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Journal articles on the topic 'Disease cycle'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

De Wolf, Erick D., and Scott A. Isard. "Disease Cycle Approach to Plant Disease Prediction." Annual Review of Phytopathology 45, no. 1 (September 8, 2007): 203–20. http://dx.doi.org/10.1146/annurev.phyto.44.070505.143329.

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2

Musacchio, Andrea, and Kristian Helin. "Cell cycle, differentiation and disease." Current Opinion in Cell Biology 25, no. 6 (December 2013): 673–75. http://dx.doi.org/10.1016/j.ceb.2013.09.003.

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3

Dwyer, Barney, Atsushi Takeda, Xiongwei Zhu, George Perry, and Mark Smith. "Ferric Cycle Activity and Alzheimer Disease." Current Neurovascular Research 2, no. 3 (July 1, 2005): 261–67. http://dx.doi.org/10.2174/1567202054368371.

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4

Grange, John, and Alimuddin Zumla. "Tuberculosis and the poverty-disease cycle." Journal of the Royal Society of Medicine 92, no. 3 (March 1999): 105–7. http://dx.doi.org/10.1177/014107689909200301.

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5

NABEL, E. G., M. BOEHM, L. M. AKYUREK, T. YOSHIMOTO, M. F. CROOK, M. OLIVE, H. SAN, and X. QU. "Cell Cycle Signaling and Cardiovascular Disease." Cold Spring Harbor Symposia on Quantitative Biology 67 (January 1, 2002): 163–70. http://dx.doi.org/10.1101/sqb.2002.67.163.

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6

Shankland, Stuart J. "Cell-cycle control and renal disease." Kidney International 52, no. 2 (August 1997): 294–308. http://dx.doi.org/10.1038/ki.1997.335.

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7

Baehr, Wolfgang, Samuel M. Wu, Alan C. Bird, and Krzysztof Palczewski. "The retinoid cycle and retina disease." Vision Research 43, no. 28 (December 2003): 2957–58. http://dx.doi.org/10.1016/j.visres.2003.10.001.

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8

Doobin, David J., Tiago J. Dantas, and Richard B. Vallee. "Microcephaly as a cell cycle disease." Cell Cycle 16, no. 3 (November 16, 2016): 247–48. http://dx.doi.org/10.1080/15384101.2016.1252591.

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9

Shankland, Stuart J. "Cell Cycle Proteins in Glomerular Disease." Kidney and Blood Pressure Research 21, no. 2-4 (1998): 213–14. http://dx.doi.org/10.1159/000025857.

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10

Griffin, Si�n V., Raimund Pichler, Mary Dittrich, Raghu Durvasula, and Stuart J. Shankland. "Cell cycle control in glomerular disease." Springer Seminars in Immunopathology 24, no. 4 (May 1, 2003): 441–57. http://dx.doi.org/10.1007/s00281-003-0120-8.

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11

Pinkerton, JoAnn V., Christine J. Guico-Pabia, and Hugh S. Taylor. "Menstrual cycle-related exacerbation of disease." American Journal of Obstetrics and Gynecology 202, no. 3 (March 2010): 221–31. http://dx.doi.org/10.1016/j.ajog.2009.07.061.

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12

Akperbekova, S. A. "Symptoms and Duration of the Menstrual Cycle and Vaccination against Coronavirus Disease (COVID-19)." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 7, no. 3 (July 2, 2022): 92–98. http://dx.doi.org/10.26693/jmbs07.03.092.

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The purpose of the study was to determine the association of COVID-19 vaccination with changes in cycle or duration of menstruation during menstrual cycles while receiving vaccine doses. Materials and methods. The study included 200 women aged from 20 to 38 who had at least three cycles after pregnancy or after using hormonal contraception. The women were vaccinated with Pfizer-BioNTech (Pfizer) and CoronaVac (Sinovac) (Sinovac Biotech) vaccines. The distribution of women by age is as follows: 20–24, 25–29, 30–34, 35–38 years. Additional characteristics included parity (nulliparous versus parous), body mass index, which was classified as underweight or normal weight, overweight or obese; education and relationship status (sustainable relationship or not). Results and discussion. Of 200 women included in the study, 110 (55.0%) patients were vaccinated, 90 (45.0%) were unvaccinated. Average age of vaccinated was 31.6 ± 2.88 years, unvaccinated – 29.3 ± 3.05 years (t = 0.55, p = 0.584). Among 110 vaccinated women, 73.6% had regular menstrual cycles before the introduction of the vaccine during the last year, among 90 unvaccinated women, 74.4% of women had regular menstrual cycles. Menstrual irregularities among those who were vaccinated and those who did not undergo COVID-19 were 11.8% and 14.5%, respectively. Symptoms appeared within a week in 27.6%. In 62.1% of cases, symptoms appeared after the first dose, in 37.9% of cases – after the second dose. There was a significant difference between menstrual irregularities during the COVID-19 pandemic and menstrual irregularities after vaccination (p < 0.001). The study showed that 26.4% of our sample complained of menstrual irregularities after vaccination against COVID-19, especially after the first dose (16.4%). The type of vaccine did not affect the frequency of menstrual disorders in these women. After vaccination, women reported significantly longer average duration of menstruation and duration of the menstrual cycle compared to their condition before vaccination. These symptoms decreased a month after vaccination. Although 27.6% had a clinically noticeable change in cycle duration by 7-8 days, this change rapidly weakened during two post-vaccination cycles. We found no significant changes in the duration of menstruation between vaccination doses. Conclusion. Among women who received vaccines against COVID-19, 26.4% of cases had menstrual irregularities. When counseling women who have received a COVID-19 vaccine, it is advisable to inform them of the possible occurrence of temporary and self-limiting menstrual irregularities in the following months

