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Biomedical subjects

D Kidd

Publications and source records attributed to D Kidd.

At least 19 recordsLinked to original sources
PubMed2005

The prevalence of headache in Behçet's syndrome.

OBJECTIVES: Behçet's syndrome is an uncommon systemic disorder that involves the nervous system in 5% of cases. Headache may arise in conjunction with such complications but also appears to occur independently. We sought to define the prevalence of headache in an unselected group of patients with Behçet's syndrome, to characterize the headache syndromes and to identify what treatments are being used. METHODS: A questionnaire was sent to an unselected group of patients through their support group newsletter. RESULTS: The results showed a prevalence of recurrent headache in 82.5% of responders; the majority exhibited symptoms that fulfilled the International Headache Society criteria for migraine, with a higher than normal prevalence of visual or sensory aura of 52%. Using the Migraine Disability Assessment (MIDAS) score for disability in migraine, 62% of responders showed moderate or severe disability. Headache treatment was poor, the majority of sufferers resorting to over-the-counter remedies; preventative treatments had rarely been prescribed. CONCLUSIONS: Recurrent headache is very common in Behçet's syndrome, is poorly treated and is associated with disablement.

Analgesics↗
PubMed2005

Paroxysmal intracranial hypertension.

We present the case of a man who presented with headache and severe papilloedema which was caused not by chronic intracranial hypertension but by paroxysms of raised intracranial pressure, and we speculate what relationship this disorder has to idiopathic intracranial hypertension.

Adult↗
PubMed2003

Chronic relapsing inflammatory optic neuropathy (CRION).

We describe the clinical characteristics and early natural history of a form of inflammatory optic neuropathy which is frequently bilateral and often painful, and is characterized by relapses and remissions. MRI scans of the brain are normal and those of the optic nerves often, but not always, show high signal abnormalities which enhance. The symptoms and signs respond well to corticosteroid treatment, although long-term immuno suppression is often necessary. The syndrome behaves in a way which is typical of the condition known as granulomatous optic neuropathy, but during a median follow-up of 8 (2-26) years in no case has evidence for systemic sarcoidosis been identified. We suggest that the disorder be named chronic relapsing inflammatory optic neuropathy (CRION).

Adult↗
PubMed2003

Expression of beta2 adrenoreceptors on peripheral blood mononuclear cells in patients with primary and secondary progressive multiple sclerosis: a longitudinal six month study.

BACKGROUND: Beta(2) adrenoreceptor expression on peripheral blood mononuclear cells is increased in progressive multiple sclerosis. This increase has been correlated with disease activity in relapsing-remitting multiple sclerosis. OBJECTIVE: To determine the beta(2) adrenoreceptor expression in primary and secondary progressive multiple sclerosis in relation to findings on magnetic resonance imaging (MRI) and clinical disease activity. METHODS: 10 patients with multiple sclerosis were studied (five with primary progressive and five with secondary progressive forms of the disease) over a period of six months. Monthly clinical and MRI assessments of the brain and spinal cord were carried out. Beta(2) adrenoreceptor expression was assessed monthly using a ligand binding assay with [(125)I]iodocyanopindolol. Expression of beta(2) adrenoceptors on peripheral blood mononuclear cells was also assessed in five normal controls over a similar period. RESULTS: The mean (SEM) value of beta(2) adrenoreceptor density for the five normal controls was 1346 (183) sites/cell, with affinity Kd of 120 (40) pM. MRI disease activity in primary progressive multiple sclerosis was reported on two occasions and on those occasions the expression of beta(2) adrenoreceptors was increased in excess of 1900 sites/cell; in the remaining 28 observations beta(2) adrenoreceptor expression was within the normal range (800 to 1900 sites/cell). In patients with secondary progressive disease, MRI disease activity was observed on 16 occasions. In these patients expression of beta(2) adrenoreceptors was increased in excess of 2000 sites/cell in all measurements except in one subject who did not show MRI activity throughout the six months period of study. The affinity of the receptors was within the normal range in all cases. CONCLUSIONS: Increased expression of beta(2) adrenoreceptors was correlated with MRI disease activity in two patients with primary progressive multiple sclerosis. In secondary progressive multiple sclerosis, increased expression of beta(2) adrenoreceptors tended not to correlate with MRI disease activity. This may reflect a persistent Th1 immune reaction in the secondary progressive form of the disease.

