Unexpected cell-specific and stress-specific NF-kappa B activation found in the inner ear in this in vivo study suggest that this approach may have

wide applications in demonstrating similar specializations of stress responses in other tissues, including the brain. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“We studied the stimulus characteristics necessary for the expression of c-fos protein in optokinetic system neurons using immunocytochemistry. Using whole-field visual motion as a stimulus, we found substantial c-fos expression in the optic tectum (TeO), the nucleus of the basal optic root (nBOR) and the pretectal nucleus lentiformis mesencephali (LM); in all cases immunostaining was seen only on the side contralateral to the eye Alvocidib molecular weight viewing whole-field unidirectional motion; the side of the brain contralateral to the eye wearing a diffuser showed no staining. In the nBOR and the LM, different regions showed a remarkable specificity of c-fos expression depending on the direction of visual motion stimulation. Neurons were stained primarily in regions known from previous electrophysiological recordings to be maximally responsive Idasanutlin to that direction of motion; little staining was seen after

motion orthogonal to the preferred motion direction. Novel, continuous visual motion stimuli, lasting more than 30 min, was required for maximal c-fos expression, suggesting that brief periods of unidirectional optic flow, as would be experienced during normal life, do not stimulate the expression of c-fos. The largest number of neurons was labeled when birds raised from hatching with one eye covered by a diffuser were exposed to full-field visual motion immediately after the diffuser was switched from one eye to the other,

so that only the previously naive eye was visually stimulated. We conclude that the expression of c-fos in the optokinetic nuclei is linked to near peak firing rates on the one hand, and the novelty and duration of the visual signals, on the other, supporting the assumption that this expression is mainly MYO10 related to stimulus contexts leading to neuronal plastic changes. (C) 2009 IBRO. Published by Elsevier Ltd. All rights reserved.”
“Recent evidence suggests that extracellular ATP modulates retinal processing and could play a role in modulating glial cells during retinal diseases. Here, we evaluated the localization of P2Y(1) receptors in the rat retina using indirect immunofluorescence immunocytochemistry. We observed labeling within defined populations of inner retinal neurons and Muller cell processes and end feet. Double labeling of P2Y(1) receptor with choline acetyltransferase revealed extensive colocalization indicating the expression of this receptor by cholinergic amacrine cells. Ganglion cell labeling for P2Y(1) receptors was also observed.

Interstage mortality was not significantly reduced by our program. However, 1-year transplant-free survival was significantly improved in patients in the Single Ventricle Program. (J Thorac Cardiovasc Surg 2011;142:1358-66)”
“Objectives: Various radionuclide-labeled somatostatin analogues are used

currently for diagnosis and therapy of neuroendocrine tumors. In particular, [Ga-68]Ga-DOTA-TOC is commonly used for diagnosis, while [Lu-177]Lu-DOTA-TATE is used for therapy. With the development of theranostics and personalized medicine where the imaging diagnosis is tailored to the subsequent radiotherapy, it is of paramount importance to investigate the relevance of the ligand exchange. The aim of this study was to compare binding capacity of [Ga-67/68]Ga-DOTA-TOC ([Ga-67/68]Ga-N-(4,7,10-(tris(carboxymethyl)-1,4,7,10-tetraazacyclododecan-1-yl)acetyl-D-Phe-c[Cys-D-Tyr-Trp-Lys-Thr-Cys]-Thr(ol)) find more and [Ga-67/68]Ga-DOTA-TATE ([Ga-67/68]Ga-N-(4,7, 10-(tris(carboxymethyl)-1,4,7,10-tetraazacyclododecan-1-yl)acetyl-D-Phe-c[Cys-D-Tyr-Trp-Lys-Thr-Cys]-Thr)

in vitro in monkey brain cryosections and in vivo in the rat, where, in contrast to transfected cell lines, there is a heterogeneous distribution of somatostatin receptor (SSTR) subtypes. The influence selleck products of various production methods of [Ga-68]Ga-DOTA-TOC and [Ga-68]Ga-DOTA-TATE on the biological performance of the tracers was also studied.

Material and Methods: [Ga-67]Ga-DOTA-TOC,

[Ga-68]Ga-DOTA-TOC, [Ga-67]Ga-DOTA-TATE and [Ga-68]Ga-DOTA-TATE were synthesized including preconcentration and purification of the generator eluate. The binding of the radioligands was assessed in vitro using autoradiography on cryosections of Rhesus monkey brains and in vivo/ex vivo using organ distribution studies in rats.

