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Biomedical subjects

P Woo

Publications and source records attributed to P Woo.

At least 109 records · Page 6Linked to original sources
PubMed1995

Juvenile chronic arthritis.

The nomenclature and classification criteria for arthritis in children should be dealt with initially as separate issues, although they are undoubtedly intertwined. The classification criteria should aim to delineate homogeneous patient populations, yet should be flexible enough to incorporate advances in disease knowledge. It should be recognized that arriving at an international consensus for classification criteria will merely provide a set of operational definitions to facilitate research, and not a set of diagnostic criteria. Indeed the only point to obtaining consensus is to begin a process of systematic ongoing review of the criteria. The labels attached to any of these diseases should facilitate accurate communication. In view of the heterogeneous nature of childhood arthritis, consideration should be given to using a broad umbrella term such as juvenile or childhood arthritis only for communicating with the lay public. Medical nomenclature should be formulated to reflect accurately homogeneous subgroups of arthritis, and should not artificially proscribe a relationship between paediatric and adult disease.

Arthritis, Juvenile↗
PubMed1995

Inflammatory cytokine responses in juvenile chronic arthritis.

The inflammatory cytokines interleukin 1 beta (IL-1 beta) interleukin 6 (IL-6), tumour necrosis factor alpha (TNF alpha) and the anti-inflammatory peptide--the interleukin 1 (IL-1) receptor antagonist--were measured in the plasma of children with juvenile chronic arthritis (JCA). In the two subgroups studied (polyarticular JCA and systemic JCA), there was good correlation between laboratory measures of disease activity C-reactive protein (CRP), erythrocyte sedimentation rate and clinical scores for disease activity. Despite higher levels of CRP in the systemic group IL-1 beta levels were lower and regression analysis recorded a difference in the relationship between CRP and IL-1 beta within the two clinical groups. In contrast, IL-6 levels were high in the systemic group and correlated with disease activity. No such correlation was observed in the polyarticular group. Five children with systemic JCA were studied during the febrile phase of their illness. IL-6 levels rose and fell with the fever. TNF alpha levels also rose and fell but out of phase with the fever. In contrast IL-1 beta levels were either undetectable throughout the febrile episode or only became detectable as the temperature reduced to normal. The IL-1 receptor antagonist was usually found in 1000-fold excess over IL-1 beta, levels rising and falling with the fever. These results demonstrate difference in the cytokine profiles and acute phase protein responses in polyarticular and systemic JCA. This would suggest different pathogenic mechanisms for these two groups of JCA with IL-6 being the more important cytokine in systemic JCA.

Acute Disease↗
PubMed1995

Increase of activated factor VIIA and haemostatic molecular markers in juvenile chronic arthritis.

Activated factor VIIa (FVIIa), von Willebrand factor antigen (vWF:Ag), D-dimer and thrombin-antithrombin III complex (TAT) were measured to monitor coagulation status in patients with juvenile chronic arthritis (JCA). Subjects included 14 patients with systemic JCA, 16 with pauciarticular JCA and 16 with polyarticular JCA without disseminated intravascular coagulopathy, thrombosis or liver dysfunction. All types of JCA showed an increase of FVIIa, D-dimer and TAT, indicating enhanced activation of coagulation. In systemic JCA only there was also characteristically an elevation of vWF:Ag. We conclude that all types of JCA constitute a state of subclinical hypercoagulopathy caused by tissue damage and that additionally systemic JCA involves a prothrombotic state associated with or precipitated by vasculitis.

Antifibrinolytic Agents↗
PubMed1995

Glottal patency during experimental seizures in piglets.

Tracheostomized cats and piglets demonstrate respiratory stimulation during experimental seizures, whereas airway intact piglets demonstrate hypoventilation and increased subglottic resistances. The purpose of this study was to characterize the role of the vocal folds in contributing to these increased subglottic resistances during experimental seizures. A controlled animal study was performed in six anesthetized, spontaneously breathing, hyperoxic piglets who had subglottic pressure and airflow measured. A fiberoptic video scope directed into the cephalad trachea recorded subglottic images of the vocal folds. Glottal area patency (GAP) was evaluated at inspiratory onset (Io), peak inspiratory pressure (Ip), and expiratory onset (Eo) for four to five consecutive breaths under baseline control, ictal, interictal, and anticonvulsant conditions. Seizures were induced with i.v. pentylenetetrazol or bicuculline. Normalized GAP was greatest at Ip under all conditions, except anticonvulsant. During ictal periods, piglets demonstrated significant reductions in mean GAP throughout the respiratory cycle (Io, 98%; Ip, 78%; Eo, 98%), compared with baseline (p < 0.001, repeat measures analysis of variance). During ictal discharges, hypoventilation and glottal obstruction resulted in significant reductions in mean arterial pH (-0.35) and PaO2 (-39 kPa) and elevations in PaCO2 (+8.1 kPa), compared with baseline conditions. During interictal conditions mean GAP at Ip was increased, whereas at Eo (-66%) GAP was reduced, compared with control. These data demonstrate that the vocal folds are tonically adducted throughout the respiratory cycle during ictal phases and have increased expiratory adduction during interictal phases of seizures induced with standard i.v. convulsants in hyperoxic piglets.