Adult↗
PubMed2001

Profiling serine hydrolase activities in complex proteomes.

Serine hydrolases represent one of the largest and most diverse families of enzymes in higher eukaryotes, comprising numerous proteases, lipases, esterases, and amidases. The activities of many serine hydrolases are tightly regulated by posttranslational mechanisms, limiting the suitability of standard genomics and proteomics methods for the functional characterization of these enzymes. To facilitate the global analysis of serine hydrolase activities in complex proteomes, a biotinylated fluorophosphonate (FP-biotin) was recently synthesized and shown to serve as an activity-based probe for several members of this enzyme family. However, the extent to which FP-biotin reacts with the complete repertoire of active serine hydrolases present in a given proteome remains largely unexplored. Herein, we describe the synthesis and utility of a variant of FP-biotin in which the agent's hydrophobic alkyl chain linker was replaced by a more hydrophilic poly(ethylene glycol) moiety (FP-peg-biotin). When incubated with both soluble and membrane proteomes for extended reaction times, FP-biotin and FP-peg-biotin generated similar "maximal coverage" serine hydrolase activity profiles. However, kinetic analyses revealed that several serine hydrolases reacted at different rates with each FP agent. These rate differences were exploited in studies that used the biotinylated FPs to examine the target selectivity of reversible serine hydrolase inhibitors directly in complex proteomes. Finally, a general method for the avidin-based affinity isolation of FP-biotinylated proteins was developed, permitting the rapid and simultaneous identification of multiple serine peptidases, lipases, and esterases. Collectively, these studies demonstrate that chemical probes such as the biotinylated FPs can greatly accelerate both the functional characterization and molecular identification of active enzymes in complex proteomes.

Animals↗
PubMed2001

Protein kinase C activation by 12-0-tetradecanoylphorbol 13-acetate in CG-4 line oligodendrocytes stimulates turnover of choline and ethanolamine phospholipids by phospholipase D and induces rapid process contraction.

Treatment of [3H]-choline- or [14C]-ethanolamine-labelled undifferentiated bipolar and differentiated multipolar CG-4 line oligodendrocytes with 12-0-tetradecanoylphorbol 13-acetate (TPA) to activate protein kinase C stimulated the release of choline or ethanolamine metabolites to the medium over controls. Ro31-8220, a PKC inhibitor, reduced TPA-stimulated release of choline- and ethanolamine-metabolites to basal levels. TPA treatment of both bipolar and multipolar cells caused rapid contraction of processes leaving rounded up cells: this effect was blocked by Ro31-8220. After 12-15 h exposure to TPA, bipolar undifferentiated CG-4 line cells extended short processes again and the cells became multipolar. Nocodozole, an agent which disrupts microtubules and caused CG-4 line cells to round up, caused increased choline or ethanolamine-metabolite release to the medium over basal levels suggesting that some release during TPA-treatment might occur due to process fragmentation. However, the transphosphatidylation reaction confirmed that phospholipase D was active in these cells. Exposure of bipolar undifferentiated CG-4 line cells to TPA resulted in down-regulatation of PKC-alpha and PKC-beta which could not be detected by Western blotting after a few hours; PKC-epsilon was down-regulated much more slowly but PKCs delta, zeta and iota were not influenced by 48 h exposure of cells to TPA. Formation of phosphatidylethanol in the transphosphatidylation reaction was markedly reduced in TPA down-regulated cells indicating a role for PKCs alpha and beta in phospholipase D activation in CG-4 line oligodendrocytes.

