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PubMed2000

Quantification of viral ribonucleic acid in plasma of cats naturally infected with feline immunodeficiency virus.

OBJECTIVE: To assess plasma viral RNA concentration in cats naturally infected with feline immunodeficiency virus (FIV). ANIMALS: 28 FIV-infected cats. PROCEDURE: Cats were categorized into 1 of the 3 following stages on the basis of clinical signs: asymptomatic (nonclinical) carrier (AC; n = 11), acquired immunodeficiency syndrome-related complex (ARC; 9), or acquired immunodeficiency syndrome (AIDS; 8). Concentration of viral RNA in plasma (copies per ml) was determined by use of a quantitative competitive polymerase chain reaction (QC-PCR) assay. Total lymphocyte count, CD4+ cell and CD8+ cell counts, and the CD4+ cell count-to-CD8+ cell count ratio were determined by use of flow cytometry. RESULTS: Plasma viral RNA concentration was significantly higher in cats in the AIDS stage, compared with cats in AC and ARC stages. Most (5/7) cats in the AIDS stage had low total lymphocyte, CD4+ cell, and CD8+ cell counts. CONCLUSIONS AND CLINICAL RELEVANCE: Concentration of plasma viral RNA is a good indicator of disease progression in FIV-infected cats, particularly as cats progress from the ARC to the AIDS stage. Determination of CD4+ and CD8+ cell counts can be used as supportive indicators of disease progression.

Animals↗

PubMed2004

Range of retinal diseases potentially treatable by AAV-vectored gene therapy.

Viable strategies for retinal gene therapy must be designed to cope with the genetic nature of the disease and/or the primary pathologic process responsible for retinal malfunction. For dominant gene defects the aim must be to destroy the presumably toxic gene product, for recessive gene defects the direct approach aims to provide a wild-type copy of the gene to the affected retinal cell type, and for diseases of either complex or unknown genetic origin, more general cell survival strategies that deal with preserving affected retinal cells are often the best and only option. Hence examples of each type of therapy will be briefly discussed in several animal models, including ribozyme therapy for autosomal dominant retinitis pigmentosa in the transgenic P23H opsin rat, beta-PDE gene augmentation therapy for autosomal recessive retinitis pigmentosa in the rd mouse, glial cell-derived neurotrophic factor (GDNF) gene therapy for autosomal dominant RP in the transgenic S334ter opsin rat and pigment epithelial cell-derived neurotrophic factor (PEDF) gene therapy for neovascular retinal disease in rodents. Each employs a recombinant AAV vectored passenger gene controlled by one of several promoters supporting either photoreceptor-specific expression or more general retinal cell expression depending on the therapeutic requirements.

Animals↗

PubMed1990

Studies of the morphology and structure of the plasma lipid transfer particle from the tobacco hornworm, Manduca sexta.

Morphological features of Manduca sexta plasma lipid transfer particle (LTP) have been investigated by electron microscopy. LTP was found to be an asymmetric particle with two major structural features: a roughly spherical head and an elongated, hinged tail. The hinge occurs approximately at the midpoint of the tail section with the two halves forming angles ranging from 30 degrees to 180 degrees. A molecular mass estimate of 1.4 x 10(6) daltons based on the dimensions of LTP suggests that multiple copies (two or three) of each of the three LTP apoproteins exist in the native complex. Limited digestion studies of LTP suggest that apoLTP-III is less susceptible to trypsin cleavage than apoLTP-I or -II, and therefore may be less exposed to the aqueous environment. Digestion for 1 h at a 1:50 trypsin-LTP protein ratio did not alter the flotation properties of LTP or its morphological features; thus, although significant proteolysis occurred, the particle retained its overall structure. Transfer activity, on the other hand, was affected by trypsin digestion with 30 +/- 14% inhibition of LTP activity occurring upon proteolysis at a 1:50 trypsin-LTP protein ratio. Treatment of LTP with phospholipase A2 resulted in the conversion of LTP-associated phosphatidylcholine and phosphatidylethanolamine to their corresponding lyso forms. Phospholipase A2 treatment did not, however, alter the SDS-PAGE profile, transfer activity, flotation pattern, or the microscopic features of LTP. These results suggest that the products of the phospholipase reaction remain associated with the particle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Non-isotopic in situ hybridization of human papilloma virus on histologic sections: an amended protocol.

