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Gulseren Sagcan,1 Zeki Dogan,2 Hafize Uzun,3 Caglar Cuhadaroglu,1 Gulfer Okumus,4 Orhan Arseven4 1Department of Chest Diseases, Faculty of Medicine, Acıbadem University, İstanbul, Turkey; 2Department of Cardiology, Faculty of Medicine, Istanbul Atlas University, Istanbul, Turkey; 3Department of Medical Biochemistry, Faculty of Medicine, Istanbul Atlas University, Istanbul, Turkey; 4Department of Chest Diseases, Faculty of Medicine, Istanbul University, İstanbul, TurkeyCorrespondence: Gulseren Sagcan, Department of Chest Diseases, Faculty of Medicine, Acıbadem University, İstanbul, Turkey, Tel +902166495751 ; +905323637953, Fax +902166495373, Email gulserensagcan@yahoo.comBackground: Acute pulmonary embolism (APE) is a common clinical condition. Its severity ranges from asymptomatic radiological findings to fatal obstructive shock. The potential circulating biomarkers have been studied to predict APE outcomes. This study aimed to explore their predictive power on prognosis in APE.Material and Method: It was a prospective observational study between March 2008 and April 2010. All consecutive patients diagnosed with APE were categorized as massive/high-risk, submassive/moderate-risk, and non-massive/low-risk. Cardiac troponin T (cTnT), myoglobin, N-terminal pro-brain natriuretic peptide (NT-proBNP), heart-type fatty acid-binding protein (H-FABP), growth differentiation factor-15 (GDF-15), and D-dimer levels were measured.Results: Of these patients, 14 (29.8%), 16 (34.0%), and 17 (36.2%) patients were categorized as low-risk, moderate-risk, and high risk-patients, respectively. There was no significant difference between the patient groups categorized based on the risk stratification in terms of demographic and clinical characteristics. The cTnT, myoglobin, HFABP, and D-dimer levels have also not differed significantly between the groups. There was a significant difference between the groups in respect of NT-proBNP and GDF-15 levels (p=0.009 and p=0.037, respectively). Nine (19.1%) patients had died by the 3rd-month follow-up. Adverse events were seen in 26 (55.3%) patients. GDF-15 had the highest area under the curve (AUC) value for predicting any adverse event (cut-off value=9.3 ng/mL, AUC=0.796, CI (confidence interval) 95%: 0.653– 0.899). NT-ProBNP was determined as the best predictor for mortality (cut-off value=229.2 pg/mL, AUC=0.889, CI 95%: 0.756– 0.964).Conclusion: Higher levels of NT-proBNP and GDF-15 were found to be associated with more severe APE, worse outcomes, and mortality.Keywords: pulmonary embolism, biomarkers, adverse clinical outcome, natriuretic peptides, growth differentiation factor-15

Copyright of Turkish Thoracic Journal / Turk Toraks Dergisi is the property of Aves Yayincilik Ltd. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Turkish Thoracic Journal / Turk Toraks Dergisi is the property of Aves Yayincilik Ltd. STI and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Heparin induced thrombocytopenia (HIT) is an important complication of heparin treatment. In this article, we presented a case of HIT who was treated with fondaparinux, which is the only alternative anticoagulant agent in our country. A 48 year-old male patient was referred to our clinic when bilateral main pulmonary arterial thromboses were detected by spiral computerized tomography after he sought consultation for chest pain, dyspnea and presyncope of 3 days duration. In the physical examination, tachypnea, tachycardia, cyanosis, hypotension, neck vein distention, hepatomegaly and hepatojugular reflux were recorded. After the diagnosis of massive PTE, unfractionated heparin (UFH) infusion was started following the treatment with r-tPA. UFH was stopped due to the rapid fall in thrombocyte count (39000/mm[3]) on the second. day of treatment. PF4-heparin antibodies detected by ELISA were positive. Anticogulant therapy was followed with fondaparinux. Oral anticoagulant therapy was started when the thrombocyt count reached >100000/mm[3] on the sixth day of treatment. [ABSTRACT FROM AUTHOR]

