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At least 73 records · Page 4Linked to original sources
PubMed2001

Test-retest reliability of the ulnar F-wave minimum latency versus ulnar distal motor latency in healthy adults.

BACKGROUND AND PURPOSE: The purposes of this study were to explore reliability of the ulnar F-wave minimum latency (Fmin) and the ulnar distal motor latency (DML) and to contrast those levels of reliability in order to reveal whether physiologic lability is the primary contributor to unwanted variability in Fmin measurements. SUBJECTS AND METHODS: Fmin and DML in the Abductor Digiti Minimi muscle were measured bilaterally by two raters in 50 healthy adults (n = 100 hands, 70 male, 30 female) with 3-14 days between testing sessions. RESULTS: Intrarater reliability (ICC 3,1) for the Fmin was 0.89 with a standard error of the measurement (SEM) of 0.77 msec. Interrater reliability (ICC 2,1) for the Fmin was 0.80 with a SEM of 1.04 msec. Intrarater reliability (ICC 3,1) for the DML was 0.71 with a SEM of 0.18 msec. Interrater reliability (ICC 2,1) for the DML was 0.76 with a SEM of 0.19 msec. DISCUSSION AND CONCLUSIONS: Contrary to our hypothesis, the Fmin had a higher reliability than the DML. The DML did not display the high reliability other investigators have reported. We conclude the Fmin is a reliable measurement when 10 supramaximal stimulations are administered to healthy, young to middle-aged adult subjects. However, no inferences were made regarding relative levels of psychologic lability for the two latencies.

Adult↗
PubMed1992

[Estimation of cancer latency using data from a case-control study with time-related factors--estimated latency for consumption of alcohol and tobacco in relation to gastric cancer].

As a practical application of theory, the susceptible exposure age and latency distribution of consumption of alcohol and tobacco in relation to stomach cancer is discussed. It was revealed that, in univariate, estimation of the susceptible exposure age of alcohol and tobacco were 15-50 years and 35-50 years. The estimated latency were 35 years and 15 years. Those of accumulative period and preneoplastic period were 30 and 10 years. In a multivariate analysis, the latency for alcohol consumption was changed to 20 years as the incubation time in preneoplastic period was prolonged by 5 years due to consumption of vegetables. This could give a theoretical interpretation of second line cancer prevention.

Adult↗
PubMed2004

Protection against wild-type murine gammaherpesvirus-68 latency by a latency-deficient mutant.

A murine gammaherpesvirus-68 (MHV-68) mutant with deregulated transcription of its ORF50 transactivator was severely impaired in latency establishment. The deregulated virus showed reduced immunogenicity, probably reflecting a lower antigen load. However, it still elicited effective immunity to a subsequent wild-type (WT) virus challenge. Infection was not completely prevented, but was very substantially reduced in extent and the long-term level of WT viral DNA in lungs and spleens remained low. Thus latency-deficient MHV-68 illustrates a possible general approach to creating attenuated gammaherpesvirus vaccines that can protect against pathogenic WT infections.

Administration, Intranasal↗
PubMed2006

Absence or overexpression of the Varicella-Zoster Virus (VZV) ORF29 latency-associated protein impairs late gene expression and reduces VZV latency in a rodent model.

Varicella-zoster virus (VZV) ORF29 encodes the viral single-stranded DNA binding protein and is expressed during latency in human ganglia. We constructed an ORF29 deletion mutant virus and showed that the virus could replicate only in cells expressing ORF29. An ORF29-repaired virus, in which ORF29 was driven by a cytomegalovirus promoter, grew to peak titers similar to those seen with the parental virus. The level of ORF29 protein in cells infected with the repaired virus was greater than that seen with parental virus. Infection of cells with either the ORF29 deletion or repaired virus resulted in similar levels of VZV immediate-early proteins but reduced levels of glycoprotein E compared to those observed with parental virus. Cotton rats infected with the ORF29 deletion mutant had a markedly reduced frequency of latent infection in dorsal root ganglia compared with those infected with parental virus (P < 0.00001). In contrast, infection of animals with the ORF29 deletion mutant resulted in a frequency of ganglionic infection at 3 days similar to that seen with the parental virus. Animals infected with the ORF29-repaired virus, which overexpresses ORF29, also had a reduced frequency of latent infection compared with those infected with parental virus (P = 0.0044). These studies indicate that regulation of ORF29 at appropriate levels is critical for VZV latency in a rodent model.

