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Biomedical subjects

O V Nielsen

Publications and source records attributed to O V Nielsen.

At least 19 recordsLinked to original sources
PubMed1995

[Hydatidosis. A survey].

With the increased influx of foreign workers, refugees and immigrants, particularly from endemic areas, we will probably see more patients with hydatid disease, chiefly hydatid disease of the liver caused by E. granulosus. Thus it is important to bring the disease to the attention of the general surgeon. The diagnosis of hydatid disease is primarily made by ultrasound and serological examination. Other tests such as CT, angiography and ERCP are as a rule only important in surgical planning and in complicated cases. Treatment is principally surgical. The choice of surgical procedure should be individualized as much as possible due to the many aspects of the disease. Drainage of residual cavities should be avoided. Preoperative evaluation by ERCP is indicated in cases complicated by biliary communication. Percutaneous drainage can be indicated in cases of recurrence and in cysts of poor accessability. Medical treatment has its place primarily pre- and postoperatively. The preferred drug is albendazole. Mebendazole is now considered obsolete. It is not possible to monitor the effect of treatment with current serological methods.

Data Collection↗
PubMed1989

Role of gastrin-releasing peptide in neural control of pancreatic exocrine secretion.

We studied the effect of electrical stimulation of the vagus nerves on the exocrine secretion of isolated perfused porcine pancreas before and after procedures that almost completely blocked the effects elicited by infusions of gastrin-releasing peptide (GRP): desensitization of the pancreas for GRP (by perfusion with high concentrations of GRP); administration of an antagonist of GRP action [D-Arg1, D-Pro2, D-Trp7,9, Leu11)-substance P]; and perfusion with Fab fragments of antibodies against GRP. Both desensitization and antagonist administration significantly (p less than 0.01) inhibited the effect of vagus stimulation on pancreatic protein secretion (by 42.1 and 33%). The inhibitory effect of anti-GRP perfusion was less pronounced (22% inhibition, 0.05 greater than p less than 0.1). The results support the notion that pancreatic, GRP-producing nerve fibers are involved in the neural control of pancreatic enzyme secretion.

Animals↗
PubMed1989

On the regulatory functions of neuropeptide Y (NPY) with respect to vascular resistance and exocrine and endocrine secretion in the pig pancreas.

We compared the effects of electrical stimulation of the splanchnic nerves and infusions of neuropeptide Y, noradrenaline or a combination of the two on pancreatic vascular resistance and exocrine and endocrine secretion. For these studies we used isolated perfused pig pancreas with preserved splanchnic nerve supply. The exocrine secretion was stimulated with physiological concentrations of secretin and cholecystokinin octapeptide. Noradrenaline and NPY at 10(-8) M both increased pancreatic perfusion pressure. Their effects were additive and similar in magnitude to that of electrical stimulation of the splanchnic nerves at 4-8 Hz. Nerve stimulation as well as NPY and noradrenaline infusions inhibited exocrine secretion, but an additive effect could not be demonstrated. Neither NPY nor noradrenaline could reproduce the stimulatory effect of nerve stimulation on glucagon secretion, nor the weak inhibitory effect on somatostatin secretion. NPY alone had no effect on insulin secretion and did not influence the inhibitory effect of noradrenaline. It is concluded that NPY is likely to cooperate with noradrenaline in the control of pancreatic blood flow, whereas its role in the control of pancreatic secretion is likely to be of minor importance, if any.

Animals↗
PubMed1988

Adenocarcinoma of the anal ducts. A series of 21 cases.

The records of 21 patients treated for adenocarcinoma of the anal ducts between 1943 and 1982 were reviewed. The patients were followed until death or current status in April 1987. The median follow-up period was eight months (range, 3 to 144 months). Fifteen patients had an erroneous diagnosis made at first physician visit resulting in a median doctor's delay of 14 months (range, 3 to 24 months) before correct treatment was carried out. Nine of the tumors were localized perianally (ischiorectal space), seven anally, and five in a fistula-in-ano. Tumors localized anally were significantly smaller and had a significantly shorter history than perianally or fistula-in-ano localized tumors (P less than .05 for each localization). Three patients with anal tumors had their diagnosis made accidentally by routine histologic examination of an excised hemorrhoid. First examination revealed distant metastases in 13 patients and follow-up examination revealed regional or distant metastases in seven patients. Modes of treatment were wide local excision (N = 3), abdominoperineal resection (N = 3), colostomy (N = 9), and radiotherapy (N = 2). Twenty of the 21 patients died within 18 months due to the cancer. One long-term survivor was observed; the patient was alive 12 years after local excision of the tumor without evidence of recurrent disease. The crude five- and 10-year survival was only 4.8 percent.

