scholarly journals Role of echography in the diagnosis of endemic goiter

1994 ◽  
Vol 40 (4) ◽  
pp. 16-19
Author(s):  
N. V. Bolotova ◽  
L. A. Lisenkova ◽  
L. A. Scheplyagina ◽  
T. V. Glukhova ◽  
A. V. Kruglov ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Endemic Goiter ◽  
Saratov Region ◽  
Ultrasonic Examination ◽  
Second Degree

Screening of 1520 children living in the Khvalynsk district of the Saratov region, including assessment of urinary excretion of iodine and ultrasonic examinations of the thyroid in children and adults, revealed endemic goiter in the region. Special attention was paid to echographic examination of the thyroid; this method was used in examinations of 161 children aged 2 to 14 with thyroid enlargement of the IIII degree. 103 (64.0 %) of there children had enlarged thyroid, in some children with diffusely enlarged thyroid of the I II dergee ultrasonic examination showed no enlargement, and in some children the gland was found even reduced in size. The greatest discrepancy between the data of palpation and ultrasonography was observed in first-degree thyroid enlargement, the least so in second-degree enlargement; in third-degree enlargement there was no such a discrepancy. Assessment of thyroid structure revealed various disorders of the organ in 29 of the 161 examined children, these disorders present both in enlarged glands and in those of normal or reduced size. Nodes that could not be palpated were detected in 2 children. Ultrasonic examinations of 56 adults aged 20 to 60 revealed changed structure of the thyroid in 35, with nodes of various sizes and localization detected in 15 of these.

Tryptophan-Niacin Metabolism in Rat with Puromycin Aminonucleoside-Induced Nephrosis

2006 ◽  
Vol 76 (1) ◽  
pp. 28-33 ◽  
Author(s):  
Yukari Egashira ◽  
Shin Nagaki ◽  
Hiroo Sanada
Keyword(s):  
Body Weight ◽  
Urinary Excretion ◽  
Enzyme Activities ◽  
Treated Group ◽  
Control Group ◽  
Puromycin Aminonucleoside ◽  
Low Level ◽  
Key Enzyme

We investigated the change of tryptophan-niacin metabolism in rats with puromycin aminonucleoside PAN-induced nephrosis, the mechanisms responsible for their change of urinary excretion of nicotinamide and its metabolites, and the role of the kidney in tryptophan-niacin conversion. PAN-treated rats were intraperitoneally injected once with a 1.0% (w/v) solution of PAN at a dose of 100 mg/kg body weight. The collection of 24-hour urine was conducted 8 days after PAN injection. Daily urinary excretion of nicotinamide and its metabolites, liver and blood NAD, and key enzyme activities of tryptophan-niacin metabolism were determined. In PAN-treated rats, the sum of urinary excretion of nicotinamide and its metabolites was significantly lower compared with controls. The kidneyα-amino-β-carboxymuconate-ε-semialdehyde decarboxylase (ACMSD) activity in the PAN-treated group was significantly decreased by 50%, compared with the control group. Although kidney ACMSD activity was reduced, the conversion of tryptophan to niacin tended to be lower in the PAN-treated rats. A decrease in urinary excretion of niacin and the conversion of tryptophan to niacin in nephrotic rats may contribute to a low level of blood tryptophan. The role of kidney ACMSD activity may be minimal concerning tryptophan-niacin conversion under this experimental condition.

