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PubMed2001

Oral anticoagulants versus antiplatelet therapy for preventing further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin.

BACKGROUND: Patients who are entered in clinical trials after a transient ischaemic attack (TIA) or non disabling ischaemic stroke have an annual risk of important vascular events (death from all vascular causes, non-fatal stroke, or non-fatal myocardial infarction) of between 4 and 11 percent. Aspirin, in a daily dose of 30mg or more, offers only modest protection after cerebral ischaemia: it reduces the incidence of major vascular events by 20 percent at most. Secondary prevention trials after myocardial infarction indicate that treatment with oral anticoagulants is associated with a risk reduction approximately twice that of treatment with antiplatelet therapy. OBJECTIVES: 1) To compare the efficacy of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischaemia of presumed arterial origin. 2) To compare the safety of oral anticoagulants and antiplatelet therapy in the secondary prevention of vascular events after cerebral ischaemia of presumed arterial origin. SEARCH STRATEGY: This review draws on the search strategy developed for the Stroke Group as a whole. Relevant trials were identified in the Specialised Register of Controlled Trials (last searched: June 2000). Authors of published trials were contacted for further information and unpublished data. SELECTION CRITERIA: Randomised trials with concealed treatment allocation on long term (> 6 months) secondary prevention after recent (< 6 months) TIA or minor ischaemic stroke of presumed arterial origin were selected. The oral anticoagulant therapy was to be of specified intensity (by means of the International Normalised Ratio (INR)) with warfarin, phenprocoumon or acenocoumarol versus a single antiplatelet drug (or combination of antiplatelet agents). DATA COLLECTION AND ANALYSIS: Two reviewers selected trials meeting the inclusion criteria and extracted details of randomisation methods, blinding of treatments and assessments, whether intention-to-treat analysis is possible from the published data, whether treatment groups are comparable with regard to major prognostic risk factors for outcomes, the number of patients who are excluded or lost to follow-up, definition of outcomes, and entry and exclusion criteria. The methodological quality of each trial was assessed by the two reviewers using these extracted data. In addition, target INR for anticoagulant treatment and dose and type of antiplatelet drug, duration of follow-up and the numbers of defined outcome events was recorded. The data were analysed according to the intention-to-treat principle. Subgroup analyses with treatment INR 2.1 - 3.6 versus INR 3.0 - 4.5 was performed. Relative and absolute risk reductions were calculated by means of the statistical software provided by the Cochrane Collaboration. MAIN RESULTS: Four trials, with a total of 1870 patients were selected. In the prevention of ischaemic stroke after cerebral ischaemia of presumed arterial origin, the available data do not allow a robust conclusion on whether anticoagulants (in any intensity) are more efficacious than antiplatelet therapy (low intensity anticoagulation RR 0.96, 95% CI 0.38 to 2.42, high intensity anticoagulation RR 1.02, 95% CI 0.49 to 2.13). Treatment with anticoagulation INR 2.1 - 3.6 does not give an importantly higher bleeding risk than treatment with antiplatelet agents (RR 1.19, 95% CI 0.59 to 2.41). It is clear that oral anticoagulants INR 3.0 - 4.5 are not safe, because they yield a higher risk of major bleeding complications (RR 9.0, 95% CI 3.9 to 21). REVIEWER'S CONCLUSIONS: For the secondary prevention of further vascular events after transient ischaemic attack or minor stroke of presumed arterial origin, there is insufficient evidence to justify the routine use of low intensity oral anticoagulants (INR 2.0 - 3.6). More intense anticoagulation (INR 3.0 - 4.5) is not safe and should not be used in this setting.

Administration, Oral↗
PubMed1992

Origins of secondary metabolism.

Secondary metabolites generally benefit their producers as poisons that protect them against competitors, predators or parasites. They are produced from universally present precursors (most often acetyl-CoA, amino acids or shikimate) by specific enzymes that probably arose by the duplication and divergence of genes originally coding for primary metabolism. Most secondary metabolites are restricted to single major taxa on the universal phylogenetic tree and so probably originated only once. But different secondary metabolic pathways have originated from different ancestral enzymes at radically different times in evolution. Secondary metabolites are most abundantly produced by microorganisms in crowded habitats and by plants, fungi and sessile animals like sponges, where chemical defence and attack rather than physical escape or fighting are at a premium. The first secondary metabolites were probably antibiotics produced in microbial mats over 3500 million years ago. These first ecosystems probably consisted entirely of eubacteria: archaebacteria and eukaryotes arose much later. As a phylogenetic context for considering the earliest origins of antibiotics I summarize a cladistic analysis of the explosive eubacterial primary diversification. This suggests that the most primitive surviving cells are the photosynthetic heliobacteria. Study of these and of the nearly as primitive chloroflexibacteria, spirochaetes and deinobacteria may provide the best evidence on the origins of secondary and primary metabolism.