Adenocarcinoma↗
PubMed1988

Long-term prognosis after radical treatment for squamous-cell carcinoma of the anal canal and anal margin.

Sixty-seven of 100 (67 percent) and 24 of 58 (41 percent) apparently radically treated patients with squamous-cell carcinoma of the anal canal (AC) and the anal margin (AM) developed recurrent disease during a median observation time of ten years (range, 0 to 38 years). A significantly higher number of patients treated for AC tumors with local excision had recurrent disease compared with patients treated with abdominoperineal resection (P less than .05). Twenty patients with AC tumors had local recurrence, 21 regional recurrence, and 26 visceral metastases. Eighteen patients with AM tumors had local recurrence, five regional, and one brain metastases. The latest recurrences among AC and AM tumor patients were diagnosed 11 and nine years after primary treatment, respectively. The estimated cure rate by the actuarial method after 15 years was 26 percent and 53 percent for AC and AM tumors, respectively. Thus, if recurrent carcinomas of the anus are to be detected early, frequent life-long control examinations are necessary. It is obvious from this study that, in order to reduce recurrent disease of carcinoma of the anus, new treatment regimens must be tried under controlled circumstances. Surgical therapies alone are clearly insufficient in the treatment of carcinoma of the anus.

Actuarial Analysis↗
PubMed1988

Role of gastrin-releasing peptide in the neural control of pepsinogen secretion from the pig stomach.

A new experimental model, the isolated perfused antrectomized pig stomach with intact vagal innervation, was shown to produce pepsinogen and gastric acid upon electrical stimulation of the vagus nerves and by intravascular administration of carbachol (from a basal value of 111 +/- 24 units of pepsin per minute and 0.044 +/- 0.012 mEq H+/min to 393 +/- 75 units of pepsin per minute and 0.102 +/- 0.022 mEq H+/min upon vagal stimulation). Vagal stimulation also increased the release of the neuropeptide gastrin-releasing peptide to the venous effluent from 0.42 +/- 0.12 to 3.1 +/- 0.95 pmol/min. Intravascular infusions of gastrin-releasing peptide at a concentration of 10(-8) mol/L resulted in a threefold increase in pepsinogen secretion and a small increase in acid output. Because gastrin-mediated effects of gastrin-releasing peptide are excluded with this preparation, our results show that gastrin-releasing peptide acts either directly or through another unknown local mediator on the pepsinogen-secreting cells. Gastrin-releasing peptide may thus participate in the vagal control of pepsinogen secretion.

Animals↗
PubMed1988

Oxyntomodulin (glicentin-(33-69)): pharmacokinetics, binding to liver cell membranes, effects on isolated perfused pig pancreas, and secretion from isolated perfused lower small intestine of pigs.

The pharmacokinetics of purified synthetic oxyntomodulin were studied after infusing it into euglycaemic pigs at two rates. The elimination of the peptide from plasma was characterized by two components, a fast one (t1/2 7.2 +/- 0.6 min) and a slow one (t1/2 20.4 +/- 3.8 min) (mean +/- S.E.M., n = 7). The metabolic clearance rate was independent of infusion rate (6.96 +/- 0.99 vs 7.44 +/- 0.98 ml/kg . min (mean +/- S.E.M., n = 7). The synthetic peptide bound to pig hepatic glucagon receptors, but with approximately 2% of the affinity of glucagon, and showed insulinotropic and somatostatinotropic effects when infused into isolated perfused pig pancreases at concentrations higher than 10(-10) M. A dose-dependent increase was also shown for pancreatic glucagon output. A naturally occurring peptide, identified as oxyntomodulin by gel filtration and HPLC, was released into the circulation from the pig lower small intestinal mucosa upon intraluminal administration of glucose, and represented 25 +/- 3.8% of the secreted glucagon-like immunoreactivity. 11 +/- 2.3% of the secreted glucagon-like immunoreactivity was indistinguishable from glucagon itself upon gel filtration; thus at least 36% of the glucagon-like immunoreactivity secreted from the intestinal mucosa is already in an active form.

