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1.
Indian Pediatr ; 59(1): 87-88, 2022 Jan 15.
Artículo en Inglés | MEDLINE | ID: mdl-34845989

RESUMEN

148 Italian children (n=148) suspected of and evaluated for COVID-19 infection during the first phase of the pandemic were followed-up for 6 months.During the follow-up period, no difference in the prevalence of new-onset respiratory, dermatological or neurological symptoms, nor in psychological distress,were observed in children who were positive and negative for SARS-CoV-2.


Asunto(s)
COVID-19 , Niño , Humanos , Pandemias , Pediatras , Atención Primaria de Salud , SARS-CoV-2
2.
Blood ; 112(3): 875-85, 2008 Aug 01.
Artículo en Inglés | MEDLINE | ID: mdl-18480424

RESUMEN

In beta-thalassemia, the mechanism driving ineffective erythropoiesis (IE) is insufficiently understood. We analyzed mice affected by beta-thalassemia and observed, unexpectedly, a relatively small increase in apoptosis of their erythroid cells compared with healthy mice. Therefore, we sought to determine whether IE could also be characterized by limited erythroid cell differentiation. In thalassemic mice, we observed that a greater than normal percentage of erythroid cells was in S-phase, exhibiting an erythroblast-like morphology. Thalassemic cells were associated with expression of cell cycle-promoting genes such as EpoR, Jak2, Cyclin-A, Cdk2, and Ki-67 and the antiapoptotic protein Bcl-X(L). The cells also differentiated less than normal erythroid ones in vitro. To investigate whether Jak2 could be responsible for the limited cell differentiation, we administered a Jak2 inhibitor, TG101209, to healthy and thalassemic mice. Exposure to TG101209 dramatically decreased the spleen size but also affected anemia. Although our data do not exclude a role for apoptosis in IE, we propose that expansion of the erythroid pool followed by limited cell differentiation exacerbates IE in thalassemia. In addition, these results suggest that use of Jak2 inhibitors has the potential to profoundly change the management of this disorder.


Asunto(s)
Diferenciación Celular , Células Eritroides/patología , Eritropoyesis , Janus Quinasa 2/genética , Talasemia beta/sangre , Animales , Apoptosis , Quinasas Ciclina-Dependientes/genética , Janus Quinasa 2/antagonistas & inhibidores , Ratones , Bazo/patología
3.
Transplantation ; 75(12): 1977-83, 2003 Jun 27.
Artículo en Inglés | MEDLINE | ID: mdl-12829897

RESUMEN

BACKGROUND: Prolonged immunodeficiency after allogeneic bone marrow transplantation (allo BMT) results in significant morbidity and mortality from infection. Previous studies in murine syngeneic BMT models have demonstrated that posttransplantation insulin-like growth factor (IGF)-I administration could enhance immune reconstitution. METHODS: To analyze the effects of IGF-I on immune reconstitution and graft-versus-host disease (GVHD) after allo BMT, we used murine models for MHC-matched and -mismatched allo BMT. Young (3-month-old) recipient mice received 4 mg/kg per day of human IGF-I from days 14 to 28 by continuous subcutaneous administration. RESULTS: IGF-I administration resulted in increased thymic precursor populations (triple negative-2 and triple negative-3) as determined on day 28 but had no effect on overall thymic cellularity. In the periphery, the numbers of donor-derived splenic CD3+ T cells were increased and these cells had an improved proliferative response to mitogen stimulation. IGF-I treatment also significantly increased the numbers of pro-, pre-, and mature B cells and myeloid cell populations in the spleens of allo BMT recipients on day 28. The administration of IGF-I in combination with interleukin 7 had a remarkable additive effect on B-cell, but not on T-cell, lymphopoiesis. Finally, we tested the effects of IGF-I administration on the development of GVHD in three different MHC-matched and -mismatched models and found no changes in GVHD morbidity and mortality. CONCLUSION: IGF-I administration can enhance lymphoid and myeloid reconstitution after allo BMT without aggravating GVHD.


Asunto(s)
Trasplante de Médula Ósea/fisiología , Enfermedad Injerto contra Huésped/prevención & control , Factor I del Crecimiento Similar a la Insulina/uso terapéutico , Linfocitos T/inmunología , Animales , Células de la Médula Ósea/citología , Células de la Médula Ósea/efectos de los fármacos , Trasplante de Médula Ósea/inmunología , Diferenciación Celular/efectos de los fármacos , Granulocitos/efectos de los fármacos , Granulocitos/fisiología , Humanos , Infusiones Parenterales , Factor I del Crecimiento Similar a la Insulina/administración & dosificación , Activación de Linfocitos/efectos de los fármacos , Complejo Mayor de Histocompatibilidad , Ratones , Ratones Endogámicos C3H , Ratones Endogámicos C57BL , Ratones Endogámicos , Linfocitos T/efectos de los fármacos , Trasplante Homólogo , Trasplante Isogénico
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