Anti-Bacterial Agents↗
PubMed2004

A shrew-sized origin for primates.

The origin of primates has had a long history of discussion and debate, with few ever considering the impact of the original body weight on subsequent primate adaptive radiations. Here, I attempt to reconstruct early primate evolution by considering the initial size of primates as well as the critical functional-adaptive events that had to occur prior to the early Eocene. Microcebus is often viewed as a living model, and thus 40-65 g might represent a practical ancestral weight for the origin of primates. I consider a smaller original body weight, likely 10-15 g in actual size, and I address the biological implications for shrew-sized primates by comparing the behavioral ecology of mouse lemurs, our smallest living primates, to another tiny-sized mammalian group, the shrews (Family Soricidae). Several behavioral and ecological characteristics are shared by shrews and mouse lemurs, and several mammalian trends are evident with decreased size. I suggest that a shrew-sized ancestral primate would have had high metabolic, reproductive, and predation rates, relatively low population densities, and a dispersed and solitary existence with a promiscuous mating system. Although small mammals like shrews provide insights concerning the ancestral size of primates, primate origins have always been tied to arboreality. I assess other potential arboreal models such as Ptilocercus and Caluromys. By combining all of this information, I try to sequence the events in a functional-adaptive series that had to occur before the early Eocene primate radiations. I suggest that all of these important adaptive events had to occur at a small body size below 50 g.

Adaptation, Physiological↗
PubMed2007

Biodistance analysis of the Moche sacrificial victims from Huaca de la Luna plaza 3C: Matrix method test of their origins.

The purpose of this study is to test two competing models regarding the origins of Early Intermediate Period (AD 200-750) sacrificial victims from the Huacas de Moche site using the matrix correlation method. The first model posits the sacrificial victims represent local elites who lost competitions in ritual battles with one another, while the other model suggests the victims were nonlocal warriors captured during warfare with nearby polities. We estimate biodistances for sacrificial victims from Huaca de la Luna Plaza 3C (AD 300-550) with eight previously reported samples from the north coast of Peru using both the mean measure of divergence (MMD) and Mahalanobis' distance (d2). Hypothetical matrices are developed based upon the assumptions of each of the two competing models regarding the origins of Moche sacrificial victims. When the MMD matrix is compared to the two hypothetical matrices using a partial-Mantel test (Smouse et al.: Syst Zool 35 (1986) 627-632), the ritual combat model (i.e. local origins) has a low and nonsignificant correlation (r = 0.134, P = 0.163), while the nonlocal origins model is highly correlated and significant (r = 0.688, P = 0.001). Comparisons of the d2 results and the two hypothetical matrices also produced low and nonsignificant correlation for the ritual combat model (r = 0.210, P = 0.212), while producing a higher and statistically significant result with the nonlocal origins model (r = 0.676, P = 0.002). We suggest that the Moche sacrificial victims represent nonlocal warriors captured in territorial combat with nearby competing polities.

Adult↗
PubMed2003

Glandular cell atypia on Papanicolaou smears: interobserver variability in the diagnosis and prediction of cell of origin.