Background: Pulmonary embolism (PE) is a common and potentially life-threatening disorder. Our study was aimed to investigate whether oxidative stress markers can be used as clinical markers in the evaluation of acute PE (APE) severity., Methods: 47 patients with objectively documented diagnosis of APE were recorded. Of these patients, 14 had low-risk PE, 16 had moderate-risk PE, and 17 had high-risk PE. 21 healthy subjects were also enrolled in this study. Ischemia-modified albumin (IMA), prooxidants-antioxidants balance (PAB), advanced protein oxidation products (AOPPs), and ferric reducing antioxidant power (FRAP) were measured as oxidative stress parameters to evaluate the role of oxidative stress., Results: In the low-risk and moderate-risk APE groups, AOPPs and PAB levels were significantly higher and FRAP levels were significantly lower than those in the control group. AOPPs and IMA levels in the patients with high-risk PE were significantly higher than those in both the low-risk and moderate-risk APE patients. There was a significant correlation between levels of AOPPs and the levels of both IMA (r: 0.462, p < 0.001) and PAB (r:0.378, p < 0.005). Serum FRAP levels were negatively correlated with PAB (r:- 0.683, p < 0.001) and AOPPs levels (r:- 0,384, p < 0.001). There was also a significant positive correlation between the serum IMA and PAB levels., Conclusions: We clearly demonstrated that reactive oxygen species formation is significantly enhanced in APE. IMA and AOPPs may be used as clinical markers in the evaluation of APE severity in clinical practice. However, further studies with larger patient populations and longer follow-up periods are required to confirm the mechanisms underlying these findings., (© 2022. The Author(s).)

Background: The aim of the study was to evaluate the frequency of recurrence and the risk factors for recurrence in patients who were diagnosed with venous thromboembolism., Methods: Between January 2005 and January 2015, a total of 412 venous thromboembolism patients (164 males, 248 females; mean age: 53.5±16.6 years; range: 19 to 95 years) were retrospectively analyzed. The demographics, underlying risk factors, comorbidities, imaging findings, and treatment data of the patients were recorded., Results: At least one transient/permanent risk factor was found in 341 (82.7%) of the index events, and the other 71 (17.2%) were idiopathic. Recurrence developed in 76 (18.4%) of the patients. The duration of the treatment in the first event was significantly longer in recurrent cases (p=0.007). The recurrence rate in patients diagnosed with only deep vein thrombosis or patients diagnosed with pulmonary thromboembolism + deep vein thrombosis was significantly higher than the patients diagnosed with only pulmonary thromboembolism (24% vs. 14.2%, respectively; p=0.007). The rate of idiopathic venous thromboembolism was higher in recurrent cases than in non-recurrent cases (26.3% vs. 15.2%, respectively; p=0.028). At the end of the first year, the mean D-dimer levels were higher in recurrent cases (p=0.034). Hereditary risk factors were also higher in recurrent cases (39.5% vs. 19.3%, respectively; p=0.031). There was no significant correlation between recurrence and mortality., Conclusion: The presence of deep vein thrombosis, idiopathic events, high D-dimer levels at the end of the first year and hereditary risk factors seem to be associated with recurrence., Competing Interests: Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article., (Copyright © 2021, Turkish Society of Cardiovascular Surgery.)

Objectives: To evaluate the characteristics of patients who developed tuberculosis while receiving tumor necrosis factor-alpha (TNF-α) antagonists and the related factors with tuberculosis., Methods: Patient's demographics, tuberculin skin test (TST), isoniazid prophylaxis and type of TNF-α antagonist were recorded. TST conversion (≥5 mm increase) was evaluated for patients who had baseline and 1-year TST., Results: Files of 1887 patients who were receiving TNF-α antagonists between August 2005 and June 2015 were evaluated. TST significantly increased at the end of 1 year (n = 748 baseline:7.36 ± 7.2 mm vs. 1 year:9.52 ± 7.5 mm, P < 0.001). One-third of patients (31.2%) who had negative TST at baseline had positive TST at 1 year. Tuberculosis developed in 22 patients (1.16%). The annual incidence of tuberculosis was 423/100 000 patient-year. TNF-α antagonist indications were ankylosing spondylitis (n = 8), inflammatory bovel diseases (n = 7) and rheumatoid arthritis (n = 4). Ten (45.5%) patients received infliximab, six (27.3%) patients received etanercept and six (27.3%) patients received adalimumab. Nineteen (86.4%) patients were under isoniazid prophylaxis. Twelve patients had extrapulmonary tuberculosis (54.5%; four lymph node, three pleura, two periton, one pericarditis, one intestinal, one joint). Atypical mycobacterium was detected in one patient. Adalimumab treatment (9.5× increase), male sex (15.6× increase) and previous tuberculosis disease history (11.5× increase) were risk factors for active tuberculosis. Conversion of TST was not found related with tuberculosis., Conclusions: Despite the high proportion of isoniazid prophylaxis, the incidence of tuberculosis in our patients receiving TNF-α antagonist was higher than the literature. Adalimumab treatment, male sex and previous tuberculosis disease history were found as risk factors for tuberculosis., (© 2017 John Wiley & Sons Ltd.)

