Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “phasing”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 433 records · Page 24Linked to original sources
PubMed2005

Acute phase reaction and acute phase proteins.

A review of the systemic acute phase reaction with major cytokines involved, and the hepatic metabolic changes, negative and positive acute phase proteins (APPs) with function and associated pathology is given. It appears that APPs represent appropriate analytes for assessment of animal health. Whereas they represent non-specific markers as biological effect reactants, they can be used for assessing nutritional deficits and reactive processes, especially when positive and negative acute phase variables are combined in an index. When such acute phase index is applied to separate healthy animals from animals with some disease, much better results are obtained than with single analytes and statistically acceptable results for culling individual animals may be reached. Unfortunately at present no cheap, comprehensive and easy to use system is available for assessing various acute phase proteins in serum or blood samples at the same time. Protein microarray or fluid phase microchip technology may satisfy this need; and permit simultaneous analysis of numerous analytes in the same small volume sample and enable integration of information derived from systemic reactivity and nutrition with disease specific variables. Applying such technology may help to solve health problems in various countries not only in animal husbandry but also in human populations.

Acute-Phase Proteins↗
PubMed2003

Complexity of the mechanisms of initiation and maintenance of DNA damage-induced G2-phase arrest and subsequent G1-phase arrest: TP53-dependent and TP53-independent roles.

Through a detailed study of cell cycle progression, protein expression, and kinase activity in gamma-irradiated synchronized cultures of human skin fibroblasts, distinct mechanisms of initiation and maintenance of G2-phase and subsequent G1-phase arrests have been elucidated. Normal and E6-expressing fibroblasts were used to examine the role of TP53 in these processes. While G2 arrest is correlated with decreased cyclin B1/CDC2 kinase activity, the mechanisms associated with initiation and maintenance of the arrest are quite different. Initiation of the transient arrest is TP53-independent and is due to inhibitory phosphorylation of CDC2 at Tyr15. Maintenance of the G2 arrest is dependent on TP53 and is due to decreased levels of cyclin B1 mRNA and a corresponding decline in cyclin B1 protein level. After transiently arresting in G2 phase, normal cells chronically arrest in the subsequent G1 phase while E6-expressing cells continue to cycle. The initiation of this TP53-dependent G1-phase arrest occurs despite the presence of substantial levels of cyclin D1/CDK4 and cyclin E/CDK2 kinase activities, hyperphosphoryated RB, and active E2F1. CDKN1A (also known as p21(WAF1/CIP1)) levels remain elevated during this period. Furthermore, CDKN1A-dependent inhibition of PCNA activity does not appear to be the mechanism for this early G1 arrest. Thus the inhibition of entry of irradiated cells into S phase does not appear to be related to DNA-bound PCNA complexed to CDKN1A. The mechanism of chronic G1 arrest involves the down-regulation of specific proteins with a resultant loss of cyclin E/CDK2 kinase activity.

Cell Cycle↗
PubMed1987

The effects of inducing a follicular phase gonadotropin secretory pattern in normal women during the luteal phase.

It has been hypothesized that the slowing of the luteinizing hormone (LH) pulse frequency in the luteal phase may be necessary for the demise of the corpus luteum, the intercycle rise in baseline follicle-stimulating hormone (FSH), or ovarian follicular development in the subsequent cycle. For assessment of the physiologic role of the luteal phase LH pulse pattern, this pattern was converted to a follicular pattern in six normal women who used exogenous gonadotropin-releasing hormone administered with a portable pump (dose 50 to 100 ng/kg subcutaneously every 90 minutes beginning in the early luteal [n = 3] and midluteal [n = 3] cycle phases). There was no significant difference between the treated and the subsequent cycle for luteal progesterone production [186.3 versus 159.0 (ng/ml) day], preovulatory follicular size (23.1 versus 22.5 mm), estradiol levels, luteal phase length (15.6 versus 14.3 days), and daily gonadotropin concentrations including the intercycle FSH rise (160.5 versus 139.1 ng/ml). A follicular phase gonadotropin pulse pattern (increased frequency, decreased amplitude) in the luteal phase had no discernible effects on the corpus luteum or on follicular development in the subsequent cycle.

Adult↗
PubMed1996

[Current status of phase I and phase II trials--experience in Habikino from 1988 to 1994].

Introduction of a new agent in the treatment for cancer will require usually three phases of investigation. A new drug will be tested in a small series of patients for toxicity and feasibility; the main objective of a phase I trial is to determine the maximum tolerated dose with a specific type of administration. Demonstration of activity is the major goal of phase II trials, which will place some confidence interval on the efficacy of the new agent. Information obtained from phase I and II studies should be the basis for phase III trials. Based upon our experience with the clinical development of CPT-11, this paper reviews the two factors which influence the quality of the phase I and II trials. Firstly, adequately designed and prepared plans for every clinical trial are essential minimum requirement. Another issue which has been frequently overlooked has been variation from the planned protocol treatment. Such variations can be due to the intolerance of the patient to toxicity as well as the individual physician's poor perceptions and the physician's intolerance of toxicity.

