Cross-linking followed by negative staining and electron microsco

Cross-linking followed by negative staining and electron microscopy suggested a globular structure. The purified TRIM5Rh-21R protein displayed E3-ligase activity in vitro and also self-ubiquitylated in the presence of ubiquitin-activating and -conjugating enzymes. The purified TRIM5Rh-21R protein specifically associated

GW4869 with human immunodeficiency virus type 1 capsid-like complexes; a deletion within the V1 variable region of the B30.2(SPRY) domain decreased capsid binding. Thus, the TRIM5Rh-21R restriction factor can directly recognize retroviral capsid-like complexes in the absence of other mammalian proteins.”
“3,4-Methylenedioximethamphetamine (MDMA, ecstasy) is a worldwide abused stimulant drug, with persistent neurotoxic effects and high prevalence among adolescents. The massive release of 5-HT from pre-synaptic storage vesicles induced by MDMA followed by monoamine oxidase B (MAO-B) metabolism, significantly increases oxidative stress at the mitochondrial level. L-Carnitine and its ester, acetyl-L-carnitine (ALC), facilitate the transport of long chain free fatty acids across the mitochondrial membrane enhancing neuronal anti-oxidative defense. Here, we show the potential of ALC against the neurotoxic effects of MDMA exposure. Adolescent

male Wistar rats were assigned to four groups: control saline solution, isovolumetric to the MDMA solution, administered i.p.; MDMA (4×10 mg/kg MDMA, i.p.); ALC/MDMA (100 mg/kg 30 min of ALC prior to MDMA, i.p.) and ALC (100 mg/kg, i.p.). Rats were killed 2 weeks after exposure and brains AMN-107 supplier were analyzed for lipid peroxidation, carbonyl formation, mitochondrial DNA (mtDNA) deletion Glycogen branching enzyme and altered expression of the DNA-encoded subunits

of the mitochondrial complexes I (NADH dehydrogenase, NDII) and IV (cytochrome c oxidase, COXI) from the respiratory chain. Levels of 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) were also assessed. The present work is the first to successfully demonstrate that pretreatment with ALC exerts effective neuroprotection against the MDMA-induced neurotoxicity at the mitochondrial level, reducing carbonyl formation, decreasing mtDNA deletion, improving the expression of the respiratory chain components and preventing the decrease of 5-HT levels in several regions of the rat brain. These results indicate potential benefits of ALC application in the prevention and treatment of neurodegenerative disorders. (C) 2009 IIBRO. Published by Elsevier Ltd. All rights reserved.”
“The rhesus monkey intrinsic immunity factor TRIM5 alpha(rh) recognizes incoming capsids from a variety of retroviruses, including human immunodeficiency virus type 1 (HIV-1) and equine infectious anemia virus (EIAV), and inhibits the accumulation of viral reverse transcripts. However, direct interactions between restricting TRIM5 alpha proteins and retroviral capsids have not previously been demonstrated using pure recombinant proteins.

This instrument is a substantially improved version of the origin

This instrument is a substantially improved version of the original academic

research instrument described previously by Stoffel and Rowlen (2005a). The addition of hydrodynamic focusing, a self-contained fluidics system and customized software for system control and data analysis has resulted in a commercially viable and available design. Baculovirus samples were provided by Protein Sciences Corporation and blinded to InDevR and Baylor College of Medicine. Protein Sciences Corporation and Baylor College of Medicine analyzed selleck the samples by plaque assay and InDevR analyzed the samples using the Virus Counter. Serial dilution of stock viruses into growth media and buffer allowed for comparison of measured versus intended concentrations. Direct log-scale comparison between pooled Virus Counter results and pooled plaque assay results indicated a linear relationship (slope = 1.1 +/- 0.2, R(2) = 0.86) with statistically significant Pearson correlation (r = 0.93, p < 0.001). (C) 2010 Elsevier B.V. All rights reserved.”
“Our current study aims to evaluate the mechanisms of tranylcypromine (TCP)-mediated

enhancement of nicotine self-administration. We replicated our previous findings which demonstrate that 1 h pretreatment with TCP (3 mg/kg, i.p.) enhances nicotine self-administration (7.5 mu g/kg/inj, i.v.) when compared with vehicle-treated rodents. We tested whether TCP-mediated enhancement of nicotine self-administration was due to MAO inhibition or off-target effects by (i) extending the TCP pretreatment time from 1 to 20 h, and (ii) evaluating the role of the individual TCP stereoisomers in nicotine self-administration studies. While 20 h and (-)TCP pretreatment induced

