Sobrevida de pacientes con cáncer gástrico en el Perú, 2009-2010 / Survival rate of patients with stomach cancer in Peru, 2009-2010

OBJETIVO: Determinar la sobrevida de pacientes con diagnóstico de cáncer gástrico en 2009-2010 en el Perú. MÉTODOS: Se realizó un estudio de tipo cohorte retrospectivo de pacientes con diagnóstico de cáncer gástrico registrados en el Sistema Nacional de Vigilancia Epidemiológica (SNVE) de la Dirección General de Epidemiología (DGE) y del Registro de Hechos Vitales (RHV) de la Oficina General de Estadística e Informática (OGEI) para los años 2009-2010. RESULTADOS: Se incluyeron 3 568 pacientes del SNVE, 51,5% eran hombres y 48,5% eran mujeres; la media de edad fue 63,9 años, 60,07% tenían 60 años o más. Se halló que 33,6% tenía adenocarcinoma de tipo intestinal, 18,7% tenía carcinoma de tipo difuso y 4,1% tenía linfoma gástrico primario. La sobrevida global fue de 29,7 ± 0,8 meses y fue mejor para los menores de 60 años (P = 0,034), para las mujeres (P = 0,014) y para el adenocarcinoma de tipo intestinal (P < 0,001). No hubo diferencias (P = 0,713) entre la sobrevida de los pacientes con linfoma gástrico y aquellos con adenocarcinoma. Para evaluar la tasa de mortalidad se incluyeron 6 069 registros de pacientes del RHV, la tasa de mortalidad nacional fue de 10,3 por cada 100 000 habitantes y las regiones con mayor mortalidad fueron Huánuco, Huancavelica y Junín. CONCLUSIONES: La sobrevida general fue de 29,7 ± 0,8 meses, las mujeres, los menores de 60 años y los pacientes con adenocarcinoma de tipo intestinal tienen mejor sobrevida. La mayor mortalidad por cáncer gástrico se concentra en las regiones más pobres del Perú, donde es probable que las condiciones de vida faciliten la alta transmisibilidad de Helicobacter pylori.

OBJECTIVE: Determine the survival rate of patients diagnosed with stomach cancer in 2009-2010 in Peru. METHODS: A retrospective cohort study was conducted of patients diagnosed with stomach cancer registered in the National Epidemiological Surveillance System (SNVE) of the Directorate General of Epidemiology (DGE) and the Register of Vital Statistics (RHV) of the General Office of Statistics and Information (OGEI) for the years 2009-2010. RESULTS: 3 568 patients of the SNVE were included; 51.5% were men and 48.5% were women; the average age was 63.9 years; 60.07% were 60 years old or older. It was found that 33.6% had intestinal type adenocarcinoma, 18.7% had diffuse type carcinoma, and 4.1% had primary gastric lymphoma. The overall survival rate was 29.7 ± 0.8 months and was better for those under 60 years (P = 0.034), for women (P = 0.014) and for intestinal type adenocarcinoma (P< 0.001). There was no difference (P = 0.713) between the survival rate of gastric lymphomas and adenocarcinomas. In order to evaluate mortality, 6 069 patient records from the RHV were included; national mortality was 10.3 per 100 000 population; the regions with the highest mortality were Huánuco, Huancavelica, and Junín. CONCLUSIONS: The general survival rate was 29.7 ± 0.8 months; women, those under 60 years, and patients with intestinal type adenocarcinoma had better survival rates. The highest mortality from stomach cancer is concentrated in the poorest regions of Peru, where it is probable that living conditions facilitate the high communicability of Helicobacter pylori.

