373 research outputs found

    Population dynamics and reproduction biology of slender mudskipper (Scartelaos tenuis) from Hormuzgan Province creeks, Persian Gulf

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    Slender Mudskipper (Scartelaos tenuis) is one of the dominant fishes in inter-tidal mud flats area. Reproduction and population parameters of 2047 Slender mudskipper were studied monthly from october 2008 to september 2009. The asymptotic length (L∞) and growth coefficient (K) were estimated as 19.43(cm) and 0.64(yr-1), respectively. The minimum and maximum T.L. was 1.1 and 19.5cm, respectively. The value of to was -8.28, and Tmax was 4.6 year. The growth equation of Von Bertalanffy was obtained at L(t) = 19.43(1- exp (-0.64(t(-0.28))) for this species. The rates of natural mortality (M) on Pauly's empirical equation, was estimated 1.51 (yr-1). Five cohorts were distinguished annualy on Bhattacharya's method with mean length of 7.89, 11.42, 13.86, 15.6 and 16.81cm. Maximum recruitment was in Seprember at 18.8 percent. Reproductive studies showed that peak of maturity season occurred in April. The female to male ratio was calculated as 1:1.47 and chi-square analysis showed that it was statistically significant deviated from 1:1. LM50 is attained at a total length of 13.3cm. The mean of absolute and relative fecundity were 6742 (±1939) and 707 (±210), respectively. The length-weight relationship was as W= 0.02735 L 2.1655, that was isometric growth. Result showed that slender mudskipper population was in congenial condition, nevertheless less not evaluated

    Cytokinin response factor 6 represses cytokinin-associated genes during oxidative stress

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    Cytokinin is a phytohormone that is well known for its roles in numerous plant growth and developmental processes, yet it has also been linked to abiotic stress response in a less defined manner. Arabidopsis (Arabidopsis thaliana) Cytokinin Response Factor 6 (CRF6) is a cytokinin-responsive AP2/ERF-family transcription factor that, through the cytokinin signaling pathway, plays a key role in the inhibition of dark-induced senescence. CRF6 expression is also induced by oxidative stress, and here we show a novel function for CRF6 in relation to oxidative stress and identify downstream transcriptional targets of CRF6 that are repressed in response to oxidative stress. Analysis of transcriptomic changes in wild-type and crf6 mutant plants treated with H2O2 identified CRF6-dependent differentially expressed transcripts, many of which were repressed rather than induced. Moreover, many repressed genes also show decreased expression in 35S:CRF6 overexpressing plants. Together, these findings suggest that CRF6 functions largely as a transcriptional repressor. Interestingly, among the H2O2 repressed CRF6-dependent transcripts was a set of five genes associated with cytokinin processes: (signaling) ARR6, ARR9, ARR11, (biosynthesis) LOG7, and (transport) ABCG14. We have examined mutants of these cytokinin-associated target genes to reveal novel connections to oxidative stress. Further examination of CRF6-DNA interactions indicated that CRF6 may regulate its targets both directly and indirectly. Together, this shows that CRF6 functions during oxidative stress as a negative regulator to control this cytokinin-associated module of CRF6-dependent genes and establishes a novel connection between cytokinin and oxidative stress response

    Rictor Phosphorylation on the THR-1135 Site Does Not Require Mammalian Target of Rapamycin Complex 2

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    available in PMC 2012 January 1.In animal cells, growth factors coordinate cell proliferation and survival by regulating the phosphoinositide 3-kinase/Akt signaling pathway. Deregulation of this signaling pathway is common in a variety of human cancers. The PI3K-dependent signaling kinase complex defined as mammalian target of rapamycin complex 2 (mTORC2) functions as a regulatory Ser-473 kinase of Akt. We find that activation of mTORC2 by growth factor signaling is linked to the specific phosphorylation of its component rictor on Thr-1135. The phosphorylation of this site is induced by the growth factor stimulation and expression of the oncogenic forms of ras or PI3K. Rictor phosphorylation is sensitive to the inhibition of PI3K, mTOR, or expression of integrin-linked kinase. The substitution of wild-type rictor with its specific phospho-mutants in rictor null mouse embryonic fibroblasts did not alter the growth factor–dependent phosphorylation of Akt, indicating that the rictor Thr-1135 phosphorylation is not critical in the regulation of the mTORC2 kinase activity. We found that this rictor phosphorylation takes place in the mTORC2-deficient cells, suggesting that this modification might play a role in the regulation of not only mTORC2 but also the mTORC2-independent function of rictor. Mol Cancer Res; 8(6); 896–906.University of Texas M.D. Anderson Cancer Center (Fellow Trust fund)American Cancer Society (M.D. Anderson Cancer Center Breast Specialized Programs of Research Excellence (RSG-09-026-01CCG01))National Institutes of Health (U.S.) (NIH grant CA133522)National Institutes of Health (U.S.) (NIH grant AI104389

    The Drosophila SH2-SH3 adapter protein Dock is expressed in embryonic axons and facilitates synapse formation by the RP3 motoneuron

