PubMed · 4641036
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H J van Geuns, H van Kessel, M van Dam, A C Drogendijk, C A van Arkel. 1972-12-23. [Diffusion from the amnion sac].. https://pubmed.ncbi.nlm.nih.gov/4641036/
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This paper describes a stable isotope dilution method for quantification of 3-hydroxyglutaric acid (3-HGA) in body fluids. The method comprises a solid-phase extraction procedure, followed by gas chromatographic separation and negative chemical ionization mass spectrometric detection. This method is selective and sensitive, and enables measurement of 3-HGA concentrations in urine-, plasma-, and CSF- samples of controls. The control ranges for 3-HGA were: urine 0.88-4.5 mmol/mol creatinine (n=12); plasma 0.018-0.10 micro mol/l (n=10), CSF 0.022-0.067 micro mol/l (n=10). We applied this method to measure 3-HGA in body fluids of three patients with glutaric aciduria type I. We also quantified 3-HGA in amniotic fluid of controls (range 0.056-0.11 micro mol/l; n=12) and in two samples from fetuses affected with glutaric aciduria type I.
The feline model of human acquired immune deficiency syndrome, feline immunodeficiency virus (FIV), was used to model maternal-to-fetal human immunodeficiency virus type 1 (HIV-1) transmission. Fetuses were collected from cats infected with clade A FIV(Petaluma) (FIV-A-Pet) and clade C FIV(PaddyGammer) (FIV-C-Pgmr). Virus was detected by DNA polymerase chain reaction (PCR) and a quantitative RNA assay that used substitutional PCR. FIV in tissue sections was assayed by DNA and RNA in situ hybridization and immunohistochemistry. Viral DNA was detected in 67% and 92% of fetuses with FIV-A-Pet and FIV-C-Pgmr, respectively. A discordance was observed between placental and fetal FIV-A-Pet localization. FIV sequestration in fetal tissues was common without detectable virus in blood (occult infection). Viral RNA was not detected in amniotic fluid or fetal plasma. In situ assays demonstrated FIV DNA but neither RNA nor antigens in placentas and fetuses. If mother-to-offspring FIV infection reflects vertical HIV-1 transmission, fetal virus exposure is common and may be occult at term.
Propionic acidemia is one of the most frequent inborn errors of metabolism caused by a deficiency of propionyl-CoA carboxylase. Methylcitric acid, a key indicator of this disorder, is increased in amniotic fluid when a fetus is affected. Therefore, the direct chemical analysis of cell-free amniotic fluid for methylcitric acid, using stable isotope dilution gas chromatography-mass spectrometry, was carried out for the prenatal diagnosis of propionic acidemia. We developed a simple, highly sensitive, and accurate method for quantitation of this polar methylcitric acid in amniotic fluids by applying a simplified urease pretreatment which we devised earlier for urine. As the recovery of methylcitric acid from amniotic fluid was as high as 91% with a coefficient of variation lower than 3% in this procedure, only 0.02 ml of sample was required for the analysis of the affected fetus. This new procedure takes 1 h for sample pretreatment, including derivatization, and 15 min for GC-MS measurement and provides final results within 1.5 h.