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PubMed2001

Association and spreading of the Drosophila dosage compensation complex from a discrete roX1 chromatin entry site.

In Drosophila, dosage compensation is controlled by the male-specific lethal (MSL) complex consisting of MSL proteins and roX RNAs. The MSL complex is specifically localized on the male X chromosome to increase its expression approximately 2-fold. We recently proposed a model for the targeted assembly of the MSL complex, in which initial binding occurs at approximately 35 dispersed chromatin entry sites, followed by spreading in cis into flanking regions. Here, we analyze one of the chromatin entry sites, the roX1 gene, to determine which sequences are sufficient to recruit the MSL complex. We found association and spreading of the MSL complex from roX1 transgenes in the absence of detectable roX1 RNA synthesis from the transgene. We mapped the recruitment activity to a 217 bp roX1 fragment that shows male-specific DNase hypersensitivity and can be preferentially cross-linked in vivo to the MSL complex. When inserted on autosomes, this small roX1 segment is sufficient to produce an ectopic chromatin entry site that can nucleate binding and spreading of the MSL complex hundreds of kilobases into neighboring regions.

Animals↗
PubMed1989

Time for spreading of compensatory mutations under gene duplication.

Evolution by compensatory mutations is accelerated by gene duplication because selective constraint is relaxed by gene redundancy. A mutation is called compensatory if it corrects the effect of an earlier deleterious mutation. Without duplication, Kimura has shown that the time for spreading of compensatory mutations is much reduced by tight linkage between the two chromosomal sites of mutations. In this report, the time for spreading with gene duplication was studied by using the diffusion equation method of Kimura, together with computer simulations. It was shown that, when 2Nv- is much less than unity, the time for spreading is greatly shortened by gene duplication as compared with the case of complete linkage between the two sites of mutations, where 2N is the effective population size (haploid) and v- is the rate of compensatory mutations. However, if 2Nv- greater than 1, gene duplication is not effective for accelerating the evolution by such mutations.

Biological Evolution↗
PubMed1990

Cytoplasmically inherited reproductive incompatibility in Tribolium flour beetles: the rate of spread and effect on population size.

This paper reports on the effects of a cytoplasmically inherited reproductive incompatibility in different genetic strains of the flour beetle, Tribolium confusum. We measured the rate of spread and the effect of host population size using different initial frequencies of infection with a cytoplasmic factor that mediates reproductive incompatibility. There were two experiments, in one the infected and uninfected lines were from the same genetic strain, b-Yugoslavia. In the other, the infected line was from the "high cannibalism" bIV strain and the uninfected line from the "low cannibalism" bI strain. We estimate that the fitness ratio of infected to uninfected in b-Yugoslavia is 0.63 and the observed rate of spread for this strain corresponds to a model of cytoplasmic inheritance that takes into account the productivity differences between the infected and cured lines. In the bI-bIV experiment, because the uninfected and infected lines are from different genetic strains, we cannot partition the effects of the cytoplasmic factor from other factors. The rate of spread in the bI-bIV experiment is faster in males and slower in females than predicted from a model of cytoplasmic inheritance. In both experiments, productivity varies with initial infection frequency; however, the relationship is not explained by a simple model that predicts lower population size at intermediate infection frequencies.

Animals↗
PubMed1993

The distribution and spreading of rare variants in the histone multigene family of Drosophila melanogaster.

We surveyed the distribution of rare variant restriction sites within and among histone gene arrays of Drosophila melanogaster using restriction fragment length polymorphism (RFLP) analysis. Seventy-three naturally occurring arrays were digested with restriction enzymes that had no recognition sites in the published histone sequence. Of the arrays surveyed, 68.5% had at least two nonconsensus restriction sites present as indicated by the presence of a small band or bands on the autoradiographs. These bands were almost always the length of a single repeat in the histone multigene family or a multiple of this length. In arrays with more than one band, intensity of the bands almost always decreased with increasing size. This shows that within these arrays variant restriction sites were predominantly located on adjacent repeats. If these bands are caused by spreading of variant sites, as is most likely, then variants spread along the array as an inverse function of distance. Overall, if a sequence spread it had a 92% probability of ending up in its nearest neighbor. This pattern may result from the noncontiguous nature of the histone family.

