Scielo RSS <![CDATA[Biological Research]]> vol. 34 num. 2 lang. en <![CDATA[SciELO Logo]]> <![CDATA[La Educación en Ciencias Biológicas demanda urgentes cambios]]> <![CDATA[LOS DERROTEROS CIENTÍFICOS DE FRANCISCO VARELA (1946-2001)]]> <![CDATA[EDUARDO DEL SOLAR OSSES 1932 - 2001]]> <![CDATA[DR. JORGE ALLENDE NUEVO MIEMBRO DE LA ACADEMIA DE CIENCIAS DE ESTADOS UNIDOS]]> <![CDATA[IMPORTANTE PARTICIPACION DE CHILE EN EL CONGRESO FEBS/PABMB 2001]]> <![CDATA[IMMEDIACY INDEX EN LA CATEGORÍA "BIOLOGY": BIOLOGICAL RESEARCH ALCANZA EL QUINTO LUGAR ENTRE SUS CONGÉNERES DE ACUERDO AL JOURNAL OF CITATION REPORTS (2000)]]> <![CDATA[CHILE INVITA A CHILE: INSTITUTO MILENIO DE BIOLOGIA FUNDAMENTAL Y APLICADA ORGANIZA ORIGINAL ENCUENTRO DE ESTUDIANTES]]> <![CDATA[VEINTICINCO AÑOS DE LA RED LATINOAMERICANA DE BIOLOGIA (RELAB)]]> <![CDATA[Methodologies for evaluation of total antioxidant activities in complex mixtures. A critical review]]> <![CDATA[Identification of Adenovirus 7h Heterogeneity in the E3 Region]]> Adenovirus genotype 7h was previously reported to be originated from a recombination event between adenovirus genotypes 7p and 3p. Based on those findings, further characterization of other adenovirus 7h strains become important to determine whether all adenovirus 7h strains arose from a single recombinational event. To explore such a possibility, 160 clinical isolates were studied after developing a PCR assay using a primer set designed to amplify the region corresponding to E3-7,7 Kd of adenovirus ADV 7p and E3-9 Kd of adenovirus 3p. The assay was able to differentiate most of the subgenus B strains from adeno 7h with the genotype 3d. The study of several adenovirus 7h clinical isolates revealed the existence of three variants of adeno7h. One of the variants, 7h3, shows a high degree of similarity with gene E3-9 Kd of ADV 3p, but lacks the corresponding AUG codon. Our results suggest that more than one recombination event may explain the detection of three different types of adenovirus 7h. The genotype variants of adeno 7h were detected in different years, indicating that the recombination events took place independently from each other. The study of the recombination region may allow further understanding of the function of several viral polypeptides in the immune response, and understanding the mechanism involved in virulence associated to adenovirus 7h. <![CDATA[Studies on parasitemia courses and mortality in mice infected with genetically distant <I>Trypanosoma cruzi </I>clonets]]> The biological characterization of bloodstream forms of eleven Trypanosoma cruzi cloned stocks, corresponding to two genetically similar clonets (<A HREF="#19">19</A> and <A HREF="#20">20</A>) and one distant clonet (39), according to multilocus enzyme electrophoresis analysis, showed dissimilar parasitemia in an experimental isogenic mouse model. While clonet 39 stocks gave low parasitemias, clonets 19 or 20 stocks gave high parasitemias, independently of the inocula (10² and 10(4) bloodstream forms) used. High parasitemia did not always associate with greater mortality. Statistical studies on mortality using a low inocula showed significantly higher mortality with clonet 39 stocks when compared to clonets 19 or 20 stocks. Finally, in order to confirm the identity of each stock studied, typing by molecular karyotype was performed before inoculating mice. <![CDATA[Genetic and cytological characterization of a developmental mutant of <I>Aspergillus nidulans</I> induced by 5-azacytidine]]> An analysis of a new medusa mutant of Aspergillus nidulans obtained by 5-azacytidine-treatment and named B116 is provided. The B116 mutant was phenotypically characterized by the production of conidiophores with reduced pigmentation and vesicles bearing multiple tiers of sterigmata. A single nuclear gene located on chromosome I is responsible for phenotypical changes in the mutant. The 5-azacytidine-altered locus, designated medA102, is recessive in heterozygous diploid and the medusa mutant is a Dp(II,I) duplication bearer that renders the strain mitotically unstable. <![CDATA[Professor Jaime Alvarez: don Quixote de la Mancha at the University]]> An analysis of a new medusa mutant of Aspergillus nidulans obtained by 5-azacytidine-treatment and named B116 is provided. The B116 mutant was phenotypically characterized by the production of conidiophores with reduced pigmentation and vesicles bearing multiple tiers of sterigmata. A single nuclear gene located on chromosome I is responsible for phenotypical changes in the mutant. The 5-azacytidine-altered locus, designated medA102, is recessive in heterozygous diploid and the medusa mutant is a Dp(II,I) duplication bearer that renders the strain mitotically unstable. <![CDATA[The autonomous axon: a model based on local synthesis of proteins]]> In the current understanding of axons, axoplasmic synthesis of proteins is negated, and it is asserted that proteins are transported from perikarya to axons. This 'transport model' in which axons are fully dependent of perikarya is seriously flawed. The 'autonomous axon' proposed here negates in turn transport of proteins, and asserts (i) local synthesis of axoplasmic proteins, corner stone of this model, (ii) existence of internal programs in axon and terminals, (iii) external control of programs resulting in local regulation of phenotype of axons and terminals, hence they are autonomous from perikarya; (iv) participation of perikarya through the fast transport in setting up the axonal programs but not in their immediate regulation. The word merotrophism (meros meaning part) denotes post-transcriptional regulation of phenotype of restricted regions of a cell. We surmise that merotrophism is at the base of many plastic phenomena. <![CDATA[Jaime Alvarez and the case against slow axoplasmic transport: some epistemological reflections]]> The 'slow axoplasmic transport theory' has been the prevailing view over the last forty years in order to explain the metabolic maintenance of neuronal axons and nerve endings. A significant amount of evidence against this theoretic interpretation of the existing experimental data has been presented by J. Alvarez, A. Giuditta and E. Koenig in an exhaustive review. They propose an alternative theoretical interpretation called the 'local synthesis model', integrating recent evidence for axon biology and regeneration. We present some epistemological considerations that reinforce the above criticisms and propositions. <![CDATA[<I>In vitro</I> approach to the chemical drive of breathing]]> Since its introduction two decades ago, the isolated brain stem-spinal cord preparation of neonatal rodents has been the preferred method used to reveal the mystery underlying the genesis of the respiratory rhythm. Little research using this in vitro approach has focused on the study of the central respiratory chemosensitivity. Some unexpected findings obtained with the brain stem-spinal cord preparation have added new questions that challenge our previous theoretic framework. Some of these findings are addressed here. <![CDATA[Microglia ­ astrocyte interaction in Alzheimer's disease: friends or foes for the nervous system?]]