Animals↗
PubMed1996

Quantitation of herpes simplex virus type 1 DNA and latency-associated transcripts in rabbit trigeminal ganglia demonstrates a stable reservoir of viral nucleic acids during latency.

In this investigation we determined the dynamics of herpes simplex virus type 1 (HSV-1) DNA and latency-associated transcripts (LAT) in the latently infected rabbit trigeminal ganglion. Rabbit eyes were infected with either the McKrae strain or the l7Syn+ strain of HSV-1. Rabbits were sacrificed between 5 and 360 days after infection and their trigeminal ganglia were analyzed for the number of HSV DNA genomes and the number of neuronal cells expressing LAT. There was no statistically significant change in the number of HSV genomes or the number of neuronal cells expressing LAT in these ganglia between 20 and 360 days after infection. For both strains, the amount of HSV DNA averaged 16.8 genomes per 100 cells, and 9.2% of the neurons expressed LAT. There were 17 to 34 HSV genomes per LAT-expressing neuronal cell. The number of LAT-expressing neurons did not change over the 360 days. Spontaneous reactivation (HSV-1 recovery in tear film) and recurrence (HSV-1-specific epithelial lesions) occurred during the period of this study; however, these events did not alter the quantity of HSV-1 DNA or the number of LAT-expressing cells. These results suggest that after the latent infection is established, the viral DNA in the ganglia does not replicate to any measurable extent over long periods of latency, since no significant change in the number of HSV genomes occurs. The results also suggest that only a very small number of latently infected neuronal cells are needed to produce infectious HSV-1 during reactivation.

Actins↗
PubMed2000

Evidence for a bidirectional element located downstream from the herpes simplex virus type 1 latency-associated promoter that increases its activity during latency.

Herpes simplex virus type 1 (HSV-1) latent infection in vivo is characterized by the constitutive expression of the latency-associated transcripts (LAT), which originate from the LAT promoter (LAP). In an attempt to determine the functional parts of LAP, we previously demonstrated that viruses harboring a DNA fragment 3' of the LAT promoter itself were able to maintain detectable promoter expression throughout latency whereas viruses not containing this element could not (J. R. Lokensgard, H. Berthomme, and L. T. Feldman, J. Virol. 71:6714-6719, 1997). This element was therefore called a long-term expression element (LTE). To further study the role of the LTE, we constructed plasmids containing a DNA fragment encompassing the LTE inserted into a synthetic intron between the reporter lacZ gene and either the LAT or the HSV-1 thymidine kinase promoter. Transient-expression experiments with both neuronal and nonneuronal cell lines showed that the LTE locus has an enhancer activity that does not activate the cytomegalovirus enhancer but does activate the promoters such as the LAT promoter and the thymidine kinase promoter. The enhancement of these two promoters occurs in both neuronal and nonneuronal cell lines. Recombinant viruses containing enhancer constructs were constructed, and these demonstrated that the enhancer functioned when present in the context of the viral DNA, both for in vitro infections of cells in culture and for in vivo infections of neurons in mouse dorsal root ganglia. In the infections of mouse dorsal root ganglia, there was a very high level of promoter activity in neurons infected with viruses bearing the LAT promoter-enhancer, but this decreased after the first 2 or 3 weeks. By 18 days postinfection, neurons harboring latent virus without the enhancer showed no beta-galactosidase (beta-gal) staining whereas those harboring latent virus containing the enhancer continued to show beta-gal staining for long periods, extending to at least 6 months postinfection, the longest time examined.

Animals↗
PubMed2003

Varicella-zoster virus open reading frame 21, which is expressed during latency, is essential for virus replication but dispensable for establishment of latency.

Varicella-zoster virus (VZV) open reading frame 21 (ORF21) is one of at least five VZV genes expressed in latently infected human and rodent ganglia. To determine whether ORF21 is required for latent and lytic infection, we deleted 99% of ORF21 from the viral genome. The ORF21 deletion mutant virus could be propagated only in a cell line expressing the ORF21 protein. Insertion of the herpes simplex virus type 1 (HSV-1) homolog of VZV ORF21, HSV-1 UL37, into the ORF21 deletion mutant failed to complement the mutant for growth in cell culture. Inoculation of cotton rats with the ORF21 deletion virus resulted in latent infection in numbers of animals similar to those infected after inoculation with the parental virus. The mean numbers of latent VZV genomes were similar in animals infected with parental and ORF21 deletion viruses. Transcription of ORF63, another latency-associated gene, was detected in ganglia from similar numbers of animals infected with the mutant and parental viruses. Thus, ORF21 is the first VZV gene expressed during latency that has been shown to be dispensable for the establishment of latent infection.

