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Biomedical subjects

P Bliss

Publications and source records attributed to P Bliss.

17 recordsLinked to original sources
PubMed2006

Improvements in dose homogeneity for tangential breast fields from a selection of combinations of library compensators.

Individually paired physical compensators are used in our centre to improve dose homogeneity for radiotherapy to the whole breast. This technical note describes the further improvements that may be achieved when all possible combinations of individual compensators within the library are considered. A retrospective study of 78 patients using a total of 16 (left-sided) and 14 (right-sided) sets of library compensators was evaluated, and the results expressed in terms of the standard deviation of the differential dose-volume histogram and the dose range within the breast volume. The mean of the standard deviations was 3.17% (uncompensated), 2.16% (paired compensators) and 1.97% (combinations) and the mean homogeneity was 15.3%, 11.8% and 11.1%, respectively.

Breast Neoplasms↗
PubMed2000

Analysis of N(alpha)-methylhistamine by gas chromatography-mass spectrometry.

A gas chromatography-electron capture mass spectrometry assay has been developed for the histamine H3 receptor agonist, N(alpha)-methylhistamine (N(alpha)-MH). The assay is linear from 50 pg-10 ng, with a limit of detection of 50 pg/ml for gastric juice and plasma, and 50 pg/sample for bacteria (10(7)-10(8) CFU) and gastric tissue (5-10 mg wet weight). The limits of quantification are 100 pg/ml for gastric juice (%RSD=1.4) and plasma (%RSD=9.4), and 100 pg/sample for bacteria (%RSD=3.9) and tissue (%RSD=5.8). N(alpha)-MH was not present in human plasma, but low levels (1.4 ng/ml and 0.4 ng/ml) were detected in two samples of human gastric juice obtained from patients infected with Helicobacter pylori.

Gas Chromatography-Mass Spectrometry↗
PubMed2000

N alpha-methylhistamine: association with Helicobacter pylori infection in humans and effects on gastric acid secretion.

Infection with the bacterium Helicobacter pylori is associated with altered gastric acid secretion and gastrointestinal disease. Recent work has suggested that N alpha-methylhistamine, produced by the bacterium and acting on histamine receptors in gastric tissue, might be involved. Gastric juice and tissue biopsies from infected patients have been analysed for the presence of N alpha-methylhistamine using a specific and sensitive assay based on gas chromatography mass spectrometry. N alpha-Methylhistamine was detected in five of seven samples of gastric juice from infected patients (5-180 pmol/ml) but was absent in nine uninfected subjects. The compound was not found in fundic and antral biopsies from both subject groups. Helicobacter pylori, cultured on agar and in broth with and without added histamine, was found not to produce detectable levels of N alpha-methylhistamine. Instillation of this compound at 10(-5) mol/l into the gastric lumen produced a significant increase in acid secretion in vivo while plasma gastrin concentration remained unchanged. N alpha-Methylhistamine in gastric juice appears therefore to be associated with infection, although this product is not generated directly by the bacterium. The concentrations found are below those required to affect acid secretion or gastrin production in vivo, although higher local concentrations may exist around a site of infection.

Gas Chromatography-Mass Spectrometry↗
PubMed1999

Gastrointestinal responses to a panel of lectins in rats maintained on total parenteral nutrition.

Total parenteral nutrition (TPN) causes atrophy of gastrointestinal epithelia, so we asked whether lectins that stimulate epithelial proliferation can reverse this effect of TPN. Two lectins stimulate pancreatic proliferation by releasing CCK, so we asked whether lectins that stimulate gastrointestinal proliferation also release hormones that might mediate their effects. Six rats per group received continuous infusion of TPN and a once daily bolus dose of purified lectin (25 mg. rat-1. day-1) or vehicle alone (control group) for 4 days via an intragastric cannula. Proliferation rates were estimated by metaphase arrest, and hormones were measured by RIAs. Phytohemagglutinin (PHA) increased proliferation by 90% in the gastric fundus (P < 0.05), doubled proliferation in the small intestine (P < 0.001), and had a small effect in the midcolon (P < 0.05). Peanut agglutinin (PNA) had a minor trophic effect in the proximal small intestine (P < 0.05) and increased proliferation by 166% in the proximal colon (P < 0.001) and by 40% in the midcolon (P < 0.001). PNA elevated circulating gastrin and CCK by 97 (P < 0.05) and 81% (P < 0.01), respectively, and PHA elevated plasma enteroglucagon by 69% and CCK by 60% (both P < 0.05). Only wheat germ agglutinin increased the release of glucagon-like peptide-1 by 100% (P < 0.05). PHA and PNA consistently reverse the fall in gastrointestinal and pancreatic growth associated with TPN in rats. Both lectins stimulated the release of specific hormones that may have been responsible for the trophic effects. It is suggested that lectins could be used to prevent gastrointestinal atrophy during TPN. Their hormone-releasing effects might be involved.