Animals↗
PubMed2001

The predictive value of gadolinium enhancement for long term disability in relapsing-remitting multiple sclerosis--preliminary results.

As short-term MRI studies are increasingly being used to monitor disease activity in multiple sclerosis (MS) it is vital to establish if short-term MRI activity is predictive of long term clinical outcome. We followed up after 5 years a group of 10 benign (relapsing-remitting MS with a disease duration > 10 years and EDSS < or = 3) and 10 early relapsing-remitting patients who previously had monthly serial MRI scans for 6 months. In the early relapsing-remitting group median EDSS at entry to the initial serial study was three and in the benign group 2.5. At 5-year follow up, five of these 20 patients had developed a definite deterioration in EDSS. The median number of new enhancing lesions detected originally in the group that had deteriorated was 11 (7-17) compared to 0 (0-5) new enhancing lesions, for those who had not deteriorated (P < 0.05). There was a trend towards a higher baseline T2 lesion load in the group with a definite change in EDSS but this was not significant This study suggests that short-term measurement of the number of gadolinium enhancing lesions may predict long term outcome in relapsing-remitting MS.

Adult↗
PubMed2000

D-TACC: a novel centrosomal protein required for normal spindle function in the early Drosophila embryo.

We identify Drosophila TACC (D-TACC) as a novel protein that is concentrated at centrosomes and interacts with microtubules. We show that D-TACC is essential for normal spindle function in the early embryo; if D-TACC function is perturbed by mutation or antibody injection, the microtubules emanating from centrosomes in embryos are short and chromosomes often fail to segregate properly. The C-terminal region of D-TACC interacts, possibly indirectly, with microtubules, and can target a heterologous fusion protein to centrosomes and microtubules in embryos. This C-terminal region is related to the mammalian transforming, acidic, coiled-coil-containing (TACC) family of proteins. The function of the TACC proteins is unknown, but the genes encoding the known TACC proteins are all associated with genomic regions that are rearranged in certain cancers. We show that at least one of the mammalian TACC proteins appears to be associated with centrosomes and microtubules in human cells. We propose that this conserved C-terminal 'TACC domain' defines a new family of microtubule-interacting proteins.

Amino Acid Sequence↗
PubMed2000

Late onset heterozygous ornithine transcarbamylase deficiency mimicking complex partial status epilepticus.

A 57 year old woman with post-traumatic complex partial seizures was admitted because of recurrent episodes of altered mental state over the preceding 4 years, each lasting up to 5 days. There was a history of dietary protein intolerance since childhood and two of her daughters had died in the neonatal period from unexplained encephalopathies. In hospital she developed fluctuating confusion, amnesia, and sudden episodes of unresponsiveness. An EEG was consistent with complex partial status epilepticus but there was no response to benzodiazepines. Nasogastric feeding and sodium valproate were given and shortly afterwards she lapsed into a deep coma. Blood ammonia and urinary orotate were raised, and genetic testing confirmed that she was a carrier of a mutation in exon 3 of the ornithine transcarbamylase gene (C to T at position 92). Treatment with protein restriction, carnitine, and sodium phenylbutyrate led to a full recovery over a period of 3 months. To our knowledge this is the oldest age of onset yet described in a manifesting carrier. She is the fifth patient with heterozygous ornithine transcarbamylase deficiency reported to have had a severe reaction to sodium valproate. Hyperammonaemic encephalopathy should be considered in patients of any age who experience fluctuating confusion.

Diagnosis, Differential↗
PubMed1999

Substratum of pleiotrophin (HB-GAM) stimulates rat CG-4 line oligodendrocytes to adopt a bipolar morphology and disperse: primary O-2A progenitor glial cells disperse similarly on pleiotrophin.

