Methods: In the present cross-sectional study, 1,602 farmers were

Methods: In the present cross-sectional study, 1,602 farmers were enrolled, 1,246 from EN and 356 from control villages. Epidemiological and medical histories were taken

and clinical and laboratory examinations performed for kidney function. Blood pressure was measured following the ESH/ESC guidelines. Results: The prevalence of hypertension in EN villages was higher than in control (50.8 vs. 46.5%, p = 0.005). There was no difference in overall selleckchem treatment, control of all and treated hypertensives between the villages. In all villages, women were treated more than men (EN 41.6 vs. 28.4%, p < 0.001; control 46.4 vs. 27.3%, p < 0.001), but better control of treated was achieved in men (EN 24.7 vs. 17.4%, p = 0.002; control 29.6 vs. 15.5%, p = 0.002). Women had lower income and level of education than men (p < 0.01). Conclusion: Hypertension is highly prevalent in endemic villages. In all villages, men had better blood pressure control despite being treated less. This finding could be explained by poorer education and income in women. Copyright (C) 2012 S. Karger AG, Basel”
“The pyramidal neurons in the hippocampus are extremely neuroplastic, and the complexity of dendritic branches can be dynamically altered in response to a variety of stimuli, including learning and stress. Recently, the teneurin family of proteins has emerged as an interneuronal and extracellular matrix signaling system

that plays a significant role in brain development and neuronal communication. Encoded on the buy JQ-EZ-05 last exon of the teneurin genes is a new family of bioactive peptides termed the teneurin C-terminal-associated peptides (TCAPs). Previous studies indicate that TCAP-1 regulates axon fasciculation and dendritic morphology

in the hippocampus. This study was aimed at understanding the molecular mechanisms by which TCAP-1 regulates these changes in the mouse hippocampus. Fluoresceinisothiocyanate (FITC)-labeled TCAP-1 binds to the pyramidal neurons of the CA2 and CA3, and dentate gyrus in the hippocampus of the mouse brain. Moreover, FITC-TCAP-1 AR-13324 research buy co-localizes with beta-dystroglycan upon binding to the plasma membrane of cultured immortalized mouse E14 hippocampal cells. In culture, TCAP-1 stimulates ERK1/2-dependent phosphorylation of the cytoskeletal regulatory proteins, stathmin at serine-25 and filamin A at serine-2152. In addition, TCAP-1 induces actin polymerization, increases immunoreactivity of tubulin-based cytoskeletal elements and causes a corresponding increase in filopodia formation and mean filopodia length in cultured hippocampal cells. We postulate that the TCAP-1 region of teneurin-1 has a direct action on the cytoskeletal reorganization that precedes neurite and process development in hippocampal neurons. Our data provides novel evidence that functionally links the teneurin and dystroglycan systems and provides new insight into the molecular mechanisms by which TCAP-1 regulates cytoskeletal dynamics in hippocampal neurons.

Earlier studies showed that three conserved motifs-motifs I, II,

Earlier studies showed that three conserved motifs-motifs I, II, and III-in the N termini of geminivirus Rep proteins are essential for function. In this study, we identified a fourth sequence, designated GRS (geminivirus Rep sequence), in the Rep N terminus that displays high amino acid sequence conservation across all geminivirus

genera. Using the selleck chemical Rep protein of Tomato golden mosaic virus (TGMV AL1), we show that GRS mutants are not infectious in plants and do not support viral genome replication in tobacco protoplasts. GRS mutants are competent for protein-protein interactions and for both double-and single-stranded DNA binding, indicating that the mutations did not impair its global conformation. In contrast, GRS mutants are unable to specifically cleave single-stranded DNA, which is required to initiate rolling-circle replication. Interestingly, the Rep proteins of phytoplasmal and algal plasmids also contain GRS-related Apoptosis inhibitor sequences. Modeling of the TGMV AL1 N terminus suggested that GRS mutations alter the relative positioning of motif II, which coordinates metal ions, and motif III, which contains the tyrosine involved in DNA cleavage. Together, these results