Regional density of glial cells in the rat corpus callosum

Axons and glial cells are the main components of white matter. The corpus callosum (CC) is the largest white matter tract in mammals; in rodents, 99% of the cells correspond to glia after postnatal day 5 (P5). The area of the CC varies through life and regional differences related to the number of axons have been previously described. Whether glial cell density varies accordingly is unknown; thus the aim of this study was to estimate glial cell density for the genu, body and splenium -the three main regions of CC-, of P6 and P30 rats. Here we report that the density of CC glial cells reduced by ~10% from P6 to P30. Even so, the density of astrocytes showed a slight increase (+6%), probably due to differentiation of glioblasts. Interestingly, glial cell density decreased for the genu (-21%) and the body (-13%), while for the splenium a minor increase (+5%) was observed. The astrocyte/glia ratio increased (from P6 to P30) for the genu (+27%), body (+17%) and splenium (+4%). Together, our results showed regional differences in glial cell density of the CC. Whether this pattern is modified in some neuropathologies remains to be explored.

Attenuation of Spinal Cord Injury-Induced Astroglial and Microglial Activation by Repetitive Transcranial Magnetic Stimulation in Rats

Spinal cord injury (SCI) causes not only loss of sensory and motor function below the level of injury but also chronic pain, which is difficult and challenging of the treatment. Repetitive transcranial magnetic stimulation (rTMS) to the motor cortex, of non-invasive therapeutic methods, has the motor and sensory consequences and modulates pain in SCI-patients. In the present study, we studied the effectiveness of rTMS and the relationship between the modulation of pain and the changes of neuroglial expression in the spinal cord using a rat SCI-induced pain model. Elevated expressions of Iba1 and GFAP, specific microglial and astrocyte markers, was respectively observed in dorsal and ventral horns at the L4 and L5 levels in SCI rats. But in SCI rats treated with 25 Hz rTMS for 8 weeks, these expressions were significantly reduced by about 30%. Our finding suggests that this attenuation of activation by rTMS is related to pain modulation after SCI. Therefore, rTMS might provide an alternative means of attenuating neuropathic pain below the level of SCI.

Intrathecal Lamotrigine Attenuates Antinociceptive Morphine Tolerance and Suppresses Spinal Glial Cell Activation in Morphine-Tolerant Rats

Glial cells play a critical role in morphine tolerance, resulting from repeated administration of morphine. Both the development and the expression of tolerance are suppressed by the analgesic lamotrigine. This study investigated the relationship between the ability of lamotrigine to maintain the antinociceptive effect of morphine during tolerance development and glial cell activation in the spinal cord. In a rat model, morphine (15 microg) was intrathecally injected once daily for 7 days to induce morphine tolerance. Lamotrigine (200 microg) was co-administered with morphine either for 7 days or the first or last 3 days of this 7 day period. Thermal nociception was measured. OX-42 and GFAP immunoreactivity, indicating spinal microglial and astrocytic activation were evaluated on day 8. Tolerance developed after 7 days of intrathecal morphine administration; however, this was completely blocked and reversed by co-administration of lamotrigine. When lamotrigine was coinjected with morphine on days 5-7, the morphine effect was partially restored. Glial cell activation increased with the development of morphine tolerance but was clearly inhibited in the presence of lamotrigine. These results suggest that, in association with the suppression of spinal glial cell activity, intrathecally coadministered lamotrigine attenuates antinociceptive tolerance to morphine.

Shank 2 expression coincides with neuronal differentiation in the developing retina

The retinal activity for vision requires a precise synaptic connectivity. Shank proteins at postsynaptic sites of excitatory synapses play roles in signal transmission into the postsynaptic neuron. However, the correlation of Shank 2 expression with neuronal differentiation in the developing retina remains to be elucidated regardless of previous evidences of Shank 2 expression in retina. Herein, we demonstrated that with progression of development, Shank 2 is initially detected in the inner plexiform layer at P2, and then intensively detected in inner plexiform layer, outer plexiform layer, and ganglion cell layer at P14, which was closely colocalized to the neurofilament expression. Shank 2 was, however, not colocalized with glial fibrillary acidic protein. Shank 2 expression was increased in the differentiated retinoblastoma cells, which was mediated by ERK 1/2 activation. Moreover, Shank 2 expression was colocalized with neurofilament at the dendritic region of cells. In conclusion, our data suggests that Shank 2 is expressed in the neurons of the developing retina and could play a critical role in the neuronal differentiation of the developing retina.

