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Inflammatory and infectious diseases are the major causes of morbidity and mortality. The identification of markers for the assessment of disease activity and response to treatment can improve long-term prognosis. The aim of this study was to evaluate platelet count, C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR) among children with inflammatory and infectious disease. This cross-sectional study was conducted in the paediatric immunology and infectious units of Shahid Madani Hospital of Khorramabad. One hundred fifty children, half boys and half girls, with diagnoses of infectious and inflammatory diseases were included in the study. Platelet count, ESR and CRP were measured at the time of hospitalization and thereafter (recovery phase). A questionnaire including demographic information, diagnosis and paraclinical data was completed. At the time of hospitalization, all 150 children had abnormal ESR, 110 (73.3%) had abnormal CRP and 12 (92%) had alterations in platelet count. At the time of discharge, one patient (0.7%) had normal ESR, 132 (88%) had normal CRP and 140 patients (93.3%) had normal platelet count. At the time of discharge, we found a significant difference between the levels of CRP and platelets in girls. This study showed that CRP level is useful during treatment follow-up. Changes in platelet count are likely to be more prevalent in girls.
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Urinary tract infection (UTI) is associated with increased health burden among paediatric patients. Vitamin D is known for its immunoregulatory effects, particularly antimicrobial activity. The aim of this study was to determine the relationship between vitamin D levels and UTIs in children referred to a hospital in Khorramabad, Iran. This case-control study was conducted on 258 children aged between 2 and 14 years; 44 children with UTI and 214 healthy children were enrolled. Patients were tested for UTI on the basis of signs and symptoms, and urine culture and analysis. Vitamin D levels were measured in children in both groups. According to the results, the two groups were significantly different in terms of sex (p 0.007). There was no significant difference between the mean vitamin D among the two groups. Vitamin D levels were not related to UTI by multivariate logistic regression. The relationship between the level of vitamin D and the incidence of UTI in children in accordance with age and sex had an odds ratio of 0.99, indicating that for a 1-unit increase in vitamin D, the odds of having a UTI decreased by 1, a correlation which was not statistically significant. According to the findings of this study, no significant correlation was found between UTI and vitamin D levels. However, the prevalence of UTI was higher in girls than boys.
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AIM: The zebrafish has emerged as a novel model for investigating cardiac physiology and pathology. The aim of this study was to investigate the atrium-specific ion channels responsible for shaping the atrial cardiac action potential in zebrafish. METHODS: Using quantitative polymerase chain reaction, we assessed the expression level of atrium-specific potassium channels. The functional role of these channels was studied by patch clamp experiments on isolated atrial and ventricular cardiomyocytes and by optical mapping of explanted adult zebrafish hearts. Finally, surface ECGs were recorded to establish possible in vivo roles of atrial ion channels. RESULTS: In isolated adult zebrafish hearts, we identified the expression of kcnk3, kcnk9, kcnn1, kcnn2, kcnn3, kcnj3 and kcnj5, the genes that encode the atrium-specific K2P , KCa 2.x and Kir 3.1/4 (KACh ) ion channels. The electrophysiological data indicate that the acetylcholine-activated inward-rectifying current, IKACh, plays a major role in the zebrafish atrium, whereas K2P 3.1/9.1 and KCa 2.x channels do not appear to be involved in regulating the action potential in the zebrafish heart. CONCLUSION: We demonstrate that the acetylcholine-activated inward-rectifying current (IKACh ) current plays a major role in the zebrafish atrium and that the zebrafish could potentially be a cost-effective and reliable model for pharmacological testing of atrium-specific IKACh modulating compounds.
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Miocardio/metabolismo , Canales de Potasio/metabolismo , Pez Cebra/metabolismo , Animales , Electrocardiografía , Atrios Cardíacos/metabolismo , Preparación de Corazón Aislado , Técnicas de Placa-Clamp , Canales de Potasio/análisisAsunto(s)
Abomaso/efectos de los fármacos , Acetaminofén/farmacocinética , Eritromicina/farmacología , Vaciamiento Gástrico/efectos de los fármacos , Ovinos/sangre , Abomaso/fisiología , Absorción , Analgésicos no Narcóticos/farmacocinética , Animales , Antibacterianos/farmacología , Área Bajo la Curva , Estudios Cruzados , FemeninoRESUMEN
In this cross-sectional study, we evaluated H. pylori seroprevalence and the relevant factors in 1518 people aged > or = 6 years from the general population of Nahavand, western Islamic Republic of Iran. Questionnaires covering sociodemographic variables were completed by interview. Blood samples were taken from each individual. Sera were tested for anti-H. pylori IgG using commercial enzyme immunoassay. Overall, seroprevalence of H. pylori was high, 71.0% (95% CI: 69.0%-73.0%). There was a gradual increase with age. Based on multivariate adjustment, only female sex and age could be considered risk factors.