Animals↗
PubMed1996

Sex and the spread of retrotransposon Ty3 in experimental populations of Saccharomyces cerevisiae.

Mobile genetic elements may be molecular parasites that reduce the fitness of individuals that bear them by causing predominantly deleterious mutations, but increase in frequency when rare because transposition increases their rates of transmission to the progeny of crosses between infected and uninfected individuals. If this is true, then the initial spread of a mobile element requires sex. We tested this prediction using the yeast retrotransposon Ty3 and a strain of Saccharomyces cerevisiae lacking Ty3. We infected replicate isogenic sexual and asexual populations with a galactose-inducible Ty3 element at an initial frequency of 1%. In two of six asexual populations, active Ty3 elements increased in frequency to 38 and 86%, due to the spread in each population of a competitively superior mutant carrying a new Ty3 insertion. Ty3 frequencies increased above 80% in all sexual populations in which transposition was induced in haplophase or in diplophase. Ty3 did not increase in frequency when active during both haplophase and diplophase, apparently because of selective sweeps during adaptation to galactose. Repressed Ty3 elements spread in sexual populations, by increasing sexual fitness. These results indicate that active Ty3 elements are more likely to become established in sexual populations than in asexual populations.

Crosses, Genetic↗
PubMed2005

The spread of drug abuse in rapidly urbanizing communities in Vientiane, Lao People's Democratic Republic.

To determine the prevalence of drug abuse in city neighborhoods in a developing country undergoing rapid urbanization, we performed a household survey on the spread of drug abuse in Vientiane, Lao People's Democratic Republic. A total of 1497 households from 17 villages were selected by the stratified random sampling method from urban districts in the city of Vientiane. Participatory style research was employed to increase both the sensitivity of detection and the reliability of information gathered. Local key players shared in the participatory process in this study. We worked with national and city officers and community leaders, as well as with neighborhood leaders who had received previous training for this survey, and conducted household surveys using face-to-face interviews. We inquired about the spread of drug abuse by asking if the families interviewed recognized drug abuse problems in their community. To examine the extent of urbanization of individual villages, the urban index was calculated by principle component analysis from the following eight indicators: income, occupation, parents' educational histories, diffusion of telephones, ownership of livestock, diffusion of plumbing for running water and distance from the Vientiane city center to the village. Distance was calculated by the Geographic Information System. Among the 17 villages included in the study, the average percentage of recognition of drug abuse in the community was 63.2%. The relationship between recognition of cases of drug abuse in the community and the urban index showed a significant correlation, with a Spearman coefficient of 0.650 (p < 0.01). The high reliability of participatory style surveys is also discussed. In conclusion, city neighborhoods in a developing country undergoing rapid urbanization showed evidence of the spread of drug abuse, which was associated with the urban index. Participatory style research activity was recommended to help raise awareness of community participation in anti-drug-abuse activities.

Adult↗
PubMed2001

Heterozygosity for the neurofibromatosis 1 (NF1) tumor suppressor results in abnormalities in cell attachment, spreading and motility in astrocytes.

Individuals with the neurofibromatosis 1 (NF1) tumor predisposition syndrome develop low-grade pilocytic astrocytomas at an increased frequency. Previously, we demonstrated that astrocytes from mice heterozygous for a targeted mutation in the Nf1 gene (Nf1+/- astrocytes) exhibit a cell autonomous growth advantage associated with increased RAS pathway activation. In this report, we extend our initial characterization of the effect of reduced Nf1 gene expression on astrocyte function by demonstrating that Nf1+/- astrocytes exhibit decreased cell attachment, actin cytoskeletal abnormalities during the initial phases of cell spreading, and increased cell motility. Whereas these cytoskeletal abnormalities were also observed in Nf1-/- astrocytes, astrocytes expressing a constitutively active RAS molecule showed increased cell motility and abnormal actin cytoskeleton organization during cell spreading, but exhibited normal cell attachment. Based on ongoing gene expression profiling experiments on human astrocytoma tumors, we demonstrate increased expression of two proteins implicated in cell attachment, spreading and motility (GAP43 and T-cadherin) in Nf1+/- and Nf1-/- astrocytes. These results support the emerging notion that tumor suppressor gene heterozygosity results in abnormalities in cell function that may contribute to the pathogenesis of non-tumor phenotypes in NF1.

