Search PubMed⌕ Search

Biomedical subjects

G Thomas

Publications and source records attributed to G Thomas.

At least 793 records · Page 44Linked to original sources

Disordered breathing during sleep in hypothyroidism.

A 58-yr-old man with hypothyroidism and sleep apnea syndrome was studied to determine the cause of the nocturnal obstructive apnea and oxygen desaturation. Control studies showed free thyroxine (T4) concentration of 0.7 ng/dl (normal, 0.8 to 2.3 ng/dl), and thyroid-stimulating hormone of 32 microIU/ml (normal, less than 12 microIU/ml). Weight, pulmonary function, arterial blood gases, minute ventilation to carbon dioxide production ratio (VE/VCO2), and the ventilatory response to exercise (delta VE/delta VCO2) were normal. Episodes of obstructive apnea (4 per hour during non-REM (NREM) and 10 per hour during REM) and oxygen desaturation (9 per hour during NREM and 11 per hour during REM) were common during sleep. Oxygen saturation ranged between 72 and 99% and 70 and 97% during NREM and REM sleep, respectively. Medroxyprogesterone acetate (MPA) therapy for 4 wk caused a reduction in awake PaCO2 (38 to 33 mm Hg), and an increase in VE/VCO2 (17%), mouth occlusion pressure (50%), and AVE/VCO2 (23%). During sleep, apneas were completely eliminated and only one episode of oxygen desaturation occurred. L-thyroxine therapy for 2 months after a placebo period caused an awake isocapnic hyperpnea with no change in PaCO2 and VE/VCO2 despite a 23% increase in VE. Mouth occlusion pressure increased 37% but delta VE/delta VCO2 was unchanged. Obstructive apnea and oxygen desaturation during sleep were completely eliminated with L-thyroxine. The patient noted completed relief of symptoms with both MPA and L-thyroxine. We concluded that the sleep apnea syndrome was the presenting manifestation of hypothyroidism in this patient and was solely responsible for his symptoms and disability.

Carbon Dioxide↗

[3-Amino-2H-1,2,4-benzothiadiazine-1,1-dioxides with antihypertensive and possibly diabetogenic activity (author's transl)].

By reaction of dialkylaminoalkylamines or omega-amino-alkylethers with 2H-1,2,4-benzothiadiazine-1,1-dioxides bearing a group in the 3-position labile towards nucleophilic substitution (Cl, CH3S, CH3CO2), the corresponding 3-substituted amino-2H-1,2,4-benzothiadiazine-1,1-dioxides are obtained. A series of these compounds exerts an antihypertensive effect in the renally hypertonic rat after oral administration and in the "two-kidney hypertensive dog" after parenteral administration. Two compounds (1 and 4) were studied thoroughly in comparison to diazoxide (16) and the known piperazino compound (17). At 10 mg/kg in the rat, diazoxide causes a marked reduction of water and electrolyte excretion but at this dosage 1 and 4 are neither diuretic nor antidiuretic. In the hyperglycaemia test on normal rats at a dosage 30--100 times that required for an antihypertensive effect, 1 and 4 show after 300 mg/kg no hyperglycaemic effect and after 1000 mg/kg p.o. a very weak one. 17 has a weak hyperglycaemic effect at 300 mg/kg diazoxide a strong one. However, intensive glucose loading studies on diabetic rats (reduced glucose-tolerance) and on metabolically healthy rats with glucose loading showed that compounds 1 and 4 as well as the piperazine derivative 17 inhibit insulin release, albeit in higher doses than does diazoxide. In animals with insulin resistance a diabetic metabolic condition occurs with high blood-sugar levels. Owing to this possible diabetogenic activity, testing and application of 1, 4 and the known 7-chloro-3-(4-methyl-1-piperazinyl)-2H-1,2,4-benzothiadiazine-1,1-dioxide for blood-sugar lowering activity to human volunteers is not considered appropriate.

Animals↗

Structure of a family of rat amylase genes.

The sequences of two cloned rat pancreatic amylase cDNAs comprising 95% of the mRNA sequence are reported. Analysis of cloned rat genomic DNA fragments using cloned cDNA probes indicates that the rat genome contains multiple closely related amylase genes in which the cDNA sequences are distributed within a region 9 kilobases in length and are interrupted by at least seven intervening sequences.

Amino Acid Sequence↗

Characteristics of prostaglandin E1 potentiation of inflammatory activity of some agents.