significant inhibition of MAO (60-90%), animals found nicotine only weakly reinforcing. Furthermore, while both (+) and (+/-) TCP treatment induced nearly 100% MAO inhibition, (+)TCP pretreated Farnesyltransferase animals took longer to acquire nicotine self-administration compared to (+/-)TCP pretreated animals. Stable nicotine self-administration in (+)TCP pretreated animals was influenced by nicotinic receptor activation but not nicotine-paired cues. The opposite was found in (+/-)TCP pretreated animals. Treatment with (-) or (+/-)TCP increased dopamine and serotonin overflow, while the (+) and (+/-)TCP treatment enhanced monoamine overflow subsequent to nicotine. Together, our data suggests TCP enhancement of nicotine self-administration are mediated through mechanisms independent of MAO inhibition, including nicotine-paired cues and monoamine uptake inhibition. (C) 2011 Elsevier Ltd. All rights reserved.”
“The ability to establish the lineage of type A H1N1 and type B human influenza virus strains using a new proteotyping approach is demonstrated. Lineage-specific signature peptides have been determined for the hemagglutinin antigen of type A H1N1 and type B influenza viruses.

However, there is a need to understand how alcohol influences the

However, there is a need to understand how alcohol influences the processing of advisory messages.

The current study used a computerised gambling simulation and investigated whether intoxication would affect the use of a decision aid. Using a double-blind repeated measures design, 16 adult males (aged 18-29) completed the Alcohol Use Disorders Identification Test and the South Oaks

Gambling Screen and played a computer blackjack program on two separate occasions, under differing doses ISRIB of alcohol. On certain conditions, the computerised decision aid gave advice to participants as to whether the odds were in their favour.

Participants were found to take longer to respond to the decision aid under higher risk conditions

when they were losing.

Alcohol intoxication may lead to problems evaluating information pertaining to risk, TPX-0005 nmr and this has implications for the use of other decision aids designed to assist intoxicated individuals. The problems processing warning information were consistent with alcohol induced ‘myopia’ where intoxicated individuals had problems processing less salient cues.”
“Cognitive dysfunction in type 1 and type 2 diabetes share many similarities, but important differences do exist. A primary distinguishing feature of type 2 diabetes is that people with this disorder often (but not invariably) do poorly on measures of learning and memory, whereas deficits in these domains are rarely seen in people with type 1 diabetes. Chronic hyperglycaemia and microvascular disease contribute to cognitive dysfunction in both type 1 and type 2 diabetes, and both disorders are associated with mental and motor slowing and decrements of similar magnitude on measures of attention and executive functioning. Additionally, both types are characterised by neural old slowing, increased

cortical atrophy, microstructural abnormalities in white matter tracts, and similar, but not identical, changes in concentrations of brain neurometabolites. Disconcertingly, the rapid rise in obesity and type 2 diabetes in all age groups might result in a substantial increase in prevalence of diabetes-related cognitive dysfunction.”
“The purpose of the present article is to review our actual knowledge on the desensitization of metabotropic glutamate receptors based on the literature available so far, with the attempt to emphasize all converging data and to give a possible explanation to those evidences that still remain controversial. 1. We review our knowledge on the regulation of mGlu receptors based on the available literature 2. We report converging data and we comment on issues that still remain controversial.

This article is part of a Special Issue entitled ‘Metabotropic Glutamate Receptors’. (c) 2012 Elsevier Ltd. All rights reserved.”
“Alcohol and nicotine are commonly co-abused.

Growth hormone receptor knockout (GHRKO), calorie restriction, an

Growth hormone receptor knockout (GHRKO), calorie restriction, and surgical visceral fat removal constitute experimental interventions to delay aging and increase life span. We examined the expression of known regulators of mitochondriogenesis: peroxisome proliferator-activated receptor gamma co-activator 1 alpha (PGC-1 alpha), adenosine monophosphate (AMP)-activated protein kinase (AMPK), sirtuin-1 (SIRT-1) and sirtuin-3 (SIRT-3), endothelial nitric oxide synthase (eNOS), nuclear respiratory factor-1, mitochondrial VX-770 manufacturer transcription factor A (TFAM), and mitofusin-2 (MFN-2) in the skeletal muscles and hearts of control and calorie-restricted female GHRKO mice and in the kidneys of male GHRKOs after

