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At least 397 records · Page 22Linked to original sources
PubMed1994

A truncated thyroxine-binding globulin due to a frameshift mutation is retained within the rough endoplasmic reticulum: a possible mechanism of complete thyroxine-binding globulin deficiency in Japanese.

We have previously reported six unrelated Japanese families having the same mutation in the TBG gene and manifesting complete TBG deficiency (TBG-CDJ). The deficiency consists of a single nucleotide deletion resulting in the production of C-terminal truncation due to a frameshift and premature termination. However, the reason for the failure to detect TBG in the serum of subjects harboring this mutation remains unknown. In this communication we investigated the mechanism of the TBG deficiency associated with TBG-CDJ. The complementary DNAs of TBG-CDJ and normal TBG (TBG-N) were expressed in COS-1 cells. Pulse-chase experiments revealed a complete absence of secretion of TBG-CDJ, whereas TBG-N was already present in the medium at time 0 and was almost entirely secreted by 3 h. In cell lysates, TBG-CDJ had a smaller molecular mass [52 kilodalton (kDa)] than TBG-N (54 kDa) and gradually decreased during the chase. Thus, failure of TBG-CDJ secretion accounts for the complete TBG deficiency. The molecular mass of TBG-CDJ (42 kDa) was also smaller than that of TBG-N (44 kDa) when synthesized in the presence of tunicamycin. These findings are consistent with the premature termination of the TBG-CDJ molecule deduced from the nucleotide sequence analysis. Intracellular TBG-N was resistant to endoglycosidase H but not TBG-CDJ, suggesting the retention of TBG-CDJ within the rough endoplasmic reticulum. Indeed, subcellular fractionation revealed that most of TBG-CDJ was located in the rough endoplasmic reticulum compartment, and TBG-N was distributed in the Golgi fractions. Our results suggested that the lack of intracellular transport of the truncated TBG molecule is the cause for the absence of immunoreactive TBG in the serum of subjects harboring the TBG-CDJ variant.

Animals↗
PubMed1979

Effects of obesity, total fasting and re-alimentation on L-thyroxine (T4), 3,5,3'-L-triiodothyronine (T3), 3,3',5'-L-triiodothyronine (rT3), thyroxine binding globulin (TBG), cortisol, thyrotrophin, cortisol binding globulin (CBG), transferrin, alpha 2-haptoglobin and complement C'3 in serum.

UNLABELLED: The effects of total fasting for 31 +/- 10 days followed by re-alimentation with an 800 calorie diet on thyroid function, i.e. T4,T3,rT3,RT3U (resin T3 uptake), and TSH, and on TBG levels in serum were studied sequentially in obese hospitalized patients (N=18). Additionally, cortisol, growth hormone, prolactin, parathyrin and free fatty acids were followed as hormonal and metabolic parameters, respectively. Further, CBG, transferrin, alpha 2-haptoglobin and complement C'3 were measured as representatives of other serum proteins. Results before fasting: T4, T3, TBG, cortisol, CBG, alpha 2-haptoglobin and complement C'3 of the obese patients were elevated when compared with healthy normal weight controls, whereas rT3, T4/TBG ratio, T3/TBG ratio, TSH, coritsol/cbg ratio, growth hormone, prolactin, parathyrin and transferrin of the obese group were normal. RT3U and fT4 index were decreased in the obese patients. Results during fasting: Significant decreases were observed during fasting for the following parameters -- T3, TBG, T3/TBG ratio, transferrin, alpha 2-haptoglobin complement C'3. rT3, T4/TBG ratio, RT3U, fT4 index and FFA increased. T4, tsh response to TRH stimulation, cortisol, CBG, cortisol/cbg ratio, parathyrin, growth hormone and prolactin did not change. Results during re-alimentation: T3, TBG, T3/TBG ratio, TSH response to TRH, transferrin, alpha 2-haptoglobin and complement C'3 increased. Conversely, fT3, RT3U, FFA, cortisol and cortisol/cbg ratio decreased whereas the other parameters did not change. CONCLUSIONS: 1) There is no evidence for primary hypothyroidism in obese patients during prolonged fasting and re-alimentation. 2) The rapid decrease of T3 and increase of RT3U after initiation of fasting are not fully explained by the observed slower decreases in TBG. 3) The alterations of T3, rT3 and RT3U resemble in their kinetics the changes in FFA levels. 4) Fasting reduced the levels of only certain serum proteins, interestingly TBG, transferrin, alpha 2-haptoglobin and complement C'3, all of which, except transferrin, are elevated in obesity. 5) The magnitude of the observed decreases does not suggest any clinically relevant deficiencies in serum proteins. 6) Re-alimentation reverses rapidly all observed changes.

Adult↗
PubMed1997

Antilymphocyte globulin (ALG) or antithymocyte globulin (ATG) with methylprednisone and oxymethalone in aplastic anaemia.

From 1986 to 1994 we treated 26 patients of aplastic anaemia between 6 to 61 years age group with ATG/ALG, Methylprednisone and Oxymethalone. Five had very severe aplastic anaemia, 16 had severe and 5 nonsevere disease. Disease was associated with hepatitis in 5 patients and with pregnancy and drug use in 2 patients each. In others no cause could be ascertained. A total of 31 courses of treatment were given (range 1-3 courses per patient). Nine patients had complete response (34.62%) and 3 had partial response (11.54%) with an overall response rate of 46.16%. Four patients died within 2 months of starting the treatment. The median follow up was 24 months (range 6-102 months) with an overall survival probality of 45% at 2 yr. At the time of evaluation 12 patients have died, 9 are alive disease-free and 5 are alive with disease. The side effects associated with therapy were tolerable and did not require cessation of therapy in any patient. We conclude that ATG/ALG with Methylprednisone and Oxymethalone is beneficial to significant number of patients with aplastic anaemia.

Adolescent↗