胎肝细胞输注对癌症病人化疗中外周血白细胞变化干预的序贯试验研究

本文自１９９１年１月以来．进行了静脉输注胎肝细胞悬液干扰化疗药物降白副反应的医学序贯试验。实验组病人静脉输注４～６月胎龄胎肝细胞悬液１６００～４０００ｍｌ（浓度５～７×１０９个／Ｌ），对照组按常规方法升白。通过２８例病人的序贯试验发现化疗期间输注胎肝细胞悬液的病人骨髓抑制发生延迟，持续时间短，程度减轻，从而为化疗正常进行提供基本条件。结论；胎肝细胞悬液输注可干扰化疗药物降白副反应的发生。     

REPAIR AND RECOVERY FOLLOWING SPINAL CORD INJURY IN A NEONATAL MARSUPIAL (MONODELPHIS DOMESTICA)

1. Repair and recovery following spinal cord injury (complete spinal cord crush) has been studied in vitro in neonatal opossum (Monodelphis domestica), fetal rat and in vivo in neonatal opossum. 2. Crush injury of the cultured spinal cord of isolated entire central nervous system (CNS) of neonatal opossum (P4–10) or fetal rats (E15–E16) was followed by profuse growth of fibres and recovery of conduction of impulses through the crush. Previous studies of injured immature mammalian spinal cord have described fibre growth occurring only around the lesion, unless implanted with fetal CNS. 3. The period during which successful growth occurred in response to a crush is developmentally regulated. No such growth was obtained after P12 in spinal cords crushed in vitro at the level of C7–8. 4. In vivo, in the neonatal (P4–8) marsupial opossum, growth of fibres through, and restoration of, impulse conduction across the crush was apparent 1–2 weeks after injury. With longer periods of time after crushing a considerable degree of normal locomotor function developed. 5. By the time the operated animals reached adulthood, the morphological structure of the spinal cord, both in the region of the crush and on either side of the site of the lesion, appeared grossly normal. 6. The results are discussed in relation to the eventual longterm possibility of devising effective treatments for patients with spinal cord injuries.     

EFFECTS OF LOSARTAN ON THE CARDIOVASCULAR SYSTEM, RENAL HAEMODYNAMICS AND FUNCTION AND LUNG LIQUID FLOW IN FETAL SHEEP

1. The angiotensin type 1 (AT₁) receptor antagonist, losartan (10 mg/kg) was infused intravenously into nine chronically catheterized fetal sheep (125–132 days gestation). Losartan reduced the fetal systolic (P < 0.01) and diastolic (P < 0.01) pressor response to 5 μg angiotensin II (AngII) i.v. from 27.4 ± 1.5 to 7.4 ± 0.9 and from 17.5 ± 1.3 to 5.4 ± 0.6 mmHg, respectively, after 1h and to 6.1 ± 0.5 and 4.4 ± 0.5 mmHg, respectively, after 2h. Maternal pressor responses to 5 μg AngII i.v. were unchanged. Fetal mean arterial pressure decreased (P < 0.05) after losartan administration, but fetal heart rate did not change. 2. Fetal haematocrit increased (P < 0.05), fetal PO₂ decreased (P < 0.01), PCO₂ did not change and pH decreased (P < 0.01), as did plasma bicarbonate levels (P < 0.01) following administration of losartan. Thus, losartan induced a fetal metabolic acidosis. 3. Fetal placental blood flow did not change following administration of losartan. In the fetal kidney, losartan caused a decrease in vascular resistance (P < 0.01) and an increase in blood flow (P < 0.05). Glomerular filtration rate decreased (P < 0.05); thus, filtration fraction decreased (P < 0.01). There was no change in the fractional reabsorption of sodium and glomerulotubular balance was maintained. Free water clearance decreased (P < 0.01) and became negative. Urine flow decreased (P < 0.01), the excretion rates of sodium, potassium and chloride did not change, but the urinary sodium:potassium ratio decreased (P < 0.05). There was a decrease in lung liquid flow (P < 0.05) following losartan. 4. It is concluded that the fetal renin-angiotensin system (RAS) is important in the maintenance of fetal arterial pressure, the regulation of fetal renal blood flow and is essential in the maintenance of fetal glomerular function. Further, these actions of AngII are mediated via functional AT₁ receptors. These effects of losartan on the fetal cardiovascular system, renal blood flow and function are similar to those observed following captopril administration. Thus, the effects of angiotensin converting enzyme (ACE) inhibition in the foetus are due to the blockade of the fetal RAS and are independent of any direct effects on bradykinin or prostaglandin levels.     