Analysis of Variance↗
PubMed1994

Use of somatic cell hybrids and fluorescence in situ hybridization to localize the functional serum amyloid A (SAA) genes to chromosome 11p15.4-p15.1 and the entire SAA superfamily to chromosome 11p15.

The serum amyloid A (SAA) superfamily consists of two acute phase genes, SAA1 and SAA2; a pseudogene, SAA3; and a constitutively expressed gene, SAA4. The SAA proteins, which are found associated with high-density lipoprotein, are believed to have an essential function. Chronic infection, inflammation, or trauma causes very high levels of the acute phase SAA proteins. This may result in the potentially fatal condition, amyloidosis, in which amyloid fibrils are deposited in the essential organs. Somatic cell hybrids have been used by several groups to map one or more of the SAA genes to chromosome 11p. We used FISH analysis and PCR amplification of DNA from 17 somatic cell hybrids carrying all or part of chromosome 11 as their only human component to fine map systematically the chromosomal location of the entire SAA superfamily. We demonstrate by these methods that the location of the entire SAA superfamily is at 11p15. Furthermore, we have demonstrated that SAA1, SAA2, and SAA4, i.e., all of the functional genes of the superfamily, map within this region to chromosome 11p15.4-p15.1.

Animals↗
PubMed1994

Aerodynamic and stroboscopic findings before and after microlaryngeal phonosurgery.

Acoustic, aerodynamic, and laryngo-video-stroboscopy (LVS) studies were done on 50 patients before and after microlaryngeal surgery for benign vocal fold lesions. Perceptual pre- and postratings were also obtained. After microlaryngeal surgery, statistically significant differences between pre- and posttreatment conditions included postoperative findings of (a) a lowering of mean flow rate, (b) an increase in glottal efficiency, and (c) an increase in maximum sound pressure level. There was no significant improvement in maximum phonation time. Stroboscopy findings showed changes of glottal configuration, linearity of the vocal fold edge, amplitude of vocal fold vibration, excursion of the mucosal wave, and periodicity. Acceptable perceptual voice quality appeared to depend on a straight vocal fold edge, good vibratory amplitude, and good mucosal wave. Improved understanding of vocal function after phonosurgery should help us refine surgical principles and techniques. The combined use of LVS and phonatory function measures is advocated.

Glottis↗
PubMed1994

The functional and psychological outcomes of juvenile chronic arthritis in young adulthood.

The functional and psychological outcome of 43 patients with polyarticular juvenile arthritis was assessed in order to evaluate the impact of disease on their quality of life. Mean disease duration was 19.7 yr (range 10-39 yr), mean age 26.7 yr (range 18-54 yr) with sex ratio 1:3 (male:female). Severe disability was present in 8% of systemic onset, 34% of RF negative (Rh-P), 38% of RF positive (Rh+P) and 86% of extended pauci-articular (ExP) juvenile arthritics-this last high percentage was due to ocular impairment. The Rh+P had more hip (100% of the group) and knee prostheses (31%) compared with Rh-P (77 and 11% respectively). The Rh+P and ExP groups were the most disabled with the highest proportions of patients with currently active disease (85 and 71% respectively). Psychological testing showed that 21% of the patients were clinically depressed and the rate increased (P = 0.06) with the degree of disability. The proportion of patients demonstrating an anxious preoccupation with their disease increased (P = 0.002) with the degree of disability. Despite this, 66% of patients were employed and 38% felt that their arthritis had no effect on their ability to form relationships.

Adult↗
PubMed1994

The fifth serum amyloid A-related gene sequence, GSAA4, is SAA3.

