En el presente trabajo se realiza la actualizacion y modernizacion de la linea de fabricacion de adhesivos en Base a Agua; para lo cual se realizaron las siguientes actividades preliminares: inventario de los equipos involucrados en el proceso, conocimiento y familiarizacion con el proceso productivo y de fabricacion, elaboracion de los planos de instrumentacion y tuberias (PI identificar y solucionar los aspectos criticos que afectan el proceso productivo y la calidad de sus productos. Seguidamente, despues de involucrarnos con el proceso y puntualizar aquellos aspectos a optimizar, procedimos a construir la propuesta para la actualizacion de la linea de fabricacion, involucrando las siguientes actividades: diseno y analisis de costos por concepto de la redistribucion de los reactores, lo cual implica una ampliacion de la estructura civil de la mezzanina de PVA y la redistribucion de las lineas de tuberias asociadas; calculos estructurales y de tuberias, ademas de considerar sus costos; disenar una nueva sala de control; recopilacion de datos para el estudio de la automatizacion; investigar y hacer el contacto con las empresas acerca de los posibles sistemas de automatizacion a implementar; solicitar cotizacion por los equipos preseleccionados, seleccionar la empresa con la mejor propuesta de sistema; disenar un esquema para el flujo de materiales; reportar el costo total del proyecto. Al final del proyecto concluimos que la propuesta servira para la optimizacion del proceso de fabricacion en general, gracias a las modificaciones y actualizaciones anteriormente nombradas.

Each May; red knots (Calidris canutus rufa) congregate in Delaware Bay during their northward migration to feed on horseshoe crab eggs (Limulus polyphemus) and refuel for breeding in the Arctic. During tire 1990s, the Delaware Bay harvest of horseshoe crabs for bait increased 10 fold, leading to a more than 90% decline in the availability of their eggs for knots. The proportion of knots achieving weights of more than 180 grains by 26-28 May, their main departure period, dropped from 0.6-0.8 to 0.14-0.4 over 1997-2007. During tire same period, the red knot population stopping in Delaware Bay declined by more than 75%, in part because the annual survival rate of adult knots wintering in Tierra del Fuego declined. Despite restrictions, the 2007 horseshoe crab harvest was still greater than the 1990 harvest, and no recovery of knots was detectable. We propose an adaptive management strategy with recovery goals and annual monitoring that, if adopted, will both allot,, red knot and horseshoe crab populations to rccover and permit a sustainable harvest of horseshoe crabs.

New information indicates that the rufa subspecies of the Red Knot comprises three biogeographically distinct populations wintering in Tierra del Fuego, Maranhão and Florida, respectively, and that the roselaari subspecies is largely or wholly confined to the Pacific coast of the Americas on passage and in winter.

Evidence indicates that a link between peptic ulcer disease (PUD) and selected psychosomatic factors may exist. A series of 70 consecutive male and female adult patients were categorized by peptic symptoms and divided into four groups: a) controls; b) gastric ulcer (GU); c) duodenal ulcer (DU); and d) chronic non-ulcer dyspepsia (CNUD). All patients were interviewed and asked to answer a questionnaire that included demographics, medical history and the incidence of negative life events. A decreased level of activity was a predominant finding in GU, DU and CNUD patients. Family history of PUD may be correlated with CNUD. Of interest was the finding that DU and CNUD patients presented a higher incidence of negative life events when compared to the other study groups. Negative life events that produce considerable stress may predispose to peptic symptoms in certain patients.

The aim of this study was to develop a model of inflammatory bowel disease (IBD) induced by colonic application of 2,4-dinitrofluorobenzene in previously sensitized BALB-c mice. During the follow-up period of 30 days we observed ulcerations, haemorrhage, necrosis, and mononuclear infiltration in the colonic mucosa of previously sensitized (experimental) and, to a lesser extent, nonsensitized (control) animals. In addition, the animals in the experimental group developed adhesions, thickening of colonic segments, stenosis, and dilatation of the colon, and some animals also developed megacolon. Oedema, mononuclear infiltration, and superficial ulcerations were observed in the ileum of experimental animals and, to a lesser extent, in the control group. In addition, the animals in the experimental group developed extraintestinal changes in the liver and spleen (that is, pericholangitis and lymphofollicular proliferation). We suggest that this model of IBD may have some value for the study of early pathogenetic mechanisms of IBD and for developing new therapeutic modalities for this condition.

The present study investigated both the healing rate (after four weeks) and the relapse rate (during six months) following treatment with the dopamine-like drugs bromocriptine (2.5 mg twice daily), amantadine (100 mg nocte), or with the H-2 blockers cimetidine (800 mg nocte), and famotidine (40 mg nocte) in 124 patients with endoscopically proven duodenal ulcer (DU). The ulcer was completely healed in 27 (amantadine), 26 (bromocriptine), 23 (cimetidine), and in 24 (famotidine) patients. Relapse was noted in 34.7% (cimetidine) and 25% (famotidine) versus 11.7% (amantadine) and 7.7% (bromocriptine) DU patients. No significant difference was found in initial healing rates. However, the relapse rate in the cimetidine-treated group was significantly higher than in all the other test groups. Additional comparisons between all the treatments categories showed a significant lower relapse rate with the dopamine-like agents. These important new results indicate that dopamine-like compounds are equally effective as H-2 blockers in inducing DU healing and may offer a promising advantage over H-2 blockers concerning their efficacy in preventing ulcer relapse in DU patients.