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13

Cole, Scott, and Bradley Voytek. "Cycle-by-cycle analysis of neural oscillations." Journal of Neurophysiology 122, no. 2 (August 1, 2019): 849–61. http://dx.doi.org/10.1152/jn.00273.2019.

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Neural oscillations are widely studied using methods based on the Fourier transform, which models data as sums of sinusoids. This has successfully uncovered numerous links between oscillations and cognition or disease. However, neural data are nonsinusoidal, and these nonsinusoidal features are increasingly linked to a variety of behavioral and cognitive states, pathophysiology, and underlying neuronal circuit properties. We present a new analysis framework, one that is complementary to existing Fourier and Hilbert transform-based approaches, that quantifies oscillatory features in the time domain on a cycle-by-cycle basis. We have released this cycle-by-cycle analysis suite as “bycycle,” a fully documented, open-source Python package with detailed tutorials and troubleshooting cases. This approach performs tests to assess whether an oscillation is present at any given moment and, if so, quantifies each oscillatory cycle by its amplitude, period, and waveform symmetry, the latter of which is missed with the use of conventional approaches. In a series of simulated event-related studies, we show how conventional Fourier and Hilbert transform approaches can conflate event-related changes in oscillation burst duration as increased oscillatory amplitude and as a change in the oscillation frequency, even though those features were unchanged in simulation. Our approach avoids these errors. Furthermore, we validate this approach in simulation and against experimental recordings of patients with Parkinson’s disease, who are known to have nonsinusoidal beta (12–30 Hz) oscillations. NEW & NOTEWORTHY We introduce a fully documented, open-source Python package, bycycle, for analyzing neural oscillations on a cycle-by-cycle basis. This approach is complementary to traditional Fourier and Hilbert transform-based approaches but avoids specific pitfalls. First, bycycle confirms an oscillation is present, to avoid analyzing aperiodic, nonoscillatory data as oscillations. Next, it quantifies nonsinusoidal aspects of oscillations, increasingly linked to neural circuit physiology, behavioral states, and diseases. This approach is tested against simulated and real data.

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14

Nagy, Zsuzsanna. "Cell Cycle-Related Protein Expression in Alzheimer's Disease and Vascular Disease." International Psychogeriatrics 15, S1 (July 2003): 77–79. http://dx.doi.org/10.1017/s1041610203009001.

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The link between Alzheimer's disease and cerebrovascular disease has been long recognized. However, the mechanisms that lead to the development of the two seemingly different pathologies are still elusive. Our studies concentrate on the understanding of the interaction between the two diseases and the deciphering of a possible common pathogenic mechanism. In this context the role of shared risk factors, such as ApoE and elevated plasma homocysteine, is also discussed.

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15

Jankowitz, Rachel C., Margaret V. Ragni, Holly L. Chapman, Elizabeth P. Merricks, Mark T. Kloos, Aaron M. Dillow, Helen Franck, and Timothy C. Nichols. "Recombinant Interleukin-11 (rhIL-11) in Women with Refractory Menorrhagia and Von Willebrand Disease." Blood 112, no. 11 (November 16, 2008): 1210. http://dx.doi.org/10.1182/blood.v112.11.1210.1210.

