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Biomedical subjects

R Otter

Publications and source records attributed to R Otter.

At least 37 records · Page 2Linked to original sources
PubMed1997

Accuracy and completeness of the registration of childhood leukaemia in The Netherlands, 1989-1992.

In the Netherlands, childhood leukaemia is recorded by the Dutch Childhood Leukaemia Study Group (DCLSG, set up in 1972) and by nine regional cancer registries which together form the Netherlands Cancer Registry (NCR, set up in 1989). The data files from the incidence years 1989-1992 of the two registries were linked in order to evaluate accuracy and completeness and to calculate and equalise the incidence rates for childhood leukaemia in The Netherlands. Unlinked records or records with disagreements (birth date, sex, type of leukaemia and incidence date) were checked by the DCLSG and by the regional cancer registries. The DCLSG recorded 431 cases of childhood leukaemia, while the NCR recorded 434 cases. After record linkage and review of the cases, it was concluded the 445 records should have been recorded as childhood leukaemia. The NCR had recorded 425 of the 445 correct cases (95.5%), but had missed 20 cases (4.5%). The DCLSG had recorded 431 of the 445 correct cases (96.9%) and had missed 14 cases (3.1%). In addition, the NCR had recorded 9 cases incorrectly as childhood leukaemia. Part of the disagreement was caused by differences in coding rules (definition of non-Hodgkin's lymphoma (NHL) and the myelodysplastic syndrome versus leukaemia). It could be concluded that the quality and completeness of the two registries was very high. Regular comparison of the recorded data will help to reveal the inherently problematic disagreement between definitions and coding.

Adolescent↗
PubMed1997

Distressed or relieved? Psychological side effects of breast cancer screening in The Netherlands.

STUDY OBJECTIVES: To assess the psychological impact of mammographic screening on women with non-malignant outcomes after attending the Netherlands' National Breast Cancer Screening Programme. DESIGN: During one year all women with false positive test results (95) in a screening area were invited for the study. Each false positive was matched with two women with normal mammograms with respect to age and municipality. A random reference group of 400 was drawn from the female population in an area not yet included in the screening programme. Experiences with screening and psychological status of subjects were assessed 8-10 weeks after screening (T1) and again after six months (T2), by interviews as well as questionnaires. References completed two questionnaires with a six months' interval. PARTICIPANTS: 74 (78%) women with false positive outcomes and 113 (59%) women with negative outcomes participated at T1, of these 65 (88%) and 105 (93%) at T2, respectively; 238 references returned questionnaires at T1 (59%), of these 143 (60%) at T2. MAIN RESULTS: At 8-10 weeks after the screening, the women who received false positive test results scored higher on most of the variables indicating psychological disfunctioning than women with normal mammograms, but did not notably differ on the same variables from the non-screened reference group. Women with normal mammograms had the lowest scores on all the variables in the study at both assessments. The same situation was observed six months later. Although 61% of the women who received false positive mammograms reported that they had experienced the "false alarm" as a stressful event, this experience had apparently no adverse effects on their psychological functioning, as assessed 8-10 weeks after screening. CONCLUSIONS: Overall, breast screening is not likely to generate adverse psychological effects in "healthy" women, even if the outcome is false positive. Differences in psychological functioning between false positives and negatives are more likely ascribable to feelings of relief in the negative group than to raised anxiety and distress in the false positive group.

Aged↗
PubMed1994

Molecular characterization of human and bovine endothelin converting enzyme (ECE-1).

A membrane-bound protease activity that specifically converts Big endothelin-1 has been purified from bovine endothelial cells (FBHE). The enzyme was cleaved with trypsin and the peptide sequencing analysis confirmed it to be a zinc chelating metalloprotease containing the typical HEXXH (HELTH) motif. RT-PCR and cDNA screens were employed to isolate the complete cDNAs of the bovine and human enzymes. This human metalloprotease was expressed heterologously in cell culture and oocytes. The catalytic activity of the recombinant enzyme is the same as that determined for the natural enzyme. The data suggest that the characterized enzyme represents the functional human endothelin converting enzyme ECE-1.

Amino Acid Sequence↗
PubMed1994

Risk of endometrial cancer after tamoxifen treatment of breast cancer.

