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En las adicciones sin sustancia psicoactiva o comportamentales como el juego patológico, la adicción a las compras, el sexo o las nuevas tecnologías, un hábito de conducta aparentemente inofensivo puede convertirse en adictivo e interferir gravemente en la vida de las personas afectadas. Este tipo de adicciones presentan características clínicas similares a aquellas con sustancia psicoactiva, como la pérdida de control, la excitación excesiva antes de realizar dicha conducta y el alivio en el momento de realizarla. El objetivo del tratamiento debe centrarse en el reaprendizaje del control de la conducta y el cambio en el estilo de vida. Las terapias más contrastadas son las de tipo conductual, cognitivo y cognitivo-conductual, así como los grupos de autoayuda; el uso de psicofármacos se reserva para el tratamiento de los trastornos comórbidos.

Los trastornos por consumo de sustancias asocian síntomas cognitivos, somáticos y comportamentales que se dan a pesar de las consecuencias negativas que supone el consumo en aspectos cruciales de la vida de los sujetos. Existe evidencia científica creciente de los cambios neurofisiológicos que acontecen en el cerebro del adicto que se manifiestan a través de su conducta compulsiva, en la que además confluyen factores psicosociales. Repasamos en esta revisión datos de actualidad al respecto de los opioides, psicoestimulantes y cannabis, así como la emergencia de nuevas drogas psicoactivas y el abuso de fármacos de prescripción.

Klebsiella pneumoniaestrains resistant to cefotaxime, ceftazidime and cefepime, but susceptible to imipenem and meropenem, were isolated from blood samples from two patients. Following treatment with meropenem, K. pneumoniae strains with reduced susceptibilities to imipenem and meropenem were isolated from the patients' stools. PCR assays and DNA sequencing showed that all the strains contain blaCTX M 15•, SDS-PAGE analysis of the outer membrane proteins did not identify OmpK35 and OmpK36 in any of the strains. The carbapenem susceptible strains were OmpK37 sufficient; however, this protein was not apparent in the strains with reduced susceptibility to carbapenems. It was concluded that resistance to extended spectrum β-lactams in the K. pneumoniae strains was due to the production of CTX-M-15, and reduced susceptibility to carbapenems was attributed to a combination of CTX-M and altered outer membrane permeability.

The microwave surface resistance of pure niobium has been measured in magnetic fields up toHc3. The surface resistance in the mixed state state was found to depend strongly on the mean free path, in contrast to the earlier theory of Caroli and Maki but in agreement with the recent theoretical work of Cerdeira, Houghton, and Maki. Neglect in the theory of the surface solution for the order parameter limits the value of making comparisons with our results except in the orientation where the steady magnetic field is perpendicular to the surface. In this orientation we have found the slope of the curve of surface resistance plotted against flux density to be proportional to mean free path, as predicted by the recent theory. The theory has been developed only for absolute zero, and so in order to make comparisons we have extrapolated an empirical scaling procedure that reduces data at different temperatures to a single curve. Estimates of the constant of proportionality in the mean-free-path dependence are limited in accuracy by the present uncertainty in the values of ?2(T). Although both the earlier and recent theories purport to deal with the anisotropy of the surface resistance when the direction of the steady magnetic field is varied with respect to the wave vector of the electromagnetic field but is kept perpendicular to the microwave current, neither includes the large shielding effects produced by the vortex-free layer that can exist at the real surface and persist up toHc3. Agreement with the mean free path dependence predicted by the recent theory could not be achieved by incorporating measurements aboveHc2 into a simple layer model to adjust the measured values of the surface resistance with the steady field parallel to the surface. However, the discrepancy between the predicted and measured anisotropies was reduced by this procedure. Other aspects of our experimental results that fall outside the range of validity of the recent theory are compared with general features established by earlier experimental and theoretical work on impure type II superconductors. In particular, the anisotropy of the surface resistance in fields just belowHc3 was found to be temperature independent, as predicted by Thompson and confirmed by Monceau and Waysand. The observed magnetic hysteresis effects in the mixed state are discussed in relation to the nascent vortex model and to the existence of an oxygen-rich surface layer.

