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Biomedical subjects

D Williams

Publications and source records attributed to D Williams.

At least 91 records · Page 5Linked to original sources
PubMed2001

Affinity purification of secreted alkaline phosphatase produced by baculovirus expression vector system.

Human secreted alkaline phosphatase (SEAP) was produced in a stably-transformed Spodoptera frugiperda Sf-9 insect cell line (Sfb4GalT) following infection with a recombinant Autographa californica multiple nuclear polyhedrovirus containing the SEAP gene under control of the polyhedrin promoter. An affinity chromatographic column prepared by linking 4-amino-benzylphosphonic acid to histidyl-expoxy-Sepharose was used to isolate SEAP from the cell supernatant following removal of cells and virus and 10-fold concentration through ultrafiltration. We found that the binding of SEAP on the affinity matrix follows the Langmuir isotherm model. In addition, either recycling SEAP sample through the column for 24 h or loading high SEAP concentrations resulted in a high-purity product. Some nonspecific binding of protein on the matrix occurred when low concentrations of SEAP sample were loaded. Finally, we found that SEAP binding occurs rapidly, i.e., within 30 min of adding the SEAP sample to the affinity matrix.

Alkaline Phosphatase↗
PubMed2001

From sterile debate to burning issue: the economics and safety dichotomy.

Surgical instruments are thought to be capable of transmitting spongiform encephalopathies from patient to patient, even after sterilisation. At the same time, there is an increasing trend to reuse devices intended for single use. This article discusses certain aspects of that apparent contradiction.

Bacterial Infections↗
PubMed2001

One step back and one, possibly two, steps forward. The different approaches to Parkinson's disease.

Parallel approaches to the development of medical treatment often experience advances in one technology sector and simultaneous setbacks in others. The potential role of medical devices and biomaterials in the treatment of neurological conditions such as Parkinson's Disease is discussed here together with the contrast between the role of devices in tackling the consequences of disease and that of drugs and cell therapies that aim to cure it.

Electric Stimulation Therapy↗
PubMed2001

Medical devices of human origin.

The introduction of the concepts of tissue engineering into medical practice especially those involving human cellular and tissue-based products has necessitated a reappraisal of some of the principles of manufacturing and quality control. This article addresses some of these issues.

Biological Products↗
PubMed2001

The new materials technology of drug delivery.

The ability to deliver pharmaceuticals to patients in the most physiologically acceptable manner has always been an important issue in medicine. Increasingly, there is evidence to suggest that new technologies and materials will have a profound impact on drug delivery in the near future. Some of these are reviewed here.

Administration, Cutaneous↗
PubMed2001

The golden anniversary of titanium biomaterials.

Titanium has become the leading structural metallic biomaterial and 50 years of clinical performance has proven its value. However, it is wise not to forget the basic laws of materials science upon which its reputation has been based.

Alloys↗
PubMed2001

War and peace in the new year.

The world has been turned upside down and changes are being forced on society from unexpected directions. It is an opportune time to consider the changes that are likely to be witnessed in the medical technology sector.

Biomedical Technology↗
PubMed2000

BMPR2 haploinsufficiency as the inherited molecular mechanism for primary pulmonary hypertension.

Primary pulmonary hypertension (PPH) is a potentially lethal disorder, because the elevation of the pulmonary arterial pressure may result in right-heart failure. Histologically, the disorder is characterized by proliferation of pulmonary-artery smooth muscle and endothelial cells, by intimal hyperplasia, and by in situ thrombus formation. Heterozygous mutations within the bone morphogenetic protein type II receptor (BMPR-II) gene (BMPR2), of the transforming growth factor beta (TGF-beta) cell-signaling superfamily, have been identified in familial and sporadic cases of PPH. We report the molecular spectrum of BMPR2 mutations in 47 additional families with PPH and in three patients with sporadic PPH. Among the cohort of patients, we have identified 22 novel mutations, including 4 partial deletions, distributed throughout the BMPR2 gene. The majority (58%) of mutations are predicted to lead to a premature termination codon. We have also investigated the functional impact and genotype-phenotype relationships, to elucidate the mechanisms contributing to pathogenesis of this important vascular disease. In vitro expression analysis demonstrated loss of BMPR-II function for a number of the identified mutations. These data support the suggestion that haploinsufficiency represents the common molecular mechanism in PPH. Marked variability of the age at onset of disease was observed both within and between families. Taken together, these studies illustrate the considerable heterogeneity of BMPR2 mutations that cause PPH, and they strongly suggest that additional factors, genetic and/or environmental, may be required for the development of the clinical phenotype.

Adolescent↗
PubMed2000

Age and seasonal variations in the prevalence of Oestrus ovis larvae among sheep in northern Jordan.