established that the GRS is a conserved, essential motif characteristic of an ancient lineage of rolling-circle initiators and support the idea that geminiviruses may have evolved from plasmids associated with phytoplasma or algae.”
“Hepatitis C virus NS3-4A is a membrane-bound enzyme complex that exhibits serine protease, RNA helicase, and RNA-stimulated ATPase activities. This enzyme complex is essential for viral genome replication and has been recently implicated in virus particle assembly. To help clarify the role of NS4A in these processes, we conducted alanine scanning mutagenesis on the C-terminal acidic domain of NS4A in the context of a chimeric genotype 2a reporter virus. Of 13 mutants tested, two (Y45A and F48A) had severe defects in replication, while seven (K41A, L44A, D49A, E50A, M51A, E52A, and E53A) efficiently replicated but had severe defects in virus particle assembly. Multiple strategies were used to identify second-site

mutations that suppressed these NS4A defects. The replication Lonafarnib datasheet defect of NS4A F48A was partially suppressed by mutation of NS4B I7F, indicating that a genetic interaction between NS4A and NS4B contributes to RNA replication. Furthermore, the virus assembly defect of NS4A K41A was suppressed by NS3 Q221L, a mutation previously implicated in overcoming other virus assembly defects. We therefore examined the known enzymatic activities of wild-type or mutant forms of NS3-4A but did not detect specific defects in the mutants. Taken together, our data reveal interactions between NS4A and NS4B that control genome replication and between NS3 and NS4A that control virus assembly.”
“Sequences of retroviral origin occupy approximately 10% of mammalian genomes.

Inflammation markers included C-reactive protein, interleukin-6,

Inflammation markers included C-reactive protein, interleukin-6, fibrinogen, and white blood cell count). Depressive symptoms were assessed, using the 10-item Centers for Epidemiological Studies Depression scale. learn more Cox proportional hazards models were used to investigate the mortality risk

associated with depression, ANS, and inflammation markers, adjusting for demographic and clinical covariates. Results: Depression was associated with ANS dysfunction (DFA(1), p = .018), and increased inflammation markers (white blood cell count, p = .012, fibrinogen p = .043) adjusting for covariates. CVD-related mortality occurred in 121 participants during a median follow-up SBC-115076 of 13.3 years. Depression was associated with an increased CVD mortality risk (hazard ratio, 1.88; 95% confidence interval, 1.23-2.86). Multivariable analyses showed that depression was an independent predictor of CVD mortality (hazard ratio, 1.72; 95% confidence interval, 1.05-2.83) when adjusting for independent HRV and inflammation predictors (DFA(1), heart rate turbulence, interleukin-6), attenuating the depression-CVD mortality association by 12.7% (p < .001). Conclusion: Autonomic dysfunction and inflammation contribute to the increased

cardiovascular mortality risk associated with depression, but a large portion of the predictive LCZ696 price value of depression remains unexplained by these neuroimmunological measures.”
“A new isolate of chicken anemia virus (CAV) was designated GD-1-12. GD-1-12 was isolated from a 12-day-old commercial broiler in Guangdong province, China, in 2012. The GD-1-12 CAV caused high mortality,

severe anemia, thymic atrophy, and subcutaneous hemorrhage in commercial broilers. Here, we report the complete genome sequence of GD-1-12 CAV and comparison with the complete genome sequence of another CAV that was isolated from human fecal samples in China (GenBank accession no. JQ690762). The genomes of the two CAV isolates shared high homology, although a deletion was identified by comparison. The findings from this study provide additional insights into the molecular characteristics of the CAV genomes and should advance knowledge for continuous monitoring and, perhaps, preventing the spread of the virus in chickens as well as in humans.”
“Background: A great deal of research has been devoted to identifying subclinical functional brain abnormalities in manganese (Mn)-exposed welders. However, no previous study has investigated morphological brain abnormalities, such as changes in brain volume, in welders. This study evaluates morphological changes in brain volume among welders, and investigates the relationship between structural brain abnormalities and subclinical dysfunction in this population.

1% lifetime risk of fatal cancer over the baseline risk

1% lifetime risk of fatal cancer over the baseline risk.

Conclusions: Forskolin datasheet At a tertiary care center with experience with managing testicular cancer 78% of patients with more than 5 years of followup exceeded current national and standard safety limits for radiation exposure. Imaging should

be done judiciously in this population at high risk for radiation overexposure.”
“The ability to examine associations between neuro psychiatric conditions and functionally relevant frontal lobe sub-regions is a fundamental goal in neuropsychiatry, but methods for identifying frontal sub-regions in MR (magnetic resonance) images are not well established. Prior published techniques have principally defined gyral regions that do not necessarily correspond to known functional divisions. We present a method in which sulcal-gyral landmarks are used to manually delimit functionally

