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Biomedical subjects

R Watson

Publications and source records attributed to R Watson.

At least 217 records · Page 12Linked to original sources

Measuring feeding difficulty in patients with dementia: multivariate analysis of feeding problems, nursing intervention and indicators of feeding difficulty.

The feeding difficulty of 196 elderly people with dementia was investigated by means of an 11-item questionnaire administered to nursing staff. The questionnaire was analysed by means of multivariate statistics, namely factor analysis. The factor analysis demonstrated that the original items could be reduced to three factors. These three factors were named: (a) patient obstinacy or passivity; (b) nursing intervention; and (c) indicator of feeding difficulty. This quantitative analysis confirms a previous qualitative distinction between items in the questionnaire and suggests avenues of research into the relationship between the factors.

Aged↗

Isolation of a matrix that binds medial Golgi enzymes.

Rat liver Golgi stacks were extracted with Triton X-100 at neutral pH. After centrifugation the low speed pellet contained two medial-Golgi enzymes, N-acetylglucosaminyltransferase I and mannosidase II, but no enzymes or markers from other parts of the Golgi apparatus. Both were present in the same structures which appeared, by electron microscopy, to be small remnants of cisternal membranes. The enzymes could be removed by treatment with low salt, leaving behind a salt pellet, which we term the matrix. Removal of salt caused specific re-binding of both enzymes to the matrix, with an apparent dissociation constant of 3 nM for mannosidase II. Re-binding was abolished by pretreatment of intact Golgi stacks with proteinase K, suggesting that the matrix was present between the cisternae.

Amino Acid Sequence↗

Measuring feeding difficulty in patients with dementia: developing a scale.

Feeding difficulty in elderly people with dementia is well documented and the need for research in this area of nursing care has been raised by several authors. One hundred and twelve elderly people with dementia were entered into a study of feeding difficulty. Data were gathered by means of a questionnaire administered to the nurses caring for the patients. The aspects of feeding difficulty which were investigated were based on reports of relevant behaviour in the literature and included refusal to eat, turning the head away, refusing to open the mouth, spitting, allowing food to drop out of the mouth and not swallowing. It was possible to arrange these different aspects of feeding difficulty under three headings: (a) refusal to eat, (b) spitting, and (c) inability to swallow, and to analyse the pattern of accumulation of these feeding difficulties by means of Guttman scale analysis. According to this analysis, the feeding difficulties investigated form a cumulative and unidimensional pattern. The implications of this pattern and the possibilities for further research are discussed.

Aged↗

Measuring feeding difficulty in patients with dementia: replication and validation of the EdFED Scale #1.

A study was conducted in order to replicate a scale which was previously reported for assessing the feeding difficulty of elderly patients with dementia. The clinical significance of the scale was also investigated. It was demonstrated that the scale was replicable in two separate nursing units. Also, it was demonstrated that, according to criteria such as its correlation with levels of nursing intervention, for example physical help, and with an indicator of feeding difficulty, namely leaving food on the plate at the end of a meal, the scale was clinically significant. The consequences and limitations of the present investigation are discussed and recommendations for future lines of enquiry are suggested. Specifically, the possibility of analysing data from such studies by the use of multivariate statistical techniques is raised.

Aged↗

Regulation of fetal muscle development by thyroxine.

We have demonstrated that fetal hypophysectomy (hypox) induces deficiencies in skin and adipose tissue development and that chronic thyroxine (T4) treatment either normalizes or enhances skin and adipose tissue development in hypox fetuses. Since hypox also induces deficiencies in muscle development we report herein results of a histochemical and biochemical analysis of muscle development conducted in studies of T4-treated hypox fetuses. Pig fetuses were hypophysectomized on day 70 of gestation and treated with T4 during two periods, i.e. 70-90 days and 90-105 days gestational age, by implanting slow-release T4 (15 mg) pellets in the lateral musculature of the hind limb. Blood, muscle and other tissue samples were obtained upon removal of fetuses at days 90 and 105 of gestation. Weights of hypox, control and T4-treated hypox fetuses were similar at the end of the early period (70-90 days) whereas T4 significantly depressed body weight (p < 0.05) during the later period (90-105 days). Muscle weights, protein, DNA and RNA concentrations and muscle fiber size were not influenced by hypox or T4 treatment. Hypox-induced deficiencies in muscle capillary-to-fiber ratios, percentage of dry matter and general morphology were normalized by T4 (p < 0.05) during both treatment periods. Lipid deposition (staining) and histochemical reactivity for an oxidative marker (NADH-TR) were enhanced (p < 0.05) by T4 during both treatment periods as revealed by computer-assisted image analysis. Histochemistry for myofibrillar (acid) ATPase showed that the hypox-impaired type II to type I fiber type conversion was not influenced by T4 treatment. Muscle developmental traits enhanced or normalized by T4 were directly or indirectly related to lipid and/or oxidative metabolism. Effects of T4 on muscle and other tissues indicate, therefore, that thyroid hormones may be key regulators of oxidative and/or lipid metabolism in the neonatal animal.

