[Small cell lung cancer associated with multiple paraneoplastic syndromes].

We report the case of a patient presenting with multiple severe electrolyte disturbances who was subsequently found to have small cell lung cancer. Upon further evaluation, she demonstrated three distinct paraneoplastic processes, including the syndrome of inappropriate antidiuretic hormone, Fanconi syndrome, and an inappropriate elevation in fibroblast growth factor-23 (FGF23). The patient underwent one round of chemotherapy, but she was found to have progressive disease. After 36 days of hospitalization, the patient made the decision to enter hospice care and later she expired.

Small cell lung cancer associated with multiple paraneoplastic syndromes / Cáncer de pulmón de células pequeñas asociado a múltiples síndromes paraneoplásicos

Abstracts We report the case of a patient presenting with multiple severe electrolyte disturbances who was subsequently found to have small cell lung cancer. Upon further evaluation, she demonstrated three distinct paraneoplastic processes, including the syndrome of inappropriate antidiuretic hormone, Fanconi syndrome, and an inappropriate elevation in fibroblast growth factor-23 (FGF23). The patient underwent one round of chemotherapy, but she was found to have progressive disease. After 36 days of hospitalization, the patient made the decision to enter hospice care and later she expired.

Resumen Se reporta el caso de una paciente que ingresó al hospital para evaluación de múltiples trastornos electrolíticos y, posteriormente, se le hizo el diagnóstico de cáncer de pulmón de células pequeñas. Tras la evaluación médica, se detectaron tres síndromes paraneoplásicos: síndrome de secreción inadecuada de hormona antidiurética, síndrome de Fanconi y elevación inapropiada del factor 23 de crecimiento de fibroblastos. Se le administró quimioterapia sin éxito, por lo cual se decidió darle tratamiento paliativo y, un tiempo después, falleció.

[Procalcitonin as a marker of intra-abdominal infection]. / La procalcitonina como marcador de infección intraabdominal.

BACKGROUND: Procalcitonin is a quite specific biomarker of infection and in recent years has shown its superiority to others markers of inflammation, such as C-reactive protein, for the diagnosis and monitoring of a variety of infections. AIM: For this reason, several researchers have studied the potential role of procalcitonin for diagnosis and management of these infections. DISCUSSION: Intra-abdominal infections are a heterogeneous group of infections that, sometimes, pose difficult challenges to physicians. The published studies have produced mixed results, leading to controversy on the utility of this marker in intra-abdominal infections. CONCLUSIONS: This review summarizes these data and discuss the utility of procalcitonin in several intra abdominal infections, including postoperative infections.

Antecedentes: la procalcitonina es un marcador bastante específico de infección y en los últimos años se ha demostrado su superioridad, con respecto a otros marcadores de inflamación como la proteína C reactiva, para el diagnóstico y vigilancia de una gran variedad de infecciones. Objetivo: resumir los datos actualmente existentes y discutir la utilidad de la procalcitonina en diversas infecciones intrabdominales, incluidas las postoperatorias. Conclusiones: los resultados de estudios hasta ahora publicados son variables, lo que genera controversia en relación con su utilidad.

The effect of oviductal deleted in malignant brain tumor 1 over porcine sperm is mediated by a signal transduction pathway that involves pro-AKAP4 phosphorylation.

The interaction between sperm and oviduct results in the selection of sperm with certain qualities. Porcine oviductal deleted in malignant brain tumor 1, DMBT1 (previously called sperm-binding glycoprotein, SBG), has been proposed to be implicated in sperm selection through acrosome alteration and suppression of motility of a subpopulation of sperm that have begun capacitation prematurely. It produces in vitro acrosome alteration and decrease of motility of boar sperm, concomitant with tyrosine phosphorylation of a 97 kDa sperm protein (p97). We hypothesized that the phosphorylation of p97 may be a link between DMBT1 sensing by a subpopulation of boar sperm and its biological effect. In this work, p97 was identified by mass spectrometry and immunoprecipitation as a porcine homologue of AKAP4. Pro-AKAP4 was localized by immunofluorescence and subcellular fractionation to the periacrosomal membranes and was shown to be tyrosine phosphorylated by DMBT1 regardless of the presence of calcium or bicarbonate, and of cAMP analogs, protein kinase A inhibitors, or a protein kinase C inductor. A processed ∼80 kDa form of AKAP4 was also detected at the tail of boar sperm, which was not tyrosine phosphorylated by DMBT1 under the conditions tested. Immunohistochemistry of testis showed presence of AKAP4 in boar sperm precursor cells. The evidence presented here supports the involvement of AKAP4 in the formation of the fibrous sheath on boar precursor sperm cells and implicates the phosphorylation of pro-AKAP4 as an early step in the signal transduction pathway gated by DMBT1 that leads to sperm selection through acrosome alteration.

Anatomy, function and regulation of neuropeptide EI (NEI).