relevant regions within the frontal lobe: primary motor cortex, anterior cingulate, deep white matter, premotor cortex regions (supplementary motor complex (SMC), frontal eye field and lateral premotor cortex) and prefrontal cortex (PFC) regions (medial PFC, dorsolateral PFC (DLPFC), inferior PFC, lateral orbitofrontal cortex (OFC) and medial OFC). Feasibility was tested by applying the protocol to brain MR data from 15 boys with attention-deficit/hyperactivity disorder (ADHD) and 15 typically developing controls, 8-12 years old. Intra- and inter-rater intraclass correlation coefficients were calculated using parcellation volumes from a subset of that group. Inter-rater results for the 22

hemisphere specific sub-regions ranged from 0.724 to 0.997, with all but seven values Selleck R428 above 0.9. Boys with ADHD showed significantly eFT-508 price smaller left hemisphere SMC and DLPFC volumes after normalization for total cerebral volume. These findings support the method as a reliable and valid technique for parcellating the frontal lobe into functionally relevant sub-regions. (C) 2009 Elsevier Ireland Ltd. All rights reserved.”
“Disorders of iron homeostasis are very common, yet the molecular mechanisms of iron regulation remain understudied. Over 20 years have passed since the first characterization of iron-regulatory proteins (IRP) as mediators of cellular iron-deficiency response in mammals through iron acquisition. However, little is known about other mechanisms necessary for adaptation to low-iron states. In this review, we present recent evidence that establishes the existence of a new iron-regulatory pathway aimed at iron conservation and optimization of iron use through suppression of nonessential iron-consuming processes. Moreover, we discuss the possible links between iron homeostasis and energy metabolism uncovered by studies of iron-deficiency response.”
“Purpose: Primary laparoscopic retroperitoneal lymph node dissection is done at our institution with therapeutic intent and it technically duplicates the open approach.

(C) 2008 Elsevier Ireland Ltd All rights reserved “

(C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Heterozygous mutations of the tissue-specific transcription factor Transmembrane Transproters modulator hepatocyte nuclear factor (HNF)1 beta, cause maturity onset diabetes of the young (MODY5) and kidney anomalies including agenesis, hypoplasia, dysplasia and cysts. Because of these renal anomalies, HNF1 beta is classified as a CAKUT (congenital anomalies of the kidney and urinary tract) gene. We searched for human fetal kidney proteins interacting with the N-terminal region of HNF1 beta using a bacterial two-hybrid system and identified five novel proteins along with the known partner DCoH. The interactions were confirmed for

four of these proteins by GST pull-down assays. Overexpression of two proteins, E4F1 and ZFP36L1, in Xenopus embryos interfered with pronephros formation. Further, in situ hybridization showed overlapping expression of HNF1 beta, E4F1 and ZFP36L1 in the developing pronephros. HNF1 beta is present largely in the nucleus where it colocalized with E4F1. However, ZFP36L1 was located predominantly in the cytoplasm. A nuclear function for ZFP36L1 was shown as it was able to reduce HNF1 beta transactivation in a selleck inhibitor luciferase reporter system. Our studies show novel proteins may cooperate with HNF1 beta in human metanephric

development and propose that E4F1 and ZFP36L1 are CAKUT genes. We searched for mutations in the open reading frame of the ZFP36L1 gene in 58 patients with renal anomalies but found none.”
“Lens epithelium-derived growth factor (LEDGF) can be alternatively spliced to produce two isoforms-LEDGFp52 and LEDGFp75, however, LEDGFp52 has rarely been investigated. The LEDGFp52 protein or its monoclonal antibody was added to primary rat retinal ganglion cell cultures and their impact on neurite number and length, and the mRNA and protein expression levels of GAP-43, NF-L and MAP2 quantified. LEDGFp52

was compared to the addition of ciliary neurotrophic factor (CNTF). LEDGFp52 protein significantly increased primary neurite growth compared to control conditions. In addition, the expression of GAP-43, NF-L and MAP2 genes and proteins were also significantly up-regulated. The positive action of the LEDGFp52 protein was similar to or more efficacious than CNTF. LEDGFp52 appears to be an important regulatory protein for the growth of cell processes. (C) 2008 Elsevier Ireland Ltd. All rights reserved.”
“Renal amyloid deposits can often be seen in primary amyloidosis (immunoglobulin light chain disease) or in secondary forms such as reactive amyloidosis as well as in several hereditary forms where a variety of mutant proteins ‘precipitate’ as amyloid plaques. However, in rare cases, amyloidosis may be identified by renal biopsy, but no definitive diagnosis could be made.

