PubMed Health⌕ Search

Biomedical subjects

A G Howatson

Publications and source records attributed to A G Howatson.

31 records · Page 2Linked to original sources
PubMed1990

Cerebral lymphomas: review of 70 cases.

Seventy cerebral lymphomas from 37 men and 33 women were reviewed and reclassified using the modified Kiel classification. Fifty two of the patients were over the age of 50 years (age range 23-85 years). Only two patients were known to be immune deficient--one case of AIDS and one renal transplant recipient. Necropsies only were performed on 31 cases, biopsies only in 23 cases, and both biopsies and necropsies in 16 cases. Systemic tumour was found in 16 of 47 necropsy cases. All the tumours available for review were classic diffuse non-Hodgkin's lymphomas. Where immunocytological studies were positive, the tumour cells were of B cell origin. None was of T cell origin, although reactive T cells in the tumours were frequently identified. It is concluded from this and other studies that the incidence of intrinsic cerebral lymphomas is increasing.

Adult↗
PubMed1990

Gastric antral vascular ectasia (watermelon stomach)--therapeutic options.

We have encountered five cases of chronic iron deficiency anaemia due to bleeding from gastric antral vascular ectasia (watermelon stomach). Two cases were associated with a lymphoma and in three cases there was evidence of portal hypertension. Two patients were treated conservatively by blood transfusions. The other patients required either surgery or tranexamic acid or endoscopic laser therapy to control the chronic haemorrhage.

Aged↗
PubMed1989

Immunolocalization of alpha interferon in liver disease.

The expression of immunoreactive alpha interferon was examined in 78 liver biopsy specimens using an indirect immunoperoxidase technique. Biopsy specimens included cases of acute viral hepatitis, chronic active hepatitis, primary biliary cirrhosis, alcoholic hepatitis, large bile duct obstruction and normal liver. Kupffer cells were positive for alpha interferon in all cases. Hepatocytes were negative for alpha interferon in normal liver but in acute viral hepatitis were positive in perivenular and necrotic areas. Hepatocytes were positive in periportal areas, associated with piecemeal necrosis, in chronic active hepatitis and primary biliary cirrhosis, and were positive in perivenular areas in alcoholic hepatitis and large bile duct obstruction. The unexpected finding of alpha interferon in hepatocytes in non-viral liver disease indicates that the presence of this substance in liver cells cannot be taken as a specific marker of viral infection.

Biomarkers↗
PubMed1988

Localization of alpha-interferon in the human feto-placental unit.

The distribution of alpha-interferon in human placental tissue was investigated by immunocytochemical study of paraffin wax-embedded tissue sections using a sheep alpha-interferon antiserum. Fifty-eight placentas of gestational ages from 8 to 40 weeks were examined. alpha-Interferon was present in the syncytiotrophoblast of the chorionic villi of all placentas and was also in macrophages in 28 cases. The appearances suggest production of interferon in human placental trophoblast and, in view of its diverse biological effects, support the concept of a role for alpha-interferon in the complex series of events required for successful gestation.

Chorionic Villi↗
PubMed1987

Pancreatic carcinogenesis: effect of secretin in the hamster- nitrosamine model.

The effect of exogenous secretin on pancreatic carcinogenesis in WO strain hamsters has been examined in the nitrosamine-ductular adenocarcinoma model. Secretin, 20 clinical U/kg, stimulated a maximal secretory response of pancreatic juice and bicarbonate when given iv. The same dose given sc for 6 weeks had no significant effect on pancreatic wet weight and DNA or RNA contents. However, when given to animals receiving N-nitrosobis(2-oxopropyl)amine [(BOP) CAS: 60599-38-4] (5 mg/kg), it reduced the latency and increased the induction rate of tumor development when compared with the carcinogen given alone to animals (secretin + BOP, 15 of 17 animals with tumors; BOP alone, 4 of 13 with tumors at 15 wk; P less than .002). These effects are consistent with secretin acting as a cocarcinogen in this model of pancreatic carcinogenesis.

Adenocarcinoma↗
PubMed1985

Pancreatic carcinogenesis-enhancement by cholecystokinin in the hamster-nitrosamine model.