Introduction: Patients with pulmonary hypertension (PH) show no symptoms at rest, but symptoms are triggered by physical activities., Objectives: The primary aim of our study was to assess physical activity of patients with PH by using an activity monitor. The secondary aim was to evaluate the correlation between the activity monitor parameters and 6-min walk distance (6MWD), activity of daily living (ADL), quality of life, WHO functional class and PH classification., Methods: Thirty-eight patients with pulmonary arterial hypertension (PAH) and seven patients with chronic thromboembolic PH were included in the study. Physical activity was assessed using a SenseWear arm band. A 6-min walk test was performed. Daily living activities were assessed using the 'nottingham extended activity of daily living index' (NEADL). For quality of life assessments, 'Minnesota living with heart failure' (MLHF) and 'Short form-36' (SF-36) surveys were used., Results: Physical activity, exercise capacity, quality of life and contribution to ADL were lower in patients with PH. These data were associated with the 6MWD, quality of life and ADL index scores. We also found weak and moderate correlations between activity monitor data and SF-36 sub-group scores, MLHF and NEADL scores (P < 0.05). For the group with PAH, idiopathic PAH patients had more exercise capacity and total energy expenditure compared with patients with scleroderma-associated PAH., Conclusion: Correlation between activity monitor data and 6MWD, most of SF-36 sub-group scores, MLHF scores and NEADL index scores suggest that activity monitor can be used in the evaluation of patients with PH., (© 2016 John Wiley & Sons Ltd.)

Introduction: Conflicting results has been achieved in a small number of clinical studies evaluating the efficiency of magnesium sulphate (MS) in COPD exacerbations. We aimed to investigate the efficiency of nebulised MS in COPD exacerbations., Patients and Methods: Twenty patients who met the study criteria were randomized into two groups. All patients were treated with O2, antibiotics and oral corticosteroids. Additionally one group received ipratropium bromide (IB) 500 µg together with MS 151 mg/dose, while the other group received IB together with placebo. The patients were followed-up with forced expiratory volume in 1 second (FEV1) and visual analogue scale dyspnea scores for 48 hours. Peak expiratory flow rates (PEFRs) were measured before and 10, 30, 60 and 120 minutes after each nebule treatment., Result: The baseline characteristics of the patients in both groups were similar. The FEV1 values measured at 24 and 48 hours did not show significant changes compared to baseline in both groups. Dyspnea scores in both groups decreased significantly in the first day, and in only MS group in the second day. The % change in the dyspnea score at the end of first day was significantly more in the MS group [-23.8% (13.6)] compared with the placebo group [-9.4% (12.9)] (p= 0.002). The % changes in PEFRs at 10 minutes [4.7 (7.5) and -3.5 (6.0), p= 0.005] and 30 minutes [8.2 (6.7) and 1.3 (5.5), p= 0.03] were significantly greater in the MS group compared with the placebo group on the first day. No side effects developed due to MS., Conclusion: Nebulised MS is a cheap, feasible and safe drug that can be added to the standart bronchodilator treatment since it provides additional relief of dyspnea in patients with COPD exacerbations. This needs to be evaluated in future clinical studies including greater number of patients.

Unlabelled: Bronchial artery embolization (BAE) is a widely used modality of treatment for massive hemoptysis which has well known complications such as chest pain, groin hematoma and transverse myelitis but systemic embolization of the material used in the procedure is very rare and was reported only four times in the literature which were all caused by the use of microspheres. Herein we report a case of a 41-year-old caucasian male who had a history of tuberculosis 10 years ago. He had BAE with polyvinyl alcohol (PVA) for the treatment of recurrent hemoptysis. After the procedure, the patient complained of severe pain on the left upper quadrant and bilateral costovertebral regions and in abdominal CT, multiple infarcts in the subcapsular area of the spleen and kidneys were observed. This is the first reported case of inadvertent systemic embolization secondary to BAE with PVA. Although the risk of systemic embolization is greater with microspheres, still potentially serious and life threatening complications may occur with PVA., Keywords: Bronchial artery emobolization; Complication; Polyvinyl alcohol.

