Search PubMed⌕ Search

Biomedical subjects

D May

Publications and source records attributed to D May.

At least 73 records · Page 4Linked to original sources
PubMed1991

Teaching mental handicap to medical students.

An innovative approach to the teaching of mental handicap to pre-clinical medical students as part of their Behavioural Sciences course is first described. The teaching is organized around a number of extended placements which allow students to interact with people with a mental handicap on a basis of equality and reciprocity. Students respond positively to the seminar, regarding it as enjoyable, interesting and relevant to their future work as doctors. Questionnaires administered to students participating in the seminar suggest that they have a generally positive image of mentally handicapped people and hold vaguely liberal views as to how they should be treated by Society. Few, however, wish to work in the mental handicap area. There is no evidence that the experience of the seminar leads to any significant change in these attitudes.

Behavioral Sciences↗
PubMed1991

Low levels of cryofibrinogenaemia and peripheral circulatory dysfunction.

Over 12 months of general internal medicine practice in a small community, three premenopausal women, and a man presented with peripheral circulatory complaints. All were found to have cryofibrinogen, a cold-precipitable abnormal fibrinogen complex, in their blood. None had cryofibrinogen levels above 100mg per 100ml. The plasma of 195 other patients were screened. Cryofibrinogen was found in only one of these samples, that of a 23 year old women with active lupus erythematosis. These case reports suggest a relationship between low levels of cryofibrinogenaemia and mild circulatory disorders.

Adolescent↗
PubMed1990

[Cardiac side effects of 5-fluorouracil].

In four patients (a 54-year-old man and three women aged 57, 60 and 65 years, respectively) with colorectal carcinoma and no obvious cardiac abnormality anginal symptoms and ECG changes occurred during chemotherapy with 5-fluorouracil at a dose of 400 and 600 mg/m2. The ECG changes consisted of descending ST depressions with preterminally negative T waves, terminally negative T waves, ventricular extrasystoles and sinus tachycardia with intermittent atrial fibrillation. The signs first appeared between the second and fourth day of treatment; in two patients they improved with glyceryl trinitrate. A few days after 5-fluorouracil had last been administered all ECG changes had disappeared. The causes of cardiotoxicity of the drug remain unknown.

Aged↗
PubMed1990

Treatment of chronic myelogenous leukemia with interferons alpha and gamma.

A 23-year-old male patient with Philadelphia chromosome (Ph) positive chronic myelogenous leukemia (CML) was treated with both IFN alpha and IFN gamma. Normalization of leukocyte counts was reached after 3 months of treatment. Southern blot analysis failed to detect the neoplastic cell clone after 19 months of therapy. Cytogenetically, complete suppression of Ph positive cells in the patient's bone marrow and blood was observed after 20 months and 25 months, respectively. This response was achieved with doses of IFN alpha and IFN gamma which were considerably lower than the dosage of IFN used in single agent therapy of CML.

Adult↗
PubMed1990

DNA-flow cytometry studies in blood and marrow cells from chronic myelogenous leukemia patients treated with interferon alpha-2b.

Cell cycle distribution in bone marrow and peripheral blood mononucleated cells was studied in patients with chronic myelogenous leukemia (CML) before and during treatment with interferon (IFN) alpha-2b. DNA-flow cytometry with ethidium bromide fluorescence was used. Highly significant differences between mononucleated cells from CML patients and normal controls were seen in peripheral blood but not in bone marrow specimens. Patients achieving hematologic remission during IFN treatment showed a cell cycle distribution in bone marrow cells and peripheral blood cells similar to normal controls.

Bone Marrow↗
PubMed1990

Intracellular mechanism responsible for reduced enzyme secretion from camostate-induced hypertrophied pancreas.