Animals↗
PubMed1988

Processing and secretion of prosomatostatin by the pig pancreas.

Antisera and radioimmunoassays against five different regions of prosomatostatin (proSS) were used for chromatographical analysis and for immunohistochemical mapping of the products of proSS in the pig pancreas. Secreted products of proSS were studied by analysis of effluent from isolated perfused pig pancreas obtained during isoproterenol stimulation. All cells that were stained with one antiserum also stained with the other antisera. Immunoreactive nerves were not observed. Isoproterenol increased equally the secretion of proSS 20-36, proSS 65-76, and proSS 79-92 immunoreactivity. The major molecular forms identified in pancreatic extracts and released from the pancreas were proSS 79-92; proSS 65-76; an N-terminally extended form of proSS 65-76; and two larger forms comprising the proSS 20-36 sequence (but not the 1-13 sequence) with and without the proSS 65-76 sequence. ProSS 1-10, 1-32 and 65-92 (somatostatin 28) were not identified.

Animals↗
PubMed1988

Effect of truncated glucagon-like peptide-1 [proglucagon-(78-107) amide] on endocrine secretion from pig pancreas, antrum, and nonantral stomach.

We studied the effect of truncated glucagon-like peptide-1 [naturally occurring GLP-1; proglucagon-(78-107) amide], a potent insulinotropic peptide from the pig ileum, on endocrine and exocrine secretion of potential gastrointestinal target organs using isolated perfused preparations of the porcine pancreas, antrum, and nonantral part of the stomach. Truncated GLP-1 significantly increased somatostatin secretion from the pancreas at 10(-10) mol/liter and more than doubled the secretion at 10(-9) mol/liter, but had no effect on either somatostatin or gastrin secretion from the antrum or on somatostatin secretion from the nonantral stomach in concentrations up to 10(-8) mol/liter. Insulin secretion from the pancreas (with 7 mmol/liter glucose in the perfusate) increased 2-fold with truncated GLP-1 at 10(-10) mol/liter and almost 5-fold at 10(-9) mol/liter. Pancreatic glucagon secretion was inhibited by 50% at 10(-10) mol/liter and by 70-80% at 10(-9) mol/liter. Full-length GLP-1 [proglucagon-(72-107)] and GLP-2 [proglucagon-(126-159)] had no effect on hormone secretion from any of the perfused organs. It is concluded that truncated GLP-1 may participate in an entero-insular control of pancreatic endocrine secretion.

Animals↗
PubMed1987

Truncated glucagon-like peptide I, an insulin-releasing hormone from the distal gut.

By hydrophobic gel permeation and high pressure liquid chromatography we isolated from pig intestinal mucosa a peptide which corresponds to proglucagon 78-107 as suggested by chromatography and determination of its N-terminal sequence. Natural and synthetic proglucagon 78-107 dose dependently and potently increased insulin secretion from the isolated perfused pig pancreas. Proglucagon 78-107 also secreted by the small intestine may participate in the hormonal control of insulin secretion.

Animals↗
PubMed1987

Does an erroneous diagnosis of squamous-cell carcinoma of the anal canal and anal margin at first physician visit influence prognosis?

Patients with squamous-cell carcinoma of the anal canal (n = 125) and its margin (n = 76) were divided into five groups: those with an erroneous diagnosis and a correct diagnosis made at first physician visit; those with a history of less than six months, between six and 18 months, and more than 18 months. Patients with canal tumors had an erroneous diagnosis made more frequently than patients with margin tumors. In both groups patients with an erroneous diagnosis had longer histories than patients with a correct diagnosis. Among patients with erroneously diagnosed canal tumor, pain, the feeling of a lump, anal discharge, and pruritus ani occurred less frequently than among correctly diagnosed patients. The prognosis was worse among patients with erroneously diagnosed canal tumors compared with correctly diagnosed patients. Such a difference could not be found among patients with margin tumors. There was a gradual worsening of the prognosis among patients with increasing length of history and canal tumors, in contrast to patients with margin tumors, in whom only a history of more than 18 months was associated with a worse prognosis.