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Abstract Von Willebrand disease (VWD) is the single most common congenital bleeding disorder, and among women, menorrhagia is the most common bleeding symptom. Although DDAVP is the treatment of choice for those with type 1 VWD, its use may be limited by tachyphylaxis, allergic reactions, or unresponsiveness. We previously showed that recombinant human IL-11 (rhIL-11, Neumega), a gp-130 signaling cytokine with hematopoietic and anti-inflammatory activity, increases VWF levels 2–3 fold when given subcutaneously daily in individuals with mild VWD, and is well tolerated. We, therefore, initiated a Phase II clinical trial to determine the efficacy and safety of rhIL-11 in women with VWD and refractory menorrhagia, despite estrogen, DDAVP, and/or other treatment. We report the results of the first four subjects, age 28–40, with VWF:RCo 0.22–0.37 U/ml at diagnosis, normal VWF multimers, and bleeding severity scores (BSS) 4–6. rhIL-11 was given in a daily subcutaneous dose of 25 mcg/kg for 4 days, followed by monthly home self-injection for up to 7 days during each of six consecutive menstrual cycles, beginning on the first day of each cycle. Menstrual bleeding severity was measured by a validated bleeding pictorial assessment chart (BPAC) (Janssen, Obstet Gynecol, 1995) and cycle severity rating (CSR), as compared with two pre-treatment baseline menstrual cycles. BPAC scores were compared with standardized cutoff score for menorrhagia of 185. Cycle severity ratings (CSR) were rated on a nominal scale, with 0=mild bleeding; 1=moderate bleeding, less than usual cycle; 2= moderately severe bleeding, not as severe as worst cycle; and 3=severe bleeding, as severe as worst cycle. The drug was well tolerated with less than grade 1 toxicity, including mild conjunctival erythema and mild fluid retention (fingers) in one each. Following treatment with rhIL-11, there was a significant reduction in BPAC and cycle severity rating during the seven days the drug was given, as compared with the first seven days in cycles prior to rhIL-11 (see Table). Cycle length also shortened, but this did not reach significance. These was an associated increase in VWF:RCo, VWF:Ag, and FVIII:C on day 4 of rhIL-11 dosing, as compared with pre-rhIL-11 levels day 1. These data suggest that rhIL-11 improves hemostasis and reduces bleeding severity when used during the first seven days of menses in women with VWD. Further studies are needed to confirm these findings. Mensural Cycle Bleeding Severity in Women with VWD With and Without rhIL-11 No. Cycles Bleeding Pictorial Chart (BPAC) No. >185 Cycle Severity Rating (CSR) Cycle Length (Day) VWF:Rco U/ml VWF:Ag U/ml FVIII:C U/ml Significance, *p<0.05; †p<0.01; ‡p=0.014 CYCLES WITHOUT rhIL-11 7 6/7 (85.7%) 2.0±5 12±5 0.92±0.13 1.16 ± 0.06 0.60±0.09 CYCLES WITH rhIL-11 15 4/15 (23.5) ‡ 1.1±0.2† 7±1 1.71±0.17† 1.70±0.17† 1.02 ± 0.12*

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16

Gilbert, Michael A., and Willard O. Granath. "WHIRLING DISEASE OF SALMONID FISH: LIFE CYCLE, BIOLOGY, AND DISEASE." Journal of Parasitology 89, no. 4 (August 2003): 658–67. http://dx.doi.org/10.1645/ge-82r.

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17

McDonald, B. A., and C. Linde. "Disease resistance and pathogen population genetic." Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (January 1, 2002): 245–48. http://dx.doi.org/10.17221/10375-pps.

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Plant pathologists have seen many boom-and-bust cycles following the deployment of resistant varieties. These cycles result when pathogen populations adapt to the presence of a major resistance gene by evolving a new population that can overcome this resistance gene. The breakdown of genetic resistance is due to the evolution of the local pathogen population because of selection for mutants, recombinants, or immigrants that are better adapted to the resistant cultivar. To understand the process that leads to breakdown of a resistance gene, we need to understand the processes that govern pathogen evolution. Population geneticists have identified five evolutionary forces that interact to affect the evolution of organisms. We ranked these risks and developed a quantitative framework to predict the risk that a pathogen will evolve to overcome major resistance genes. Our hypothesis is that much of the durability of resistance genes is due to the nature of the pathogen population rather than to the nature of the resistance gene. The framework we developed can be used as a hypothesis to test against a large number of plant pathosystems. The underlying principles of the framework can be tested individually or in combination according to the available knowledge of the population genetics for any pathogen. We propose that this framework can be used to design breeding strategies to break the boom-and-bust cycle and lead to durable resistance.

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18

Bowser, Robert, and Mark A. Smith. "Cell cycle proteins in Alzheimer's disease: Plenty of wheels but no cycle." Journal of Alzheimer's Disease 4, no. 3 (July 23, 2002): 249–54. http://dx.doi.org/10.3233/jad-2002-4316.

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19

Prentki, Marc, and S. R. Murthy Madiraju. "Glycerolipid Metabolism and Signaling in Health and Disease." Endocrine Reviews 29, no. 6 (July 7, 2008): 647–76. http://dx.doi.org/10.1210/er.2008-0007.

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Abstract Maintenance of body temperature is achieved partly by modulating lipolysis by a network of complex regulatory mechanisms. Lipolysis is an integral part of the glycerolipid/free fatty acid (GL/FFA) cycle, which is the focus of this review, and we discuss the significance of this pathway in the regulation of many physiological processes besides thermogenesis. GL/FFA cycle is referred to as a “futile” cycle because it involves continuous formation and hydrolysis of GL with the release of heat, at the expense of ATP. However, we present evidence underscoring the “vital” cellular signaling roles of the GL/FFA cycle for many biological processes. Probably because of its importance in many cellular functions, GL/FFA cycling is under stringent control and is organized as several composite short substrate/product cycles where forward and backward reactions are catalyzed by separate enzymes. We believe that the renaissance of the GL/FFA cycle is timely, considering the emerging view that many of the neutral lipids are in fact key signaling molecules whose production is closely linked to GL/FFA cycling processes. The evidence supporting the view that alterations in GL/FFA cycling are involved in the pathogenesis of “fatal” conditions such as obesity, type 2 diabetes, and cancer is discussed. We also review the different enzymatic and transport steps that encompass the GL/FFA cycle leading to the generation of several metabolic signals possibly implicated in the regulation of biological processes ranging from energy homeostasis, insulin secretion and appetite control to aging and longevity. Finally, we present a perspective of the possible therapeutic implications of targeting this cycling.