BACKGROUND: The 2001 Bethesda System recommended qualification of atypical glandular cells (AGC) to indicate the site of origin and separated endocervical adenocarcinoma in situ (AIS) from "AGC favor neoplastic" as a specific diagnostic category. To the authors' knowledge, the literature evaluating the reproducibility of Papanicolaou (Pap) smear diagnosis of glandular cell abnormalities with emphasis on the cell of origin is limited. The aim of the current study was to investigate whether a variety of benign to neoplastic glandular lesions can be reliably classified on Pap smear with regard to diagnosis and cell of origin. METHODS: Twenty-three conventional Pap smears (CPS) with glandular cellular changes varying from benign to adenocarcinoma (ACA) were reviewed by six observers. They were asked to categorize each smear according to cell of origin (endocervical vs. endometrial) and diagnosis (benign, AGC, or ACA). Kappa statistics were used to evaluate interobserver agreement and correlation of interobserver agreement with experience. RESULTS: There was no consensus among observers for both the origin of the cells and the diagnosis. Interobserver agreement for site was poor (kappa < 0.4) especially in the AGC category. Unanimous agreement for site was reached for 7 of 23 smears (30%). Two of five endocervical AIS were classified as endometrial and another two were classified as benign by four observers. Interobserver agreement was poor in all diagnostic categories (kappa < 0.4) and showed slight correlation with level of experience. Unanimous agreement for diagnosis was reached for only 2 smears (9%). Three of 11 (27%) smears demonstrating preneoplastic/neoplastic processes were diagnosed as benign by 3 observers. Three (25%) benign CPS were diagnosed as ACA by 2 observers. Accurate prediction of the final histologic diagnosis by observers varied from 30% to 87% and did not correlate closely with experience. CONCLUSIONS: Cytologic diagnosis of glandular lesions by CPS was problematic and suffered from significant interobserver subjectivity.

Adenocarcinoma↗
PubMed2006

Locus coeruleus neurons originate in alar rhombomere 1 and migrate into the basal plate: Studies in chick and mouse embryos.

We investigated in the mouse and chick the neuroepithelial origin and development of the locus coeruleus (LoC), the most important noradrenergic neuronal population in the brain. We first studied the topography of the developing LoC in the hindbrain, using as markers the key noradrenergic marker gene Dbh and the transcription factors Phox2a and Phox2b (upstream of Dbh). In both mouse and chicken, LoC neurons first appear arranged linearly along the middle one-third of the alar plate of rhombomere 1 (r1), collinear to a reference ventricular longitudinal band that early on expresses Phox2a and Phox2b in the alar plate of r2 and later expands to r1. Double-labeling experiments with LoC markers (Dbh or Phox2a) and either alar (Pax7 and Rnx3) or basal (Otp) genetic markers suggested that LoC cells migrate from their origin in the alar plate to a final position in the lateral basal plate. To corroborate these suggestions experimentally and determine the precise origin of the LoC, we fate mapped the LoC in the chick at stage HH11 by using quail-chick homotopic grafts. The experimental results confirmed that the LoC originates in the alar plate throughout the rostrocaudal extent of r1 and ruled out a rostrocaudal translocation. They also corroborated a ventralward tangential migration of LoC cells into the lateral basal plate, where the postmigratory LoC primordium is located. Comparisons with neighboring alar r1-derived cell populations established that LoC neurons originate outside the cerebellum, in a matrix area intercalated dorsoventrally between the sources of the prospective vestibular and trigeminal columns.

Animals↗
PubMed1976

Cells of origin of entorhinal cortical afferents to the hippocampus and fascia dentata of the rat.

The pathway from the entorhinal cortical region to the hippocampal formation has previously been shown to be comprised of two sub-systems, one of which projects predominantly to the ipsilateral fascia dentata and regio inferior of the hippocampus proper, and a second which projects bilaterally to regio superior. The goal of the present investigation was to determine if these two pathways might originate from different cell populations within the entorhinal area. The cells of origin of these entorhinal pathways were identified by retrograde labeling with horseradish peroxidase (HRP). Injections which labeled the entorhinal terminal fields in both the fascia dentata and regio superior resulted in the retrograde labeling of two populations of cells in the entorhinal area. Ipsilateral to the injection, HRP reaction product was found in the cells of layer II (predominantly stellate cells) and the cells of layer III (predominantly pyramidal cells). Contralateral to the injections, however, the reaction product was found almost exclusively in the cells of layer III. With selective injections of the entorhinal terminal field in regio superior, only the cells of layer III were labeled, but these were labeled bilaterally. Selective injection of the entorhinal terminal field in the fascia dentata, however, resulted in the labeling of cells of layer II, but not of layer III, and these cells of layer II were labeled almost exclusively ipsilaterally. A very small number of labeled cells in layer II were, however, found contralateral to the injection as well. No labeled cells were found either in the presubiculum or parasubiculum following injections of the hippocampal formation. These cell populations were found capable of retrograde transport of HRP, however, since cells in both presubiculum and parasubiculum were labeled following HRP injections into the contralateral entorhinal area. These results suggest that the projections to the fascia dentata originate from the cells of layer II, while the projections to regio superior originate from the cells of layer III of the entorhinal region proper. The very slight crossed projection from the entorhinal area to the contralateral area dentata probably originates from the small population of cells in layer II which are labeled following HRP injections in the contralateral area dentata.