The authors report on their experience with an HPV non-radioactive in situ hybridization kit and describe the favorable results gained with the amended protocol, which are as follows: 1. The application of a decreased amount of both the probe and the chromogen substrate did not alter the quality of reactions. Therefore we were able to make 60 reactions instead of the originally suggested 21. 2. The proteolytic enzyme digestion time could be prolonged by changing proteinase-K for pepsin which intensifies the signal of hybridization. 3. By changing the order of hybrid detection and posthybridization washing, we succeeded in removing the excess amount of probe-ABC-AP-BAAV-ABC-AP conglomerates without losing the target sequence. 4. Using alkaline phosphatase or ABC-AP-BAAV-ABC-AP complex instead of peroxidase it was possible to demonstrate a very low number of gene copies, even if they were not detectable following the original instructions.

Adult↗

PubMed2005

Temporal fluctuation of nuclear pore complex localization by single diffusing mRNP complexes.

There is now compelling evidence that messenger ribonucleoprotein (mRNP) complexes after the release from the transcription/processing sites execute essentially unhindered Brownian movements in the nucleoplasm and target nuclear pore complexes (NPCs) by chance encounter. For the majority of genes expressed in eukaryotic cells, only single/few transcript copies are generated, which reinforces the stochastic nature of NPC localization. In this paper, I analyse the NPC localization by freely diffusing single mRNPs and discuss the implications for the temporal progression of gene expression and consecutive processes associated with the gene products. To this end, a walk-and-capture model is considered, assuming a spherical nuclear compartment with a partially absorbing boundary. Perfect absorption and perfect reflection mark the extreme outcomes. For this model, the closed-form analytic solution of the first-passage time probability density function (FPT p.d.f.), the mean passage time and variance have been obtained. The FPT p.d.f. enables to calculate the probability that single mRNPs localize the nuclear boundary and dock to NPCs within certain time windows. For freely moving mRNP complexes in osteosarcoma cell nuclei, a mean apparent diffusion coefficient (D) of 0.04 microm2 s(-1) (range 0.01-0.09 microm2 s(-1)) has been reported. Assuming a nuclear radius of 8 microm and D=0.04 microm2 s(-1), the position-averaged minimum mean passage time min for the considered model is 1.8 min, which presupposes perfect absorption of the mRNP complex at the first encounter with the nuclear boundary. In this case, the probability of capture in the time interval (0, min) is 0.67. In smaller sized yeast cell nuclei with a radius of 0.8 mum and D=0.04 microm2 s(-1), single diffusing mRNPs would localize an NPC within tens of seconds, rather than minutes.

Active Transport, Cell Nucleus↗

PubMed1998

Probing the structure of complex macromolecular interactions by homolog specificity scanning: the P1 and P7 plasmid partition systems.

The P1 plasmid partition locus, P1 par, actively distributes plasmid copies to Escherichia coli daughter cells. It encodes two DNA sites and two proteins, ParA and ParB. Plasmid P7 uses a similar system, but the key macromolecular interactions are species specific. Homolog specificity scanning (HSS) exploits such specificities to map critical contact points between component macromolecules. The ParA protein contacts the par operon operator for operon autoregulation, and the ParB contacts the parS partition site during partition. Here, we refine the mapping of these contacts and extend the use of HSS to map protein-protein contacts. We found that ParB participates in autoregulation at the operator site by making a specific contact with ParA. Similarly, ParA acts in partition by making a specific contact with ParB bound at parS. Both these interactions involve contacts between a C-terminal region of ParA and the extreme N-terminus of ParB. As a single type of ParA-ParB complex appears to be involved in recognizing both DNA sites, the operator and the parS sites may both be occupied by a single protein complex during partition. The general HSS strategy may aid in solving the three-dimensional structures of large complexes of macromolecules.

Amino Acid Sequence↗

PubMed2006

Crystal structure and mechanism of TraM2, a second quorum-sensing antiactivator of Agrobacterium tumefaciens strain A6.

Quorum sensing is a community behavior that bacteria utilize to coordinate a variety of population density-dependent biological functions. In Agrobacterium tumefaciens, quorum sensing regulates the replication and conjugative transfer of the tumor-inducing (Ti) plasmid from pathogenic strains to nonpathogenic derivatives. Most of the quorum-sensing regulatory proteins are encoded within the Ti plasmid. Among these, TraR is a LuxR-type transcription factor playing a key role as the quorum-sensing signal receptor, and TraM is an antiactivator that antagonizes TraR through the formation of a stable oligomeric complex. Recently, a second TraM homologue called TraM2, not encoded on the Ti plasmid of A. tumefaciens A6, was identified, in addition to a copy on the Ti plasmid. In this report, we have characterized TraM2 and its interaction with TraR and solved its crystal structure to 2.1 A. Like TraM, TraM2 folds into a helical bundle and exists as homodimer. TraM2 forms a stable complex (K(d) = 8.6 nM) with TraR in a 1:1 binding ratio, a weaker affinity than that of TraM for TraR. Structural analysis and biochemical studies suggest that protein stability may account for the difference between TraM2 and TraM in their binding affinities to TraR and provide a structural basis for L54 in promoting structural stability of TraM.