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Infecciones por Helicobacter/epidemiología , Helicobacter pylori , Adolescente , Adulto , Distribución por Edad , Anciano , Anticuerpos Antibacterianos/sangre , Distribución de Chi-Cuadrado , Niño , Estudios Transversales , Femenino , Infecciones por Helicobacter/sangre , Infecciones por Helicobacter/inmunología , Helicobacter pylori/inmunología , Humanos , Inmunoglobulina G/sangre , Irán/epidemiología , Masculino , Persona de Mediana Edad , Análisis Multivariante , Vigilancia de la Población , Factores de Riesgo , Estudios Seroepidemiológicos , Distribución por Sexo , Factores Socioeconómicos , Adulto JovenRESUMEN
In this cross-sectional study, we evaluated H. pylori seroprevalence and the relevant factors in 1518 people aged > /= 6 years from the general population of Nahavand, western Islamic Republic of Iran. Questionnaires covering sociodemographic variables were completed by interview. Blood samples were taken from each individual. Sera were tested for anti-H. pylori IgG using commercial enzyme immunoassay. Overall, seroprevalence of H. pylori was high, 71.0% [95% CI: 69.0%-73.0%]. There was a gradual increase with age. Based on multivariate adjustment, only female sex and age could be considered risk factors
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Infecciones por Helicobacter , Estudios Seroepidemiológicos , Estudios Transversales , Población , Encuestas y Cuestionarios , Inmunoglobulina G , Factores de Riesgo , Factores de Edad , Factores Sexuales , Helicobacter pyloriRESUMEN
Andersen-Tawil syndrome (ATS) is an autosomal dominant multisystem disorder characterized by developmental, cardiac, and neuromuscular abnormalities. Approximately 70% of patients have mutations in KCNJ2, resulting in dysfunction of the inward-rectifying potassium channel Kir2.1. Variable expression complicates the diagnosis of ATS, which in many cases, is not made until years after the first recognized symptom. To better define the distinctive clinical features of ATS and facilitate earlier diagnosis, we conducted a prospective, standardized evaluation of 10 subjects with confirmed KCNJ2 mutations. Detailed anthropometric, neurological, and cardiac evaluations were performed. Using this approach, we identified novel skeletal and dental findings and proposed additional diagnostic criteria for ATS dysmorphology.
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Anomalías Múltiples/genética , Síndrome de Andersen/genética , Mutación/genética , Canales de Potasio de Rectificación Interna/genética , Anomalías Múltiples/diagnóstico , Adolescente , Adulto , Síndrome de Andersen/patología , Antropometría , Arritmias Cardíacas/genética , Niño , Estudios de Cohortes , Femenino , Predisposición Genética a la Enfermedad , Humanos , Masculino , Enfermedades del Sistema Nervioso/genética , Linaje , Fenotipo , Estudios Prospectivos , Anomalías Dentarias/genéticaRESUMEN
Periodic paralyses (PPs) are rare inherited channelopathies that manifest as abnormal, often potassium (K)-sensitive, muscle membrane excitability leading to episodic flaccid paralysis. Hypokalaemic (HypoPP) and hyperkalaemic PP and Andersen-Tawil syndrome are genetically heterogeneous. Over the past decade mutations in genes encoding three ion channels, CACN1AS, SCN4A and KCNJ2, have been identified and account for at least 70% of the identified cases of PP and several allelic disorders. No prospective clinical studies have followed sufficiently large cohorts with characterized molecular lesions to draw precise conclusions. We summarize current knowledge of the clinical diagnosis, molecular genetics, genotype-phenotype correlations, pathophysiology and treatment in the PPs. We focus on unresolved issues including (i) Are there additional ion channel defects in cases without defined mutations? (ii) What is the mechanism for depolarization-induced weakness in Hypo PP? and finally (iii) Will detailed electrophysiological studies be able to correctly identify specific channel mutations? Understanding the pathophysiology of the potassium-sensitive PPs ought to reduce genetic complexity, allow subjects to be stratified during future clinical trials and increase the likelihood of observing true clinical effects. Ideally, therapy for the PPs will prevent attacks, avoid permanent weakness and improve quality of life. Moreover, understanding the skeletal muscle channelopathies will hopefully lead to insights into the more common central nervous system channel diseases such as migraine and epilepsy.