Differential astroglial responses in the spinal cord of rats submitted to a sciatic nerve double crush treated with local injection of cultured Schwann cell suspension or lesioned spinal cord extract: implications on cell therapy for nerve repair

PURPOSE: Reactive astrocytes are implicated in several mechanisms after central or peripheral nervous system lesion, including neuroprotection, neuronal sprouting, neurotransmission and neuropathic pain. Schwann cells (SC), a peripheral glia, also react after nerve lesion favoring wound/repair, fiber outgrowth and neuronal regeneration. We investigated herein whether cell therapy for repair of lesioned sciatic nerve may change the pattern of astroglial activation in the spinal cord ventral or dorsal horn of the rat. METHODS: Injections of a cultured SC suspension or a lesioned spinal cord homogenized extract were made in a reservoir promoted by a contiguous double crush of the rat sciatic nerve. Local injection of phosphate buffered saline (PBS) served as control. One week later, rats were euthanized and spinal cord astrocytes were labeled by immunohistochemistry and quantified by means of quantitative image analysis. RESULTS: In the ipsilateral ventral horn, slight astroglial activations were seen after PBS or SC injections, however, a substantial activation was achieved after cord extract injection in the sciatic nerve reservoir. Moreover, SC suspension and cord extract injections were able to promote astroglial reaction in the spinal cord dorsal horn bilaterally. Conclusion: Spinal cord astrocytes react according to repair processes of axotomized nerve, which may influence the functional outcome. The event should be considered during the neurosurgery strategies.

OBJETIVO: Astrócitos reativos participam de vários mecanismos após lesões do sistema nervoso central e periférico, os quais incluem neuroproteção, brotamento neuronal, neurotransmissão e dor neuropática. As células de Schwann (CS), um tipo de glia periférica, também reagem com a lesão do nervo, podendo interferir com o reparo e cicatrização, crescimento de fibras e regeneração neuronais. Investigamos aqui a possibilidade da terapia celular para o reparo do nervo ciático poder alterar o padrão da ativação astrocitária nos cornos anterior e posterior da medula espinal do rato. MÉTODOS: Suspensão de CS cultivadas ou extrato homogeneizado de medula espinal lesada de rato foram inoculados num reservatório feito a partir de dois esmagamentos aplicados no nervo ciático do rato distantes 0,5mm entre si. Injeção local de salina tamponada serviu como controle. Os ratos foram mortos uma semana após e os astrócitos da medula espinal marcados por método imunohistoquímico e quantificados por análise de imagem. RESULTADOS: No corno anterior da medula, ipsilateral à lesão, ativação astrocitária leve foi vista após as injeções de tampão ou CS, entretanto, ativação celular intensa foi observada nesta região com a inoculação neural do extrato homogeneizado de tecido medular lesado. Adicionalmente, as inoculações de CS e de extrato homogeneizado de tecido medular promoveram forte reação astrocitária no corno dorsal da medula espinal, bilateralmente. CONCLUSÕES: Os astrócitos da medula espinal reagem em função do processo de reparo do nervo lesado, o que pode influenciar o resultado funcional esperado, algo que deve ser considerado durante o planejamento da estratégia neurocirúrgica.

Extracellular HIV-1 Tat enhances monocyte adhesion by up-regulation of ICAM-1 and VCAM-1 gene expression via ROS-dependent NF-kappaB activation in astrocytes