Agrobacterium tumefaciens↗

PubMed1999

Cortical, auditory, event-related potentials in response to periodic and aperiodic stimuli with the same spectral envelope.

OBJECTIVE: 1) To determine whether the N1-P2 acoustic change complex is elicited by a change of periodicity in the middle of an ongoing stimulus, in the absence of changes of spectral envelope or rms intensity. 2) To compare the N1-P2 acoustic change complex with the mismatch negativity elicited by the same stimuli in terms of amplitude and signal to noise ratio. DESIGN: The signals used in this study were a tonal complex and a band of noise having the same spectral envelope and rms intensity. For elicitation of the acoustic change complex, the signals were concatenated to produce two stimuli that changed in the middle (noise-tone, tone-noise). Two control stimuli were created by concatenating two copies of the noise and two copies of the tone (noise-only, tone-only). The stimuli were presented using an onset-to-onset interstimulus interval of 3 sec. For elicitation of the mismatch negativity, the tonal complex and noise band stimuli were presented using an oddball paradigm (deviant probability = 0.14) with an onset-to-onset interstimulus interval of 600 msec. The stimuli were presented via headphones at 80 dB SPL to 10 adults with normal hearing. Subjects watched a silent video during testing. RESULTS: The responses to the noise-only and tone-only stimuli showed a clear N1-P2 complex to the onset of stimulation followed by a sustained potential that continued until the offset of stimulation. The noise-tone and tone-noise stimuli elicited an additional N1-P2 acoustic change complex in response to the change in periodicity occurring in the middle. The acoustic change complex was larger for the tone-noise stimulus than for the noise-tone stimulus. A clear mismatch negativity was elicited by both the noise band and tonal complex stimuli. In contrast to the acoustic change complex, there was no significant difference in amplitude across the two stimuli. The acoustic change complex was a more sensitive index of peripheral discrimination capacity than the mismatch negativity, primarily because its average amplitude was 2.5 times as large. CONCLUSIONS: These findings indicate that both the acoustic change complex and the mismatch negativity are sensitive indexes of the neural processing of changes in periodicity, though the acoustic change complex has an advantage in terms of amplitude. The results support the possible utility of the acoustic change complex as a clinical tool in the assessment of peripheral speech perception capacity.

Adult↗

PubMed1987

Mechanism of dexamethasone 21-mesylate antiglucocorticoid action: I. Receptor-antiglucocorticoid complexes do not competitively inhibit receptor-glucocorticoid complex activation of gene transcription in vivo.

The actions of dexamethasone 21-mesylate (DM) have been studied in two recently developed cultured murine cell lines containing approximately 200 copies of episomal minichromosome. This minichromosome contains the glucocorticoid regulatory element in the mouse mammary tumor virus long terminal repeat fused upstream of v-rasH sequences in a totally defined primary sequence environment. The levels of v-rasH mRNA were measured as an index of glucocorticoid regulated expression of this chimeric gene. In addition, expression of the endogenous single copy mouse metallothionein I (MT-I) gene was monitored simultaneously. DM was found to be an essentially pure antagonist of dexamethasone (dex)-stimulated expression of both the episomal chimeric gene and the endogenous MT-I gene. The covalent labeling efficiency by DM of glucocorticoid receptors in intact cells approached 100%, surpassing previously observed whole cell DM labeling efficiencies. These results strengthen the hypothesis that covalent complex formation is responsible for antiglucocorticoid action. The efficiency of whole cell nuclear binding of covalent receptor-DM complexes was found to be approximately 50% of that seen with receptor-dex complexes. Analyses of long terminal repeat initiated v-rasH mRNA and MT-I mRNA inductions by dex in cells previously exposed to a subsaturating concentration of DM indicated that receptor-DM complexes do not inhibit by a competitive mechanism the transcriptional activation of these glucocorticoid responsive genes by receptor-dex complexes. These results do not rule out the possibility, however, that covalent receptor-DM complexes may still bind to the biologically active nuclear sites. The implications of this result concerning the mechanism of DM irreversible antiglucocorticoid action are discussed.

