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  • 1
    ISSN: 1432-1440
    Keywords: Parathyroid ; Crisis ; Kidney ; Bone ; Turnover
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Parathyroid crisis occurring in primary hyperparathyroidism is characteized by extremely high circulating levels of parathyroid hormone and acute onset of severe hypercalcemia. We describe a 62-year-old woman with parathyroid crisis probably due to an intraturnoral hemorrhage. Renal dysfunction reduced the effectiveness of preoperative management and continued to deteriorate for 5 days after parathyroidectomy. The normalization of serum calcium after parathyroidectomy delayed and it took 6 days. Maintenance of renal function is important for pre- and postoperative courses of the present case. The rapid decrease in serum parathyroid hormone after parathyroidectomy was followed by a rapid and transient (about fivefold) increase in serum alkaline phosphatase with peak value on the 10th postoperative day. This indicated that reversal phase from bone resorption (accelerated by parathyroid hormone) to bone formation lasted about 10 days under the conditions of the present case.
    Type of Medium: Electronic Resource
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  • 2
    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
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 38 (1996), S. 243-244 
    ISSN: 1432-1920
    Keywords: Key words Anatomical localisa- ; tion ; Single-photon emission computed tomography ; Wernicke's aphasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We introduce a simple method for localising brain images an anatomical templates. Our method does not need expensive software or hardware and may be useful for clinical investigation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 38 (1996), S. 243-244 
    ISSN: 1432-1920
    Keywords: Anatomical localisation ; Single-photon emission computed tomography ; Wernicke's aphasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We introduce a simple method for localising brain images an anatomical templates. Our method does not need expensive software or hardware and may be useful for clinical investigation.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1076
    Keywords: TRH ; Prolactin ; Hyperthyroidism ; Turner syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma prolactin (PRL) response to synthetic thyrotropin-releasing hormone (TRH) was studied in 26 prepubertal and 19 pubertal children with constitutional short stature, 7 patients with Turner's syndrome and 10 patients with hyperthyroidism. The mean basal concentrations of plasma PRL did not differ among groups. In prepubertal children PRL responses to TRH were comparable in both sexes, while pubertal children plasma PRL levels after TRH in females were significantly higher (P〈0.05) than those in age-matched males. Plasma PRL levels after TRH in patients with Turner's syndrome were significantly higher (P〈0.05) than those in age-matched males, but were not significantly different from those in age-matched females. Plasma PRL response to TRH was markedly suppressed in patients with hyperthyroidism before treatment, but it returned to normal after treatment when patients became euthyroid. A significant correlation (P〈0.05) between peak concentrations of plasma PRL after TRH stimulation and plasma T3 but not T4 levels was observed. These data suggest that a sex difference in TRH-stimulated PRL secretion appears around puberty and that plasma PRL response to TRH is suppressed in children with hyperthyroidism. The magnitude of plasma PRL response to TRH is closely correlated with the severity of hyperthyroidism when judged by plasma T3 but not T4 concentrations.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-1076
    Keywords: Prolactin ; Arginine ; Hyperthyroidism ; Primary hypothyroidism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma prolactin (PRL) response to arginine was examined in 16 prepubertal and 18 pubertal children with constitutional short stature, 5 patients with hyperthyroidism and 4 patients with primary hypothyroidism. The mean basal concentration of plasma PRL was significantly higher (P〈0.01) in primary hypothyroidism than in other groups. Arginine infusion elicited significant (P〈0.05) rises in plasma PRL in all groups. The maximal increment of plasma PRL above the baseline level after arginine stimulation was significantly larger (P〈0.05) in pubertal than in prepubertal females and was significantly smaller (P〈0.05) in patients with hyperthyroidism than in age- and sex-matched controls. There was no sex difference in arginine-stimulated PRL secretion. These data suggest that arginine produces a significant increase in plasma PRL and the PRL response to arginine was greater in pubertal than in prepubertal children. Plasma PRL response to arginine is suppressed in children with hyperthyroidism and the basal plasma PRL is markedly elevated in primary hypothyroidism.
    Type of Medium: Electronic Resource
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  • 7
    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
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular neurobiology 18 (1998), S. 709-719 
    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
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