Results and Discussion: The tracer production method was improved in terms of higher robustness, simplification and good manufacturing practice (GMP) relevance. The synthesis variation did not influence the biological performance of the tracers. There was no statistically significant difference observed in the binding of [Ga-67/68]Ga-DOTA-TOC Tobramycin and [Ga-67/68]Ga-DOTA-TATE either in brain cortex in vitro or in rat biodistribution and uptake in SSTR-positive tissues such as pancreas, adrenals and pituitary. The uptake in these organs was precluded by the excess of octreotide (Sandostatin). The 10-fold higher affinity to SSTR2 of DOTA-TATE as compared to DOTA-TOC known from studies in transfected cells was reflected in a slightly more intense binding of [Ga-67/68]Ga-DOTA-TATE than of [Ga-67/68]Ga-DOTA-TOC in the monkey brain sections in vitro, but not in vivo in the rat.

Conclusion: A robust Ga-68-labeling method was introduced.

None of the 12 normal- and disease-control muscle biopsies contained conformational or PHF-1 immunoreactive tau. This first demonstration of conformational tau in s-IBM, because of its abundance in non-atrophic muscle fibers, suggests that it might play an early role in s-IBM PHFs formation and thus be pathogenically important. (C) 2011 Elsevier Ireland Ltd. All rights reserved.”
“Objective: The Levitronix CentriMag (Levitronix LLC, Waltham, Mass) ventricular assist system

is designed for temporary left, right, or biventricular support. Advantages include ease of use, excellent reliability, and low thrombosis risk,. which may allow wider application of short-term support and improved outcomes in patients with Cobimetinib cardiogenic shock. This multi-institutional study evaluated

safety, effectiveness, and outcomes of the CentriMag in patients with cardiogenic shock.

Methods: Thirty-eight patients were supported at 7 centers. Patients included 12 after cardiotomy, 14 after myocardial infarction, and 12 with right ventricular failure after implantable left ventricular assist device placement. Devices were implanted in left (n = 8), right (n = 12), or biventricular (n = 18) configuration. Support was continued until recovery, transplantation, or implantation see more of long-term ventricular assist device.

Results: Mean support duration for the entire cohort (n = 38) was 13 days (1-60 days), with 47% of patients (18/38) surviving 30 days after device removal. Mean CentriMag biventricular support (n = 18) duration was 15 days (1-60 days), with 44% (8/18) surviving at 30 days. Mean CentriMag right ventricular support with a commercially available

left ventricular assist device (n = 12) duration was 14 days (1-29 days), with 58%(7/12) surviving at 30 days. Complications included bleeding (21%), infection (5%), respiratory failure (3%), hemolysis (5%), and Dimethyl sulfoxide neurologic dysfunction (11%). There were no CentriMag or pump failures.

Conclusions: In this preliminary study, the CentriMag provided short-term support for patients with cardiogenic shock with a low incidence of device-related complications and no device failures. (J Thorac Cardiovasc Surg 2011;141:932-9)”
“Huntington disease (HD) is caused by the expansion of polyglutamine (polyQ) repeats in the amino-terminal of hungtintin (htt). PolyQ-expanded htt forms intracellular ubiquitinated aggregates in neurons and causes neuronal cell death. Here, utilizing a HD cellular model, we report that Tollip, an ubiquitin binding protein that participates in intracellular transport via endosomes, co-localizes with and stimulates aggregation of polyQ-expanded amino-terminal htt. Furthermore, we demonstrate that Tollip protects cells against the toxicity of polyQ-expanded htt.

