The major histocompatibility complex: its genes and their roles in antigen presentation.
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Biomedical subjects
Publications and source records attributed to C Hewitt.
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AIMS: To determine the status of cystic fibrosis patients, their mode of diagnosis and source of medical care in New Zealand. METHODS: A database was established in 1988 to record clinical information on individuals with cystic fibrosis in New Zealand. Three hundred and two cystic fibrosis patients were identified and clinical information on 248 obtained. RESULTS: Thirty five per cent of patients at diagnosis had gastrointestinal and pulmonary and 33% had gastrointestinal symptoms alone. Ninety three infants were diagnosed after a positive screening test and confirmatory sweat test. The mean age at diagnosis overall was 1.8 years, while 61% of children were diagnosed before one year of age. 74.2% of patients were said to be pancreatic insufficient, 4% pancreatic sufficient and in 22% the results were unavailable or unknown. Medical care was provided by 28 sources comprising paediatricians, physicians or combined clinics. One cystic fibrosis clinic cared for more than 40 patients. Sixty-one per cent of cystic fibrosis subjects were colonised with Staphylococcus aureus at some time, and 44% were reported to be colonised with Pseudomonas aeruginosa. CONCLUSIONS: Common clinical features of cystic fibrosis have been characterised for New Zealand patients. It is unknown to what extent the clinical features of the disease and source of medical care in New Zealand are responsible for previously reported survival for the condition but it is planned to examine serial measurements of growth, nutrition, pulmonary function and survival and it is hoped that these measurements will be the subject of a further report.
This research among a sample of 1,915 Mississippi adolescents investigated whether lonely adolescents who use illicit substances were at increased risk of hopelessness. Relative risk of scoring within the severe hopelessness range was 6.9 for non-substance users who were lonely and 4.2 for substance users who were not lonely. Yet, relative risk for severe hopelessness in substance-using lonely adolescents was 25.2. Lonely, substance-using adolescents were 25 times more likely to be severely hopeless than the reference group composed of non-substance using, not-lonely adolescents. Lonely adolescents who get drunk also were 15.9 times more likely to be severely hopeless than the reference group. Because hopelessness often is an indicator of suicidal behavior, these results may have important implications for school health adolescent suicide prevention efforts.
The case is described of a lady who developed dysphagia and dysphonia misdiagnosed first as hysteria, then as myasthenia gravis, one year after a Cloward's operation for cervical disc disease. After a bout of coughing the bony dowel was expelled and the correct diagnosis was made.
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BACKGROUND AND OBJECTIVES: Intraspinally administered alpha 2-adrenergic agonists produce analgesia in part by causing spinal acetylcholine and nitric oxide (NO) release. Clonidine-induced analgesia is enhanced by subarachnoid neostigmine and inhibited by N-methyl-L-arginine (NMLA), a blocker of NO synthesis. The authors tested whether dexmedetomidine, an alpha 2-adrenergic agonist with greater intrinsic efficacy than clonidine, would be similarly affected by neostigmine and NMLA. METHODS: Drugs were administered subarachnoid to 22 chronically prepared ewes, and antinociception was determined by a noxious mechanical stimulation. Sheep received subarachnoid saline, neostigmine, or NMLA, followed by cumulative doses of clonidine or dexmedetomidine. Neostigmine was injected either 20 or 60 minutes prior to beginning cumulative dosing with the alpha 2-adrenergic agonist. RESULTS: Both clonidine and dexmedetomidine produced dose-dependent antinociception with similar potency (ED50 was 61 +/- 26 micrograms for clonidine and 65 +/- 24 micrograms dexmedetomidine). Neostigmine pretreatment 20 minutes before dosing potentiated clonidine's dose response (ED50 was reduced to 6.8 +/- 2.3 micrograms), but had no effect on dexmedetomidine (ED50 27 +/- 6.1 micrograms). Neostigmine pretreatment 60 minutes before dosing potentiated both clonidine (ED50 was reduced to 11.8 +/- 5.1 micrograms) or dexmedetomidine (ED50 was reduced to 10 +/- 2.1 micrograms). The NMLA did not affect antinociception from dexmedetomidine. CONCLUSIONS: These data are in agreement with previous hemodynamic studies suggesting that neostigmine has a slow onset of action after subarachnoid administration. That clonidine is potentiated more than dexmedetomidine by neostigmine pretreatment at 20 minutes likely may reflect the lower intrinsic efficacy of clonidine. Alternatively, since acetylcholine can cause NO synthesis, lack of effect of NMLA on dexmedetomidine implies that analgesia from this drug is less reliant on acetylcholine-NO mechanisms than clonidine. The large potentiation observed between neostigmine and these alpha 2-adrenergic agonists carries important clinical implications.