Animals↗

PubMed2006

Breakpoint structure reveals the unique origin of an interspecific chromosomal inversion (2La) in the Anopheles gambiae complex.

Paracentric chromosomal inversions are major architects of organismal evolution and have been associated with adaptations relevant to malaria transmission in anopheline mosquitoes. The processes responsible for their origin and maintenance, still poorly understood, can be illuminated by analysis of inversion breakpoint sequences. Here, we report the breakpoint structure of chromosomal inversion 2La from the principal malaria vector Anopheles gambiae and its relatives in the A. gambiae complex. The distal and proximal breakpoints of the standard (2L+a) arrangement contain gene duplications: full-length genes and their truncated copies at opposite ends. Intact genes without pseudogene copies in the alternative arrangement (2La) imply that 2L+a is derived and was viable despite damage to genes, because duplication preserved gene function. A unique origin for the interspecific 2La inversion was challenged previously by indirect genetic evidence, but breakpoint sequences determined from members of the A. gambiae complex strongly suggest their descent from a single event. The derived position of 2L+a, long considered ancestral in this medically important group, has significant implications for the phylogenetic history and the evolution of vectorial capacity in the A. gambiae complex.

Animals↗

PubMed2000

Genetic control of oxidative phosphorylation and experimental models of defects.

Energy in the form of ATP is continually produced by all cells for normal growth and function. Anaerobic glycolysis can provide enough ATP for some cells, but energetic cells such as cardiomyocytes and neurons require a more efficient ATP supply, which can only be provided by mitochondrial oxidative phosphorylation. Invented by bacteria that became symbiotically associated with other bacteria to form eukaryotic cells billions of years ago, oxidative phosphorylation carries with it a genetic legacy that is unique. The mitochondrial oxidative phosphorylation complexes are assembled from protein subunits encoded by both the mitochondrial genome (mtDNA) and the nuclear genome (nDNA, located in the chromosomes). The mtDNA is a remnant genome of the bacterial progenitor of mitochondria, and (unlike the biparental diploidy that characterizes the nuclear genome) is present in thousands of copies per cell, is replicated through life, and is inherited (cytoplasmically) only from the female parent. Oxidative phosphorylation comprises five multimeric enzyme complexes that act as a redox pathway, passing electrons from oxidizable intermediates produced by the metabolism of food to molecular oxygen in the mitochondrial matrix, while producing an electrochemical gradient by pumping protons into the intermembranal space. The proton (hydrogen ion) gradient across the inner mitochondrial membrane is used by the H+-transporting ATP synthase to produce ATP from ADP and inorganic phosphate, with the protons released into the mitochondrial matrix then combining with electronated oxygen to form water. Many of the details regarding the control of the synthesis of oxidative phosphorylation enzyme complexes remain to be elucidated. Transmitochondrial cell culture systems have been developed so that defective oxidative phosphorylation can be studied in a controlled nuclear background. Such systems may soon enable the development of mtDNA 'knockout' mice in order to better model mtDNA transmission and mitochondrial disease.

3T3 Cells↗

PubMed2004

IS6110 mediates increased transcription of the phoP virulence gene in a multidrug-resistant clinical isolate responsible for tuberculosis outbreaks.

Drug resistance in Mycobacterium tuberculosis complex strains is solely due to chromosomal mutations that could affect bacterial virulence. Molecular epidemiology studies have shown that resistant strains are less likely to be clustered than susceptible strains. However, a few multidrug-resistant (MDR) M. tuberculosis complex strains have been described as causing outbreaks, suggesting that they have restored virulence or increased transmission. One of the biggest MDR tuberculosis outbreaks documented to date was caused by the B strain of M. bovis. Restriction fragment length polymorphism fingerprinting revealed that the B strain contains two copies of IS6110. Here, we mapped and sequenced the regions flanking the two copies of IS6110 in the B strain. Ligation-mediated PCR showed that one of these IS6110 copies is located within the promoter region of phoP, a transcriptional regulator that is essential for M. tuberculosis virulence. We used PCR to screen 219 MDR M. tuberculosis complex strains (90.4% of all MDR isolates) isolated in Spain between 1998 and 2002 and found that the B strain was the only strain that contained a copy of IS6110 in the phoP promoter. To determine whether IS6110 affects phoP promoter activity in the B strain, we individually cloned the phoP gene and its promoter region (including IS6110 from the B strain and the equivalent region from M. tuberculosis without IS6110 as a control) into a mycobacterial replicative plasmid and transformed M. smegmatis with the resulting plasmid. Primer extension analysis showed that phoP transcription was strongly upregulated when the promoter region contained IS6110, as in the case of the B strain.