Recently, it has become apparent that microRNAs (miRNAs) also contribute to EBV’s oncogenic properties; recombinant EBVs

that lack the BHRF1 miRNA cluster display a reduced ability to selleck chemical transform B lymphocytes in vitro. Furthermore, infected cells evince a marked upregulation of the EBNA genes. Using recombinant viruses that lack only one member of the cluster, we now show that all three BHRF1 miRNAs contribute to B-cell transformation. Recombinants that lacked miR-BHRF1-2 or miR-BHRF1-3 displayed enhanced EBNA expression initiated at the Cp and Wp promoters. Interestingly, we find that the deletion of miR-BHRF1-2 reduced the expression level of miR-BHRF1-3 and possibly that of miR-BHRF1-1, demonstrating that the expression of one miRNA can potentiate the expression of other miRNAs located in the same cluster. Therefore, the phenotypic traits of the miR-BHRF1-2 null mutant could result partly from reduced miR-BHRF1-1 and miR-BHRF1-3 expression levels. Nevertheless, using an miR-BHRF1-1 and miR-BHRF1-3 double mutant, we could directly assess and confirm the contribution of miR-BHRF1-2 to B-cell transformation. Furthermore, we found that the potentiating effect

of miR-BHRF1-2 on miR-BHRF1-3 synthesis can be reproduced with simple expression plasmids, provided that both miRNAs are processed from the same transcript. Therefore, this enhancing effect does not result from an idiosyncrasy of the EBV genome but rather reflects a general property of these miRNAs. This study highlights the advantages Z-IETD-FMK of arranging the BHRF1 miRNAs in clusters: it allows the synchronous and synergistic expression of genetic elements that cooperate to transform their target cells.”
“Introduction Mirtazapine is a racemic antidepressant with a multireceptor profile. Previous studies have shown that the enantiomers of mirtazapine have different

Ureohydrolase pharmacologic effects in the brain of laboratory animals.

Materials and methods In the present study, we used positron emission tomography (PET) and autoradiography to study effects of (R)- and (S)-[(11)C]mirtazapine in the human brain. Detailed brain imaging by PET using three methods of kinetic data analysis showed no reliable differences between regional binding potentials of (R)- and (S)-[(11)C]mirtazapine in healthy subjects.

Results Autoradiographic studies carried out in whole hemispheres of human brain tissue showed, however, that (R)- and (S)-mirtazapine differ markedly as inhibitors of [(3)H]clonidine binding at alpha(2)-adrenoceptors.

Conclusions The multireceptor binding profiles of mirtazapine enantiomers, along with individual differences between subjects, may preclude PET neuroimaging from demonstrating reliable differences between the regional distribution and binding of (R)- and (S)-[(11)C]mirtazapine in the living human brain.

Unbalanced CREB/ICER expression needs to be considered a pathogenetic feature in leukemogenesis. The molecular characterization of this pathway

could be useful for novel therapeutic strategies.”
“Background Schistosoma japonicum causes an infection involving humans, livestock, and snails and is a significant cause of morbidity in China.

Methods We evaluated a comprehensive control strategy in two intervention villages and two control Selleck LY3023414 villages along Poyang Lake in the southeastern province of Jiangxi, where annual synchronous chemotherapy is routinely used. New interventions, implemented from 2005 through 2007, included removing cattle from snail- infested grasslands, providing farmers with mechanized farm equipment, improving sanitation by supplying

tap water and building lavatories and latrines, providing boats with fecal- matter containers, and implementing an intensive health- education program. During the intervention period, we Gemcitabine supplier observed changes in S. japonicum infection in humans, measured the rate of infection in snails, and tested the infectivity of lake water in mice.

Results After three transmission seasons, the rate of infection in humans decreased to less than 1.0% in the intervention villages, from 11.3% to 0.7% in one village and from 4.0% to 0.9% in the other ( P< 0.001 for both comparisons). The rate of infection in humans in control villages fluctuated but remained at baseline levels. In intervention villages, the percentage of sampling sites with infected snails decreased from 2.2% to 0.1% in one grassland area and from 0.3% to no infection in the other ( P< 0.001 for both comparisons). The rate of infection in mice after exposure to lake water decreased from Methisazone 79% to no infection ( P< 0.001).

Conclusions A comprehensive control strategy based on interventions to reduce the rate of transmission of S. japonicum infection from cattle and humans to snails was highly effective. These interventions have been adopted as the national strategy to control schistosomiasis in China.”
“Recent retrospective studies

of heterogeneously treated patients have suggested that chromosomal aberrations of the MYC gene locus indicate an unfavorable prognosis in diffuse large B-cell lymphoma (DLBCL). Here, we investigated the prognostic impact of MYC aberrations analyzed by interphase fluorescence in situ hybridization in 177 patients with de novo DLBCL treated within the two prospective, randomized trials non-Hodgkin’s lymphoma NHL-B1 and NHL-B2. MYC aberrations were detected in 14 DLBCL (7.9%). In a univariate analysis compared with MYC-negative DLBCL, MYC-positive cases showed a significantly shorter overall survival (OS) (P = 0.047) and relevantly, though not significantly, shorter event-free survival (EFS) (P = 0.062).

