Pub Date : 1994-01-01DOI: 10.1093/OXFORDJOURNALS.QJMED.A068916
C. Winearls, F. Sanderson
{"title":"Treatment of aggressive idiopathic membranous glomerulonephritis.","authors":"C. Winearls, F. Sanderson","doi":"10.1093/OXFORDJOURNALS.QJMED.A068916","DOIUrl":"https://doi.org/10.1093/OXFORDJOURNALS.QJMED.A068916","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 4 1","pages":"199-201"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/OXFORDJOURNALS.QJMED.A068916","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61292657","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-01-01DOI: 10.1093/OXFORDJOURNALS.QJMED.A068919
V. Dhillon, S. McCALLUM, D. Latchman, D. Isenberg
We have previously shown that the 90 kDa heat-shock protein (hsp90) is notably elevated in lupus patients with active neuro-psychiatric (NP) and/or cardio-respiratory (CR) disease. This elevation is dependent upon enhanced transcription of the hsp90 beta gene. Serial studies have shown that changes in hsp90 levels have a high level of sensitivity for changes in activity of NP, CR, haematological and renal SLE. We now present evidence that overexpression of hsp90 in lupus patients is associated with the presence of the anti-phospholipid syndrome, and with the absence of the HLA allo-/haplotypes most commonly found in this particular cohort of patients. We conclude that the upregulation of hsp90 expression in SLE has a genetic basis, and that this may be directly involved in pathogenesis in subsets of patients with this disease.
{"title":"Elevation of the 90 kDa heat-shock protein in specific subsets of systemic lupus erythematosus.","authors":"V. Dhillon, S. McCALLUM, D. Latchman, D. Isenberg","doi":"10.1093/OXFORDJOURNALS.QJMED.A068919","DOIUrl":"https://doi.org/10.1093/OXFORDJOURNALS.QJMED.A068919","url":null,"abstract":"We have previously shown that the 90 kDa heat-shock protein (hsp90) is notably elevated in lupus patients with active neuro-psychiatric (NP) and/or cardio-respiratory (CR) disease. This elevation is dependent upon enhanced transcription of the hsp90 beta gene. Serial studies have shown that changes in hsp90 levels have a high level of sensitivity for changes in activity of NP, CR, haematological and renal SLE. We now present evidence that overexpression of hsp90 in lupus patients is associated with the presence of the anti-phospholipid syndrome, and with the absence of the HLA allo-/haplotypes most commonly found in this particular cohort of patients. We conclude that the upregulation of hsp90 expression in SLE has a genetic basis, and that this may be directly involved in pathogenesis in subsets of patients with this disease.","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 4 1","pages":"215-22"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/OXFORDJOURNALS.QJMED.A068919","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61292682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chest pain with normal coronary arteries.","authors":"J W Paulley","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 1","pages":"69"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19132058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-01-01DOI: 10.1093/OXFORDJOURNALS.QJMED.A068915
R. Souhami
{"title":"Drug-DNA interactions: new discoveries and possibilities for cancer treatment.","authors":"R. Souhami","doi":"10.1093/OXFORDJOURNALS.QJMED.A068915","DOIUrl":"https://doi.org/10.1093/OXFORDJOURNALS.QJMED.A068915","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 4 1","pages":"195-7"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/OXFORDJOURNALS.QJMED.A068915","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61292650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chest pain with normal coronary arteries.","authors":"P B Fowler","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 1","pages":"68-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19132057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
T Ezri, S Kunichezky, A Eliraz, D Soroker, D Halperin, A Schattner
We review current concepts about the clinical manifestations, diagnosis and treatment of patients with bronchiolitis obliterans (BO) with emphasis on clinical/pathological correlations and recent developments. BO is a relatively rare disease, but its incidence is probably higher than generally believed and is continuously rising, partly because of better recognition, but also because of increased exposure to industrial fumes, and its occurrence in lung transplantation. BO is characterized histologically by varying degrees of obliteration of the lumen of the respiratory bronchioles by organizing connective tissue often extending into the alveoli ('proliferative' BO with organizing pneumonia--BOOP) or by more extensive fibrosis and scarring of the more proximal, conductive bronchioles ('constrictive' BO). Diverse clinical conditions have been associated with the development of BO, notably viral and mycoplasma infection, toxic fume exposure and immune reactions in the setting of a collagen vascular disease, drug reaction or organ transplantation. The clinical course and features of BO may vary considerably according to the aetiology, histological pattern and stage of the disease. The most common presentation is that of a progressive dry cough and dyspnea, associated with diffuse patchy interstitial lung infiltrates on chest X-ray. In the more advanced cases, lung function tests show either restrictive or obstructive defects, depending on the extent of alveolar involvement, and hypoxemia without CO2 retention. The diagnosis is often possible on clinical grounds, however, in a seriously ill patient uncertainty should be resolved by tissue diagnosis, preferably by open lung biopsy. Treatment is based on symptomatic therapy. The use of corticosteroids is controversial, but common. Patients with BOOP are exceptional, in that there may be no underlying condition ('idiopathic' BOOP or cryptogenic organizing pneumonia--COP), a restrictive ventilatory defect is usual and the response to corticosteroids often remarkable.
