Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030305 (pancreatitis)
 16,014 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute edematous pancreatitis was produced in rats by subcutaneous administration of caerulein. Pancreas weight, pancreas histology and plasma amylase were used as endpoints to quantitate the severity of the syndrome. A caerulein dose of 10 micrograms/kg.hour produced the most severe pancreatitis, whereas at 5 micrograms/kg.hour the values were half-maximal. The pancreatic lesions were characterized by edema, formation of cytoplasmic vacuoles, leukocytic infiltration, necrosis, and with time (12-hour caerulein infusion) dilated acini. Cholecystokinin octapeptide also produced pancreatitis when given at ten times the dose required for caerulein (50 micrograms/kg.hour instead of 5 micrograms/kg.hour). Carbachol did not induce pancreatitis. Two prostaglandins, 16,16-dimethyl prostaglandin E2 injected subcutaneously and prostaglandin E2 infused subcutaneously, dose dependently prevented caerulein-induced pancreatitis (pancreatic edema, leukocytic infiltration, and necrosis) and reduced the number and size of intracellular vacuoles. The ED50 were 15 to 25 micrograms/kg for 16,16-dimethyl prostaglandin E2 and 90 micrograms/kg.hour for prostaglandin E2. Neither prostaglandin, given at doses inhibiting the development of pancreatitis, prevented the retardation of gastric emptying caused by caerulein, a finding suggesting that the prostaglandins may act specifically on the effect of caerulein on the pancreas but not on caerulein receptors in gastric smooth muscle. Indomethacin, an inhibitor of prostaglandin synthesis, and methscopolamine bromide, an anticholinergic agent, had no effect on caerulein-induced pancreatitis. We concluded that prostaglandins of the E type prevent the development of caerulein-induced pancreatitis. The mechanism by which prostaglandins protect the pancreas may involve stabilization of lysosomes within the acinar cells and inhibition of intracellular activation of pancreatic digestive enzymes.
 ...
PMID:Prevention by prostaglandins of caerulein-induced pancreatitis in rats. 246 59

We reported a case of motor neuropathy with pyramidal sign following prolonged administration of a high dose of muscle relaxant, pancuronium bromide (Myoblock). A 40-year-old male was admitted to our hospital with acute episode of pancreatitis. He was treated with artificial ventilation and Myoblock to manage delirious state, disseminated intravascular coagulation and multiple organ failure. Total dose of 823 mg (24 mg/day) of Myoblock was given intravenously over 36 days. After Myoblock was discontinued, he regained his consciousness and marked muscle weakness with atrophy was noted in both limbs, more severe in distal lower limbs, without any noticeable sensory and sphincter disturbances. Motor nerve conduction studies showed normal nerve conduction velocities with markedly decreased amplitude of compound muscle action potentials. Repetitive nerve stimulation studies revealed decrement response after tetanic stimulation, which disappeared later. Needle EMG showed active denervation potentials and marked polyphasic motor unit potentials. Muscle biopsy revealed neurogenic muscle atrophy with fragmented acetylcholine esterase-positive postsynaptic sites. Sural nerve biopsy showed slight to moderate degree of axonal degeneration of myelinated fibers. Clinical, electrophysiological, and pathological studies above indicated that the main affected sites were neuromuscular junctions including the terminal twigs of motor neurones and postsynaptic membrane, and pyramidal tracts, predominant in lower limbs. About one month after the recognition of the muscle weakness, his muscle strength improved gradually, however, spasticity with hyperreflexia and pathologic reflexes of both legs were found, and became more prominent thereafter. Intensive physiotherapy and rehabilitation led improvement to the point that he became able to ambulate with walking-aids about 7 months later, but marked spasticity persisted.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[A case of motor neuropathy with pyramidal sign due to prolonged administration of high dose of pancuronium bromide (Myoblock)]. 840 81

Necrotizing panniculitis due to potassium-bromide is a drug induced allergic reaction following stimulation of lymphocytes as demonstrated for the first time by a lymphocyte transformation test (LTT). We named the disease "halogen panniculitis" because of similar generally known reactions to iodides and describe the typical symptoms in three own cases. Bromoderma tuberosum tends to be a similar kind of allergy. For the first time pancreatitis to potassium bromide in men has been observed, which has already been described in epileptic dogs treated with potassium bromide.
 ...
PMID:[Halogen-induced panniculitis caused by potassium bromide]. 841 44

1. Cypridina luciferin analogues, 2-methyl-6-(p-methoxyphenyl)-3,7- dihydroimidazo[1,2-a]pyrazin-3-one (MCLD) and 2-methyl-6-phenyl-3,7-dihydroimidazo[1,2-a]pyrazin-3-one(CLA ), react with O2- or 1O2 to emit light in visible region. Such chemiluminescences were used for the detection of O2- or 1O2 in activated leukocyte systems and myeloperoxidase (granulocyte-extract) + Br- + H2O2 systems in vitro. 2. The mechanisms of MCLA (CLA)-dependent luminescence is described in detail. Superoxide generated from sinusoidal cells in acute ethanol intoxication of rats was detected by MCLA-dependent luminescence from the surface of perfused rat liver (organ luminescence). 3. Furthermore, with alive animals, O2- generated in the lung of rats with necrotized pancreatitis and that in the stomach of rats after ischemia/reperfusion were detected by their organ luminescences.
 ...
PMID:Detection of active oxygen species in biological systems. 987 66

In a retrospective study, at least 10% of dogs receiving potassium bromide/phenobarbital combination therapy, compared with 0.3% of dogs receiving phenobarbital monotherapy, had probable pancreatitis. Pancreatitis may be a more frequent and more serious adverse effect of potassium bromide/phenobarbital combination therapy than has been reported previously.
 ...
PMID:Pancreatitis associated with potassium bromide/phenobarbital combination therapy in epileptic dogs. 1090 78