A case of a cavernous hemangioma of the right frontal lobe of the brain is reported. The lesion showed a myriad of tiny discrete calcifications and was associated with a well-circumscribed uptake on technetium brain scan and positive findings on cerebral angiography. The patient has done well since excision of the hemangioma.

The updated Vitek Yeast Biochemical Card (YBC) was compared with the API 20C by using 409 germ tube-negative yeasts and Geotrichum spp. that were either clinical or proficiency sample isolates. The API 20C was the reference standard. The 409 isolates represented nine genera and 21 species. Morphology agars were inoculated and interpreted for each isolate. The API 20C identified 406 isolates (99.3%), while the Vitek YBC identified 367 (89.7%). Both systems identified the majority of yeasts after 24 h of incubation--73.4% were identified by the API 20C and 77.4% were identified by the Vitek YBC. The Vitek 24-h reading had some incorrect identifications. These included 14 isolates of Candida tropicalis that were identified as Candida parapsilosis (91 to 97% reliability) and 3 isolates of Candida krusei that were called Blastoschizomyces capitatus (Geotrichum capitatum), Candida rugosa, and Candida zeylanoides. In total, the Vitek YBC misidentified 30 isolates, while the API 20C misidentified 3 isolates. In addition, results for 14 isolates with the Vitek YBC were listed under the category "no identification." Morphology agars were required for identification with 89 isolates (21.9%) when the API 20C was used and with 50 isolates (12.6%) when the Vitek YBC was used. Apart from the price of the Vitek instrument, the API 20C costs $1.28 more per test than the Vitek YBC. Overall, the updated Vitek YBC compares favorably with the API 20C in the identification of common yeasts such as Torulopsis glabrata, C. parapsilosis, and Cryptococcus neoformans. However, problems were encountered with the Vitek system in the identification of C. tropicalis, C. krusei, Trichosporon spp., and some Cryptococcus spp. The routine use of morphology agars with either method is recommended.

Swainsonine, an alpha-mannosidase inhibitor found in the Australian plant Swainsona canescens and in spotted locoweed, was tested for its effect on the degradation of endocytosed proteins in rat liver cells. The compound inhibited the release of proteolytically derived breakdown products from endocytosed glycoproteins but not from nonglycoproteins. Fifty per cent inhibition of the degradation of 125I-asialofetuin occurred at a concentration of swainsonine in the medium of 6 X 10(-7) M. In the presence of the inhibitor, there was an increased cellular accumulation of the glycoproteins corresponding quantitatively to the decreased degradation, so that total uptake was the same in the presence or absence of the inhibitor. The excess 125I-labeled material which accumulated within cells under these conditions was found entirely in the lysosomal peak on Percoll density gradient centrifugation and migrated on sodium dodecyl sulfate-polyacrylamide gel electrophoresis with a mobility indistinguishable from that of the original material. Thus, the inhibition of breakdown occurs prior to any conversion of the protein to intermediates of detectably smaller size. In contrast to the results with swainsonine, degradation of both glycoproteins and nonglycoproteins was inhibited by chloroquine and by 3-methyladenine. The findings with 3-methyladenine are in conflict with earlier reports in the literature on the effect of this compound on degradation of endocytosed proteins.

A study designed to assess the relative efficacy of chlorpromazine and Serenace in the control of chronic schizophrenics is described. Twenty-five cases were selected for the study and were randomly allocated to treatment. The condition of the patients was assessed at fortnightly intervals over the eight-week duration of trial period. No significant differences in side-effects emerged in patients on chlorpromazine and Serenace in the dosages administered. The statistically significant trends all showed a superiority of Serenace above chlorpromazine which was in accord with the clinical picture.

