The cholinesterase activity of myoneural junctions from frog twitch and tonic muscles

Résumé La distribution de l'activité cholinestérasique dans des faisceaux de jonctions myoneurales séparés des fibres cloniques et toniques de muscles de grenouille a été étudiée par une méthode radiochimique. Les jonctions myoneurales de fibres cloniques ont montré une plus forte activité cholinestérasique que celles de fibres toniques. Il est suggéré que la différence d'activité enzymatique est liée à la différence fonctionnelle des deux types de fibres.     

t-Haplotypes of the mouse may involve a change in intercalary DNA.

The naturally occurring t-haplotypes of the mouse exhibit a set of peculiar genetic properties, including strong suppression of crossing over in the segment of chromosome 17 between the loci of T and H--2. Study of the genetics of mutant haplotypes suggests that the observed effects on meiosis and embryonic development may be due to an altered form of intercalary DNA (iDNA) in the relevant chromosomal region (band 17B).     

EDRF coordinates the behaviour of vascular resistance vessels

Constriction of vascular smooth muscle in response to the stimulus of raised intravascular pressure--the myogenic response--represents a positive feedback mechanism which, if unopposed, could theoretically lead to instability in the intact circulation. Dilation in response to increased intraluminal flow would provide an opposing feedback mechanism which could confer overall stability. Flow-dependent dilation in conduit vessels is mediated by endothelium-derived relaxing factor (EDRF), but the relationship between flow and EDRF activity has not been studied in resistance vessels in situ. We here demonstrate that EDRF can coordinate the aggregate hydrodynamic properties of an intact network. Under control conditions, EDRF maintains a fourth-power relationship between diameter and flow so that the pressure gradient in each vessel asymptotically approaches a constant value at high flow rates. Basal EDRF release may also maintain a similar spatial distribution of flow at different flow rates, even under conditions of moderate pharmacological constriction.     

Transgenic mice with inducible dwarfism

The pituitary gland, composed of the anterior, intermediate and posterior lobe, represents a principal regulatory interface through which the central nervous system controls body physiology. The ontogeny of the growth hormone (GH) and prolactin (Prl) producing cells of the anterior pituitary has been analysed in transgenic mice, using the thymidine kinase obliteration system (TKO). Cells expressing the herpes virus 1 thymidine kinase (HSV1-TK) gene acquire pharmacological sensitivity to synthetic nucleosides such as FIAU (1-(2-deoxy-2-fluoro-beta-delta-arabinofuranosyl)-5-iodouracil), whose metabolites kill dividing cells. Consequently we created transgenic mice carrying the HSV1-TK gene under the control of either the rat growth hormone or the rat prolactin promoter. If transgenic mice expressing HSV1-TK in somatotropes (GH-producing cells) are treated with FIAU, they develop as dwarfs. The anterior pituitary in these animals is nearly devoid of both somatotropes and lactotropes (Prl-producing cells). By contrast, transgenic mice expressing HSV1-TK in the lactotropes, treated with FIAU, have anatomically and histologically normal pituitaries. Because toxicity depends on cell division, we conclude that Prl expression and lactotrope differentiation are post-mitotic events. These results indicate that both somatotropes and lactotropes derive from a common GH-expressing stem-somatotrope. Unexpectedly, the stemsomatotrope is still present in the adult animal and is capable of repopulating the pituitaries of treated animals with mature GH and Prl producing cells.     

Preparation and photochromic properties of NiAl-NO3- LDHs/LDPE composite

Nanoscale NiAl-NO3-LDHs with good crystallinity have been synthesized by a method, Separate Nucleation and Aging Steps (SNAS). An NiAl-NO3-LDHs/LDPE composite was prepared by blending NiAl-NO3-LDHs and LDPE in a heated double-roller mixer. The color of this composite changed from olive green to steel gray under UV irradiation. After heating at 80oC for 2 h, the color returned to olive green. The effect of varying the amount of added NiAl-NO3-LDHs and UV exposure time on the photochromic properties of the composite has been investigated. The results showed that the photochromic phenomenon becomes more apparent with increasing amount of NiAl-NO3-LDHs. When the amount reaches 5%, the composite exhibits good photochromic properties and reproducibility. The color change rate of the composite reaches a maximum when the irradiation time exceeds 20 min. The addition of LDPE improves the photochromic cyclability of NiAl-NO3-LDHs significantly. The addition of nanoscale NiAl-NO3-LDHs also improves the mechanical properties of LDPE to some extent.     

Mutant alpha subunits of Gi2 inhibit cyclic AMP accumulation

One or more of three Gi proteins, Gi1-3, mediates hormonal inhibition of adenylyl cyclase. Whether this inhibition is mediated by the alpha or by the beta gamma subunits of Gi proteins is unclear. Mutations inhibiting the intrinsic GTPase activity of another G protein, the stimulatory regulator of adenylyl cyclase (Gs), constitutively activate it by replacing either of two conserved amino acids in its alpha subunit (alpha s). These mutations create the gsp oncogene which is found in human pituitary and thyroid tumours. In a second group of human endocrine tumours, somatic mutations in the alpha subunit of Gi2 replace a residue cognate to one of those affected by gsp mutations. This implies that the mutations convert the alpha i2 gene into a dominantly acting oncogene, called gip2, and that the mutant alpha i2 subunits are constitutively active. We have therefore assessed cyclic AMP accumulation in cultured cells which stably or transiently express exogenous wild-type alpha i2 complementary DNA or either of two mutant alpha i2 cDNAs. The results show that putatively oncogenic mutations in alpha i2 constitutively activate the protein's ability to inhibit cAMP accumulation.     

Deletion polymorphism in the gene for angiotensin-converting enzyme is a potent risk factor for myocardial infarction.

Factors involved in the pathogenesis of atherosclerosis, thrombosis and vasoconstriction contribute to the development of coronary heart disease. In a study comparing patients after myocardial infarction with controls, we have explored a possible association between coronary heart disease and a variation found in the gene encoding angiotensin-converting enzyme (ACE). The polymorphism ACE/ID is strongly associated with the level of circulating enzyme. This enzyme plays a key role in the production of angiotensin II and in the catabolism of bradykinin, two peptides involved in the modulation of vascular tone and in the proliferation of smooth muscle cells. Here we report that the DD genotype, which is associated with higher levels of circulating ACE than the ID and II genotypes, is significantly more frequent in patients with myocardial infarction (n = 610) than in controls (n = 733) (P = 0.007), especially among subjects with low body-mass index and low plasma levels of ApoB (P < 0.0001). The ACE/ID polymorphism seems to be a potent risk factor of coronary heart disease in subjects formerly considered to be at low risk according to common criteria.