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Root growth is often restricted by genetics, cultural factors, and adverse environmental conditions. The application of plant biostimulants can help to promote root growth and to guarantee optimal shoot growth and productivity. An innovative biopolymer-based biostimulant (Quik-Link, Italpollina S.p.A., Rivoli Veronese, Italy) for boosting root growth and improving nutrient uptake by plants was tested in three experiments. In the first experiment, tobacco leaf explants cultured in vitro under Murashige and Skoog basal medium enriched with 1 mL L-1 of Quik-Link showed regeneration of roots while no roots were detected from leaf explants cultured without the addition of Quik-Link in the medium. In the second experiment carried out under greenhouse conditions, tomato plants were transplanted in pots filled with a sandy soil and irrigated after two days from transplanting with a solution containing the biostimulant at three concentrations corresponding to 0, 0.12 or 0.24 mL plant-1. After 12 days from transplanting, tomato plants treated with 0.24 mL plant-1 of biostimulant exhibited a higher root dry biomass and root to shoot ratio than control plants. In the third experiment, carried under field conditions, treatments were defined by a factorial combination of two fertilization levels (conventional and low input fertilization with half-dose of fertilizers used in conventional fertilization plan) and two Quik-Link application rates (0 and 12 L ha-1). Biostimulant application increased marketable yield by 19.2 and 9.7%, under reduced and conventional fertilization regimes, respectively. Quik-Link application increased N, P, and Fe in tomato leaves at flowering/fruit set stage. Fruit quality parameters were only affected by fertilization level with an increase of soluble solids contents with the reduced rate of mineral fertilizers.

In 31 campi dei principali areali di coltivazione italiani sono stati valutati 38 genotipi, di cui 12 al primo anno di prova. La cultivar mediamente più produttiva è ri sultata LG anubis, al primo anno, con indice 108 e medie superate in 25 prove su 31 totali (81% dei campi), caratterizzata da peso ettolitrico e tenore proteico leggermente inferiori alle medie (-0,1 e -0,4 punti, rispettivamente).

Plant biostimulants, including microbial and non-microbial based products, have been successfully used to improve agriculture productivity due to their ability to stimulate nutrient uptake, plant growth and to improve tolerance to abiotic stresses. An open field experiment was carried out on processing tomato (Solanum lycopersicum L.) with the aim to evaluate the effect of microbial and non-microbial plant biostimulant applications on yield, yield components, nutritional and functional quality attributes as well as on economic profitability. Two treatments were tested: untreated control and biostimulant treatments (mycorrhizal fungi and Trichoderma koningii in combination with vegetal extracts). All plant biostimulants were applied through fertigation during the growing season. Biostimulant applications increased the marketable yield by 15% compared to untreated tomato plants. The higher marketable yield in biostimulant-treated plants was attributed to an increase of mean fruit weight and not to the number of fruits per plant. Physiological parameters, such as SPAD index and fluorescence, were not affected by biostimulant applications. Vitamin C and lycopene were boosted by biostimulant applications while no significant differences were observed for total soluble solids and pH of fruit juice. The better crop productivity observed in the current trial could be attributed to the better nutritional status in biostimulant-treated tomato in terms of higher N concentration. Our findings can assist processing tomato growers in adopting innovative and sustainable tools such as plant biostimulants to boost crop productivity to a level resulting in higher economic returns.

Mitochondria are highly dynamic organelles, whose morphology can vary from an elongated and interconnected network to fragmented units. In recent years, outstanding discoveries have linked mitochondrial morphology to the regulation of an increasing number of biological processes, such as biosynthetic pathways, oxidative phosphorylation and ATP production, calcium buffering, and cell death. Here we describe two of the main methods used to analyze the mitochondrial length in fixed cells and the mitochondrial fusion rate in live cells. Moreover, we focus one of the protocols on T cells, as an example of non-adherent cells, which present some particularities and difficulties in the analysis of mitochondrial shape. We also discuss the main mouse models carrying a mitochondrial targeted fluorescent protein, an invaluable tool to deeply investigate in vivo mitochondrial morphology.