Base Sequence↗
PubMed1995

Cytomegalovirus latency and latency-specific transcription in hematopoietic progenitors.

Latency-associated transcripts have been detected in human cytomegalovirus (CMV)-infected granulocyte-macrophage progenitors and have been shown to be encoded from both DNA strands in the ie1/ie2 region of the viral genome. One class includes differentially spliced transcripts that extends exon 1 by initiating at two novel start sites 292 and 356 nucleotides in the ie1/ie2 promoter/enhancer region, upstream of the start site used during productive infection. The other class includes an unspliced transcript antisense to ie1 exons 2,3, and 4. These transcripts are specific to latently infected cells and are not detected during productive infection of human fibroblast cells. Several open reading frames are found within these cytomegalovirus latency-specific transcripts (CLTs), including one 94 codons long that begins in the extended exon 1 region and is predicted to remain open through the exon1/2 and exon 2/3 splice junctions. Expression of latent transcripts was detected in bone marrow-derived hematopoietic samples from CMV-seropositive healthy donors but not from seronegative donors.

Base Sequence↗
PubMed1981

Latency in the ascending auditory pathway determined using continuous sounds: comparison between transient and envelope latency.

The gross responses from the cochlea (round window) and two nuclei of the ascending auditory pathway of the rat in response to tone and noise bursts (compound action potentials) were compared with those recorded in response to continuous tones and noise that was amplitude modulated with pseudorandom noise. The cross-correlation function between: (1) the averaged response to the sounds that were amplitude modulated with the pseudorandom noise, and (2) one period of the pseudorandom noise, were obtained. The compound action potentials and the cross-correlation functions both had a series of peaks. The two functions had a similar morphology. The latency of the peaks in the cross-correlation showed less dependence on sound intensity than did the latency of the peaks in the compound action potentials.

Animals↗
PubMed1996

Different effect of height on latency of leg and foot short- and medium- latency EMG responses to perturbation of stance in humans.

In standing humans, platform perturbations evoked short- (SLR) and medium-latency responses (MLR) in soleus (Sol), tibialis anterior (TA) and flexor digitorum brevis (FDB) muscles. The latency of all responses significantly increased with subjects' height. The slope of the regression lines for the MLRs versus height was significantly steeper than that for the SLRs. The conduction velocity of the afferent fibres mediating the FDB MLR, calculated on the basis of the regression, was 17.5 m/s. These findings indicate that the MLRs are transmitted through afferent fibres slower than those mediating the SLRs. While the latter fibres are spindle group Ia afferents, the former are suggested to be group II fibres.

Adolescent↗
PubMed2003

Serial analysis of gene expression predicts structural differences in hippocampus of long attack latency and short attack latency mice.

The genetically selected long attack latency (LAL) and short attack latency (SAL) mice differ in a wide variety of behavioural traits and display differences in the serotonergic system and the hypothalamus-pituitary-adrenocortical (HPA)-axis. Serial analysis of gene expression (SAGE) was used to generate a hippocampal expression profile of almost 30 000 genes in LAL and SAL mice. Using SAGE, we found differential expression of 191 genes. Among these were genes involved in growth, signal transduction, and cell metabolism. The SAGE study was supported by GeneChip analysis (Affymetrix). Strikingly, both SAGE and GeneChips showed a higher expression of numerous cytoskeleton genes, such as cofilin and several tubulin isotypes in LAL mice. LAL mice also showed a higher expression of several calmodulin-related genes and genes encoding components of a MAPK cascade, namely raf-related oncogene and ERK2. The findings were confirmed by in situ hybridization. Our results of differential expression of cytoskeleton and signal transduction genes therefore suggest differential regulation of the raf/ERK pathway that may be related to structural differences in the hippocampus of LAL and SAL mice. As stress-related disorders, such as depression, are also linked to differential regulation of the HPA-axis and the serotonergic system and are associated with altered hippocampal morphology, differential regulation of these genes may be involved in the pathogenesis of these diseases.

Aggression↗
PubMed1987

Repeater F waves: a comparison of sensitivity with sensory antidromic wrist-to-palm latency and distal motor latency in the diagnosis of carpal tunnel syndrome.