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20

MORI, OSAMU, HIROSHI HACHISUKA, YASUHIKO MAEYAMA, and YOICHIRO SASAI. "Cell Cycle Analyses of Extramammary Paget's Disease." Kurume Medical Journal 40, no. 3 (1993): 129–32. http://dx.doi.org/10.2739/kurumemedj.40.129.

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21

Shea, Thomas B. "Folate, the methionine cycle, and Alzheimer's disease." Journal of Alzheimer's Disease 9, no. 4 (August 7, 2006): 359–60. http://dx.doi.org/10.3233/jad-2006-9401.

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22

Shankland, Stuart J. "Cell cycle regulatory proteins in glomerular disease." Kidney International 56, no. 4 (October 1999): 1208–15. http://dx.doi.org/10.1046/j.1523-1755.1999.00709.x.

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23

Fowler, Brian. "The folate cycle and disease in humans." Kidney International 59, s78 (February 2001): 221–29. http://dx.doi.org/10.1046/j.1523-1755.2001.07851.x.

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24

Fowler, Brian. "The folate cycle and disease in humans." Kidney International 59 (February 2001): S221—S229. http://dx.doi.org/10.1046/j.1523-1755.2001.59780221.x.

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25

Shankland, Stuart J., and Mouhannad Al’Douahji. "Cell Cycle Regulatory Proteins in Glomerular Disease." Nephron Experimental Nephrology 7, no. 3 (May 28, 1999): 207–11. http://dx.doi.org/10.1159/000020603.

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26

Hanif, J., S. S. M. Jawad, and R. Eccles. "The nasal cycle in health and disease." Clinical Otolaryngology and Allied Sciences 25, no. 6 (June 2000): 461–67. http://dx.doi.org/10.1046/j.1365-2273.2000.00432.x.

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27

Grahammer, Florian, and Tobias B. Huber. "Aberrant podocyte cell cycle in glomerular disease." Cell Cycle 15, no. 17 (July 29, 2016): 2237–38. http://dx.doi.org/10.1080/15384101.2016.1205413.

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28

Hansmannel, Franck, David Mann, Corinne Lendon, Jean Jacques Hauw, Geoffroy Laumet, Anne Marie Ayral, Julien Chapuis, et al. "P4-101: Urea cycle and Alzheimer's disease." Alzheimer's & Dementia 5, no. 4S_Part_15 (July 2009): P461. http://dx.doi.org/10.1016/j.jalz.2009.04.769.

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29

Marshall, Caroline B., and Stuart J. Shankland. "Cell Cycle and Glomerular Disease: A Minireview." Nephron Experimental Nephrology 102, no. 2 (2006): e39-e48. http://dx.doi.org/10.1159/000088400.

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30

Piccolo, Stefano, and Eduard Batlle. "Editorial overview: Cell cycle, differentiation and disease." Current Opinion in Cell Biology 31 (December 2014): v—vi. http://dx.doi.org/10.1016/j.ceb.2014.10.003.

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31

Vissing, John, and Ronald G. Haller. "A diagnostic cycle test for McArdle's disease." Annals of Neurology 54, no. 4 (September 25, 2003): 539–42. http://dx.doi.org/10.1002/ana.10725.

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32

Wang, Yi-Xin, Jennifer J. Stuart, Janet W. Rich-Edwards, Stacey A. Missmer, Kathryn M. Rexrode, Leslie V. Farland, Kenneth J. Mukamal, et al. "Menstrual Cycle Regularity and Length Across the Reproductive Lifespan and Risk of Cardiovascular Disease." JAMA Network Open 5, no. 10 (October 25, 2022): e2238513. http://dx.doi.org/10.1001/jamanetworkopen.2022.38513.

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ImportanceMenstrual cycle characteristics may be associated with an increased risk of cardiovascular disease (CVD). However, existing studies are limited, and few have explored the mediating role of established CVD risk factors.ObjectiveTo explore the associations of menstrual cycle characteristics across the reproductive lifespan with the risk of CVD and to what extent these associations were mediated by hypercholesterolemia, chronic hypertension, and type 2 diabetes.Design, Setting, and ParticipantsThis cohort study prospectively followed Nurses’ Health Study II participants between 1993 and 2017 who reported menstrual cycle regularity and length for ages 14 to 17 years and 18 to 22 years at enrollment in 1989 and updated current cycle characteristics in 1993 (at ages 29 to 46 years). Data analysis was performed from October 1, 2019, to January 1, 2022.ExposuresMenstrual cycle regularity and length across the reproductive lifespan.Main Outcomes and MeasuresIncident CVD events of interest, including fatal and nonfatal coronary heart disease (CHD; myocardial infarction [MI] or coronary revascularization) and stroke.ResultsA total of 80 630 Nurses’ Health Study II participants were included in the analysis, with a mean (SD) age of 37.7 (4.6) years and body mass index of 25.1 (5.6) at baseline. Over 24 years of prospective follow-up, 1816 women developed their first CVD event. Multivariable Cox proportional hazards models showed that, compared with women reporting very regular cycles at the same ages, women who had irregular cycles or no periods at ages 14 to 17, 18 to 22, or 29 to 46 years had hazard ratios for CVD of 1.15 (95% CI, 0.99-1.34), 1.36 (95% CI, 1.06-1.75), and 1.40 (95% CI, 1.14-1.71), respectively. Similarly, compared with women reporting a cycle length of 26 to 31 days, women reporting a cycle length 40 days or more or a cycle too irregular to estimate from ages 18 to 22 or 29 to 46 years had hazard ratios for CVD of 1.44 (95% CI, 1.13-1.84) and 1.30 (95% CI, 1.09-1.57), respectively. Mediation analyses showed that subsequent development of hypercholesteremia, chronic hypertension, and type 2 diabetes only explained 5.4% to 13.5% of the observed associations.Conclusions and RelevanceIn this cohort study, both irregular and long menstrual cycles were associated with increased rates of CVD, which persisted even after accounting for subsequently established CVD risk factors.