The role of the pancreaticotrophic hormone cholecystokinin (CCK) in modifying the pancreatic response to carcinogen has been examined in the hamster-nitrosamine pancreatic cancer model. Exogenous CCK, 30 IDU kg-1, stimulated a maximal pancreatic secretory response when given intravenously and caused hypertrophy and hyperplasia of the pancreas when given subcutaneously over a period of 6 weeks (pancreatic wet weight, mg per 100 g body weight, controls 295.6 +/- 61; CCK treated 466.4 +/- 77, P less than 0.001). When the same dose of CCK was given to animals receiving N-nitrosobis (2-oxopropyl)amine (BOP; 5 mg kg-1 weekly) there was a reduction in latency period and increase in induction rate of tumour development (CCK + BOP vs. BOP alone, 12 animals with tumours vs. 2 at 15 weeks; P less than 0.02). These effects are consistent with CCK acting as a co-carcinogen or promoter of pancreatic carcinogenesis in this model.

Adenocarcinoma↗
PubMed1980

TNM (1978) in bladder cancer: use and abuse.

Modifications to the TNM classification for bladder cancer, introduced in 1979, are described. The use of this classification was evaluated in 106 new patients. It proved to be satisfactory for in situ and papillary tumours but major problems occurred in attempting to separate superficially invasive from deeply invasive tumours. Several aspects of this classification require further consideration and modifications are proposed.

Humans↗
PubMedDate not supplied

Placental synthesis of oestriol in Down's syndrome pregnancies.

In the second trimester, oestriol is synthesized in the placenta and secreted into the maternal circulation. 16alpha-hydroxy dehydroepiandrosterone sulphate (16alpha-OH-DHEAS) is formed in the fetal liver by hydroxylation of dehydroepiandrosterone sulphate (DHEAS) and transported to the placenta where it undergoes desulphation by steroid sulphatase (STS) and aromatization to oestriol. Maternal serum levels of unconjugated oestriol (UE3) are lower in Down's syndrome pregnancies than in unaffected pregnancies in the second trimester. The underlying cause of this variation was investigated in placenta, fetal liver, maternal serum and amniotic fluid from Down's syndrome pregnancies by measuring the levels of UE3, DHEAS and STS in appropriate tissues and in corresponding samples from unaffected pregnancies. UE3 levels, expressed as multiples of the control median at the appropriate gestation (MOM), were lower in placental tissue (0.52 MOM), maternal serum (0.65 MOM) and amniotic fluid (0.61 MOM) than in unaffected pregnancies. There was a significant correlation between placental and maternal serum levels of UE3 in the Down's syndrome cases. The median STS activity in placental tissue from Down's syndrome pregnancies (1.14 MOM) was not significantly different from that of the control pregnancies (1. 01 MOM), suggesting that placental turnover of the fetal precursor DHEAS is not reduced. However, levels of DHEAS were reduced in maternal serum (0.69 MOM), placental tissue (0.54 MOM) and fetal liver (0.65 MOM) from Down's syndrome pregnancies. Thus, a diminished supply of the fetal precursor DHEAS may be the cause of the decreased placental production of UE3 in Down's syndrome pregnancies in the second trimester.

Arylsulfatases↗
PubMedDate not supplied

Placental and maternal serum inhibin-A and activin-A levels in Down's syndrome pregnancies.

The objective of this study was to analyse the levels of inhibin-A and activin-A in maternal serum and placental tissue from Down's syndrome (DS) pregnancies. Inhibin-A and activin-A levels were determined by specific immunoassays and individual results were expressed as multiples of the control median (MoM) at the appropriate gestation. Immunohistochemistry was used to localize inhibin alpha and beta(A)-subunits in a selection of placental sections. In DS pregnancies, median inhibin-A levels were found to be significantly elevated to 1.46 MoM (P< 0.05) in placental extracts, and 2.06 MoM (P< 0.0001) in maternal serum, when compared with uncomplicated pregnancies. Median activin-A MoMs were also elevated in placental extracts and maternal serum to 1.62 MoM (P< 0.01), and 1.26 MoM (P< 0.05), respectively. Immunohistochemistry revealed that the alpha subunit of inhibin-A and the beta(A)subunit of inhibin-A and activin-A were mainly localized to the trophoblastic layer of placental villi. Semiquantitative studies of staining intensity revealed a trend towards stronger staining of placental trophoblasts and stroma of DS tissues, although this was statistically significant only for beta(A)subunit staining of trophoblasts (P< 0.05). These results support the hypothesis that maternal serum levels of inhibin-A and activin-A are elevated due to increased production in the placenta, and increased immunostaining of trophoblasts suggests that this may be due to increased production in the trophoblasts.

Activins↗