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61.
Luciani P Ferruzzi P Arnaldi G Crescioli C Benvenuti S Nesi G Valeri A Greeve I Serio M Mannelli M Peri A 《The Journal of clinical endocrinology and metabolism》2004,89(3):1332-1339
Selective Alzheimer's disease indicator-1 (seladin-1) is a novel gene with antiapoptotic activity that is down-regulated in vulnerable brain regions in Alzheimer's disease. This gene encodes 3-beta-hydroxysterol Delta-24-reductase (DHCR24), which converts desmosterol into cholesterol. In the adrenal cortex, increased expression of seladin-1/DHCR24, which appears to be modulated by ACTH, has been recently reported in cortisol-secreting adenomas, compared with the adjacent atrophic tissue. In our study, we measured the expression level of seladin-1/DHCR24 in cortisol- (n = 18) and aldosterone-secreting (n = 16) adrenocortical adenomas, in carcinomas (n = 17), and in normal adrenal glands (n = 8) by quantitative real-time RT-PCR. The amount of seladin-1/DHCR24 mRNA was significantly reduced in carcinomas (total RNA, 2.5 +/- 0.8 pg/ micro g) compared with the other groups (P < 0.01). Western blot analysis confirmed the mRNA results. Similarly, in adrenal malignancies, significantly reduced levels of expression of the ACTH receptor gene were found. In the adrenal cancer cell line H295R and in primary cultures from adrenocortical cells, ACTH (1 nM) and forskolin (10 micro M) effectively increased seladin-1/DHCR24 expression, confirming that seladin-1/DHCR24 is modulated by the ACTH/cAMP-driven pathway. In summary, this is the first demonstration that seladin-1/DHCR24 expression is reduced in adrenal cancer, suggesting that it might be viewed as a new potential marker of adrenal malignancies. 相似文献
62.
Carolina Ciacci Daniela Gennarelli Gabriella Esposito Raffaella Tortora Francesco Salvatore Lucia Sacchetti 《Clinical gastroenterology and hepatology》2006,4(5):635-638
BACKGROUND & AIMS: Celiac disease (CD) has been associated with several genetic disorders, but has not been associated with hereditary fructose intolerance (HFI). METHODS: We identified CD in 4 female patients affected by HFI from among 38 Italian HFI patients. RESULTS: Three of these patients were children in whom the CD-associated signs were hypertransaminasemia, failure to thrive, low weight, and short stature, whereas the adult patient had protracted diarrhea notwithstanding a fructose-free diet. The incidence of CD in our group of HFI patients was higher (>10%) than in the general population (1%-3%) (P<.02). CONCLUSIONS: The possibility of an association between these 2 gastrointestinal disorders is important, particularly in the management of HFI patients with persisting symptoms. 相似文献
63.
Thyroid destruction leading to endemic myxoedematous cretinism is highly prevalent in central Africa, where iodine (I) and selenium (SE) deficiencies as well as thiocyanate (SCN) overload are combined. All three factors have been studied experimentally in the etiology of the disease, but they have never been studied in combination. In a model using rats, we have previously shown that combining I and SE deficiencies increases the sensitivity of the thyroid to necrosis after iodide overload, an event unlikely to occur in the African situation. To develop a model that would more closely fit with the epidemiological findings, we have determined whether an SCN overload would also result in thyroid necrosis as does the I overload. The combination of the three factors increased by 3.5 times the amount of necrotic cells, from 5.5 +/- 0.3% in the I-SE+ thyroids to 18.9 +/- 1.6% in the I-SE-SCN-overloaded ones. Methimazole administration prevented the SCN-induced necrosis. SE- thyroids evolved to fibrosis, whereas SE+ thyroids did not. TGFbeta was prominent in macrophages present in SE- glands. Thyroid destruction in central Africa might therefore originate from the interaction of three factors: I and SE deficiencies by increasing H(2)O(2) accumulation, SE deficiency by decreasing cell defense and promoting fibrosis, and SCN overload by triggering follicular cell necrosis. 相似文献
64.
