Wrong biochemistry results. Companies and Medical Devices Agency must act to prevent wrong results.
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Biomedical subjects
Publications and source records attributed to K Lawton.
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The NIM1 (for noninducible immunity, also known as NPR1) gene is required for the biological and chemical activation of systemic acquired resistance (SAR) in Arabidopsis. Overexpression of NIM1 in wild-type plants (hereafter referred to as NIM1 plants or lines) results in varying degrees of resistance to different pathogens. Experiments were performed to address the basis of the enhanced disease resistance responses seen in the NIM1 plants. The increased resistance observed in the NIM1 lines correlated with increased NIM1 protein levels and rapid induction of PR1 gene expression, a marker for SAR induction in Arabidopsis, following pathogen inoculation. Levels of salicylic acid (SA), an endogenous signaling molecule required for SAR induction, were not significantly increased compared with wild-type plants. SA was required for the enhanced resistance in NIM1 plants, however, suggesting that the effect of NIM1 overexpression is that plants are more responsive to SA or a SA-dependent signal. This hypothesis is supported by the heightened responsiveness that NIM1 lines exhibited to the SAR-inducing compound benzo(1,2,3)-thiadiazole-7-car-bothioic acid S-methyl ester. Furthermore, the increased efficacy of three fungicides was observed in the NIM1 plants, suggesting that a combination of transgenic and chemical approaches may lead to effective and durable disease-control strategies.
AIMS: Previous studies have suggested that the self-reporting of smoking amongst diabetic patients is unreliable, and that objective markers such as breath carbon monoxide (CO) or urinary cotinine are needed. As these studies have been mostly in young Type 1 diabetic patients, the reliability of smoking history has been assessed in a large group of older Type 2 diabetic patients. METHODS: Two hundred and ninety-nine Type 2 diabetic patients were investigated for smoking habits by unstructured questionnaire, breath CO, and urinary ratio. RESULTS: Mean age of the group was 63 (range 30-80) years and 41% were female. Direct questioning suggested 77 (26%) to be smokers, and of these 852 had raised (>1 microg/mg) urinary cotinine-creatinine , and 71% raised (>8 p.p.m.) breath CO. Assuming urinary cotinine-creatinine as the 'gold standard', the sensitivity, specificity and positive predictive values for questionnaire were 97%, 95% and 85%, respectively; and for breath CO they were 74%, 98%, and 93%. CONCLUSION: It is concluded that at least in this population of Type 2 diabetic patients, a structured smoking history appeared to identify current smokers with good accuracy.
Recent work has demonstrated that plants have endogenous defence mechanisms that can be induced as a response to attack by insects and pathogens. There are two well-studied examples of these induced defence responses. Systemic acquired resistance (SAR) results in increased resistance to a broad spectrum of pathogens throughout a plant in response to localized necrosis caused by pathogen infection. The second example is the systemic induction of proteinase inhibitors to deter feeding by herbivores following an initial event of feeding. In addition, there is now preliminary evidence for other induced defence response pathways. By understanding the breadth of induced defence responses and the mechanisms used to control these pathways, novel plant protection strategies may be developed for use in agronomic settings. Rather than reducing crop losses caused by pests or pathogens by using chemicals that are designed to kill the offending organism, the plant's own defence mechanisms can be used to limit damage due to pests. Novel crop protection strategies based on genetic or chemical regulation of these induced responses show great potential. The first example of a crop protection product that acts by inducing an endogenous defence response pathway is now on the market. Bion reduces the level of pathogen infection in plants by activating SAR.