We have reviewed the neurobiology of stress ulcers from animal models to potential pharmacotherapeutic mechanisms. The evidence strongly supports the hypothesis that certain stress-related gastric lesions are 'braindriven' events which may be more effectively managed through central manipulations than by altering local, gastric factors. Recent advances in the use of anxiolytic and antidepressant drugs in the management of stress-related gastric mucosal injury further supports the contention that a brain-gut axis, which may have nervous, peptidergic and classic monoaminergic components, modulates the intricate and complicated pattern of communication between the brain and the stomach. Delineation of the precise pathways which make up this communication as well as their manipulation by various pharmacological agents will be the focus of future research endeavour.

The present study investigated both the healing rate (after four weeks) and the relapse rate (during six months) following treatment with the dopamine-like drugs bromocriptine (2.5 mg twice daily), amantadine (100 mg nocte), or with the H2 blockers cimetidine (800 mg nocte), and famotidine (40 mg nocte) in 124 patients with endoscopically proven duodenal ulcer (DU). The ulcer was completely healed in 27 (amantadine), 26 (bromocriptine), 23 (cimetidine), and in 24 (famotidine) patients. Relapse was noted in 34.7% (cimetidine) and 25% (famotidine) versus 11.7% (amantadine) and 7.7% (bromocriptine) DU patients. No significant difference was found in initial healing rates. However, the relapse rate in the cimetidine-treated group was significantly higher than in all the other test groups. Additional comparisons between all the treatment categories showed a significantly lower relapse rate with the dopamine-like agents. These important new results indicate that dopamine-like compounds are equally effective as H2 blockers in inducing DU healing and may offer a promising advantage over H2 blockers concerning their efficacy in preventing ulcer relapse in DU patients.

Specific polyclonal antibodies raised against synthetic thyrotropin-releasing hormone (TRH) infused intracerebroventricularly (ICV) significantly decreased gastric lesions induced by cold restraint stress. The antiulcer effect of immunologic blockade of brain TRH was specific. Normal rabbit serum or antibodies raised against somatostatin, α-MSH, Leu-enkephalin, gonadotropin-releasing hormone and atrial natriuretic factor were ineffective. These findings suggest that brain TRH may play an important role in experimental stress ulcer formation.

Increasing evidence indicates that thyrotropin-releasing hormone (TRH), and endogenous brain-gut peptide may play a role in experimental ulcerogenesis. Potential interactions between TRH and imipramine (a typical tricyclic antidepressant (TCA] on the development of TRH-induced gastric lesions have not been investigated. Imipramine (0.05, 0.5 and 5 mg/kg, i.p.) dose-dependently inhibited gastric lesion formation induced by intracisternal (i.c.) administration of TRH (1 micrograms). In addition, imipramine (5 mg/kg, i.p.) significantly decreased gastric acid secretion in response to i.c. TRH (1 microgram) in rats with pyloric ligation. These findings suggest the TCAs may be effective drug agents against centrally initiated gastric ulcerations. The mechanism of this response probably involves blockade of cholinergic (muscarinic) and H2 histamine receptors.

In previous work we have determined that intracameral (IC) administration of neurotensin (NT) produces strong miosis in rabbits. However, the pharmacological mechanism of this response remains undetermined. Blockade of alpha and beta-adrenoceptor subtypes with phenoxybenzamine and propranolol, blockade of M1 muscarinic receptors with atropine or blockade of mu opioid receptors with naloxone did not affect NT-induced miosis. Of interest however was the observation that destruction of ocular dopamine (DA) nerve endings with 6-hydroxydopamine (6-OHDA) + desmethylimipramine (DMI), or blockade of D-2 DA receptors with haloperidol significantly inhibited the miotic response to IC NT. These findings indicate that an intact iridic DA pathway is required for the expression of NT-induced miosis.

This study evaluated the effect of ACTH and several ACTH fragments on the development of gastric glandular lesions induced by cold-restraint stress in rats. Intracerebroventricular administration of ACTH1–39 dose-dependently (0.1–10 μg) inhibited stress gastric lesion formation. Studies with smaller molecular weight forms of ACTH (in a dose equimolar to 10 μg of ACTH1–39) revealed that ACTH1–13 and ACTH1–10 were also protective. The ACTH fragments ACTH5–10, ACTH34–39 and ACTH1–17 were without effect. Immunoneutralization of endogenous brain ACTH1–39 significantly increased stress gastric lesion severity. Antisera raised against synthetic somatostatin, gonadotropin-releasing hormone, and L-enkephalin were ineffective. These results with ACTH coupled with our previous demonstration of a protective effect of β-endorphin suggest that specific brain pro-opiomelanocortin gene products modulate gastric mucosal integrity in response to stress. Brain ACTH ACTH fragments Stress ulcers ACTH antiserum Male rats