In rats pretreated with indomethacin, injection of PGE1 (prostaglandin E1) with carrageenan potentiated the carrageenan paw oedema. This effect of PGE1, was maximal when it was injected together with carrageenan, there being a reduction in the action of PGE1 if carrageenan injection was delayed after PGE1 injection. PGE1 induced potentiation of increase in plasma protein leakage induced by intradermal injections of bradykinin and histamine also depended on the injection of PGE1 along with these agents. Thus oedema enhancement by PGE1 differs from its action in pain, where PGs cause a long lasting sensitization of the injected area for the actions of other algesics. Since vasodilation may be a mechanism of oedema enhancement by PGs, the ability of adenosine and papaverine to mimic PGE1 in paws and skins of rats were examined. Adenosine was active whereas papaverine was inactive in this respect. To clarify this difference, the vasodilatory properties of PGE1, adenosine and papaverine were assessed by their ability to antagonize NA response in perfused rat mesenteric blood vessels. Only papaverine was effective in antagonising the NA response. Thus, PGE1 and adenosine which potentiated the oedema inducing actions of other agents showed no vasodilatory properties and papaverine, a vasodilator, had no oedema potentiating actions.

Adenosine↗

Regulation of 40S ribosomal protein S6 phosphorylation in Swiss mouse 3T3 cells.

Addition of serum to resting cultures of Swiss mouse 3T3 cells causes an immediate multiple phosphorylation of 40S ribosomal protein S6. After 60 min of stimulation, changing to medium containing no serum led to the net dephosphorylation of S6. During this same period, a second protein, as yet unidentified, became increasingly phosphorylated. Incubation of cells with cycloheximide prior to the addition of serum almost completely blocked the activation of protein synthesis. There was no effect on the serum-induced phosphorylation of S6. If cells were stimulated in the presence of cAMP phosphodiesterase inhibitors theophylline or SQ 20006, both S6 phosphorylation and the activation of protein synthesis were inhibited. Stimulation of cells with serum also led to an immediate drop in total intracellular cAMP levels. This was blocked by prostaglandin E1 (PGE1), which caused a 10 fold increase in total intracellular cyclic AMP. However, PGE1 had no effect on protein synthesis or S6 phosphorylation.

Animals↗

4-Thiouridine triggers both growth delay induced by near-ultraviolet light and photoprotection.

4-Thiouridine, a rare nucleoside present in Escherichia coli tRNAs, has been recently proposed to be the major chromophore leading to near-ultraviolet (315-400-nm)-induced growth delay. Here this is established by the isolation of mutants exhibiting a reduced growth delay. The selection procedure involves several successive cycles of 365-nm illumination of the cells in the stationary phase, followed by growth for two or three generations. After the eighth cycle, the level of 4-thiouridine in the culture decreases to 20% of the original level and all individual clones tested show a 4-thiouridine deficiency. One mutant exhibiting a complete lack of 4-thiouridine in its tRNAs has been characterized. In the dark the growth characteristics of the mutant and of the parental strain are indistinguishable. In contrast after near-ultraviolet illumination the nuv mutation abolishes the growth delay and considerably reduces the photoprotection efficiency.

Escherichia coli↗

Clinical characteristics, DNA repair, and complementation groups in xeroderma pigmentosum patients from Egypt.

Xeroderma pigmentosum (XP) has been reported to be unusually frequent among Middle Eastern populations. This report describes the first survey of DNA repair characteristics among Egyptians. Sixteen XP patients were contacted, and biopsies from eight were analyzed for unscheduled DNA synthesis, strand breakage during pyrimidine dimer excision, and complementation groups. The patients were equally distributed between Complementation Groups A and C. Unscheduled synthesis and strand breaks were significantly higher in Group C than in Group A cells. Central nervous system disorders were found in all of the Group A patients and in none of the Group C patients. No clinical symptoms were observed in the heterozygotes. A 2-month-old sib of an XP patient was free of symptoms, but unscheduled synthesis and strand breakage in cultures from this sib were the same as in the related XP homozygote. From the relative frequencies of each complementation group found in various parts of the world, we offer a hypothesis concerning the relative sizes and roles for gene products specified by the alleles or genes corresponding to each complementation group.

Adolescent↗

Multiple phosphorylation of ribosomal protein S6 during transition of quiescent 3T3 cells into early G1, and cellular compartmentalization of the phosphate donor.

At 5 min after quiescent cells are induced to enter G1 there is a large increase in the amount of 32P incorporated into 40S ribosomal protein S6. Here we show that changes in the specific activities of 32Pi and [gamma-32P]ATP in stimulated as compared to quiescent cultures do not account for this large increase. Instead, we demonstrate by decreased electrophoretic mobility on two-dimensional polyacrylamide gels that this increase is due to a quantitative increase in the total amount of phosphate incorporated into S6. Furthermore, pulse-chase experiments show that the phosphate that is incorporated into S6 is metabolically stable during at least the first 60 min of induction and that the incorporation of 32P into S6 responds immediately to the replacement of 32Pi by Pi in the medium, in contrast to [gamma-32P]ATP which changes very slowly. Thus, the S6 phosphate donor must be a compartment separate from that of the total cellular ATP.

Adenosine Triphosphate↗