“
“Earlier studies suggest that opioid receptors in the ventral tegmental area, but not the nucleus accumbens (NAc), play a role in relapse to drug-seeking behavior. However, environmental stimuli that elicit relapse also release

the endogenous opioid beta-endorphin in the NAc. Using a within-session extinction/reinstatement paradigm in rats that self-administer cocaine, we found that NAc infusions of the muopioid receptor (MOR) agonist DAMGO moderately reinstated responding on the cocaine-paired lever at low doses (1.0-3.0 ng/side), whereas the delta-opioid receptor (DOR) agonist DPDPE induced greater responding at higher doses (300-3000 ng/side) that also enhanced inactive lever responding. Using doses of either agonist that induced responding on only the cocaine-paired lever, we found that DAMGO-induced responding CP673451 mouse was blocked selectively by pretreatment with the MOR antagonist, CTAP, whereas DPDPE-induced responding was selectively blocked by the DOR antagonist, naltrindole. Cocaine-primed reinstatement was blocked

by intra-NAc CTAP but not naltrindole, indicating a role for endogenous OICR-9429 supplier MOR-acting peptides in cocaine-induced reinstatement of cocaine-seeking behavior. In this regard, intra-NAc infusions of beta-endorphin (100-1000 ng/side) induced marked cocaine-seeking behavior, an effect blocked by intra-NAc pretreatment with the MOR but not DOR antagonist. Conversely, cocaine seeking elicited by the enkephalinase inhibitor thiorphan (1-10 mu g/side) was blocked by naltrindole but not CTAP. MOR stimulation in more dorsal caudate-putamen sites was ineffective, whereas DPDPE infusions induced cocaine seeking. Together, these findings establish

distinct roles for MOR and DOR in cocaine relapse and suggest that NAc MOR could be an important therapeutic target to neutralize the effects of endogenous beta-endorphin release on cocaine relapse. Neuropsychopharmacology (2009) 34, 1946-1957; doi: 10.1038/npp.2009.28; published online 11 March 2009″
“Severe acute respiratory syndrome (SARS), which is caused by a novel coronavirus (CoV), is a highly communicable disease with the lungs as the major pathological target. Although Atezolizumab chemical structure SARS likely stems from overexuberant host inflammatory responses, the exact mechanism leading to the detrimental outcome in patients remains unknown. Pulmonary macrophages (M phi), airway epithelium, and dendritic cells (DC) are key cellular elements of the host innate defenses against respiratory infections. While pulmonary M phi are situated at the luminal epithelial surface, DC reside abundantly underneath the epithelium. Such strategic locations of these cells within the airways make it relevant to investigate their likely impact on SARS pathogenesis subsequent to their interaction with infected lung epithelial cells. To study this, we established highly polarized human lung epithelial Calu-3 cells by using the Transwell culture system.

Active surveillance started on the date of the second biopsy. Actuarial rates of remaining on active surveillance were calculated and univariate Cox regression was used to assess predictors of discontinuing active surveillance.

Results: With a median followup of 29 months 43 patients ultimately received active treatment. The 2 and 5-year probabilities of remaining on active surveillance INCB018424 were 91% and 75%, respectively. Patients with cancer on the second biopsy (HR 2.23, 95% CI 1.23-4.06, p = 0.007) and a higher number of cancerous cores from the 2 biopsies combined (p = 0.002) were more likely to undergo treatment.

Age, prostate specific antigen, clinical stage, prostate volume and number of total biopsy cores sampled were not predictive of outcome. Skeletal metastases developed in 1 patient 38 months after starting active surveillance. Of the 43 patients undergoing delayed treatment 41 (95%) are without disease progression at a median of 23 months following treatment.