Animals↗
PubMed1998

Effect of PACAP-27 on 14C-aminopyrine accumulation in isolated rabbit parietal cells.

Pituitary adenylate cyclase-activating polypeptide (PACAP) is present in gastric mucosa, but its direct effect on parietal cells is unknown. We examined this using 14C-aminopyrine uptake in elutriated rabbit cells. PACAP-27 had no effect on basal cells but significantly increased the response to histamine (10(-4) M) at 10(-9) M and to carbachol (10(-4) M) in the presence of ranitidine (10(-4) M) at 10(-7) M and 10(-8) M. PACAP (6-38), an antagonist of PACAP, inhibited the effect of PACAP-27 on carbachol-stimulated cells. Vasoactive intestinal peptide had no significant effect. In conclusion, PACAP-27 has a direct additive effect on stimulated rabbit parietal cells in vitro.

Aminopyrine↗
PubMed1997

How does Helicobacter pylori cause mucosal damage? Its effect on acid and gastrin physiology.

Helicobacter pylori infection increases gastric acid secretion in patients with duodenal ulcers but diminishes acid output in patients with gastric cancer and their relatives. Investigation of the basic mechanisms may show how H. pylori causes different diseases in different persons. Infection of the gastric antrum increases gastrin release. Certain cytokines released in H. pylori gastritis, such as tumor necrosis factor alpha and specific products of H. pylori, such as ammonia, release gastrin from G cells and might be responsible. The infection also diminishes mucosal expression of somatostatin. Exposure of canine D cells to tumor necrosis factor alpha in vitro reproduces this effect. These changes in gastrin and somatostatin increase acid secretion and lead to duodenal ulceration. But the acid response depends on the state of the gastric corpus mucosa. The net effect of corpus gastritis is to decrease acid secretion. Specific products of H. pylori inhibit parietal cells. Also, interleukin 1 beta, which is overexpressed in H. pylori gastritis, inhibits both parietal cells and histamine release from enterochromaffin-like cells. H. pylori also promotes gastric atrophy, leading to loss of parietal cells. Factors such as a high-salt diet and a lack of dietary antioxidants, which also increase corpus gastritis and atrophy, may protect against duodenal ulcers by decreasing acid output. However, the resulting increase of intragastric pH may predispose to gastric cancer by allowing other bacteria to persist and produce carcinogens in the stomach.

Animals↗
PubMed1996

Incidence and possible aetiological factors in the development of pelvic insufficiency fractures following radical radiotherapy.

Five patients out of a total of 183 treated with radical radiotherapy for carcinoma of cervix at The Royal Marsden Hospital from 1991 to 1994 inclusive have developed severe pelvic fractures. Two patients had rheumatoid arthritis, one of whom died as a result of the radiation induced damage. This patient developed radiological evidence of radionecrosis within 1 month of completing radiotherapy. There are very few reports in the literature of such a rapid onset. We suggest that the presence of a connective tissue disorder in a patient with other risk factors such as steroid use, old age and osteopenia should alert the clinician to the risk of radionecrosis following radical irradiation.

Aged↗
PubMed1994

Incidence of second brain tumours after pituitary irradiation in Edinburgh 1962-1990.