visceral fat removal or sham surgery. Expression of PGC-1

alpha in skeletal muscles, AMPK, SIRT-1, SIRT-3, eNOS, and MFN-2 in the heart and PGC-1 alpha, AMPK, SIRT-3, eNOS, and MFN-2 in kidneys was increased in GHRKO mice but was not affected by calorie restriction or visceral fat removal. GHRKO SRT2104 mice have increased expression of key regulators of mitochondriogenesis, which is not improved further by calorie restriction or visceral fat removal.”
“Scores of compounds ameliorate cognitive deficits or neuropathology in transgenic mouse models of Alzheimer’s disease (AD), yet these triumphs in mice have not translated into successful therapies for people. Why have studies in mice failed to predict results of human trials? We argue that most transgenic mouse ‘models of AD’ actually simulate the asymptomatic

phase of the disease, and the results of interventional studies in these mice should be considered in the context of disease prevention. In addition, recent advances in imaging technology and biomarker discovery should aid in comparisons of mouse and human neurological status and, importantly, might nearly allow us to predict better the response of people to drugs tested in mice.”
“Catatonia is an infrequent but severe condition in young people. Organic diseases may be associated and need to be investigated though no specific recommendations and guidelines are available.

We extensively reviewed the literature of all the cases of organic catatonia in children and adolescents from January 1969 to June 2007. We screened socio-demographic characteristics, organic diagnosis, clinical characteristics and treatment.

We found 38 cases of children and adolescents with catatonia due to an organic condition. The catatonic syndrome occurred in 21 (57%) females and 16 (43%) males. The mean age of patients was 14.5 years (+/-3.39) [range=7-18 years], and three died from their condition. The organic conditions included infectious diseases (N= 10), neurological conditions (N=10), toxic induced states (N= 12) and genetic conditions including inborn errors of metabolism (N=6). The onset was dominantly acute, and the clinical presentation most frequently stuporous. Although benzodiazepines were recommended as primary symptomatic treatment.

These findings suggest that allogeneic HSCT may overcome the unfa

These findings suggest that allogeneic HSCT may overcome the unfavorable impact of t(6; 9)(p23; q34) as an independent prognostic factor. Leukemia (2012) 26, 461-464; doi:10.1038/leu.2011.229; published online 26 August 2011″
“Introduction: The sigma(1) ligands are considered to be a new class of potential therapeutic agents for several types of central nervous system disorder.

Carbon-11-labeled 1-[2-(3,4-dimethoxyphenyl)ethyl]-4-(3-phenylpropyl)piperazine ([C-11]SA4503) was shown to be a promising PET ligand for mapping sigma(1) receptors, and was applied to measure receptor occupancy with several therapeutic drugs in the living human brain. In this study, we applied this technique for preclinical in vivo screening of novel sigma(1) selective agonists.

Methods: Six newly synthesized piperazine derivatives containing arylalkylamine groups and cyclohexylamine derivatives containing phenyl groups were selected and tested for their in vivo sigma(1) receptor binding with [C-11]SA4503.

The test compounds were administered by intravenous co-injection or oral administration. The in vivo receptor binding of [C-11]SA4503 was evaluated by a tissue dissection method at a single time point.

Results: Our in vivo screen identified the most promising candidate of novel sigma(1) agonist in the piperazine derivatives. Some correlations between in vitro affinity and in vivo receptor blocking rate were observed when considering LY2606368 oral bioavailability. In vivo receptor blocking of piperazine derivatives after oral administration may be predictable by simple co-injection study.

Conclusion: Ligand selection

with [C-11]SA4503 by the in vivo receptor binding assay was performed successfully. This technique is a practical and high-throughput method that can directly evaluate blood-brain barrier permeability, receptor binding, and bioavailability of drug candidates at the same time. (C) 2012 Elsevier Inc. All rights reserved.”
“The PcF protein from Phytophthora cactorum is the first member of the “”PcF toxin family”" from the plant see more pathogens Phytophthora spp. It is able to induce withering in tomato and strawberry leaves. The lack of sequence similarity with other proteins hampers the identification of the molecular mechanisms responsible for its toxicity. Here, we show that the six cysteines form a disulphide pattern that is exclusive for PcF and essential for the protein withering activity. The NMR solution structure identifies a novel fold among protein effectors: a helix-loop-helix motif. The presence of a negatively charged surface suggests that it might act as a site of electrostatic interaction. Interestingly, a good fold match with Ole e 6, a plant protein with allergenic activity, highlighted the spatial superimposition of a stretch of identical residues. This finding suggests a possible biological activity based on molecular mimicry.

