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Biomedical subjects

P Woo

Publications and source records attributed to P Woo.

At least 127 records · Page 7Linked to original sources
PubMed1993

HLA-B27 subtypes in the spondarthropathies.

The spondarthropathy (Sp)-associated HLA-B27 antigen includes at least seven subtypes, B*2701-07, of which 01, 02, 05 and 07 occur in Caucasians. This study examined the B27 subtype distribution in British patients with Sp. The 133 HLA-B27+ subjects comprised 94 European Caucasian Sp (58 ankylosing spondylitis (AS), 22 reactive arthritis (ReA; 11 sexually acquired (SARA), 11 enteric (EReA)), eight undifferentiated Sp (USp), and six pauciarticular juvenile-onset chronic arthritis (pJCA)) patients, and 34 healthy Caucasian controls, together with four Asian Indian and one Chinese. 35S-labelled B27 was immunoprecipitated with anti-B27 MoAbs, and subtyped according to isoelectric point (pI) following isoelectric focussing. The use of B27 MoAb permitted subtype assignment without full class I HLA typing. The vast majority (95%) were B*2705 (Caucasian controls 31/34; AS 55/58; ReA 21/22; USp 8/8, and pJCA 6/6; Indian control 1/1 and AS 2/3; Chinese pJCA 1/1), and the remainder B*2702. No B*2701 or 07 subjects were identified. AS occurs in both B*2702 and 05 subjects, and we extend this observation to small numbers of ReA and of Indian AS subjects. This implicates molecular features shared between B27 subtypes, rather than subtype-determining regions of the antigen, in Sp pathogenesis.

Antibodies, Monoclonal↗
PubMed1993

Polyarteritis nodosa associated with streptococcus.

Twelve children are described with an essentially benign vasculitic illness in association with streptococcal infection. They demonstrated characteristic clinical features of nodular cutaneous polyarteritis with fever. Laboratory findings showed an acute phase response associated with raised antistreptolysin and antihyaluronidase titres in all patients and a positive throat culture for beta haemolytic streptococcus in three patients. Ten required corticosteroids. Two patients had systemic involvement with abnormal arteriography; both had appreciably raised white cell counts (> 40 x 10(9)/l). They may represent a subset of poststreptococcal vasculitis, requiring cytotoxic treatment for effective disease control.

Acute-Phase Reaction↗
PubMed1993

Partial thyroarytenoid myectomy: an animal study investigating a proposed new treatment for adductor spasmodic dysphonia.

A new surgical procedure with potential application for the treatment of adductor spasmodic dysphonia was performed on ten rabbits to assess surgical effects on laryngeal function. Using an external approach, partial unilateral thyroarytenoid (TA) muscle excision was performed through a thyroplasty cartilage window. The contralateral side was left undisturbed as a control. The animals were studied acutely and at 3 months using videolaryngoscopy. Electrophysiologic measurements were recorded at 3 months. The procedure was well tolerated by all animals, with no postoperative infection or aspiration. At 3 months, spontaneous and evoked (recurrent laryngeal nerve stimulation) TA muscle electromyographic potentials were measurable bilaterally. TA compound muscle action potential amplitudes were reduced on the side of myectomy. The threshold of recurrent laryngeal nerve stimulation needed to produce observable vocal fold adduction was increased on the side operated on. Perioperative and long-term (3 months) videolaryngoscopy demonstrated preservation of laryngeal competence with good true vocal cord adduction. Histologic analysis with whole organ sections showed replacement of excised muscle with loose fibroareolar tissue. No evidence of muscle regeneration was observed. The vocal ligament and vocal fold mucosa were intact and undistorted in all specimens. This procedure is technically simple and appears to effectively result in a functional yet weakened TA muscle. Because myectomy includes motor unit end-plate excision, problems associated with reinnervation may be circumvented. TA myectomy may be applicable in patients with focal laryngeal dystonia to decrease muscle spasm.

Animals↗
PubMed1992

Interleukin 1 induces NF-kappa B through its type I but not its type II receptor in lymphocytes.