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Parálisis Periódicas Familiares , Animales , Inhibidores de Anhidrasa Carbónica/uso terapéutico , Genotipo , Humanos , Activación del Canal Iónico , Ratones , Ratones Noqueados , Modelos Animales , Músculo Esquelético/metabolismo , Músculo Esquelético/patología , Mutación , Parálisis Periódicas Familiares/diagnóstico , Parálisis Periódicas Familiares/tratamiento farmacológico , Parálisis Periódicas Familiares/genética , Fenotipo , Potasio/metabolismo , Potasio/uso terapéutico , Canales de Potasio/genética , Canales de Potasio/metabolismo , Canales de Sodio/genética , Canales de Sodio/metabolismoRESUMEN
The Shiraz Organ Transplant Center in southern Iran has been performing all liver transplantations in Iran and certain neighboring countries for 12 years. This study evaluated the 140 operations performed from April 1993 through November 2004. Sixty-one percent of the recipients were men and 39% were women. The average recipient age was 29.9 +/- 14.0 years. One hundred twenty-eight patients has a full-size cadaveric transplant. Most frequent causes of cirrhosis were cryptogenic and viral. An acute rejection episode occurred in 47.5% of cases, and two episodes in 8%. Most frequent short-term complications included respiratory, neurologic, and biliary problems. The 1-, 2-, and 3-year patient survival rates were 92%, 89%, and 85%, respectively. The experience that the Shiraz Organ Transplant Center has had with liver transplantation indicated success comparable to that noted in other reports. The calculated trend suggests that a goal of 100 transplantations for 2005 is within reach.
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Trasplante de Hígado/fisiología , Adolescente , Adulto , Femenino , Humanos , Irán , Hepatopatías/clasificación , Hepatopatías/cirugía , Trasplante de Hígado/métodos , Masculino , Estudios Retrospectivos , Resultado del TratamientoRESUMEN
BACKGROUND: Mutations in KCNJ2, the gene encoding the inward-rectifying K+ channel Kir2.1, cause the cardiac, skeletal muscle, and developmental phenotypes of Andersen-Tawil syndrome (ATS; also known as Andersen syndrome). Although pathogenic mechanisms have been proposed for select mutations, a common mechanism has not been identified. METHODS: Seventeen probands presenting with symptoms characteristic of ATS were evaluated clinically and screened for mutations in KCNJ2. The results of mutation analysis were combined with those from previously studied subjects to assess the frequency with which KCNJ2 mutations cause ATS. RESULTS: Mutations in KCNJ2 were discovered in nine probands. These included six novel mutations (D71N, T75R, G146D, R189I, G300D, and R312C) as well as previously reported mutations R67W and R218W. Six probands possessed mutations of residues implicated in binding membrane-associated phosphatidylinositol 4,5-bisphosphate (PIP2). In total, mutations in PIP(2)-related residues accounted for disease in 18 of 29 (62%) reported KCNJ2 -based probands with ATS. Also reported is that mutation R67W causes the full clinical triad in two unrelated males. CONCLUSIONS: The novel mutations corresponding to residues involved in Kir2.1 channel-PIP2 interactions presented here as well as the overall frequency of mutations occurring in these residues indicate that defects in PIP2 binding constitute a major pathogenic mechanism of ATS. Furthermore, screening KCNJ2 in patients with the complex phenotypes of ATS was found to be invaluable in establishing or confirming a disease diagnosis as mutations in this gene can be identified in the majority of patients.
