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Biomedical subjects

T R Terry

Publications and source records attributed to T R Terry.

12 recordsLinked to original sources
PubMed1995

UK studies on suramin therapy in hormone resistant prostate cancer.

New insights regarding the biology of hormone resistant CaP have shown that major growth factors other than testosterone are responsible for cellular proliferation of androgen resistant prostate cancer cells. In vitro studies have confirmed the efficacy of growth factor inhibitors such as suramin in reducing cellular proliferation of androgen dependent LNCaP and independent PC-3 CaP cell lines as well as CaP cells obtained by primary culture. Initial clinical trials using high dose suramin (peak serum concentration 250-300 micrograms/ml) as monotherapy in patients with hormone resistant CaP have shown some promise, but the duration of response to therapy has been short lived and suramin toxicity is a problem. To minimize toxicity without reducing anti-tumour activity, studies evaluating its use in combination with other cytotoxic drugs are attractive in CaP. Suramin and doxorubicin, tumour necrosis factor and EMP have shown synergy in vitro. However, in a phase II clinical trial using combination therapy with low dose suramin (140 micrograms/ml) and mitomycin C in 32 patients, there was one complete response and six partial responses, and in 15 patients, the disease had stabilized. The median time to treatment failure was 103 days, and the median survival was 209 days. This regimen caused significant toxicities. The present study has shown that the combination of EMP 280 mg twice a day and suramin 1 g weekly infusions for 6 weeks, compared to EMP 280 mg alone, showed a statistically significant difference in the rate of depression of PSA levels after 3 and 6 months of treatment (p < 0.01) and a statistically significant reduction in bone pain and requirement for analgesics in patients on combination therapy-100% compared to 0% for patients on EMP alone.

Aged↗
PubMed1993

Percutaneous nephrostomies.

A review was made of 127 percutaneous nephrostomies (PCN) in 106 patients with benign (74 patients) and malignant (32 patients) urinary tract obstruction. Data on underlying aetiology, complications, subsequent management and long-term management are presented. The study confirms that PCN is an effective and safe method of providing temporary or prolonged urinary diversion in obstruction. Its use in pelvic malignancy should be determined by the likelihood of obtaining worthwhile prolonged palliation in individual patients.

Adolescent↗
PubMed1987

Intraduct enterokinase is lethal in rats with experimental bile-salt pancreatitis.

Controlled intraduct infusion and peri-acinar dispersal of 100 microliter buffer containing sodium glycodeoxycholate (GDOC) at concentrations of 8.5, 17 and 34 mmol/l in rats caused a progressively severe acute pancreatitis from which none of the animals died over the experimental period. Infusion of affinity-purified active human enterokinase in buffer did not cause pancreatitis, presumably because of the inability of the macromolecule to gain access to its specific intracellular substrate trypsinogens. The addition of enterokinase 200 ng to GDOC 34 mmol/l in the infusate resulted in a severe systemic disturbance and a form of acute necrotizing pancreatitis which was uniformly and rapidly lethal. This effect was not seen when equimolar trypsin was substituted for enterokinase. These findings show that enterokinase specifically increases the lethality of experimental bile salt pancreatitis and suggest that this bile-borne enzyme may in some cases pose a significant clinical threat.

Acute Disease↗
PubMed1986

Small bowel ulceration in patients receiving non-steroidal anti-inflammatory drugs for rheumatoid arthritis.

Evidence is presented for a non-specific ulcerative process in the small bowel of patients with rheumatoid arthritis. All three cases presented with lower gastrointestinal bleeding; on withdrawal of non-steroidal anti-inflammatory drugs no further bleeding occurred. Non-steroidal anti-inflammatory drugs may lead to small bowel ulceration in inhibiting mucosal glycoprotein synthesis and increasing intestinal permeability.

Aged↗
PubMed1985

The generation of lysolecithin by enterokinase in trypsinogen prophospholipase A2 lecithin mixtures, and its relevance to the pathogenesis of acute necrotising pancreatitis.

The cascade enterokinase-trypsinogen-prophospholipase A2 lecithin, generating trypsin, phospholipase A2 and lysolecithin, respectively, was studied in vitro using a novel phospholipase A2 assay. The rate of enterokinase catalysed activation of trypsinogen was maximal at 4 mmol/1 glycodeoxycholic acid; higher concentrations of bile salt progressively inhibited enterokinase activity. Net phospholipase A2 activity in reaction mixtures was critically dependent on the trypsin/prophospholipase A2 molar ratio. Lecithin hydrolysis by phospholipase A2 was dependent on the bile salt/lecithin molar ratio and was optimal at 1.25 to 1. The addition of enterokinase to lecithin and bile salt mixtures, containing trypsinogen and prophospholipase A2 at presumed pathophysiological concentrations, resulted in the generation of concentrations of lysolecithin lytic for pancreatic acinar cells within 5 min. These findings would support the concept that the entry of bile containing active enterokinase into the pancreatic duct system in vivo may in some cases be involved in the initiation of necrotising acute pancreatitis in man.

Acute Disease↗
PubMed1983

Biliary excretion of enterokinase in rats: studies in alcoholic rats with fatty liver.

Ethanol-associated fatty liver was induced in rats fed a nutritionally deficient liquid diet containing 36% of total calories as ethanol. Control rats received the same diet with sucrose substituted isocalorically for ethanol. After 40 days, hepatic lipid content of the ethanol-maintained animals was four-fold greater than controls and ultrastructural changes in hepatocytes were well established. Clearance of intravenously administered human enterokinase from the circulation as well as bile flow were, however, the same in both groups. The proportion of enterokinase appearing in catalytically active form in bile after intravenous injection was substantially greater in the ethanol-maintained animals than the isocaloric controls; the difference was highly significant (p less than 0.001) and reached two- to four-fold after 70 days on the diet. These findings would suggest that the ability of hepatocytes to degrade enterokinase cleared from the blood may be bypassed or impaired by prolonged ethanol consumption and a deficient diet. Catalytically active enterokinase in bile may participate in the development of some types of acute necrotising pancreatitis.

Animals↗