtained by using a multi-pinholed lead plate. the vertical plane, including the central axis and tube axis, was decided upon by observing the symmetry of focal images. the central axis was designated as a line through the center of focus parallel to the target surface lying in the vertical plane. A method to determine the manipulation of the central axis in any direction is presented.

Radiography↗

PubMedDate not supplied

Simultaneous inhibition of renal phospholipase A(2) and glutathione synthesis by manoalide and DL-buthionine sulfoximine induces acute tubular dysfunction in rats.

We have previously demonstrated that gentamicin-induced acute renal failure is mediated by the consumption of renal glutathione (GSH) and accumulation of oxidized phospholipids in tubular epithelial cells as a result of inhibition of phospholipase A(2) (PLA(2)) activity. Based on these results, we tested the hypothesis that the simultaneous inhibition of PLA(2) and GSH synthesis induces acute renal failure similar in characteristics to gentamicin-induced acute renal failure. Male Sprague-Dawley rats kept under standard laboratory conditions were administered 3 mmol/kg of DL-buthionine sulfoximine (BSO; gamma-glutamylcysteine synthetase inhibitor) and 30 microg/kg of manoalide (PLA(2) inhibitor), following which significant elevations in serum creatinine and urinary lysosomal enzyme levels (elevation of N-acetyl-beta-D-glucosaminidase activity) were observed. The renal tissue GSH content was reduced in the group that received both BSO and manoalide as compared with the group that received manoalide alone. The renal tissue GSH content was also reduced in the group that received BSO alone. The renal tissue concentration of 2-thiobarbituric-acid-reactive substances increased rapidly, followed by an increase in renal tissue total phospholipid concentration in the group that received both BSO and manoalide. In contrast, the activity of PLA(2) in renal tissue decreased in the group that received both BSO and manoalide as compared with the groups that received BSO alone or physiological saline. In conclusion, concomitant administration of BSO and manoalide induces renal tubular damage and acute renal failure in rats, similar in characteristics to gentamicin-induced nephrotoxicity, whereas administration of BSO or manoalide alone did not. These results suggest that both inhibition of PLA(2) and GSH depletion are necessary for the induction of acute renal failure.

Acetylglucosaminidase↗

PubMedDate not supplied

A case of partial carnitine palmitoyltransferase deficiency in a patient undergoing chronic hemodialysis.

A 71-year-old male undergoing hemodialysis for chronic renal failure presented with proximal muscle weakness. He had normal levels of serum creatine phosphokinase. The results of nerve conduction velocity studies and a needle-exploration electromyogram were normal. Ultrasonography revealed adenomatous enlargement of the parathyroid glands, and he had marked elevation of the serum parathormone level. The level of serum free carnitine before hemodialysis was significantly lower than normal, while the acyl/free ratio was high. However, the muscle carnitine content was within the normal range. Interestingly, partial inactivation of carnitine palmitoyltransferase activity in the muscle was observed in association with the elevation of the serum parathormone level. Uremic myopathy in this case may be caused not only by abnormal carnitine metabolism but could also be attributable to the partial carnitine palmitoyltransferase deficiency associated with secondary hyperparathyroidism.

Aged↗

PubMedDate not supplied

[Relation of electrocardiographic features and distribution of hypertrophy in hypertrophic non-obstructive cardiomyopathy during childhood].

The relationship between the electrocardiographic features and the distribution of ventricular hypertrophy in pediatric patients with hypertrophic non-obstructive cardiomyopathy (HNCM) aged from 6 to 16 years (mean 11.6 years) was studied during a period of 6 months to 10 years (mean 3.9 years). Hypertrophy in the three segments (anterior septum, lateral free wall, posterior free wall) of the left ventricle in 17 patients with HNCM was evaluated by two-dimensional echocardiography (short-axis cross section of the left ventricle) at the end-diastolic period. The 17 patients were divided into four groups according to the echocardiographic findings as follows: Group A: hypertrophy in the ventricular anterior septum with or without posterior septum (eight patients). Group B: hypertrophy in both the ventricular septum and lateral left ventricular free wall (three patients). Group C: hypertrophy in the lateral left ventricular free wall (three patients). Group D: hypertrophy in the posterior left ventricular free wall with or without posterior septum (three patients). The incidence of electrocardiographic abnormalities in each group was analyzed using serial standard 12-lead electrocardiography. Electrocardiographic abnormalities and the distribution of the ventricular hypertrophy were related as follows: Lateral free wall: increased SV1 + RV6 (p < 0.05), ST-T change in leads V5.6 (p < 0.01). Posterior free wall: ST-T change in leads II.aVF (p < 0.05). Electrocardiographic abnormalities in HNCM patients in the hypertrophy were: Group A: abnormal Q waves in leads II.III.aVF (75%) and V5.6 (50%), high voltage R waves in leads II.III.aVF (25%) and V1 (38%), low voltage R waves in leads V2.3 (13%) and V5.6 (38%), and ST-T changes in leads I.aVL (25%), II.aVF (13%) and V2-4 (50%). Group B: abnormal Q waves in leads II.III.aVF (33%), high voltage R wave in lead V1 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V2.3 (33%) and V5.6 (33%), and ST-T changes in leads I.aVL (33%), II.aVF (33%), V2-4 (67%) and V5.6 (67%). Group C: abnormal Q waves in leads I.aVL (33%) and V5.6 (33%), high voltage R waves in leads II.III.aVF (33%), V1 (67%) and V5.6 (33%), increased SV1 + RV6 (67%), low voltage R waves in leads V5.6 (33%) and ST-T changes in leads II.aVF (33%), V2-4 (33%) and V5.6 (67%).

Adolescent↗