Spontaneous colitis cystica profunda in captive tamarins

Of the 232 tamarins (133 Saguinus mystax and 99 Saguinus labiatus) that died at the Center for Reproduction and Conservation of Nonhuman Primates in Iquitos, Peru from January 1987 to December 1990, 23 monkeys (9.9%) were diagnosed as having chronic colitis. Typically, the cecal and colonic mucosa was greyish and small yellowish cysts, measuring 1–4 mm, were found randomly distributed bulging the mucosa. Microscopically, colitis cystica profunda was diagnosed additionally in six more animals, giving a total of 29 cases (12.5%). This is the first report to our knowledge that describes colitis cystica profunda in a nonhuman primate.     

13C-N.M.R. characterizations of the sarsasapogenin disaccharides,the filiferins a and b: 2-O-(β-d-xylopyranosyl)- and 2-O(β-d-glucopyranosyl)-β-d-galactopyranosides

Filiferin B is identical to timosaponin A-III, which had previously been shown to be 3-O-[2-O-(β-d-glucopyranosyl)-β-d-galactopyranosyl]sarsasapogenin. A larger-scale isolation of filiferin B from the seeds of Yucca filifera led to the isolation of filiferin A, now shown to be 3-O-[2-O-β-d-xylopyranosyl)-β-d-galactopyranosyl]-sarsasapogenin. The presence of the xylose residue was established by way of hydrolysis. 8-Methoxycarbonyloctyl 2-O-(β-d-glucopyranosyl)-β-d-galactopyranoside was synthesized to serve as a model for interpretation of the ¹³C-n.m.r. spectrum of filiferin B. The information thus gained, together with the ¹³C-n.m.r. spectra of other, simple model-compounds, permitted assignment of the structure for filiferin A. 8-Methoxycarbonyloctyl 2-O-(α-d-glucopyranosyl)-β-d-galactopyranoside was also synthesized.     

A parametrization of the CT number of a substance and its use for stoichiometric calibration

A method to carry out stoichiometric calibrations of CT scanners employed in radiotherapy treatment planning is proposed. The method is based on a simple parametrization of the CT number of a substance, which involves only two variables to describe the substance (electron density and one effective atomic number) and one parameter to describe the beam. The method was tested experimentally on a group of beams. A set of no tissue-like substances of known densities and elemental compositions were employed as calibrators. CT number-to-density curves (RED curves) were calculated with the proposed parametrization and compared to those measured with a commercial density phantom. Differences between the electron densities assigned by the calculated RED curves and the measured ones were in the range 0.009–0.019 (RMS). The proposed method may be employed to carry out accurate stoichiometric calibrations by using only one suitable substance as calibrator, not necessarily tissue-like.     

Endometriosis: New concepts in the pathogenesis

Endometriosis is a gynaecological disease defined by the histological presence of endometrial glands and stroma outside the uterine cavity. Though there are several theories, research scientists remain unsure as to the definitive cause(s) of endometriosis. Considering the relevant health problems caused by endometriosis, all new information on the pathogenesis of this disease, may have important clinical implications. Goal of this article is to summarize the latest advances in the pathogenesis of endometriosis, with particular emphasis on the embryological theory, that has been recently re-proposed. The possible clinical implications of these findings will be discussed.     

Phosphatidic Acid Induces Ligand-independent Epidermal Growth Factor Receptor Endocytic Traffic through PDE4 Activation

Endocytosis modulates EGFR function by compartmentalizing and attenuating or enhancing its ligand-induced signaling. Here we show that it can also control the cell surface versus intracellular distribution of empty/inactive EGFR. Our previous observation that PKA inhibitors induce EGFR internalization prompted us to test phosphatidic acid (PA) generated by phospholipase D (PLD) as an endogenous down-regulator of PKA activity, which activates rolipram-sensitive type 4 phosphodiesterases (PDE4) that degrade cAMP. We found that inhibition of PA hydrolysis by propranolol, in the absence of ligand, provokes internalization of inactive (neither tyrosine-phosphorylated nor ubiquitinated) EGFR, accompanied by a transient increase in PA levels and PDE4s activity. This EGFR internalization is mimicked by PA micelles and is strongly counteracted by PLD2 silencing, rolipram or forskolin treatment, and PKA overexpression. Accelerated EGFR endocytosis seems to be mediated by clathrin-dependent and -independent pathways, leading to receptor accumulation in juxtanuclear recycling endosomes, also due to a decreased recycling. Internalized EGFR can remain intracellular without degradation for several hours or return rapidly to the cell surface upon discontinuation of the stimulus. This novel regulatory mechanism of EGFR, also novel function of signaling PA, can transmodulate receptor accessibility in response to heterologous stimuli.