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La contaminación con hongos, bacterias y levaduras causa grandes pérdidas en la micropropagación comercial de especies vegetales y en los trabajos de investigación. El control de la contaminación in vitro es fundamental para aumentar la eficiencia de la micropropagación. Este trabajo evaluó la acción bacteriostática y/o bactericida del PPM (Plant Preservative Mixture) para controlar la contaminación con Pseudomonas, y su efecto sobre el crecimiento in vitro de caña de azúcar. La bacteria se aisló de material vegetal contaminado. Las concentraciones de PPM fueron: T1 (0,06); T2 (0,125); T3 (0,250); T4 (0,500); T5 (0,750); T6 (1,00) y T7 (0 mL/L), incorporadas al medio de cultivo MS (1962). La bacteria se sembró en tubos con 5 repeticiones. El crecimiento bacteriano se evaluó con extendidos microscópicos. Usando concentraciones inhibitorias del crecimiento bacteriano y un testigo sin PPM, se evaluó su efecto en el crecimiento de macollos. Se colocaron 6 macollos de 2-4 cm por frasco, con 10 repeticiones. Se evaluó el número, longitud y peso fresco de macollos. T3, T4, T5 y T6 inhibieron el crecimiento bacteriano, con acción bactericida. El PPM no tuvo efectos inhibitorios sobre longitud, peso fresco y número de macollos. T5 presentó mayor uniformidad en el desarrollo de los macollos. Fungi, bacteria and yeast contamination causes several lost in the commercial micro dissemination of vegetal species and in research works. The control of in vitro contamination is essential to increase the micro dissemination efficiency. This work evaluated bacteristatic and/or bactericidal action of PPM (Plant Preservative Mixture) to control the contamination with Pseudomonas, and the effect on the "in vitro" sugarcane growth. The bacterium was isolated from contaminated vegetal material. PPM concentrations were: T1 (0.06); T2 (0.125); T3 (0.250); T4 (0.500); T5 (0.750 ); T6 (1) and T7 (0 mL/L) incorporated to the MS (1962) culture medium. The bacterium was sown in tubes with 5 replications. The bacterial growth was evaluated doing microscopic extended. Using inhibitory concentrations of the bacterial growth and a control without PPM, it was evaluated the effect on the bunches growth. Six bunches of 2-4 cm long were put in each bottle with 10 replications. Number; length and fresh weight of bunches were evaluated. T3, T4, T5 and T6 inhibited the bacterial growth with bactericidal action. There was no inhibitory effects of PPM on the length, fresh weight and number of bunches. T5 presented major uniformity in the development of the bunches.

Adults with growth hormone (GH) deficiency (GHD) have impaired health, which improves with GH replacement. GHD in adulthood leads to impairment in body composition and structure functions as well as to deranged lipoprotein and carbohydrate metabolism leading to increased cardiovascular morbidity. Therefore the transition adolescent in whom severe GHD is confirmed has to continue GH replacement with an appropriate age-related dosage. All short children who have been treated with rhGH for classical and non-classical GHD should be suspected as potentially GHD in adulthood though only in classical organic and idiopathic forms is severe GHD likely to be confirmed. GHD must be shown biochemically by single provocative testing. Insulin-induced hypoglycemia (ITT) and GHRH + arginine are the tests of choice provided that appropriate cutoff limits are assumed; these tests show good specificity and sensitivity. Testing with GHRH + GH secretagogues is another reliable alternative. Low IGF-I levels can be definitive evidence of persistent severe GHD in patients with genetic GHD or panhypopituitarism, but normal IGF-I levels do not rule out severe GHD. Individual titration of the rhGH dose is recommended and measurement of IGF-I levels is needed for monitoring the adequacy of replacement. The mean GH dose for replacement in the transition adolescent, however, is still higher than in adulthood; after puberty the rhGH dose should be progressively decreased in the following years (probably up to 25 years old) in order to obtain optimal peak bone mass.