During the period March 1996-July 1997, 417 heads of Awassi sheep slaughtered at the Irbid Abattoir (northern Jordan) were examined for the three larval instars (L1, L2 and L3) of Oestrus ovis. Of the 417 heads, 242 (58%) were infested with O. ovis larvae. Larval numbers were highly aggregated. The lowest number of larvae and the lower quartile were both zero, whilst the median was two and the upper quartile was 12. The highest number of larvae recovered from one head was 151. All three larval instars were observed in each month of the year. July and October had the highest proportions of L1, 75 and 78%, respectively, among infected animals (adjusted for age). The number of larvae increased with age. Infestation with live larvae was associated with inflammatory responses in the upper respiratory tract and with catarrhal or purulent discharge. The percentage of infested sheep and the mean monthly total number of larvae/sheep peaked in the warmer part of the year. Most larvae were L1 except during the spring when L2 and L3 predominated. Distribution analysis demonstrates that the numbers of larvae recovered in the sheep population followed a negative-binomial distribution. Furthermore, the negative-binomial constant k for each month correlated with the monthly prevalence.

Abattoirs↗
PubMed2000

Promoter trapping of a novel medium-chain acyl-CoA oxidase, which is induced transcriptionally during Arabidopsis seed germination.

The first step of peroxisomal fatty acid beta-oxidation is catalyzed by a family of acyl-CoA oxidase isozymes with distinct fatty acyl-CoA chain-length specificities. Here we identify a new acyl-CoA oxidase gene from Arabidopsis (AtACX3) following the isolation of a promoter-trapped mutant in which beta-glucuronidase expression was initially detected in the root meristem. In acx3 mutant seedlings medium-chain acyl-CoA oxidase activity was reduced by 95%, whereas long- and short-chain activities were unchanged. Despite this reduction in activity lipid catabolism and seedling development were not perturbed. AtACX3 was cloned and expressed in Escherichia coli. The recombinant enzyme displayed medium-chain acyl-CoA substrate specificity. Analysis of beta-glucuronidase activity in acx3 revealed that, in addition to constitutive expression in the root axis, AtACX3 is also up-regulated strongly in the hypocotyl and cotyledons of germinating seedlings. This suggests that beta-oxidation is regulated predominantly at the level of transcription in germinating oilseeds. After the discovery of AtACX3, the Arabidopsis acyl-CoA oxidase gene family now comprises four isozymes with substrate specificities that encompass the full range of acyl-CoA chain lengths that exist in vivo.

Acyl-CoA Oxidase↗
PubMed2000

CL100/MKP-1 modulates JNK activation and apoptosis in response to cisplatin.

Treatment of cells with cisplatin induces a sustained activation of the stress activated protein kinase SAPK/JNK and the mitogen-activated protein kinase p38. Activation of JNK by cisplatin is necessary for the induction of apoptosis. Expression of the MAPK phosphatases CL100/MKP-1 and hVH-5 selectively prevents JNK/SAPK activation by cisplatin in a dose dependent fashion and results in protection against cisplatin-induced apoptosis. In contrast, expression of the ERK-specific phosphatase Pyst1 inhibits JNK/SAPK activity only when expressed at very high levels and does not confer protection against cisplatin. Furthermore, expression of a catalytically inactive mutant of CL100 in 293 cells decreases the IC50 for cisplatin and increases the toxicity of transplatin. This effect seems to be mediated by an increase in JNK activity since p38 activity is unaffected. These results suggest that dual-specificity MAPK phosphatases may be candidate drug targets in order to optimize cisplatin based therapeutic protocols.

Antineoplastic Agents↗
PubMed2000

Fluorescence in situ hybridization detection of two telomeres on the short arm of a derived chromosome 16 in an infant with thrombocytopenia.

We report a case of severe thrombocytopenia with an abnormal bone marrow karyotype described by G-banding analysis as t(16;21)(p?13;q11). Using fluorescence in situ hybridization (FISH) analysis with whole chromosome paints, the chromosome rearrangement was shown to be more complex, with the additional cryptic involvement of the long arm of chromosome 3. The chromosome rearrangement involved the breakpoints 3q26, 16p13.3, and 21q11; this rearrangement has not been previously described. The size of genomic material translocated from the chromosome 16 homologue was too small to be detected by chromosome paint. A 16p-specific telomeric probe was hybridized to locate the translocated 16p material. The 16p telomeric unique sequence DNA was retained on the der(16) chromosome, indicating a more distal breakpoint. This study demonstrates that telomeric translocations can occur that would be undetected by telomeric-specific FISH probes.

Bone Marrow Cells↗