Thirty-five thousand six hundred supramaximal shocks were applied to 209 healthy and 147 entrapped median nerves (carpal tunnel syndrome--CTS) to characterize the backfiring behavior of the alpha motor neuron pool of abductor pollicis brevis in health and the modifying effect of a compressive neuropathy. A contraction of the normal subpopulation of active F-wave generators was found in CTS, while active neurons backfired at higher than normal frequencies (p less than 0.001). These modifications in spinal behavior are reflected in the % Repeater F-wave value, whose sensitivity in the detection of CTS approaches that of sensory wrist-to-palm latency estimation. This technique offers an alternative to latency measurement in the diagnosis of CTS. An economical strategy for the electrodiagnosis of CTS is proposed.

Adolescent↗
PubMed2004

Noxious stimuli evoke a biphasic flexor reflex composed of A delta-fiber-mediated short-latency and C-fiber-mediated long-latency withdrawal movements in mice.

The nociceptive flexor reflex was studied in mice, focusing in particular on movement. Electrical stimuli delivered to the ventral aspect of the toe through a pair of needle electrodes inserted subcutaneously elicited a biphasic withdrawal reflex that was composed of short- and long-latency movements of the ipsilateral hind paw. The first response had a lower activation threshold compared with the second movement. Similar biphasic responses were observed in the afferent volley recorded from the sciatic nerve as well as in the electromyographic activity recorded from the femoris biceps muscle. Tetrodotoxin, applied over the sciatic nerve, abolished the first movement, but the second response was preserved, revealing that the first movement was elicited by the activation of myelinated Adelta-fibers, whereas the second movement was mediated by unmyelinated C-fibers. Thus, simultaneous activation of Adelta- and C-fibers leads to separate, but sequentially occurring withdrawal movements of the hind paw in mice. Systemic administration of morphine suppressed the withdrawal reflex, which was attributable to a preferential reduction of the Adelta-fiber-mediated short-latency component. This method will be useful for understanding how Adelta-fiber- and C-fiber-mediated nociceptive reflexes are affected by drugs in the whole animal system.

Animals↗
PubMed1998

Shorter latencies of components of middle latency auditory evoked potentials in congenitally blind compared to normal sighted subjects.

A previous study which reported shorter latencies of the Nb component of AEP-MLRs in congenitally blind compared to normal sighted subjects, formed the basis for the present study. The blind subjects had received a rehabilitation program from the age of 4 years onwards, which may have influenced auditory function. Hence the present study was designed to compare the AEP MLRs of normal sighted subjects with age-matched blind subjects who had not undergone early rehabilitation. Auditory evoked potentials (0 to 100 ms. range) were recorded in 10 congenitally blind subjects (average age = 22.4 +/- 4.9 yrs.) and an equal number of age-matched subjects with normal vision. There were two repetitions per subject. The peak latencies of both the Pa (maximum positive peak between Na and 35 ms.) and Nb (maximum negative peak between 38 and 52 ms.) waves was significantly shorter in congenitally blind compared to normal sighted subjects. Since the Pa and Nb waves are believed to be generated by the superior temporal cortex (Heschl's gyrus), it appears that processing at this neural level occurs more efficiently in the blind. Also, in spite of the absence of an early rehabilitation program the present subjects showed the same auditory changes as those reported earlier.

Adaptation, Physiological↗
PubMed1989

[Inter-individual variability of mean latencies in the dynamic topography of short latency visual evoked potentials and the origin of brainstem potentials evaluated by the dipole tracing method in normal subjects].

To determine the normal pattern of the short latency visual evoked potentials (SVEP) in clinical diagnosis, in a previous report, the normal responses were classified into the following three types: uniform type, brainstem dominant type and occipital dominant type, according to the strength of the potentials. In the present report the latencies of N40 and P50, which constitute the SVEP, were investigated. In addition, the burst origin of these potentials was investigated using the dipole tracing method for P50 obtained through dynamic topography. Optic nerve potentials of N40 appeared first in the anterior region (from 37.1msec to 40.4msec following the stimulus) after the fourth retinal oscillatory potentials and soon extended to the posterior region (after about 2msec). This potential appeared in approximately about 65%, because of the low amplitude. P50 appeared 45.8-53.6msec after the stimulus about 100% and burst 2-4 times in the same place. Using the dipole tracing method, the origin of P50 was estimated to the near the deep center of the brain, probably around the brainstem. The same results were obtained using dynamic topography.