One of characteristic features of AIDS-related encephalitis and dementia is the infiltration of monocytes into the CNS. HIV-1 Tat was demonstrated to facilitate monocyte entry into the CNS. In this study, we examined the effect of HIV-1 Tat on the expression of adhesion molecules, generation of reactive oxygen species (ROS) and NF-kappaB activation in CRT-MG human astroglioma cells. Treatment of CRT-MG cells with HIV-1 Tat protein significantly increased protein and mRNA levels of ICAM-1 and VCAM-1, as measured by Western blot analysis and RT-PCR, indicating that Tat increases these protein levels at an mRNA level. In addition, Tat induced the activation of NF-kappaB in astrocytes. Treatment of CRT-MG with NF-kappaB inhibitors led to decrease in Tat-induced protein and mRNA expression of ICAM-1 and VCAM-1. Furthermore, HIV-1 Tat protein increased ROS generation. Inhibition of Tat-induced ROS generation by N-acetyl cysteine, vitamin C and diphenyl iodonium suppressed Tat-induced NF-kappaB activation, ICAM-1 and VCAM-1 expression, and monocyte adhesion in CRT-MG. These data indicate that HIV-1 Tat can modulate monocyte adhesiveness by increasing expression of adhesion molecules such as ICAM-1 and VCAM-1 via ROS- and NF-kappaB-dependent mechanisms in astrocytes.

Cytotoxicity effect of alkaloidal extract from Prosopis juliflora Sw. D.C. (Algaroba) pods on glial cells

Prosopis juliflora is largely used for feeding cattle and humans. Neurological signals have been reported in cattle due to intoxication with this plant. In this study, an alkaloidal fraction (AF) obtained from P. juliflora pods was tested on astrocyte primary cultures. Astrocytes display physiological functions essential to development, homeostasis and detoxification in the central nervous system (CNS). These cells are known for their role on energetic support and immune response in the CNS. Concentrations between 0.03 to 30 µg/ml AF were assayed for 24 - 72 h. The mitochondrial activity, assayed by MTT test, showed cytotoxicity at 30 µg/ml AF after 24 h. At concentrations ranging between 0.3 - 3 µg/ ml, the AF induced an increase on mitochondrial activity, indicating cell reactivity. lmmunocytochemistry assay for GFAP cytoskeletal protein, revealed alterations on cell morphology after treatment with 0.3 - 3 µg/ ml AF for 72 h. This result corroborates with western blot analysis when ceUs treated with 0.3 - 3 I-µg/ml AF for 72 h showed GFAP upregulation. The vimentin expression was not significantly altered in all tested concentrations. These results suggest that alkaloids induce astrocyte reactivity and might be involved in the neurotoxic effects induced by P. juliflora consumption.

A Prosopis juliflora é amplamente utilizada na alimentação humana e de várias espécies animais, especialmente bovinos. Quadros de intoxicação por esta planta, nesta espécie, têm sido relatados, principalmente quando a mesma é oferecida como única fonte alimentar, desencadeando uma doença de sintomatologia nervosa. Neste estudo, objetivou-se avaliar os efeitos in vitro da fração de alcalóides totais (F A) extraída das vagens da Prosopis juliflora utilizando cultura primária de astrócitos obtidos do córtex cerebral de ratos como modelo de estudo. A avaliação da atividade mitocondrial pelo teste do MTT demonstrou a citotoxicidade em 30 µg/ ml da FA após 24 h. As concentrações de 0,3 e 3 µg/ ml da FA induziram um aumento da atividade mitocondrial, indicando reatividade celular. Testes imunocitoquimicos para a GFAP, principal proteína de citoesqueleto de astrócitos, revelaram alterações morfológicas nas células após tratamento com 0,3 e 3 µg/ml da FA por 72 h. Tais resultados são consoantes à análise desta proteína por westernblot, quando as culturas foram tratadas com 0,3 e 3 µg/ml da FA por 72 h, demonstrando interferências na regulação da expressão da GFAP. A expressão de vimentina não foi significativamente alterada em nenhuma das concentrações testadas. Estes resultados sugerem que os alcalóides da P.juliflora induzem a reatividade astrocitária, o que pode estar envolvido nos efeitos neurotóxicos providos pelo consumo desta planta.

