Biomedical subjects
Publications and source records attributed to M R Watts.
A mode-evolution-based polarization splitter suitable for high-index-contrast systems and directly integratable with a recently reported on-polarization rotator is described and its performance verified through both finite-difference time-domain and eigenmode expansion simulations. For a device length of 200 microm, greater than 22 dB of extinction is obtained across a 1.45-1.75-microm bandwidth.
For the first time to our knowledge, designs for mode-evolution-based integrated polarization rotators requiring only a pair of waveguide core layers are presented. Finite-difference time-domain and eigenmode expansion simulations demonstrate the near-ideal performance of the approach. In contrast with approaches based on mode coupling, no significant wavelength sensitivity is observed.
INTRODUCTION: Older patients are the most prevalent age cohort requiring bronchoscopy. Prior sedation should be offered to improve patient comfort and operator technical ease. Older patients have increased sensitivity to centrally acting drugs increasing the procedural risk. This perceived risk may limit access to bronchoscopy in older patients. There have been no systematic prospective placebo-controlled studies in older patients. We compared a novel premedication regimen-oral temazepam plus nebulised Lignocaine (new treatment) to an established regimen of intravenous alfentanyl (control). METHODS: Consecutive patients 75 years and older referred for bronchoscopy were considered. Twenty-five patients were randomly assigned to each group. The primary outcome measure was the lowest oxygen saturation recorded from the administration of IV drugs and for 30 min post-bronchoscopy. RESULTS: The lowest mean oxygen saturation in the new treatment group was 92.2% (90.3-94.2) and in the control group 91.1% (89.2-93.1). This was not statistically different (P = 0.370). There were no adverse events. CONCLUSION: This is the largest prospective study to date on an older population undergoing bronchoscopy supporting previous retrospective findings regarding the safety of this procedure. Determined by oxygen saturations there is no difference in safety between premedication regimens comprising oral temazepam/nebulised lignocaine or intravenous alfentanyl.
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Three cases of periorbital necrotising fasciitis are described, one occurring in a three-year-old child. The cases in adults required debridement of necrotic tissue, in one of whom there was extensive disease involving the face and orbital fat. It is probable that the early stages of this condition are under-recognised; the importance of early signs and intensive treatment of this life-threatening disease are illustrated.
The Hong Kong H3N2 subtype of influenza A virus appeared in 1968 and since then has caused epidemics of varying degrees of severity. We describe a community outbreak of influenza A H3N2 which occurred in members of a bowls club in an English rural village in late April 1989. The explosive onset, high attack rate (34/41 = 83 per cent) in those exposed, and the clinical presentation initially suggested a toxic or allergic aetiology. Twenty-three persons consulted their general practitioners; before the diagnosis was made all cases were considered to merit antibiotic therapy and 17/23 were prescribed steroids or bronchodilators on account of persisting severe wheeze and chest tightness. One of the 23 was admitted to hospital. There were no deaths. Influenza vaccination is recommended for people at special risk but protective efficacy is relatively low and short-lived. Only two of the group had received influenza vaccination since the beginning of October 1988 and both became symptomatic. The use of amantadine for the prevention and early treatment of influenza A in selected situations merits serious consideration, provided the diagnosis is made sufficiently early.
The subcellular distribution of T-2 mycotoxin and its metabolites was studied in isolated rat livers perfused with [3H]T-2 toxin. After a 120-min perfusion, the distribution of radiolabel was to bile 53%, perfusate 38% and liver 7%. Livers were fractionated into mitochondria, endoplasmic reticulum (smooth and rough), plasma membrane and nuclei. Plasma membrane fractions contained 38% of the radiolabel within 5 min, decreasing to less than 1% at the end of the 120-min perfusion. Smooth endoplasmic reticulum contained 27% of the radiolabel by 5 min and increased to 43% over the 120-min perfusion. The mitochondrial fraction contained 3% of the radiolabel by 30 min and increased to 10% after 120-min perfusion. Label in the nuclear fraction remained constant at 7% from 30 to 120 min. By 15 min, only the parent toxin was detected in the mitochondrial fraction. In the other fractions, radiolabel was associated with HT-2, 4-deacetylneosolaniol, T-2 tetraol, and glucuronide conjugates. Glucuronide conjugates accounted for radiolabel eliminated via the bile. The time course for distribution of radiolabel in liver suggested an immediate association of [3H]T-2 with plasma membranes and a subsequent association of toxin and metabolites with endoplasmic reticulum, mitochondria and nuclei, the known sites of action of this toxin.
