Fertility-sparing treatment of a primary retroperitoneal mucinous cystadenocarcinoma.
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Adult↗
Biomedical subjects
T M Chang
Publications and source records attributed to T M Chang.
Numerical investigation of non-Newtonian microcirculatory blood flow in hepatic lobule.
The circulation in the liver is unique at macroscopic and microscopic levels. At the macroscopic level, there is an unusual presence of portal and arterial inputs rather than a single arterial input. At the microscopic level, a series of microenvironments in the acinar system is essential in controlling the functional characteristics of hepatic parenchymal cells. Since the hemodynamics is much less studied in the multifunctional liver, an attempt is made to study the hepatic hemodynamics in a segment of a hepatic lobular structure, that is made up of high-pressure oxygenated arteriole, low-pressure nutrient-rich portal venule, fenestrated sinusoidal space and hepatic venule. Our goal is to dispel some of the myths of this complex vascular bed by means of finite volume blood flow simulation. Flow features like high-velocity gradients near the fenestrations, flow reversal and Dean vortices in the sinusoidal space are analyzed within the non-Newtonian framework. Since no distinct exact or numerical solutions are available for this complex vascular bed, the present simulated results are compared with the available clinical observations. Results revealed that the pressure plays a key role in hepatic blood flow.
Humans↗
Clinical analysis and literature review of massive duodenal diverticular bleeding.
A duodenal diverticulum (DD) appears in 2.5% of upper gastrointestinal (UGI) examinations and up to 22% of endoscopic retrograde cholangiopancreaticographies (ERCP) and autopsies. Most of these patients are asymptomatic, but the lesion is occasionally associated with bleeding, inflammation, perforation, obstruction of the duodenum or biliary-pancreatic duct (or both), fistula formation in the bile duct, and bezoar formation inside the diverticulum. A total of 816 patients have undergone ERCP examination at our institution since January 1987, and 100 (12.25%) of them have DD. Seven (7%) patients presented with bloody or tarry stools from massive UGI bleeding followed by shock. Only two could be diagnosed by UGI endoscopy preoperatively. The lesions were demonstrated in angiographic studies in another four cases. However, only one was correctly interpreted and one required reoperation after a correct repeat endoscopic finding. The lesions in the other two patients were identified by thorough exploration during laparotomy. The remaining case was diagnosed by intraoperative endoscopy via pyloroduodenotomy. Six underwent surgical intervention, and one was successfully treated by expectant treatment. Three (50%) had leakage from the duodenotomy but recovered uneventfully with conservative treatment. In conclusion, we believe that DD bleeding is more frequent than usually thought. A high index of suspicion should be raised in cases of UGI bleeding when more obvious and common causes have been excluded by routine endoscopy. Aggressive but careful endoscopic examination combined with accurate angiography can help us diagnose most of the cases preoperatively. Diverticulectomy is an effective surgical procedure, though it is associated with a considerable leakage rate. The morbidity is minimal if we can identify the lesion earlier and evacuate the lesion without delay.
Angiography↗
Long-term results of duodenectomy with highly selective vagotomy in the treatment of complicated duodenal ulcers.
BACKGROUND: Highly selective vagotomy and complete circular or partial duodenectomy have been applied to complicated duodenal ulcer for many years. These procedures seem to provide better clinical results than truncal vagotomy and antrectomy. METHODS: A retrospective analysis was conducted of 120 patients with complicated duodenal ulcer who underwent surgical treatment between 1986 and 1999. Patients with obstruction were treated with either circular complete (17) or partial duodenectomy (3) combined with highly selective vagotomy or truncal vagotomy and antrectomy (37). Those with perforation were treated primarily with highly selective vagotomy and partial duodenectomy, highly selective vagotomy alone, or truncal vagotomy and pyloroplasty. Every patient was followed up either by a clinic visit (75%) or questionnaire to determine the presence of ulcer pain, dumping, diarrhea, vomiting, weight loss, and Visick grade. RESULTS: Long-term follow-up of patients treated with duodenectomy and highly selective vagotomy for obstruction showed that 94% had sustained weight gain whereas more than half of those treated with truncal vagotomy and antrectomy had weight loss. In patients with perforation, duodenectomy and highly selective vagotomy offered no advantage over highly selective vagotomy alone. CONCLUSIONS: Highly selective vagotomy and complete circular or partial duodenectomy provide fewer sequelae and better weight gain long term than truncal vagotomy and antrectomy for patients with obstructing duodenal ulcers.
