按尿分析对钚全身负荷量的估算方法

直至几年前,工作人员钚全身负荷量的估算总是依据Langham氏尿排出方程Yu=0.002t~(-0.74),式中Yu是Pu注入后第t天在尿中的分数。此方程是从1945年和1946年注射了钚的某些严重病人以及少数被钚事故污染的工作人员的尿分析资料推导出的。近年来发现,Langham氏模式常导致Pu体负荷量的明显高估,特别是在远期。其依据来自Pu职业辐照人员尿排出资料与其死后尸体解剖资料的比较以及对曼哈顿计划工作人员预期的与观测到的长期模式之间的差异,也来自于二例Langham氏实验对     

肾前性肾功能衰竭,从肾代偿向失代偿的有害转变

肾前性肾功能衰竭(prerenal failure)一词,传统上用来描述肾结构完好而肾小球灌流障碍所致肾功衰竭的临床综合征。过去认为,流至肾小球血液的减少,促使肾小球滤过率下降,从而发生氮质血症。目前我们对这一综合征的了解,比早先的简单公式复杂得多。我们认为,这种情况下的肾功能,通常是有助     

Determination of tryptamine in rat brain by gas chromatography-mass spectrometry

Tryptamine (TA) occurs in trace levels in the brain, but its role in the central nervous system is not clear. However, there is evidence that TA may be a neuromodulator since it binds to specific binding sites in the brain. TA was measured as a diheptafluorobutyryl derivative in rat whole brain by capillary gas chromatography—mass spectrometry using negative chemical ionization (NCI) and single ion monitoring (SIM). d₄-TA was used as the internal standard. The ions m/z 532 and m/z 536 were monitored to identify TA and d₄-TA, respectively and to calculate the concentration of TA in rat whole brain which was found to be 0.19 ± 0.08 ng g⁻¹ (n = 8). The results confirm the earlier TA concentrations measured by GC—MS using positive electron impact ionization. However, NCI improved the signal/noise ratio of the method increasing its sensitivity for TA.     

Trisomy 22 in acute myeloid leukemia: a marker for myeloid leukemia with monocytic features and cytogenetically cryptic inversion 16

Trisomy 22 is an uncommon chromosomal abnormality in acute myeloid leukemia. Recent studies, however, have shown an association between trisomy 22 and acute myeloid leukemia with a monocytic component, and in particular, acute myelomonocytic leukemia with marrow eosinophilia. Furthermore, it has also been suggested that trisomy 22 was in fact only a secondary chromosomal change occurring in acute myeloid leukemia with inv(16). In this report, we analyze the morphological, cytogenetic, and molecular findings of three cases of acute myeloid leukemia with trisomy 22 but without cytogenetic evidence of inv(16). The results indicate a consistent association between trisomy 22 and inv(16), the latter being cytogenetically cryptic in some cases. This finding is of potential diagnostic and therapeutic significance.     

Novel mutations in type 2 Gaucher disease in Chinese and their functional characterization by heterologous expression

We investigated 10 unrelated Chinese patients with type 2 Gaucher disease and performed ex vivo expression for the novel mutations to characterize their functional defects. These patients were diagnosed by enzymatic assays and clinicopathologic features over the past five years in a national centre in China. Genomic DNA was sequenced by a two-stage PCR approach for mutations in the functional GBA gene. Novel mutations were expressed with baculovirus-transfected Sf21 cells. Six novel mutations were found (in traditional nomenclature): P122L, Y363C, N382K, L383R, L385P, and M416V. Review of reported mutations indicated clustering of type 2 mutations in three regions of the GBA gene. Expression of novel mutations revealed that the enzyme defect could arise from one of two mechanisms: loss of catalytic activity (Y363C and M416V) or enzyme instability (P122L and N382K).     

Altered responsiveness to stress and NMDA following prenatal exposure to cocaine

Pregnant Sprague--Dawley rats were treated once daily with 40-mg/kg cocaine or saline from gestation days (GD) 12 to 21. A third group of pregnant dams was used as a pairfed control. Male and female offspring were examined for stress endurance response as determined by the cold-water swim test on postnatal days (PND) 21, 30, 40, and 60. Male and female offspring exposed to cocaine in utero were found to have diminished tolerance and altered hormonal response to stress. Moreover, prenatal cocaine exposure has been associated with significant increases in severity of N-methyl-D-aspartate (NMDA; 35 mg/kg) behavioral responses (tail twitches, wetdog shaking, and convulsion) as compared to control. Examining the experimental groups for pain sensitivity using the tail-flick and the hot-plate methods indicated that prenatal cocaine exposure altered pain sensitivity. NMDA receptor binding studies showed an increase in receptor density in the hippocampus and hypothalamus of the cocaine-treated group. These results indicate that gestational cocaine exposure is associated with long-term alterations in response to stress, NMDA receptor, and pain sensitivity in the rat offspring.