Animals↗
PubMed1991

The spread of human immunodeficiency virus type 2 into Europe: a geographical analysis.

Geographically-related computer databases on the global incidence of HIV-1 and HIV-2 infection are being maintained in the Department of Geography at the University of Cambridge, England. Using the information they contain, the original geographical heartlands of HIV-2 infection are identified as former Portuguese and French colonies in West and South Central Africa. The same databases permit the reconstruction of the diffusion corridors by which the virus is spreading from these heartlands into Europe. The reconstruction shows that, as a result of traditional links with their former colonies, the main areas of infection in Europe are Portugal and France. These countries have subsequently acted as diffusion nodes for the spread of the virus to other parts of Europe. The patterns of spread thus differ fundamentally from those by which HIV-1 infection arrived in and is moving through Europe.

Acquired Immunodeficiency Syndrome↗
PubMed1993

Thresholds and stability analysis of models for the spatial spread of a fatal disease.

A simple two-class (susceptibles and infectives) model describing the dynamics of a fatal disease in a variable-size population is presented and analysed. Spatial dependence is introduced into the model by considering two different mechanisms for the geographic spread of the disease: nonlocal interaction between susceptibles and infectives, and migratory spread of the animals. The steady states and their stability for these spatially dependent models are deduced; no spatially heterogeneous steady states were possible. For nonlocal interaction, there were two spatially uniform steady states: the trivial state (no infectives or susceptibles), which was unstable, and the endemic state (constant proportion of the population infected), which was locally asymptotically stable. With migratory spread, the number of spatially uniform steady states was dependent on the boundary conditions imposed. With hostile (Dirichlet) boundary conditions, only the trivial steady state was possible and its local stability found to depend on the rate of diffusion of the total population. With no-flux (Neumann) boundary conditions, the steady states are the trivial and endemic states; these were unstable and locally asymptotically stable, respectively.

Animals↗
PubMed1992

Poliovirus spreads from muscle to the central nervous system by neural pathways.

A transgenic mouse model was used to address an unsolved question in the pathogenesis of poliomyelitis: how poliovirus invades the central nervous system (CNS). LD50 values for intramuscular and intracerebral inoculation of poliovirus in transgenic mice expressing poliovirus receptors (TgPVR mice) were similar. After intramuscular inoculation with poliovirus, paralysis was observed first in the inoculated limb. In contrast, localization of initial paralysis to the inoculated limb was not observed in normal mice inoculated intramuscularly with the mouse-adapted P2/Lansing poliovirus strain. After intramuscular inoculation, infectious poliovirus was first detected in the inferior segment of the spinal cord, then in the superior spinal cord and the brain. Sciatic nerve transection blocked poliovirus spread to the spinal cord after inoculation into the hindlimb footpad of TgPVR mice. These results demonstrate that in TgPVR mice, poliovirus spreads from muscle to the CNS through nerve pathways and that expression of the poliovirus receptor plays an important role in viral spread by this route.

Animals↗
PubMed1999

Cell spreading distinguishes the mechanism of augmentation of T cell activation by integrin-associated protein/CD47 and CD28.

Integrin-associated protein (IAP/CD47) is a 50 kDa transmembrane protein initially defined as a regulator of beta3 integrin-mediated functions in neutrophils. IAP also can synergize with the TCR in T cell activation independent of beta3 integrins. To analyze the mechanism for IAP synergy with TCR, we expressed in Jurkat cells a chimeric molecule, consisting of the CD16 extracellular domain, the CD7 transmembrane domain and the TCR zeta chain cytoplasmic tail (CD16-7-zeta), which on its own is unable to induce IL-2 production. Ligation of IAP acted in synergy with TCR to induce IL-2 transcription and synthesis, but failed to synergize with the signal generated by CD16-7-zeta, while CD28 was a potent co-stimulator with both TCR and CD16-7-zeta. The failure of IAP to activate Jurkat together with CD16-7-zeta correlated with a lack of c-Jun N-terminal kinase, but not extracellular-signal-regulated kinase activation. Jurkat adhesion to anti-IAP, but not anti-CD28, induced cell spreading and the same domains of IAP required for augmentation of T cell activation were required to induce cell spreading. IAP synergy with TCR signaling likely results from its ability to stimulate adhesion to a ligand-expressing surface or antigen-presenting cell (APC), rather than from initiation of a novel signaling cascade. We conclude that a major role for ligation of IAP in T cell activation is to enhance the efficiency of TCR signaling by causing T cells to spread on an APC or surface.