Acetaminophen Inhibits Spinal Prostaglandin E2Release after Peripheral Noxious Stimulation 

1999 ◽  
Vol 91 (1) ◽  
pp. 231-239 ◽  
Author(s):  
Uta S. Muth-Selbach ◽  
Irmgard Tegeder ◽  
Kay Brune ◽  
Gerd Geisslinger
Keyword(s):  
Spinal Cord ◽  
Urinary Excretion ◽  
Dorsal Horn ◽  
Formalin Test ◽  
Intraperitoneal Administration ◽  
Noxious Stimulation ◽  
Cyclooxygenase Inhibitor ◽  
Nociceptive Processing ◽  
Pge2 Release

Background Prostaglandin play a pivotal role in spinal nociceptive processing. At therapeutic concentrations, acetaminophen is not a cyclooxygenase inhibitor. inhibitor. Thus, it is antinociceptive without having antiinflammatory or gastrointestinal toxic effects. This study evaluated the role of spinal prostaglandin E2 (PGE2) in antinociception produced by intraperitoneally administered acetaminophen. Methods The PGE2 concentrations in the dorsal horn of the spinal cord were measured after formalin was injected into the hind paw of rats. The effect of antinociceptive doses of acetaminophen (100, 200, and 300 mg/kg given intraperitoneally) on PGE2 levels and flinching behavior was monitored Spinal PGE2 and acetaminophen concentrations were obtained by microdialysis using a probe that was implanted transversely through the dorsal horn of the spinal cord at L4. Furthermore, the effects of acetaminophen on urinary prostaglandin excretion were determined. Results Intraperitoneal administration of acetaminophen resulted in a significant decrease in spinal PGE2 release that was associated with a significant reduction in the flinching behavior in the formalin test Acetaminophen was distributed rapidly into the spinal cord with maximum dialysate concentrations 4560 min after intraperitoneal administration. Urinary excretion of prostanoids (PGE2, PGF2alpha, and 6-keto-PGF1alpha) was not significantly altered after acetaminophen administration. Conclusions The data confirm the importance of PGE2 in spinal nociceptive processing. The results suggest that antinociception after acetaminophen administration is mediated, at least in part, by inhibition of spinal PGE2 release. The mechanism, however, remains unknown. The finding that urinary excretion of prostaglandins was not affected might explain why acetaminophen is antinociceptive but does not compromise renal safety.

scholarly journals The Leading Global Experiences in the Application of Equitable Economy and Solidarity

2018 ◽  
Vol 2 (2) ◽  
pp. 1-12
Author(s):  
Aied Malika ◽  
Abdelli Mohammed El Amine
Keyword(s):  
Social Justice ◽  
Legal Framework ◽  
The State ◽  
Geographical Region ◽  
Labor Organizations ◽  
Personal Initiative ◽  
Voluntary Contribution ◽  
Vertical Cooperation ◽  
Second Degree

This study is designed to highlight the important role of the growing role played by the equitable economy and solidarity in building a balanced and integrated into the society, characterized by the values of solidarity in the framework of the spirit of the voluntary contribution and the spirit of the personal initiative, as well as the principles of equity and social justice that seeks this economy established and consolidated, the study found that the pilot experiences for both the state of Canada, Ecuador, Brazil, Finland, France, Spain, the reputation and excellence by relying primarily on the legal framework for this sector and organized the second degree of integration of all segments of society in the form of labor organizations for each category but every geographical region, the study recommended in the end to adopt the principle of integration and horizontal and vertical cooperation between these organizations in order to achieve effectiveness More competitive.

scholarly journals Studies on the role of taurine in Friedreich's ataxia

1984 ◽  
Vol 11 (S4) ◽  
pp. 610-615 ◽  
Author(s):  
B. Lemieux ◽  
R. Giguère ◽  
D. Shapcott
Keyword(s):  
Urinary Excretion ◽  
Muscle Mass ◽  
Friedreich’S Ataxia ◽  
Friedreich's Ataxia ◽  
Control Groups ◽  
Creatinine Excretion

AbstractNew studies were undertaken to verify the previous findings of increased urinary excretion of taurine, in the basal state and after challenge with a taurine load, in Friedreich's disease. Particular attention was paid to possible causes of error such as weight, muscle mass, creatine and creatinine excretion, variability with time and appropriate control groups. Although the overall findings were confirmed, their interpretation is open to question because of all these factors of error. Many possibilities must still be further explored to account for the apparent taurine retention defect observed in many cases of Friedreich's disease.

