Myalgic encephalomyelitis.
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Biomedical subjects
Publications and source records attributed to S Powell.
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We retrospectively reviewed the records of 71 patients to determine the epidemiologic and clinical features of pleural tuberculosis in patients with and without AIDS and compared the composition of pleural fluid in these two groups of patients. By age, race, sex, and country of birth, the 21 AIDS and 50 non-AIDS patients with pleural tuberculosis were comparable. However, the AIDS patients were more likely to be intravenous drug abusers than the non-AIDS patients (15/21 vs 6/50, p less than .001). The clinical presentation of each group was similar except that the AIDS patients were more likely to present without respiratory symptoms (4/21 vs 0/50, p less than .001). Pleural fluid and pleural biopsy analyses were not different in the two groups. However, AIDS patients had significantly more chest roentgenographic infiltrates (10/21 vs 11/50, p less than .05), hilar/mediastinal adenopathy (4/21 vs 1/51, p less than .007) and a higher prevalence of bilateral effusions (6/21 vs 5/50, p less than 0.05). AIDS patients were also more likely to have sputum smear/culture positive (10/19 vs 9/49, p less than .001) for mycobacteria. The yield for acid-fast bacilli culture of pleural fluid was higher than previously reported (60%) regardless of AIDS status. Thus, AIDS patients with pleural tuberculosis may present without respiratory symptoms, but otherwise do not differ clinically and epidemiologically from non-AIDS patients. Radiologic and mycobacterial data suggest that pleural tuberculosis in AIDS patients is often part of disseminated mycobacterial infection.
Three cases of death after 40 years of differentiated thyroid cancer are presented. Prolonged follow-up identified relapses in patients assumed to have been cured. Thus the case is argued for intensive initial therapy comprising near-total thyroidectomy (including excision of any macroscopic nodal disease) and ablative iodine-131 therapy in addition to thyroid hormone suppression.
Although the clinical and epidemiologic features of progressive disseminated histoplasmosis (PDH) in the acquired immunodeficiency syndrome (AIDS) have been well described, the pathologic and pulmonary aspects remain to be fully defined. A retrospective review of three patients and a prospective study of four more with PDH and AIDS recently admitted to an inner city hospital in a non-endemic area were used to elucidate these features more fully. All patients were men aged 23 to 46 years, born in endemic areas, who had immigrated to the US seven to 15 years before the onset of their illnesses. Five had been exposed to human immunodeficiency virus (HIV) through intravenous drug use (one was also a homosexual), and two through heterosexual contacts. Respiratory symptoms were evident in five of the seven patients, fever in seven, weight loss in seven, hepatomegaly in four, splenomegaly in three, peripheral adenopathy in three, and gastrointestinal symptoms in three. PDH was the initial or only opportunistic infection in five patients. Bilateral nodular infiltrates (4/7), bilateral interstitial infiltrates (2/7), and mediastinal adenopathy associated with pleural effusion (1/7) were the chest roentgenographic findings. Histoplasma capsulatum was isolated from five of five bronchoalveolar lavages, four of four transbronchial biopsies, one of one endobronchial biopsy, one of one brushing, one of one pleural biopsy, three of three lymph node biopsies, two of two bone marrow biopsies, one of one liver biopsy, and three of four peripheral blood smears. Granuloma formation was seen in only three of 12 biopsies. There were ten or more fungi per monocyte in almost all tissues, some with extracellular forms.(ABSTRACT TRUNCATED AT 250 WORDS)
We have previously reported that continuous in vitro passage in the presence of 3T3 feeders of a non-tumorigenic adenoma-derived epithelial cell line, designated PC/AA, resulted in its becoming immortal. At early passage PC/AA was normal diploid, whereas every cell of PC/AA late passage had an isochromosome 1(q) which led us to suggest that abnormalities of chromosome 1 may be involved in tumour progression. We now report the isolation of a 3T3-feeder-independent variant of early-passage PC/AA, designated PC/AA/FI, which was immortal in vitro and remained non-tumorigenic. Each cell of PC/AA/FI again has an isochromosome 1(q), like the late-passage PC/AA. However, with PC/AA/FI it is the other chromosome 1 of the homologous pair which is involved in the formation of the isochromosome 1(q). This is possible to determine because of the polymorphic centromeric heterochromatin on chromosome 1 of the early-passage PC/AA. With the late-passage PC/AA (grown with 3T3 feeders) the homologue with the large C-band has given rise to an isochromosome 1(q) whereas with PC/AA/FI it is the other homologue with the smaller C-band which has given rise to this isochromosome. Both the immortal PC/AA/FI and the immortal PC/AA late passage, therefore, have independent abnormalities involving chromosome 1. These results indicate that chromosome 1 may be involved in in vitro immortalization.
We report on two patients with mosaic tetrasomy of 8p[46,XY/47,XY,+i(8p)], a previously unreported cytogenetic anomaly. The first patient had a low percentage of tetrasomic (secondary trisomic) cells in lymphocytes and fibroblasts, an only mildly abnormal phenotype, and a rather benign clinical course. The second patient had a considerably larger percentage of tetrasomic cells in lymphocytes and fibroblasts, and had more severe congenital anomalies that led to his death at 8 months. A characteristic phenotype +i(8p) is suggested but not yet established. The manifestations of these two patients resemble those of mosaic trisomy 8 and mosaic trisomy 8p, with rib and vertebral abnormalities, absent corpus callosum, and enlarged cerebral ventricles.