Conclusions: With a median followup of 29 months active surveillance for select

patients appears to be safe and associated with a low risk of systemic progression. Cancer at restaging biopsy and a higher total number of cancerous cores are associated with a lower likelihood of remaining on active surveillance. A restaging biopsy should be strongly considered to finalize eligibility for active surveillance.”
“When the 34 kDa kinase S3I-201 solubility dmso domain of human spleen tyrosine kinase (Syk-KD) was expressed as a C-terminally His-tagged protein in baculovirus-infected Sf-21 insect cells, the purified protein included two forms that migrated slightly differently in SDS-polyacrylamide gel electrophoresis. Intact mass analysis and LC-MS/MS peptide mapping showed that the major and faster-migrating Celastrol product had the intended amino-acid sequence and 0-6 phosphorylations. This material accounted

for about 95% of the purified protein. The minor product was Syk-KD with a 26 amino-acid N-terminal extension. The result suggested the existence of an upstream alternative site for the initiation of translation, and this proved to be an ACG codon derived from the pBacPAK9 vector used to express Syk-KD. The ACG codon was preceded and followed by Kozak-type sequence elements (a purine in the 3 position and a G in the +4 position) that would have enhanced the viability of initiation at ACG. The initiating amino-acid residue was Met for both minor and major products, and both forms of the protein were alpha-N-acetylated. For the minor product, protein intact mass analysis and peptide mapping both gave results in agreement with the sequence predicted from the DNA.

E1A-13S is essential for activating viral transcription in the early phase of infection. Coimmunoprecipitation assays showed that E1A-13S preferentially interacts with only one (PML-II) of at least six nuclear human PML isoforms. Deletion mapping located the interaction site within E1A conserved region 3 (CR3), which was previously described as the transcription factor binding region of E1A-13S. Indeed, cooperation with PML-II enhanced E1A-mediated transcriptional activation,

while deleting the SUMO-interacting motif (SIM) of PML proved even more effective. Our results suggest that in contrast to PML NB-associated antiviral defense, PML-II may help transactivate viral gene expression and therefore play a novel role in activating Ad transcription during the early viral life cycle.”
“The development of treatments for Alzheimer’s disease (AD) is currently shifting away from the correction www.selleckchem.com/products/jq-ez-05-jqez5.html of neurotransmitter abnormalities and from attempts to remove the pathognomonic protein deposits. Drug discovery is heading towards novel types of pharmacological interventions which are aimed at more central and upstream pathophysiological events. The large number of upcoming treatment targets can be grouped into two major categories. The first category consists of antecedents of beta amyloid peptide (A beta) and TAU deposition including A beta

Tozasertib research buy production, degradation and clearance, TAU hyperphosphorylation and aggregation. The second consists of protectors against neuronal dysfunction and premature death such as mitochondrial functioning, nerve growth and regeneration, and neuronal membrane integrity. It is hoped

that some of these strategies will not only have larger symptomatic effects than the currently available drugs but also an impact on the underlying neurodegeneration. Since the novel treatments will be typically administered Florfenicol over years they must meet high standards of safety, drug-drug compatibility, and tolerability. Probably the most important target groups for novel treatments are carriers of mutations causing AD, and individuals with minor cognitive impairment representing a pre-dementia stage of the disease. To minimise incorrect case identifications, drug development must be paralleled by improved diagnostic techniques. Novel pharmacological strategies may be cost-effective if disability and need of full-time care can be postponed or prevented without prolonging time lived with dementia or extending survival. We are uncertain whether the advent of novel disease-retarding strategies will revolutionise the management of AD. Symptomatic treatments will continue to be needed, and psychosocial approaches will retain an essential role in supporting affected individuals and their families. (C) 2010 Elsevier Inc. All rights reserved.

(C) 2013 Elsevier Masson SAS. All rights reserved.”
“factors Tideglusib play an important role in the understanding of clinical response to antipsychotic treatments. We aimed to assess the effect of the catechol-O-methyltransferase (COMT) genotype in the short-term (6 weeks) clinical response of 161 first-episode

psychosis patients. COMT genotype was not related to clinical response at 6 weeks. Val homozygote patients showed higher negative symptoms than Met homozygote patients. The COMT Val158 genotype seems to be related to the severity of negative symptoms rather than to clinical response. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Batai virus (BATV) is a widely distributed but poorly studied member of the Orthobunyavirus genus in the family Bunyaviridae and is of particular interest as a known participant in natural reassortment events. Both research and surveillance efforts on this and other related viruses have been hampered https://www.selleckchem.com/products/Temsirolimus.html by the lack of available full-length sequence data covering all three genomic segments. Here, we report the complete genome sequence of four BATV strains (MM2222, Chittoor/IG-20217, UgMP-6830, and MS50) isolated from various geographical locations. Based on these data, we have determined that strain MS50 is in fact unrelated to BATV and likely represents as a novel genotype in the genus Orthobunyavirus.”
“Aim of the study. – The objective of this preliminary study was to evaluate the effectiveness, in terms of

fall reduction, of an in-home strategy that we have developed Etomidate for elderly falters. We also aimed at

finding links between the expected changes in the data obtained in static posturography and in clinical balance tests through our program.