{"title":"Bronchiolitis obliterans--current concepts.","authors":"T Ezri, S Kunichezky, A Eliraz, D Soroker, D Halperin, A Schattner","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>We review current concepts about the clinical manifestations, diagnosis and treatment of patients with bronchiolitis obliterans (BO) with emphasis on clinical/pathological correlations and recent developments. BO is a relatively rare disease, but its incidence is probably higher than generally believed and is continuously rising, partly because of better recognition, but also because of increased exposure to industrial fumes, and its occurrence in lung transplantation. BO is characterized histologically by varying degrees of obliteration of the lumen of the respiratory bronchioles by organizing connective tissue often extending into the alveoli ('proliferative' BO with organizing pneumonia--BOOP) or by more extensive fibrosis and scarring of the more proximal, conductive bronchioles ('constrictive' BO). Diverse clinical conditions have been associated with the development of BO, notably viral and mycoplasma infection, toxic fume exposure and immune reactions in the setting of a collagen vascular disease, drug reaction or organ transplantation. The clinical course and features of BO may vary considerably according to the aetiology, histological pattern and stage of the disease. The most common presentation is that of a progressive dry cough and dyspnea, associated with diffuse patchy interstitial lung infiltrates on chest X-ray. In the more advanced cases, lung function tests show either restrictive or obstructive defects, depending on the extent of alveolar involvement, and hypoxemia without CO2 retention. The diagnosis is often possible on clinical grounds, however, in a seriously ill patient uncertainty should be resolved by tissue diagnosis, preferably by open lung biopsy. Treatment is based on symptomatic therapy. The use of corticosteroids is controversial, but common. Patients with BOOP are exceptional, in that there may be no underlying condition ('idiopathic' BOOP or cryptogenic organizing pneumonia--COP), a restrictive ventilatory defect is usual and the response to corticosteroids often remarkable.</p>","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 1","pages":"1-10"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7108655/pdf/87-1-1.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19132124","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-01-01DOI: 10.1093/OXFORDJOURNALS.QJMED.A068920
G. Warwick, C. G. Geddes, J. Boulton-Jones
Twenty-one patients with membranous nephropathy, heavy proteinuria and progressive renal failure were treated with alternating monthly cycles of corticosteroids and chlorambucil for six months. Four patients received repeat courses. After a median period of follow-up of 39 months, three patients had died, six were receiving renal replacement therapy or had serum creatinine > 500 mumol/l, and one had progressive renal failure. Eleven patients had either stable or improved renal function, as judged by serum creatinine concentration. Of these eleven, four patients were in partial remission (daily protein excretion 0.2-2.0 g), and two were in complete remission. There was a tendency for those who received intravenous methylprednisolone to have a more favourable outcome. There was a high incidence of side-effects, with significant complications related to drug therapy observed in > 50% of subjects. Although individual patients appeared to respond well, sometimes dramatically, these results are less encouraging than other reports. We would urge caution in the use of this form of therapy, particularly in older patients who may have occult neoplasms, impaired glucose intolerance or pre-existing cardiac disease.