Adult↗
PubMed1987

The effect of gastrin-releasing peptide on the endocrine pancreas.

The 27-amino acid peptide gastrin releasing peptide (GRP-(1-27] was infused at 4 dose levels (0.01, 0.1, 1.0, and 10 nM) into the arterial line of the isolated perfused porcine pancreas. Infusions were performed at 3 different perfusate glucose levels (3.5, 5.0, and 8.0 mM) and at two levels of amino acids (5 and 15 mM). GRP-(1-27) stimulated insulin and pancreatic polypeptide secretion and inhibited somatostatin secretion in a dose-dependent manner. Glucagon secretion was unaffected by infusion of GRP under all circumstances. The effect of GRP-(1-27) on insulin secretion was enhanced with increasing perfusate glucose levels, whereas the effects upon somatostatin and pancreatic polypeptide secretion were independent of perfusate glucose levels. The responses to GRP were unaffected by elevation of the concentration of amino acids in the perfusate. The effects of GRP were unaffected by atropine at 10(-6) M. The localization of GRP within the porcine pancreas, its release during electrical stimulation of the vagus nerve, and its potent effects upon pancreatic endocrine secretion make it conceivable that the peptide participates in parasympathetic regulation of pancreatic endocrine secretion.

Animals↗
PubMed1987

Gastrin-releasing peptide in the porcine pancreas.

The presence of gastrin-releasing peptide (GRP) was studied in extracts of porcine pancreata. Gel filtration and high-pressure liquid chromatographic profiles of these extracts as monitored with both C-terminally and N-terminally directed radioimmunoassays against GRP showed pancreatic GRP to consist of one main form, namely the 27-amino acid peptide originally extracted from porcine stomach, and small amounts of a C-terminal fragment identical with the C-terminal 10-amino acid peptide. Gastrin-releasing peptide-like immunoreactivity released from the isolated perfused porcine pancreas during electrical vagal stimulation was shown by gel filtration to consist of the same two forms. By use of immunocytochemical techniques employing an antiserum directed against its N terminus, GRP was localized to varicose nerve fibers in close association with the exocrine tissue of the porcine pancreas in particular. Some fibers were found penetrating into pancreatic islets also. Immunoreactive nerve cell bodies as well as fibers were found within intrapancreatic ganglia. The potency of GRP in stimulating exocrine as well as endocrine secretion from the porcine pancreas, its presence in close contact with both acini and islets, and its release during vagal stimulation indicate that GRP may have a role in the parasympathetic regulation of endocrine and exocrine secretion from the pig pancreas.

Animals↗
PubMed1987

VIP and PHI in the pig pancreas: coexistence, corelease, and cooperative effects.

The human vasoactive intestinal polypeptide (VIP) precursor contains a sequence, a peptide with an N-terminal histidine and C-terminal methionine (PHM), which is 93% homologous to the porcine intestinal peptide, (PHI) a peptide having N-terminal histidine and C-terminal isoleucine amide, suggesting that PHI could be a product of the porcine VIP precursor. If so, VIP-producing nerves would be expected to produce and release PHI in addition to VIP. We studied this in the pig pancreas. By immunohistochemistry, we identified nerve cell bodies in local ganglia and nerve fibers that were both PHI and VIP immunoreactive, innervating exocrine as well as endocrine structures. During electrical stimulation of the vagus nerve supply to the isolated perfused pig pancreas, a synchronous and approximately equimolar release of immunoreactive PHI and VIP was observed. Both responses were abolished by hexamethonium and could be copied by cholinergic agonists. Infusions of PHI and VIP at 10(-9) M stimulated the exocrine secretion of fluid and bicarbonate, and the effect of a combination of the two peptides was additive. In addition, both peptides stimulated insulin as well as glucagon secretion. By gel chromatography the VIP immunoreactivity in the venous effluent corresponded precisely to synthetic VIP, but only 24% of the PHI immunoreactivity corresponded to synthetic PHI; a larger peptide (mol wt 5,000-7,000) was responsible for the majority. The biological activity of this component is unknown. The results suggest that both VIP and PHI, released from intrapancreatic nerve fibers, participate in the parasympathetic control of pancreatic secretion.