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33

Quarmby, Lynne M., and Jeremy D. K. Parker. "Cilia and the cell cycle?" Journal of Cell Biology 169, no. 5 (May 31, 2005): 707–10. http://dx.doi.org/10.1083/jcb.200503053.

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A recent convergence of data indicating a relationship between cilia and proliferative diseases, such as polycystic kidney disease, has revived the long-standing enigma of the reciprocal regulatory relationship between cilia and the cell cycle. Multiple signaling pathways are localized to cilia in mammalian cells, and some proteins have been shown to act both in the cilium and in cell cycle regulation. Work from the unicellular alga Chlamydomonas is providing novel insights as to how cilia and the cell cycle are coordinately regulated.

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34

Gusella, James F. "The Genetic Research Cycle in Human Disease: The Huntington's Disease Paradigm." Journal of Medical Sciences 2, no. 1 (February 10, 2009): 29–32. http://dx.doi.org/10.2174/1996327000902010029.

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35

Colbach, Nathalie, Philippe Lucas, and Jean-Marc Meynard. "Influence of Crop Management on Take-All Development and Disease Cycles on Winter Wheat." Phytopathology® 87, no. 1 (January 1997): 26–32. http://dx.doi.org/10.1094/phyto.1997.87.1.26.

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Wheat was assessed at four crop growth stages for take-all (Gaeumannomyces graminis var. tritici) in a series of field trials that studied the effects of five wheat management practices: sowing date, plant density, nitrogen fertilizer dose and form, and removal/burial of cereal straw. An equation expressing disease level as a function of degree days was fitted to the observed disease levels. This equation was based on take-all epidemiology and depended on two parameters reflecting the importance of the primary and secondary infection cycles, respectively. Early sowing always increased disease frequency via primary infection cycle; its influence on the secondary cycle was variable. Primary infection and earliness of disease onset were increased by high density; however, at mid-season take-all was positively correlated to the root number per plant, which was itself negatively correlated to plant density. At late stages of development, neither plant density nor root number per plant had any influence on disease. A high nitrogen dose increased both take-all on seminal roots and severity of primary infection cycle but decreased take-all on nodal roots and secondary infection cycle. Ammonium (versus ammonium nitrate) fertilizer always decreased disease levels and infection cycles, whereas straw treatment (burial versus removal of straw from the previous cereal crop) had no influence.

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36

Wang, Yingjie, Qiuju Chen, and Yun Wang. "Effects of Different Endometrial Preparation Regimens during IVF on Incidence of Ischemic Placental Disease for FET Cycles." Journal of Clinical Medicine 11, no. 21 (November 2, 2022): 6506. http://dx.doi.org/10.3390/jcm11216506.

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We conducted this retrospective cohort study aiming to compare the different pregnancy outcomes of endometrial preparation regimens on ischemic placental disease in a frozen embryo transfer cycle. The study included a total of 9351 women who had undergone therapy at our single tertiary hospital from January 2015 to July 2020. The women were divided into three groups depending on their endometrial regimens: natural cycle, stimulation cycle, hormone replacement therapy cycle. The data were analyzed after propensity score matching, then we used multiple linear regression to study the relationship between ischemic placental disease and endometrial regimens, adjusted by confounding factors including age, body mass index, and score of propensity score matching. We performed univariate logistic regression, as well as multivariate logistic regression for ischemic placental disease, small for gestational age infant, placental abruption. and pre-eclampsia, respectively, listing the odds ratio and p-values in the table. As a result, risk of ischemic placental disease and small for gestational age infant were detected as higher in stimulation cycles compared to natural cycles before or after adjustment. Hormone replacement therapy cycles conferred a higher risk of pre-eclampsia and preterm delivery compared to natural cycles. No difference was found between stimulation cycles and hormone replacement therapy cycles, regardless of whether they are adjusted or not. In summary, more pharmacological intervention in endometrial preparation was associated with a higher risk of ischemic placental disease related symptoms than natural cycles for endometrial preparation in women undergoing frozen embryo transfer. Our findings supported that minimizing pharmacological interventions during endometrial preparation when conditions permit has positive implications for improving pregnancy outcomes.