Bacterial Proteins↗

PubMed1972

Effect of growth conditions on the formation of the relaxation complex of supercoiled ColE1 deoxyribonucleic acid and protein in Escherichia coli.

Colicinogenic factor E1 (ColE1) is present in Escherichia coli strain JC411 (ColE1) cells to the extent of about 24 copies per cell. This number does not appear to vary in situations which give rise to twofold differences in the amount of chromosomal deoxyribonucleic acid (DNA) present per cell. If cells are grown in the absence of glucose, approximately 80% of the ColE1 molecules can be isolated as strand-specific DNA-protein relaxation complexes. When glucose is present in the medium, only about 30% of the plasmid molecules can be isolated as relaxation complexes. Medium shift experiments in which glucose was removed from the medium indicate that within 15 min after the shift the majority (>60%) of the plasmid can be isolated as relaxation complex. This rapid shift to the complexed state is accompanied by a two- to threefold increase in the rate of plasmid replication. The burst of replication and the shift to the complexed state are both inhibited by the presence of chloramphenicol. Inhibition of protein synthesis in log cultures by the addition of chloramphenicol or amino acid starvation allows ColE1 DNA to continue replicating long after chromosomal replication has ceased. Under these conditions, noncomplexed plasmid DNA accumulates while the amount of DNA that can be isolated in the complexed state remains constant at the level that existed prior to treatment. In the presence of chloramphenicol, there appears to be a random dissociation and association of ColE1 DNA and "relaxation protein" during or between rounds of replication.

Bacterial Proteins↗

PubMed1998

Association of germline p53 mutation with MLL segmental jumping translocation in treatment-related leukemia.

Segmental jumping translocations are chromosomal abnormalities in treatment-related leukemias characterized by multiple copies of the ABL and/or MLL oncogenes dispersed throughout the genome and extrachromosomally. Because gene amplification potential accompanies loss of wild-type p53, we examined the p53 gene in a case of treatment-related acute myeloid leukemia (t-AML) with MLL segmental jumping translocation. The child was diagnosed with ganglioneuroma and embryonal rhabdomyosarcoma (ERMS) at 2 years of age. Therapy for ERMS included alkylating agents, DNA topoisomerase I and DNA topoisomerase II inhibitors, and local radiation. t-AML was diagnosed at 4 years of age. The complex karyotype of the t-AML showed structural and numerical abnormalities. Fluorescence in situ hybridization analysis showed multiple copies of the MLL gene, consistent with segmental jumping translocation. A genomic region including CD3, MLL, and a segment of band 11q24 was unrearranged and amplified by Southern blot analysis. There was no family history of a cancer predisposing syndrome, but single-strand conformation polymorphism (SSCP) analysis detected identical band shifts in the leukemia, ganglioneuroma, ERMS, and normal tissues, consistent with a germline p53 mutation, and there was loss of heterozygosity in the ERMS and the t-AML. Sequencing showed a CGA-->TGA nonsense mutation at codon 306 in exon 8. The results of this analysis indicate that loss of wild-type p53 may be associated with genomic instability after DNA-damaging chemotherapy and radiation, manifest as a complex karyotype and gene amplification in some cases of t-AML.

Acute Disease↗

PubMed2003

Structure, organization and expression of the genes encoding mitochondrial cytochrome c(1) and the Rieske iron-sulfur protein in Chlamydomonas reinhardtii.

The sequence and organization of the Chlamydomonas reinhardtii genes encoding cytochrome c(1) ( Cyc1) and the Rieske-type iron-sulfur protein ( Isp), two key nucleus-encoded subunits of the mitochondrial cytochrome bc(1) complex, are presented. Southern hybridization analysis indicates that both Cyc1 and Isp are present as single-copy genes in C. reinhardtii. The Cyc1 gene spans 6404 bp and contains six introns, ranging from 178 to 1134 bp in size. The Isp gene spans 1238 bp and contains four smaller introns, ranging in length from 83 to 167 bp. In both genes, the intron/exon junctions follow the GT/AG rule. Internal conserved sequences were identified in only some of the introns in the Cyc1 gene. The levels of expression of Isp and Cyc1 genes are comparable in wild-type C. reinhardtii cells and in a mutant strain carrying a deletion in the mitochondrial gene for cytochrome b (dum-1). Nevertheless, no accumulation of the nucleus-encoded cytochrome c(1) or of core proteins I and II was observed in the membranes of the respiratory mutant. These data show that, in the green alga C. reinhardtii, the subunits of the cytochrome bc(1) complex fail to assemble properly in the absence of cytochrome b.