Since large trials have been set up to assess whether tamoxifen decreases the risk of breast cancer in healthy women, it has become important to investigate the drug's potential adverse effects, including occurrence of endometrial cancer. We undertook a case-control study in the Netherlands to assess the effect of tamoxifen on the risk of endometrial cancer after breast cancer. Through the population-based Netherlands Cancer Registry and two older, hospital-based, registries, we identified 98 patients who had endometrial cancer diagnosed at least 3 months after a diagnosis of primary breast cancer. Detailed information about treatment was obtained for all these patients, and for 285 controls, who were matched to the cases for age, year of breast cancer diagnosis, and survival time with intact uterus. Tamoxifen had been used by 24% of patients with subsequent endometrial cancer and 20% of controls (relative risk 1.3 [95% CI 0.7-2.4]). Women who had used tamoxifen for more than 2 years had a 2.3 (0.9-5.9) times greater risk of endometrial cancer than never users. There was a significant trend of increasing risk of endometrial cancer with duration of tamoxifen use (p = 0.049), and also with cumulative dose (p = 0.046). The duration-response trends were similar with daily doses of 40 mg or 30 mg and less. These findings support the hypothesis that tamoxifen use increases the risk of endometrial cancer. This oestrogenic effect on the endometrium was not related to the dose intensity. Physicians should be aware of the higher risk of endometrial cancer in tamoxifen users.

Aged↗
PubMed1989

Alterations in the protein-synthesis, -degradation and/or -secretion rates in hepatic subcellular fractions of selenium-deficient mice.

Single mouse livers were subfractionated by differential centrifugation and isopycnic centrifugation on sucrose or metrizamide gradients and separated into subcellular compartments. The fractionation procedure was highly reproducible and yielded essentially similar results in different preparations of livers from selenium-adequate (Se+) and selenium-deficient (Se-) mice that were fed on a Torula-yeast-based diet containing less than 10 parts per 10(9) of selenium for at least 16 weeks. Mice of both dietary groups were injected intraperitoneally with 370 kBq of L-[U-14C]leucine, and 48 h later 1.85 MBq of L-[4,5-3H]leucine was injected intraportally. After another 1 h, the livers were removed and subjected to subcellular fractionation. Incorporation of the 3H label into proteins of the subcellular fractions was taken as a measure of relative protein-synthesis rate. The ratio of the 3H to the 14C protein-bound label of the same fractions was used as an estimate of relative protein-degradation and/or -secretion rate. The results showed a statistically significant 180% increase in protein-synthesis rate in the endoplasmic reticulum and a 80% increase in relative protein-degradation and/or -secretion rate in the same compartment. A significant decrease in the 3H/14C ratio, by 40 and 30% respectively, was observed in the Golgi fraction and in liver homogenate. The observed changes suggest a highly regulated hepatic response to selenium deficiency.

Animals↗
PubMed1989

Subcellular distribution of selenium in deficient mouse liver.

Selenium (Se)-deficient mice were labelled in vivo with single pulses of [75Se]selenite, and the intrahepatic distribution of the trace element was studied by subcellular fractionation. At 1 h after intraperitoneal injection of 3.3 or 10 micrograms of Se/kg body weight, 15% of the respective doses were found in the liver. Accumulation in the subcellular fractions followed the order: Golgi vesicular much greater than lysosomal greater than cytosolic = microsomal greater than mitochondrial, peroxisomal, nuclear and plasma-membrane fraction. At a dose of 3.3 micrograms/kg, more than 90% of the hepatic Se was protein-bound. When cross-contamination was accounted for, the following specific Se contents of the subcellular compartments were extrapolated: Golgi apparatus, 7.50 pmol/mg; cytosol, 0.90 pmol/mg; endoplasmic reticulum, 0.80 pmol/mg; mitochondria, 0.49 pmol/mg; nuclei, lysosomes, peroxisomes and plasma membrane, less than 0.4 pmol/mg. At 10 micrograms/kg, a roughly 2-3-fold increase in Se content of all fractions was found without major changes in the intrahepatic distribution pattern. An extraordinary rise in the cytosolic fraction was due to an apparently non-protein-bound Se pool. At 24 h after dosing, total hepatic Se had decreased to 6% of the initial dose and had become predominantly protein-bound. The 60% decrease in hepatic Se was reflected in a similar fall in the subcellular levels of the trace element. The Golgi apparatus still had the highest specific Se content, although accumulation was 5 times less than that after 1 h. The cytosolic pool accounted for 50% of the hepatic Se at both labelling times. After 1 h the Golgi apparatus was, with 19%, the second largest intrahepatic pool, followed by the endoplasmic reticulum with 16%. The high affinity and fast response of the Golgi apparatus to Se supplementation of deficient mice is interpreted in terms of a predominant function of this cell compartment in the processing and the export of Se-proteins from the liver.