Afferent Pathways↗
PubMed1981

Cells of origin of pathways descending to the spinal cord in two chondrichthyans, the shark Scyliorhinus canicula and the ray Raja clavata.

The cells of origin of pathways descending to the spinal cord in the shark Scyliorhinus canicula and in the ray Raja clavata have been demonstrated by using the horseradish peroxidase (HRP) technique. Following HRP injections in the spinal cord of Scyliorhinus (fourth to sixth segment) and of Raja (15th to 20th segment) labeled neurons could be identified in the rhombencephalon, the mesencephalon, and in the diencephalon. Cells of origin of diencephalic nuclei, which project to the spinal cord, were observed in the nucleus periventricularis hypothalami and in the thalamus ventralis pars medialis which can in this respect be considered hypothalamic. Descending pathways from mesencephalic structures originate from the interstitial nucleus of the fasciculus longitudinalis medialis, the tectum mesencephali, the nucleus intercollicularis, the tectotegmental junction zone, and from diffusely arranged tegmental neurons. A contralateral rubrospinal pathway could be recognized in Raja, but not in Scyliorhinus. Rhombencephalic cells of origin of pathways descending to the spinal cord were found in all parts of the reticular formation, i.e., the nucleus raphes inferior, the nucleus reticularis inferior, medius, superior, and isthmi, in two vestibular nuclei, and in three nuclei, which have been tentatively indicated as nucleus B, F, and G. Furthermore cells of origin of descending pathways have been found in the nucleus tractus descendens nervi trigemini, in the nucleus funiculi lateralis, and in the nucleus tractus solitarii. The descending pathways of the two species studied have been compared with those of other vertebrates. It is concluded that the basic pattern in the organization of descending pathways to the spinal cord, as proposed by ten Donkelaar ('76) for terrestrial vertebrates, also holds for cartilaginous fishes.

Animals↗
PubMed1984

Histological and ultrastructural studies on the origin of caudal neural crest cells in mouse embryos.

The origin of neural crest cells was studied histologically and ultrastructurally in caudal regions of mouse embryos at 8.5-11 days of gestation (day of vaginal plug = day 0). The neural tube of caudal regions develops in two different phases, called primary and secondary neurulation. The primary (more cranial) portion of the neural tube originates from the ectodermal neural plate, whereas the secondary (most caudal) portion originates from the tail bud. We asked in this study: Do neural crest cells of caudal regions originate exclusively from the developing primary portion of the neural tube and, subsequently, migrate into areas undergoing secondary neurulation; or do some of these cells originate from the tail bud, with the secondary portion of the neural tube, forming in situ in caudal areas? Most embryos were preserved with fixative containing cetylpyridinium chloride (CPC) to facilitate the identification of neural crest cells, which stain darkly after exposure to CPC during fixation. Our results suggest that there are two sources of neural crest cells in caudal regions: the neuroectoderm of the neural folds flanking the closing posterior neuropore, and the tail bud. Neural crest cells derived from the neuroectoderm are designated as the primary neural crest, because they form in conjunction with the primary portion of the neural tube during primary neurulation, whereas neural crest cells derived from the tail bud are designated as the secondary neural crest, because they form in conjunction with the secondary portion of the neural tube during secondary neurulation.

Animals↗
PubMed1985

Embryonic development of the rat cerebellum. III. Regional differences in the time of origin, migration, and settling of Purkinje cells.