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Anomalías Múltiples/genética , Arritmias Cardíacas/genética , Mutación , Parálisis/genética , Fosfatidilinositol 4,5-Difosfato/metabolismo , Canales de Potasio de Rectificación Interna/genética , Anomalías Múltiples/diagnóstico , Anomalías Múltiples/patología , Arritmias Cardíacas/diagnóstico , Sitios de Unión , Femenino , Predisposición Genética a la Enfermedad , Humanos , Masculino , Debilidad Muscular/genética , Parálisis/diagnóstico , Linaje , Fenotipo , Canales de Potasio de Rectificación Interna/química , Canales de Potasio de Rectificación Interna/metabolismo , SíndromeRESUMEN
PURPOSE: To examine the amount of sHLA-I in malignant pleural and peritoneal effusions and its possible role in natural immune defense. METHODS: Three groups of patients (75 patients with malignancy, 21 with infection, and 27 with other diseases) were studied for sHLA-I value using an ELISA method. Cytolytic activity of freshly isolated pleural and peritoneal effusion-associated lymphoid (EAL) cells from 14 of cases with malignancy were examined and compared to that of ten non-cancerous patients. EAL cells were co-cultured with the autologous cell-free effusions immediately after collection and 3 days after incubation with IL-2. RESULTS: The mean value of sHLA-I in effusions was 1.01+/-1.36 micro g/ml, 0.97+/-1.20 micro g/ml, and 0.49+/-0.45 micro g/ml, respectively. Despite higher mean sHLA-I levels in malignant and infected patients, no significant difference between these groups was observed ( P >0.05). Generally, the amount of sHLA-I in peritoneal effusions was higher than that for pleural effusions, but the difference was not significant. There were also no statistical differences in the sHLA-I levels between sub-groups of patients with malignancy. EAL cells' killing activity in malignant and infected effusions was 68.15+/-11.73 and 78.28+/-14.41, respectively ( P=0.08). No correlation between sHLA-I level and NK activity of EAL cells from the patients was found. Almost all malignant cases after exposure to cell-free effusions displayed an increase in NK activity (from 68.66+/-11.13 to 74.2+/-12.39, P=0.042) and a decrease in LAK activity (74.5+/-18.30 vs 67.72+/-16.46, P=0.040). Whereas, the same experiment performed for non-malignant effusions showed a decrease in both NK activity and LAK activity. Changes in NK and LAK activity were not correlated with the amount of sHLA-I in the effusions. CONCLUSION: The presence of sHLA-I, particularly in malignant effusions, suggests a role for these molecules in tumor immunity in the peritoneal or plural environment; however, at least with these group of patients, sHLA-I appears not to be a unique determining factor on EAL cells' killing activity.
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Líquido Ascítico/inmunología , Antígenos de Histocompatibilidad Clase I/inmunología , Células Asesinas Activadas por Linfocinas/inmunología , Células Asesinas Naturales/inmunología , Derrame Pleural Maligno/inmunología , Supervivencia Celular , Técnicas de Cocultivo , Citotoxicidad Inmunológica , Ensayo de Inmunoadsorción Enzimática , HumanosRESUMEN
Voltage-gated channels are normally opened by depolarization and closed by repolarization of the membrane. Despite sharing significant sequence homology with voltage-gated K(+) channels, the gating of hyperpolarization-activated, cyclic-nucleotide-gated (HCN) pacemaker channels has the opposite dependence on membrane potential: hyperpolarization opens, whereas depolarization closes, these channels. The mechanism and structural basis of the process that couples voltage sensor movement to HCN channel opening and closing is not understood. On the basis of our previous studies of a mutant HERG (human ether-a-go-go-related gene) channel, we hypothesized that the intracellular linker that connects the fourth and fifth transmembrane domains (S4-S5 linker) of HCN channels might be important for channel gating. Here, we used alanine-scanning mutagenesis of the HCN2 S4-S5 linker to identify three residues, E324, Y331, and R339, that when mutated disrupted normal channel closing. Mutation of a basic residue in the S4 domain (R318Q) prevented channel opening, presumably by disrupting S4 movement. However, channels with R318Q and Y331S mutations were constitutively open, suggesting that these channels can open without a functioning S4 domain. We conclude that the S4-S5 linker mediates coupling between voltage sensing and HCN channel activation. Our findings also suggest that opening of HCN and related channels corresponds to activation of a gate located near the inner pore, rather than recovery of channels from a C-type inactivated state.