Effects of ischemia and anoxia on cell activation and cell cycle of cultured astrocytes in vitro / 华中科技大学学报（医学）（英德文版）

To examine the effects of ischemia and anoxia on cell activation and cell cycle of astrocytes in vitro, the cell cycles and the proliferation of astrocytes in different time points after ischemia and anoxia were studied by flow cytometry and BrdU labeling and the expression of GFAP and cyclin D1 was detected by the fluorescence immunochemistry. After ischemia and anoxia in vitro, the astrocytes in S phase were significantly increased as compared with those in the normal group and the proliferating ability of the astrocytes was highest 6 h after the treatment as revealed by BrdU pulse labeling, but the astrocytes in S phase and proliferating ability were decreased after 6 h. At the early stages of ischemia and anoxia, the positive staining intensity of GFAP was increased, peaked at 6th h, while 12 h after the ischemia and anoxia, the positive staining intensity of GFAP became weak, and the expression of cyclin D1 was gradually increased after the ischemic and anoxic damage. It is concluded that astrocytes are activated to proliferate and enter new cycle events by ischemia and anoxia, and cyclin D1 is implicated in the proliferation and repair of astrocytes. The cell cycle events are closely associated with the proliferation and activation of astrocytes.

Human Brain Astrocytes Mediate TRAIL-mediated Apoptosis after Treatment with IFN-gamma

TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1beta TNF-alphaor IFN-gamma TRAIL was induced in cultured fetal astrocytes. In particular, IFN-gammainduced the highest levels of TRAIL in cultured astrocytes. When astrocytes were pre-reated with IFN-gamma they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-gamma modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain.

Human Brain Astrocytes Mediate TRAIL-mediated Apoptosis after Treatment with IFN-gamma

TNF-related apoptosis inducing ligand (TRAIL) expressions were studied in primary human brain astrocytes in response to pro-inflammatory cytokines. When astrocytes were treated with IL-1beta TNF-alphaor IFN-gamma TRAIL was induced in cultured fetal astrocytes. In particular, IFN-gammainduced the highest levels of TRAIL in cultured astrocytes. When astrocytes were pre-reated with IFN-gamma they induced apoptosis in TRAIL-sensitive Peer cells. Our results suggest that IFN-gamma modulates the expression of TRAIL in astrocytes, which may enhance cytotoxic sensitivity of infiltrating immune cells or brain cells other than astrocytes during inflammation of brain.

Immunochemical and morphometric features of astrocyte reactivity vs. plaque location in Alzheimer's disease

The quantitative relationship between glial fibrillary acidic protein (GFAP) hyper-reactivity and -amyloid protein (AP) deposition was investigated by double immunoperoxidase labeling of hippocampal and entorhinal cortex sections from five Alzheimer´s disease (AD) cases and five age-matched controls. AP plaques, which were absent in controls, were found in all AD samples, without significant differences in number or perimeter according to their location among the regions studied. In contrast, the mean number of GFAP (+) cells was significantly greater in the hippocampus than in the entorhinal cortex from AD cases (49 vs.39). Although at lower values (30 vs. 20), predominance of astrocyte hyperplasia in hippocampus as compared with entorhinal cortex was also found in control samples. Concomitant astrocyte hypertrophy, as defined by surface density (Sv) values of GFAP-immunoreactive material exceeding those of control means, affected a similar proportion of cells in the hippocampus (73%) and the entorhinal cortex (74%) from AD cases. Since an increased number of GFAP (+) cells in the hippocampus was not accompanied by an increased number and/or perimeter of neighbouring plaques, such differential hyper-reactivity in samples from AD patients, as well as in those with normal aging, seems to depend partially on the regional location of the involved astrocyte.

Immortalized rat astrocyte strain genetically modified by rat preprogalanin gene / 华中科技大学学报（医学）（英德文版）