Annals of the New York Academy of SciencesVolume 597, Issue 1 p. 28-35 The Role of Brain Peptides in the Pathogenesis of Experimental Stress Gastric Ulcersa DANIEL E. HERNANDEZ, Corresponding Author DANIEL E. HERNANDEZ Brain-Gut Research Laboratory Division of Gastrointestinal and Liver Diseases Department of Medicine University of Southern California School of Medicine Los Angeles, California 90033bAddress for correspondence: Dr. Daniel E. Hernandez, Department of Medicine, Division of Gastroenterology, University of Southern California, 2025 Zonal Avenue, Los Angeles, California 90033.Search for more papers by this author DANIEL E. HERNANDEZ, Corresponding Author DANIEL E. HERNANDEZ Brain-Gut Research Laboratory Division of Gastrointestinal and Liver Diseases Department of Medicine University of Southern California School of Medicine Los Angeles, California 90033bAddress for correspondence: Dr. Daniel E. Hernandez, Department of Medicine, Division of Gastroenterology, University of Southern California, 2025 Zonal Avenue, Los Angeles, California 90033.Search for more papers by this author First published: July 1990 https://doi.org/10.1111/j.1749-6632.1990.tb16155.xCitations: 12 a This work was supported in part by National Institutes of Health Grants EY-05830 and RR 5356–27. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume597, Issue1Neurobiology of Stress UlcersJuly 1990Pages 28-35 RelatedInformation

Annals of the New York Academy of SciencesVolume 597, Issue 1 p. 239-247 The Role of the Hypothalamic-Pituitary-Thyroid Axis in Stress Gastric Ulcers GEORGE A. MASON, GEORGE A. MASON Department of Psychiatry and Biological Sciences Research Center University of North Carolina Chapel Hill, North Carolina 27599Search for more papers by this authorDANIEL E. HERNANDEZ, DANIEL E. HERNANDEZ Brain-Gut Research Laboratory Division of Gastrointestinal and Liver Diseases Department of Medicine University of Southern California School of Medicine Los Angeles, California 9003Search for more papers by this author GEORGE A. MASON, GEORGE A. MASON Department of Psychiatry and Biological Sciences Research Center University of North Carolina Chapel Hill, North Carolina 27599Search for more papers by this authorDANIEL E. HERNANDEZ, DANIEL E. HERNANDEZ Brain-Gut Research Laboratory Division of Gastrointestinal and Liver Diseases Department of Medicine University of Southern California School of Medicine Los Angeles, California 9003Search for more papers by this author First published: July 1990 https://doi.org/10.1111/j.1749-6632.1990.tb16172.xCitations: 4AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume597, Issue1Neurobiology of Stress UlcersJuly 1990Pages 239-247 RelatedInformation

Clinical and laboratory evidence indicates that the brain exerts major control on the gastrointestinal tract. Specific brain loci and circuits that send efferent viscerotropic projections to the gut have been described. A variety of aminergic and peptidergic neurotransmitters have been shown to occur along these cerebrogastrointestinal pathways and to influence motor and secretory functions of the gut. Some of the newly identified peptides have been shown to influence the development of gastroduodenal ulcers. Findings with thyrotropin-releasing hormone (TRH) indicate that this endogenous tripeptide induces a full spectrum of gut effects, prominent among which is production of gastric ulcers. By contrast, other peptides including β-endorphin, neurotensin, and bombesin induce gut effects opposite to those of TRH, namely, inhibition of gastric acid and motility and prevention of experimental ulcers. These laboratory findings suggest that ulcer disease may represent a brain-driven event, which may be the result of a neurochemical imbalance within the brain. Further neurobiological research will generate additional data on brain-gut interactions and will probably disclose new information to explain certain functional and organic disorders of the gut.

High-affinity and saturable membrane-bound dopamine binding sites have been characterized in rat and human gastrointestinal tissues. Although their role in experimental ulcerogenesis has been suggested, dopamine receptor activity in peptic ulcer disease has not been investigated. Radioligand binding studies were performed with mucosal tissue homogenates obtained from the antrum and duodenum of six male healthy volunteers and six male duodenal ulcer patients. The binding assay was performed in triplicate with a crude membrane fraction using [3H] dopamine as a ligand at a final concentration of 1 nM at 22 °C in the dark. Nonspecific binding (which usually comprised about 30% of total binding) was determined in the presence of a 100-fold excess of unlabeled dopamine. A significant (P<0.05) increase of [3H]dopamine binding was found in duodenal mucosa of duodenal ulcer patients. [3H]Dopamine binding in stomach (antrum) of normal and duodenal ulcer patients did not differ significantly. These findings provide preliminary evidence for a role of dopamine receptors in duodenal ulcer and suggest that biochemical abnormalities of gut dopamine function may be operative in the pathogenesis of peptic ulcer disease.