Animals↗
PubMed1989

Primary extranodal and nodal non-Hodgkin's lymphoma. A survey of a population-based registry.

In a population-based registry, there were 580 patients with non-Hodgkin's lymphoma (NHL); 236 had primary extranodal lymphoma (41%). The initial localization of the primary extranodal lymphomas varied markedly, although 36% were primary gastrointestinal lymphomas. Histological classification was performed by a regional panel of pathologists according to the Kiel Classification and the International Working Formulation. Twelve per cent of the patients with nodal NHL had a localized disease in contrast to 40% with primary extranodal NHL. Low grade lymphomas were encountered in 30 and 10% of the patients with primary nodal and extranodal NHL, respectively. Recurrence-free survival rate for patients with localized low-grade malignancy and disseminated intermediate grade NHL is significantly better for extranodal lymphoma than for nodal NHL. Patients with disseminated high-grade extranodal NHL had the worst prognosis of all. We conclude that primary nodal and primary extranodal lymphomas should be considered as distinctive and separate entities.

Adolescent↗
PubMed1989

Primary gastrointestinal non-Hodgkin's lymphoma in a population-based registry.

In a population-based registry of 580 patients with non-Hodgkin's lymphoma (NHL) 54 patients had a primary gastric lymphoma, 42 an intestinal, 113 a primary extranodal lymphoma localised elsewhere than in the gastrointestinal tract and 371 a primary nodal NHL. Histological specimens were reviewed by a panel of pathologists and classified according to the Kiel classification and the International Working Formulation. The 4-year survival rates for primary gastric, intestinal, other extranodal and nodal NHL ranged from 50 to 60%; the 4-year recurrence-free survival rates were 50%, 35%, 19% and 19%, respectively. Among patients with localised intermediate-grade disease survival for those with gastric NHL was better than for those with intestinal lymphoma. Because it is population-based, our study cohort was not subjected to exclusion due to age, performance scale, etc. and therefore provides a more realistic picture of the occurrence and presentation of as well as prognosis for lymphoma in the population.

Adult↗
PubMed1989

Malignant lymphoma of the gastrointestinal tract and mesentery. A clinico-pathologic study of the significance of histologic classification. NHL Study Group of the Comprehensive Cancer Center West.

A series of 92 malignant lymphomas of the gastrointestinal tract and mesentery obtained from a population-based registry was studied to assess whether the newly defined concept of mucosa-associated lymphoma has clinical relevance. The cases were grouped according to localization; gastric, intestinal, and mesenteric lymphoma. All cases were reviewed histologically, graded according to the Working Formulation, and reclassified according to the Kiel classification, which was modified to include the categories low- and high-grade mucosa-associated lymphoma. Clinical data, as well as staging and follow-up data, were related to both the original diagnosis and the diagnosis after reclassification. The results showed that the distribution of the types of lymphoma is related to site: centroblastic lymphoma was predominant in the stomach, lymphoblastic in the bowel, and follicular centroblastic-centrocytic in the mesentery. Gastrointestinal lymphoma was disseminated in approximately 50% of the patients at presentation. Survival analysis revealed that classification according to the original Kiel classification and grading according to the Working Formulation provided important prognostic information, whereas introduction of mucosa-associated lymphoma as an entity did not. It was concluded that modification of current classifications to include a separate category for mucosa-associated lymphoma is not useful.

Gastrointestinal Neoplasms↗
PubMed1987

Alterations in the intermediary metabolism of selenium-deficient mice.