The human serum amyloid A (SAA) gene family consists of two acute phase genes, SAA1 and SAA2; a pseudogene, SAA3 and a fourth gene, SAA4. The existence of SAA4 was first described in this laboratory. Subsequently, Sack & Talbot isolated a clone, designated GSAA4, which had homology to SAA3. The clone was described as the same as SAA4 and was characterized as a pseudogene. However, our restriction site and sequence analyses of SAA4 demonstrated that SAA4 and GSAA4 are separate entities. SAA4 encodes a functional, constitutively expressed protein. Recently, the GSAA4 clone has been reported by Sellar & Whitehead as constituting a fifth SAA-related sequence. However, we have demonstrated that GSAA4 has striking homology with the 3' terminus of SAA3 in the reverse orientation. Furthermore, computer analyses strongly indicate that the GSAA4 or fifth SAA-related sequence is in fact, a clone from the SAA3 locus. We have amplified, isolated and sequenced fragments from genomic DNA which demonstrate that the GSAA4 sequence is the correct sequence of the 3' region of SAA3. The SAA family must therefore still be viewed as consisting of four SAA loci at present.

Amino Acid Sequence↗
PubMed1994

Oxidation of LDL to a biologically active form by derivatives of nitric oxide and nitrite in the absence of superoxide. Dependence on pH and oxygen.

A key factor in atherogenesis is oxidation of LDL in the subendothelial space. In the normal vessel wall or in the thickened intima of diseased vessels, this space is rich in nitric oxide (NO.) released from endothelial cells, smooth muscle cells, and macrophages. To determine whether NO. has a role in LDL oxidation, we exposed human LDL to NO. under aerobic and anaerobic conditions and at acidic and neutral pH. Spectrophotometric detection of beta-carotene in the LDL was used as a marker for LDL oxidation. Depletion of beta-carotene was observed in LDL treated with NO. under aerobic conditions but not under anaerobic conditions. In contrast, treatment of LDL with sodium nitrite did not require oxygen for beta-carotene depletion, although depletion was increased when O2 was present. Furthermore, low pH greatly accelerated LDL oxidation by either NO. gas or by nitrite (NO2-). Depletion of beta-carotene corresponded with formation of conjugated dienes, increased susceptibility to further oxidation, and aggregation of apolipoprotein B-100, but did not increase electrophoretic mobility of LDL. Also, nitrite-oxidized LDL demonstrated biological properties similar to minimally oxidized LDL, including stimulation of monocyte adhesion and inhibition of lipopolysaccharide-induced neutrophil binding to endothelium. These results indicate that NO. under certain circumstances may contribute to oxidative modification of LDL and may have a role in atherogenesis.

Animals↗
PubMed1994

Diagnosis and treatment of persistent dysphonia after laryngeal surgery: a retrospective analysis of 62 patients.

Sixty-two patients with persistent or recurrent dysphonia after laryngeal surgery underwent interdisciplinary voice evaluation, laryngostroboscopy, and objective measurements of vocal function. The causes of persistent dysphonia were attributed to vocal fold scarring (n = 22), residual mass lesion (n = 8), residual inflammation (n = 13), recurrent mass (n = 4), and hyperfunctional voice disorder (n = 7). Laryngoscopy often showed excessive ventricular compression and anterior-to-posterior laryngeal compression. Ventricular dysphonia was often a compensatory gesture in response to poorly mobile vocal fold membranes. Stroboscopy was able to document a number of abnormalities which included abnormalities of laryngeal configuration, vibratory asymmetry, reduction of amplitude, and mucosal wave. Using a diversified approach consisting of medical therapy, voice therapy, and repeat surgery, better vocal function was able to be restored in the majority of patients. An interdisciplinary approach to the dysphonic patient after laryngeal surgery was most useful in defining the pathology and refining a treatment rehabilitation program.

Adult↗
PubMed1994

Treatment of growth retardation in juvenile chronic arthritis with recombinant human growth hormone.

OBJECTIVE: To evaluate the effect of recombinant human growth hormone (rhGH) on the linear growth of children with persistently active juvenile chronic arthritis (JCA), most of whom were receiving steroid therapy. All of them were severely growth retarded, but had adequate GH secretion. METHODS: After monitoring height velocity for one year, children were treated for the following year with either 12 IU/m2 or 24 IU/m2 of rhGH. During this period disease activity, drug treatment, dietary intake and bone maturation as well as linear growth were documented. RESULTS: There was a significant increase in height velocity in almost all children during the treatment period. Children with mild to moderate disease activity grew at a better rate than those with very active disease. Children with polyarticular disease responded better than those with systemic JCA. Those children receiving high dose rhGH grew significantly more than those on the low dose regimen. Bone maturation did not exceed chronological age. CONCLUSION: We conclude the rhGH significantly increases the height velocity during one year of treatment. However, its effect on ultimate adult height remains unknown. Thus extensive longterm studies are required to evaluate the risk benefit ratio of this costly treatment.

Adolescent↗
PubMed1993

The role of NF-kappa B and NF-IL6 transactivating factors in the synergistic activation of human serum amyloid A gene expression by interleukin-1 and interleukin-6.