The aim of this study was to evaluate exercise performance in patients affected by anorexia nervosa.We studied 19 patients (all females, mean age 23.1 +/- 5.2 years) affected by anorexia nervosa (mean weight 37.3 kg, body mass index 14.04 +/- 1.4 kg/m2) and 20 constitutionally thin women, matched for age, height and physical activity, with a body mass index19 kg/m2. All these women underwent clinical examination, standard ECG and a cardiopulmonary stress test.Patients affected by anorexia nervosa showed a lower heart rate and systolic blood pressure at peak exercise (148.8 +/- 13.8 vs 171 +/- 9.2 b/min, p0.001, and 130 +/- 9.5 vs 152 +/- 11.2 mmHg, p0.001), work load (85.5 +/- 15.1 vs 117.2 +/- 20.3 W, p0.001), rate-pressure product (19 371 +/- 2391 vs 25,986 +/- 2218 b/min/mmHg, p0.001), oxygen uptake (VO2) at rest and maximum VO2 (5.4 +/- 1.7 vs 7.1 +/- 1.1 ml/kg/min, p0.001, and 28.08 +/- 6.3 vs 40.2 +/- 7.1 ml/kg/min, p0.001), anaerobic threshold (15.7 +/- 1.9 vs 20.4 +/- 2.1 ml/kg/min, p0.001), VO2 during exercise (9.5 +/- 1.2 vs 12.8 +/- 1.3 ml/min/W, p0.001), maximum minute ventilation (34.5 +/- 9.9 vs 48.4 +/- 10.3 /min, p0.001), and oxygen pulse (7.2 +/- 2 vs 10.9 +/- 2.4 ml/b, p0.001).These data show an abnormal working capacity and cardiovascular responses to exercise in patients affected by anorexia nervosa. The low VO2, both at rest and during exercise, allows them to maintain a relatively high level of physical activity, which contributes to increase the energy expenditure needed for weight loss.

Acute-phase reactants have recently been shown to have a short-term and possibly long-term prognostic value in acute coronary syndromes. The aim of the present study was to retrospectively verify whether serum levels of inflammation markers can predict the occurrence of early and late cardiac events after myocardial infarction.We reevaluated 58 consecutive patients (43 men and 15 women, mean age 66 +/- 12 years) admitted to our Center during 1993 with a first myocardial infarction. Patients with non-cardiac causes of inflammation were excluded, as well as patients with a left ventricular ejection fraction40%. From the first blood sample obtained at admission, we evaluated C-reactive protein (CRP) and alpha1-acid glycoprotein (alpha1-AGP) serum levels, the erythrocyte sedimentation rate (ESR), fibrinogen levels, and the white blood cell (WBC) count. We also evaluated the highest level of serum cardiac markers. Follow-up data were collected for 55 patients in June 1999.Five in-hospital and 13 delayed cardiac deaths occurred. The mean follow-up of current survivors was 5.9 +/- 0.4 years. Patients in whom cardiac death occurred had significantly higher CRP (7.4 +/- 4.1 vs 3.0 +/- 2.4 mg/dl, p0.001) and alpha1-AGP levels (160 +/- 38 vs 113 +/- 24 mg/dl, p0.001), ESR (63 +/- 30 vs 37 +/- 25 mm/hour, p0.001), and WBC count (13,727 +/- 3,853 vs 10,936 +/- 3,358/mm3, p = 0.004). At multivariate analysis, higher alpha1-AGP (p0.001) and CRP serum levels (p = 0.02) were independent predictors of cardiac death. Patients in whom cardiac events occurred during follow-up showed higher CRP (5.7 +/- 3.7 vs 1.6 +/- 1.5 mg/dl, p0.001) and alpha1-AGP levels (140 +/- 36 vs 101 +/- 23 mg/dl, p0.001) and ESR (50 +/- 30 vs 34 +/- 26 mm/hour, p = 0.06). Higher alpha1-AGP (p0.001) and CRP serum levels (p = 0.03) were independent predictors of the occurrence of cardiac events.The present study shows that CRP and alpha1-AGP have an independent prognostic value in patients presenting with a first, uncomplicated myocardial infarction. Assays of these markers may help to better stratify patients hospitalized for acute coronary syndromes.

To investigate whether motoneurons react to signals deriving from target inflammation, we studied the facial motor nucleus after injections of phytohaemagglutinin in the snout of adult rats. This plant lectin is a tool widely used to induce proliferation and activation of T lymphocytes, and we observed marked lymphocyte infiltration in the injected facial muscles. Retrograde labelling of motoneurons was not detected after peripheral injections of fluorochrome-conjugated phytohaemagglutinin. Nitric oxide synthase, revealed by NADPH-diaphorase histochemistry, OX-42-immunoreactive microglia, and expression of the cell death repressor gene bcl-2, investigated with nonradioactive in situ hybridization and immunohistochemistry, were evaluated in the facial nucleus. Daily phytohaemagglutinin injections for 4 days, mimicking repeated muscle exposure to inflammatory stimuli, resulted after 2-day survival in NADPH-diaphorase induction in motoneurons and marked activation of the surrounding microglia. Quantitative image analysis of NADPH-diaphorase staining, and OX-42 immunoreactivity and microglial cell counts indicated highly significant increases with respect to saline-injected control cases. The occurrence of a neuroprotective retrograde response was evaluated monitoring bcl-2 expression. Following single phytohaemagglutinin administration, bcl-2 mRNA was significantly upregulated at 6 h in facial motoneurons and returned to basal levels at 24 h. Bcl-2 immunoreactivity was markedly upregulated at 24 h and was still significantly higher than in controls at 7 days, when concomitant NADPH-diaphorase induction in motoneurons and microglia activation was also observed. No degenerative features were observed in motoneurons after phytohaemagglutinin injections at the examined time-points. The data point out that local muscle inflammation retrogradely elicits gene activation in motoneurons and their microenvironment.