Two hundred and ninety-six patients irradiated for pituitary adenoma in Edinburgh between 1962 and 1990 were reviewed. The number of subsequent tumours was noted. The expected incidence of tumours was estimated, based on data from the Scottish Cancer Registry, for an age and sex matched population. One malignant brain tumour was found; the expected incidence was 0.3 (95% CI 0-12). One meningioma was reported. Thirty non-CNS tumours were found, compared with an expected incidence of 17.5 (95% CI 12-26). We see no reason at present to alter our practice as a result of radiation induced neoplasia in this group, although close follow-up continues.

Adenoma↗
PubMed1994

Photodynamic therapy for villous adenomas of the colon and rectum.

Endoscopic thermal laser therapy of colorectal villous adenomas is associated with a high recurrence rate due to incomplete tumor ablation, as treatment over carries a risk of perforation. Photodynamic therapy has been shown to be a promising in the treatment of small malignant tumors, and may be useful for benign adenomas. Eight patients with nine colosigmoid villous adenomas measuring 1-5 cm in length were treated with photodynamic therapy using either haematoporphyrin derivative or Photofrin as photosensitizer and multiple (4-16) applications of interstitial photoirradiation with red light (630 nm, 100 mW x 500 s per application). All but one adenoma had previously been incompletely treated with Nd-YAG laser therapy. Some skin sensitivity to light was seen in one patient. Seven adenomas were eradicated (follow-up 9-56 months, median = 12) as judged by follow-up endoscopy and biopsy. No local complications were seen. Substantial necrosis was produced in the other two adenomas, but they were not completely destroyed, probably due to inadequate light. PDT holds promise in the non-surgical management of villous adenomas, particularly after initial tumour debulking with the Nd-YAG laser.

Adenoma, Villous↗
PubMed1993

An assessment of the clinical usefulness of two serum markers, CA15 3 and HMFG 2 in localized and metastatic breast cancer.

CA 15 3 is a circulating glycoprotein defined by two monoclonal antibodies (115 D 8 and DF 3) with good specificity for breast cancer. Tumour-associated antigens have been detected by the monoclonal antibody HMFG 2 using a low pH ELISA method. We compare the values obtained using these two assays in patients with localized and metastatic breast cancer. CA 15 3 and HMFG 2 levels were measured in 61 patients, 24 localized and 37 metastatic, evaluated by standard biochemical and radiological testing. Of the patients with metastatic disease 78.4 per cent had an elevated CA 15 3 level whereas only 8.3 per cent of patients with localized disease had an elevated level (chi 2 = 28.2 p = 0.001); 29.8 per cent of patients with metastatic disease had elevated HMFG 2 levels while among those with localized disease 16.7 per cent had elevated levels (chi 2 = 0.57 p = NS). We conclude that only CA 15 3 is a useful marker in advanced disease.

Adult↗
PubMed1992

Endometrial carcinoma: does the addition of intracavitary vault caesium to external beam therapy postoperatively result in improved control or increased morbidity?

A retrospective analysis of treatment for endometrial carcinoma is reported here. From 1987 to 1989, 138 patients were referred to the oncology department following total abdominal hysterectomy and bilateral salpingo-oophorectomy for endometrial cancer. Forty-seven patients were not prescribed postoperative radiotherapy; 31 had Stage I well differentiated adenocarcinoma with minimal myometrial invasion, while the remaining 16 patients were considered unfit for postoperative radiotherapy. There were no instances of local relapse amongst the 31 patients with minimal myometrial invasion. The remaining 91 patients all received external beam irradiation to the pelvis and, according to the preference of the individual therapist, 51 were prescribed additional intracavitary vault caesium-137. Patients receiving postoperative radiotherapy were analysed according to whether or not they received additional intracavitary vault caesium. The two groups were also analysed for incidence of vaginal vault recurrence and treatment related morbidity. In the group receiving additional intracavitary treatment more patients had Stage II or III disease (P < 0.05), and had greater depth of myometrial invasion (P < 0.05). Vaginal vault recurrence was not observed in patients receiving intracavitary therapy in addition to external beam therapy. Four patients (10%) receiving external beam therapy alone developed vaginal vault recurrence. The incidence of Kottmeier-Perez grade 2 or 3 bowel toxicity following treatment was significantly higher in those patients receiving combined treatment (18% vs. 2.5%; P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenocarcinoma↗