The time of origin, site of origin, migratory path and settling pattern of the Purkinje cells of the cerebellar hemispheres, anterior vermis, and posterior vermis were investigated in thymidine radiograms and plastic-embedded materials from rat embryos ranging in age from 15 to 22 days. In the hemispheres there is a rostral-to-caudal cytogenetic gradient: the Purkinje cells of lobulus simplex, crus I, and crus II are produced earlier than the Purkinje cells of the paramedian lobule and paraflocculus, followed by the Purkinje cells of the flocculus. The Purkinje cells of the vermis, in general, are generated later than those of the hemispheres, and with a reverse gradient from caudal to rostral: the Purkinje cells of the posterior vermis (lobules X-VI) being produced ahead of the Purkinje cells of the anterior posteriorly directed wedge of early-produced Purkinje cells through the vermis. Evidence was obtained that the Purkinje cells of the hemispheres derive from the lateral cerebellar primordium capping the lateral recess of the fourth ventricle anteriorly. The Purkinje cells of the anterior vermis originate from the subisthmal cerebellar primordium medially lining the isthmal canal. The Purkinje cells of the posterior vermis originate in the postisthmal cerebellar primordium overlying the tela choroidea caudally. The young Purkinje cells migrate from the neuroepithelium to the surface of the cerebellum in a strictly caudal-to-rostral order, paralleling the spread of the EGL superficially from posteroventral to anterodorsal. This pattern is independent of the time of origin of Purkinje cells. In the posterior vermis the earliest-settling Purkinje cells of the uvula follow a short radial course, and a discrete Purkinje layer is formed 3 days after they are generated. In the anterior vermis the Purkinje cells of lobulus centralis, which follow an anterodorsal migratory course, are still settling on day E22, 7 days after their production, presumably awaiting the fusion of the cerebellar base anteriorly. The fissura prima forms medially at the interface region of Purkinje cells derived from the postisthmal and subisthmal cerebellar primordia. For 1-2 days after their settling, the Purkinje cells of the newly forming lobules can be distinguished by certain cytological criteria from the Purkinje cells in the more caudally-situated, earlier-settled lobules.

Animals↗
PubMed1989

Development of the rat thalamus: IV. The intermediate lobule of the thalamic neuroepithelium, and the time and site of origin and settling pattern of neurons of the ventral nuclear complex.

Short-survival, sequential, and long-survival thymidine radiograms of rat embryos, fetuses, and young pups were analyzed in order to examine the time of origin, settling pattern, migratory route, and site of origin of neurons of the ventral nuclear complex of the thalamus. Quantitative examination of long-survival radiograms established that the bulk of the neurons of the ventral nuclear complex are generated between days E14 and E16 but with statistically significant differences between its three nuclei. The ventrobasal nucleus is the oldest component (97% of the cells are generated on days E14 and E15); the ventrolateral nucleus is next (82% of the cells are generated on days E14 and E15); and the ventromedial nucleus is last (51% of the cells are generated on days E14 and E15). In addition to this caudal-to-rostral (from the ventrobasal nucleus to the ventrolateral nucleus) and lateral-to-medial (from the ventrobasal nucleus to the ventromedial nucleus) internuclear gradients, there are lateral-to-medial and ventral-to-dorsal intranuclear neurogenetic gradients within the ventrobasal and ventrolateral nuclei. Qualitative examination of short and sequential survival thymidine radiograms indicate that the neurons of the ventral nuclear complex originate in the unique intermediate thalamic neuroepithelial lobule, which is distinguished from the rest of the thalamic neuroepithelium by the presence of a mitotically active secondary neuroepithelial matrix. Two sublobules can be distinguished in the intermediate lobule during the early stages of thalamic development. On the basis of their location and chronological pattern of cell production and differentiation, it is inferred that the neurons of the ventrobasal nucleus originate in the earlier differentiating, posteroventrally situated inverted sublobule, and the neurons of the ventrolateral nucleus are produced in the later differentiating, anterodorsally situated everted sublobule. The neurons of the ventromedial nucleus appear to originate from the intermediate neuroepithelial lobule after its two sublobules are no longer distinguishable. The heavily labeled neurons generated soon after injection on day E15 form a wave front that translocates in a lateral direction at a steady rate of 215 microns/day. Examination of methacrylate-embedded materials showed that, in day E15 rats the actively migrating cells are spindle-shaped, with their long axis oriented horizontally. The far-laterally situated differentiating cells (the oldest neurons) become vertically oriented by day E16. Associated with this change in polarity, vertically oriented fibers appear among the cells. These fibers can be traced to the inte

Animals↗
PubMed1989

Development of the rat thalamus: VI. The posterior lobule of the thalamic neuroepithelium and the time and site of origin and settling pattern of neurons of the lateral geniculate and lateral posterior nuclei.