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37

Pall, Martin L. "Pulmonary Hypertension Is a Probable NO/ONOO− Cycle Disease: A Review." ISRN Hypertension 2013 (September 4, 2013): 1–27. http://dx.doi.org/10.5402/2013/742418.

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The NO/ONOO− cycle is a primarily local biochemical/physiological vicious cycle that appears to cause a series of chronic inflammatory diseases. This paper focuses on whether the cycle causes pulmonary arterial hypertension (PAH) when located in the pulmonary arteries. The cycle involves 12 elements, including superoxide, peroxynitrite (ONOO−), nitric oxide (NO), oxidative stress, NF-κB, inflammatory cytokines, iNOS, mitochondrial dysfunction, intracellular calcium, tetrahydrobiopterin depletion, NMDA activity, and TRP receptor activity. 10 of the 12 are elevated in PAH (NMDA?, NO?) and 11 have documented causal roles in PAH. Each stressor that initiates cases of PAH acts to raise cycle elements, and may, therefore, initiate the cycle in this way. PAH involves a primarily local mechanism as required by the cycle and the symptoms and signs of PAH are generated by elements of the cycle. Endothelin-1, which acts as a causal factor in PAH, acts as part of the cycle; its synthesis is stimulated by cycle elements, and it, in turn, increases each element of the cycle. This extraordinary fit to the principles of the NO/ONOO− cycle allows one to conclude that PAH is a NO/ONOO− cycle disease, and this fit supports the cycle as a major paradigm of chronic inflammatory disease.

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38

Peh, Woei Ling, Kate Middleton, Neil Christensen, Philip Nicholls, Kiyofumi Egawa, Karl Sotlar, Janet Brandsma, et al. "Life Cycle Heterogeneity in Animal Models of Human Papillomavirus-Associated Disease." Journal of Virology 76, no. 20 (October 15, 2002): 10401–16. http://dx.doi.org/10.1128/jvi.76.20.10401-10416.2002.

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ABSTRACT Animal papillomaviruses are widely used as models to study papillomavirus infection in humans despite differences in genome organization and tissue tropism. Here, we have investigated the extent to which animal models of papillomavirus infection resemble human disease by comparing the life cycles of 10 different papillomavirus types. Three phases in the life cycles of all viruses were apparent using antibodies that distinguish between early events, the onset of viral genome amplification, and the expression of capsid proteins. The initiation of these phases follows a highly ordered pattern that appears important for the production of virus particles. The viruses examined included canine oral papillomavirus, rabbit oral papillomavirus (ROPV), cottontail rabbit papillomavirus (CRPV), bovine papillomavirus type 1, and human papillomavirus types 1, 2, 11, and 16. Each papillomavirus type showed a distinctive gene expression pattern that could be explained in part by differences in tissue tropism, transmission route, and persistence. As the timing of life cycle events affects the accessibility of viral antigens to the immune system, the ideal model system should resemble human mucosal infection if vaccine design is to be effective. Of the model systems examined here, only ROPV had a tissue tropism and a life cycle organization that resembled those of the human mucosal types. ROPV appears most appropriate for studies of the life cycles of mucosal papillomavirus types and for the development of prophylactic vaccines. The persistence of abortive infections caused by CRPV offers advantages for the development of therapeutic vaccines.

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Allen, Shari N. "Urea cycle disorder." Mental Health Clinician 2, no. 12 (June 1, 2013): 398–401. http://dx.doi.org/10.9740/mhc.n155467.

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Urea cycle disorder is a rare genetic disorder in which there is a full or partial deficiency in the enzymes of the urea cycle, causing a defect in the metabolism of excess nitrogen, and leading to hyperammonemia. This article reviews the clinical presentation, diagnosis, treatment, and drug-disease state implications of urea cycle disorders.

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Woyach, Jennifer A., Amy S. Ruppert, Farrukh Awan, Jeffrey A. Jones, Sharon Waymer, Gerard Lozanski, Natarajan Muthusamy, and John C. Byrd. "A Phase II Study of the Fc Engineered CD19 Antibody MOR208 in Combination with Lenalidomide for Patients with Chronic Lymphocytic Leukemia (CLL)." Blood 126, no. 23 (December 3, 2015): 2953. http://dx.doi.org/10.1182/blood.v126.23.2953.2953.