To understand the mechanisms by which large increases in serum amyloid A (SAA) occur during the acute phase response, human hepatoma cells were transfected with SAA2 gene reporter plasmids and stimulated with combinations of cytokines. Although interleukin-1 (IL-1) and interleukin-6 (IL-6) stimulated transcription from this promoter individually, addition of both mediators produced a response between two and nine times greater than the expected additive response. This synergistic activation was dependent on the integrity of at least two cis-acting sequences in the SAA2 enhancer. The SAA2 NF-kappa B site was required functionally for the response to both IL-1 and IL-6 alone as well as for synergistic activation; however, IL-6 did not directly induce binding of nuclear proteins to the NF-kappa B sequence. A NF-IL6 site was required for full induction by IL-1 and IL-6, and also mediated strong transactivation by recombinant NF-IL6. Furthermore, transfected NF-IL6 synergized strongly with co-transfected NF-kappa B, particularly with RelA (p65). However synergy between IL-1 and IL-6 was only partly reduced by mutation of the NF-IL6 site, indicating further levels of interaction in addition to the NF-kappa B/NF-IL6 cooperativity.

Base Sequence↗
PubMed1993

Serum amyloid P component scintigraphy and turnover studies for diagnosis and quantitative monitoring of AA amyloidosis in juvenile rheumatoid arthritis.

OBJECTIVE: To evaluate aspects of the natural history of AA amyloidosis complicating juvenile rheumatoid arthritis (JRA), and its response to therapy with chlorambucil. METHODS: Scintigraphy and 7-day turnover studies were performed in JRA patients with histologically proven (n = 35) or clinically suspected (n = 30) AA amyloidosis, following intravenous injection of 123I and 125I-labeled serum amyloid P component (SAP). Prospective monitoring studies were performed over 2-3 years in 20 patients with amyloidosis. All but 2 amyloidosis patients were treated with chlorambucil. RESULTS: Positive scanning results were obtained in all patients in whom imaging was performed within 12 years of positive biopsy findings of amyloid and in 5 patients with clinically suspected amyloidosis. Negative scanning results with normal SAP metabolism, indicating regression of amyloid, were obtained in 4 patients whose amyloidosis had been in full clinical remission for more than 12 years. Prospective monitoring studies in patients whose JRA-associated inflammatory activity was in remission demonstrated regression of amyloid in 8 patients and no substantial changes in 8 others; however, in 4 further patients with active inflammation, there was accumulation of amyloid. There was a very poor correlation between the amount of amyloid present at a particular site and the resultant organ dysfunction. CONCLUSION: Radiolabeled SAP scintigraphy and turnover studies are useful complementary tools in the diagnosis, screening, and quantitative monitoring of type AA amyloidosis in JRA. The amyloid deposits may progress and/or regress at different rates in different anatomic sites over short periods.

Adolescent↗
PubMed1993

Gastro-duodenal damage due to non-steroidal anti-inflammatory drugs in children.

Thirteen juvenile chronic arthritis patients with abdominal symptoms related to non-steroidal anti-inflammatory drug therapy were endoscoped before and after a 6-week course of either misoprostol or ranitidine therapy. Major presenting symptoms were generalized abdominal pain and nausea. Symptoms did not correlate well with endoscopic findings which revealed no evidence of ulceration and minimal erosive damage. Five patients had mild erythema or gastritis. Bleeding lesions were confined to small numbers of petechiae. Following treatment with either misoprostol or ranitidine, patients improved symptomatically without a corresponding improvement on endoscopic and histological examination of stomach and duodenum. Both treatments were well tolerated.

Adolescent↗
PubMed1993

Study of antibodies to histones and histone synthetic peptides in pauciarticular juvenile chronic arthritis.

The objective of this study was to determine the prevalence of histone antibodies in early onset pauciarticular juvenile chronic arthritis (JCA), and to assess any association with disease activity in terms of arthritis or uveitis. Forty-four children with early onset pauciarticular JCA have been assessed prospectively using clinical and laboratory parameters. Sera were collected from these patients during clinical follow-up. Some of them had serial measurements during the period of study. Patient sera were analysed for histone antibodies by ELISA. A further study using 30 synthetic peptides of calf thymus core histones was performed by ELISA. Seventy-five per cent of children have IgM antibodies to histone, usually to more than one type. The highest values were anti H3 and H4 antibodies. There was no correlation between the level of anti-histone antibodies and anterior uveitis. There were increased levels of IgG antibodies to histone peptides, in particular the N- and C-terminal peptides of H3 in 70.5% of children. Antibodies to H3 peptides tend to be in patients with chronic anterior uveitis (P = 0.04).

Antibodies↗