Role of 20-hydroxyeicosatetraenoic acid in the renal and vasoconstrictor actions of angiotensin II

2002 ◽  
Vol 283 (1) ◽  
pp. R60-R68 ◽  
Author(s):  
Magdalena Alonso-Galicia ◽  
Kristopher G. Maier ◽  
Andrew S. Greene ◽  
Allen W. Cowley ◽  
Richard J. Roman
Keyword(s):  
Urinary Excretion ◽  
Intravenous Infusion ◽  
Pressor Response ◽  
Maximal Response ◽  
Epoxyeicosatrienoic Acids ◽  
Ang Ii ◽  
Hydroxyeicosatetraenoic Acid ◽  
Peripheral Vasculature ◽  
Oxide Synthase

The present study examined the effects of ANG II on the renal synthesis of 20-hydroxyeicosatetraenoic acid (20-HETE) and its contribution to the renal vasoconstrictor and the acute and chronic pressor effects of ANG II in rats. ANG II (10−11 to 10−7mol/l) reduced the diameter of renal interlobular arteries treated with inhibitors of nitric oxide synthase and cyclooxygenase, lipoxygenase, and epoxygenase by 81 ± 8%. Subsequent blockade of the synthesis of 20-HETE with 17-octadecynoic acid (1 μmol/l) increased the ED50 for ANG II-induced constriction by a factor of 15 and diminished the maximal response by 61%. Graded intravenous infusion of ANG II (5–200 ng/min) dose dependently increased mean arterial pressure (MAP) in thiobutylbarbitol-anesthetized rats by 35 mmHg. Acute blockade of the formation of 20-HETE with dibromododecenyl methylsulfimide (DDMS; 10 mg/kg) attenuated the pressor response to ANG II by 40%. An intravenous infusion of ANG II (50 ng · kg−1 · min−1) in rats for 5 days increased the formation of 20-HETE and epoxyeicosatrienoic acids (EETs) in renal cortical microsomes by 60 and 400%, respectively, and increased MAP by 78 mmHg. Chronic blockade of the synthesis of 20-HETE with intravenous infusion of DDMS (1 mg · kg−1 · h−1) or EETs and 20-HETE with 1-aminobenzotriazole (ABT; 2.2 mg · kg−1 · h−1) attenuated the ANG II-induced rise in MAP by 40%. Control urinary excretion of 20-HETE averaged 350 ± 23 ng/day and increased to 1,020 ± 105 ng/day in rats infused with ANG II (50 ng · kg−1 · min−1) for 5 days. In contrast, urinary excretion of 20-HETE only rose to 400 ± 40 and 600 ± 25 ng/day in rats chronically treated with ANG II and ABT or DDMS respectively. These results suggest that acute and chronic elevations in circulating ANG II levels increase the formation of 20-HETE in the kidney and peripheral vasculature and that 20-HETE contributes to the acute and chronic pressor effects of ANG II.

scholarly journals The role of the Ah locus in hexachlorobenzene-induced porphyria. Studies in congenic C57BL/6J mice

1988 ◽  
Vol 254 (1) ◽  
pp. 245-254 ◽  
Author(s):  
M E Hahn ◽  
T A Gasiewicz ◽  
P Linko ◽  
J A Goldstein
Keyword(s):  
Urinary Excretion ◽  
Causative Factor ◽  
Ah Receptor ◽  
Lipid Levels ◽  
Uroporphyrinogen Decarboxylase ◽  
Hepatic Lipid ◽  
Congenic Strains ◽  
Cytosolic Protein ◽  
Hepatic Microsomes