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Abstract MOR208 is an Fc engineered CD19 monoclonal antibody which has been shown in a Phase I trial in patients with relapsed and refractory CLL to be generally well tolerated and have preliminary efficacy, with an overall response rate (ORR) of 30% by IWCLL 2008 guidelines (Woyach et al, Blood 2014). Compared to non-engineered CD19 monoclonal antibodies, MOR208 has significantly enhanced antibody dependent cellular cytotoxicity (ADCC), which can be further augmented in vitro with the addition of lenalidomide. Given the in vitro synergy of these agents, acceptable individual safety profiles, and efficacy of each as a single agent, we chose to combine MOR208 and lenalidomide in patients with both previously treated and previously untreated CLL. This study is a single institution phase II trial of MOR208 in combination with lenalidomide with an initial safety run-in as part of each cohort. MOR208 was given at a dose of 1 mg/kg on cycle 1 day 1, then 9 mg/kg on days 2, 8, 15, and 22 of cycle 1, and then on day 1 of cycles 2-12. Lenalidomide was started at a dose of 2.5 mg daily on cycle 1 day 8 and given continuously. The dose of lenalidomide could be escalated up to 10 mg daily in patients without toxicity. After 12 cycles, lenalidomide could be continued indefinitely in responding patients. Toxicity was assessed using the National Cancer Institute's Common Criteria for Adverse Events v4.0 for non-hematologic toxicity, and IWCLL 2008 guidelines for hematologic toxicity. Disease response by IWCLL 2008 guidelines was assessed at cycle 7 day 1 and at the end of cycle 12. This study will enroll 20 patients with treatment-naïve CLL and 20 patients with relapsed/refractory CLL. At this time, 7 patients with relapsed/refractory disease and 5 patients with treatment-naïve disease have been enrolled and evaluated. The most common toxicities observed related to protocol therapy have been infusion related reactions, fatigue, thrombocytopenia, and neutropenia. In patients with relapsed disease, all toxicities except neutropenia have been grade 1 or 2, and 2 patients experienced grade 3 neutropenia. Of the 5 patients with treatment-naïve CLL, two experienced significant infusion reactions on cycle 1 day 1 that prevented further administration of MOR208. After a protocol amendment escalating steroid premedication, no further grade 3 infusion reactions have been observed. While the majority of patients were able to escalate lenalidomide to either 5 or 10 mg, all patients had lenalidomide eventually dose reduced to 2.5 mg daily due to cytopenias, rash, or fatigue. This combination has shown preliminary efficacy. In the cohort of patients with relapsed disease, two experienced progressive disease during cycle 2 and cycle 5 respectively. The remaining 5 patients achieved stable disease (SD, n=3) or a partial response (PR, n=2) at cycle 7 day 1, with one patient converting to PR by cycle 12. Three patients completed 12 cycles of therapy, and the remaining two completed 12 cycles and now remain on lenalidomide alone at cycle 18 and cycle 19 respectively. In the cohort of patients with treatment-naïve disease, three patients completed more than 1 day of therapy. All of these patients achieved a PR at cycle 7 day 1, and are now in cycle 10 (n=1) or cycle 11 (n=2). In conclusion, this Phase II trial in progress demonstrates preliminary safety and activity of the combination of MOR208 and lenalidomide in patients with CLL. This combination also has the potential to positively modulate the immune system, and detailed correlative studies are evaluating T cell and NK cell function in these patients. Trial accrual is ongoing and updated results will be presented at the meeting. Disclosures Jones: AbbVie: Research Funding; Pharmacyclics LLC, an AbbVie Company: Consultancy, Research Funding. Byrd:Acerta Pharma BV: Research Funding.

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Liang, Feng, and Yi Wang. "Coronary heart disease and atrial fibrillation: a vicious cycle." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 1 (January 1, 2021): H1—H12. http://dx.doi.org/10.1152/ajpheart.00702.2020.

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The population suffering from coronary heart disease (CHD) complicated by atrial fibrillation (AF) is rising rapidly. A strong correlation between the two diseases has been reported, and the many common risk factors they share may play prominent roles in their development. In addition, CHD can directly promote the progression of AF by affecting reentry formation, focal ectopic activity, and neural remodeling. At the same time, AF also affects CHD through three aspects: 1) atherosclerosis, 2) the mismatch of blood supply and oxygen consumption, and 3) thrombosis. In conclusion, CHD and AF can aggravate each other and seem to form a vicious cycle. For patients with CHD complicated by AF, principal studies and guidelines have focused on antithrombotic treatment and rhythm control, which are paramount for these patients. Of note, our review sheds light on the strategies to break the cycle of the two diseases, which may be fundamental to treat these patients and optimize the benefit.

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Kharadi, Roshni R., Jeffrey K. Schachterle, Xiaochen Yuan, Luisa F. Castiblanco, Jingyu Peng, Suzanne M. Slack, Quan Zeng, and George W. Sundin. "Genetic Dissection of the Erwinia amylovora Disease Cycle." Annual Review of Phytopathology 59, no. 1 (August 25, 2021): 191–212. http://dx.doi.org/10.1146/annurev-phyto-020620-095540.

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Fire blight, caused by the bacterial phytopathogen Erwinia amylovora, is an economically important and mechanistically complex disease that affects apple and pear production in most geographic production hubs worldwide. We compile, assess, and present a genetic outlook on the progression of an E. amylovora infection in the host. We discuss the key aspects of type III secretion–mediated infection and systemic movement, biofilm formation in xylem, and pathogen dispersal via ooze droplets, a concentrated suspension of bacteria and exopolysaccharide components. We present an overall outlook on the genetic elements contributing to E. amylovora pathogenesis, including an exploration of the impact of floral microbiomes on E. amylovora colonization, and summarize the current knowledge of host responses to an incursion and how this response stimulates further infection and systemic spread. We hope to facilitate the identification of new, unexplored areas of research in this pathosystem that can help identify evolutionarily susceptible genetic targets to ultimately aid in the design of sustainable strategies for fire blight disease mitigation.