Antigens, CD↗
PubMed2004

High frequency transfer and horizontal spread of apramycin resistance in calf faecal Escherichia coli.

OBJECTIVES: The aminoglycoside apramycin has been used extensively in animal husbandry in the UK since 1978. This study aimed to determine both whether calves that had never been treated with aminoglycoside antibiotics harboured apramycin-resistant (apr(R)) commensal Escherichia coli, and the mode of spread of the resistance gene. METHODS: Apr(R) E. coli from weekly calf faecal samples were typed by pulsed-field gel electrophoresis, antibiotic resistance phenotype, plasmid restriction profiles and plasmid transfer frequencies. RESULTS: During 4 months of weekly sampling, six of 11 calves were found to harbour apr(R) E. coli. All apr(R) E. coli (45) were cross-resistant to gentamicin and tobramycin, which are both used in human medicine. Resistance was conferred by the aac(3)IV gene, present on three different conjugative plasmids. Two of these plasmids also mediated tetracycline and streptomycin resistance. One plasmid demonstrated very high transfer frequencies and was found in three different genotypes. CONCLUSIONS: We report the presence of apr(R) commensal E. coli in cattle that have never been treated with aminoglycosides. The presence of one conjugative plasmid in three different genotypes is evidence of horizontal spread of this plasmid. This is the first report of a very high transfer frequency of apr(R) plasmid, demonstrating horizontal spread in the commensal flora of food animals.

Acetyltransferases↗
PubMed2003

Pathological assessment of intraductal spread of carcinoma in relation to surgical margin state in breast-conserving surgery.

BACKGROUND: Spreading of carcinoma has been considered to be a prognostic factor for local failure after breast-conserving therapy. The extensive intraductal component (EIC) was defined as when the component of intraductal carcinoma constitutes more than 25% of the primary tumor with intraductal foci. However, the definition of EIC was based on the predominance of intraductal component surrounding the invasive lesions and not on the segmental anatomy. We designated carcinoma extension as the intraductal spread of carcinoma (ISC) along with the duct-lobular system by three-dimensional (3-D) reconstruction analysis. This study was initiated to simplify the method of two-dimensional (2-D) pathological examination based on 3-D mapping. METHODS: Thirty-four specimens from breast cancer patients were subjected to 3-D reconstruction. We investigated the correlation between actual extension of intraductal carcinoma and EIC defined by 2-D examination or ISC grading defined by 3-D reconstruction. Furthermore, using another 62 histological mappings, we investigated how correctly the simplified 2-D method using several paraffin blocks reflected the actual carcinoma spread and margin state. RESULTS: Carcinoma extension over 2 cm was observed in 64% specimens that were EIC positive and 26% specimens that were EIC negative. In contrast, according to the ISC grading defined by 3-D reconstruction, none of the specimens with a low grade of ISC demonstrated carcinoma extension over 2 cm. Carcinoma extension over 2 cm was observed in 71% of specimens with a high grade of ISC, thus demonstrating a correlation between carcinoma extension and ISC grading. In addition, the simplified 2-D method using only several blocks reflected both the 3-D ISC grading and surgical margin state. CONCLUSIONS: We conclude that ISC grading correlates with carcinoma extension and surgical margin state. From a clinical point of view, the simplified 2-D examination using paraffin blocks may contribute to routine surgical pathology in evaluating the degree of carcinoma extension in breast-conserving therapy.

Adult↗
PubMed2006

Relaxin expression from tumor-targeting adenoviruses and its intratumoral spread, apoptosis induction, and efficacy.