Adult↗
PubMed1990

Subnormal follicular-phase serum progesterone levels and elevated follicular-phase serum estradiol levels in young women with insulin-dependent diabetes.

In a search for possible hormonal reasons for the loss of protection from myocardial infarction seen in diabetic women, serum levels of estradiol, progesterone, and luteinizing hormone were compared throughout a menstrual cycle (17 points) in eight healthy nonsmoking women and five otherwise healthy nonsmoking insulin-dependent diabetic women. The total length of the menstrual cycle and the lengths of the follicular and luteal phases did not differ between the groups. During the periovulatory and luteal phases, there was no significant intergroup difference with respect to any of the three hormones. During the follicular phase, in both groups, there was a plateau in serum progesterone concentration, with the level approximately 42% lower in the diabetic group (12.0 +/- 6.6 ng/dl versus 20.7 +/- 5.7; P less than 0.0001). Follicular-phase serum estradiol showed a rising curve in both groups; day-by-day comparison (days -10 to -3 before the luteinizing hormone peak) showed consistently higher levels in the diabetic group (mean, 108 pg/ml versus 95 pg/ml; P less than 0.001). The follicular-phase serum estradiol to progesterone ratio was nearly twice as high in the diabetic group as in the normal group (8.9 versus 4.6), a difference that was highly significant. The finding of elevated serum estradiol and subnormal serum progesterone concentrations during the follicular phase is so far unique to women with insulin-dependent diabetes mellitus. The possibility that this pronounced abnormality in diabetic women may be related to coronary disease merits testing in suitable in vivo and in vitro models of atherogenesis.

Adult↗
PubMed1983

Plasma gonadotropin and sex steroid hormone levels during early, midfollicular, and midluteal phases of women with luteal phase defects.

Thirteen women with luteal phase defects (LPD) confirmed by endometrial biopsies and 14 with histologically normal endometria were studied for early follicular and midfollicular phase follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels and for midluteal phase progesterone, estrogen, testosterone, and prolactin levels. The results showed that the women with LPD had significantly lower FSH levels and FSH/LH ratios in the early and midfollicular phases. LH levels, however, were similar in the LPD and normal women. During the midluteal phase, the LPD women showed significantly lower levels of progesterone and estrogen and normal levels of testosterone and prolactin. These findings reaffirm the prevailing concept that events surrounding follicular growth and development can indeed influence the quality of that cycle's corpus luteum. Furthermore, LPD as a result of hyperprolactinemia appears to be a different entity from that due to inadequate follicular phase FSH.

Adnexal Diseases↗
PubMed2003

Flow cytometric analysis of aneuploidy and S-phase fraction in chronic myeloid leukemia patients: role in early detection of accelerated phase.

We studied S-phase fraction (SPF) and aneuploidy in peripheral blood leucocytes of patients with chronic myeloid leukemia (CML) in chronic phase (CML-CP, n=41), accelerated phase (CML-AP, n=6), and control subjects (n=12) with an aim to find out their role in early detection of accelerated phase. The SPF and aneuploidy were studied through flow-cytometry using LT-Mod. Fit software. Mean SPF value in CML-AP (9.28+/-3.46%) and in CML-CP (4.76+/-2.30%) were significantly higher than in normal controls (0.28+/-0.21%), (P<0.005, P<0.001). CML-CP patients having higher SPF (>7%) converted to accelerated phase within 18 months of follow-up while those with lower SPF (<7%) did not. Aneuploidy was present in 34.14% of CML-CP and all patients of CML-AP whereas no control subjects showed aneuploidy. Among CML-CP patients having SPF >7%, 86% developed aneuploidy during follow-up as compared to 18.50% of CML-CP with less than 7% SPF. We conclude that peripheral blood SPF and aneuploidy could be important parameters for prediction of evolution to accelerated phase in CML patients.

Adult↗
PubMed2005

Differential effects of ferulic acid and p-coumaric acid on S phase distribution and length of S phase in the human colonic cell line Caco-2.

Ferulic acid (FA) and para-coumaric acid (p-CA) may mediate the protective effects of whole-grain cereals against colon cancer. Therefore, the effects of FA and p-CA on the metabolic activity, proliferation, cell cycle phase distribution, and kinetics of the colonic endothelial tumor cell line Caco-2 was studied. Both compounds at 1500 microM decreased the number of cells to 43-75% of control after 2-3 days of treatment. Cell cycle phase distribution and cell cycle kinetics were determined by flow cytometric analysis after bromodeoxyuridine labeling. Each compound at 1500 microM decreased the proportion of cells in the G(1) phase and increased the proportion of cells in the S and G(2) phases. Treatment with 1500 microM FA significantly increased the length of the S phase, while p-CA did not. It was concluded that FA and p-CA inhibited cell proliferation by presumably affecting different cell cycle phases, and this warrants further investigations because this inhibition may be one explanation for the diet-related protection against cancer.