Patients and methods. – Twelve elderly patients living at home who were diagnosed as falters (5 males and 7 females; 77.9 +/- 4.1 years) participated in the study. Our multimodal intervention lasted 6 months. Before this period, and one year later, an evaluation was conducted using cognitive (MMSE), clinical balance tests (i.e. Berg Balance Scale, Balance One leg, Timed Up and Go, and Functional Reach tests) and static posturography (where the area of body sway, velocity and medio-lateral and antero-posterior amplitudes were recorded twice, first with eyes open and then with eyes closed).

Results. – Among the 12 patients who were diagnosed as falters, eight became non-fallers. When comparing data obtained after the intervention with those obtained beforehand, we found significant changes in all of the clinical balance tests and in the posturographic-derived variables indicating improvements in the balance control in our group of subjects. We also found significant correlations between the changes in the Berg Balance Scale scores and the changes in the area of body sway data, in antero-posterior amplitude both with eyes open and with eyes closed, and also in the media lateral amplitude in the eyes closed condition.

Conclusions.

As a defense mechanism in prostate cancer cells, the fatty acid synthesis pathway harnesses

its oxidizing power for improving the redox balance despite conditions of extreme hypoxia, potentially altering Cu-ATSM hypoxia selectivity.

Methods: Human prostate tumor-cultured cell lines (PC-3, 22Rv1, LNCaP and LAPC-4), were treated with a fatty acid synthase (FAS) inhibitor (C75, 100 mu M) under anoxia. The 64 Cu-ATSM uptake in these treated cells and nontreated anoxic cells was then examined. Fatty acid synthase expression level in each cell line was subsequently quantified by ELISA. An additional study was performed in PC-3 cells to examine the relationship between the restoration of 64 Cu-ATSM hypoxia selectivity and the concentration of C75 (100, 20, 4 or 0.8 mu M) administered to the cells.

Results: Inhibition of fatty acid synthesis

with C75 resulted in a significant increase selleck chemicals in (CU)-C-64 -ATSM retention in prostate tumor cells in vitro under anoxia over 60 min. Inhibition studies demonstrated higher uptake values of 20.9 +/- 3.27%, 103.0 +/- 32.6%, 144.2 +/- 32.3% and 200.1 +/- 79.3% at 15 min over control values for LAPC-4, PC-3, LNCaP and 22Rv1 cells, respectively. A correlation was seen (R-2 =.911) with FAS expression plotted against percentage change in Cu-64-ATSM uptake with C75 treatment.

Conclusions: 3-MA ic50 Although Cu-ATSM has clinical relevance in the PET imaging of hypoxia in many tumor types, its translation to the imaging of prostate cancer may

be limited by the overexpression of FAS associated with prostatic malignancies. (C) 2008 Elsevier Inc. All rights reserved.”
“Template switching between copackaged human immunodeficiency virus type 1 (HIV-1) genomic RNAs is genetically silent when identical RNAs are copackaged but yields recombinants when virions contain two distinct RNAs. Sequencing has revealed that errors at retroviral recombination junctions are infrequent, suggesting that template switching is not intrinsically mutagenic. Here, we tested the hypothesis that template Verteporfin cell line switching may instead contribute to replication fidelity. This hypothesis predicts that reverse transcription of a single-copy gene will be more error prone than replication in the presence of a second copy. To test this, HIV-1-based vectors containing both lacZ and the puromycin resistance marker were expressed either alone or with an excess of an “”empty”" vector lacking lacZ and puro. This resulted in virions with either RNA homodimers or haploid genomes with only a single lacZ-puro RNA. In untreated cells, lacZ inactivation rates suggested that haploid vector reverse transcription was slightly more error prone than that of homodimerized pseudodiploid vectors. Haploid reverse transcription was at least threefold more error prone than pseudodiploid-templated synthesis when slowed by hydroxyurea treatment or stopped prematurely with zidovudine.