Adult↗
PubMed2001

The effect of latency-associated transcript on the herpes simplex virus type 1 latency-reactivation phenotype is mouse strain-dependent.

Herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) null mutants reactivate poorly in the rabbit ocular model. The situation in mice is less clear. Reports concluding that LAT null mutants reactivate poorly in the mouse explant-induced reactivation (EIR) model are contradicted by a similar number of reports of normal EIR of LAT(-) mutants in mice. To determine if the EIR phenotype might be mouse strain-dependent we infected BALB/c and Swiss Webster mice with LAT(-) or LAT(+) virus and assessed EIR in individual trigeminal ganglia. Compared to LAT(+) virus, LAT(-) virus reactivated poorly in Swiss Webster mice (P<0.05). In contrast, the EIR phenotype of these viruses was similar in BALB/c mice (P>0.1). Thus, LAT appeared to have a much greater impact on the EIR phenotype in Swiss Webster mice than in BALB/c mice. The mouse strain therefore appeared consequential in the HSV-1 EIR phenotype in mice.

Animals↗
PubMed1994

Two open reading frames (ORF1 and ORF2) within the 2.0-kilobase latency-associated transcript of herpes simplex virus type 1 are not essential for reactivation from latency.

The herpes simplex virus type 1 (HSV-1) latency-associated transcripts (LATs) are dispensable for establishment and maintenance of latent infection. However, the LATs have been implicated in reactivation of the virus from its latent state. Since the reported LAT deletion and/or insertion variants that are reactivation impaired contain deletions in the putative LAT promoter, it is not known which LAT sequences are involved in reactivation. To examine the role of the 2.0-kb LAT in the process of reactivation and the functional importance of the putative open reading frames (ORF1 and ORF2) contained within the 2.0-kb LAT, we have constructed an HSV-1 variant that contains a precise deletion and insertion within the LAT-specific DNA sequences using site-directed mutagenesis. The HSV-1 variant FS1001K contains an 1,186-bp deletion starting precisely from the 5' end of the 2.0-kb LAT and, for identification, a XbaI restriction endonuclease site insertion. The FS1001K genome contains no other deletions and/or insertions as analyzed by a variety of restriction endonucleases. The deletion in FS1001K removes the entire 556-bp intron within the 2.0-kb LAT, the first 229 nucleotides of ORF1, and the first 159 nucleotides of ORF2 without having an affect on the RL2 (ICP0) gene. Explant cocultivation reactivation assays indicated that this deletion had a minimal effect on reactivation of the variant FS1001K compared with the parental wild-type virus using a mouse eye model. As expected, Northern (RNA) blot analyses have shown that the variant virus (FS1001K) does not produce the 2.0-kb LAT or the 1.45- to 1.5-kb LAT either in vitro or in vivo; however, FS1001K produces an intact RL2 transcript in tissue culture. These data suggest that the 2.0-kb LAT putative ORF1 and ORF2 (or the first 1,186 bp of the 2.0-kb LAT) are dispensable for explant reactivation of latent HSV-1.

Animals↗
PubMed1997

The latency-associated promoter of herpes simplex virus type 1 requires a region downstream of the transcription start site for long-term expression during latency.

The latency-associated transcript (LAT) promoter of herpes simplex virus type 1 (HSV-1) is unique among the many promoters on the viral genome in that it remains active during the latent state. We have previously shown that a DNA fragment comprising the LAT promoter element through the cap site, when moved from the LAT locus to the glycoprotein C gene, is capable of only short-term expression. These and other data suggested that an HSV DNA element from the repeat region, not included in the LAT promoter itself, might be needed to preserve long-term expression. Based on a number of recombinant viruses, we narrowed our search for this putative element to a region 3' of the LAT transcription start site. In the present study, we have shown that a 1.1-kb DNA fragment containing the putative long-term expression element (LTE) is able to restore latent-phase gene expression to the LAT promoter. The element appeared to function best when it was placed in its natural location, which is 3' of the LAT promoter; however, partial function was obtained when the LTE was inserted upstream of the LAT promoter in the reverse direction. These data indicate that the LAT promoter region is more complex than originally anticipated and that in addition to requiring both core promoter and neuronal transcription factor binding sites, the promoter requires a specific region of DNA to prevent its shutoff during a latent infection.

Animals↗