The clinical diagnosis is not reliable in pulmonary thromboembolism (PTE) because the symptoms are mostly nonspecific. Different clinical prediction rules for PTE have been described recently. These rules are used to aid clinicians in assigning a pre-test probability to patients with clinical signs and symptoms of disease. The aim of this study was to assess the clinical probability of PTE using three different models (Wells, Wicki and modified Hyers scores) and to find their power to determine PTE probability. Clinical probabilities of patients with PTE were determined with Wells, Wicki and modified Hyers scores. Cramer's, contingency coefficient (CC), Spearman's rho, Kendal's tau-b and kappa tests were used for statistical analysis. The study included 248 patients (119 male, 129 female; mean age= 57 +/- 16.7 years). Although 61.3% of the patients were assigned high clinical probability with modified Hyers score, 56% and 50% of them were assigned moderate clinical probability with Wicki and Wells scores, respectively. The correlations of the clinical probabilities was low according to kappa correlation test and moderate according to the Cramer's, CC, Spearman's rho and Kendal's tau-b tests among these three scores. In conclusion, modified Hyers score showed higher percentage of high probability compared to Wells and Wicki scoring systems and the best correlation was found between the modified Hyers and Wells scores.

The aim of this study was to investigate the hereditary thrombophilic risk factors in patients with venous thromboembolism (VTE) and whether these risk factors play a different role in patients with isolated pulmonary embolism (PE) as compared with patients with deep vein thrombosis (DVT) and patients with PE + DVT. The protein C (PC), protein S, antithrombin activities, homocysteine levels, and factor V Leiden (FVL) G1691A and prothrombin G20210A mutations were evaluated in 191 patients with VTE and 191 controls. The prevalence of FVL and PC deficiency were higher in patients (P = .003 and P = .02, respectively). There was no significant difference for the other risk factors. The combination of thrombophilic risk factors was significantly higher in patients with DVT + PE as compared with patients with isolated PE or DVT (P = .04). In conclusion, the most important hereditary risk factors for VTE in this study were the FVL mutation and PC deficiency.

Alveolar echinococcosis, which is caused by Echinococcus multilocularis, is a very aggressive and potentially fatal infestation which always affects the liver primarily and metastasizes to any part of the body. Imaging studies are usually highly suspicious of carcinoma or sarcoma, and biopsy may provide the first indication of infection. We report a case of disseminated alveolar echinococcosis with liver, lung, and bone involvement mimicking a metastatic malignancy.

Two silent polymorphisms (807C/T and 873G/A) within glycoprotein Ia (GPIa) gene have been implicated in increased risk of developing thrombosis and myocardial infarction in affected individuals. The aim of this study was to investigate the GPIa gene polymorphism in patients with venous thromboembolism (VTE). A multiplexed allele specific-polymerase chain reaction (AS-PCR)-based method was used to determine the GPIa 807T/873A allele frequency in 77 patients with VTE and 106 healthy controls. The allelic frequency for 807T/873A was 33% in the patient group and 38% in the control group. The allelic frequency for 807C/873G was 66% in the patient group and 62% in the control group. The genotypic frequencies were 8% for 807TT/873AA, 42% for 807CC/GG, and 50% for 807CT/GA in the patient group. In the control group, the frequencies were 12% for 807TT/873AA, 35% for 807CC/873GG, and 52% for 807CT/873GA. As a result, the glycoprotein Ia 807C/T and 873G/A dimorphisms were not shown as risk factors for VTE.

Heparin induced thrombocytopenia (HIT) is a life-threatening complication that can be seen in the course of heparin treatment. The syndrome is much likely to be seen during treatment with standard heparin but it can also be seen due to low molecular weight heparins. In this article, we presented a case of HIT who was given low molecular weight heparin for prophylaxis that developed massive pulmonary thromboembolism. The patient was successfully treated with lepirudin infusion and no complications due to treatment was seen.