Health service reforms have led to relocation of care of the chronic mentally ill from institutions to the community, with subsequent demands on the primary health care team. Few studies have attempted to identify satisfactory models of care for this patient group. This study explores the impact of the employment of a community psychiatric nurse (CPN) by a general practice in Aberdeen city to co-ordinate care of discharged long-stay psychiatric patients resettled in hostels. A similar general practice with a comparable group of registered patients was selected as a control group. Patient health outcome was measured using the Health of the Nation Outcome Scales (HoNOS) and service providers' views on dedicated psychiatric care within general practice were explored using qualitative methods. Improvements in communication, liaison and drug management were reported in the intervention practice. A primary care-based CPN service dedicated to the care of the chronic mentally ill promoted a smooth transfer of care from long-term institutionalized care to the community setting.
BACKGROUND: There are no large published studies of the prevalence of seasonal affective disorder (SAD) among UK populations. AIM: To determine the prevalence of SAD among patients attending a general practitioner (GP). METHOD: Patients aged 16-64 consulting their GPs in Aberdeen during January were screened with the Seasonal Pattern Assessment Questionnaire (SPAQ). SPAQs were also mailed to 600 matched patients, who had not consulted their GP during January. Surgery attenders who fulfilled SPAQ criteria for SAD were invited for interview to determine whether they met criteria for SAD in DSM-IV and the Structured Interview Guide for the Hamilton Rating Scale for Depression--Seasonal Affective Disorder Version (SIGH-SAD). RESULTS: Of 6161 surgery attenders, 4557 (74%) completed a SPAQ; 442 (9.7%) were SPAQ cases of SAD. Rate of caseness on the SPAQ did not differ between surgery attenders and non-attenders. Of 223 interviewed SPAQ cases of SAD, 91 (41%) also fulfilled DSM-IV and SIGH-SAD criteria. CONCLUSIONS: There is a high prevalence of SAD among patients attending their GPs in January in Aberdeen; this is likely to reflect a similar rate in the community.
This study examines the impact of the employment of a community psychiatric nurse (CPN), dedicated to the care of patients with chronic mental illness, on general practice workload. Although the consultation rate with general practitioners for mental health reasons was significantly lower after CPN intervention, no differences were found in the total consultation rate.
The NIM1 (for noninducible immunity) gene product is involved in the signal transduction cascade leading to both systemic acquired resistance (SAR) and gene-for-gene disease resistance in Arabidopsis. We have isolated and characterized five new alleles of nim1 that show a range of phenotypes from weakly impaired in chemically induced pathogenesis-related protein-1 gene expression and fungal resistance to very strongly blocked. We have isolated the NIM1 gene by using a map-based cloning procedure. Interestingly, the NIM1 protein shows sequence homology to the mammalian signal transduction factor I kappa B subclass alpha. NF-kappa B/I kappa B signaling pathways are implicated in disease resistance responses in a range of organisms from Drosophila to mammals, suggesting that the SAR signaling pathway in plants is representative of an ancient and ubiquitous defense mechanism in higher organisms.
Cigarette smoke is potentially capable of generating a high free radical load in the body and many patients with diabetes are smokers. This study was designed to investigate the relationship between long-term smoking and free radical activity in young adult insulin-dependent diabetic patients with no evidence of macrovascular disease. Eight-five patients (48 male) aged 17-40 years were studied. Mean duration of diabetes was 10.5 years (0.08-33) and 39 were cigarette smokers. All had normal serum creatinine levels. The free radical markers measured were: thiobarbituric acid reactive substances, glutathione peroxidase, and superoxide dismutase. No significant differences in thiobarbituric acid reactive substances, glutathione peroxidase, or superoxide dismutase, were found between the diabetic smokers and non-smokers. Also no difference was found comparing the diabetic patients with 40 non-diabetic control subjects (20 smokers). Persistent albuminuria was present in 16 patients (10 microalbuminuria) and free radical marker concentrations in these subjects were similar to the normoalbuminuric patients. This data suggests that any increase in free radical activity due to cigarette smoke is adequately scavenged in young adults with diabetes who are free of significant macrovascular disease.