Animals↗

The role of Myb proteins in normal and neoplastic cell proliferation.

The c-myb protooncogene is the prototype of a gene family that contains two other recently described members, A-myb and B-myb. The c-myb gene encodes a transcription regulatory protein, c-Myb, that has distinct DNA-binding domain structure and binding specificity compared with unrelated transcription factors. All three members of the myb protein family, however, display a high degree of homology within their DNA-binding domain, suggesting that they may regulate transcription of a similar set of target genes. We examine here whether, by implication, the individual members of the myb gene family play analogous roles within the cell, in particular focusing on their potential functions in the control of cell proliferation. Expression of both c-myb and B-myb is subject to regulation in the cell cycle, transcripts of these genes being induced within the G1 phase of the cell cycle and persisting at maximal levels through S phase. Consistent with this timing of expression, inhibition of c-Myb and B-Myb synthesis by treatment of cells with anti-sense oligonucleotides indicates that both proteins are required for transition from the G1 to S phase of the cell cycle. The c-Myb and B-Myb proteins cannot be considered as analogs, however, as they show certain differences in trans-activation activity of their target genes. Moreover, while superficially similar, expression of c-myb and B-myb is not coordinated, and it is conceivable that their products have quite distinct functions in the regulation of cell proliferation. The ubiquitous expression of B-myb in cycling cells and its strict regulation during late G1 suggest a universal function for B-Myb in G1 to S phase transition. Consistent with this conclusion, B-myb transcription is controlled by the transcription factor E2F, which has been implicated in cell cycle regulation of a number of genes involved in DNA synthesis. The restricted tissue tropism of c-myb expression and its regulation by certain growth factors such as IL-2 suggest a specific function in transduction of extrinsic proliferation (and differentiation) signals. The role of A-myb in the cell remains to be determined; however, its expression shows no correlation with cell cycling, implying that it has no direct role in cell proliferation. Recent data show that the necessity for c-myb function in proliferation of a number of cell types provides a promising opportunity for intervention in the treatment of certain tumors.

Animals↗

The influence of human growth hormone (GH) and thyroxine (T4) on the differentiation of adipose tissue in the fetus.

Late term fetuses from genetically obese dams have slightly larger fat cells, greater adipose tissue lipoprotein lipase (LPL) activities, elevated levels of thyroid hormones, and depressed growth hormone (GH) levels when compared to fetuses from lean dams. We have investigated the influence of thyroid hormone and GH status per se on these and other adipose tissue traits by chronically treating hypophysectomized (hypox) fetuses (day 70) between day 90 and 105 of gestation with either thyroxine (T4) or human GH. Treatment with T4 decreased body weights (P<.05), increased serum T4 levels (P<.05), and enhanced skin and hair development (P<.05). Quantitative analysis of sections of perirenal and subcutaneous adipose tissue indicated that T4 increased LPL activity (P<.05), slightly increased fat cell size, and more than doubled (P<.05) lipid accretion. A hypox induced deficit in fat cell cluster number in the outer layer of subcutaneous tissue was normalized by T4 (P<.05). Conversely, human GH (hGH) treatment had no influence on body weight, increased serum hGH levels, decreased fat cell size (P<.05) and LPL activity (P<.05) but had no influence on lipid accretion. Quantitative analysis of adipose tissue sections provided direct and indirect evidence of a "critical" or "sensitive" period between 90 and 105 days, since fetal hypox at day 70 severely impeded preadipocyte recruitment/replication during this period. Furthermore, T4 but not GH effectively normalized this hypox-induced deficiency in preadipocyte development. Therefore, T4 may have a major role in preadipocyte recruitment/replication during late fetal life.

Adipocytes↗

Estimating selective advantage of two alleles in discrete time.

A class of estimators for the selective advantage, s, in a Wright-Fisher model with two alleles, variable population size, and genic selection is derived via martingale theory. Explicit expressions are given for these estimators which only involve simple computation. The optimal estimate among this class of estimators is obtained. Asymptotic results are readily established by an application of a martingale central limit theorem. The performance of this optimal estimator is compared to known estimators by means of a simulation study.

Alleles↗

Kinetic PCR analysis: real-time monitoring of DNA amplification reactions.

We describe a simple, quantitative assay for any amplifiable DNA sequence that uses a video camera to monitor multiple polymerase chain reactions (PCRs) simultaneously over the course of thermocycling. The video camera detects the accumulation of double-stranded DNA (dsDNA) in each PCR using the increase in the fluorescence of ethidium bromide (EtBr) that results from its binding duplex DNA. The kinetics of fluorescence accumulation during thermocycling are directly related to the starting number of DNA copies. The fewer cycles necessary to produce a detectable fluorescence, the greater the number of target sequences. Results obtained with this approach indicate that a kinetic approach to PCR analysis can quantitate DNA sensitively, selectively and over a large dynamic range. This approach also provides a means of determining the effect of different reaction conditions on the efficacy of the amplification and so can provide insight into fundamental PCR processes.