The role of the Ah locus in hexachlorobenzene (HCB)-induced porphyria and the possible involvement of P-450 cytochromes P(1)450 and P(3)450 in the pathogenesis of this disease were investigated in two congenic strains of C57BL/6J mice that differ only at this locus. Female B6-Ahb mice (Ah receptor: approximately 30-70 fmol/mg of cytosolic protein) and B6-Ahd mice (Ah receptor: undetectable) were pretreated with iron (500 mg/kg) and then fed a diet containing 0 or 200 p.p.m. of HCB for up to 17 weeks. Mice from the two strains consumed similar amounts of HCB. Urinary excretion of porphyrins was increased after 7 weeks of HCB treatment in B6-Ahb mice, and after 15 weeks was over 200 times greater than that of mice given iron only. In B6-Ahd mice, porphyrin excretion did not begin to increase until after 13 weeks, and after 15 weeks was only six times greater than that of controls. Similar differences were seen in the 15-week hepatic porphyrin concentrations (B6-Ahb: 1110 +/- 393; B6-Ahd: 17.6 +/- 14.5; controls: approximately 0.20 nmol/g). Uroporphyrinogen decarboxylase (EC 4.1.1.37) activity was diminished by 70 and 20% in B6-Ahb B6-Ahd mice respectively after 15 weeks of treatment with HCB. Cytochromes P(1)450 and P(3)450 were measured in hepatic microsomes (microsomal fractions) by radioimmunoassay and immunoblotting, using antisera raised against the orthologous rat isoenzymes P450c and P450d. HCB induced small amounts of a protein recognized by anti-P450c (P(1)450) in B6-Ahd mice, but not in B6-Ahd mice. Relatively large amounts of a protein recognized by anti-P450d (P(3)450) were induced in both strains, but to a somewhat greater extent in the B6-Ahb mice. The hepatic accumulation of HCB at 15 weeks was greater in B6-Ahb than in B6-Ahd mice, in association with elevated hepatic lipid levels in the former strain. The results of this experiment indicate that the Ah locus influences the susceptibility of C57BL/6J mice to HCB-induced porphyria and are consistent with the suggestion that the sustained induction of P(3)450 and/or P(1)450 may be a causative factor in the development of this disease.

scholarly journals Accelerated hepatic haem catabolism in the selenium-deficient rat

1977 ◽  
Vol 168 (1) ◽  
pp. 105-111 ◽  
Author(s):  
R F Burk ◽  
M A Correia
Keyword(s):  
Urinary Excretion ◽  
Sodium Dodecyl Sulphate ◽  
Gel Electrophoresis ◽  
Polyacrylamide Gel Electrophoresis ◽  
Sodium Dodecyl ◽  
Fold Increase ◽  
Microsomal Cytochrome ◽  
Haem Oxygenase ◽  
Cytochrome P 450

1. Hepatic microsomal cytochrome P-450 concentrations are lower in selenium-deficient rats treated with phenobarbital for 4 days than in similarly treated control rats. 2. No defect in haem synthesis was found on the basis of measurements of delta-aminolaevulinate synthase (EC 2.3.1.37), delta-aminolaevulinate dehydratase (EC 4.2.1.24) and ferrochelatase (EC 4.99.1.1) activities, and urinary excretion of delta-aminolaevulinate, porphobilinogen, uroporphyrin and coproporphyrin. 3. No defect in apo-(cytochrome P-450) separated by sodium dodecyl sulphate/polyacrylamide-gel electrophoresis. 4. An increase in haem catabolism was found. An 8-fold increase in hepatic microsomal haem oxygenase (EC 1.14.99.3) activity occurred in selenium-deficient rats after phenobarbital treatment, compared with a less than 2-fold increase in control rats. Also excretion of 14CO in the breath after administration of delta-amino[5-14C]laevulinate was greater by phenobarbital-treated selenium-deficient rats than by similarly treated controls. 5. These studies demonstrate that the defective induction of cytochrome P-450 by phenobarbital in selenium-deficient rats is accompanied by increased haem catabolism. This could be due to increased breakdown of cytochrome P-450 or to catabolism of haem before it attaches to the apo-cytochrome. The role of selenium in stabilizing cytochrome P-450 and/or in protecting haem from breakdown remains to be determined.

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