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Nagamani, Sandesh C. S., Saima Ali, Rima Izem, Deborah Schady, Prakash Masand, Benjamin L. Shneider, Daniel H. Leung, and Lindsay C. Burrage. "Biomarkers for liver disease in urea cycle disorders." Molecular Genetics and Metabolism 133, no. 2 (June 2021): 148–56. http://dx.doi.org/10.1016/j.ymgme.2021.04.001.

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Soodaeva, S. K., I. A. Klimanov, and L. Yu Nikitina. "Particularities of nitric oxide cycle in respiratory disease." Russian Pulmonology 26, no. 6 (January 1, 2016): 753–59. http://dx.doi.org/10.18093/0869-0189-2016-26-6-753-759.

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Quereda, Victor, and Marcos Malumbres. "Cell cycle control of pituitary development and disease." Journal of Molecular Endocrinology 42, no. 2 (November 5, 2008): 75–86. http://dx.doi.org/10.1677/jme-08-0146.

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The pituitary gland regulates diverse physiological functions, including growth, metabolism, reproduction, stress response, and ageing. Early genetic models in the mouse taught us that the pituitary is highly sensitive to genetic alteration of specific cell cycle regulators such as the retinoblastoma protein (pRB) or the cell cycle inhibitor p27Kip1. The molecular analysis of human pituitary neoplasias has now corroborated that cell cycle deregulation is significantly implicated in pituitary tumorigenesis. In particular, proteins involved in cyclin-dependent kinase regulation or the pRB pathway are altered in nearly all human pituitary tumors. Additional cell cycle regulators such as PTTG1/securin may have critical roles in promoting genomic instability in pituitary neoplasias. Recent experimental data suggest that these cell cycle regulators may have significant implications in the biology of putative progenitor cells and pituitary homeostasis. Understanding how cell cycle regulation controls pituitary biology may provide us with new therapeutic approaches against pituitary diseases.

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Hansmannel, Franck, Adeline Sillaire, M. Ilyas Kamboh, Corinne Lendon, Florence Pasquier, Didier Hannequin, Geoffroy Laumet, et al. "Is the Urea Cycle Involved in Alzheimer's Disease?" Journal of Alzheimer's Disease 21, no. 3 (September 2, 2010): 1013–21. http://dx.doi.org/10.3233/jad-2010-100630.

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García-Osta, Ana, Jinya Dong, María Jesús Moreno-Aliaga, and Maria Javier Ramirez. "p27, The Cell Cycle and Alzheimer´s Disease." International Journal of Molecular Sciences 23, no. 3 (January 21, 2022): 1211. http://dx.doi.org/10.3390/ijms23031211.

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The cell cycle consists of successive events that lead to the generation of new cells. The cell cycle is regulated by different cyclins, cyclin-dependent kinases (CDKs) and their inhibitors, such as p27Kip1. At the nuclear level, p27Kip1 has the ability to control the evolution of different phases of the cell cycle and oppose cell cycle progression by binding to CDKs. In the cytoplasm, diverse functions have been described for p27Kip1, including microtubule remodeling, axonal transport and phagocytosis. In Alzheimer’s disease (AD), alterations to cycle events and a purported increase in neurogenesis have been described in the early disease process before significant pathological changes could be detected. However, most neurons cannot progress to complete their cell division and undergo apoptotic cell death. Increased levels of both the p27Kip1 levels and phosphorylation status have been described in AD. Increased levels of Aβ42, tau hyperphosphorylation or even altered insulin signals could lead to alterations in p27Kip1 post-transcriptional modifications, causing a disbalance between the levels and functions of p27Kip1 in the cytoplasm and nucleus, thus inducing an aberrant cell cycle re-entry and alteration of extra cell cycle functions. Further studies are needed to completely understand the role of p27Kip1 in AD and the therapeutic opportunities associated with the modulation of this target.

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Bahn, Rebecca S. "Pathophysiology of Graves’ Ophthalmopathy: The Cycle of Disease." Journal of Clinical Endocrinology & Metabolism 88, no. 5 (May 1, 2003): 1939–46. http://dx.doi.org/10.1210/jc.2002-030010.

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Mulhall, JP, J. Branch, T. Lubrano, and TV Shankey. "Perturbation of cell cycle regulators in Peyronie’s disease." International Journal of Impotence Research 13, S5 (December 2001): S21—S28. http://dx.doi.org/10.1038/sj.ijir.3900771.

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Mancini, Anthony J., Hilary E. Baldwin, Lawrence F. Eichenfield, Sheila Fallon Friedlander, and Albert C. Yan. "Acne Life Cycle: The Spectrum of Pediatric Disease." Seminars in Cutaneous Medicine and Surgery 30, no. 3 (September 2011): S2—S5. http://dx.doi.org/10.1016/j.sder.2011.07.003.

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