A Spanish version of the Family Assessment Device

Introduction  

This paper presents the results of a study on the psychometric properties of an authorized Spanish version of the McMaster Family Assessment Device, a self-report measure of family functioning.     

Panhypopituitarism as first manifestation of a lung cancer

Pituitary metastases of solid tumours are infrequent, specially as a first manifestation. When they happen, they are usually due to breast or lung cancer and are asymptomatic or produce diabetes insipidus. It is very strange that they produce hormonal deficiency. We present a case report of a bronchogenic adenocarcinoma in a 65-year-old man which began with panhypopituitarism, diabetes insipidus and visual alterations. Magnetic resonance imaging revealed a large sellar mass, with clivus infiltration and invading the right cavernous sinus. The biopsy result was adenocarcinoma metastases from lung cancer.     

N3-arylspiroimidazolidine-2,4-diones N3-arylspiroimidazolidine-2-thio-4-ones and 4-hydroxy derivatives. Synthesis and anthelmintic activity

The synthesis of new N3-arylciclohexanespiroimidazolidine-2,4-diones, N3-arylciclohexanespiroimidazolidine-2-tio-4-ones and the 4-hydroxy derivatives is described and their structures discussed on the basis of I.R. and 1H-N.R.M. data. The anthelmintic activity of these compounds was tested.     

Inhibition of Intestinal Pyrimidine Nucleoside Phosphorylases

The activity of 5-deoxy-5-fluorouridine (dFUR) depends on its activation to 5-fluorouracil (FU) by pyrimidine nucleoside phosphorylases. These enzymes are found in tumors and normal tissues, with the highest activity in the small intestines. The present study examined the inhibition of dFUR phosphorolysis in intestinal tissues. dFUR metabolism in intestinal homogenates was inhibited by uracil (U), uridine (UR), and thymidine (TdR), which are the normal substrates for the phosphorylases. Conversely dFUR reduced the metabolism of these inhibitors. A good agreement was found between the observed data and the computer-fitted data using the equations for competitive inhibition between dFUR and the inhibitors. In the absence of inhibitors, the V _max of dFUR phosphorolysis was 47.1 ± 4.9 µM/min and the apparent K _m was 910 ± 167 µM. The V _max was unaltered by the inhibitors, while the K _m was increased with increasing inhibitor concentrations. The maximal inhibition of dFUR metabolism by UR and TdR was about 80%. The K _i,'s were 372 µM for U, 87.2 µM for UR, and 112 µM for TdR and are orders of magnitude higher than their reported endogenous serum concentrations. The rate of dFUR phosphorolysis to FU in the intact intestinal epithelial crypt cells, indicated by the ratio of FU to dFUR in the intracellular fluid, was reduced by UR in a concentration-dependent fashion. These data indicate that the naturally occurring pyrimidines inhibit competitively the dFUR metabolism by the intestinal phosphorylases, that this inhibition occurs at concentrations much higher than the circulating endogenous levels, and that phosphorolysis is the major route of dFUR metabolism.     

Inverse association between smoking and idiopathic Parkinson's disease

An evaluation is made of the effect of smoking during the period of life between 20 and 50 years of age and idiopathic Parkinson's disease in a case-control study carried out in Navarra. An inverse association is observed: for the number of smokers (OR = 0.66, CI 90% 0.41-1.05); for the number of years smoking (OR =0.22, CI 90% 0.05-0.97); and for the quantity of cigarettes smoked (z = 2.2298, p = 0.02). Likewise, a dose-response relationship exists between the number of cigarettes consumed and the risk of Parkinson's disease (p = 0.01). The same effect is maintained on analysing the data by matching 1:1 (OR = 0.59, CI 90% 0.31-1.10). All of this contributes to giving consistency to the protective effect of smoking against idiopathic Parkinson's disease. The anti-oxidant status, measured by means of different parameters in peripheral blood, is lower in the cases than in the tests for reduced glutathione (GSH) (p = 0.001) and is an independent variable with respect to smoking.     

Body weight gain after administration of antipsychotic drugs: correlation with leptin, insulin and reproductive hormones

Excessive body weight gain, hyperprolactinemia and low gonadal steroid serum levels are often observed during chronic administration of antipsychotic drugs (AP). Clinical and experimental findings suggest that leptin, the peptidic hormone involved in long-term body weight regulation, and reproductive hormones are interrelated. Therefore, we assessed circulating leptin levels in healthy, lean women (n = 12) and men (n = 7) before and after short-term administration of the AP sulpiride (SUL, 200 mg/day). In addition, we studied psychotic obese (n = 9) and lean women (n = 13) under chronic treatment with diverse AP. No significant weight changes were observed after SUL administration in healthy women--initial weight: 54.9+/-2.6 Kg; final weight: 55.04+/-2.6, NS. Leptin levels did not change either: 11.9+/-1.5 ng/ml. vs. 10.6+/-1.3, NS. By contrast, a small, but significant weight gain was found in SUL-treated men--60.6+/-1.9 Kg. vs. 61.3+/-2.1, p = 0.004. Leptin and insulin levels were significantly higher after SUL administration--leptin: 2.77+/-0.22 ng/ml. vs. 13.9+/-2.5, p=0.035; insulin: 3.59+/-0.17 mIU/ml vs. 8.81+/-0.81, p = 0.0001. In these subjects, leptin levels positively correlated with body weight change (p = 0.006), and serum prolactin change (p = 0.001). Obese psychotic women (Body Mass Index, BMI, Kg/m2 = 31.5+/-1.03) displayed higher leptin levels than non-obese psychotic women (BMI = 25.5+/-0.52): 26.8+/-4.8, vs. 12.8+/-3.4 ng/ml, p = 0.006. In these women, a significant positive correlation was found between leptin levels and BMI (p = 0.0001), and between leptin and basal insulin levels (p = 0.001). These results show that the expected circulating leptin elevation which is observed when body weight raises, is preserved in people treated with AP drugs.