This review is focused on the anatomy, role and behavior of neuropeptide-glutamic acid-isoleucine (NEI), providing a general report on the neuropeptide. In addition to hormone release, this peptide also takes part in the regulation of grooming behavior and locomotor activity. NEI is produced by cleavage of prepro-MCH that probably takes place at the Lys(129)-Arg(130) and Arg(145)-Arg(146) sites (the glycine residue on the C-terminus of NEI strongly suggests that this peptide is amidated). This same prohormone is also the precursor of MCH, widely studied in relation to food and water intake, and NGE, of which little is known. NEI and MCH are extensively colocalized throughout the central nervous system (CNS), and NEI is also present in peripheral tissues. The latter is also effective in stimulating luteinizing hormone (LH) release and, to a lesser extent, FSH from primary pituitary cell cultures. In addition to releasing LH from the medial eminence, NEI also acts directly on gonadotropes. Lastly, this neuropeptide also acts at the CNS level on gonadotropin-releasing hormone (GnRH) neurons.

Reanimación protocolizada del shcok séptico / Protocolized reanimation of septic shock

Severe sepsis and septic shock are pathologies with an increasing incidence in the world. Annually, in the USA 200.000 people die because of severe sepsis, the same number that die because of a myocardial infarction, being this last disease much more common. In Chile, a multicentric study found a 40 percent of prevalence of severe sepsis in critically ill patients, with amortality of 27 percent. In this scenario, it becomes of great importance the appropriate and integral management of this condition, by means of an early diagnosis and the implementation of anaggressive protocolized resuscitation, guided by clear goals. During the first stage of the resuscitation cristalloids and/ or colloids can be used, in order to expand the intravascular space, searching for CVP around 8 to 12 mmHg. In case of hypotension refractory to the administration of fluids, it is recommended to start with increasing doses of norepinephrin untila MAP of 65 - 75 mmHg is achieved. The intensity of the septic shock can be stratified according to the requirements of norepinephrine. It is of great importance to obtain blood cultures of the patients and to start with empiric antibiotic therapy as soon as possible. The initial metabolic goal must be the normalization of the central venous oxygen saturation. The implementation of the resuscitation bundle during the first six hours, since the diagnose of severe sepsis is done, increases the chances of surviving. Protocols of sedation and analgesia, and the use of protective mechanical ventilation is highly recommended. The use of hydrocortisone and human recombinant protein C in selected patients, may have a beneficial result in the outcome.Vasopressin, terlipressin and high-volume hemofiltration can be used as rescue measures for the most severe patients.

Isolation of temperature-sensitive yeast GPI-anchoring mutants.

We are using a genetic approach to explore the synthesis and function of glycosylphosphatidylinositol (GPI). We have developed a novel strategy to isolate Saccharomyces cerevisiae mutants blocked in GPI anchoring by screening colonies of mutagenized yeast cells for those that fail to incorporate [3H]inositol into protein. Among our isolates are strains blocked in mannosylation of the GPI-anchorprecursor, and strains defective in the synthesis of N-acetylglucosaminyl phosphatidylinositol (GlcNAc-PI). We have characterized one mutant, gpi1, further. This strain is defective in GlcNAc-PI synthesis and is temperature-sensitive for growth. Completion of the first step in GPI assembly is therefore required for the growth of the unicellular eukaryote S. cerevisiae. We have isolated plasmids that complement the gpi1 mutation from S. cerevisiae genomic DNA-and fission yeast cDNA libraries.

Metabolism of GPIs in mammalian cells.

In Trypanosoma brucei, glycosylphosphatidylinositol (GPI) anchors of proteins and free GPIs with identical structures have been characterized. This identity provides strong presumptive evidence that the free GPIs are in fact precursors of the GPI anchors on proteins. In mammalian tissues, however, rather consistent differences in the structures of free GPIs and GPI anchors are observed. The terminal GPIs produced by the mammalian biosynthetic pathway differ from GPI anchors in being almost exclusively fatty acid acylated on the inositol residue, having a greater number of phosphoethanolamine residues, and perhaps in containing a greater percentage of diacylglycerol components. While in principle these differences could be reconciled by remodeling reactions before or after attachment of GPI anchors, it is possible that some of the mammalian free GPIs play cellular roles other than as anchor precursors. We have approached this question by studying the lifetimes of the last three GPIs on the biosynthetic pathway, denoted H6, H7 and H8, in K562 cells and in a K562 mutant designated class K that is devoid of GPI-anchored proteins. Pulse-chase metabolic labeling with [3H]-mannose indicated that H6 was a precursor of H7 and H8 and that the H8 lifetime was more than one hour in the parental cells and even longer in the mutant. Preliminary data indicated that the majority of each of the three GPIs was localized in the plasma membrane fraction rather than the endoplasmic reticulum. These observations argue that mammalian GPIs are not utilized exclusively as GPI anchor precursors.