As these studies attempt to exploit the intensity information con

As these studies attempt to exploit the intensity information contained in the MS/MS spectra, a critical step required for a meaningful comparison of this information between MS/MS spectra is peak intensity normalization. We here describe a procedure for quantifying the efficiency of different published normalization methods in terms of the quartile coefficient of dispersion (qcod) statistic.

The quartile coefficient of dispersion is applied to measure the dispersion of the peak intensities between redundant MS/MS spectra, allowing the quantification of the differences in computed peak intensity reproducibility between the different normalization methods. We demonstrate that our results are independent of the data set used in the evaluation procedure, allowing us to provide generic guidance on the choice of normalization method to apply in a certain MS/MS pipeline application.”
“It S3I-201 mw PD0332991 cost is postulated that disruptions of glutamatergic signalling may underlie the pathophysiology of psychosis and schizophrenia. A strong body of evidence indicates that antagonism of the N-methyl-d-aspartate receptor (NMDAR) leads to similar molecular, cellular, cognitive and behavioural changes in rodents and/or humans to those that have been identified to occur in psychosis. One of the main

loci of change appears to comprise the hippocampus, raising the question as to whether changes in hippocampal glutamatergic transmission may drive changes in GABAergic and dopaminergic-mediated signalling in schizophreniform diseases. NMDAR antagonists such as MK801, PCP and ketamine all elicit similar psychosis-related effects, with MK801 inducing the most potent psychotomimetic PF-6463922 supplier reactions.

Treatment with MK801 is associated with a loss of hippocampal synaptic plasticity, hippocampusdependent learning and cognitive deficits. These findings have raised the question as to whether targeting the NMDA receptors or its modulators could prove an effective strategy in treatment of psychosis and schizophrenia. Specifically, the otherwise untreatable negative and cognitive symptoms of schizophrenia currently comprise the highest research priority. A single injection with MK801 has been used to emulate first-episode psychosis in animals. This treatment induces both psychosis-related acute effects but interestingly also persisting consequences, which might be more sensitive as indicators of drug efficacy. Here, we review the current status of the field with regard to the MK801 animal model of firstepisode psychosis and its relevance for the glutamate hypothesis of schizophrenia. Furthermore, we argue that synaptic plasticity may be a better assay for assessing novel schizophrenia therapeutics than behavioural evaluation.

This article is part of the Special Issue entitled ‘Glutamate Receptor-Dependent Synaptic Plasticity’. (C) 2013 Elsevier Ltd.

Here, we investigated the effect of lactic acid on the expression

Here, we investigated the effect of lactic acid on the expression and cellular distribution of AQP 4 in cultured rat astrocytes. After 24 h of incubation, the AQP4 expression AZD9291 in vitro level increased maximally with 35 mM lactic acid. The AQP4 expression levels also increased with hydrochloric acid or acetic acid. In contrast, with sodium lactate, the AQP4 levels did not increase. The increase in AQP4 expression level occurred without a significant increase in AQP4 mRNA expression

level by lactic acid. Under the conditions of de novo protein synthesis inhibition with cycloheximide, lactic acid increased the AQP4 expression level. Furthermore, lactic acid increased the AQP4 expression level on the cell surface of the astrocytes, as determined by a cell surface biotinylation assay and immunocytochemical examination. The increase in AQP4 expression level on the cell membrane of astrocytes induced by lactic acid may be a new regulation mechanism of AQP4 in the brain. (c) 2008 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“Recognition of immunoglobulin G (IgG) by surface receptors for the Fc Histone Methyltransferase inhibitor domain of immunoglobulin G (Fc gamma), Fc gamma Rs, can trigger both Immoral and cellular

immune responses. Two human cytomegalovirus (HCMV)encoded type I transmembrane receptors with Fc gamma-binding properties (vFc gamma Rs), gp34 and gp68, have been identified on the surface of HCW-infected cells and are assumed to confer protection against IgG-mediated immunity. Here we show that Fc gamma recognition by both vFc gamma Rs occurs independently Tucidinostat order of N-linked glycosylation of Fc gamma, in contrast with the properties of host Fc gamma Rs. To gain further insight into the interaction with Fc gamma, truncation mutants of the vFc gamma R gp68 ectodomain were probed for Fc gamma binding, resulting in localization of the Fc gamma binding site on gp68 to residues 71 to 289, a region including an immunoglobulin-like domain. Gel filtration and biosensor binding experiments revealed