To construct an immortalized rat astrocyte strain genetically modified by rat preprogalanin gene (IAST/GAL) and detect its galanin (GAL) expression and secretion, a cDNA fragment of rat GAL in plasmid of pBS KS(+)-GAL was inserted into eukaryotic expression vector pcDNA3.1 (+) by DNA recombinant technology, then the restriction enzyme digestion and DNA sequencing were carried out to evaluate the recombinant. The pcDNA3.1 (+)-GAL and pcDNA3.1 (+) construct were transfected into immortalized rat astrocyte strain (IAST) by lipofectamine and the population of cells which stably integrated the construct was selected with 600 microg/mL G418. Individual clones were screened and expanded into clonal cell strains. Detection of Neo gene was used to validate the success of the transfection. Immunocytochemical staining, RT-PCR and radioimmunoassay were used to detect the expression and secretion level of GAL. The recombinant had been successfully constructed by restriction enzyme digestion and DNA sequencing. Detection of Neo gene showed that the pcDNA3.1 (+)-GAL and pcDNA3.1 (+) have been successfully transfected into IAST. After selection by using G418, IAST/GAL and IAST/Neo cell strains were obtained. IAST/GAL, IAST/Neo and IAST were immunostained positively for GAL, but the GAL average optical density of IAST/GAL was significantly higher than that of IAST/Neo and IAST (P0.05). It was concluded that IAST/GAL strain was constructed successfully and it might provide a basis for the further study of pain therapy.

Regulation of astroglia on synaptic plasticity in the CA1 region of rat hippocampus / 华中科技大学学报（医学）（英德文版）

The regulation of astroglia on synaptic plasticity in the CA1 region of rat hippocampus was examined. Rats were divided into three groups: the newly born (< 24 h), the juvenile (28-30 days) and the adult groups (90 - 100 days), with each group having 20 animals. The CA1 region of rat hippocampus was immunohistochemically and electron-microscopically examined, respectively, for the growth of astroglia and the ultrastructure of synapses. The high performance liquid chromatography was employed to determine the cholesterol content of rat hippocampus. In the newly-born rats, a large number of neurons were noted in the hippocampal CA1 region of the newly-born rats, and few astroglia and no synaptic structure were observed. In the juvenile group, a few astroglias and some immature synapses were found, which were less than those in adult rats (P < 0.01). The cholesterol content was 2.92 +/- 0.03 mg/g, 11.20 +/- 3.41 mg/g and 12.91 +/- 1.25 mg/g for newly born, the juvenile and the adult groups, respectively, with the differences among them being statistically significant (P < 0.01). Our study suggests that the astrocytes may play an important role in the synaptic formation and functional maturity of hippocampal neurons, which may be related to the secretion of cholesterol from astrocytes.

An improved method for directional differentiation and efficient production of neurons from embryonic stem cells in vitro / 华中科技大学学报（医学）（英德文版）

To establish a method of directional differentiation and efficient production of neurons from embryonic stem cells (ES cells) in vitro, based on the 4-/4+ protocol described by Bain, a new method was established to induce ES cells differentiating into neurons by means of three-step differentiation using all-trans retinoic acid (ATRA) combined with astrocyte-conditioned medium (ACM) in Vitro. The totipotency of ES cells was identified by observation of cells' morphology and formations of teratoma in immunocompromised mice. The cells' differentiation was evaluated continuously by the detection of the specific cellular markers of neural stem cells, neurons and astrocytes, including nestin, NSE and GFAP using immunohistochemistry assay. The NSE positive cells' ratio of the differentiated cells was determined by flow cytometry. It was found that the transparent circular clusters surrounding embryoid bodies induced with combining induction protocol formed just after 24 h and gradually enlarged later. This phenomenon could not be observed in EBs induced only by ATRA. The NSE positive cells' ratio in the cells induced with ATRA and ACM was higher than that of the cells induced by ATRA at different time points of differentiation, and finally reached up to 73.5% among the total differentiated population. It was concluded that ES cells could be induced into neurons with high purity and yield by means of inducing method combining with ATRA and ACM.

Forskolin promotes astroglial differentiation of human central neurocytoma cells

Human central neurocytoma is a kind of the brain tumors that are usually found in anterior part of the lateral ventricles. In this study, we established conditions that allowed proliferation of neurocytoma cells culture and analyzed characteristics of neurocytoma cells in vitro. For in vitro, a condition that used for culturing neural stem cells and contained basic fibroblast growth factor (bFGF) provided high proliferation. RT-PCR analaysis showed that nestin was found in neurocytoma cells, indicating that the neurocytomas possess neural stem cell properties. Interestingly, treatment of neurocytoma cells with forskolin increased expression of glial fibrillary acidic protein with a concomitant decrease in the nestin expression. Forskolin also induced morphological changes of neurocytoma cells to adopt an astrocyte-like phenotype. The results suggest that neurocyotma cells may have properties of multipotent neural stem cells.