Adolescent↗
Bioencapsulated hepatocytes for experimental liver support.
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Animals↗
Neurohormonal control of exocrine pancreas.
The exocrine pancreas is regulated by various hormonal factors derived from the gut through hormone-hormonal and neurohormonal interactions. Physiologic stimuli entering the upper small intestine elicit the release of intestinal hormones and activate sensory reflex mechanisms from the intestinal mucosa to stimulate or inhibit exocrine pancreatic secretion. In addition, the endocrine pancreas, intrapancreatic nerves, and some extrapancreatic neural pathways, with or without mediation by the vagus nerve, are known to participate in regulation of exocrine pancreatic secretion. It has been established that two key intestinal hormones, secretin and cholecystokinin (CCK), in physiologic doses, act through the vagal afferent pathway and interact with each other as well as with other gut hormones. The releases of these two hormones are mediated through the corresponding releasing peptides. In the past few years, the roles of secretin- and CCK-releasing peptides have become more clearly defined. The participation of several neurotransmitters and regulatory peptides in the regulation of exocrine pancreatic secretion has also been established. In addition, neurotransmitters and neuropeptides released from the central nervous system may participate in the regulation of pancreatic secretion. It is conceivable that a few neurotransmitters and neuropeptides are involved in each neural regulatory pathway. However, their roles and sites of action in each pathway remain to be determined.
Journal Article↗
Present status of modified hemoglobin as blood substitutes and oral therapy for end stage renal failure using artificial cells containing genetically engineered cells.
Artificial cell or bioencapsulation has been developed for use in bioartificial organs, drug delivery, blood substitutes, and other areas. Recent rapid advances in modified hemoglobin blood substitutes have resulted in advance stages of Phase III clinical trials. Another area of use is in oral therapy, using artificial cells microencapsulated with genetically engineered cells for use in end stage renal failure and other conditions.
Administration, Oral↗
Roles of 5-HT receptors in the release and action of secretin on pancreatic secretion in rats.
5-Hydroxytryptamine (serotonin, 5-HT) is a hormone and neurotransmitter regulating gastrointestinal functions. 5-HT receptors are widely distributed in gastrointestinal mucosa and the enteric nervous system. Duodenal acidification stimulates not only the release of both 5-HT and secretin but also pancreatic exocrine secretion. We investigated the effect of 5-HT receptor antagonists on the release of secretin and pancreatic secretion of water and bicarbonate induced by duodenal acidification in anesthetized rats. Both the 5-HT(2) receptor antagonist ketanserin and the 5-HT(3) receptor antagonist ondansetron at 1-100 microg/kg dose-dependently inhibited acid-induced increases in plasma secretin concentration and pancreatic exocrine secretion. Neither the 5-HT(1) receptor antagonists pindolol and 5-HTP-DP nor the 5-HT(4) receptor antagonist SDZ-205,557 affected acid-evoked release of secretin or pancreatic secretion. None of the 5-HT receptor antagonists affected basal pancreatic secretion or plasma secretin concentration. Ketanserin or ondansetron at 10 microg/kg or a combination of both suppressed the pancreatic secretion in response to intravenous secretin at 2.5 and 5 pmol x kg(-1) x h(-1) by 55-75%, but not at 10 pmol x kg(-1) x h(-1). Atropine (50 microg/kg) significantly attenuated the inhibitory effect of ketanserin on pancreatic secretion but not on the release of secretin. These observations suggest that 5-HT(2) and 5-HT(3) receptors mediate duodenal acidification-induced release of secretin and pancreatic secretion of fluid and bicarbonate. Also, regulation of pancreatic exocrine secretion through 5-HT(2) receptors may involve a cholinergic pathway in the rat.
Animals↗
MEK inhibits secretin release and pancreatic secretion: roles of secretin-releasing peptide and somatostatin.
