Characterization and potential applications of progenitor-like cells isolated from horse amniotic membrane.

The aim of this work was to isolate, for the first time, progenitor-like cells from the epithelial (AECs) and mesenchymal (AMCs) portions of the horse amniotic membrane, and to define the biological properties of these cells. AECs displayed polygonal epithelial morphology, while AMCs were fibroblast-like. Usually, six to eight passages were reached before proliferation decreased, with 13.08 and 26.5 cell population doublings attained after 31 days for AECs and AMCs, respectively. Immunocytochemical studies performed at passage 3 (P3) showed that both cell populations were positive for the expression of specific embryonic markers (TRA-1-60, SSEA-3, SSEA-4 and Oct-4). Meanwhile, RT-PCR performed at P1 and P5 showed expression of mesenchymal stem/stromal cell markers (CD29, CD105, CD44 and CD166) with negativity for CD34 at P1, although this marker began to be expressed by P5. The cells also expressed MHC-I at both P1 and P5, but lacked MHC-II expression at P1. Both AECs and AMCs demonstrated high plasticity, differentiating in vitro toward the osteogenic, adipogenic, chondrogenic and neurogenic lineages. Equine amnion-\derived cells could also be frozen and recovered without loss of their functional integrity in terms of morphology, presence of specific stemness markers and differentiation ability, although the renewal capacity was lower than that observed for freshly isolated cells. To investigate potential therapeutic effects and cell tolerance in vivo, horse amnion-derived cells were allogeneically injected into three horses with tendon injuries, resulting in a quick reduction in tendon size and ultrasonographic cross-sectional area measurements. These results suggest that horse amnion-derived cells may be useful for cell therapy applications.

[Is the reduction of the plasma levels of endothelin in the acute and sub-acute stage of myocardial infarct one of the beneficial effects of early treatment with ace inhibitors?]. / La riduzione dei livelli plasmatici dell'endotelina nelle fasi acute e sub-acute dell'infarto miocardico e uno degli effetti benefici del precoce trattamento con ace-inibitori?

BACKGROUND: Studies showed that endothelin-1 (ET-1) was increased in the acute myocardial infarction (AMI). Experimental studies reported that captopril was able to reduce ET-1 secretion. In addition increased levels of ET-1 were reported as a negative prognostic index. The study was aimed to verify whether captopril was able to reduce plasma ET-1 levels in the acute and subacute phases of AMI. METHODS: Forty five patients, hospitalized for suspected anterior AMI within 4 h since the onset of symptoms, suitable for thrombolysis (first episode), in Killip class 1-2, were randomized (double blind) into two groups: Group A (23 patients, pts), 7 females and 16 males, received captopril 6.25 mg orally (as first dose) 2-4 h after starting thrombolysis, and the doses of captopril were successively increased up to 25 mg every 8 h. Group B: (22 pts), 5 females and 17 males, received placebo after thrombolysis. All the patients met the reperfusion criteria. RESULTS: The two groups were similar for age, sex, CK peak, ejection fraction, end systolic volume and risk factors. Plasma ET levels were checked on admission, and 2, 12, 24, 48, 72 hours, after starting thrombolysis. Mean concentrations of ET +/- SD: Group A: basal 1.50 +/- 0.67, at 2 h 2.31 +/- 1.24, 12 h 1.84 +/- 1.45, 24 h 1.30 +/- 0.72, 48 h 0.95 +/- 0.50, 72 h 0.60 +/- 0.15 fmol/ml (p < 0.001). Group B: basal 1.58 +/- 0.83, at 2 h 2.38 +/- 1.35, 12 h 2.33 +/- 1.71, 24 h 1.80 +/- 1.41, 48 h 1.46 +/- 0.88, 72 h 0.93 +/- 0.44 fmol/ml (p < 0.001). Difference between the two groups was significant at 48 h (p < 0.05), and 72 h (p < 0.001). CONCLUSIONS: Our data suggest that captopril affects plasma endothelin levels in the acute and subacute phases of AMI. In addition, our results seem to be an additional support to the beneficial effects of early captopril treatment in patients with AMI.

Effects of the administration of captopril, metoprolol and of the captopril-metoprolol combination as adjuvant therapy during thrombolysis in acute myocardial infarction.

UNLABELLED: The aim of the study was to verify, during thrombolysis in patients with anterior acute myocardial infarction, the safety and effects of beta-blockers or ACE-inhibitors and their combination in the short and long term. One-hundred sixty-six patients hospitalized within 4 h from the onset of the symptoms (first episode), eligible for thrombolysis, Killip class I-II, were randomized (single blind) into four groups. Group A (42 patients) received 6.25 mg captopril (orally) 15 min before thrombolysis and metoprolol (i.v.) not later than 1 h, and orally afterwards. Group B (42 patients) received 6.25 mg captopril 15 min before thrombolysis. Group C (37 patients) received metoprolol not later than 1 h. Group D (45 patients) received thrombolysis only. Later (day 3), groups C and D also received captopril. We checked ventricular arrhythmias (first 2h) from thrombolysis, creatine kinase peak, creatine kinase peak normalization time, late ventricular arrhythmias at Holter test pre-discharge (Lown's class > 2). At follow-up (mean 30.5 +/- 2 months), mortality was evaluated for reinfarction and ventricular failure. Age and sex were similar. RESULTS: Early ventricular arrhythmias: Group A, five cases; Group B, five cases; Group C, 15 cases; Group D, 16 cases. Creatine kinase peak: Group A, 1875 +/- 220 U/l; Group B, 1566 +/- 168 U/l; Group C, 2274 +/- 212 U/l; Group D 2103 +/- 232 U/l. Creatine kinase peak normalization time: Group A, 57.7 +/- 3 h; Group B, 58.1 +/- 3 h; Group C, 72.7 +/- 3 h; Group D, 69.5 +/- 2 h (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Neurologic symptoms in fat embolism syndrome: case report.

We present a case of FES (fat embolism syndrome) with very serious neurologic signs (convulsions, deep coma, decerebrate response to noxious stimuli), without lung lesions. Nuclear magnetic resonance imaging revealed vascular alterations of the cerebral hemisphere, truncus, and cerebellum. The patient recovered without neurologic sequelae.

[Two cases of accidental hypothermia]. / Due casi di ipotermia accidentale.

We report two cases of accidental and moderate hypothermia in drug/addict subjects who came to our attention in coma, shock and respiratory distress, metabolic acidosis and characteristic ECG alterations. We used the methods of minimal invasivity to rewarm them, with good results. The two cases had a different clinical course: the first one presented some important cardiac and respiratory problems, that required 30 days of permanence in our ICU, while the second one had a quick resolution. We believe that the critical time for arrhythmias goes beyond the hypothermic period.