Protective Effects of N-acetylcysteine and Selenium against Doxorubicin Toxicity in Rats

To investigate the neutralizing effect of N-acetylcysteine (NAC) and selenium (Se) aganist doxorubicin (DOX) toxicity in rats, NAC (140 mg/kg, p.o.) and Se (0.5 mg/kg, p.o.) were administered for 2 days before DOX injection and then 3 times a week. Cell viability and the level of lipid peroxidation were examined in cultured-rat astrocytes. Severe morphologic changes in the kidney of DOX group; thickening of Bowmans capsule, presence of multifocal tubular casts were observed, but not in the other treated groups. Vacuoles in some hepatic cells and focal aggregation of stellate macrophages were also detected in DOX group, but not in the other treated groups. However, the severe inhibition of spermatogenesis was found in all treated groups. The cell viability of DOX (10 mg/ml) treated group and NAC (5 mM) or Se (0.001 mg/ml) combinedtreated group was 52.5+/-2.0 % , 85.3+/-4.5 % and 75.5+/-1.6 %, respectively. In MDA (malondialdehyde) assay, the level of lipid peroxidation on DOX (10 mg/ml), NAC (5 mM) and Se (0.001 mg/ml) was 0.77+/-0.06, 0.35+/-0.06 and 0.54+/-0.11 nmol/mg protein, respectively. Thus, it is known that NAC and Se have protective effects in kidney and liver but not in the testes. Morphological change was not detected in brain and heart in all groups for experiment period. From this in vitro study, it is known that NAC and Se protect well the astrocytes against DOX induced-cell damage.

Cross-talk between neurons and glia: highlights on soluble factors

The development of the nervous system is guided by a balanced action between intrinsic factors represented by the genetic program and epigenetic factors characterized by cell-cell interactions which neural cells might perform throughout nervous system morphogenesis. Highly relevant among them are neuron-glia interactions. Several soluble factors secreted by either glial or neuronal cells have been implicated in the mutual influence these cells exert on each other. In this review, we will focus our attention on recent advances in the understanding of the role of glial and neuronal trophic factors in nervous system development. We will argue that the functional architecture of the brain depends on an intimate neuron-glia partnership

Cell differentiation increases astrocyte phagocytic activity: a quantitative analysis of both GFAP labeling and pas-stained yeast cells

Since efficiency of phagocytic potential in activated astrocytes is still a subject of controversy, an attempt was made to quantify simultaneously phagocytic activity and astrocyte differentiation. Resorting to Junin virus, known to induce astrocyte activation, infected vs control samples of cultured rat astroglial cells were serially harvested up to day 12 post-inoculation (pi), and subjected to a triple staining procedure consisting in immunoperoxidase labeling of GFAP, periodic acid-Schiff (PAS) reaction in added baker's yeast cells and hematoxylin for nuclear staining of the whole cell monolayer. Adopting GFAP labeling as a specific marker of astrocyte differentiation, the immunoprecipitate development over time was measured. Direct calculation of the initial reaction rate was feasible given its linear behavior during the first 10 min, so that GFAP amount was regarded proportional to peroxidase activity. As determined by digital image analysis, mean optical density (MOD) values of GFAP in infected samples increased from 0.618 + 0.082 at day 1 pi to 0.825 + 0.125 at day 3, leveling off at 1.010 + 0.101 as from day 9, while control unifected samples remained unchanged at roughly 0.6 during the entire observation period. In turn, phagocytosis was quantified by PAS staing densitometry, whose intensity varied according to wall degradation of yeast cells. MOD levels of PAS-stained phagocytized yeast cells were significantly lower (p <0.05) in efected vs control cultures at 48 and 72 h following their addition to the astroglial monolayer. According to simultaneous quantification of two components of astrocyte response to viral infection, it is concluded that phagocytic activity increases with astrocyte differentiation.