Esophagogastric decompression and enteral feeding following cholecystectomy: a controlled, randomized prospective trial

One hundred fourteen patients scheduled to undergo elective cholecystectomy were prospectively randomized into one of four treatment groups to study the potential benefits of esophagogastric decompression with and without immediate postoperative enteral nutrition. Group I was the control, and patients received only iv fluids and were allowed to eat as tolerated. Group II patients received iv fluids and esophagogastric decompression. Group III patients received esophagogastric decompression and enteral sterile water through the duodenal feeding lumen. Group IV patients received esophagogastric decompression and infusion of an elemental diet through the feeding lumen. The surgical techniques were standardized for all patients. The results of the study indicated no statistically or clinically significant differences among any of the treatment groups regarding; (1) need for parenteral analgesics or antiemetics, (2) tolerance of regular diet, (3) postoperative day of discharge, and (4) postoperative day that other discharge criteria were met. It is concluded that there is no objective benefit to the routine use of esophagogastric decompression with or without enteral nutrition in elective cholecystectomy patients.     

Functional changes in canine saphenous veins after cryopreservation.

This study was designed to determine the functional characteristics of the endothelium, smooth muscle and nerve terminals of cryopreserved veins. Freshly harvested and cryopreserved canine saphenous veins were cut into rings. In some rings, the endothelium was removed. Cryopreserved veins were stored at -196 degrees C for at least 3 weeks prior to use. All rings contracted in a concentration-dependent manner to depolarization with KCl and to alpha-adrenergic stimulation; the maximal tensions were significantly less in cryopreserved than in freshly harvested veins. Calcium ionophore A23187 caused greater relaxations in rings with than without endothelium in freshly harvested and cryopreserved veins. These relaxations were reduced significantly by methylene blue and NG-monomethyl-L-arginine (L-NMMA) only in fresh veins. Cocaine-sensitive uptake of H3-norepinephrine was reduced following cryopreservation. Immediately after cryopreservation, the production of prostacyclin was elevated. The calcium ionophore A23187 stimulated production of prostacyclin only in freshly harvested veins. Tissue content of endothelin did not change following cryopreservation. These results suggest that cryopreservation of canine saphenous veins alters nerve terminals and decreases the ability of the smooth muscle to contract. The endothelium releases an endothelium-derived relaxing factor and prostanoids following cryopreservation but the ability to synthesize nitric oxide is probably reduced. These changes following cryopreservation may affect patency of the veins when used as arterial grafts.     

Follistatin and activin A production by the male reproductive tract

Follistatin is a binding protein for the activin and inhibin family of hormones, regulating their biological activity. In the male reproductive tract, the interaction of these factors is likely to be involved in the regulation of the proliferation of several cell types. We have investigated the presence of follistatin and activin A in seminal plasma using specific immunoassays and have localized follistatin and activin/inhibin subunits in the adult human testis, prostate and seminal vesicle to establish their likely sources. High concentrations of immunoreactive follistatin were present in seminal plasma in normal men (mean 97.9 ng/ml; 1.43 ng/ml in peripheral plasma) and were similar in men with oligo/azoospermia and following vasectomy. Follistatin immunoreactivity was localized to both Leydig and Sertoli cells of the testis, and to epithelial cells of the prostate gland and seminal vesicle, which are likely to be the predominant sources of the hormone in seminal plasma. Activin A was also present in seminal plasma in normal men but was undetectable following vasectomy, thus deriving from the testis. Consistent with this finding, the betaA-subunit was immunolocalized in Sertoli and Leydig cells but was not present in seminal vesicle or prostate gland. The functional significance of the high concentrations of follistatin secreted into seminal plasma by the prostate gland and/or seminal vesicle is uncertain, but they may regulate the biological activity of testis-derived activin A and inhibin B.      

Priming of the oxidative burst in human neutrophils by physiological agonists or cytochalasin B results from the recruitment of previously non-responsive cells.

Using a sensitive flow cytometric assay, which measures the intracellular oxidation of 2'7' dichlorofluorescein (DCFH) by H2O2, we have assessed, at a single-cell level, the effects of a variety of physiological priming agonists and cytochalasin B (CB) on purified populations of neutrophils stimulated at different points along the signal response transduction pathway. Pretreatment of purified neutrophils with the physiological priming agonists monocyte interleukin-8 (IL-8), granulocyte-monocyte colony-stimulating factor (GM-CSF), platelet-activating factor (PAF), IL-1 beta, tumour necrosis factor-alpha (TNF-alpha), IL-6, and non-stimulatory doses of formyl-methionyl-leucyl-phenylalanine (FMLP), resulted in an increased percentage of cells generating an oxidative burst in response to subsequent receptor stimulation with FMLP. CB had a similar but much more pronounced effect on cellular recruitment to a receptor-mediated responsive state. Activation of protein kinase C (PKC) using the phorbol ester phorbol myristate acetate (PMA) resulted in a heterogeneous response, with all cells generating H2O2, but with two populations differing in their magnitude of response. Physiological priming agonists had no effect on the heterogeneity of the PMA response. However, pretreatment with CB dramatically altered the PMA response, producing a homogeneous population highly responsive to stimulation with PKC. In contrast, direct stimulation of G proteins with fluoride (A1F-4) was primed both by physiological priming agonists and by CB. These results demonstrate that priming of neutrophils by physiological agonists involves changes at the level of signal transduction which enable a previously non-responsive cell to respond to a secondary stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Meal patterns of normal, untreated bulimia nervosa and recovered bulimic women