that, unlike host Fc gamma Rs but similar to the herpes simplex virus type I (HSV-1) Fc receptor gE-gI, gp68 binds to the C(H)2-C(H)3 interdomain interface of the Fc gamma dimer with a nanomolar affinity and a 2:1 stoichiometry. Unlike gE-gI, which binds Fc gamma at the slightly basic pH of the. extracellular milieu but not at the acidic pH of endosomes, the gp68/Fc gamma complex is stable at pH values from 5.6 to pH 8.1. These data indicate that the mechanistic details of Fc binding by HCMV gp68 differ from those of host Fc gamma Rs and from that of HSV-1 gE-gI, suggesting distinct functional and recognition properties.”
“We studied hippocampal cellular proliferation and neurogenesis processes in a model of transient global cerebral ischemia in gerbils by labelling dividing cells with 5-Bromo-2′-deoxyuridine (BrdU).

Stimulation of the DNA damage response was dependent on viral DNA

Stimulation of the DNA damage response was dependent on viral DNA replication. Inhibition of the DNA damage response prevented both the increase in SfP53 accumulation and H2AX phosphorylation and also caused a 10- to 100-fold reduction

in virus production, along with HDAC inhibitor decreased viral DNA replication and late gene expression. However, silencing of Sfp53 expression by RNA interference did not significantly affect AcMNPV replication or induction of apoptosis by a mutant of AcMNPV lacking the antiapoptotic gene p35, indicating that these processes are not dependent on SfP53 in Sf9 cells.”
“Objective: This study examined whether the manganese superoxide dismutase (MnSOD) gene Ala-9Val single-nucleotide polymorphism (SNP) is associated with neuroleptic-induced tardive dyskinesia (TD) and the severity of the abnormal involuntary movements in Korean schizophrenic patients.

Method: We investigated whether the MnSOD gene Ala-9Val SNP is associated with TD in Korean schizophrenic patients with (n=83) and without(n= 126)TD who were matched for exposure to anti psychotics and other relevant variables.

Results: Logistic

regression analysis revealed that being older(p=0.026) was a risk factor for TD, but that there was no significant association between MnSOD gene and TD, Abnormal involuntary movements were more severe in carriers of the Ala allele than in noncarriers (p=0.044).

Conclusion: These findings do not support that the MnSOD CAL-101 cost gene Selleckchem NU7026 Ala-9Val SNP is associated with TD in Korean schizophrenic patients. However, this polymorphism might be related to the severity of abnormal involuntary movements in this population. (c) 2008 Elsevier Inc. All rights reserved.”
“Nonsyndromic orofacial clefts have a multifactorial etiology, involving both genetic and environmental factors. Although linkage and candidate gene studies have attempted to elucidate the underlying genetic architecture, only the interferon regulatory factor 6 (IRF6) gene

has been identified as causative. The recent introduction of high-throughput genotyping technologies has enabled researchers to perform genome-wide association studies (GWAS). Four GWAS of nonsyndromic cleft lip with or without cleft palate have been conducted, and these have identified five new chromosomal loci. One locus, located in an intergenic region of chromosome 8q24, has been implicated in all GWAS and constitutes a major susceptibility locus. This review describes the latest genetic findings for nonsyndromic orofacial clefts and discusses their biological and functional implications.”
“Traumatic Brain Injury (TBI) is a major cause of morbidity and mortality in civilian and military populations. Interleukin-1beta (IL-1 beta) is a pro-inflammatory cytokine with a key role in the inflammatory response following TBI and studies indicate that attenuation of this cytokine improves behavioral outcomes.

In addition, we detected a significant number of mutations fixed

In addition, we detected a significant number of mutations fixed in the complete

genome consensus sequence of the final viral populations. Among the mutations, events of convergent JIB04 evolution with important phenotypic characteristics occurred in several independent clones. One common change, V35I, in the nuclear localization signal of the p17 protein appeared in four viruses of three different lineages. Other common alterations mapped in position E196K of the reverse transcriptase or in position S316K of the V3 loop of the gp120 residue that is associated with the X4/R5 phenotype. Together with this mutational analysis, we studied the quasispecies heterogeneity of the initial and final viruses, revealing that fitness increase correlated with an augmentation

in the genetic heterogeneity of viral quasispecies. However, while heterogeneity was mostly FK506 clinical trial composed of synonymous (dS) mutations in the first 10 passages performed, at passage 21 it switched to nonsynonymous (dN) substitutions, with significant differences in dN – dS values between passages 11 and 21. In summary, the HIV-1 in vitro fitness recovery depicts a multiphase process occurring first by generation of mutations followed by fixation of the beneficial ones, depicting a classical Darwinian process.”