including the inferior fronto-occipital fasciculus (IFOF), uncina

including the inferior fronto-occipital fasciculus (IFOF), uncinate fasciculus (UF), and superior longitudinal fasciculus (SLF). Declines in average FA in these tracts, and in average FA of the right inferior longitudinal

fasciculus (ILF), were associated with increased time to completion on the set-shifting subtask of the TMT but not with the simple sequencing subtask. FA values in these tracts were strong mediators of the effect of age on set-shifting performance. Automated tractography methods can enhance PI3K inhibitor our understanding of the fiber systems involved in performance of specific cognitive tasks and of the functional consequences of age-related changes in those systems. (C) 2009 Elsevier Ltd. All rights reserved.”
“Apart from its regulatory role in protease ( PR) activation, little GKT137831 is known about the function of the human immunodeficiency virus type 1 transframe protein p6* in the virus life cycle. p6* is located between the nucleocapsid and PR domains in the Gag-Pol polyprotein precursor and is cleaved by PR during viral maturation. We have recently reported that the central region of p6* can be extensively mutated without abolishing viral infectivity and replication in vitro. However, mutagenesis of the entire p6*-coding sequence in the proviral context is not feasible

without affecting the superimposed

frameshift signal or the overlapping p1-p6(gag) sequences. To overcome these limitations, we created a novel NL4-3-derived provirus by displacing the original frameshift signal to the 3′ end of the gag gene, thereby uncoupling the p6* gene sequence from the p1-p6(gag) reading frame. The resulting virus (AL) proved to be replication competent in different cell cultures and thus represents an elegant tool for detailed analysis of p6* function. Hence, extensive deletions or substitutions were introduced into the p6* gene sequence of the AL provirus, and effects on particle release, protein processing, Unoprostone and viral infectivity were evaluated. Interestingly, neither the deletion of 63% of all p6* residues nor the partial substitution by a heterologous sequence affected virus growth and infectivity, suggesting that p6* is widely dispensable for viral in vitro replication. However, the insertion of a larger reporter sequence interfered with virus production and maturation, implying that the length or conformation of this spacer region might be critical for p6* function.”
“Deficits in working memory (WM) and executive cognitive control are core features of schizophrenia. However, findings regarding functional activation strengths are heterogeneous, partly due to differences in task demands and behavioral performance.

Conclusion: Our results indicate differences in cerebral activati

Conclusion: Our results indicate differences in cerebral activation patterns due to different perceptions of high-calorie food images, modulated by feelings of hunger or satiety, among AN patients with modulation by subjective ratings of food valence. Copyright (C) 2010 S. Karger AG, Basel”
“Herpes simplex virus 2 (HSV-2) strains containing mutations in the virion host shutoff (vhs) protein are attenuated for replication compared with wild-type virus in mouse embryonic fibroblasts (MEFs). However, CDK inhibitor HSV-2 vhs mutants replicate to near wild-type levels in the absence of the RNA-activated protein kinase (PKR). PKR is one of several kinases that phosphorylates

the eukaryotic initiation factor 2 alpha (eIF2 alpha) to inhibit translation initiation, and we previously found that more of the phosphorylated form of eIF2 alpha accumulates in MEFs infected with HSV-2 vhs mutants than with wild-type virus. Here, we show that this increase in phosphorylated eIF2 alpha is primarily PKR dependent. Using selleck chemical MEFs expressing nonphosphorylatable eIF2 alpha, we demonstrate that phosphorylated eIF2 alpha is the primary cause of attenuated replication of HSV-2 vhs mutants and that attenuation correlates with decreased accumulation of viral proteins. Normally, HSV antagonizes eIF2 alpha phosphorylation through the action of

