一些保肝药物对原代培养大鼠肝细胞糖原合成功能的影响

本文参照PO Seglen的方法并加以修改,建立了原代培养大鼠肝细胞糖原合成功能的测定体系。观察到联苯双酯既能使正常肝细胞合成糖原增加88%,又能保护肝细胞完全拮抗四氯化碳对其功能的损伤;银耳多糖能使四氯化碳对肝细胞糖原合成功能的损伤减轻57%;去甲斑蝥素10μg/ml能增加肝细胞糖原合成,浓度增加到100μg/ml时,此作用减弱,1000μg/ml则明显抑制糖原的合成,而且在10～100μg/ml浓度时,即能加强四氯化碳的损伤作用;100μg/ml CL₁₅₀₀和熊果酸二钠单独应用可增加肝细胞糖原合成,但与四氯化碳同时应用,反而加重对糖原合成的抑制作用。     

Secretion of vascular endothelial growth factor/vascular permeability factor from human luteinized granulosa cells is human chorionic gonadotrophin dependent

Vascularization is a prominent event during corpus luteum formation, providing low density lipoproteins for steroid biosynthesis and enabling transport of secreted steroids. The process of vascularization is controlled by specific regulators. Vascular endothelial growth factor (VEGF), otherwise named vascular permeability factor (VPF), induces endothelial cell proliferation as well as angiogenesis in vivo and increases capillary permeability. Here we report the expression of VEGF/VPF mRNA by cultured human luteinized granulosa cells (GC) for at least 10 days. Without HCG VEGF/VPF expression declined after day 4 and by day 10 was reduced to approximately 30% of the value at day 4. However, after culture in the presence of 1 U/ml human chorionic gonadotrophin (HCG), expression of VEGF/VPF mRNA by GC was four times greater than control experiments by day 10, and increased 100% from day 4 to day 10. Simultaneously, HCG supplementation increased VEGF/VPF secretion by GC. Medium VEGF/VPF on day 3 was 13 pM without and 11 pM with HCG. Medium VEGF/VPF on day 10 was 6 pM without HCG and 29 pM with HCG. These results suggest that vascularization of the corpus luteum is induced by HCG-mediated effects of VEGF/VPF.      

The UTX gene escapes X inactivation in mice and humans

We recently have identified a ubiquitously transcribed mouse Y chromosome gene, Uty , which encodes a tetratricopeptide repeat (TPR) protein. A peptide derived from the UTY protein confers H-Y antigenicity on male cells. Here we report the characterization of a widely transcribed X-linked homologue of Uty , called Utx , which maps to the proximal region of the mouse X chromosome and which detects a human X-linked homologue at Xp11.2. Given that Uty is ubiquitously transcribed, we assayed for Utx expression from the inactive X chromosome (Xi) in mice and found that Utx escapes X chromosome inactivation. Only Smcx and the pseudoautosomal Sts gene on the mouse X chromosome have been reported previously to escape inactivation. The human UTX gene was also found to be expressed from Xi. We discuss the significance of these data for our understanding of dosage compensation of X-Y homologous genes in humans and mice.      

The mouse Mid1 gene: implications for the pathogenesis of Opitz syndrome and the evolution of the mammalian pseudoautosomal region

We have recently reported isolation of the gene responsible for X- linked Opitz G/BBB syndrome, a defect of midline development. MID1 is located on the distal short arm of the human X chromosome (Xp22. 3) and encodes a novel member of the B box family of zinc finger proteins. We have now cloned the murine homolog of MID1 and performed preliminary expression studies during development. Mid1 expression in undifferentiated cells in the central nervous, gastrointestinal and urogenital systems suggests that abnormal cell proliferation may underlie the defect in midline development characteristic of Opitz syndrome. We have also found that Mid1 is located within the mouse pseudoautosomal region (PAR) in Mus musculus , while it seems to be X- specific in Mus spretus. Therefore, Mid1 is likely to be a recent acquisition of the M. musculus PAR. Genetic and FISH analyses also demonstrated a high frequency of unequal crossovers in the murine PAR, creating spontaneous deletion/duplication events involving Mid1. These data provide evidence for the first time that genetic instability of the PAR may affect functionally important genes. In addition, we show that MID1 is the first example of a gene subject to X-inactivation in man while escaping it in mouse. These data contribute to a better understanding of the molecular content and evolution of the rodent PAR.      