Chornic exogenous administration of cholecystokinin octapeptide (CCK8) to rats led to a reduced sensitivity of pancreatic acinar cells to both CCK8 and carbachol stimulation without changes in affinity or number of CCK or muscarinic receptors. In addition, repeated feeding of camostate, a synthetic protease inhibitor which stimulates endogenous CCK release, desensitized the response of the acini to caerulein. This study investigates whether an altered postreceptor signal transduction mechanism is responsible for the reduced amylase secretion. Four days of camostate treatment significantly increased pancreatic weight, protein and amylase, but not DNA content, indicating organ hypertrophy, CCK8 and carbachol stimulated amylase release from acini, isolated from camostate-treated rats, was significantly reduced without shifting the dose response curve compared to controls. There was no difference in total phosphoinositide turnover between the groups. In addition, CCK8 and carbachol stimulated 45Ca efflux and calcium ionophore stimulated amylase release were similar in both groups. These results indicate that the release of calcium from intracellular stores and the utilization of intracellular calcium to drive amylase secretion is not affected in the hypertrophied pancreas. In contrast, incubation of acini from camostate-treated rats with TPA (a phorbol ester which directly stimulates protein kinase C) showed a 48% reduction in amylase secretion. This suggests that a regulatory mechanism is present at the level of protein kinase C or beyond, which is responsible for the decrease in amylase release in the hypertrophied pancreas.

Amylases↗
PubMed1989

Phase I study of recombinant human tumor necrosis factor alpha in advanced malignant disease.

A phase I study with recombinant human tumor necrosis factor alpha (rhuTNF-alpha; Knoll AG, Ludwigshafen, FRG) in patients with advanced malignant disease was undertaken to evaluate drug toxicity (organ specificity, time course, predictability, reversibility, maximal tolerated dose), effectiveness, antigenicity and pharmacokinetics. TNF was administered as a test dose followed by daily i.v. infusions for 5 days, every 3 weeks (single i.v. infusion lasting 10 min, TNF dissolved in 50 ml 5% human albumin). Dosage was increased in groups of 3 or 4 patients from 0.04 mg/m2 to 0.28 mg/m2. A total of 19 patients with different cancers, including seven large-bowel carcinomas, three chronic myelogenous leukemias, three hypernephromas, two small-cell lung cancers, one malignant melanoma, one malignant lymphoma, one rhabdomyosarcoma and one fibrosarcoma were treated. Major side-effects were chills and fever (maximum 40.4 degrees C, median 38.7 degrees C, 19/19), headache (12/19), nausea and vomiting (12/19) and pronounced (greater than 20%) hypotension (4/19). Acute side-effects could be diminished by paracetamol or indomethacin pretreatment, and with one possible exception no tachyphylaxis to TNF was noted. Mild renal toxicity was seen during TNF treatment. Pharmacokinetic studies showed a serum half-life (t1/2) ranging from 11 min to 17 min for doses from 0.04 mg/m2 to 0.16 mg/m2 and prolonged clearance with t1/2 ranging from 54 min to 70 min in the 0.20-0.28 mg/m2 dose range. No objective antitumor effects were observed in this phase I study.

Adenocarcinoma↗
PubMed1988

[The dose of alpha interferon in induction and maintainance therapy of hairy cell leukemia].

The efficacy of different doses of interferon (IFN) alpha in the induction therapy of hairy cell leukemia was studied. Recombinant IFN alpha-2b was administered subcutaneously every second day at an initial dose of 4 x 10(6) U/m2 (7 patients), 2 x 10(6) U/m2 (14 patients) and 1 x 10(6) U/m2 (13 patients). Each dose was effective to induce a normalization of blood cell counts and a reduction of bone marrow infiltration in the majority of patients treated. A delayed increase in granulocyte counts, however, was noted in patients treated with 1 x 10(6) U/m2, and 2 of them only achieved a partial hematological remission after 1 year of treatment. After the induction of stable remission, patients were randomized into 2 different schedules of maintenance therapy. Five of 7 patients receiving IFN alpha-2b at a total dose of 1 x 10(6) U twice a week, and 6/8 patients treated with 2 x 10(6) U once weekly, respectively, received this therapy for 1 year and remained in stable remission.

Adult↗
PubMed1987

Treatment of chronic myelogenous leukemia with recombinant interferon alfa-2b.