It is not known whether one or both of the interleukin 1 (IL1) receptors mediates the induction of the DNA-binding protein NF-kappa B. Nuclear extracts of the murine lines EL4.NOB.1 and 70Z/3, which bear the type I (80 kDa) and type II (67 kDa) IL1 receptor, respectively, were analyzed by an electrophoretic mobility shift assay. A 265-base pair sequence of the human serum amyloid A gene or a synthetic oligonucleotide each containing the NF-kappa B site were used as the DNA probes. IL1 induction of NF-kappa B was rapid (optimal at 15-30 min) and transient in both cell types. The IL1 receptor antagonist (IL1ra), which binds strongly to the type I receptor, inhibited the NF-kappa B response in both cell lines. IL1ra did not bind to the type II receptor on 70Z/3 cells as judged by competition for binding with 125I-IL1 alpha. When 125I-IL1ra binding to 70Z/3 cells was measured, a small number (10/cell) of high affinity sites (Kd = 5 x 10(-12) M) were detected. These were likely to have been type I receptor because an antibody to this inhibited the NF-kappa B induction in 70Z/3 cells (as well as EL4). Potential signal transduction mechanisms involving protein kinase C or oxygen radicals were studied. Phorbol 12-myristate 13-acetate induced NF-kappa B with a similar time course to IL1 in 70Z/3 but only after 4 h in EL4.IL1 was unaffected by a protein kinase C inhibitor (staurosporine). H2O2 did not mimic IL1, and IL1 was not inhibited by an antioxidant. The type I receptor mediates the induction of NF-kappa B in response to IL1 via a signaling mechanism that still remains to be identified.

Animals↗
PubMed1992

Analysis of the genomic and derived protein structure of a novel human serum amyloid A gene, SAA4.

We have determined the structure of the novel SAA gene, SAA4. The gene is 6.2 kb in length and comprises three introns and four exons. Introns 2 and 3 are significantly longer than those of the other human SAA genes. We have sequenced the exons and junction fragments and have shown that the sequence is the same as c-SAA[1] and does not correspond to the pseudogene carried on GSAA4[2]. The predicted SAA4 protein sequence has an eight amino acid insertion relative to the other human SAA proteins and is more closely related to rabbit and mouse SAA proteins than to the other human SAA proteins, or to those of animal species which also possess an insertion. We have analysed the predicted SAA4 protein relative to the other human SAA proteins and have identified three important structural regions. We predict that region 1 of SAA4 represents a lipid binding domain. Region 2 forms an extensive, distinctive, hydrophobic beta sheet region in place of a helical region. In region 3, SAA4 is the only SAA protein having an alpha helix which is not amphipathic. We predict that the SAA4 protein retains a modified function of the conserved region, retains the Ca2+ binding site, has an amino terminal surface site and has a potentially distinct secretion pattern. Together, these differences indicate a distinct function from those of the other SAA proteins.

Amino Acid Sequence↗
PubMed1992

Acquired laryngomalacia: epiglottis prolapse as a cause of airway obstruction.

Epiglottis prolapse during inspiration is an unusual cause of upper airway obstruction. It occurs primarily in patients who have lost pharyngeal airway support because of previous surgery or after head injury and coma. Eight cases of epiglottis prolapse are presented. One patient had epiglottis prolapse after resection of floor of mouth cancer and another after laryngeal fracture. The rest of the cases were seen in patients recovering from head injury and coma. Videolaryngoscopy shows the larynx to assume an ovoid shape within the pharynx. There is loss of the usual anterior to posterior pharyngeal and laryngeal dimension. The epiglottis is in a more horizontal position at rest. During inspiration, the epiglottis prolapses into the endolarynx, causing subtotal airway obstruction. Laryngeal obstruction due to epiglottis prolapse can prevent decannulation in the head-injured and can be the cause of obstructive sleep apnea. Endoscopic carbon dioxide laser epiglottectomy was successful in management of these cases.

Adult↗
PubMed1992

Intraoperative laryngeal electromyographic assessment of patients with immobile vocal fold.

The differential diagnosis of laryngeal ankylosis versus paralysis is occasionally difficult in patients with immobile vocal folds. Eight patients with acute and chronic evidence of vocal fold immobility were investigated by intraoperative electromyography (IEMG) during planned microlaryngoscopy. Bipolar hook wire electrodes were inserted into the thyroarytenoid muscle, of which the electrical activity was monitored during neuromotor blockade and emergence from anesthesia. The normal side and the side with ankylosis or stenosis showed normal IEMG activity. There was progressive recruitment of larger motor units during recovery from muscle relaxation. Patients with laryngeal paralysis failed to show such recruitment patterns. Thus, IEMG can be used as a diagnostic tool during operative laryngoscopy to differentiate neuromotor injury from anatomic causes of vocal fold immobility. The advantages of IEMG are its ease of application and certainty of electrode position. It can also be used to monitor recurrent nerve integrity and detect early laryngospasm. Further IEMG clinical study is warranted.

Adult↗
PubMed1992

Dysphonia in the aging: physiology versus disease.