Cigarette smoke is capable of generating free radicals. In this study markers of free radical activity (thiobarbituric acid reactivity, superoxide dismutase and glutathione peroxidase) were measured in young adult smoking and non-smoking volunteers. No significant differences were found in any of the free radical markers between the two groups. The number of leucocytes was elevated and a positive correlation was found between the number of leucocytes and thiobarbituric acid reactivity in the smokers. The results from this study suggest that any free radical activity generated from long term cigarette smoking in young adults is adequately scavenged.
The prevalence of smoking amongst a group of 77 diabetic teenagers aged 11-18 years attending two paediatric clinics was determined using a questionnaire and urine cotinine assay. Five individuals were identified as definite smokers with two further individuals being probable smokers, all of whom were aged 15 years or more. This low prevalence (9%) is in contrast to a 48% prevalence in a young adult diabetic clinic. Many diabetic teenagers appear to acquire a regular smoking habit after leaving the paediatric clinic so it is important that health education is targeted at this group.
Complementary DNA clones encoding acidic and basic isoforms of the class III chitinase were isolated from Nicotiana tabacum. The clones share ca. 65% identity, are equally homologous to the class III chitinases from cucumber and Arabidopsis, and are members of small gene families in tobacco. An acidic class III chitinase was purified from the intercellular fluid of tobacco leaves infected with tobacco mosaic virus (TMV). Partial amino acid sequencing of the protein confirmed that it was encoded by one of the cDNA clones. The mRNAs of the class III chitinases are coordinately expressed in response to TMV infection, both in infected and uninfected tissue. The acidic and basic class III chitinases constitute previously undescribed pathogenesis-related proteins in tobacco.
The influence of exposure to tobacco smoke on maternal serum alpha-fetoprotein (AFP) levels at 16 wk gestation was examined. Urinary cotinine levels were used to quantify exposure to tobacco smoke. Significantly higher levels of maternal serum AFP were found in 101 women who had more than 1.0 microgram cotinine/mg urinary creatinine compared with 180 women whose urinary cotinine levels were below this level [(mean +/- SD) 1.23 +/- 0.64 and 1.06 +/- 0.54 respectively; 95 per cent CI of difference of means 0.01-0.31; P < 0.05]. There was a mild albeit statistically significant correlation between urinary cotinine levels and maternal serum AFB (r 0.099; P < 0.05). However, the difference in maternal serum AFP levels between the two groups was not found to be significant, when adjustments for maternal body mass index were made.
The smoking habits of 300 consecutive pregnant women and of other members of their household were obtained by interview at 16 and 32 weeks' gestation and after delivery. Urine samples for estimation of cotinine were collected at the same times during pregnancy and on admission in labour. Both self-reports of active maternal smoking and urinary cotinine levels were significantly associated with lighter babies but urinary cotinine correlated the better. Active maternal smoking was associated with a decrease in birth-weight of 12 g for every cigarette smoked in a day while there was a decrease of 25 g in birth-weight for every microgram of cotinine/mg of urinary creatinine. Passive maternal smoking was associated with a decrease of 66 g in mean birth-weight but this decrease was not statistically significant. Self-reports of active and passive smoking accounted for 43% of the variation in urinary cotinine levels suggesting that urinary cotinine assays can be used to assess and monitor exposure to tobacco smoke in pregnancy.
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The various clinical types of depression may correspond to biochemically distinct forms of the condition. If these could be characterized, antidepressant treatment might be tailored to correction of the underlying biochemical change(s) in individual patients. In particular, the selective actions of clomipramine and maprotiline on the serotonergic and noradrenergic systems respectively might be exploited therapeutically. Studies of the clinical response to these two antidepressants included tests of urinary 5-hydroxy-indoleacetic acid (5-HIAA) excretion and of serum thyroxine levels. While thyroid stimulation tests may prove of value for investigating depressed patients, urinary 5-HIAA levels are inconvenient, subject to extraneous influences and hard to interpret in terms of brain chemistry. (An alternative is proposed in the next paper.)