Setting: Undergraduate training on tuberculosis at Istanbul Medical School., Objective: To assess whether tuberculosis-related questions asked in chest medicine examinations comply with the World Health Organization's (WHO) learning objectives for tuberculosis training, and to investigate students' skills in interpreting radiology and smears with respect to tuberculosis., Design: Tuberculosis questions set for 4th year medical students (n = 838) were compared with WHO objectives (n = 23): 122 students were each asked to interpret 10 chest X-rays which had been read by three experts as 'typical tuberculosis lesions', 'normal' or 'non-tuberculosis lesions'; 114 students were also each given five smears which had been interpreted by an expert as 'negative' or 'positive' with respect to acid-fast-bacilli (AFB), and were asked to interpret them., Results: Questions covered only nine of the WHO objectives. Among 117 types of questions, 91 (77.8%) were about clinical-radiological findings, treatment and drugs; 334 (65.1%) of 513 X-rays with typical tuberculosis lesions, 77 (21.1%) of 364 normal X-rays and 87 (25.4%) of 343 X-rays with non-tuberculosis lesions were identified as tuberculosis (kappa 0.45). Of 369 AFB-positive smears, 149 (40.4%) were evaluated as false negative, and of 185 AFB-negative smears, 48 (25.9%) were evaluated as false positive (kappa 0.49)., Conclusion: Examination questions set on tuberculosis at Istanbul Medical School do not adequately reflect WHO learning objectives. Students' skills in interpreting radiology and smears suggest that their practical training on tuberculosis is insufficient.

Constitutively activating mutations of the thyrotropin (TSH) receptor have been identified as a molecular cause of toxic adenomas, nonautoimmune familial hyperthyroidism, and sporadic congenital hyperthyroidism. By analyzing genomic DNA from a toxic adenoma, we detected a novel somatic mutation in codon 601, tyrosine to asparagine (Y601N), a residue located in the carboxyterminal part of the fifth transmembrane helix. This codon is also notable for the presence of a polymorphic variant, Y601H. These two naturally occurring substitutions (Y601N and Y601H) were analyzed together with an artificial mutation, Y601F, to study the role of this residue for receptor function further. Transient transfection assays revealed that the Y601N mutation results in constitutive activation of the cyclic adenosine monophosphate (cAMP) pathway, but that it is unable to couple to Gq/11. Y601H and Y601F do not display basal activity while retaining responsiveness to TSH, but also lose the ability to induce inositol phosphate accumulation in response to TSH. These studies define Y601N as a mutation that selectively activates the cAMP pathway, and they confirm that Y601H is not a silent polymorphism. In conclusion, residue Y601 has an important role for the characteristic constitutive basal activity of the TSH receptor and coupling to Gq/11.

Constitutively activating mutations in the thyrotropin (TSH) receptor have been identified as a major molecular cause of hyperfunctioning thyroid adenomas. A smaller subset of these benign tumors is caused by constitutive activation of the adenylyl cyclase cascade by somatic mutations in the Gsalpha gene. In this study, we analyzed hyperfunctioning thyroid adenomas from seven Brazilian patients for TSH receptor and G(s)alpha gene mutations. Solitary autonomous thyroid adenomas were identified by ultrasound and scintigraphy, and DNA was extracted from adenomatous and periadenomatous tissue. Exons 9 and 10 of the TSH receptor gene, and exons 8 and 9 of the G(s)alpha gene, were amplified by polymerase chain reaction (PCR) and subjected to direct sequence analysis. Six of seven adenomas harbored heterozygous mutations known to confer constitutive activity to the TSH receptor. In one case, aspartate 619 was substituted by glycine (D619G). In four adenomas, alanine 623 was replaced by valine (A623V). Both residues are located in the third intracellular loop. In one instance, aspartate 633 located in the sixth transmembrane domain was replaced by tyrosine (D633Y). In this patient, one allele also contained a change of aspartate 727 to glutamate (D727E). This substitution is thought to be a polymorphic variant of the wild-type but it has also been associated with toxic multinodular goiters. Functional comparison of D727 with E727 did not reveal differences in basal or TSH-stimulated cyclic adenosine monophosphate (cAMP)-dependent luciferase activity in transiently transfected cells. These results demonstrate a high prevalence of activating TSH receptor mutations in toxic adenomas in this small series from Brazil (approximately 86%). These findings are in agreement with reports from other countries with a marginal iodine intake but contrast with studies from regions with a high iodine intake where these mutations appear to be less prevalent.