Short-survival, sequential, and long-survival thymidine radiograms of rat embryos, fetuses, and young pups were analyzed in order to determine the time of origin, site of origin, migratory route, and settling pattern of neurons of the dorsal lateral geniculate (LGD), ventral lateral geniculate (LGV), and lateral posterior (LP) nuclei of the thalamus. Quantitative examination of long-survival radiograms established that the neurons of the LGD are produced on days E14 and E15. Within the LGD there is an external-to-internal neurogenetic gradient; the majority (77%) of neurons of the external half are generated on day E14, while in the internal half the majority (64%) of neurons originate on day E15. The late-generated LGD neurons are located in the termination field of the uncrossed fibers of the optic tract. Examination of short-survival radiograms indicated that the neurons of the LGD originate in a discrete neuroepithelial eversion situated ventral to the pineal rudiment and dorsal to the putative neuroepithelium of the ventral nuclear complex. In sequential radiograms from rats injected with 3H-thymidine on day E15 and killed on days E16 and E17, the migration of young LGD neurons was followed in a posterolateral direction to the formative lateral geniculate body. By day E17, the day when the optic tract fibers begin to disperse over the lateral surface of the posterior diencephalon, the distribution of early and late-generated neurons of the LGD resembles that seen in young pups. As a whole, the neurons of the LGV are produced earlier than the neurons of the LGD. The bulk of LGV neurons are generated on days E14 and E15 in a caudal-to-rostral intranuclear neurogenetic gradient. Caudal LGV neurons are generated mainly on day E14 (82%), while a substantial proportion of rostral neurons (32%) are generated on day E15. Examination of short-survival and sequential radiograms suggest that the LGV neurons originate in an inverted sublobule situated beneath the putative neuroepithelium of the LGD. At anterior levels the putative inverted sublobule of the LGV merges imperceptibly with the neuroepithelium that produces the neurons of the lateral habenular nucleus. Like the neurons of the LGD and LGV, so also those of the LP are generated on days E14 and E15, but the neurogenetic gradients are different. There is a lateral-to-medial gradient within the LP as a whole. Peak production of neurons is on day E14 laterally (58%) and on day E15 medially (59%).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

An extended secondary structure model for the TMV assembly origin, and its correlation with protection studies and an assembly defective mutant.

Recognition of the unique internal assembly origin on tobacco mosaic virus (TMV) RNA by the disk aggregate of the viral coat protein probably involves an extended region of the RNA (larger than that coated by a single disk) folded into a specific conformation. A secondary structure model is proposed for the RNA preferentially coated by limiting amounts of coat protein disks on the basis of partial nuclease digestion data. Part of this sequence can form three symmetrically spaced hairpins with marginally stable base paired sequences at the tips of the stems. The pattern of progressive protection of the RNA from nuclease attack during assembly suggests that these three hairpins are successively coated by the first three disks to add. The spacing of these hairpins is identical to that of three hairpins in the pseudo assembly origin (part of the coat protein gene homologous to the assembly origin). In Ni 2519, a TMV mutant whose assembly is defective at high temperature because it can no longer discriminate between the true and pseudo assembly origins, a point mutation has occurred near the tip of the third metastably base paired stem of the true assembly origin which would disrupt its structure and alter one copy of a repeated heptanucleotide. This suggests an important role for the ordered and cooperative recognition of successive loops in determining the specificity of assembly.

Journal Article↗
PubMed1985

Conservation of genes and their organization in the chromosomal replication origin region of Bacillus subtilis and Escherichia coli.

The organization of six open reading frames which were deduced from the nucleotide sequence of some 10 kb from the replication origin region of Bacillus subtilis resembles the organization of the genes in the rnpA-dnaA-gyrB region of the Escherichia coli chromosome. Based on the detection of homology with the E. coli genes the open reading frames were found to represent the Bacillus 'rnpA', 'rpmH', 'dnaA', 'dnaN', recF and gyrB genes. Only the latter two have also been defined by genetic analysis. Two regulatory regions containing nine and four copies of a repeating sequence, DnaA-box, which is identical with the DnaA protein-binding sequence repeated four times in the E. coli origin of replication, flank the 'dnaA' gene of B. subtilis. One or both of them are proposed to function as origins in the initiation of chromosomal replication. Transcription of the 'dnaA' gene of Bacillus starts in one of these regions and appears to be coupled to initiation of chromosomal replication. We propose that the conserved gene organization in the 'dnaA'-'gyrB' region of B. subtilis is representative of the replication origin region of a primordial replicon. The oriC sequence of E. coli has either been translocated to its present location 44 kb away from the primordial origin or has independently evolved there.

Amino Acid Sequence↗
PubMed2006

Clonal analysis favours a monoclonal origin for serous borderline tumours with peritoneal implants.

