LHRH-A对孕中期大鼠抗妊娠作用的研究

本文观察了[D-Ala⁶,Pro⁹-Ethylamide¹⁰]-LHRH(LHRH-A)对孕中期大鼠的抗妊娠作用。结果显示:在孕9～11d sc 200μg/d LHRH-A,血浆孕酮水平自第二次给药后明显下降(P<0.05),给药大鼠均流产终止妊娠;LHRH-A的抗妊娠作用可被醋酸甲地孕酮所拮抗;LHRH-A对体外培养的假孕大鼠和孕d 9大鼠黄体细胞分泌孕酮有明显的直接抑制作用。     

Biocompatibility studies on biodegradable polyester-based composites of human osteoblasts: a preliminary screening.

A series of biodegradable composites with natural hydroxyapatite, designed for possible use in orthopedics applications, were preliminarily screened for biocompatibility by employing primary cultures of human osteoblasts in a direct contact method. The cells were seeded at low density onto the materials under investigation and allowed to grow for 2 weeks. They then were analyzed for morphology, proliferation, viability, alkaline phosphatase activity (AP), osteocalcin (OC) production, and extracellular matrix mineralization. The results showed that all materials have good biocompatibility. Cell viability tests demonstrated that in all cases the values were comparable to the control, and the addition of hydroxyapatite always resulted in an enhancement of performance with respect to the plain polymer. AP and OC analysis confirmed that all composites allowed the expression of phenotypic markers. Scanning electron microscopy provided direct evidence of intense cell adhesion and proliferation on the tested materials.     

Can a non-tumorigenic dose of carcinogen cause two or more errors in a cell?

Cancer is believed to be the result of a multistep process, beginning with a single alteration in a cell's genome. Here the hypothesis that a few cells may receive two or more hits after the application of a non-tumorigenic or higher dose of carcinogen is proposed. Preneoplastic lesions that arise from such doubly-hit cells may be few in number, but may more easily undergo tumor formation and tumor progression. This hypothesis augments the multihit model of carcinogenesis and explains much data that the single, first-hit assumption cannot.     

Hemorrhagic vascular complications of endoscopic transsphenoidal surgery.

Two hundred and fifty consecutive patients operated on by an endoscopic endonasal transsphenoidal approach were retrospectively analyzed in order to evaluate hemorrhagic vascular complications occurring during or after the surgical procedure and their appropriate management. Vascular complications of endoscopic transsphenoidal surgery are identical to those of a microsurgical transsphenoidal approach. Damage to the sphenopalatine artery and to the internal carotid artery (ICA), which are the most frequent vascular troubles, may require technical tricks because of some aspects connected to the approach itself and of the physical properties of the endoscope. Furthermore, the progress in interventional neuroradiology in the last decades offers new solutions in respect to the past, where the use of the surgical microscope was already a tremendous progress. The anatomic substrate of each complication is discussed, along with the peculiar surgical details related to it.     

Compression of the sigmoid of gynecological origin]

The authors report a case of extrinsic stenosis of the sigmoid colon due to inflammation of the uterus and adjoining parts. Attention is drawn to the possibility that the radiological images of this condition may be similar to neoplastic diseases.     

GGA1 acts as a spatial switch altering amyloid precursor protein trafficking and processing

The beta-amyloid (Abeta) precursor protein (APP) is cleaved sequentially by beta-site of APP-cleaving enzyme (BACE) and gamma-secretase to release the Abeta peptides that accumulate in plaques in Alzheimer's disease (AD). GGA1, a member of the Golgi-localized gamma-ear-containing ARF-binding (GGA) protein family, interacts with BACE and influences its subcellular distribution. We now report that overexpression of GGA1 in cells increased the APP C-terminal fragment resulting from beta-cleavage but surprisingly reduced Abeta. GGA1 confined APP to the Golgi, in which fluorescence resonance energy transfer analyses suggest that the proteins come into close proximity. GGA1 blunted only APP but not notch intracellular domain release. These results suggest that GGA1 prevented APP beta-cleavage products from becoming substrates for gamma-secretase. Direct binding of GGA1 to BACE was not required for these effects, but the integrity of the GAT (GGA1 and TOM) domain of GGA1 was. GGA1 may act as a specific spatial switch influencing APP trafficking and processing, so that APP-GGA1 interactions may have pathophysiological relevance in AD.     

Endogenous aspartate release in the rat hippocampus is inhibited by M2 'cardiac' muscarinic receptors

The release of endogenous aspartic acid elicited by depolarization of rat hippocampus synaptosomes with 15 mM KCl was totally calcium-dependent. Acetylcholine (ACh) added to the superfusion medium inhibited the K(+)-evoked release of aspartate in a concentration-dependent manner. The effect of ACh was mimicked by oxotremorine and carbachol. It was insensitive to the nicotinic receptor antagonist mecamylamine but blocked by the non-selective muscarinic receptor antagonist atropine. Further pharmacological characterization of the muscarinic receptor involved showed that the ACh effects was insensitive to the M1 selective muscarinic receptor antagonists pirenzepine and dicyclomine. However, the inhibition by ACh of aspartate release was counteracted by 11-[[2-[(diethylamino)methyl]-1-piperidinyl]acetyl]-5,11-dihydro-6H- pyrido-[2-3-b][1,4]benzodiazepine-6-one (AF-DX 116), a selective M2 'cardiac' receptor antagonist. The calcium dependence of the release of aspartate and its regulation through presynaptic receptors are suggestive of a transmitter role for this excitatory amino acid. Moreover, the similarities between the present results and those previously obtained with glutamate are compatible with the idea that aspartate and glutamate are co-released in the rat hippocampus.