Enuresis and body worn alarms.
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Biomedical subjects
Publications and source records attributed to M Knapp.
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Systemic lupus erythematosus (SLE) is a complex disease which is partly determined by genetic factors which influence susceptibility to the disease phenotype. In this association study we try to define the high risk haplotypes which are responsible for this disease, together with other environmental factors. In many other association studies a set of SLE patients is compared to a set of controls. The basic assumption about the underlying population is that the disease and control sample should originate from the same genetic population, which is not always completely satisfied in many studies. Therefore, we analyse our family data by applying the Haplotype Frequency Difference (HFD) Method, which constructs its internal control group from those haplotypes not transmitted to the affected individual. Results partially conform with other studies, showing that the haplotypes B8 DR3 as well as B7 DR2 have a high positive association with SLE. When the DR locus was analyzed alone, we found besides the alleles DR2 and DR3 a negative association for DR1, DR5, and DR6.
There is a tendency in discussions of mental health policy and psychiatric practice to talk of the cost of a treatment, facility, or policy and to ignore variations. These variations can be considerable, which alone suggests they should not be overlooked, and they can be explored and perhaps exploited to improve the delivery of services. This article describes a theoretical framework for the examination of cost differences, applies it to a particularly rich data base on people with long-term mental health problems moving from hospital to the community, and uses the empirical evidence to address four key policy questions. The study finds encouragingly strong positive associations between costs, needs, and outcomes. It also uncovers significant cost-effectiveness differences between the public and private sectors and between community accommodation types.
The prenatal and postnatal human ontogeny of the central benzodiazepine receptor was investigated in six different brain regions between week 24 postconception and age 14 years. Binding studies, which were performed with [3H]flunitrazepam [( 3H]FNZ), revealed a steep increase in receptor density postnatally in frontal cortex and cerebellum. Bmax values were higher in medulla oblongata, pons, and thalamus than in cortex and cerebellum up to week 26. After that, receptor densities declined significantly in medulla and olive. The same tendency was apparent in pons, whereas receptor density remained unchanged in thalamus. The early ontogeny of the benzodiazepine receptor was also evaluated in fluorographs [( 3H]FNZ) and immunoblots using the alpha 1-subunit-specific monoclonal antibody (mAb) bd-24. Specific radiolabeled proteins with molecular weights of 53K and 59K were visible in cortical membranes from gestational week 8, the earliest time investigated. During further development, the intensity of the 53K band increased without changes in the 59K band. As in other species, postmortem proteolysis in human brain led to a specifically labeled peptide of 47K. The mAb bd-24 immunolabeled only the 53K protein and the 47K peptide.
In 16 healthy and 16 asymptomatic asthmatic children (age range 5-8 yr; 8 girls, 24 boys) we studied the influence of breathing frequency on the results and the diagnostic value of body plethysmographic measurements. Airway resistance (Raw), specific airway resistance (SRaw), and thoracic gas volume (TGV) were measured during breathing (or breathing efforts against a closed shutter) at 0.4, 1, and 2 Hz. SRaw was computed by a simplified procedure directly from flow at the mouth vs. box volume-curves. The diagnostic value of each parameter was assessed as the percentage of correctly classified healthy and asthmatic subjects by means of discriminant analysis. When frequency was increased from 0.4 to 1 and 2 Hz mean TGV rose by 5 and 14% in healthy children and by 11 and 21% in asthmatic children, respectively. From 0.4 to 1 Hz mean Raw decreased by 16% (P = 0.002) in healthy children and by 25% (P = 0.0004) in asthmatic children. The differences in Raw between both groups decreased with frequency (3.5, 1.8, and 1.5 cm H2O.L-1.s at 0.4, 1, and 2 Hz, respectively) and those of TGV increased (0.13, 0.21, and 0.23 L). SRaw showed similar frequency characteristics as Raw. As intra-group variability changed in parallel with the differences the diagnostic value of the parameters remained constant with frequency. Simplified SRaw alone and TGV combined with Raw exhibited no differences in their diagnostic values (81-84% correctly classified).(ABSTRACT TRUNCATED AT 250 WORDS)
In this paper four principal topics are addressed: (a) the policy and political contexts in which demands arise for cost information; (b) the nature and phasing of those demands; (c) the basic rules of empirical costs research for meeting those demands; and (d) concomitant implications for the design, execution and interpretation of their research. Mental health care policy or practice changes which ignore costs, or which embody cost information without obeying or recognizing the four basic rules, can only be of dubious validity, or can only be used to answer a limited range of questions. But, as the illustrative studies show, it need not be an horrendous, or ideologically compromising or scientifically complex task to add a cost dimension to the evaluation of mental health services. There are enough examples in the literature of bad costs research to demonstrate that it is not as simple as some people think, but there are also enough examples of good research to encourage further attempts.
