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This study has investigated the potential of environmental electron microscopy techniques for studying the structure of polymer-based electronic devices. Polymer blend systems composed of F8BT and PFB were examined. Excellent contrast, both topographical and compositional, can be achieved using both conventional environmental scanning electron microscopy (ESEM) and a transmission detector giving an environmental scanning transmission electron microscope (ESTEM) configuration. Controllable charging effects present in the ESEM were observed, giving rise to a novel voltage contrast. This shows the potential of such contrast to provide excellent images of phase structure and charge distributions.

The development of environmental scanning electron microscopy has opened the way for the examination of a wide variety of new sample types that were previously inaccessible to conventional scanning electron microscope techniques. With the advent of such a new methodology comes also the potential for new contrast mechanisms. We investigated the use of environmental scanning electron microscopy on semiconducting organic polymer materials. We observed contrast from these materials in secondary electron images, this contrast being attributed to differences in electron yield due to the polymer's electronic structure. Further study of these materials, and specifically the influence of film thickness on signal, has indicated a significant effect as the secondary electrons move through the sample. Systematic studies such as these are needed for a full understanding of the relationship between electronic properties and signal and, hence, the ability to probe structure-property relationships in greater depth.

1. Electrical field stimulation (EFS) (1-10 Hz, 30 V, 2 ms) of frog oesophageal body strips resulted in frequency-dependent non-adrenergic, non-cholinergic (NANC) relaxations. 2. Tetrodotoxin (TTX) (10(-6)-10(-5) M) had no effect on EFS evoked relaxations with a 2 ms pulse width. At a pulse width of 0.5 ms only the responses to the highest frequency (10 Hz) were significantly inhibited by TTX at 10(-5) M. Relaxation at 2 ms pulse width were unaffected by omega-conotoxin (10(-6) M), nifedipine (10(-6) M) or cobalt (5 x 10(-4) M). 3. NG-nitro-L-arginine (L-NOARG) (10(-6)-10(-4) M), a nitric oxide synthase (NOS) inhibitor, caused a concentration-dependent inhibition of the EFS-induced NANC relaxant responses. The inhibitory effect of L-NOARG was both prevented and reversed by L-arginine but not D-arginine (5 x 10(-3) M). 4. The phosphodiester type V inhibitor (PDE V), SK&F 96231 (10(-7)-10(-4) M), caused a concentration-dependent potentiation of both the percentage relaxation and the duration of the relaxant responses to EFS. 5. ODQ (10(-7)-10(-5) M), a guanylate cyclase inhibitor, produced a concentration-dependent inhibition of EFS-evoked NANC relaxations. 6. Oxyhaemoglobin (10(-6) M), which binds nitric oxide (NO), inhibited NANC relaxations to EFS. 7. The NO donor sodium nitroprusside (SNP) (10(-8)-10(-4) M) produced a concentration-dependent inhibition of evoked tone. L-NOARG (10(-4) M) had no effect on the SNP evoked relaxations. Preincubation with oxyhaemoglobin (10(-6) M) caused a reduction in the SNP (10(-6)-10(-5) M) induced relaxations. 8. These results suggest NO is the relaxant transmitter of the frog oesophageal body and the source of NO may be non-neuronal.

1. The effects of NG-nitro-L-arginine (L-NOARG), a nitric oxide synthase inhibitor, and SK&F 96231, a phosphodiesterase type V inhibitor, on electrical field stimulated (EFS) nonadrenergic noncholinergic (NANC) relaxations of rat fundal strips, guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus, and guinea-pig taenia caeci were investigated. 2. Reproducible repeated control random EFS frequency-response curves were obtained for all three tissues. 3. Depending on the frequency of stimulation, L-NOARG (10(-4)-5 x 10(-3) M) caused either a complete or partial inhibition of the NANC-induced relaxations of the rat fundal strips and the guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus, but not of the guinea-pig taenia caeci. The inhibitory action of L-NOARG was partially or totally reversed, depending on the tissue, by L-arginine (5 x 10(-3) M). 4. SK&F 96231 (10(-6)-10(-4) M) caused a concentration- and frequency-dependent potentiation of both the size and duration of the EFS-induced NANC relaxant response of rat fundal strips and guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus, but not of the guinea-pig taenia caeci. 5. Zaprinast, another phosphodiesterase type V inhibitor (10(-6)-10(-4) M) caused a concentration- and frequency-dependent potentiation of the NANC relaxant responses to EFS of rat fundal strips. 6. SK&F 96231 and zaprinast alone (10(-6)-10(-4) M) caused a concentration-dependent relaxation of the agonist-induced tone of all three tissues with the maximum degree of relaxation found to be in the order stomach < ileum < caecum. This is the reverse order for ability of SK&F 96231 to potentiate relaxant responses to EFS. 7. These results suggest NO is involved in the NANC nerve-mediated relaxation of rat fundal strips and guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus, but not the guinea-pig taenia caeci.

Thyroxine replacement dose in 70 patients with post-radioiodine (for Graves' thyrotoxicosis) hypothyroidism was compared with that in 34 patients with autoimmune hypothyroidism matched for age and sex and diagnosed during the same period. Median replacement dose in the post-radioiodine group (100 micrograms daily) was significantly lower (P = 0.006) than in the autoimmune hypothyroid group (137.5 micrograms daily). Furthermore there was marked variation in the time elapsing from onset of post-radioiodine hypothyroidism to achievement of a given maintenance dose. These findings may be explained by persistence of non-TSH mediated thyroid function, after radioiodine therapy for Graves' thyrotoxicosis. The observations indicate the potential risk of overtreatment with thyroxine in post-radioiodine hypothyroidism unless the dose is carefully titrated against serum TSH levels. Final thyroxine requirements may not be evident in the initial phase of treatment and patients with apparently low maintenance thyroxine requirements require long-term follow up.

SUMMARY Ten patients with metastatic pancreatic endocrine tumours were treated with the long-acting somatostatin analogue octreotide (SMS 201–995). Three patients showed no response, clinically or biochemically, and treatment was therefore withdrawn. The seven remaining patients continued treatment for a median period of 28 months (range 13–54 months). Treatment was initially effective, symptoms improved and the concentrations of tumour-related hormones were reduced. Worsening of symptoms and rising levels of tumour-related hormone concentrations occurred a median of 5 months (range 1–6 months) after the start of therapy and were initially reversed by increasing the dose of octreotide over a median of 10 months (range 6–16 months). However, after a median of 13 months (range 5–34 months) at the maximum dosage, symptoms recurred and were no longer responsive to a further increase in dosage of octreotide or other therapeutic measures. All patients died within a period of 5 months once this resistant phase of their illness had been reached.