Transmyocardial laser revascularization (TMLR) aims to improve perfusion of the ventricular wall via laser-created transmural channels. We present the results of TMLR with a holmium laser as sole therapy in patients with angina refractory to medical treatment and extensive coronary artery disease unsuitable for angioplasty or coronary artery by-pass grafting.From November 1995 to February 1997, twenty-two patients underwent isolated TMLR with a holmium laser. Five patients (23%) were female; the mean age was 67 +/- 7 years (range 53 to 74 years). Previous myocardial revascularization procedures had been performed in 17 patients (77%). Mean preoperative angina class was 3.4 +/- 0.5 and unstable angina was present in 7 patients (32%).There were no hospital deaths. The only postoperative complications were transient supraventricular arrhythmias in 6 patients (27%). Each patient received a mean of 33 +/- 8 channels in 27 +/- 13 minutes. There were two late deaths, 40 days and 4 months after TMLR, due to stroke and myocardial infarction, respectively. Mean follow-up duration was 8 +/- 5 months (range 40 days-15 months). The mean number of hospitalizations due to angina fell from 4.9 +/- 1.5 in the 6 months before TMLR to 1.5 +/- 1.0 in the 6 months following surgery (p0.001). At follow-up, mean angina class had significantly improved (1.8 +/- 0.6, p0.001), as well as effort tolerance, which increased from a mean of 3.5 +/- 1.4 minutes to 5.1 +/- 1.7 minutes (p = 0.01). 201Tl SPECT at 3 and 6 months did not show any significant changes in the segmental perfusion of the lased and unlased areas.TMLR with a holmium laser is a simple procedure with low operative mortality and morbidity. Short-term results confirm that clinical improvement is obtained in most patients, although this is not supported by significant changes in myocardial perfusion at short-term follow-up.

To evaluate the changes of left ventricular diastolic and systolic function and the timing of these changes in the early stages of acute myocardial infarction, serial echocardiograms were performed in 10 male patients (mean age of 56 years) with acute myocardial infarction, undergoing reperfusion by thrombolysis (recombinant tissue plasminogen activator). Echocardiograms were performed before reperfusion and 3, 6, 12, 24, 48, 72 hours, 7 and 14 days after thrombolysis. Significant differences of heart rate, systolic and diastolic blood pressure, left ventricular end diastolic volume, end-systolic volume and ejection fraction were not found. The mean regional wall motion index improved from 1.02 +/- 0.50 to 0.89 +/- 0.51 (p less than 0.05) at 48 hours; to 0.79 +/- 0.46 (p less than 0.01) at 72 hours; to 0.69 +/- 0.43 (p less than 0.001) at 7 days and to 0.61 +/- 0.40 at 14 days (p less than 0.001). The deceleration time decreased from 223 +/- 33 to 169 +/- 30 ms (p less than 0.001) 24 hours after reperfusion without further improvement. E peak velocity and E/A ratio significantly increased at 72 hours, while A peak velocity was not statistically different. A slow and progressive recovery of left ventricular function occurred after thrombolysis in acute myocardial infarction. Left ventricular diastole improves earlier while regional systolic function improves slowly till the hospital discharge.