The effect of swainsonine, an inhibitor of Golgi alpha-mannosidase II and lysosomal alpha-mannosidase, on the synthesis, processing, and turnover of two glycoproteins, lysosomal beta-galactosidase and lysosomal beta-glucuronidase, has been studied in cultured mouse peritoneal macrophages. No effect of the inhibitor on the relative rates of synthesis of the precursor form of either enzyme was observed. On the other hand, carbohydrate processing of beta-galactosidase and beta-glucuronidase was markedly altered by swainsonine, consistent with a blockage by the inhibitor of the removal of the alpha-1,3- and alpha-1,6-linked mannose residues which occurs in normal processing. In homogenates of both normal and swainsonine-treated cells, the precursor forms of the enzymes were found exclusively in the light membrane fraction on Percoll gradients and the mature forms exclusively in the lysosomal fractions indicating that translocation from Golgi to lysosomes and proteolytic processing in the lysosome were not impaired by the presence of abnormal oligosaccharide side chains. There was no detectable effect of swainsonine during a 4-day chase period on the total cellular turnover of these enzymes which involves two processes, secretion and degradation. In the absence of swainsonine, secretion represented about 40% of the total turnover of beta-galactosidase and about 50% with beta-glucuronidase. The presence of swainsonine increased these proportions to about 60 and 70%, respectively.

Sera from military personnel found to have antibodies to hepatitis B surface antigen (anti-HBS) in an epidemiological study of a hepatitis B outbreak were tested for persistence of that antibody 1 year later. Initially, 64% of the anti-HBS-positive sera reacted in passive hemagglutination tests with erythrocytes coated with hepatitis B surface antigen of both ayw and adw subtypes; the remaining sera reacted only with adw-coated erythrocytes (19%) or ayw-coated erythrocytes (17%). After 1 year, anti-HBS was detectable by passive hemagglutination tests in 87% of individuals with initial antibody to both subtypes but in only 41% and 16% (P less than 0.001) of those initially reacting only to adw- or ayw-coated erythrocytes, respectively. Seropositivity for anti-HBS correlated best with history of contact with jaundiced people (20.3%) and duty in Asia.

Rat liver lysosomes, isolated from metrizamide gradients by the method of Wattiaux et al. (Wattiaux, R., Wattiaux-de Coninck, S., Ronveaux-Dupol, M.F., and Dubois, F. (1978) J. Cell Biol. 78, 349-368) took up from the medium and degraded several marker protein preparations, viz. 125I-asialofetuin, [35S]methionine-labeled hemoglobin, and [3H]leucine-labeled rat liver cytosol proteins. Rates were indistinguishable for all the markers, indicating that uptake was by a nonspecific process analogous to fluid pinocytosis. No effect of added MgATP or K+ was observed. Lysosomal degradation of all the markers was inhibited by 10(-4) M chloroquine. Swainsonine, on the other hand, at 10(-5) M, inhibited the breakdown only of the glycoprotein, 125I-asialofetuin. In the presence of the inhibitors, there was an accumulation of markers in the lysosomes in amount corresponding to the decreased breakdown, indicating that uptake was unaffected. Degradation and inhibition were measured at pH 7.0, 6.0, and 5.0 with both intact lysosomes and with lysosomes disrupted by the addition of 0.2% Triton X-100. Degradation with intact lysosomes was relatively independent of pH. On the other hand, activity with disrupted lysosomes was negligible at pH 7.0 and rose rapidly with decreasing pH. Inhibition by 10(-4) M chloroquine and 10(-5) M swainsonine with intact lysosomes decreased sharply with decreasing pH and did not occur with disrupted lysosomes.

The uptake by rat yolk sacs of native invertase and invertase which was deglycosylated by treatment with endo-beta-N-acetylglucosaminidase was compared. The initial rate of uptake of the deglycosylated enzyme was severalfold greater and its accumulation leveled off much earlier than that of the native enzyme. Uptake rates of the deglycosylated and native forms of the enzyme were proportional to their concentration in the medium in the range employed and were inhibited about 85% by 10(-6) M glucagon in both cases. After preloading of yolk sacs with native invertase, the tissue level of activity remained relatively constant over a subsequent 6-h time period, while with the deglycosylated form, activity declined substantially. Since this difference appears not to be attributable to differences in thermal stability, it is suggested that the deglycosylated form of the protein is more susceptible to intracellular proteolytic digestion. In vitro studies on the digestion of these two forms of invertase by trypsin are consistent with this suggestion.

Five disinfectants or soaps were tested to determine if any could be responsible for false-positive results obtained with the Latex-Crypto Antigen Detection System kit (Immuno-Mycologics, Inc., Norman, Okla.). Three disinfectants or soaps (Derma soap, 7X, and Bacdown) produced false-positive agglutination after repeated washing of ring slides during testing of a known negative cerebrospinal fluid specimen.