Biomedical subjects
A Rachmel
Publications and source records attributed to A Rachmel.
Acute acalculous cholecystitis in an infant: a case report.
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Rise in plasma growth hormone in response to exogenous LRH in Klinefelter's syndrome.
In a group of sixteen patients with Klinefelter's syndrome (KS) aged from 2 years 8 months to 31 years, a study was made of the plasma growth hormone (hGH) response to LRH (50 micrograms/m2 i.v.; n=16), TRH (200 micrograms i.v.; n=14) and insulin-induced hypoglycaemia (0.1 u R.I,/kg i.v.; n=6). There was a rise in hGH following LRH from a level below 5 ng/ml during fasting to a level above 8 ng/ml (P less than 0.001) in nine (56.3%) of the sixteen patients tested; a similar response was found in only one of a control group of fifteen boys matched for age. TRH stimulation led to a rise in hGH in one of the fourteen KS patients tested, with none in the control group. Insulin-induced hypoglycaemia elicited a normal response of hGH in the six KS patients tested, from 1.8 +/- 0.7 to 16.5 +/- 3.7 ng/ml, (M +/- SD, P less than 0.001). Basal prolactin (PRL) levels were normal in the KS patients (9.4 +/- 4.1 ng/ml, M +/- SD) but the response to TRH stimulation was significantly higher (63.3 +/- 40 ng/ml; P less than 0.01) than that of the control group (30 +/- 15 ng/ml). Plasma gonadotrophin levels and the response to LRH stimulation were increased in all of the KS patients except those below the age of 13. Plasma TSH levels and the response to TRH stimulation as well as the levels of serum thyroxine were found to be normal in all the KS patients tested. The abnormal rise of hGH following LRH stimulation and of PRL following TRH stimulation suggests a disturbance in the neuroendocrine regulation mechanisms of these hormones in KS.
Furosemide 1-O-acyl glucuronide. In vitro biosynthesis and pH-dependent isomerization to beta-glucuronidase-resistant forms.
A biosynthetic acyl-type glucuronic acid conjugate of furosemide was isolated from in vitro incubation of pregnenolone-16 alpha-carbonitrile-induced rat liver microsomes containing UDP-glucuronyltransferase activity, furosemide, and UDP-glucuronic acid. Furosemide 1-O-acyl glucuronide (FG) was specifically hydrolyzed by beta-glucuronidase (BG) and was also labile to alkaline hydrolysis. FG concentration decreased at an apparent first order rate when incubated at 37 degrees C in buffer solution of pH values greater than 6.0 with only moderate hydrolysis of the conjugate at pH values less than 8.5. Formation of rearrangement forms of FG that were resistant to BG but labile to alkaline hydrolysis accounted for most of the disappearance of FG at this pH range. Radiochemical labeling of the conjugate with either 14C-furosemide or 14C-UDP-glucuronic acid was detected in the BG-resistant isomerization products of FG as they were separated by HPLC. The structure of FG and its isomerization products was further verified by negative ion thermospray liquid chromatography/mass spectrometry. The abundant (M - 1)-ion at mass 505, the aglycone fragment at m/z 329, and the characteristic sugar fragment ion of mass 175 were found in the spectra of FG and three additional isomers. An ion at m/z 221 was noted only in the case of the parent conjugate and thus may prove to be a characteristic ion for 1-O-acyl-linked glucuronides under negative ion thermospray. In vivo as well as in vitro rearrangement of FG to BG-resistant forms might affect the results of furosemide disposition studies which use BG hydrolysis to determine FG formation.