A chart review from 151 dysphonic patients over the age of 60 was done to define aging related voice disorders. Overwhelmingly, patients suffered from dysphonia due to disease processes associated with aging rather than to physiologic aging alone. These include: 1. central neurological disorders affecting laryngeal function (e.g., stroke, Parkinson's disease, essential tremor, Alzheimer's disease); 2. benign vocal fold lesions (e.g., Reinke's edema, benign and dysplastic epithelial lesions); 3. inflammatory disorders (e.g., laryngitis sicca, medication effect); 4. laryngeal neoplasia; and 5. laryngeal paralysis. Typical laryngeal findings of vocal fold bowing and breathiness consistent with presbylarynges were present in only six patients. Presbylarynges is not a common disorder and should be a diagnosis of exclusion made only after careful medical and speech evaluation.

Aged↗
PubMed1991

Constitutive and NF-kappa B-like proteins in the regulation of the serum amyloid A gene by interleukin 1.

Serum amyloid A (SAA) is a major acute-phase protein whose chronic production by the liver can lead to the fatal disorder of secondary amyloidosis. Control of SAA is mediated by several inflammatory cytokines, including interleukin 1 (IL-1). To study the cis-acting regulatory elements responsible for constitutive and IL-1-induced expression, DNA constructs containing varying lengths of the promoter region from the human SAA2 beta gene 5' to the bacterial reporter gene, chloramphenicol acetyltransferase (CAT), were generated and transfected into human hepatoma cells, HepG2. Both positive and negative regulatory elements were found in the 5' flanking region of the human SAA2 beta gene. The more proximal region contains an IL-1 enhancer sequence GGGACTTTCC (SAA kappa B1; between -82 and -91), the binding site for the ubiquitous transcription factor NF-kappa B. IL-1 induction of the binding of nuclear factor to this sequence is maximal between 5 min and 30 min after incubation with IL-1 and negative in cells incubated for 60 min or longer. Mutation of the SAA kappa B1 sequence to a nonbinding form of NF-kappa B (CTCACTTTCC) abolishes the IL-1 effect. The SAA 5' region also contained an upstream repressor element, shown by transfection experiments. Within this element, a second NF-kappa B binding site (SAA kappa B2; -626 to -635) was found, and mutation of SAA kappa B2 to a non-NF-kappa B-binding form results in an increase in both constitutive + IL-1 stimulated SAA transcription.(ABSTRACT TRUNCATED AT 250 WORDS)

Amyloid↗
PubMed1991

Studies in vivo and in vitro of serum amyloid P component in normals and in a patient with AA amyloidosis.

Pure serum amyloid P component (SAP) was isolated from a normal donor pool, from individuals with the different genotypes of an MspI restriction fragment length polymorphism (RFLP) linked to the SAP gene, and from a patient with AA amyloidosis. The SAP preparations were all identical and all behaved as a single homogeneous species in polyacrylamide gel electrophoresis, isoelectric focussing, reverse-phase chromatography, binding in vitro to phosphoethanolamine-Sepharose (binding constant 2.4 x 10(7) l/mol) and AL amyloid fibrils (1.6 x 10(8) l/mol), and binding to amyloid deposits in vivo in mice with casein-induced amyloidosis. The in vivo metabolism of 125I-SAP from a single donor was normal and identical in three healthy individuals representing the three different MspI RFLP genotypes. There is thus no frequent polymorphism of SAP in normal subjects, and SAP altered with respect to the characteristics studied here is not a necessary condition for pathogenesis of systemic AA amyloidosis.

Amyloidosis↗
PubMed1991

The human acute-phase serum amyloid A gene family: structure, evolution and expression in hepatoma cells.

Serum amyloid A (SAA) proteins are a group of phylogenetically conserved acute-phase reactants. Evidence is presented here for the existence of four genetic loci for the human serum amyloid A (SAA) genes. The first locus was defined by three contiguous lambda clones spanning approximately 30 kb which contained a single SAA gene encoding apoSAA1 beta. Allelic variants were isolated at the second locus: a novel clone encoding apoSAA2 alpha was distinguished from SAA2 beta (previously known as SAAg9, Ref.1) by a His/Arg polymorphism at residue 71.SAA1 and SAA2 found in the high density lipoprotein fraction of acute-phase plasma were approximately 90% homologous at the nucleotide level. Homology in the 5' flanking regions was reflected functionally with similar transcriptional responses to inflammatory cytokines in transfected hepatoma cells. A further novel gene, SAA4, was isolated from a cosmid library and mapped 10 kb downstream of SAA2. The locus defining SAA3 has been described elsewhere. Polymorphisms were detected at both SAA1 and SAA2 loci by Southern analysis and the entire SAA region mapped to discrete fragments by pulsed field analysis. The four genes account for all the hybridizing bands present on Southern analyses in a Caucasian population.

Base Sequence↗