The acinar cell culture plays a very important role in research of pancreatic pathophysiology. The aim of this study was to establish a long-term culture of human (foetal) pancreatic acinar cells in standardized nutrient media with supplements. Acinar cells were prepared from pancreatic tissues obtained from aborted foetus (> or =35 weeks) with no prior pancreatic complications by collagenase digestion and cultured using different media and supplements. The purity and phenotype of acinar cells was confirmed by various staining techniques and FACS. The acinar cell proliferation was determined at different time intervals by Bromo-deoxyuridine (BrdU) incorporation, and metabolic enzyme activity was analysed. The acini could be cultured and maintained in Ham's F-12 K/M199 media in the presence of 5% BSA, 0.1 mg/ml STI, 10 ng/ml EGF, and 10% FCS with the same morphological appearance as that of freshly prepared for 12 days with maximum viability of 80-85% and formation of monolayer without extracellular matrix. A significant BrdU incorporation of acinar cells in primary culture was observed which was maximum (105%) at day four. Higher amylase and lipase activity was seen in freshly isolated acinar cells which decreased with time of the culture. The established human pancreatic acinar cell culture may act as an excellent model to study exocrine dysfunction or pancreatitis in response to acinar cell injury.
 ...
PMID:Primary culture of pancreatic (human) acinar cells. 1824 27

Potassium bromide, phenobarbital, or a combination of both is commonly used in the treatment of canine epilepsy. Several cases of clinical pancreatitis have been reported in dogs after treatment with potassium bromide, but the risk of elevated serum canine pancreatic lipase immunoreactivity concentrations in dogs treated with potassium bromide and/or phenobarbital has not previously been evaluated in a large group of dogs. This study suggests an increased risk for elevated serum canine pancreatic lipase immunoreactivity concentrations and possibly pancreatitis in dogs treated with potassium bromide or phenobarbital alone or in combination.
 ...
PMID:Serum pancreatic lipase immunoreactivity concentrations in dogs treated with potassium bromide and/or phenobarbital. 1841 45

High-throughput studies to determine differential immune (humoral) response to diseases are becoming of increasing interest because the information they provide can help in early diagnosis as well as monitoring of therapeutics. Protein microarrays are a high-throughput and convenient technology that can be applied to the study of the humoral response. Proteins can be arrayed on slides and then probed with serum from different classes of patients to observe differences that may exist among autoantibodies that reflect differences in disease states. However, such studies may be difficult to interpret due to the weak overall signal response of such protein microarrays. We propose that this weak signal response is due to the physical positioning of the disease proteins that renders them sterically hindered from binding partners in the serum. In this study, we hypothesize that reducing the complexity and size of the disease proteins by chemical digestion using cyanogen bromide (CNBr) may enhance the overall signal from the humoral response and facilitate visualization of disease-specific responses in various classes of serum. A modified protein microarray methodology using CNBr digestion is presented here. The new workflow was applied to a set of 10 serum samples from healthy subjects, 10 from patients with chronic pancreatitis and 10 from patients diagnosed with pancreatic cancer and the results were compared to results obtained in the absence of CNBr digestion. CNBr digestion allowed the identification of 10 additional autoantibodies that responded to serum, 5 of which were unique to pancreatitis and cancer sera. This new methodology may increase the sensitivity of microarray studies measuring autoantibodies in serum.
 ...
PMID:Enhanced detection of autoantibodies on protein microarrays using a modified protein digestion technique. 1845 26

Sphincter of Oddi manometry (SOM) is the gold standard for assessing sphincter of Oddi dysfunction (SOD), but is considered a diagnostic sensitivity of 30-80% and associated with significant complications of pancreatitis. Electromyography (EMG) of sphincter of Oddi (SO) using a circular electrode (CE) may be useful in improving diagnostic accuracy and reducing complications. To evaluate the feasibility and reliability of the CE, we record myoelectric activity of SO in rabbits using the CE to compare with the traditional needle electrode (NE). The CE was prepared using a double-channel biogel catheter with two silver rings at the head of the catheter. The CE was then inserted into the lumen of the SO through the duodenal papilla, and myoelectric activity was recorded in the SO in 30 rabbits. An EMG recorded using an NE was performed at the same time, when the SO was in basal state, after injection of cholecystokinin and N-butylscopolamine bromide. Electromyographs recorded by the two methods were then evaluated. Satisfactory SO EMGs were acquired using the CE without any injury. Simultaneous recording revealed a very similar traces and one-to-one correspondence of SO spike bursts (SOSB). Linear regression analysis showed a significant direct correlation between the two methods for SOSB duration and amplitude. The results suggested that CE was comparable with NE in terms of recording efficacy. The CE also has advantages of easy fixation, accurate localisation, broad applicability and ease of achieving satisfactory outcomes without trauma, compared with the NE.
 ...
PMID:The feasibility and reliability of using circular electrode for sphincter of Oddi electromyography in anaesthetised rabbits. 1921 Jun 27

The field of Emergency Care Medicine is a very dynamic part of the Medical Science. That is why there is a huge amount of publications on this topic every year. This article is my personal selection of recently published scientific work on pulmonary embolism, classification of circulatory shock, betablockers in acute decompensated heart failure, advanced cardiac life support, subarachnoid hemorrhage, inhalation therapy with ipratropium-bromide, community acquired pneumonia, diverticulosis, gout and pancreatitis. Last but not least there is a choice of prophylactic interventions, you might not yet be aware of. Some of the discussed publications may help you manage the next patient you'll encounter, when you're on call next time.
 ...
PMID:[News in emergency medicine 2009]. 1984 80


1 2 Next >>