Amino Acid Sequence↗

PubMed2003

Hexamerization of RepA from the Escherichia coli plasmid pKL1.

The Escherichia coli plasmid pKL1 is one of the smallest bacterial plasmids. It encodes a single, autoregulating structural gene, repA, responsible for replication and copy number control. The oligomerization of RepA was previously proposed as the basis of a strategy for pKL1 copy number control. To elucidate the oligomerization properties of RepA in solution, RepA was expressed in E. coli; purified by ion exchange and hydrophobic chromatography; and examined in solution by spectrapolarimetry, light scattering, sedimentation velocity, and equilibrium ultracentrifugation. RepA behaved as a concentration-dependent equilibrium of dimers and hexamers. Conformational parameters of the RepA hexameric complex were determined. These results support the proposed autogenous regulatory model whereby RepA hexamers negatively regulate repA expression thereby affecting the copy number control of pKL1. RepA of pKL1 is the first plasmid replication initiation protein documented to be in dimeric-hexameric forms.

Base Sequence↗

PubMed1996

[Amplification and expression of c-erbB2 oncogene in normal, hyperplastic, and malignant endometria].

OBJECTIVE: To study the correlation of development and survival with amplification of c-erbB2 oncogene in endometrial carcinoma. METHODS: The amplification and expression of c-erbB2 oncogene were determined from formalin-fixed, paraffin-embedded tissues of 25 normal, 31 hyperplastic, and 72 malignant samples of the endometrium in 128 patients, using differential polymerase chain reaction (DPCR) and an immunohistochemical technique. RESULTS: Amplified c-erbB2 (2 to 12 copies) were found in two of 25 (8.0%) normal, 15 of 31 (48.4%) hyperplastic, and 45 of 72 (62.5%) malignant samples. When the results of DPCR were compared with those of the immunohistochemical method, the negative findings concide well with one another, i.e., nonamplification was associated with the absence of immunoreactivity. It was noted that the amplified c-erbB2 was found more significantly in complex and a typical hyperplasias than in simple hyperplasias. The high-level c-erbB2 amplification (at least five copies) was significantly correlated with the histological grade of endometrial carcinoma and vascular or lymphatic invasion. No correlation was seen between c-erbB2 amplification and overall survival in the present group of patients. CONCLUSIONS: The amplified c-erbB2 may play a potential role in the early development of some endometrial carcinomas. The high-level c-erbB2 amplification may identify a subset of aggressive endometrial carcinoma that involves vascular or lymphatic invasiveness and poor cell differentiation playing the role of a marker for clinical prognosis.

Endometrial Hyperplasia↗

PubMed1999

Organizational strategies mediate nonverbal memory impairment in obsessive-compulsive disorder.

BACKGROUND: Previous neuropsychological studies of obsessive-compulsive disorder (OCD) have indicated impaired executive functioning and nonverbal memory. The extent to which impaired executive functioning impacts nonverbal memory has not been established. The current study investigated the mediating effects of organizational strategies used when copying a figure on subsequent nonverbal memory for that figure. METHODS: We examined neuropsychological performance in 20 unmedicated subjects with OCD and 20 matched normal control subjects. Subjects were administered the Rey-Osterrieth Complex Figure Test (RCFT) and neuropsychological tests assessing various aspects of executive function. RESULTS: OCD subjects differed significantly from healthy control subjects in the organizational strategies used to copy the RCFT figure, and they recalled significantly less information on both immediate and delayed testing. Multiple regression analyses indicated that group differences in immediate percent recall were significantly mediated by copy organizational strategies. Further exploratory analyses indicated that organizational problems in OCD may be related to difficulties shifting mental and/or spatial set. CONCLUSIONS: Immediate nonverbal memory problems in OCD subjects were mediated by impaired organizational strategies used during the initial copy of the RCFT figure. Thus, the primary deficit was one affecting executive function, which then had a secondary effect on immediate memory. These findings are consistent with current theories proposing frontal-striatal system dysfunction in OCD.

Adult↗