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  • 1
    ISSN: 1432-0584
    Keywords: Anemia ; Burst-promoting activity Cimetidine ; Elderly ; T lymphocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Erythroid stem cell proliferation is regulated by lymphokines and erythropoietin. The helper subset of T lymphocytes is known to produce the erythroid growth factor IL-3 or burst-promoting activity (BPA), while the suppressor subset seems to inhibit the erythroid growth. Leukocyte-conditioned media derived from white cells of nonanemic elderly were reported to provide defective support to the erythropoiesis. In two groups of elderly, nonanemic and anemic, we studied the ability of T lymphocytes to stimulate the BFU-E growth and the in vitro effect of cimetidine, as a drug that inhibits the suppressor T lymphocytes. Culture data were then compared with the peripheral blood lymphocyte picture. The study shows that defective mononuclear cell support to the BFU-E growth, namely due to reduced absolute number of the T4 subset of T lymphocytes, can be observed in both anemic and nonanemic elderly. It is suggested that isolated defective BPA production is not always sufficient to induce anemia. In most cases, anemia of unexplained origin in senescence would be due to the concomitance of both BFU-E impairment and defective BPA production. The simultaneous evaluation of BFU-E growth, lymphokine production, and the T-lymphocyte blood picture offers the best way to investigate the erythropoiesis of the elderly.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Annals of hematology 64 (1992), S. 221-223 
    ISSN: 1432-0584
    Keywords: BFU-E ; BPA ; Cimetidine ; T lymphocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of cimetidine, an inhibitor of suppressor T lymphocytes, on the burst-promiting activity (BPA) of normal T lymphocytes has been studied. Cimetidine has been shown to increase the BPA of normal T lymphocytes, both when added to the culture and when T lymphocytes were preincubated for 1 h with it. Cimetidine had no direct effect on the in vitro growth of burstforming units (BFU-E). Our results show that CD 8 suppressor T lymphocytes inhibit the in vitro growth of BFU-E in normal conditions, either directly or through inhibition of BPA of CD 4 helper T lymphocytes. Cimetidine has proved to be a useful tool for investigating the hematological role of T-lymphocyte subsets in normal and pathological conditions.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neurological sciences 17 (1996), S. 211-214 
    ISSN: 1590-3478
    Keywords: Transient global amnesia ; Cerebral ischemia ; Epilepsy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario L'amnesia globale transitoria (TGA) è caratterizzata dall'insorgenza improvvisa di incapacità a memorizzare, amnesia retrograda, ripetitività delle domande, in assenza di altri segñi o sintomi neurologici. La fisiopatologia dell'anmesia globale transitoria è incerta; sono stati proposti meccanismi tromboembolici, epilettici e metabolici. Abbiamo studiato 25 pazienti affetti da TGA nei quali sono state praticate le indagini cliniche, laboratoristiche, strumentali di base, E.E.G., TC, cerebrale, ecodoppler dei tronchi sovraaortici. E stata dimostrata una maggiore incidenza di ipertensione arteriosa e di ipercolesterolemia. Inoltre abbiamo riscontrato una maggiore frequenza di alterazioni elettroencefalografiche nei pazienti con TGA di minore durata. Viceversa le lesioni ischemiche riscontrate alla TC cerebrale sono risultate più frequenti nei pazienti con TGA di maggiore durata. Questi dati, sebbene statisticamente non significativi, sembrano confermare l'ipotesi che la TGA sia una sindrome eterogenea, comprensiva di una forma pura, e una forma ischemica.
    Notes: Abstract Transient global amnesia (TGA) has been defined as the presence of an impairment of short-term memory, retrograde amnesia and repetitive queries, without any other neurological signs or symptoms. The precise pathophysiology of TGA is unclear, although thromboembolic, epileptic, migrainous and metabolic mechanisms have been suggested. We have studied the clinical, biohumoral, electroencephalographic and neuro-imaging data relating to 25 patients with TGA, and found a prevalence of hypertension and hypercholesterolemia. We also found a higher incidence of electrical changes in the patients whose TGA was of shorter duration, whereas brain CT scans revealed ischemic lesions more frequently in the patients with TGA of longer duration. Our findings seem to confirm the hypothesis that TGA is a heterogenous clinical syndrome consisting of pure and ischemic forms.
    Type of Medium: Electronic Resource
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