Serous borderline tumours (SBTs) of the ovary were originally classified as such because the vast majority behave in a remarkably indolent manner, even in the presence of widespread tumour deposits, termed implants, and/or lymph node involvement. The pathogenesis of the implants is currently unknown. Two major hypotheses have been proposed: the first favours a monoclonal origin, arguing that the peritoneal lesions derive from neoplastic cells that are shed from the primary ovarian tumour. The second hypothesis favours a polyclonal origin as a result of a field defect of susceptible Müllerian cells from which multiple independent tumours arise. To test both hypotheses, genome-wide allelotyping and B-RAF/K-RAS mutation analyses were employed to assess clonality in 25 metachronous or synchronous tumours from ten SBT patients. Loss of heterozygosity (LOH) profiling and K-RAS/B-RAF mutation analysis showed concordance of the genetic changes in all sites in 21 tumours from eight patients who were informative. These results favour a common origin, underscored by a likelihood ratio (probability of common origin/probability of independent origin) ranging from 2.43 to 7,662,850. In conclusion, this study strongly supports the hypothesis that both non-invasive and invasive implants arise as a consequence of spread from a single ovarian site.

DNA Mutational Analysis↗
PubMed2002

Differentiation of the geographical origin of durum wheat semolina samples on the basis of isotopic composition.

The identification of the geographical origin of foods is attracting great interest from consumers and producers since it may be used as a criterion for guaranteeing quality and authenticity. Stable isotope techniques can provide useful information on the origin of food products. The natural abundance isotopic ratios of carbon, oxygen and nitrogen were determined and a comparison made between the isotopic content of samples originating from Italy and those of samples originating from other countries (Canada, Turkey, Australia). A correlation was found between the isotopic composition and geographical origin of the samples. The relationship between isotopic content and the latitude has been confirmed.

Australia↗
PubMed1994

A search for an essential function of the replication origin ARS1 in the life cycle of Saccharomyces cerevisiae.

We have investigated the significance of the chromosomal replication origin, ARS1, during the entire life cycle of yeast. This was done by substituting the chromosomal copy with a series of ars1 deletion mutants. It was shown that the ARS1 replication origin is not essential for mitotic or premeiotic DNA replication since no effect on growth, chromosomal loss rate and spore viability was observed in the ars1 mutant strains. We conclude that replication origins are abundantly, present in the yeast genome and that the removal of a single replication origin is compensated for by replication forks emanating from neighbouring origins.

Chromosomes, Fungal↗
PubMed1998

The origin of the subepicardial mesenchyme in the avian embryo: an immunohistochemical and quail-chick chimera study.

It has been proposed that the subepicardial mesenchymal cells (SEMC) originate from the primitive epicardium and also from migration of extracardiac mesenchyme from the liver area. We have studied the possibility of an origin of SEMC through transformation of the proepicardial mesothelium, as well as the potential of the early proepicardium to generate epicardium and SEMC in quail-chick chimeras. The study was carried out in quail and chick embryos between HH16 and HH29 stages. Most proepicardial cells, mesothelial as well as mesenchymal, were cytokeratin and vimentin immunoreactive, suggesting a cytoskeletal shift from the epithelial to the mesenchymal type. Furthermore, we immunolocated, in the proepicardial mesothelium, three proteins specifically expressed during the endothelial-mesenchymal transition of the endocardial cushions, namely the JB3/fibrillin-associated antigen, the ES/130 protein and the smooth muscle cell alpha-actin. Grafts of proepicardial tissue from HH16-17 quail embryos into chick embryos of the same age originated large areas of donor-derived epicardium, including mesothelial, mesenchymal, and vascular cells. The donor-derived primitive epicardium showed segment-specific features, being squamous and adhered to the myocardium on the atrial wall and showing morphological signs of ingression in the atrioventricular groove and outflow tract. These morphological traits together with the distribution of vimentin, the ES/130 protein, and the JB3/fibrillin-associated antigen suggested a localized transformation of some epicardial mesothelial cells into mesenchyme. Most of the donor-derived cells, mesothelial and mesenchymal, showed the vascular marker QH1, which frequently colocalized with cytokeratin. Heterotopic grafts of quail splanchnopleura into the pericardial cavity of chick embryos originated a squamous, epicardial-like, cytokeratin-immunoreactive cell layer on the heart surface, as well as a few QH1(+) subepicardial and intramyocardial cells. The results suggest that a substantial part of the subepicardial mesenchyme, including the progenitors of the cardiac vessels, originates from the transformation of proepicardial and epicardial mesothelial cells into mesenchyme, and that the epicardial transition could be driven by a segment-specific myocardial signal.

Animals↗