Male albino mice were pair-fed a torula yeast-based selenium-deficient (Se-) diet containing 10 ppb selenium for 4 months, while a control group (Se+) received a similar diet supplemented with 330 ppb selenium as Na2SeO3. In addition to previously observed modulations of drug-metabolizing enzymes (Reiter, R. and Wendel, A. (1985) Biochem. Pharmacol. 34, 2287-2290), an increase of 6-phosphogluconate dehydrogenase activity and succinate dehydrogenase activity in liver by about 60% was found. In vivo, an increased 14CO2 exhalation from a tracer dose of glucose either labeled in the C-1- or C-6 position was observed in selenium-deficient mice. However, no difference in the total CO2 exhalation of Se(-)- as compared to Se+-mice was detectable. In line with the assumption that Se(-)-mice have an increased glucose turnover, Se(-)-mice exhibited a greater glucose tolerance when treated with an oral glucose load of 2.5 mg glucose/kg body weight. Also, the Se(-)-mice had a lower blood glucose level as compared to Se+-controls (89 +/- 3 versus 110 +/- 12 mg glucose/100 ml blood). Further in vitro experiments with red blood cells from Se(-)-mice showed that erythrocytes did not contribute to an increased CO2 formation from glucose via the pentose phosphate shunt. No significant differences between Se(-)- and Se+-animals were found in the profile of urinary metabolites, including ketone bodies and nitrogen excretion. These findings suggest a hitherto unknown involvement of selenium in specific regulatory sites of intermediary metabolism.

Animals↗
PubMed1987

Biological efficacy of partial hepatectomy and hepatopoietin in long-term selenium-deficient mice.

After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.

Animals↗
PubMed1986

Increased proliferative activity in selenium-deficient mouse liver.

Male albino NMRI mice were fed a selenium-deficient (Se-), torula yeast-based diet containing less than 10 ppb Se for at least 2 months (Se-) while a control group received the same diet supplemented (Se+) with 330 ppb Se as Na2SeO3. The Se-(-)animals showed multiple enzyme modulations of liver enzyme activities indicating that they were in a severely Se- state. No significant difference in the basic DNA synthesis rate of Se-(-)animals compared to Se+ controls was measured. However, when liver cell proliferation was induced by either hepatopoietin pretreatment or by partial hepatectomy, an about 3-fold increase in DNA replication rates was found in Se- compared to controls. We conclude that the enhanced proliferative activity in Se- mouse liver is expressed in an emergency situation.

Animals↗
PubMed1984

A novel biologically active seleno-organic compound--II. Activity of PZ 51 in relation to glutathione peroxidase.

The anti-inflammatory compound 2-phenyl-1,2-benzoisoselenazol-3(2H)-on (PZ 51) catalysed GSSG formation from GSH in the presence of hydroperoxides in an NADPH/GSSG reductase system with the following rates (delta log GSH/min per molar selenium): 1.1 X 10(6) with H2O2, 1.2 X 10(6) with butylhydroperoxide, 1.7 X 10(6) with cumenehydroperoxide. The reaction catalysed by the sulphur analogue of PZ 51 was negligible. Similar results were obtained in a direct assay of GSH-Px activity based on GSH estimation by dithionitrobenzoate. The activation energy of the reaction was determined as 55 kJ/mol . deg in the presence of 30 mumol/1 PZ 51 compared to 36.5 kJ/mol . deg obtained in the presence of 1 nmol/1 pure GSH-Px isolated from bovine red blood cells. In mouse liver microsomes, NADPH-dependent aminopyrine dealkylation was totally inhibited in the presence of 50 mumol/1 PZ 51. In vivo experiments with Se-deficient mice showed that the Se-moiety of PZ 51 is not available for the synthesis of the selenoenzyme GSH-Px after dietary treatment or i.p. doses up to 25 mg Se as PZ 51 per kg body wt. After oral administration of labelled PZ 51, unlike with selenite, no radioactivity was incorporated into GSH-Px within 48 hr. The data suggest that several similarities between PZ 51 and the active site of GSH-Px exist, resulting in the capability of the compound to catalyse the GSH-Px reaction. An extracellular pharmacodynamic action of the drug seems likely.

Animals↗