We investigated the mechanism of action of methionine enkephalin (MEK) on HCl-stimulated secretin release and pancreatic exocrine secretion. Anesthetized rats with pancreatobiliary cannulas and isolated upper small intestinal loops were perfused intraduodenally with 0.01 N HCl while bile and pancreatic juice were diverted. The effect of intravenous MEK on acid-stimulated secretin release and pancreatic exocrine secretion was then studied with or without coinfusion of naloxone, an anti-somatostatin (SS) serum, or normal rabbit serum. Duodenal acid perfusate, which contains secretin-releasing peptide (SRP) activity, was collected from donor rats with or without pretreatment with MEK, MEK + naloxone, or MEK + anti-SS serum, concentrated by ultrafiltration, and neutralized. The concentrated acid perfusate (CAP), which contains SRP bioactivity, was infused intraduodenally into recipient rats. MEK increased plasma SS concentration and inhibited secretin release and pancreatic fluid and bicarbonate secretion dose-dependently. The inhibition was partially reversed by naloxone and anti-SS serum but not by normal rabbit serum. In recipient rats, CAP increased plasma secretin level and pancreatic secretion. CAP SRP bioactivity decreased when it was collected from MEK-treated donor rats; this was partially reversed by coinfusion with naloxone or anti-SS serum. These results suggest that in the rat, MEK inhibition of acid-stimulated pancreatic secretion and secretin release involves suppression of SRP activity release. Thus the MEK inhibitory effect appears to be mediated in part by endogenous SS.
Animals↗
Pancreatic phospholipase A2 from the small intestine is a secretin-releasing factor in rats.
A secretin-releasing activity exists in the upper small intestine and pancreatic juice in the rat and the dog. Group I pancreatic phospholipase A2 (PLA2) in canine pancreatic juice and porcine pancreatic PLA2 stimulate the release of secretin from both STC-1 cells and a secretin-producing cell (S cell)-enriched preparation isolated from rat duodenal mucosa. We investigated the distribution and release of pancreatic PLA2-like immunoreactivity in the gastrointestinal tract and the role of PLA2 on the release of secretin and pancreatic exocrine secretion in response to duodenal acidification in anesthetized rats. PLA2-like immunoreactivity was detected in the mucosa throughout the gastrointestinal tract. High concentrations of PLA2 were found in both the small intestine and the pancreas. Duodenal acidification significantly increased the release of PLA2 from the upper small intestine (385% over basal secretion). Intravenous infusion of an anti-PLA2 serum (anti-PLA2) dose-dependently inhibited the release of secretin and pancreatic exocrine secretion in response to duodenal acid perfusion. Preincubation of the concentrate of intestinal acid perfusate (10-fold) from donor rats with the anti-PLA2 significantly suppressed its stimulation of secretin release and pancreatic exocrine secretion in recipient rats. We conclude that pancreatic PLA2 also functions as a secretin-releasing factor in the small intestine that mediates acid-stimulated release of secretin in rats.
Animals↗
Procedures for microencapsulation of enzymes, cells and genetically engineered microorganisms.
Methods to microencapsulate enzyme, cells, and genetically engineered cells have been described in this article. More specific examples of enzyme encapsulation include the microencapsulation of xanthine oxidase for Lesch-Nyhan disease; phenylalanine ammonia lyase for pheny, ketonuria and microencapsulation of multienzyme systems with cofactor recycling for multistep enzyme conversions. Methods for cell encapsulation include the details for encapsulating hepatocytes for liver failure and for gene therapy. This also includes the details of a novel two-step method for encapsulation of high concentrations of smaller cells. Another new approach is the detailed method of the encapsulation of genetically engineered Escherichia coli DH5 cells for lowering urea, ammonia, and other metabolites in kidney or, liver failure and other diseases.
Animals↗
Two future generations of blood substitutes based on polyhemoglobin-SOD-catalase and nanoencapsulation.
This paper discusses our research on two new generation blood substitutes. One is based on the crosslinking of hemoglobin, superoxide dismutase(SOD) and catalase (CAT) to form polyhemoglobin-SOD-CAT. This is being investigated for use in conditions with potential problems related to ischemia-reperfusion injuries as in severe hemorrhagic shock, stroke and other conditions. The second one is based on biodegradable polymeric nanocapsules containing hemoglobin and enzymes. In this form, the hemoglobin and enzymes are separated from the external environment. Furthermore, modifications of the polymeric membrane can result in increase in circulation time.
Animals↗
A secretin releasing peptide exists in dog pancreatic juice.