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Activación del Canal Iónico/fisiología , Canales Iónicos/química , Canales Iónicos/fisiología , Potenciales de la Membrana/fisiología , Proteínas Musculares , Alanina , Secuencia de Aminoácidos , Sustitución de Aminoácidos , Animales , Encéfalo/metabolismo , Clonación Molecular , Femenino , Humanos , Canales Regulados por Nucleótidos Cíclicos Activados por Hiperpolarización , Ratones , Modelos Moleculares , Datos de Secuencia Molecular , Mutagénesis Sitio-Dirigida , Oocitos/fisiología , Técnicas de Placa-Clamp , Mutación Puntual , Canales de Potasio/química , Canales de Potasio/fisiología , Estructura Secundaria de Proteína , Proteínas Recombinantes/química , Proteínas Recombinantes/metabolismo , Eliminación de Secuencia , Xenopus laevisRESUMEN
Andersen's syndrome is characterized by periodic paralysis, cardiac arrhythmias, and dysmorphic features. We have mapped an Andersen's locus to chromosome 17q23 near the inward rectifying potassium channel gene KCNJ2. A missense mutation in KCNJ2 (encoding D71V) was identified in the linked family. Eight additional mutations were identified in unrelated patients. Expression of two of these mutations in Xenopus oocytes revealed loss of function and a dominant negative effect in Kir2.1 current as assayed by voltage-clamp. We conclude that mutations in Kir2.1 cause Andersen's syndrome. These findings suggest that Kir2.1 plays an important role in developmental signaling in addition to its previously recognized function in controlling cell excitability in skeletal muscle and heart.
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Arritmias Cardíacas/genética , Cromosomas Humanos Par 17 , Facies , Parálisis Periódicas Familiares/genética , Canales de Potasio de Rectificación Interna , Canales de Potasio/genética , Alelos , Secuencia de Aminoácidos , Animales , Canales de Calcio/genética , Cartilla de ADN , Salud de la Familia , Femenino , Expresión Génica , Ligamiento Genético , Genotipo , Humanos , Masculino , Mutación Missense , Canal de Sodio Activado por Voltaje NAV1.4 , Oocitos/fisiología , Técnicas de Placa-Clamp , Linaje , Fenotipo , Canales de Sodio/genética , XenopusRESUMEN
Unsuitability of the in-situ right gastroepiploic artery in coronary bypass grafting occurs. Sometimes free-grafting can be performed, although this should not be considered in patients with a diseased ascending aorta. We describe the successful use of the left gastric artery as an alternative in-situ arterial conduit in a patient with a severely atherosclerotic ascending aorta.
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Puente de Arteria Coronaria/métodos , Anciano , Aorta , Enfermedades de la Aorta/complicaciones , Arteriosclerosis/complicaciones , Femenino , HumanosRESUMEN
The configuration of cardiac action potentials varies considerably from one region of the heart to another. These differences are caused by differential cellular expression of several types of K(+) channel genes. The channels encoded by these genes can be grouped into several classes depending on the stimulus that permits the channels to open and conduct potassium ions. K(+) channels are activated by changes in transmembrane voltage or binding of ligands. Voltage-gated channels are normally the most important players in determining the shape and duration of action potentials and include the delayed rectifiers and the transient outward potassium channels. Ligand-gated channels include those that probably have only minor roles in shaping repolarization under normal conditions but, when activated by extracellular acetylcholine or a decrease in the intracellular concentration of ATP, can substantially shorten action potential duration. Inward rectifier K(+) channels are unique in that they are basically stuck in the open state but can be blocked in a voltage-dependent manner by intracellular Mg(2+), Ca(2+), and polyamines. Other K(+) channels have been described that provide a small background leak conductance. Many of these cardiac K(+) channels have been cloned in the past decade, permitting detailed studies of the molecular basis of their function and facilitating the discovery of the molecular basis of several forms of congenital arrhythmias. Drugs that block cardiac K(+) channels and prolong action potential duration have been developed as antiarrhythmic agents. However, many of these same drugs, as well as other common medications that are structurally unrelated, can also cause long QT syndrome and induce ventricular arrhythmia.
