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  • 1
    Electronic Resource
    Electronic Resource
    The modulatory effect of endogenous parathyroid hormone on the action of hydrochlorothiazide in pseudohypoparathyroidism type I (1994)
    Springer
    Calcified tissue international 54 (1994), S. 473-476 
    Details
    ISSN: 1432-0827
    Keywords: Pseudohypoparathyroidism ; Thiazide ; Kidney ; Bone ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract We compared the effect of orally administered 100 mg of hydrochlorothiazide (HCTZ) among eight patients with pseudohypoparathyroidism (PHP) type I, 11 patients with idiopathic hypoparathyroidism (IHP), and 12 patients with primary hyperparathyroidism (1oHPT). Patients with PHP type I or with IHP were studied during the treatment with 1α-hydroxylated metabolites of vitamin D3. HCTZ raised serum levels of calcium (Ca) in 1oHPT (P〈0.001) and PHP type I (P〈0.01) but did not increase urinary excretion of Ca. Serum parathyroid hormone (PTH) in PHP type I decreased (P〈0.02) after HCTZ administration in response to the increase in serum Ca. HCTZ did not raise serum levels of Ca in IHP but increased urinary excretion of Ca in this group (P〈0.01). HCTZ suppressed tubular reabsorption of phosphate (P) in IHP (P〈0.01) and 1oHPT (P〈0.05) but not in PHP type I. Urinary excretion of cAMP did not change after HCTZ administration in PHP type I, IHP, or 1oHPT. Endogenous PTH modulated the effects of HCTZ on Ca mobilization from bone and renal reabsorption of Ca in PHP type I with normal or high serum levels of PTH and in 1oHPT with high serum levels of PTH. The inhibitory effect of HCTZ on renal tubular reabsorption of P (probably from proximal tubules) was independent of PTH. The resistance to this inhibitory effect of HCTZ on P reabsorption in PHP type I suggested a proximal tubular dysfunction in this disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00334326
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Resetting of parathyroid hormone secretion after vitamin D3 treatment in hypoparathyroidism and after parathyroid adenectomy in primary hyperparathyroidism (1995)
    Springer
    Calcified tissue international 57 (1995), S. 30-34 
    Details
    ISSN: 1432-0827
    Keywords: Parathyroid hormone ; Hypoparathyroidism ; Vitamin D3 ; Hyperparathyroidism ; Parathyroidectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine , Physics
    Notes: Abstract The relationship between parathyroid hormone (PTH) secretion and extracellular calcium (Ca) level is reciprocal causality. The equilibrium operating point determines basal PTH secretion rate and basal extracellular Ca level. We studied how this equilibrium was achieved in the subjects with decreased PTH secretion or decreased parathyroid glands number. Basal/maximum ratio of serum PTH, which reflects the basal secretory state of parathyroid glands, was increased in 9 hypoparathyroid patients treated with vitamin D3 (VD3) [7 patients with idiopathic hypopar-athyroidism (IHP), and two patients with postsurgical hypoparathyroidism] and in seven of nine parathyroid adenectomized patients. There was a negative correlation between the ratio and basal serum Ca level in the patients with IHP after VD3 treatment (r=0.7167, P〈0.05) and in the patients after parathyroid adenectomy (r=0.7760, P〈0.05). The regression curves in these two groups coincided regardless of the difference in maximum PTH secretion rate, which suggested that the basal secretory state of parathyroid glands was determined by extracellular Ca level in a similar manner in these subjects. There was a sigmoidal relationship between basal/maximum ratio of serum PTH and basal serum Ca level, when the data were collected from 15 hypoparathyroid patients before or after VD3 treatment, 9 parathyroid adenectomized patients, and 10 normal subjects (r=0.9057, P〈0.001). This sigmoidal curve is thought to represent the fundamental relationship between the basal secretory state of parathyroid glands and extracellular Ca level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00298993
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  • 3
    Electronic Resource
    Electronic Resource
    Stress Protein Inductions After Brain Ischemia (1998)
    Springer
    Cellular and molecular neurobiology 18 (1998), S. 709-719 
    Details
    ISSN: 1573-6830
    Keywords: HSP72 ; HSC73 ; HSP60 ; cytochrome c oxidase ; ischemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract 1. Hippocampal CA1 neurons are the most vulnerable to transient cerebral ischemia. However, the mechanism has not been fully understood. 2. The mRNAs for 72-kd (HSP72) and 73-kd (HSC73) heat shock proteins (HSPs), which are located mainly in the cytoplasm, were greatly induced together in CA1 cells, with a peak at 1–2 days in gerbils. However, immunoreactive HSP72 protein was only minimally expressed in CA1 neurons. 3. The mRNA for mitochondrial HSP60 began to increase at 3 hr in CA1 cells and was sustained until 1 day. 4. The level of mRNA for cytochrome c oxidase subunit I (COX-I) progressively decreased in CA1 neurons after a transient ischemia and completely disappeared at 7 days. The activity of cytochrome c oxidase (COX) protein also showed an early decrease in CA1 cells and was followed by a reduction in the level of COX-I DNA after 2 days. 5. These results suggest that HSP gene inductions were inhibited at the translational level but that mitochondrial DNA expression was disturbed at the transcriptional level. A disturbance of mitochondrial DNA expression could cause progressive failure of energy production of CA1 cells that eventually results in neuronal cell death.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020694205003
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  • 4
    Electronic Resource
    Electronic Resource
    DNA Fragmentation and HSP72 Gene Expression by Adenovirus-Mediated Gene Transfer in Postischemic Gerbil Hippocampus and Ventricle (1998)
    Springer
    Metabolic brain disease 13 (1998), S. 211-223 
    Details
    ISSN: 1573-7365
    Keywords: Gene transfer ; lacZ gene ; ischemia ; apoptosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A replication defective adenoviral vector containing the E. coli lacZ gene (AdCMVnLacZ) was directly injected into right hippocampus and lateral ventricle immediately after 5 min of transient global ischemia in gerbils. The relations between the lacZ gene expression and DNA fragmentation or heat shock protein 72 (HSP72) immunoreactivity were examined up to 21 days post ischemia. The lacZ gene was transiently expressed at 1 day in the hippocampus except around the CA1 region, while a large number of the periventricular cells strongly expressed the lacZ gene from 8 h to 7 days. In CA1 layer terminal deoxynucleotidyl dUTP nick end labeling (TUNEL) positive cells, which were present only adjacent to the needle track at 8 h to 1 day, became more extensive in the whole CA1 layer at 3 to 7 days. TUNEL-positive cells were also detected around the DG at 1 day, around the needle track at 8 h to 3 days, and in the choroid plexus cells at 7 days HSP72 staining was detected in the subiculum at 1 to 3 days, the dentate granule cells at 8 h to 1 day, and in the CA3 or CA4 pyramidal cells at 1 to 3 days. Some lacZ expressing cells were double-positive with HSP72 in DG, while the majority of those were distinguished from the TUNEL-positive cells. Pyramidal neurons were almost completely lost in the CA1 sector at 7days after the ischemia. The present study demonstrates the successful LacZ gene transfer into the hippocampus and ventricle of postischemic gerbil brain except in the vulnerable CA1 layer by adenoviral vector injection. However adenovirus-mediated gene transfer may induce indirect apoptotic cell death in the DG and ventricle, in addition to direct traumatic injury around the needle track.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1023224025407
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    Paper (German National Licenses)
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