胎儿食管肌间神经丛胆碱能神经元的定位定量研究

用引产后死亡的正常胎儿（３２￣４０周，１５个）食管，将其分颈部，胸部上、中、下，腹部食管５部分。对各部位食管肌间神经丛内胆碱能神经元，进行光镜（ｃｈＡＴ、ＡＣｈＥ）和电镜（ＡｃｈＥ）酶组织化学定位、定量观察。结果表明，胆碱能神经元的分布及细胞内酶含量，在食管各部位不同，ＡＣｈＥ在电镜下定位于粗面内质网。这一研究结果，不仅将使食管胆碱能神经支配及其生理功能等基础理论知识，得到进一步阐明、丰富和发展；     

The development of the stria vascularisin the human foetus

The development of the stria vascularis in the human cochlea was studied in step sections of 81 human foetal temporal bones. The stria vascularis primordium can be identified as a ridge of epithelial cells on the lateral wall of the cochlear duct. The first signs of differentiation appear at the 11th week, but it is not until the 17th–18th week that the typical trilaminar structure is observed. The appearance of similar cells with notched nuclei in both marginal and mesenchymal layers at this stage suggests the possibility that some of the intermediate cells may be of epithelial origin. By the 21st week, the overall appearance resembles that of the adult structure. This occurs 1week after the opening of the tunnel of Corti, and possibly marks the onset of cochlear function.     

Diazepam metabolism in human foetal and adult liver

Summary Diazepam was metabolized by human foetal liver microsomes to N-desmethyldiazepam and N-methyloxazepam as early as the 13th week of gestation. The metabolic activity was lower than that of microsomes from adult human liver. Diazepam was shown mainly to be hydroxylated to N-methyloxazepam at substrate concentrations higher than 0.1 mM. Diazepam levels above 1.0 mM were inhibitory to the overall metabolic reaction. SKF 525-A inhibited diazepam metabolism by foetal liver microsomes at a concentration of 0.1 mM. The addition of diazepam to foetal and adult human liver microsomes resulted in a type II spectral change. Its inhibition by carbon monoxide indicated that biotransformation of diazepam was performed by the cytochrome P-450-linked mono-oxygenase system.     

Foetal cystic abdominal masses

Foetal abdominal cysts are frequently found on routine antenatal ultrasound. Various sonographic features might help in their differential diagnosis. However, a definitive diagnosis is often not made until postnatal life, and detection of an intra‐abdominal cyst antenatally rarely alters obstetric management. A review of possible causes of a foetal abdominal cyst is presented.     

Oral cadmium exposure during rat pregnancy: assessment of transplacental micronutrient transport and steroidogenesis at term

Diet is the main source of cadmium (Cd) exposure. Gastrointestinal absorption increases during pregnancy. Cadmium accumulated in the placenta may interfere with nutrient transport to the foetus. Data on the potential of Cd to act as a steroid disruptor of pregnancy are limited. We evaluated the effects of oral Cd exposure during pregnancy on placental function in micronutrient transfer to the foetus and steroidogenesis in Wistar rats (regular 4‐day cyclers) that mated with unexposed males. Pregnant rats were randomly assigned to a Cd group exposed orally to 50 mg Cd l^–1 (CdCl₂xH₂O dissolved in demineralized water), ≈7.5 mg Cd kg^–1 a day, during 20 days of gestation and control (supplied with demineralized water). Non‐pregnant rats were treated under the same experimental conditions. On day 20, all of the rats were killed and samples were taken for element analyses (by electrothermal atomic absorption spectrometry). Progesterone and testosterone were measured in serum and placenta‐derived samples (by immunoenzymometric assay and/or enzyme‐linked immunosorbent assay). In the exposed rats, Cd increased in blood and organs, more in pregnant rats, and in placenta and foetus whereas zinc increased in liver. Iron decreased in maternal organs and in foetus, whereas zinc decreased in maternal kidney and placenta. Liver copper was lower and kidney copper higher in all pregnant vs. non‐pregnant rats. Steroids in serum and placenta did not change. In conclusion, oral Cd exposure during rat pregnancy does not affect progesterone and testosterone at term. Transplacental iron and zinc handover are disrupted, which may put at risk the maintenance of foetal nutrition and viability. Copyright © 2014 John Wiley & Sons, Ltd.     

Reference ranges of Doppler parameters of foetal pulmonary artery segments between 19 and 39 weeks of gestation

Objective: To determine reference ranges of Doppler parameters of foetal pulmonary artery segments.

Methods: A prospective cross-sectional study was conducted to evaluate 150 healthy singleton pregnancies between 19 and 39 weeks of gestation. The proximal, middle and distal segments of the foetal pulmonary artery were assessed. The following Doppler parameters were evaluated: pulsatility index (PI) and peak systolic velocity (PSV). The mean, standard deviation (SD) and maximum and minimum values were determined for each Doppler parameter. Pearson’s correlation coefficient (r) was used to assess the correlation between the foetal pulmonary artery segments. Polynomial regression was performed, and adjustments were made using the coefficient of determination (R²).

Results: The mean PI values (mean?±?SD) in the proximal, middle and distal arterial segments were 2.99?±?0.61, 2.25?±?0.96 and 1.31?±?0.58, respectively. The mean PSVs in the proximal, middle and distal segments were 50.68?±?16.63, 24.396?±?11.86 and 12.08?±?3.66?cm/s, respectively. Significant differences were observed between the PI and PSV values from the different segments (p?<?0.0001). A correlation between each Doppler parameter and gestational age was observed, and it was better represented using linear equations.

Conclusion: We successfully determined the reference ranges for Doppler parameters of foetal pulmonary artery segments between 19 and 39 weeks of gestation.