DNA↗

Measuring feeding difficulty in patients with dementia: perspectives and problems.

The feeding problems of demented elderly people are well documented and the need for research into the assessment of feeding difficulty and intervention by nurses has been raised. The present paper reviews the literature in this area of care and outlines the problems which exist in attempting to investigate the feeding difficulty of demented patients. Demented elderly people display a range of behaviours related to feeding including excessive eating in the early stages of dementia and then difficulty with feeding, refusal to eat and, finally, inability to self-feed at all. The problems with research in this area revolve around the issue of measurement of feeding difficulty. There are problems in deciding what to measure and in how measurements should be made which are clinically meaningful. A possible strategy for investigating the feeding difficulty of demented elderly patients is suggested which includes the design of a tool for measurement and the application of single-case studies. Any tool which is used for measurement should enable researchers, in the first instance, and then clinicians to categorize the feeding difficulty of individual patients. Moreover, such a tool should also be sufficiently sensitive to respond to change in feeding ability. The single-case methodology is considered to be the most ethically and statistically appropriate for research with this particular group of patients.

Activities of Daily Living↗

Function of the ypt2 gene in the exocytic pathway of Schizosaccharomyces pombe.

The ypt2 gene of the fission yeast Schizosaccharomyces pombe encodes a member of the ypt/rab family of small GTP-binding proteins, related in sequence to Sec4p of Saccharomyces cerevisiae but closer to mammalian rab8. We have introduced a mutation into the gene corresponding to a mutation identified in ypt1, in which a conserved valine residue was altered to asparagine. The mutated ypt2 gene was introduced into the S. pombe genome by gene replacement. The resulting strain was temperature-sensitive for growth. Normal growth was restored by introduction of a plasmid-borne wild-type ypt2 cDNA or by cDNA for rab8 but not by various other rab or ypt sequences. At restrictive temperature the mutant cells accumulated the secretory protein acid phosphatase in a form that appeared to be fully glycosylated and acquired a population of vesicles detectable by electron microscopy. Thus the ypt2 protein, and by inference rab8, appear to function in the last stage of the secretory pathway.

Acid Phosphatase↗

Schizosaccharomyces pombe ypt5: a homologue of the rab5 endosome fusion regulator.

The ypt/rab proteins are a family of small GTP-binding proteins thought to be required for different stages of membrane traffic. From the fission yeast Schizosaccharomyces pombe we have isolated and characterized ypt5, a gene encoding a homologue of rab5, a mammalian protein apparently involved in regulating fusion of early endosomes. Recombinant ypt5 protein bound GTP. The ypt5 gene was found to be essential for viability on minimal media, but ypt5-disrupted cells grew slowly on some rich media and accumulated a population of small vesicles not observed in wild-type cells. Canine rab5 cDNA could replace the ypt5 gene in S. pombe and restore normal growth and viability. Ypt5 protein expressed in mammalian cells colocalized with the transferrin receptor to early endosomes. Thus, molecular aspects of the early endocytic pathway may be conserved between mammalian cells and S. pombe and hence may be amenable to genetic analysis.

Amino Acid Sequence↗

Clinical expression of systemic lupus erythematosus in patients with C4A deficiency.

We studied 121 patients with systemic lupus erythematosus (SLE), of whom 119 were complement typed. Both black and white patients with SLE were more likely than racially matched controls to have a C4A null allotype. Patients with homozygous C4A deficiency had less proteinuria than other patients (p = 0.02) and both homozygous and heterozygous C4A-deficient patients (p = 0.05) had fewer seizures than other patients. Anti-dsDNA, anti-Sm, anti-Ro, and anticardiolipin antibodies were less common in patients with homozygous C4A deficiency, with heterozygous C4A-deficient patients intermediate in frequency between homozygous C4A-deficient and normal patients with SLE. Both homozygous and heterozygous C4A-deficient patients (p < 0.005) had higher C3 levels than other patients, and heterozygous C4A-deficient patients had higher, not lower, C4 levels (p < 0.002), compared with non-C4A-deficient patients. C4A gene deletion was found in 23.4% of patients. C4A gene deletion was associated with subacute cutaneous lupus erythematosus (p = 0.04) and Sjögren syndrome (p = 0.02) in patients with SLE. Both anti-dsDNA (p = 0.04) and anticardiolipin (p = 0.04) were found less frequently in patients with C4A gene deletion. Patients with C4A gene deletion had lower C4 levels than patients with C4A deficiency from other mechanisms. We conclude that the presence of 1 or 2 C4A null allotypes and the presence of a C4A gene deletion identify subgroups of patients with SLE that differ in clinical, laboratory, and autoantibody characteristics from other patients with SLE.

Adolescent↗