A rapid screening test for thalassaemic trait.
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Biomedical subjects
Publications and source records attributed to A Camagna.
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INTRODUCTION: Even if infrequent, a digital necrosis after chemotherapy can occur in cancer patients. The gemcitabine is generally well tolerate; the cutaneous toxic ulcerations only in 0.3% of the cases induces the suspension of the treatment. CLINICAL CASE: A 70 year old patient, female, with a bladder cancer, after a trans-urethral resection, is submitted to adjuvant chemotherapy with Gemcitabine 1700 mg (total dose/die), with administration in the days 1st and 8th, while in the 15th day was not effected because, to distance of 3-4 days from the second administration, appear paresthesies of the fingers of the hands, together with Raynaud type phenomenon, 38-39 degrees C intermittent fever, digital necrosis and fingertips gangrene. Laboratory: (Normal): RF; AutoAb: AMA, ASMA, APCA, anti-DNA; ENA; lupus anti-coagulant; Ab-anti-cardiolipin; C3-C4, CIC; homocysteine, anti-thrombin, protein C, protein S, mutation of the factor V of Leiden, plasminogen, alfa 2-antiplasmin. (Altered): Auto-antibody: ANA (on Hep-2): positive (title 1/160, speckled pattern), cryoglobulin positive, ESR 29; Instrumental examinations: Superior Limbs Angiograpy: Occlusion of the digital arteries proper of 2nd, 3rd and 4th finger of the hands. Electromyography Inferior Arts: normal. Superior Arts: bilateral suffering of the median nerve at the carpal tunnel. Biopsy of the hand cutis: Hyperkeratosis, acanthosis and papillomatosis of the skin. Arterial vases with signs of endothelioangiitis and aspecific inflammation. CONCLUSIONS: Even if acronecrosis of the superior limbs is a rare effect of the gemcitabine, we would recommend particular caution in the administration of this drug in patient with known autoimmune disorders.
IL-6 preferentially promotes the DNA synthesis of human peripheral blood CD8+, rather than CD4+, lymphocytes in presence of PHA: this effect is observed in serum-free cultures of greater than 99% purified CD8+ lymphocytes. However, IL-6 is able to stimulate DNA synthesis of CD8+ lymphocytes triggered by a mitogenic anti-CD2 mAb, but not by anti-CD3 mAb: these results suggest that IL-6 selectively induces activation of CD8+ lymphocytes through the CD2 rather than the CD3 pathway. Limiting dilution analysis indicates that accessory cells are not required to mediate the action of IL-6 on CD8+ cells. Furthermore, this action is not blocked by addition of mAb neutralizing either IL-2 or IL2R, thus suggesting that IL-6 does not act via IL-2. CD8+ lymphocytes grown in the presence of PHA + IL-6 incorporate (3H)-thymidine to the same extent as those stimulated with PHA + IL-2, but do not increase in number until day 6 of culture. It is hence apparent that the stimulating activity of IL-6 on CD8+ lymphocytes is restricted to the GO----S phase progression, but does not lead to mitosis. IL-6 receptors are expressed on resting CD4+ and CD8+ lymphocytes: their expression is significantly enhanced on both activated CD4+ and CD8+ cells. Scatchard analysis of (125I)-IL-6 binding data showed the presence of high (Kd, 3 x 10(-10) M) and low (Kd, 6 x 10(-8) M) affinity IL6R on both lymphocyte populations. Similarly, mRNA encoding IL6R was detected in both CD4+ and CD8+ lymphocytes. Thus, our studies indicate that IL-6 directly and selectively stimulates the GO----S progression of CD8+ lymphocytes in the presence of mitogen and absence of IL-2: this phenomenon may be of interest for the elucidation of mechanisms activating cytotoxic T lymphocytes.