No abstract

Mycobacterial cell wall-DNA complex has shown antineoplastic activity in patients with bladder cancer with less toxicity than that associated with bacillus Calmette-Guerin administration. The tolerance and efficacy of mycobacterial cell wall-DNA complex might hold promise for the treatment of carcinoma in situ of the bladder.

Objective-To examine the use of balloon angioplasty in the treatment of native adult aortic coarctation.Design-Haemodynamic and angiographic studies to establish the diagnosis of aortic coarctation were established before carrying out the procedure in all patients.Setting-All the studies and angiographic procedures were performed in a large district general hospital within the departments of cardiology and radiology. There was careful perioperative monitoring. The mean hospital stay was three days.Patients-15 adult patients (with clinical, haemodynamic, and angiographic evidence of native aortic coarctation) were considered for this treatment. 13 were offered balloon angioplasty. One was excluded, as there was no significant gradient across the lesion. One patient had complete atresia at the site of the coarctation.Interventions--Percutaneous transluminal balloon angioplasty was carried out with balloon catheters diameter 2 mm less than the diameter of the aorta immediately below the left subclavian artery to minimise the possibility of tearing the aortic wall.Main outcome measures-Abolition or significant reduction of the preoperative gradient was achieved in all 13 patients treated. shed work suggests that the older the child at angioplasty the less is the likelihood of restenosis, and in one adult series of eight cases, the results at one year follow up were good (0% restenosis).2 We describe our experience with 15 adults. This is the first series reported by a British centre. Patients and methodsBetween March 1987 and March 1991 angiography with a view to angioplasty was performed on 15 patients (10 men and five women) with native aortic coarctation. The age range was 16 to 60 (mean 35 53) years. The first five patients underwent diagnostic catheterisation with angioplasty as a separate procedure, whereas we offered our last 10 patients angiography and angioplasty as a combined procedure.Eleven (73%) of the 15 patients presented with hypertension, one (6-6%) with breathlessness, one (6-6%) with a possible hypoplastic

We have demonstrated for the first time that a conditioned medium from a human cell strain can induce morphologically mature mast cells that express Fc epsilon RI and three mast cell-specific proteases from normal bone marrow progenitor cells. In contrast, recombinant human Kit ligand induced the differentiation of mast cells that were tryptase-positive but negative for chymase, carboxypeptidase, and Fc epsilon RI. This data indicates that factors other than Kit ligand are critical for inducing the differentiation and maturation of mast cells in the human. The HBM-M cell was originally derived from a patient with mastocytosis. As mastocytosis is thought to represent a reactive hyperplasia rather than a mast cell malignancy, the factor secreted by the HBM-M cell strain could well be responsible for the mast cell hyperplasia seen in some patients with mastocytosis.

The most common abnormality of the platelets in 43 patients with a variety of myeloproliferative syndromes was impaired or absent aggregation when stimulated with collagen and adrenaline. Eight unselected cases studied in more detail showed a normal prostaglandin synthesis pathway as evidenced by normal aggregation with arachidonic acid and the production of normal amounts of malonyldialdehyde. Mixing experiments with aspirin-tested platelets showed correction of the abnormal adrenaline and collagen responses and confirmed that the nature of the defect was different from that induced by aspirin. Stimulation of "myeloproliferative" platelets with thrombin after blocking the prostaglandin pathway with aspirin resulted in reduced aggregation, indicating either a deficiency of the storage pool of adenine nucleotides in the platelets or an abnormality of a membrane receptor for thrombin.