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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of dietary pectin on apparent ileal and fecal digestibilities of protein and amino acids and on pancreatic secretions was studied in two experiments with growing pigs (initial weight 70 kg). Four barrows were fitted with simple T-cannulas for collection of ileal digesta; another four barrows were fitted with permanent re-entrant cannulas for collection, sampling and subsequent return of pancreatic juice. Dietary pectin included at a level of 7.5 g/100 g in a cornstarch-based diet significantly depressed apparent ileal and fecal protein and amino acid digestibilities. This depression in the small intestine could be attributed to both an increase in endogenous protein secretions and a decrease in the efficiency of digestion. In the large intestine, pectin was used by intestinal microbes as the principal energy source to catabolize nitrogenous compounds and to stimulate bacterial nitrogen assimilation, thus altering the amino acid profile of protein voided in feces. The inclusion of pectin did not affect the flow of pancreatic juice or the total secretion of protein, lipase, trypsin and chymotrypsin. However, there was a significantly lower secretion of alpha-amylase, which was a direct result of the replacement of starch by pectin. The results demonstrate that pectin may have a detrimental effect on the processes of protein digestion and absorption but does not affect the secretion of pancreatic proteolytic enzymes in pigs.
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PMID:Dietary pectin's effect on ileal and fecal amino acid digestibility and exocrine pancreatic secretions in growing pigs. 791 17

Proteolytic enzymes, lipase, kinins, and other active peptides liberated from the inflamed pancreas convert inflammation of the pancreas, a single-organ disease of the retroperitoneum, to a multisystem disease. Adult respiratory distress syndrome, in addition to being secondary to microvascular thrombosis, may be the result of active phospholipase A (lecithinase), which digests lecithin, a major component of surfactant. Myocardial depression and shock are suspected to be secondary to vasoactive peptides and a myocardial depressant factor. Coagulation abnormalities may range from scattered intravascular thrombosis to severe disseminated intravascular coagulation. Acute renal failure has been explained on the basis of hypovolemia and hypotension. The renin-angiotensin alterations in acute pancreatitis (AP) as mediators of renal failure need to be studied. Metabolic complications include hypocalcemia, hyperlipemia, hyperglycemia, hypoglycemia, and diabetic ketoacidosis, of which hypocalcemia has been long recognized as an indicator of poor prognosis. The pathogenesis of hypocalcemia is multifactorial and includes calcium-soap formation, hormonal imbalances (e.g., parathyroid hormone, calcitonin, glucagon), binding of calcium by free fatty acid-albumin complexes, and intracellular translocation of calcium. Subcutaneous fat necrosis, arthritis, and Purtscher's retinopathy are rare. The various prognostic criteria of AP and other associated laboratory abnormalities are manifestations of systemic effects. Early recognition and appropriated management of these complications have resulted in improved prognosis of severe AP.
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PMID:Acute pancreatitis: a multisystem disease. 804 85

A feeding experiment was carried out over 42 d with four groups of broiler chickens fed experimental diets formulated to provide no supplementation, 20 mg zinc bacitracin, 60 mg salinomycin, or both feed additives in combination. During the fifth week of the experiment, four chickens from each pen were killed, and the contents of gizzard, duodenum, jejunum, ileum, ceca, and rectum were separately collected and pooled. In all intestinal segments, the pH and the concentration of lactic acid were measured, and the numbers of anaerobic bacteria, coliforms, lactic acid bacteria, lactobacilli, enterococci, and Clostridium perfringens were counted. In homogenates of pancreas obtained from four animals, the activities of amylase, lipase, trypsin, and chymotrypsin were measured. A significant growth-promoting effect was observed in the group receiving zinc bacitracin in combination with salinomycin. Zinc bacitracin significantly reduced the number of coliform bacteria in the ileum and increased the activities of amylase and lipase in pancreas homogenates. Supplementation with salinomycin and zinc bacitracin, alone or in combination, resulted in significantly lower counts of C. perfringens as well as Lactobacillus salivarius, which was a dominant lactic acid bacterium found in broiler intestinal contents. High numbers of these lactobacilli may play a role in broiler growth depression related to competition in nutrient uptake or impaired fat absorption due to bile acid deconjugation.
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PMID:Effect of zinc bacitracin and salinomycin on intestinal microflora and performance of broilers. 1102 77