Sporadic congenital hypothyroidism is most commonly caused by developmental abnormalities of the thyroid gland. More rarely, it is due to defects in gene products involved in the regulation of the hypothalamic-pituitary-thyroid axis or thyroid hormone synthesis. Loss of function mutations in the thyrotropin (TSH) receptor have been shown to result in resistance to biologically active TSH. In complete resistance to TSH, the thyroid gland is hypoplastic and unable to synthesize and secrete sufficient amounts of thyroid hormones. In partial resistance, referred to as euthyroid hyperthyrotropinemia, the size of the gland and the thyroid hormone levels are normal at the expense of an elevated TSH. Four patients with sporadic congenital hypothyroidism and properly located hypoplastic thyroid glands were included in this study. Serum TSH concentrations were 150 mU/L or higher, serum thyroglobulin levels were within normal limits (6.1 to 8.2 ng/mL; normal range: 2.1 to 32 ng/mL), and thyroid autoantibodies were absent. The coding region of the TSHbeta subunit gene, the TSH receptor gene, and exons 8 and 9 of Gsalpha were analyzed by direct sequencing and found to be normal in all patients. One patient was heterozygous for a G to A transition in the TSHbeta gene resulting in a substitution of alanine by threonine at position -7 of the signal peptide. This substitution was also found in her euthyroid father. In addition, Southern analysis of the TSH receptor gene excluded major structural alterations. These findings support previous reports that indicate that TSH resistance is genetically heterogeneous. In addition to mutations in the TSH receptor or the Gsalpha genes, other genetic defects can lead to an identical phenotype. These observations also suggest that TSH receptor mutations might be a relatively rare cause of congenital thyroid hypoplasia.

Acute exacerbations, most of which are due to lower respiratory tract infections, cause great morbidity and mortality in patients with chronic obstructive pulmonary disease (COPD) and most of these are due to lower respiratory tract infections. The aim of this study was to determine the causative organism and the effects of azithromycin, ampicillin sulbactam (sultamicillin), ciprofloxacin and cefaclor monohydrate therapy in COPD. One hundred and six patients with COPD in acute exacerbation were randomized into four groups for empiric antibiotic treatment following lung function tests and sputum examination. The most common strains isolated from sputum were Haemophilus influenzae (30.8%), Streptoccocus pneumoniae (12%) and Moraxella catarrhalis (7.7%). Azithromycin, sultamicillin, ciprofloxacin and cefaclor monohydrate were found to be effective in treating COPD exacerbations.

The thyroid hormone receptor splice variant, alpha2, is unable to bind thyroid hormone (T3) and has been proposed to function as an endogenous inhibitor of T3 action. In this report, we examined further the DNA sequence requirements for alpha2 binding to thyroid hormone response elements (TREs) in an attempt to identify response elements that mediate potent inhibition by alpha2. Heterodimers of alpha2 and retinoid X receptor were found to bind to a subset of TREs (DR4, direct repeats spaced by 4 bp) in which selected flanking and spacer sequences enhanced interactions with the AGGTCA core binding sequence. Despite the optimization of the TRE-binding sites, alpha2 remained a weak dominant negative inhibitor of TRE-driven transcription. A promoter interference assay was also developed for testing inhibition by alpha2. In these studies, alpha2 blocked gene transcription, but it required cotransfected retinoid X receptor, and it was not as potent as unliganded thyroid hormone receptors. These results led to the hypothesis that alpha2 might be deficient in interactions with nuclear receptor corepressors. Consistent with this view, alpha2 did not silence basal transcription in its native form or when linked to Gal4. Alpha2 also failed to interact with corepressors (NCoR and SMRT) in both gel shift assays and mammalian two-hybrid assays. We conclude that alpha2 is a weak antagonist of thyroid hormone action because it binds weakly to a limited repertoire of response elements, and it does not interact with corepressors. Thus, alpha2 may be able to compete with thyroid hormone receptors for binding to a limited group of target sites, but it is not able to actively inhibit transcription.

We report a patient with bilateral facial palsy due to a non-Hodgkin lymphoma. He was initially diagnosed to have a facial paralysis of unknown aetiology. Three months after this original diagnosis, he developed a non-Hodgkin lymphoma which was treated successfully with chemotherapy, and his palsy consequently returned to normal.

A 62-year old farmer woman from the northeastern, very rainy part of Turkey has been collecting large amounts of green and brown involucral hazel-nut leaves for subsequent use as fuel. For the last 20 years she had been complaining of cough, respiratory distress and intermittent fever. In the course of years of continual antigen exposure she developed the clinical and x-ray signs of fibrosis of the lung. Bronchoalveolar lavage produced the typical cell pattern of chronic exogenous allergic alveolitis with predominant CD8 cells. Serum analysis yielded high titres of IgG antibodies against mould fungi partly obtained from hazel-nut husk cultures, as well as thermophilic actinomycetes.