Pleiotrophin (HB-GAM), an extracellular matrix-associated protein with a high content of basic amino acid residues, is expressed in the central nervous system during late pre- and early post-natal development and promotes neurite outgrowth in vitro. Here, we show that, on a substratum of pleiotrophin formed from a 5 or 10 microg/ml solution, undifferentiated rat CG-4 line oligodendrocytes adopt a bipolar morphology and disperse over the substratum, as we have previously shown with poly-L-lysine (Rumsby et al. Neurosci. Res. Commun. 23:101-109, 1998). On pleiotrophin substrata formed from coating solutions of 1 microg/ml and below, CG-4 line cells form aggregates and do not disperse, as is also the case with poly-L-lysine. The same dispersing effect is observed with rat primary 0-2A progenitor glial cells on pleiotrophin substrata from solutions of 5 and 10 microg/ml: 0-2A cells aggregate together on pleiotrophin substrata formed from lower concentrations and do not disperse. A pleiotrophin substratum enhances proliferation of CG-4 line oligodendrocytes and primary 0-2A progenitor glial cells. The results show that pleiotrophin provides a substratum that can influence progenitor oligodendrocyte morphology, aid cell dispersion, and perhaps also enhance progenitor oligodendrocyte cell growth.

Animals↗
PubMed1999

Cortical lesions in multiple sclerosis.

Although previous studies have shown that the lesions of multiple sclerosis may involve the cerebral cortex, there is little published research on the prevalence and distribution of such lesions. Using neuropathological techniques and MRI, a series of studies has been undertaken in order to assess this, in particular to identify their relationship to cortical veins. A serial MRI study showed that the use of gadolinium proffered an increase in cortical lesion detection of 140% and showed that 26% of active lesions arose within or adjacent to the cortex. In a post-mortem study, MRI under-reported lesions subsequently analysed neuropathologically, particularly those arising within the cortex. In a further 12 cases examined, 478 cortical lesions were identified, of which 372 also involved the subcortical white matter. Seven different lesion types were identified; the majority arose within the territory of the principal cortical veins, whilst the remaining quarter arose within the territory of the small branch or superficial veins. Small cortical lesions are common in multiple sclerosis and are under-reported by MRI. Investigation of the cortical venous supply shows how such lesions may arise, and why the majority also involve the underlying white matter.

Adult↗
PubMed1999

Neurological complications in Behçet's syndrome.

The neurological complications of Behçet's syndrome have not been characterized with clarity. We present the clinical features, imaging characteristics and CSF findings of a series of 50 patients seen at the National Hospital for Neurology and Neurosurgery over the past 10 years. In this series, vascular complications had a low prevalence, whereas involvement of the brainstem was common; spinal cord lesions, hemisphere lesions and meningoencephalitis also occurred. Optic neuropathy, vestibulocochlear and peripheral nerve involvement occurred, but were rare. The prognosis for recovery was in general good, and the majority of those followed-up over a median of 3 years (range 1-19 years) had only single attacks. One-third of patients underwent further attacks, and four underwent progressive deterioration leading to disability. Factors suggesting a poor prognosis are repeated attacks, incomplete recovery, progressive disease course and a high level of CSF leucocytosis during acute attack. These data should be of help in the further definition of the clinical characteristics of this rare neurological disorder and in the planning of treatment trials.

Adult↗
PubMed1999

Spatz-Lindenberg disease: a rare cause of vascular dementia.

BACKGROUND: Isolated cerebral thromboangiitis obliterans (Spatz-Lindenberg disease) is not well recognized as a cause of vascular dementia. CASE DESCRIPTION: A 58-year-old woman presented with dementia and pyramidal signs. Neuroimaging showed multiple areas of white matter change. Brain biopsy showed intimal thickening of the walls of leptomeningeal and intraparenchymal arteries, almost to complete occlusion, with an intact internal elastic lamina and media and without inflammation or infiltration. The cortex showed only moderate gliosis. CONCLUSIONS: Spatz-Lindenberg disease should be considered in the differential diagnosis of vascular dementia. Additional studies of its pathogenesis are required to determine appropriate treatment.

Cerebrovascular Disorders↗