In order to examine the meal pattern characteristics associated with bulimia nervosa the meal patterns of 19 untreated bulimia nervosa, 12 recovered bulimics, and 21 normal controls spontaneously eating in their natural environments were compared. Subjects reported in a diary everything they either ate or drank for seven consecutive days. Meal pattern correlations included comparisons of the groups in regard to meal size (and binge size), meal frequency, premeal and postmeal intervals, deprivation ratios, satiety ratios, stomach contents, and composition of meals and binges. Results indicated that, although total reported intake was normal, only 33% of the total calories consumed by the untreated bulimia nervosa subjects were not followed immediately by purging. Both purged and unpurged binges were twice as large as their meal sizes which did not differ from normal. It is hypothesized that the caloric restriction of the untreated bulimics is binge/purge specific, and is used by them as a form of weight control. The recovered group showed a lack of responsivity to the signals that influence meal size and intermeal intervals in normals including impaired social facilitation of eating. They also had larger meal sizes, and greater frequency of meals. It is theorized that recovered bulimics employ other, as yet unspecified, means of food intake restriction resulting in an abnormal feeding pattern.     

The A427 anchorage-independence assay as a screening tool to identify potential chemopreventive agents

An in vitro model for screening potential chemopreventive agents using inhibition of anchorage-independent growth of a human lung tumor cell line, A427, is described. A427 cells were selected for the model development, as they are known to be tumorigenic in animals, can grow in soft agarose, and their growth can be inhibited by a well-known chemopreventive agent, 13-cis-retinoic acid. Cells are plated on agarose, allowed to develop colonies for 28 days, the stained colonies are enumerated, and the inhibition of spontaneous colony formation measured. A cytotoxicity test is used concurrently with anchorage independent assay for measuring the relative survival of cells to ensure that any observed inhibition of anchorage independent growth is due to the biological activity of the chemopreventive agents, as it uses human cells as substrates rendering the efficacy data feasible for direct extrapolation to humans.     

A longitudinal study of maternal serum inhibin-A, inhibin-B, activin-A, activin-AB, pro-alphaC and follistatin during pregnancy

Maternal serum concentrations of inhibin-A, inhibin-B, activin-A, activin-AB, pro-alphaC-related inhibin forms, total follistatin, steroids and gonadotrophins were measured longitudinally in six normal singleton pregnancies. Maternal venous blood was collected randomly during a spontaneous follicular phase prior to donor insemination, at 5, 7, 9, 11, 16, 20, 24, 28, 32 and 36 weeks after the first missed menses and in the early puerperium. Steroid and gonadotrophin profiles conformed to previous reports. While at week 5 of gestation inhibin-A, activin-A and follistatin concentrations were similar to those at the follicular phase, all three increased progressively (P < 0.001) to maximal concentrations in week 36: approximately 48-fold (3740 +/- 1349 ng inhibin-A/ml), approximately 22-fold (6109 +/- 1443 ng activin-A/ml) and approximately 10-fold (3563 +/- 418 ng follistatin/ml) higher. Pro- alphaC concentrations reached a maximum in weeks 5 (approximately 5- fold, P < 0.001) and 36 (1027 +/- 174 pg/ml, P < 0.01). Inhibin-B (71 +/- 23 pg/ml prior to pregnancy) was undetectable (<12 pg/ml) between week 5-16 of gestation but increased slightly in the third trimester (26 +/- 7 pg/ml in week 36). Activin-AB was undetectable throughout pregnancy. Post-partum concentrations of inhibin-A (41 +/- 12 ng/ml), inhibin-B (<12 pg/ml), activin-A (950 +/- 149 pg/ml), pro-alphaC (128 +/- 22 pg/ml) and follistatin (990 +/- 79 ng/ml) were substantially lower than at week 36 of gestation. The activin-A:follistatin ratio increased from 0.5 in week 5 to 1.8 in week 36, suggesting that more free activin-A is available in the maternal circulation during late pregnancy.