{"title":"Prednisolone and chlorambucil therapy for idiopathic membranous nephropathy with progressive renal failure.","authors":"G. Warwick, C. G. Geddes, J. Boulton-Jones","doi":"10.1093/OXFORDJOURNALS.QJMED.A068920","DOIUrl":"https://doi.org/10.1093/OXFORDJOURNALS.QJMED.A068920","url":null,"abstract":"Twenty-one patients with membranous nephropathy, heavy proteinuria and progressive renal failure were treated with alternating monthly cycles of corticosteroids and chlorambucil for six months. Four patients received repeat courses. After a median period of follow-up of 39 months, three patients had died, six were receiving renal replacement therapy or had serum creatinine > 500 mumol/l, and one had progressive renal failure. Eleven patients had either stable or improved renal function, as judged by serum creatinine concentration. Of these eleven, four patients were in partial remission (daily protein excretion 0.2-2.0 g), and two were in complete remission. There was a tendency for those who received intravenous methylprednisolone to have a more favourable outcome. There was a high incidence of side-effects, with significant complications related to drug therapy observed in > 50% of subjects. Although individual patients appeared to respond well, sometimes dramatically, these results are less encouraging than other reports. We would urge caution in the use of this form of therapy, particularly in older patients who may have occult neoplasms, impaired glucose intolerance or pre-existing cardiac disease.","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 4 1","pages":"223-9"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/OXFORDJOURNALS.QJMED.A068920","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61292709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chest pain with normal coronary arteries.","authors":"I H Mills","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 1","pages":"68"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19132056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The role of serotonin 5HT2 receptor antagonism in the control of coronary artery disease.","authors":"M I Noble, A J Drake-Holland","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 1","pages":"11-6"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"19132125","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 1994-01-01DOI: 10.1093/OXFORDJOURNALS.QJMED.A068921
N. Tandon, R. Metcalfe, D. Barnett, A. Weetman
Efficient antigen presentation requires the provision of a costimulatory signal, the best characterized of which is B7/BB1. It is unclear whether thyroid cells expressing class II molecules can present autoantigens to T cells, although this has been suggested as an important mechanism in the initiation of Graves' disease and Hashimoto's thyroiditis. We have found that thyroid cells from patients with thyroid autoimmunity do not express B7/BB1 in vivo or in vitro, even after activation with the cytokines interleukin-1 or gamma-interferon, or with a phorbol ester. Increased numbers of CD20+ B cells and CD14+ dendritic cells expressing B7/BB1 were found in intrathyroidal lymphocyte preparations from such patients compared to peripheral blood. These results suggest that conventional antigen-presenting cells rather than thyroid cells provide B7/BB1 costimulatory activity in autoimmune thyroid disease, and argue against a role for the thyroid cells themselves in autoantigen presentation to T cells via the B7/BB1 pathway.
{"title":"Expression of the costimulatory molecule B7/BB1 in autoimmune thyroid disease.","authors":"N. Tandon, R. Metcalfe, D. Barnett, A. Weetman","doi":"10.1093/OXFORDJOURNALS.QJMED.A068921","DOIUrl":"https://doi.org/10.1093/OXFORDJOURNALS.QJMED.A068921","url":null,"abstract":"Efficient antigen presentation requires the provision of a costimulatory signal, the best characterized of which is B7/BB1. It is unclear whether thyroid cells expressing class II molecules can present autoantigens to T cells, although this has been suggested as an important mechanism in the initiation of Graves' disease and Hashimoto's thyroiditis. We have found that thyroid cells from patients with thyroid autoimmunity do not express B7/BB1 in vivo or in vitro, even after activation with the cytokines interleukin-1 or gamma-interferon, or with a phorbol ester. Increased numbers of CD20+ B cells and CD14+ dendritic cells expressing B7/BB1 were found in intrathyroidal lymphocyte preparations from such patients compared to peripheral blood. These results suggest that conventional antigen-presenting cells rather than thyroid cells provide B7/BB1 costimulatory activity in autoimmune thyroid disease, and argue against a role for the thyroid cells themselves in autoantigen presentation to T cells via the B7/BB1 pathway.","PeriodicalId":54520,"journal":{"name":"Quarterly Journal of Medicine","volume":"87 4 1","pages":"231-6"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1093/OXFORDJOURNALS.QJMED.A068921","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"61292766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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