Summary. Myelodysplastic syndromes (MDS) are a group of clonal disturbances with defective cellular differentiation. Vitamin D3 (VD) analogues can act on the differentiation and maturity of different cell lines. We studied the effects of VD on a series of patients with MDS in an open-design trial. Nineteen patients, 12 men and seven women, with MDS were included. Patients were 74·8 Ϯ 5·6 years (mean Ϯ SD), seven had refractory anaemia with ringed sideroblasts, five had refractory anaemia, one had refractory anaemia with excess of blasts and six had chronic myelomonocytic leukaemia. All the patients were in a low to intermediate risk group. Mean follow-up period was 26·21 months, range 9-75. Responders were defined as follows: granulocyte or platelet count increase by 50%, or haemoglobin increase of 1·5 g/dl or transfusion needs decrease by 50%. The first five patients received 266 mg of calcifediol three times a week and the other 14 received calcitriol (0·25-0·75 mg/d). Response was observed in 11 patients. In the calcifedioltreated group, one case responded, three were nonresponders, and one showed progression. In the calcitriol group, 10 were responders (two with major response), and four were non-responders. No correlation was observed between baseline levels of vitamin D metabolites and the presence of response. No hypercalcaemia was observed. Treatment with vitamin D3 metabolites could induce a longstanding response of the haematological disturbance in some low-intermediate risk MDS patients without inducing hypercalcaemia.
It is unlikely that HIV-1 infects human osteoblasts in vivo; therefore, the hypothesis that these cells could act as local HIV-1 reservoirs should be reconsidered.
There is conflicting evidence favoring both the use of human serum (HS) and of human serum albumin (HSA) in human islet culture. We evaluated the effects of HS versus HSA supplementation on 1) in vitro b-cell viability and function and 2) in vivo islet graft revascularization, islet viability, b-cell death, and metabolic outcome after transplantation. Islets isolated from 14 cadaveric organ donors were cultured for 3 days in CMRL 1066 medium supplemented with HS or HSA. After 3 days in culture, b-cell apoptosis was lower in HS group (1.41 ± 0.27 vs. 2.38 ± 0.39%, p = 0.029), and the recovery of islets was 77 ± 11% and 54 ± 1% in HS-and HSAcultured groups, respectively. Glucose-stimulated insulin secretion (GSIS) was higher in HS group (29.4, range 10.4-99.9, vs. 22.3, range 8.7-70.6, p = 0.031). In vivo viability and revascularization was determined in HSand HSA-cultured islets transplanted into the anterior chamber of the eye of Balb/c mice (n = 14), and b-cell apoptosis in paraffin-embedded mouse eyes. Islet viability and b-cell apoptosis were similar in both groups. Revascularization was observed in one graft (HS group) on day 10 after transplantation. Islet function was determined in streptozotocin (STZ)-diabetic nude mice (n = 33) transplanted with 2,000 IEQs cultured with HS or HSA that showed similar blood glucose levels and percentage of normoglycemic animals over time. In conclusion, human islets cultured in medium supplemented with HS showed higher survival in vitro, as well as islet viability and function. The higher in vitro survival increased the number of islets available for transplantation. However, the beneficial effect on viability and function did not translate into an improved metabolic evolution when a similar number of HSA-and HS-cultured islets was transplanted.
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