Caco-2 Cells↗
PubMed1966

Growth phases of Mycoplasma in liquid media observed with phase-contrast microscope.

Razin, Shmuel (University of Connecticut, Storrs), and Benjamin J. Cosenza. Growth phases of Mycoplasma in liquid media observed with phase-contrast microscope. J. Bacteriol. 91:858-869. 1966-Growth of 11 Mycoplasma strains in liquid media was followed by phase-contrast microscopy. A similar pattern of development was common to all strains. Branching filaments, 0.3 to 0.4 mu thick, characterized the early logarithmic phase of growth. The length of the filaments varied according to the strain tested and the growth medium. Addition of oleic acid to the medium induced the formation of very long filaments by M. laidlawii strain B. Upon aging, the filaments were found to break up into chains of coccoid elements. These chains further fragmented to yield shorter chains and single coccoid elements, which characterized the stationary and decline phases of growth. The size of the coccoid elements increased from 0.3 to 0.4 mu, when formed in the filaments, to 0.6 to 0.8 mu after being released from the chains. Further increase in the size of the cells took place at the decline phase of growth, leading to the formation of very large cells reaching a diameter of 10 to 20 mu. However, these large cells had the appearance of empty vesicles and were apparently nonviable as indicated by viable-count experiments.

Culture Media↗
PubMed2005

Phase-space formulation for phase-contrast x-ray imaging.

Phase-space formulation based on the Wigner distribution has been presented for analyzing phase-contrast image formation. Based on the statistical nature and affine canonical covariance of Wigner distributions in the phase space, we show that the partial coherence effects of incident x-ray wave field on image intensity are simply accounted for by a multiplication factor, which is the reduced complex degree of coherence of the incident x-ray wave field. We show especially that with the undulator sources one cannot obtain the phase-contrast intensity by summing over the contributions from all electron positions, since the van Cittert-Zernike theorem fails in general for undulators. We derive a comprehensive formula that quantifies the effects of partial spatial coherence, polychromatic spectrum, body attenuation, imaging-detector resolution, and radiation dose on phase-contrast visibility in clinical imaging. The results of our computer modeling and simulations show how the formula can provide design guidelines and optimal parameters for clinical x-ray phase-contrast imaging systems.

Algorithms↗
PubMed1996

Uncoupling of M-phase kinase activation from the completion of S-phase by heat shock.

Chronic exposure of asynchronous HeLa cell cultures to 41.5 degrees C leads to an accumulation of cells in the S-phase, spontaneous premature chromosome condensation, and loss of clonogenicity (M.A. Mackey, S. L. Anolik, and J. L. Roti Roti. Cancer Res., 52: 1101-1106, 1992). In this report, we show that increases in histone H1 kinase activity during 41.5 degrees C exposure occur coincidentally with the appearance of premature chromosome condensation. Furthermore, this kinase activity is shown to be associated with M-phase kinase complexes containing cyclin B1. These increases in the activity of M-phase kinase were found to occur concomitantly with an elevation in cyclin B1 mRNA and an accumulation of cyclin B1 protein. Because cyclin B1 transcription begins in the S-phase, it is probable that the heat-induced delay in the S-phase allows the accumulation of abnormally high cyclin B1 levels. Elevated cyclin B1 levels could then account for the observed abrogation of the cell cycle checkpoint, which usually assures that mitosis does not proceed until DNA replication is complete. This involvement of M-phase kinase in heat-induced cytotoxicity demonstrates the importance of the coordinate regulation of the processes of DNA replication and entry into mitosis.

Cell Cycle↗
PubMed2004

Modern diagnostics in chronic myeloproliferative diseases (CMPDs).

According to the new WHO classification a group of chronic myeloproliferative diseases (CMPDs) were defined: chronic myeloid leukemia (CML), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia and hypereosinophilic syndrome (CEL/HES), polycythemia vera (PV), chronic idiopathic myelofibrosis (with extramedullary hematopoiesis, CIMF), essential thrombocythemia (ET), and so called CMPD/unclassifiable. As clinical features and laboratory findings differ widely between these diseases several diagnostic approaches are mandatory at diagnosis for classification and are needed also for follow up studies, especially for the measurement of minimal residual disease (MRD). We here outline the laboratory set up at diagnosis and during follow up in CMPDs with specific focus on the respective therapeutical consequences. Only by using a comprehensive diagnostic panel including cytomorphology, cytogenetics, and molecular genetic methods establishing the correct diagnosis, optimizing treatment as well as evaluating treatment response is possible in CMPDs today.

Blood Cell Count↗