Animals↗
PubMed1987

GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion.

We extracted gastrin-releasing peptide (GRP) and its C-terminal decapeptide corresponding to 6.4 and 6.8 pmol/g from pig antrum mucosa. By immunohistochemistry GRP was localized to mucosal, submucosal, and myenteric nerve fibers. A few nerve cell bodies were also identified. Using isolated perfused pig antrum with intact vagal innervation, we found concomitant, atropine-resistant release of GRP and gastrin during electrical stimulation of the vagal nerves. Intra-arterial GRP at 10(-11)-10(-10) mol/l caused up to fivefold, dose-dependent increases in gastrin secretion; higher doses were less effective and completely desensitized the gastrin cells for the lower doses. After desensitization, vagal stimulation no longer produced gastrin secretion. The substance P antagonist [D-Arg, D-Pro, D-Trp, Leu]-substance P, described as also antagonizing the actions of bombesin, decreased the gastrin response to GRP and abolished the effect of vagal stimulation. The available evidence strongly suggests that GRP nerves are responsible for the stimulatory vagal effects on gastrin secretion in the pig.

Animals↗
PubMed1987

GRP-producing nerves control antral somatostatin and gastrin secretion in pigs.

By immunohistochemistry, nerve fibers containing gastrin-releasing polypeptide (GRP)-like immunoreactivity were identified close to the somatostatin (SS)-producing cells of the gastric antral mucosa. We, therefore, studied the possible role of GRP in the control of antral SS secretion by use of isolated perfused pig antrum with intact vagus nerve supply. Electrical stimulation of the vagus nerves at 4 Hz increased the antral release of GRP up to 10-fold and increased SS output 2- to 3-fold. Atropine at 10(-6) M had no effect on these responses. Intra-arterial GRP increased SS secretion significantly at 10(-10) M and eightfold at 10(-8) M, whereas gastrin secretion was stimulated significantly at 10(-11) M and maximally at 10(-10) M and inhibited at 10(-8) M. Preperfusion with a GRP antagonist ([D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P) or Fab fragments of antibodies against GRP abolished the effects of vagus stimulation on gastrin and somatostatin output. Gastrin in concentrations up to 10(-7) M was without effect on SS secretion. We conclude that electrical stimulation of the vagus nerves increases antral SS gastrin secretion and that GRP is a likely transmitter.

Animals↗
PubMed1987

Autonomic nervous control of fundic secretion of somatostatin and antral secretion of gastrin and somatostatin in pigs.

By selective catheterization of gastric veins, we studied the secretion of gastrin and somatostatin from the antrum and of somatostatin from the gastric fundus-corpus region in anaesthetized pigs with or without acute adrenalectomy. The secretion was studied during electrical stimulation of the vagus nerves and the splanchnic nerves and simultaneous irrigation of gastric lumen with fluids of high, low, and neutral pH. The corpus-fundus somatostatin response to vagal stimulation was biphasic with a short-lasting initial increase followed by a lasting inhibition, which was little influenced by intraluminal pH or adrenalectomy. In pigs with intact adrenals, antral somatostatin secretion was increased by vagal stimulation, whereas in adrenalectomized pigs, the effect was inhibitory. The vagally induced inhibition was abolished when the intragastric pH was kept at pH 2. The antral gastrin secretion was strongly stimulated by vagal stimulation. The magnitude of the secretory response was inversely related to the pre-stimulatory somatostatin levels, but not to the nerve stimulation responses. Splanchnic stimulation increased arterial blood pressure and gastric blood flow, but had inconsistent effects on somatostatin and gastrin secretion.

Adrenalectomy↗