The present tests, in male Wistar rats, center around the trophic and functional changes of the pancreatic gland (R G), both exocrine and endocrine, induced by different types of autonomic nervous interruptions. First Group of Tests: Following one year celiac ganglionectomy (CG), nonpancreatectomized (Non-Pt) rats showed, basally, in blood, a drop of glucose (G), without changes of insulin (I). At autopsy, the CG animals showed an increase of the pancreatic we weight, of the total protein, of the RNA but not DNA. In the Pt. 95% rats, superimposing CG triggered, on the one hand, a drop to control values of the raised G blood levels, and on the other, a rise of I Besides, in feces, a rising of chymotrypsin concentration. At autopsy, in the PG, an increase of total protein and of RNA. Second Group of Tests: CG, after 6 months, induced, in blood, both basally and a 2 h glucose tolerance test, significant opposite enzyme activities changes in respect to C. Indeed, as amylase (A) was increased, that of lipase (L) was depressed. When alcohol feeding (AF) was superimposed to CG rats, a reversal of the L values was observed. The latter reached levels significantly higher those of the C. In in-vitro tests, the isolated islets of CG disclosed to release more I to the bath medium than those of the C animals. Third Group of Tests: Analyzing, in conscious animal, the L excretory changes in the basal bile pancreatic secretion (BB-PS) induced by chronic (2 months interruption of the autonomic nervous innervation of the PG, it was found that CG, truncal vagotomy (V), the association of CG + V, peri-Vaterian duodenotomy (PV-D), but not bilateral splachicectomy (Spl), inhibit, significantly the L output. It was also shown that superimosing AF to the V or CG + V animals reverted to C values the I depressed levels. In acute interruptions (24 h) of the autonomic nervous innervation of the PG: CG, V, P. V-D, the depression in the BBPS is highly significant, more than 40%. From these three sets of experiments it is concluded that: Firstly, CG increases the regenerative and functional capacity of both the exocrine pancreas. This is distinctively evident when the secretory mass is reduced like in the Pt. 95% series of animals. CG probably exerts its effects suppressing the releasing of some negative reins: adrenergic, pepdidergic (galanin). Secondly, CG evokes modifications of the normal Islet-pancreon inter-relationships. The rising of A and the drop of L in blood elicited by this type of autonomic nervous interruption probably reflects an increased release of I by the Langerhans islet. Thirdly, CG, the same as V. CG + V and P.V-D, but not Spl, depress the intrapancreatic cholinergic tone. This might by at the basis of the depression of L excretion in the BB-PS. The reversion to C Through the coupling of chronic alcohol intoxication to the autonomic decentralized PG would be a reflection of an increased sensitivity to ethanol of the intrapancreatic ganglionic neurons. The augmented acetylcholine release at the nerve terminal would lead to a high intrapancreatic cholinergic tone that, in the end, might be at the basis of the reversal changes induced in the autonomic decentralized PG by the chronic ethanol intoxication.
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PMID:[Autonomic nervous system and pancreas. (Analysis of the influence of different types of autonomic denervation in glandular regeneration phenomena and the interactions of the exocrine-endocrine-Axis)]. 1108 17

A 13-year-old, male cocker spaniel presented with a history of inappetence, depression and reluctance to stand. The dog had multiple, ulcerated skin lesions which were diagnosed as panniculitis by histopathology. A diagnosis of pancreatitis was made on the basis of markedly elevated serum lipase concentrations, abdominal ultrasonography which showed an abnormal lobulated area of hypoechoic tissue in the body and right lobe of the pancreas, and a fine needle biopsy from this area which revealed large numbers of degenerate neutrophils. After treatment with antibiotics and prednisolone, the dog made a full clinical recovery and was free of clinical signs for four months. The dog was euthanased five months later and postmortem examination revealed chronic, active pancreatitis and a pancreatic adenoma. This is the first report of antemortem diagnosis of pancreatitis and panniculitis in a dog.
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PMID:Panniculitis associated with pancreatitis in a cocker spaniel. 1257 Mar 49