The planning of long-term care in the community as an alternative to in-patient care requires accurate information on the likely expense of altering the balance of provision. Unfortunately, as very few long-stay psychiatric hospitals have yet closed, the planning of these resource requirements has had to proceed in a vacuum. By examining the costs of community reprovision for the first 136 people to leave Claybury and Friern Hospitals, a prediction equation has been estimated from existing data which links the hospital-assessed characteristics (including psychiatric symptoms and behavioural problems) of these people to the subsequent cost of community care. About a third of the observed variation in these costs can be explained statistically by these 'baseline' characteristics. However, the first cohorts exhibit fewer behavioural problems and other symptoms of mental illness, they have been in hospital for shorter lengths of time, and they are younger. The prediction equation for the leavers is thus used to extrapolate community costs for those hospital residents yet to leave. It is found that community costs are lower than hospital costs, not just for the first cohorts of leavers, but for the full populations of the two hospitals scheduled to close.
Evidence of strong genetic markers in Crohn's disease (CD) is still absent. Many investigations have focused on HLA antigens, with conflicting results. To obtain more detailed information on the relation of HLA to the disease, we used the HLA data from 269 CD patients to compute the maximum-likelihood estimates of HLA gene and haplotype frequencies. These results provide further evidence that HLA B44 and Cw5 do indeed play a role in the development of CD. Furthermore, it is conceivable from our results that HLA Cw7 may protect against being affected with this disease.
Resistance and reactance of the respiratory tract of 40 healthy newborn were measured by means of the polyfrequent oscillation method. Mean resistance had frequency-dependent values between 20.91 and 9.63 cm H2O per litre per second and mean reactance between -29.11 and -3.81 cm H2O/1/s. The resistance--but not the reactance--was found to depend on the body length and the body weight of the infants.
Inflammatory bowel diseases (IBD) as Crohn's disease (CD) and ulcerative colitis (UC) are believed to have a genetic basis. Additional factors are supposed to promote the development of IBD. However, apart from a few reports of HLA associations which await confirmation by other groups strong associations to (a) particular genetic marker(s) are still lacking. We here report on previously unobserved associations of CD to MNSS and UC to the immunoglobulin heavy chain allotype Gm 1,-2,10. We suggest that these factors play a role in a wider spectrum of genetic markers for the development of IBD.
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In the scope of the ECCDS, established to test the efficacy of prednisolone and/or sulfasalazine in Crohn's disease, the relationships of blood chemistry and CDAI to histology of rectal mucosa were studied in 115 patients by means of univariate and multivariate statistical analyses. Laboratory and histologic markers of inflammation tend to be correlated. But these correlations are definitively weak. Thus, the predictive value of histology for blood chemistry or CDAI is very low. Laboratory indices and CDAI are relatively inaccurate means of assessing disease severity at tissue level and vice versa.
Filaggrin is degraded to amino acids in the stratum corneum. We tested the hypothesis that the resulting high concentrations of amino acids might be involved in the control of keratinocyte maturation. An amino acid mixture, with the composition of the filaggrin breakdown products, inhibited the growth of cultured human keratinocytes at 0.1 M. Inhibition of protein synthesis was progressive with time. After 24-h exposure, 50% inhibition occurred at 0.3-0.4 M amino acids. When the cultures were incubated with the amino acids for 7 days, the concentration giving half-inhibition was reduced to 0.2 M. No change was observed in the pattern of keratin synthesis, although synthesis of protein with Mr of 36,000 was disproportionately inhibited. It is concluded that filaggrin breakdown products are not involved in the control of keratinocyte differentiation.
We have raised an anti-idiotypic antibody against the cell surface IgM of the murine BCL1 tumor cells. This antiserum reacts exclusively with the IgM expressed on the tumor cells and detects a unique population of cells in the spleen and blood of the tumor-bearing mice. When these cells are stimulated in vitro with LPS, they secrete an IgM bearing the same idiotype as the cell surface Ig. These results are discussed in terms of a model for the immunotherapy of a chronic lymphocytic leukemia-like syndrome in mice.