BACKGROUND: The use of oncolytic adenoviruses as cancer gene therapy is limited by their uneven penetration and distribution in tumors. We investigated whether the expression of the cell matrix-degradative protein relaxin by adenovirus could improve adenovirus distribution and penetration in tumors. METHODS: We generated relaxin-expressing, replication-incompetent (dl-lacZ-RLX) and -competent (Ad-deltaE1B-RLX) adenoviruses by inserting a relaxin gene into the E3 adenoviral region. Controls were parental adenoviruses (dl-lacZ and Ad-deltaE1B) and phosphate-buffered saline (PBS) (vehicle). Replication-incompetent viruses, which do not lyse cells, were used to assess transduction efficiency. Viral spread in tumor spheroids, made by dissecting tumor tissue into homogeneous fragments, was assessed by reporter gene (i.e., lacZ) expression. Tumor growth inhibition was assessed by injecting adenoviruses into xenograft tumors in athymic mice (n = 8 or 9). Overall survival was assessed by the Kaplan-Meier method. Extracellular matrix was examined with Masson's trichrome staining. Therapeutic efficacy was evaluated by assessing spontaneous pulmonary metastasis in the B16BL6 melanoma mouse model and growth inhibition of orthotopically implanted hepatoma (n = 4-6). All statistical tests were two-sided. RESULTS: In tumor spheroids and established solid tumors in vivo, transduction with dl-lacZ-RLX, compared with parental virus or vehicle, elicited higher transduction efficiency and viral spread throughout the tumor mass. Infection with Ad-deltaE1B-RLX, compared with parental virus, elicited greater viral persistence and spread, leading to increased survival (e.g., 100%, 95% confidence interval [CI] = 63.1% to 100%, for C33A tumor-bearing mice treated with Ad-deltaE1B-RLX, and 50%, 95% CI = 15.7% to 84.3%, for C33A tumor-bearing mice treated with Ad-deltaE1B). Infection with Ad-deltaE1B-RLX substantially decreased the collagen content of tumor tissue but not of adjacent normal tissue, compared with noninfected tissues. Intratumoral injection of Ad-deltaE1B-RLX inhibited the formation of lung metastases in mice (PBS = 268 mg of metastatic tumor per mouse and Ad-deltaE1B-RLX = 10 mg; difference = 258 mg, 95% CI = 94 to 426; P = .003, Mann-Whitney test). Systemic treatment with Ad-deltaE1B-RLX completely inhibited the growth of Hep1 hepatocellular carcinomas (PBS = 20.2 mg of tumor per mouse and Ad-deltaE1B-RLX = 0 mg; difference = 20.2 mg, 95% CI = 3.7 to 36.7; P = .004, Mann-Whitney test). CONCLUSION: Extracellular matrix degradation by relaxin expressed by adenoviruses increased viral distribution and tumor penetration, inhibited tumor growth and metastasis, and increased survival of mice.

Adenoviridae↗
PubMed1984

The spread of sequence variants in Rattus satellite DNAs.

The genus Rattus has two related families of satellite DNA: Satellite I consists of tandem arrays of a 370 base pair repeat unit which is a dimer of two 185 base pair portions (a, b) which are about 60% homologous. Satellite I' consists of tandem arrays of a 185 base pair repeat unit (a') which is about 85% homologous to a and 60% homologous to b. R. norvegicus contains only satellite I but R. rattus contains both satellites I and I'. We examined certain aspects of satellite DNA evolution by comparing the spacing at which variant repeat units of each satellite have spread among non-variant repeat units in these two species. With but one exception, in R. rattus, 15 different variant repeat units have spread among non-variant repeat units of satellite I, with a spacing equal to the length of the (a,b) dimer. Similarly, fourteen different variant repeat units of the monomeric satellite I' have mixed among non-variant repeat units with a spacing equal to the length of the (a') monomer. These results suggest that a mechanism involving homologous interaction among satellite sequences could account for the spread of variant family members. We also found that a sequence variant present in certain portions of the dimeric repeat unit of satellite I is more efficiently amplified (or less efficiently corrected) than variants occurring in other regions. This was not true for the monomeric repeat unit of satellite I'.

Animals↗
PubMed1991

Estimating the 1978-1990 and future spread of human immunodeficiency virus type 1 in subgroups of homosexual men.