Interferon alfa-2b (Intron A; Schering-Plough) was administered to 36 patients with chronic myeloid leukemia (CML) at an initial dose of 4 X 10(6) IU/m2 daily subcutaneously, adapted to changes in leukocyte counts during the course of treatment. Of 32 patients who could be fully evaluated (20 men and 12 women; median age, 34 years) 29 were in the chronic phase, one had a blast crisis and two had accelerated phase disease. Hematologic remission was achieved in 20 of the 32 patients, while a partial hematologic remission was obtained in 10. Elevated pretreatment white-cell counts returned to normal in 25 patients after 3-40 weeks. There was a parallel decrease in platelet counts after an average treatment time of six weeks and in lactate dehydrogenase, after 2-20 weeks. In conclusion, administration of interferon alfa-2b resulted in a relatively rapid cell reduction in chronic phase CML. The long-term effect of this treatment on the course of the disease and the place of interferon alfa-2b in the overall concept of CML treatment remains to be evaluated.

Adult↗
PubMed1986

Atypical fibroxanthoma of the skin with metastasis.

Cutaneous atypical fibroxanthoma (AFX) occurs in elderly persons as a small nodule or ulcernodule in actinically damaged skin of the head and neck area. The vast majority of AFX behave in a benign manner, and metastasis is rare. Eight examples of metastasizing AFX are reported. Factors that portend aggressive behavior and metastasis are vascular invasion, recurrence, deep tissue invasion, tumor necrosis and, possibly, defective or depressed host resistance. The metastasizing primary AFX were located on the head, and the metastasis involved the structures in the region of the parotid gland.

Adult↗
PubMed1986

Trypsin suppression of pancreatic enzyme secretion. Differential effect on cholecystokinin release and the enteropancreatic reflex.

We have recently demonstrated that intraduodenal perfusion of trypsin inhibits phenylalanine-stimulated pancreatic enzyme secretion by suppression of release of cholecystokinin (CCK). It is not known whether trypsin in the duodenum inhibits pancreatic secretion stimulated by a cholinergic mechanism. To investigate this question gastrointestinal intubation and perfusion were performed in 12 healthy subjects. Volume and osmoreceptors in the duodenum, which are known to elicit pancreatic secretion through cholinergic pathways, were stimulated by infusing increasing volumes (1.0, 2.5, and 5.0 ml/min) of normal saline or increasing osmolality (300, 400, 500 mosmol) of NaCl solution. Increasing the rates of intraduodenal perfusion of normal saline or increasing the osmolality of the duodenal perfusates caused a dose-related increase in pancreatic trypsin and chymotrypsin outputs without affecting basal plasma CCK levels (0.9 +/- 0.1 pM). The volume- or osmolality-stimulated pancreatic secretions were abolished by atropine, but not by intraduodenal perfusion of trypsin. In contrast, intraduodenal perfusion of phenylalanine (10 mM) produced a significant increase in plasma CCK levels (6.7 +/- 0.8 pM) and a three- to fourfold increase in pancreatic enzyme outputs. Perfusion of the duodenum with bovine trypsin (1 g/L) reduced the plasma CCK levels to basal values and significantly attenuated the phenylalanine-stimulated enzyme secretion to 63% +/- 4% of control. Simultaneous administration of atropine and intraduodenal perfusion of trypsin completely abolished the pancreatic enzyme response to phenylalanine stimulation. These studies indicate that the intestinal phase of human pancreatic enzyme secretion is under both hormonal and neural control. Intraduodenal trypsin inhibits only pancreatic secretion mediated by CCK release, and not that mediated by cholinergic mechanisms. These observations suggest that feedback regulation of pancreatic enzyme secretion is stimulus specific.

Adult↗
PubMed1986

Cholecystokinin mediates feedback regulation of pancreatic enzyme secretion in rats.