Long-term remission from life-threatening hypercoagulable state associated with lupus anticoagulant (LA) following rituximab therapy 总被引:3,自引:0,他引:3
Rituximab, a chimeric monoclonal CD20 antibody, is useful in the treatment of B-cell lymphomas and certain autoimmune diseases. We report a successful outcome of rituximab for life threatening hypercoagulable state associated with lupus anticoagulant (LA). A 30-year-old woman initially presented 10 years ago with DVT and positive serology for SLE and LA. While on Coumadin, she suffered from recurrent DVT in the legs and arms, pulmonary emboli, Budd-Chiari syndrome, mesenteric vein thrombosis, bone infarcts, recurrent strokes, and chronic ITP. All measures including plasmapheresis and monthly IV cyclophosphamide were of no benefit. She was recently admitted with spontaneous subdural hematoma with INR of 3.8. Upon discontinuation of anticoagulation for surgical drainage, she developed acute abdomen from thrombosis and recurrent DVT. Because she had failed prior standard measures, 4 weekly infusions of rituximab (375 mg/m2) were given following 2 rounds of plasmapheresis. Subsequently, she made a remarkable recovery over the next month and has been free of thrombosis on Coumadin for over 15 months. LA, IgM antibodies to cardiolipin, and B2GP1 were consistently positive. After rituximab therapy, LA became negative and IgM antibodies to cardiolipin decreased and ITP went into remission. Rituximab induced a lasting remission in a woman suffering from life-threatening hypercoagulable state associated with LA. Her clinical remission was associated with disappearance of LA. 相似文献
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66.
Piero Barbanti MD PhD Cinzia Aurilia MD Sabina Cevoli MD PhD Gabriella Egeo MD PhD Luisa Fofi MD Roberta Messina MD Antonio Salerno MD Paola Torelli MD Maria Albanese MD PhD Antonio Carnevale MD Francesco Bono MD Domenico D'Amico MD Massimo Filippi MD Claudia Altamura MD PhD Fabrizio Vernieri MD EARLY Study Group 《Headache》2021,61(9):1351-1363
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69.
Zsóka Weiszhár András Bikov Gabriella Gálffy Lilla Tamási Ildikó Ungvári Csaba Szalai György Losonczy Ildikó Horváth 《Journal of clinical immunology》2013,33(2):496-505
Background
The alternative pathway of the complement system is known to play a role in the generation of asthmatic airway inflammation, but its regulatory complement protein, factor H has not been investigated in this disease.Purpose
Our aim was to determine the local bronchial complement factor H (CFH) levels in asthma, and to investigate its relationship with complement activation, systemic CFH concentrations and clinical characteristics of patients.Methods
Induced sputum and plasma were collected from 21 healthy and 26 asthmatic subjects, and complement factor H and SC5b-9 concentrations were assessed by ELISA. Total protein concentrations were determined by biuret-reaction based microassay system from induced sputa.Results
CFH was detectable in 81 % of healthy and 100 % of asthmatic subjects, while SC5b-9 exceeded the detection limit in 62 % of healthy subjects and 85 % of asthmatic patients. Sputum CFH concentrations and CFH/protein ratios were increased in samples from asthmatic patients, and correlated with loss of lung function, asthma control, severity and medication intensity, but not with plasma CFH concentrations. Sputum CFH/protein ratios were in positive correlation also with sputum eosinophilic cell counts in asthma. SC5b-9 concentrations were not higher in the asthmatic sputa, although they correlated with sputum CFH concentrations.Conclusions
CFH level is elevated on asthmatic airway surface, and may be associated with uncontrolled inflammation in asthma. 相似文献70.
Carmen Barba Massimo Cossu Renzo Guerrini Giancarlo Di Gennaro Flavio Villani Luca De Palma Laura Grisotto Alessandro Consales Domenica Battaglia Nelia Zamponi Piergiorgio dOrio Martina Revay Michele Rizzi Sara Casciato Vincenzo Esposito Pier Paolo Quarato Roberta Di Giacomo Giuseppe Didato Chiara Pastori Giusy Carfi Pavia Simona Pellacani Giulia Matta Mattia Pacetti Gianpiero Tamburrini Elisabetta Cesaroni Gabriella Colicchio Giampaolo Vatti Sofia Asioli Massimo Caulo Carlo Efisio Marras Laura Tassi 《Epilepsia》2021,62(1):128-142