Anatomical connections of auditory and lateral line areas of the dorsal telencephalon (Dm) in the osteoglossomorph teleost, Gnathonemus petersii

Local field potentials evoked either by auditory or by mechanosensory (water displacement) lateral line stimuli were recorded in sensory subregions of the telencephalic nucleus dorsalis pars medialis (Dm) in the weakly electric fish Gnathonemus petersii. The neural tracer Neurobiotin was injected into these two physiologically defined subregions. A reciprocal connection between the two subregions of Dm, as well as cell bodies and terminals in other telencephalic regions, whose distribution was somewhat different for the two injection types, were found. The course of labeled fibers outside the telencephalon was similar after injections in both Dm regions. Fibers were seen running through the lateral forebrain bundle (lfb) to the ventral surface area of the brain within the diencephalic preglomerular region (PGv). Within a narrow streak along the ventral side of the brain densely arranged cell bodies were labeled. The locations of labeled cells within PGv were indistinguishable after tracer was injected into either acoustical or lateral line areas of Dm. Only after injection into the mechanosensory Dm region labeled cell bodies were found in the anterior preglomerular nucleus (PGa), in addition. When crystals of the fluorescent tracer DiI were inserted in the ventral part of PGv, a path of labeled fibers similar to that after telencephalic injections was found. Labeled terminals, but no cell bodies, were located both in the acoustical and in the mechanosensory regions of Dm as well as in several other telencephalic areas. Even though sensory regions in Dm that process acoustical and mechanical stimuli are segregated and unimodal, they both receive input from neurons of PGv. The specificity of the mechanosensory region of Dm might originate from the additional input from PGa and from other endbrain areas.     

Emergence of behavioural states in fetuses of type-1-diabetic women

The aim of this study was to investigate the effects of tightly controlled maternal (type-1-)diabetes mellitus on the development of fetal behavioural states. Seventeen diabetic women, who required insulin (White's class C predominantly) and were treated with continuous subcutaneous insulin infusion (CSII) therapy, participated in the study. Adjustment to an insulin-pump occurred before conception or during early pregnancy. In all diabetic women (near-)normoglycemia was achieved during pregnancy, with glycosylated hemoglobin-values within the normal range (6-8.5%). Fifty-three 2-h recordings of fetal heart rate, uterine contractions and of real-time ultrasound scanning for fetal body movements, breathing and eye movements were obtained from the 17 fetuses. The fetuses were longitudinally studied between 32 and 40 weeks post menstrual age, at intervals of 2 weeks. The 3 state variables, fetal heart rate, body movements and eye movements, were analyzed for the presence of combinations meeting the definitions of the four fetal behavioural states. Findings in the fetuses of diabetic women were compared with those obtained from 28 low risk fetuses. The criteria of states were met in only 3 of 8 fetuses studied at 38 weeks and in one of two studied at 40 weeks. For comparison: in low risk fetuses studied at 38 and 40 weeks, states were present in 70% and 90% of the cases, respectively. This poorly developed state organization exhibited by the near term fetuses of the diabetic group, was related to maternal parity, but not to pre- or postconceptional onset of CSII-treatment. Fetuses of nulliparous diabetic women showed more often asynchrony of transitions (greater than 3 min) and interruption of periods of concordant association. This resulted in significantly higher percentages of 'no-coincidence' and in low incidence of behavioural states as compared with control fetuses of nulliparous women. In the few multiparous diabetic cases studied near term the development of fetal behavioural states was normal. We conclude therefore that, despite tight control of maternal diabetes, the development of behavioural states is disturbed in fetuses of nulliparous diabetic women.     

A new heparin fragment decreases liver ischemia-reperfusion injury

<正>To the Editor:Ischemia-reperfusion injury following surgery and transplantation can lead to irreversible multiorgan failure.Intracellular calcium overload is associated to cellular death during ischemiareperfusion.A recently discovered heparin fragment (HF),trisulfated disaccharide (TD),that acts on sodium-calcium exchanger(NCX) decreasing intracellular Ca²⁺,showed effectiveness on protecting hepatocytes from ischemia-reperfusion injury [1],