Previous studies have shown that trypsin and chymotrypsin in the duodenum exert a negative-feedback regulation on pancreatic enzyme secretion in the rat. The mechanism responsible for this physiological phenomenon is unknown. By use of a specific and sensitive bioassay based on amylase release from isolated pancreatic acini, the role of cholecystokinin in the negative-feedback regulation of exocrine pancreatic secretion was examined. Rats were prepared with duodenal cannulas and pancreaticobiliary cannulas. Diversion of pancreaticobiliary juice resulted in a threefold increase in pancreatic protein output and an increase of plasma cholecystokinin from a basal level of 0.5 +/- 0.08 pM cholecystokinin octapeptide (CCK-8) to 16 +/- 4 pM CCK-8. Perfusion of trypsin (2 mg/h) or pancreaticobiliary juice returned pancreatic protein output to basal levels and plasma cholecystokinin to 2.1 +/- 1.2 and 0.33 +/- 0.1 pM, respectively. The inhibitory effect of trypsin on cholecystokinin release was enzyme and site specific, since inhibition of cholecystokinin release was not observed with perfusion of amylase into the duodenum or with trypsin into the ileum. Intravenous infusion of proglumide abolished the increase in pancreatic secretion following diversion of pancreaticobiliary juice. Intraduodenal perfusion of lidocaine, infusion of tetrodotoxin into the superior mesenteric artery, or intravenous infusion of atropine inhibited the rise in plasma cholecystokinin seen with diversion of pancreaticobiliary juice. These studies suggest that feedback regulation of pancreatic enzyme secretion in the rat is mediated by release of cholecystokinin. Furthermore, the feedback mechanism is neurally mediated, involving a cholinergic pathway.

Animals↗
PubMed1986

[Ileus of the large intestine caused by endometriosis. Report of 2 cases and review of the literature].

Two cases of distal colonic obstruction due to endometriosis prompted the authors to elaborate on problems implied in diagnosis and therapy of this rare cause of ileus. Accurate preoperative diagnosis was usually not obtainable from case histories, endoscopy, and X-ray checks. Only emergency operations should be performed on ileus cases (colostomy, Hartmann's operation). Hormonal and surgical treatment should then be continued in consultation with the gynaecologist. Resections should be minimised and mutilating interventions (rectal amputation) avoided.

Colectomy↗
PubMed1985

The life-space diary: a measure of mobility in old people at home.

Thirty people aged 64 and over living at home were asked to complete a "life-space diary" for 1 month during which they were invited to attend a gait laboratory for measurements of gait and balance. Twenty-eight subjects completed the diary satisfactorily, and 24 of these also undertook the laboratory tests. The diary was acceptable and gave a good indication of the subject's mobility. There was a close correlation between mobility as derived from the diary and the laboratory measurements of gait speed and mean sway path. The diary is worthy of further evaluation as an objective record of mobility in old people at home.

Activities of Daily Living↗
PubMed1983

Stimulation of pepsinogen release from isolated gastric glands by cholecystokininlike peptides.

Gastric glands isolated from rabbit stomach were employed to study the regulation of pepsinogen secretion by peptide hormones. Cholecystokinin octapeptide (CCK-OP) stimulated pepsinogen secretion with an ED50 of about 1 nM. Caerulein was as effective as CCK-OP but less potent (ED50, 10 nM). Gastrin (HG-17) was found to be a weak stimulus, being only about 20% as effective as CCK-OP or caerulein. Sulfation of CCK-OP and caerulein was found to be important for potency but did not alter efficacy. Peptide stimulation of pepsinogen secretion was unaffected by cimetidine, atropine, or propranolol. Combinations of peptides resulted in less-than-additive responses, as did the combination of peptides with carbachol. In contrast, combination of peptides with isoproterenol resulted in additive responses. Accumulation of the weak base aminopyrine was used to measure acid formation by the gastric glands. The peptides gastrin, CCK-OP, and caerulein were found to be equally effective in stimulating acid formation. The peptide stimulation of pepsinogen secretion was inhibited by dibutyryl cGMP, whereas stimulation of acid formation was not inhibited by the cyclic nucleotide. The results indicate that gastric glands contain at least two peptide receptors distinguishable by sensitivity to dibutyryl cGMP. The peptide receptor associated with pepsinogen secretion appears to be selective for CCK relative to gastrin.

Adenylyl Cyclases↗