Canine pancreatic juice has been shown to stimulate exocrine pancreatic secretion in the dog. In the present study we investigated whether there is a secretin-releasing peptide in canine pancreatic juice. Pancreatic juice was collected from the dogs with Thomas gastric and duodenal cannulas while pancreatic secretion was stimulated by intravenous administration of secretin at 0.5 microg/kg/h and CCK-8 at 0.2 microg/kg/h, respectively. The pancreatic juice was separated into three different molecular weight (MW) fractions (Fr) by ultrafiltration (Fr 1; MW > 10,000, Fr 2; MW=10,000-4,000 and Fr 3; MW < 4,000), respectively. All the fractions were bioassayed in anesthetized rats. Fraction 3 dose-dependently and significantly stimulated pancreatic juice flow volume from 78.0% to 99.4% (p<0.05) and bicarbonate output from 128.9% to 202.1% (p<0.01), respectively. Plasma secretin concentration also increased from 1.2 +/- 0.5 pM to 5.0 +/- 0.8 pM and 6.0 +/- 1.0 pM (p<0.05). None of these fractions increased pancreatic protein secretion or plasma CCK level. The stimulatory effect of Fraction 3 on pancreatic secretion and the release of secretin was completely abolished by treatment with trypsin (1 mg/ml for 60 min at 37 degrees C) but not by heating (100 degrees C, 10 min). Intravenous injection of a rabbit anti-secretin serum, which rendered plasma secretin almost undetectable in rat plasma, also abolished Fr 3-stimulated pancreatic secretion of fluid and bicarbonate secretion. These observations suggest that a secretin-releasing peptide exists in the canine pancreatic juice. It is trypsin-sensitive and heat-resistant. This peptide may play a significant physiological role on the release of secretin and regulation of exocrine pancreatic secretion.
Animals↗
Canine vagus nerve stores cholecystokinin-58 and -8 but releases only cholecystokinin-8 upon electrical vagal stimulation.
Cholecystokinin-58 has been shown to be the major form of cholecystokinin (CCK) released to the circulation upon lumenal stimulation of the small intestine in humans and dogs. In anesthetized dogs, electrical vagal stimulation evokes pancreatic exocrine secretion that is in part mediated through the release of CCK. We studied the molecular form of CCK stored in canine vagus nerves and that released into circulation upon electrical vagal stimulation. Gel filtration and radioimmunoassay of the water and acid extracts of canine vagus nerves indicated CCK-8 (35%) and CCK-58 (65%) as the major molecular forms in the vagus nerve. Both forms of CCK isolated from the vagal extracts were equally bioactive as the standard CCK-8 and CCK-58, respectively, in stimulation of amylase release from isolated rat pancreatic acini. Analysis of plasma collected after electrical vagal stimulation indicated that CCK-8 is the only form released into the circulation. The release of CCK-8 upon electrical vagal stimulation was not affected by application of lidocaine to the upper small intestinal mucosa, suggesting that it was released from vagal nerve terminals.
Animals↗
The development and first clinical use of semipermeable microcapsules (artificial cells) as a compact artificial kidney. 1970.
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Animals↗
Red blood cell substitutes.
Soluble polymerized haemoglobin (polyhaemoglobin) is now in a phase III clinical trials. Patients have received up to 20 units (10 litres) in trauma surgery and other surgery. Polyhaemoglobin can be stored for more than 1 year. Haemoglobin solutions have no blood group antigen and can be used as a 'universal donor' oxygen carrier. They can also be sterilized. With a circulation half-life of 24 hours they are undergoing trials for peri-operative use. For conditions with potential for ischaemia-reperfusion injuries, a new polyhaemoglobin-superoxide dismutase-catalase, which can reduce oxygen radicals, is being developed. Recombinant human haemoglobin has been tested in clinical trials, and a new type of recombinant human haemoglobin that has low affinity for nitric oxide is being developed for clinical trials. To increase the circulation time, artificial red blood cells have been prepared with a bilayer lipid membrane (haemoglobin liposomes) or with a biodegradable polymer membrane-like polylactide (haemoglobin nanocapsules). Synthetic chemicals such as perfluorochemicals are also being developed and tested in clinical trials as red blood cell substitutes.