We report about two cases of thyroid metastases, with neoplastic thrombosis of the jugular vein, originating from a renal clear cell carcinoma and arising respectively 5 and 18 years after the original nephrectomies.The first patient had also a synchronous transitional cell carcinoma of the bladder and a poorly differentiated prostatic adenocarcinoma, further complicating the location of the primary sources of the metastases. The metastases of the first case were firstly diagnosed by mean of fine needle aspiration biopsy, and subsequently histologically confirmed. Histochemical (diffuse PAS-positive cytoplasms) and immunohistochemical stains (wide spectrum cytokeratins low molecular cytokeratins+, Ck8+, CD10+, Vimentin+, Ck20-, Ck7-, Ck19-, PSA-, thyreoglobulin-, TTF-) performed both on cytologic and histological material helped to define the metastases as oriinating from the renal clear cell carcinoma. For the first patient, the other two possible primary sources were ruled out and a possible primary thyroid tumor with clear cell change was also excluded for both patients.

There is now wide consensus that, within an appropriate clinical context, GH deficiency (GHD) in adults must be shown biochemically by provocative testing of GH secretion and that appropriate cut-off limits have to be defined for each provocative test. Insulin-induced hypoglycemia (ITT) is indicated as the test of choice, and severe GHD, to be treated with recombinant human GH replacement, is defined by a GH peak response to ITT of less than 3 micrograms/L. GHRH + arginine (GHRH + ARG) is one of the most promising tests in alternative to ITT. In fact, it has been reported as a potent, reproducible, and age-independent test and that it is able to distinguish between GHD and normal adults. The aim of the present study was to compare the GH response to ITT and GHRH + ARG in a large group of hypopituitary adults (n = 40; 29 male and 11 female; age: 36.4 +/- 2.1 yr). The third centile limit of the peak GH response to ITT has been reported as 5 micrograms/L, whereas in our lab, that to GHRH + ARG is 16.5 micrograms/L. In hypopituitary adults, the mean peak GH response to ITT (1.5 +/- 0.2 micrograms/L, range: 0.1-8.5 micrograms/L) was lower (P0.001) than that to GHRH + ARG (3.0 +/- 0.4 micrograms/L, range 0.1-12.0 micrograms/L), though there was positive correlation (r = 0.61, P0.001) between the GH responses to the 2 tests. The peak GH response to GHRH + ARG, but not that to ITT, was positively (though weakly) associated with insulin-like growth factor-I levels (r = 0.35, P0.03). Childhood and adult onset GHD patients, as well as patients with single and multiple pituitary insufficiencies, had similar peak GH responses to ITT or GHRH + ARG. Analyzing individual GH responses, 4/40 (10%) of the hypopituitary patients had GH peaks higher than 5 micrograms/L after ITT; moreover, 3 other patients (7%) had GH peaks, after ITT, higher than 3 micrograms/L. On the other hand, after GHRH + ARG, all patients had GH peaks lower than 16.5 micrograms/L, whereas 21/40 (52.5%) had GH peaks higher than 3 micrograms/L. Because 3 micrograms/L is the arbitrary cut-off for ITT, the third centile limit of which is 5 micrograms/L, we arbitrarily considered 9 micrograms/L as the cut-off point for GHRH + ARG. It is noteworthy that 37/40 (92.5%) patients had a GH peak, after GHRH + ARG, below this limit. In conclusion, our present results confirm that the ITT test is a reliable provocative test for the diagnosis of adult GHD, whereas they show that the GHRH + ARG test is, at least, as sensitive as the ITT test (provided that appropriate cut-off limits are considered). Note that even the arbitrary cut-off point below which severe GHD is demonstrated has to be appropriate to the potency of the test.

A model of the d.c. operation of the GaAs Bipolar Mode Field Effect Transistor (BMFET) is presented. The model in based on a approximate, closed-form solution of the fundamental transport equations, and includes some two-dimensional effects that were not included in previously developed models of silicon BMFET structures. A comparison with the characteristics of a experimental device shows that the incorporation of the 2D effects allows an accurate modeling of the GaAs device.