Methods used in clinical practice to increase the damping of a transducer hydraulically coupled to an intraarterial blood-pressure monitoring system often decrease the undamped natural frequency of the system. This leads to spuriously high systolic and low diastolic pressure readings. The ROSE damping device is being marketed as a possible solution to the problem. We tested the dynamic response of three different catheter systems, with various pressure-tubing lengths of 1 to 7 feet (30.5 to 213.4 cm), with and without the ROSE damping device. The device was able to substantially increase damping and at the same time maintain the undamped natural frequency. Typically it increased the damping coefficient from a minimum of 0.17 +/- 0.01 to a minimum of 0.33 +/- 0.01, while never significantly decreasing the undamped natural frequency. In testing a sample of 25 devices we did observe, however, a wide variability in damping characteristics among different devices. Damping coefficients ranged between 0.19 and 1.20.
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We have compared sequencing of cloned "polymerase chain reaction" (PCR) products and the direct sequencing of PCR products in the examination of individuals from six families affected with alpha 1-antitrypsin (AAT) deficiency. In families where paternity was in question we confirmed consanguinity by DNA fingerprinting using a panel of locus-specific minisatellite probes. We demonstrate that direct sequencing of PCR amplification products is the method of choice for the absolutely specific diagnosis of AAT deficiency and can distinguish normals, heterozygotes and homozygotes in a single, rapid and facile assay. Furthermore, we demonstrate the reproducibility of the PCR and a rapid DNA isolation procedure. We have also shown that two loci can be simultaneously amplified and that the PCR product from each locus can be independently examined by direct DNA sequencing.
A non-tumorigenic epithelial cell line designated PC/AA, derived from a large pre-malignant colorectal adenoma from a patient with familial polyposis coli (also referred to as hereditary adenomatosis of the colon and rectum) has become immortal in vitro. PC/AA has been passaged in vitro continuously for over 4 years and shows no signs of senescence. At early passage, PC/AA has a normal diploid karyotype but with late passage is showing signs of progression, becoming aneuploid and displaying signs of morphological transformation. Every cell examined of late-passage PC/AA has an isochromosome (1q), and one other marker chromosome which is probably derived from an additional chromosome 8. The majority of cells examined have 48 chromosomes. Despite showing signs of progression in vitro, late-passage PC/AA has remained non-tumorigenic in athymic nude mice and retained morphological differentiation characteristics of colonic cells, in particular the ability to synthesize and secrete mucin. Two other cell lines derived from small adenomas did not become immortal in vitro and were also non-tumorigenic in athymic nude mice. The isolation of an immortal pre-malignant human epithelial cell line could prove invaluable in studies on human carcinogenesis and tumour progression. Our results, showing that only a large adenoma and no small adenomas have given rise to immortal cell lines, raise the possibility that the acquisition of in vitro immortality is associated with a relatively late stage in the adenoma-carcinoma sequence. The possible involvement of chromosome 1 in tumour progression is discussed.
The region of the brachial plexus in the root of neck and axilla was examined by computed tomography (CT) in 62 patients attending the Royal Marsden Hospital. Forty-two of these patients had been treated by surgery and subsequent radiotherapy for carcinoma of the breast. Computed tomography was able to identify varying grades of abnormality that were ascribed to radiation fibrosis. Twenty-eight patients had neurological symptoms affecting the arm or hand on the treated side and CT changes were seen in 96%. The grading and significance of these CT abnormalities is discussed. The patients had been treated by two different radiotherapy techniques (three-field and four-field) which utilised either a large or small treatment fraction. The higher grades of abnormality on CT were seen in 57% of those treated with the large fraction size and 27% of those treated with the small fraction size. However, the changes on CT did not relate to the different radiotherapy techniques.
A case of spinal cord compression in an oncology patient is presented. The compression was caused by minimal expansion of a vertebral body involved by a metastatic deposit impinging on a previously asymptomatic lipomatous spinal cord tumour. Nuclear magnetic resonance imaging clearly demonstrated both the vertebral metastasis and the intramedullary and extramedullary components of the lipomatous tumour in a single noninvasive investigation.
We have presented a case of primary testicular carcinoid in an otherwise asymptomatic 50-year-old white man treated by right orchiectomy; a postoperative abdominal CT scan was normal. Histologically and cytologically the tumor resembled carcinoids of midgut origin. Most primary testicular carcinoid tumors are not clinically functional, and thus the diagnosis is not suspected preoperatively.
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Iliocaval compression syndrome is a significant disorder in a number of patients who have lower extremity venous complaints. The diagnosis may be suspected by positive findings on exercise strain gauge venous plethysmography and unilaterally increased ambulatory venous pressures. The diagnosis is confirmed by ascending and, in some instances, descending venography which demonstrates the iliocaval compression with or without intraluminal web formation. Transstenosis pressure gradients may be measured to confirm the hemodynamic significance of the lesion. We advocate direct operative repair of the iliocaval junction with rerouting of the iliac artery and excision of the iliocaval webs with cephalic vein patch angioplasty. It provided good results in the present study when coupled with an adjunctive regimen of perioperative subcutaneous heparin and warfarin. Further investigation into the exact prevalence and significance of the iliocaval compression syndrome is needed. Only an aggressive approach to patients with lower extremity venous complaints will help clarify the exact prevalence and natural history of this disorder.
The peripheral blood of sarcoidosis patients has been shown to have abnormalities in the T Lymphocyte subsets. There is a consistent reduction in the helper/suppressor T Lymphocyte ratio caused by an increase in suppressor cell percentage as determined by monoclonal antibodies. These findings suggest that the peripheral blood T Lymphocyte subsets may be a useful adjunct for determining the underlying immunological cellular dysfunction in sarcoidosis patients.
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