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Arritmias Cardíacas/metabolismo , Mutación , Canales de Potasio/metabolismo , Animales , Arritmias Cardíacas/genética , Sistema de Conducción Cardíaco/efectos de los fármacos , Humanos , Síndrome de QT Prolongado/inducido químicamente , Síndrome de QT Prolongado/genética , Síndrome de QT Prolongado/metabolismo , Canales de Potasio/genética , Taquicardia Ventricular/inducido químicamente , Torsades de Pointes/inducido químicamenteRESUMEN
A 15-year-old girl presented with persistent fevers, night sweats, leukocytosis, an elevated erythrocyte sedimentation rate, and a 13-pound weight loss over 2 months. Duplex Doppler scans, computed tomographic scan, and magnetic resonance imaging studies were suggestive of Takayasu's arteritis. Left ventricular dysfunction occurred during the episode of active disease, and an endomyocardial biopsy demonstrated increased HLA-DR (human leukocyte antigen-DR) on the endothelium and evidence of immune complex deposition in the walls of small vessels. One year later, after treatment with corticosteroids and resolution of clinical symptoms, repeat endomyocardial biopsy revealed focal interstitial fibrosis and persistent immune complex deposition. These results indicate that the inflammatory, vasculitic process affecting the large vessels in Takayasu's arteritis may also involve the endomyocardium and its small vessels resulting in ventricular dysfunction.
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Miocarditis/complicaciones , Miocardio/patología , Arteritis de Takayasu/complicaciones , Disfunción Ventricular Izquierda/fisiopatología , Adolescente , Aorta/patología , Síndromes del Arco Aórtico/complicaciones , Síndromes del Arco Aórtico/fisiopatología , Cateterismo Cardíaco , Femenino , Técnica del Anticuerpo Fluorescente , Humanos , Miocarditis/diagnóstico , Miocarditis/tratamiento farmacológico , Miocardio/ultraestructura , Arteritis de Takayasu/diagnóstico , Arteritis de Takayasu/tratamiento farmacológico , Disfunción Ventricular Izquierda/diagnósticoRESUMEN
INTRODUCTION: The long QT syndrome (LQT) is caused by mutations in genes encoding ion channels that modulate the duration of ventricular action potentials. One of these genes, KVLQT1, encodes an alpha subunit that coassembles with another subunit, hminK, to form the cardiac slow delayed rectifier (I(Ks)) K+ channel. METHODS AND RESULTS: The functional effects of seven mutations in KVLQT1 were assessed using two-microelectrode voltage clamp and the Xenopus oocyte expression system. Most mutations in KVLQT1 caused loss of function when expressed alone. Oocytes were also injected with equal amounts of wild-type (WT) KVLQT1 and mutant KVLQT1 cRNA (with or without coinjection of hminK) and the resulting currents compared to currents induced by WT KvLQT1 alone. A341V, R190Q, or G189R KVLQT1 subunits did not affect expression of WT KvLQT1. The other mutations in KVLQT1 caused a variable degree of dominant-negative suppression of I(Ks). The order of potency for this effect was G345E > G306R = V254M > A341E. CONCLUSIONS: LQT1-associated mutations in KVLQT1 caused a spectrum of dysfunction in I(Ks) and KvLQT1 channels. The degree of I(Ks) dysfunction did not correlate with the QTc interval or the presence of symptoms in the respective gene carriers. In contrast to previous reports, we found that loss of function mutations are not exclusive to recessively inherited LQT.
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Síndrome de QT Prolongado/genética , Mutación Missense , Canales de Potasio con Entrada de Voltaje , Canales de Potasio/genética , Animales , Femenino , Genotipo , Humanos , Canales de Potasio KCNQ , Canal de Potasio KCNQ1 , Síndrome de QT Prolongado/etiología , Fenotipo , Canales de Potasio/fisiología , XenopusRESUMEN
In this study, the effect of increasing doses of aspirin on the neurite outgrowth of Dorsal Root Ganglia (DRG) was investigated. DRG were cultured in complete medium (DMEM + 10% FCS +100 ng/ml NGF + collagen Type1 in substratum in 96 multiwell plate) in the presence of concentration of 1.25, 2.5, 5 and 10 mM aspirin. The neurite outgrowth of DRG was followed in comparison with controls that lack aspirin. 10 mM aspirin treated DRG showed delayed neurite outgrowth and after 7 days it reached the same DRG neurite outgrowth control wells after 18 hrs. This growth has delayed approximately one week and showed no further development and in such stage the cells became apoptos. However at concentrations of 1.25, 2.5, 5 mM of aspirin, outgrowth was observed after 18-24 hrs. Although the rate of growth was lower than control, it was not significant. In the other experiment, when DRG cultured for one week in complete medium then treated with aspirin, at 10 mM, DRG neurite outgrowth was stopped, while it was continued in the control. It seem that the aspirin affected DRG became apoptosis.