We investigated the effect of T-2 toxin on rat liver mitochondrial protein synthesis. Isolated rat liver mitochondria were supplemented with an S-100 supernatant from rat liver and an external ATP-generating system. We used an in vitro assay employing cycloheximide, an inhibitor of cytoplasmic protein synthesis, and chloramphenicol, an inhibitor of mitochondrial protein synthesis, to distinguish mitochondrial protein synthesis from the cytoplasmic process. Amino acid incorporation into mitochondria was dependent on the concentration of mitochondria and was inhibited by chloramphenicol. The rate of uptake of [3H]leucine into mitochondrial protein was unaffected by the addition of T-2 toxin and was not a rate-limiting step in incorporation. However, 0.02 micrograms/ml of T-2 toxin decreased the rate of protein synthesis by isolated mitochondria by 50%. The degree of protein synthesis inhibition correlated with the amount of T-2 toxin taken up by the mitochondria. While T-2 toxin is known to inhibit eukaryotic protein synthesis, this is the first time T-2 was shown to inhibit mitochondrial protein synthesis.
T-2 toxin is a potent cytotoxic metabolite produced by the Fusarium species. The fate and distribution of 3H-labeled T-2 toxin were examined in male guinea pigs. Radioactivity was detected in all body tissues within 30 min after an im injection of an LD50 dose (1.04 mg/kg) of T-2 toxin. The plasma concentration of trichothecene molar equivalents versus time was multiphasic, with an initial absorption half-life equal to or less than 30 min. Bile contained a large amount of radioactivity which was identified as HT-2, 4-deacetylneosolaniol, 3'-hydroxy HT-2, 3'-hydroxy T-2 triol, and several more-polar unknowns. These T-2 metabolites are excreted from liver via bile into the intestine. Within 5 days, 75% of the total radioactivity was excreted in urine and feces at a ratio of 4 to 1. The appearance of radioactivity in the excreta was biphasic. Metabolic derivatives of T-2 excreted in urine were T-2 tetraol, 4-deacetylneosolaniol, 3'-hydroxy HT-2, and several unknowns. These studies showed a rapid appearance in and subsequent loss of radioactivity from tissues and body fluids. Only 0.01% of the total administered radioactivity was still detectable in tissues at 28 days. The distribution patterns and excretion rates suggest that liver and kidney are the principal organs of detoxication and excretion of T-2 toxin and its metabolites.
A double-blind trial was carried out in 177 patients with acute symptomatic urinary tract infections to assess the efficacy and tolerability of nitrofurantoin plus sulphadiazine at two dosage levels. Patients were allocated, at random, to receive 7-days' treatment with either 50 mg nitrofurantoin plus 150 mg sulphadiazine 3-times daily or 100 mg nitrofurantoin plus 500 mg sulphadiazine 3-times daily, and were followed-up 10 to 14 days later. Only the 73 (41%) patients with significant bacteriuria on entry were included in the analysis of the efficacy results. There were no statistically significant differences between the two treatments either in bacteriological cure rates, which were approximately 90% in both groups, or in the complete or partial resolution of symptoms, recorded in over 90% of patients at the 2-week follow-up visit. The main side-effects recorded were anorexia, nausea, vomiting and/or headache, and were fewer in the group treated with the lower dosage.
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