> Brain glial cells secrete several molecules that can modulate the survival of neurons after various types of damage to the CNS. Activated microglia and astrocytes closely associate to amyloid plaques in Alzheimer Disease (AD). They could have a role in the neurotoxicity observed in AD because of the inflammatory reaction they generate. There is controversy regarding the individual part played by the different glial cells, and the interrelationships between them. Both astrocytes and microglia produce several cytokines involved in the inflammatory reaction. Moreover, the same cytokines may have different effects, depending on their concentration and the type of cells in the vicinity. In turn, the events occurring in response to injury may lead to changes in the nature and relative concentration of the various factors involved. To learn about these putative glial interrelationships, we examined some effects of astrocytes on microglial activation <![CDATA[Muscle cell outside and inside: the nascent approach of a clinician]]> Understanding muscle cell in disease and health is an unfinished process. Following the lead of Jaime Alvarez, I have had the opportunity of working on two complementary approaches to this field. One is the study of muscle cell surface molecules. Both synaptic muscle molecules, such as the asymmetric form of acetylcholinesterase, and extrasynaptic molecules, such as the extracellular matrix proteoglycans, are regulated by the motor nerve activity. This illustrates one of Jaime's teachings: cell phenotypes are a dynamic process that reflects the influence of other cells (<A HREF="#0">Alvarez, 2001</A>). Proteoglycans have many functions, including growth factor receptors. Studying them in muscular dystrophy will contribute to the comprehension of the muscle regeneration failure, characteristic of this disease. Muscle cells are highly dependent upon energy production, and the mitochondriae produce most of it. These organelles are unique in having their own genome. Mutations in these genes have recently been recognized as the cause of human disease and originally in muscle pathology. The physiopathology of these diseases is summarized here <![CDATA[Nitric oxide and carotid body chemoreception]]> Nitric oxide (NO) has been proposed as an inhibitory modulator of carotid body chemosensory responses to hypoxia. It is believed that NO modulates carotid chemoreception by several mechanisms, which include the control of carotid body vascular tone and oxygen delivery and reduction of the excitability of chemoreceptor cells and petrosal sensory neurons. In addition to the well-known inhibitory effect, we found that NO has a dual (dose-dependent) effect on carotid chemoreception depending on the oxygen pressure level. During hypoxia, NO is primarily an inhibitory modulator of carotid chemoreception, while in normoxia NO increased the chemosensory activity. This excitatory effect produced by NO is likely mediated by an impairment of mitochondrial electron transport and oxidative phosphorylation, which increases the chemosensory activity. The recent findings that mitochondria contain an isoform of NO synthase, which produces significant amounts of NO for regulating their own respiration, suggest that NO may be important for the regulation of mitochondrial energy metabolism and oxygen sensing in the CB. <![CDATA[Genomic imprinting and human chromosome 15]]> Genomic imprinting is a reversible phenomenon that affects the expression of genes depending on their parental origin. The best characterized human disorders resulting from an alteration of the imprinting process are Angelman and Prader-Willi syndromes. They are due to the lack of active maternal or paternal genes, respectively, from chromosome region 15q11q13. Most cases arise via interstitial deletions. We review evidence that other common cytogenetic alterations of this region, interstitial and supernumerary duplications, could be the reciprocal products of the deletions and are also affected by the imprinting phenomenon, given the predominance of maternally-derived duplications in patients ascertained due to developmental delays or autistic features. <![CDATA[Targeting and fusion proteins during mammalian spermiogenesis]]> Regulated exocytosis is controlled by internal and external signals. The molecular machinery controlling the sorting from the newly synthesized vesicles from the Golgi apparatus to the plasma membrane play a key role in the regulation of both the number and spatial location of the vesicles. In this context the mammalian acrosome is a unique vesicle since it is the only secretory vesicle attached to the nucleus. In this work we have studied the membrane trafficking between the Golgi apparatus and the acrosome during mammalian spermiogenesis. During bovine spermiogenesis, Golgi antigens (mannosidase II) were detected in the acrosome until the late cap-phase spermatids, but are not found in testicular spermatozoa (maturation-phase spermatids). This suggests that Golgi-acrosome flow may be relatively unselective, with Golgi residents retrieved before spermiation is complete. Surprisingly, rab7, a protein involved in lysosome/endosome trafficking was also found associated with the acrosomal vesicle during mouse spermiogenesis. Our results suggest that the acrosome biogenesis is associated with membrane flow from both the Golgi apparatus and the endosome/lysosome system in mammalian spermatids.