ICP34.5, which redirects protein phosphatase 1 alpha (PP1 alpha) to dephosphorylate eIF2 alpha during infection. We show that ICP34.5 does not accumulate efficiently in MEFs infected with HSV-2 vhs mutant viruses, suggesting that the accumulation of phosphorylated eIF2 alpha and the attenuated phenotype of HSV-2 vhs mutants in MEFs result from a deficiency in ICP34.5.”
“Introduction: Pharmacogenetic factors may explain some of the interindividual variability of response to antidepressants in depressed patients. We focused on P-glycoprotein (P-GP), whose expression depends on a functional polymorphism of the ABCB1 gene (C3435T variants: dbSNP: rs1045642), the 3435CC

genotype being linked Doxorubicin clinical trial to a high level of P-GP expression. Acting as an efflux pump at the blood-brain barrier, P-GP reduces the intracellular penetration of many drugs. Little is known about the interaction between P-GP and response to antidepressants. The objective of this study is to assess whether the response to antidepressants in depression differs in patients with the 3435CC genotype as compared to patients with the 3435CT and 3435TT genotypes. Methods: 117 in-patients with a major depressive episode requiring a new antidepressant treatment were enrolled in this prospective naturalistic 4-week study. Response to antidepressants was assessed using the Hamilton Depression Rating Scale, the Beck Depression Inventory, the Clinician Global Impression Improvement and Therapeutic Index, and weight change. ABCB1 genotyping was performed using the Taqman method.

Donors overall used GPR15 better than did recipients However, wh

Donors overall used GPR15 better than did recipients. However, while several individual pairs showed donor/recipient differences for GPR15 and/or other coreceptors, the direction of the differences was inconsistent, and several pairs had unique alternative coreceptor patterns that were conserved across the transmission barrier. CCR5/CCR2b chimeras revealed that recipients as a group were more sensitive than were donors to replacement of the CCR5 extracellular loops with corresponding regions of CCR2b, but significant differences in this direction were not consistent within pairs. These data show that sexual transmission

does not select for enhanced macrophage tropism, nor for preferential use of any alternative coreceptor. Recipient Envs are somewhat more constrained than are donors in flexibility of CCR5 use, but this pattern is not universal for all pairs, indicating that it is not an absolute requirement.”
“B7 homolog 1 (B7-H1) is a recently discovered immunoresistance protein that is regulated posttranscriptionally after PTEN loss in

malignant glioma, a deadly form of brain tumor. Here, the impact of gamma-interferon-mediated activation of B7-H1 was investigated in glioblastoma patients with PTEN loss. Lymphocytes and T cells were selected for apoptosis assays after 1 : 1 coculture with autologous glioma cells. Gamma interferon treatment of PTEN-deficient tumors resulted in superinduction of B7-H1 protein that correlated with increased T-cell apoptosis, an effect dependent upon activation of the PI3-kinase pathway. The combination GDC973 of PTEN loss and gamma-interferon exposure in glioblastoma patients results in an exceptionally immunoresistant phenotype that may negate adaptive immunity through induction of T-cell apoptosis. NeuroReport 20:1597-1602 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.”
“Human papillomavirus type 16 (HPV16) has been identified as being the most common etiological agent leading to cervical cancer. Despite having a clear understanding of the role of HPV16 in oncogenesis, details of how HPV16 traffics during infection are poorly understood. HPV16 has been

determined to enter via clathrin-mediated endocytosis, but the subsequent steps of HPV16 infection remain unclear. There is emerging evidence that several Methocarbamol viruses take advantage of cross talk between routes of endocytosis. Specifically, JCV and bovine papillomavirus type 1 have been shown to enter cells by clathrin-dependent endocytosis and then require caveolin-1-mediated trafficking for infection. In this paper, we show that HPV16 is dependent on caveolin-1 after clathrin-mediated endocytosis. We provide evidence for the first time that HPV16 infection is dependent on trafficking to the endoplasmic reticulum (ER). This novel trafficking may explain the requirement for the caveolar pathway in HPV16 infection because clathrin-mediated endocytosis typically does not lead to the ER.

OBJECTIVE: To analyze whether ICG can

be used to analyze

OBJECTIVE: To analyze whether ICG can

be used to analyze and confirm perfusion Selumetinib order changes early after SAH.

METHODS: We prospectively enrolled 11 patients with acute SAH within the past 24 hours and 14 patients undergoing surgery for unruptured aneurysms. Cortical ICG videography was performed, and offline analysis included the arterial, parenchymal, and venous cortical compartment. Transit times, signal gradient, maximum of fluorescence intensity, and the area under the curve were calculated as surrogate markers for perfusion characteristics.

RESULTS: Arterial, parenchymal, and venous transit times were comparable in both groups. The velocity of signal change in SAH patients was significantly lower in all 3 compartments

(P < .001, P < .01, P < .001, respectively), as was the peak fluorescence intensity (P < .001). In SAH patients, fluorescence intensity did not vary between areas with and without diffuse cortical blood. Area under the curve analysis showed significantly lower Selleck PD0325901 values in SAH patients compared with the control group (P < .001).