Actions of endocannabinoids in the cerebellum can be demonstrated following distinct stimulation protocols in Purkinje cells. First, depolarization-induced elevations of intracellular Ca2+ lead to the suppression of neurotransmitter release from both inhibitory and excitatory afferents. In another case, postsynaptic group I metabotropic glutamate receptors (mGluRs) trigger a strong inhibition of the glutamatergic inputs from parallel and climbing fibers. Both pathways involve endocannabinoids retrogradely acting on type 1 cannabinoid receptors (CB1Rs) at presynaptic terminals. Here, we show that group I mGluR activation also depresses GABAergic transmission at the synapses between molecular layer interneurons and Purkinje cells. Using paired recordings, we found that application of the group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine reduced the evoked IPSCs in Purkinje cells. This effect was independent of postsynaptic Ca2+ increases and was completely blocked by a CB1R antagonist. Experiments performed with the GTP-analogues GDP-betaS and GTP-gammaS provided evidence that endocannabinoids released after G-protein activation can also inhibit GABAergic inputs onto nearby, unstimulated Purkinje cells. Block of the enzymes DAG lipase or phospholipase C reduced the group I mGluR-dependent inhibition, suggesting that 2-arachidonyl glycerol could act as retrograde messenger. Finally, group I mGluR activation by brief bursts of activity of the parallel fibers induced a short-lived depression of spontaneous IPSCs via presynaptic CB1Rs. Our results reveal a mechanism with potential physiological importance, by which glutamatergic synapses induce an endocannabinoid-mediated inhibition of the GABAergic inputs onto Purkinje cells.
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PMID:Group I metabotropic glutamate receptors inhibit GABA release at interneuron-Purkinje cell synapses through endocannabinoid production. 1515 47

The wake-promoting neuropeptides orexins (hypocretins) play a crucial role in controlling neuronal excitability and synaptic transmission in the CNS. In this study, using whole-cell patch-clamp recordings in an acute dorsal raphe nucleus (DRN) slice preparation, we report that orexin B (Orx-B) depresses the evoked glutamate-mediated synaptic currents in DRN 5-HT neurons. The Orx-B-induced depression is accompanied by an increase in the paired-pulse ratio and the coefficient of variance, suggesting a presynaptic site of action. Orx-B also reduces the frequency but not the amplitude of miniature EPSCs, indicating that depression of glutamatergic transmission is mediated by a decrease in glutamate release. Surprisingly, the Orx-B-induced inhibition of glutamatergic transmission is abolished by postsynaptic inhibition of G-protein signaling with GDPbetaS, suggesting that this effect is signaled by postsynaptic orexin receptors and expressed presynaptically, presumably through a retrograde messenger. Interestingly, the Orx-B-induced depression of glutamate release is mimicked and occluded by the cannabinoid receptor agonist WIN 55,212-2, and is abolished by the CB1 cannabinoid receptor antagonist AM 251. These results imply that the Orx-B-induced depression of glutamatergic transmission to DRN 5-HT neurons is mediated by retrograde endocannabinoid release. Examination of downstream signaling pathways involved in this response indicates that the effect of Orx-B requires the activation of phospholipase C and DAG lipase enzymatic pathways but not a rise in postsynaptic intracellular calcium. Therefore, our findings reveal a previously unsuspected mechanism by which postsynaptic orexin receptors can modulate glutamatergic synaptic transmission to DRN 5-HT neurons.
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PMID:The wake-promoting peptide orexin-B inhibits glutamatergic transmission to dorsal raphe nucleus serotonin neurons through retrograde endocannabinoid signaling. 1567 70

Anuran tadpoles (Rana pirica) are induced to develop a higher tail and a bulgy body as predator-specific morphological responses when they are exposed to predatory larval salamanders. Subtractive hybridization was performed using induced tadpole body skin and normal tadpoles' body skin. A total of 196 clones showed higher expression, and 104 clones showed lower expression, when they formed bulgy bodies. In the subtraction, carboxypeptidase B, trypsinogen, elastase I, fibrinogen, elastase II, triacyl-glycerol lipase, and alpha1-antitrypsin genes showed lower expression. In contrast, RT-like protein, bullous pemphigoid antigen, phosphoserine aminotransferase, uromodulin, tetranectin, chaperonin-like protein, zinc finger protein, osteonectin, aldehyde dehydrogenase, Sec 23A protein, and ribosomal protein showed higher gene expression. Microarray analysis was also performed using this subtracted cDNA (nine replicates). Results of the microarray data essentially corresponded with those of the subtraction data, and the degree of the suppressed genes was much stronger than that of the expressed genes. Carboxypeptidase B showed the strongest suppression, and its inhibition range was from 1/100 to 3/100 compared with that of control body skin. Strong suppression was also observed with trypsinogen, elastase I, fibrinogen, and elastase II as well. These results can be interpreted as increases of fibrinolysis by strong depression of both carboxypeptidase B and other genes simultaneously, resulting in the retention of blood vessels and facilitating the circulation of blood. Expression was observed in phosphoserine aminotransferase, aldehyde dehydrogenase, RT-related protein, chaperonin-like protein, tetranectin, bullous pemphigoid antigen, uromodulin, and Sec 23A protein. They were significantly (p<0.05) increased and were at least 1.5 times greater compared with the control. From the appearance, it seems that the bulgy shaped body is highly connecting to the bullous pemphigoid (BP) antigen that causes the skin blistering disorder, and tetranectin and uromodulin may be related to the extracell matrix through myogenesis, protein secretion, and ion transport, respectively. Since the RT-related protein gene derived from retrotransposon (L1) is known to disrupt mammalian transcriptomes, retrotransposon may be involved with phenotypic plasticity for morphological defense by Rana prica against predator threat.
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PMID:Genetic basis of phenotypic plasticity for predator-induced morphological defenses in anuran tadpole, Rana pirica, using cDNA subtraction and microarray analysis. 1582 62