Blood Substitutes↗
Endogenous nitric oxide mediates pancreatic exocrine secretion stimulated by secretin and cholecystokinin in rats.
Nitric oxide (NO) is one of the important biologic mediators in regulation of gastrointestinal (GI) functions, but the influence of NO on the release of secretin and cholecystokinin (CCK) and exocrine pancreatic secretion has not been adequately investigated in the rat. The aim of this study was to determine the role of NO on endogenous and exogenous secretin- or CCK-stimulated pancreatic exocrine secretion both in anesthetized and conscious rats. Experiments were carried out in four different groups of rats with duodenal pancreatobiliary cannulas and jugular vein catheters. Group 1: During duodenal infusion of 0.05N HCl or 15% casein (pH 7.0), N-nitro-L-arginine (NNA), an inhibitor of NO-synthase in graded doses (2.5, 5, 10 mg/kg/h), was infused intravenously. Group 2: One hour after starting intravenous secretin at 5 pmol/kg/h or intravenous CCK-8 at 0.06 microg/kg/h, NNA in graded doses was administered intravenously. Group 3: In conscious rats, NNA (5 mg/kg/h) was given intravenously for 1 hour after a meal. Group 4: L-Arginine at 100 mg/kg/h was infused intravenously during the period of NNA (5 mg/kg/h) infusion in groups 1, 2, and 3. Pancreatic juice was collected at 30-minute intervals to measure volume, as well as output of bicarbonate and protein. At the end of the experiment, plasma secretin, vasoactive intestinal polypeptide (VIP) and CCK levels were determined by radioimmunoassay (RIA). NNA dose dependently inhibited the pancreatic secretion of fluid and bicarbonate stimulated by duodenal acidification, exogenous secretin, and a meal. NNA dose dependently inhibited the pancreatic secretion of protein stimulated by duodenal infusion of casein, exogenous CCK, and a meal. L-Arginine significantly reversed the NNA-induced inhibition of pancreatic secretion in all experiments. NNA did not alter significantly the plasma levels of secretin, VIP, and CCK. Our results indicated that endogenous NO plays a significant role in the regulation of pancreatic exocrine secretion stimulated by secretin and CCK. However, NO does not influence the release of secretin, VIP, or CCK in the rat.
Animals↗
Inhibition of gastric acid secretion in rat stomach by PACAP is mediated by secretin, somatostatin, and PGE(2).
Pituitary adenylate cyclase-activating polypeptide (PACAP), existing in two variants, PACAP-27 and PACAP-38, is found in the enteric nervous system and regulates function of the digestive system. However, the regulatory mechanism of PACAP on gastric acid secretion has not been well elucidated. We investigated the inhibitory action of PACAP-27 on acid secretion and its mechanism in isolated vascularly perfused rat stomach. PACAP-27 in four graded doses (5, 10, 20, and 50 microg/h) was vascularly infused to determine its effect on basal and pentagastrin (50 ng/h)-stimulated acid secretion. To study the inhibitory mechanism of PACAP-27 on acid secretion, a rabbit antisecretin serum, antisomatostatin serum, or indomethacin was administered. Concentrations of secretin, somatostatin, PGE(2), and histamine in portal venous effluent were measured by RIA. PACAP-27 dose-dependently inhibited both basal and pentagastrin-stimulated acid secretion. PACAP-27 at 10 microg/h significantly increased concentrations of secretin, somatostatin, and PGE(2) in basal or pentagastrin-stimulated state. The inhibitory effect of PACAP-27 on pentagastrin-stimulated acid secretion was reversed 33% by an antisecretin serum, 80.0% by an antisomatostatin serum, and 46.1% by indomethacin. The antisecretin serum partially reduced PACAP-27-induced local release of somatostatin and PGE(2). PACAP-27 at 10 microg/h elevated histamine level in portal venous effluent, which was further increased by antisomatostatin serum. However, antisomatostatin serum did not significantly increase acid secretion. It is concluded that PACAP-27 inhibits both basal and pentagastrin-stimulated gastric acid secretion. The effect of PACAP-27 is mediated by local release of secretin, somatostatin, and PGE(2) in isolated perfused rat stomach. The increase in somatostatin and PGE(2) levels in portal venous effluent is, in part, attributable to local action of the endogenous secretin.
Animals↗