CONCLUSION: Cortical ICG videography and analysis are feasible during surgery. Patients early after SAH have a significantly lower velocity of signal change, lower peak of fluorescence intensity, and lower overall area under the curve, but similar transit times. This technique can be used to quantify perfusion alteration, in this case, acute SAH, and may be used as an adapted

measurement tool for intraoperative therapy.”
“The papillomavirus E1 helicase is recruited by E2 to the viral Aprepitant origin, where it assembles into a double hexamer that orchestrates replication of the viral genome. We previously identified the cellular WD40 repeat-containing protein p80/UAF1 as a novel interaction partner of E1 from anogenital human papillomavirus (HPV) types. p80 was found to interact with the first 40 residues of HPV type 31 (HPV31) E1, and amino acid substitutions within this domain abrogated the maintenance of the viral episome in keratinocytes. In this study, we report that these p80-binding substitutions reduce by 70% the ability of E1 to support transient viral DNA replication without affecting its interaction with E2 and assembly at the origin in vivo. Microscopy studies revealed that p80 is relocalized from the cytoplasm to discrete subnuclear foci by E1 and E2. Chromatin immunoprecipitation assays further revealed that p80 is recruited to the viral origin in an E1- and E2-dependent manner. Interestingly, overexpression of a 40-amino- acid-long p80-binding peptide, derived from HPV31 E1, was found to inhibit viral DNA replication by preventing the recruitment of endogenous p80 to the origin. Mutant peptides defective for p80 interaction were not inhibitory, demonstrating the specificity of this effect.

This study addressed the hypothesis that atrium-specific drug del

This study addressed the hypothesis that atrium-specific drug delivery through an amiodarone-eluting epicardial patch reduces vulnerability to atrial tachyarrhythmias, whereas ventricular and plasma drug concentrations are minimized.

Methods: Right atrial epicardiums of goats were fitted with electrodes and a bilayered patch (poly[ethylene glycol]-based matrix and poly[lactide-co-caprolactone] backing layer) loaded with amiodarone (10 mg per patch, n=10) or without drug (n=6). Electrophysiologic parameters (atrial effective refractory period, conduction time, and rapid atrial response to burst pacing) and amiodarone

levels in plasma and tissue were measured during 1 month’s follow-up.

Results: Epicardial application of amiodarone-eluting patches produced persistently higher drug concentrations in the right atrium than in Ispinesib research buy the left atrium, ventricles, and extracardiac tissues by 2 to 4 orders of magnitude. Atrial effective refractory period and conduction time increased, whereas rapid atrial Selleck SGC-CBP30 response inducibility decreased significantly (P<.05) during the 1-month

follow-up compared with that seen in animals treated with drug-free patches. Amiodarone concentrations in plasma remained undetectably low (<10 ng/mL).

Conclusions: Atrium-specific drug delivery through an amiodarone-eluting patch produces therapeutic atrial drug concentrations, whereas ventricular and systemic drug levels are minimized. This study demonstrates that sustained targeted drug delivery to a specific heart chamber is feasible and might reduce the risk for ventricular and extracardiac adverse effects. Epicardial application of amiodarone-eluting patches is a promising strategy to prevent postoperative atrial fibrillation. (J Thorac Cardiovasc Surg 2010; 140: 904-10)”
“BACKGROUND: The number of spine operations performed in the elderly population is rising.

OBJECTIVE: To identify and describe perioperative and postoperative complications in patients 70 years and older who have undergone minimally invasive lumbar interbody spine fusion.


A retrospective analysis was performed on 66 consecutive patients aged 70 years or older who underwent a minimally invasive interbody lumbar fusion. Electronic medical records were analyzed for patient demographics, ADAMTS5 procedures, and perioperative and postoperative complications.

RESULTS: Between 2000 and 2009, 66 patients with an average age of 74.9 years (range, 70-86 years) underwent 68 lumbar interbody fusions procedures. The mean follow-up was 14.7 months (range, 1.5-50 months). The minimally invasive approaches included 41 cases of extreme lateral interbody fusion and 27 minimally invasive transforaminal lumbar interbody fusions. We observed 5 major (7.4%) and 17 minor (25%) complications. The 5 major complications consisted of 4 cases of interbody graft subsidence and 1 adjacent level disease. There were no intraoperative medical complications.