The aggressive and heterogeneous nature of lung cancer has thwarted efforts to reduce mortality from this cancer through the use of screening. The advent of low-dose helical computed tomography (CT) altered the landscape of lung-cancer screening, with studies indicating that low-dose CT detects many tumors at early stages. The National Lung Screening

Trial (NLST) was conducted to determine whether screening with low-dose CT could reduce mortality from lung cancer.


From August 2002 through April 2004, we enrolled 53,454 persons at high risk for lung cancer at 33 U. S. medical centers. Participants were randomly assigned to undergo three annual screenings with either low-dose CT MK5108 molecular weight (26,722 participants) or single-view posteroanterior chest radiography (26,732). Data were collected on cases of lung cancer and deaths from lung cancer that occurred through December 31, 2009.


The rate of adherence to screening was more than 90%. The rate of positive screening tests was 24.2% with low-dose CT and 6.9% with radiography over all three rounds. A total of 96.4% of the positive screening results in the low-dose CT group and 94.5% in the radiography group were false positive results. The incidence of lung cancer was 645 cases per 100,000 person-years (1060 cancers) in the low-dose CT group, as compared with 572 cases per 100,000 person-years (941 cancers) in the radiography group (rate ratio, 1.13; 95% confidence interval [CI], 1.03 to 1.23).

CONCLUSION: Results of this study strongly suggests that associat

CONCLUSION: Results of this study strongly suggests that associative analysis was able to accurately identify ELTD1 as a putative glioma-associated

biomarker. The detection of ELTD1 was also validated in both rodent and human gliomas and may serve as an additional biomarker for gliomas in preclinical and clinical diagnosis of gliomas.”
“Malaria causes a worldwide annual mortality of about a million people. Rapidly evolving drug-resistant species of the parasite have created a pressing need for the identification of new drug targets and vaccine candidates. By developing fractionation protocols to enrich parasites from low-parasitemia patient samples, we have carried out the first ever proteomics analysis of clinical isolates of early stages of Plasmodium falciparum (Pf) and P. vivax. Patient-derived malarial parasites were directly processed and analyzed using Apoptosis inhibitor shotgun proteomics approach using high-sensitivity MS for protein identification. Our study revealed about 100 parasite-coded gene products that included many known drug targets such as Pf hypoxanthine guanine phosphoribosyl transferase, Pf L-lactate dehydrogenase, and Plasmepsins. In addition, our study reports the expression of several parasite proteins in clinical ring stages that have never been reported in the ring stages of the laboratory-cultivated parasite strain. This proof-of-principle study

represents a noteworthy step forward in our understanding of pathways elaborated by the parasite within the malaria patient and will pave Cell Cycle inhibitor the way towards identification of new drug and vaccine targets that can aid malaria therapy.”
“BACKGROUND: Arteriovenous

malformation (AVM) treatment is multidisciplinary, and the patient may undergo embolization, neurosurgery, or radiosurgery combined. Great improvement in endovascular techniques was provided by the introduction of Onyx with different kinds of approach.

OBJECTIVE: To evaluate the efficacy and the safety of Onyx embolization of brain AVMs with the double arterial catheterization technique (DACT).

METHODS: see more This was a retrospective study. From January 2006 until June 2011, 61 AVMs eligible for the DACT were treated. Forty-one of the 61 AVMs were treated with single arterial catheterization technique and 20 of 61 with DACT; patient age and Spetzler-Martin AVM grade were similar in the 2 groups.

RESULTS: In the DACT group, we obtained complete occlusion of the nidus in all small AVMs, whereas in the single arterial catheterization technique group, we obtained complete occlusion in only 1 of the 36% of the cases. Among the medium-size AVMs, there were no significant differences in the 2 groups, but we performed fewer procedures per patient when we used the DACT (1.4 vs 2.2). In the DACT group, we observed fewer hemorrhagic complications (3.4% vs 12.5% per procedure) and lower morbidity (5% vs 7% per patient) and mortality (0% vs 2.4%) rates.