The authors studied the historical spread of human immunodeficiency virus type 1 (HIV-1) infection in homosexual/bisexual men and projected its future spread in these men using data from an AIDS-free cohort recruited during late 1984 in Baltimore, Maryland; Chicago, Illinois; Los Angeles, California; and Pittsburgh, Pennsylvania. Dates of preentry seroconversion in HIV-1 seroprevalent men were estimated using study entry values of hematologic variables influenced by HIV-1 infection. The authors used survival methods incorporating truncation to determine numbers/dates of seroconversion for men with a pre-1984 AIDS diagnosis who were selectively excluded by design from the 1984 AIDS-free cohort. Overall, the annual seroconversion hazard rose progressively from 0.4% in 1978 to 13.8% in 1983, dropped to 4.6% in 1985, and remained relatively stable at 1.1-2.2% from 1986 to 1990. By January 1990, almost 46% of men who were seronegative in 1978 had seroconverted. The authors estimated historical rates of spread by city, age, education, and ethnicity to examine the effects of these factors in the early and continuing stages of the HIV-1 epidemic. There were striking differences among cities with respect to pre-1985 seroconversion rates but not with respect to post-1985 seroconversion rates. Age, education, and ethnicity were all associated with 1978-1990 seroconversion rates. Future seroconversion among homosexual men was predicted assuming that the "stabilized" 1986-1990 hazards (stratified by age) observed here will be representative of future rates. Truncated Kaplan-Meier methods gave the probability of a seronegative 20-year-old man's remaining seronegative in subsequent years. Such a man has a 20.2% chance of seroconverting before reaching the age of 25 years (a 4.4% yearly hazard). The annual hazard drops to 2.5% between 25 and 30 years, to about 1.5% between 30 and 45 years, and to 1.0% between 45 and 55 years. The overall probability of seroconversion prior to age 55 years is about 50%, with seroconversion still continuing at and after age 55. Given that this cohort consists of volunteers receiving extensive anti-HIV-1 transmission education, the future seroconversion rates of the general homosexual population may be even higher than those observed here.

Adult↗
PubMed2005

The effects of the spread of hatch and interaction with delayed feed access after hatch on broiler performance until seven days of age.

Delay in access to feed for 1-d-old chicks impairs posthatch growth. It is a standard practice that 1-d-old chicks are deprived of feed for about 48 h before they are placed on farms. During incubation, there is a spread of 24 to 48 h for late versus early hatching. As spread of hatch increases, number of chicks that are feed-deprived for a longer time before free access (IA) to feed and water increases. In this current study, we investigated the effects of time delay in feed access on chick juvenile relative growth (RG: a measure of speed of growth) up to d 7, taking into consideration the duration of egg storage and spread of hatch. Our results confirmed that delay in feed access caused weight loss during holding time and depressed growth rate after access to feed. The magnitude of the effect depended on the hatching period within the hatching window. It also depended on whether the biological age (BA) or the chronological age (CA) of the chick was considered. Immediate access to feed produced significantly different results depending on CA or BA. Both ways, the method seemed to benefit the late hatchers. This finding contrasts with the effect of delayed feeding in which early hatchers benefited more. Long duration of egg storage depressed RG not only of chicks with immediate access to feed but also in those denied access after hatch. Delay in feed access significantly aggravated the effects of long egg storage duration on RG. Triiodothyronine levels were lower in feed-deprived chicks, and the effect was greater in late hatchers. It is concluded that the beginning of delay in feed access should be determined from the time of hatch not at the end of hatch. It is suggested that the adverse effects of delay in feed access can be reduced by providing a source of energy in hatching baskets or during transportation.

Aging↗
PubMed2002

The role of tumor lymphangiogenesis in metastatic spread.

The high mortality rates associated with cancer can be attributed to the metastatic spread of tumor cells from the site of their origin. Tumor cells invade either the blood or lymphatic vessels to access the general circulation and then establish themselves in other tissues. Clinicopathological data suggest that the lymphatics are an initial route for the spread of solid tumors. Detection of sentinel lymph nodes by biopsy provides significant information for staging and designing therapeutic regimens. The role of angiogenesis in facilitating the growth of solid tumors has been well established, but the presence of lymphatic vessels and the relevance of lymphangiogenesis to tumor spread are less clear. Recently, the molecular pathway that signals for lymphangiogenesis and relatively specific markers for lymphatic endothelium have been described allowing analyses of tumor lymphangiogenesis to be performed in animal models. These studies demonstrate that tumor lymphangiogenesis is a major component of the metastatic process and implicate members of the VEGF family of growth factors as key mediators of lymphangiogenesis in both normal biology and tumors.

Animals↗