The significance of U-wave inversion during coronary arterial spasm was investigated in 188 consecutive ergometric tests performed in 69 patients. All patients had previously undergone coronary arteriography which had clearly shown coronary spasm either at rest or after a single 0.4 mg injection of ergometrine. The ergometrine tests were then performed at the patient's bedside using a standard protocol with injection of incremental doses of ergometrine: 0.05, 0.1, 0.2 and 0.4 mg every 5 minutes with 12-lead ECG recordings every minute. Fifty of the 59 patients with positive tests had classical signs of spasms: ST elevation or depression and/or T wave inversion; the other 9 patients had inversion of the U wave alone (2 cases) or associated with classical ST segment changes in the remaining cases. The 10 other patients had no ECG changes although 2 of them suffered typical anginal pain. Negative U waves were observed in 4 of the 12 patients with spasm of the left anterior descending artery, accompanied by ST elevation in the anterior wall leads. A negative U wave would appear to be a sign of less ischaemia than the classical ECG changes because anginal pain is less common: 4 out of 9 cases in which U wave inversion was a very early change, 8 out of 9 cases in which it was the first or only abnormality. The recognition of a negative U wave increases the sensitivity of the electrocardiogram during resting angina and allows earlier treatment of coronary spasm with nitrate derivatives after an ergometrine test.

To evaluate the utility of echo-Doppler (ED; PW, CW and color), 67 patients affected by pure mitral stenosis (20 M, 47 F, mean age 52 years) were submitted to ED examination. Right and left cardiac catheterization were performed in 20 patients within 24 hours before ED. Mitral area obtained by Doppler method (Hatle's formula) correlated highly with both echo-2 dimensional and hemodynamic area (r = 0.93, p less than 0.001; r = 0.95, p less than 0.001 respectively). It was possible to calculate systolic pulmonary pressure, in patients with tricuspid incompetence, (43.9 +/- 14.9 mmHg, range 25-80) which correlated significantly (r = 0.95, p less than 0.001) with hemodynamic data (40.2 +/- 12.7 mmHg, range 20-70). The left atrial-left ventricular pressure gradient was 15.6 +/- 6.9 mmHg, range 6-32; the mean pressure gradient was 8.4 +/- 3.7 mmHg, range 3-17; the pressure half time 170.2 +/- 62.3 ms, range 83-330. We observed different types of direction of transmitral jets: centrally directed (n = 34); forward antero-lateral wall (n = 28); toward interventricular septum (n = 5). The transmitral jets presented 4 different appearances: scimitar-shaped (n = 28); candle flame (n = 24); mushroom (n = 9); double-jets (n = 6). No correlation was observed between the different types of transmitral jets (direction and appearance) and the parameters obtained by Doppler (PW and CW): velocities, pressure half-time, gradients. Thus, Doppler echocardiography permits a complete anatomic and functional evaluation of patients with pure mitral stenosis. We have not observed any correlation between the hemodynamic data and the different types of transmitral jets visualized by color Doppler.

Eighteen previously untreated patients with histologically confirmed small-cell lung cancer were treated with high-dose epirubicin (course 1, 100 mg/m2; courses 2–6, 140 mg/m2, day 1), every 3 weeks. Overall response rate was 33% (95% confidence limits, 14–52%), including two complete and four partial responses. The response rates for limited (n = 11) and extensive (n = 7) disease patients were 45% and 14%, respectively. With a median follow-up of 18 months, estimated 2-year survival of all patients was 29% and the median duration of response 18.5 months. The dose-limiting toxicity was myelosuppression, with a median granulocyte nadir of 1,150/mm3; 39% of patients had neutropenic fever. Nausea/ vomiting, alopecia, and stomatitis were the most common non hematological toxicities, usually mild to moderate. Acute cardiac toxicity was unusual and no episodes of congestive heart failure were observed. Cumulative doses of 800 mg/m2 were associated with moderate cardiotoxicity (grade 2), as assessed by endomyocardial biopsy and electron microscopy analysis. These results indicate that epirubicin, at the present doses and schedule, is an active single agent in patients with small-cell lung cancer, with acceptable general and moderate cardiac toxicity.

In the isolated perfused rat heart the main released purine catabolite is uric acid. Furthermore purine nucleosides and bases added to the perfusion buffer are oonverted into uric acid at the passage through the coronary circulation. In the human heart a low xanthine oxidase activity has been observed, however few data are available on the release of uric acid. In this work we have determined the purine catabolites by HPLC in deproteinated blood samples collected from the aorta and coronary sinus in human patients submitted to routine cardiac catheterization, whole blood concentration of uric acid increased from 105 ± 21 uM in aortic blood to 189 ± 25 uM in coronary sinus blood, while the concentrations of xanthine and hypoxanthine were slightly decreased or in a few patients were unchanged. Only trace amounts of inosine and adenosine could be detected. The amount of the released uric acid is consistent with the xanthine oxidase activity in human heart. From these results it appears that in the human heart under rest conditions uric acid is the main purine catabolite and that the purine output exceeds the reuptake. In basal conditions the net purine output (including uric acid) should correspond to myocardial de novo synthesis of purine nucleotides. The formation of uric acid must be taken into account in the study of purine metabolism also in human heart.