Endocannabinoids (eCBs) act as retrograde messengers at inhibitory synapses of the hippocampal CA1 region. Current models place eCB synthesis in the postsynaptic pyramidal cell and the site of eCB action at cannabinoid receptors located on presynaptic interneuron terminals. Four responses at the CA1-interneuron synapse are attributed to eCBs: depolarization-induced suppression of inhibition (DSI), G-protein-coupled receptor-mediated enhancement of DSI (DeltaDSI), persistent suppression of evoked inhibitory postsynaptic currents (eIPSCs), and finally, mGluR-dependent long-term depression (iLTD). It has been proposed that all are mediated by the eCB, 2-arachidonoyl glycerol, yet there is evidence that DSI does not arise from the same underlying biochemical processes as the other responses. In view of the increasing importance of eCB effects in the brain, it will be essential to understand the mechanisms by which eCB effects are produced. Our results reveal new differences in the biochemical pathways by which the eCB-dependent responses are initiated. Both U73122, a phospholipase C antagonist, and RHC-80267, a diacylglycerol (DAG) lipase antagonist, prevented eCB-dependent iLTD induction by 3,5-dihydroxyphenylglycine (DHPG). However, mAChR activation does not cause eCB-dependent iLTD. Neither enzyme inhibitor affects DSI, and persistent eCB-dependent eIPSC suppression induced by either mGluRs or mAChRs is unaffected by U73122. On the other hand, inhibition of DAG lipase prevents persistent eCB-dependent eIPSC suppression triggered by mAChRs. The results show that the biochemical pathways for the various eCB-dependent responses differ and might therefore be independently manipulated.
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PMID:Multiple mechanisms of endocannabinoid response initiation in hippocampus. 1620 81

Long-term changes in synaptic efficacy produced by high-frequency stimulation (HFS) of glutamatergic afferents to the rat dorsolateral striatum exhibit heterogeneity during early stages of postnatal development. Whereas HFS most often induces striatal long-term potentiation (LTP) in rats postnatal day 12 (P12)-P14, the same stimulation tends to induce long-term depression (LTD) at ages P16-P34. Previous studies have shown that striatal LTD induction depends on retrograde endocannabinoid signaling and activation of the CB1 cannabinoid receptor. It is also known that levels of one of the primary endogenous CB1 receptor agonists, anandamide (AEA), increases during development in whole-brain samples. In the present study, we sought to determine whether this developmental increase in AEA also takes place in striatal tissue and whether increased AEA levels contribute to the postnatal switch in the response to HFS. We observed a pronounced increase in striatal levels of AEA, but not the other major endogenous cannabinoid 2-arachidonoylglycerol (2-AG), during the postnatal period characterized by the switch from LTP to LTD. Furthermore, application of synthetic AEA during HFS in field recordings of slices from P12-P14 rats allowed for induction of LTD whereas blocking the CB1 receptor during HFS in animals P16-P34 resulted in expression of LTP. However, blocking 2-AG synthesis with the DAG-lipase inhibitor tetrahydrolipstatin did not alter HFS-induced striatal LTD. In addition, synaptic depression produced by a synthetic CB1 agonist was similar across development. Together, these findings suggest that the robust developmental increase in striatal AEA may be the key factor in the emergence of HFS-induced striatal LTD.
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PMID:Anandamide regulates postnatal development of long-term synaptic plasticity in the rat dorsolateral striatum. 1732 38


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