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    The Dock SH2-SH3 domain adapter protein, a homolog of the mammalian Nck oncoprotein, is required for axon guidance and target recognition by photoreceptor axons in Drosophila larvae. Here we show that Dock is widely expressed in neurons and at muscle attachment sites in the embryo, and that this expression pattern has both maternal and zygotic components. In motoneurons, Dock is concentrated in growth cones. Loss of zygotic dock function causes a selective delay in synapse formation by the RP3 motoneuron at the cleft between muscles 7 and 6. These muscles often completely lack innervation in late stage 16 dock mutant embryos. RP3 does form a synapse later in development, however, because muscles 7 and 6 are normally innervated in third-instar mutant larvae. The absence of zygotically expressed Dock also results in subtle defects in a longitudinal axon pathway in the embryonic central nervous system. Concomitant loss of both maternally and zygotically derived Dock dramatically enhances these central nervous system defects, but does not increase the delay in RP3 synaptogenesis. These results indicate that Dock facilitates synapse formation by the RP3 motoneuron and is also required for guidance of some interneuronal axons The involvement of Dock in the conversion of the RP3 growth cone into a presynaptic terminal may reflect a role for Dock-mediated signaling in remodeling of the growth cone's cytoskeleton

    Best practices for documentation of psychotropic drug-drug interactions in an adult psychiatric clinic

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    Introduction: Psychotropic drug-drug interactions (DDIs) contribute to adverse drug events, but many go undetected or unmanaged. Thorough documentation of potential DDIs can improve patient safety. The primary objective of this study is to determine the quality of and factors associated with documentation of DDIs in an adult psychiatric clinic run by postgraduate year 3 psychiatry residents (PGY3s). Methods: A list of high-alert psychotropic medications was identified by consulting primary literature on DDIs and clinic records. Charts of patients prescribed these medications by PGY3 residents from July 2021 to March 2022 were reviewed to detect potential DDIs and assess documentation. Chart documentation of DDIs was noted as none, partial, or complete. Results: Chart review identified 146 DDIs among 129 patients. Among the 146 DDIs, 65% were not documented, 24% were partially documented, and 11% had complete documentation. The percentage of pharmacodynamic interactions documented was 68.6% with 35.3% of pharmacokinetic interactions documented. Factors associated with partial or complete documentation included diagnosis of psychotic disorder (p = .003), treatment with clozapine (p = .02), treatment with benzodiazepine-receptor agonist (p<.01), and assumption of care during July (p = .04). Factors associated with no documentation include diagnosis of “other (primarily impulse control disorder)” (p<.01) and taking an enzyme-inhibiting antidepressant (p<.01). Discussion: Investigators propose best practices for psychotropic DDI documentation: (1) description and potential outcome of DDI, (2) monitoring and management, (3) Patient education on DDI, and (4) patient response to DDI education. Strategies to improve DDI documentation quality include targeted provider education, incentives, and electronic medical record “DDI smart phrases.

    Effectiveness and safety of apixaban vs warfarin among venous thromboembolism patients at high-risk of bleeding

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    This study evaluated effectiveness and safety of apixaban versus warfarin among venous thromboembolism patients at high-risk of bleeding (defined as having at least one of the following bleeding risk factors: ≄75 years; used antiplatelet, NSAIDs, or corticosteroids; had prior gastrointestinal bleeding or gastrointestinal-related conditions; late stage chronic kidney disease). Adult venous thromboembolism patients initiating apixaban or warfarin with ≄1 bleeding risk factor were identified from Medicare and four commercial claims databases in the United States. To balance characteristics between apixaban and warfarin patients, stabilized inverse probability treatment weighting was conducted. Cox proportional hazards models were used to estimate the risk of recurrent venous thromboembolism, major bleeding, and clinically relevant non-major bleeding. In total, 88,281 patients were identified. After inverse probability treatment weighting, the baseline patient characteristics were well-balanced between the two cohorts. Among venous thromboembolism patients at high-risk of bleeding, apixaban was associated with significantly lower risk of recurrent venous thromboembolism, major bleeding and clinically relevant non-major bleeding. No significant interactions were observed between treatment and number of risk factors on major bleeding and clinically relevant non-major bleeding or between treatment and type of bleeding risk factors on any of the outcomes. In conclusion, apixaban was associated with significantly lower risk of recurrent venous thromboembolism and bleeding among venous thromboembolism patients at high-risk of bleeding. Effects were generally consistent across subgroups of patients with different number or type of bleeding risk factors

    Oral anticoagulants for nonvalvular atrial ïŹbrillation in frail elderly patients: insights from the ARISTOPHANES study

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    Background Patient frailty amongst patients with nonvalvular atrial fibrillation (NVAF) is associated with adverse health outcomes and increased risk of mortality. Additional evidence is needed to evaluate effective and safe NVAF treatment in this patient population. Objectives This subgroup analysis of the ARISTOPHANES study compared the risk of stroke/systemic embolism (S/SE) and major bleeding (MB) amongst frail NVAF patients prescribed nonvitamin K antagonist oral anticoagulants (NOACs) or warfarin. Methods This comparative retrospective observational study of frail, older NVAF patients who initiated apixaban, dabigatran, rivaroxaban or warfarin from 01JAN2013‐30SEP2015 was conducted using Medicare and 3 US commercial claims databases. To compare each drug, 6 propensity score‐matched (PSM) cohorts were created. Patient cohorts were pooled from 4 databases after PSM. Cox models were used to estimate hazard ratios (HR) of S/SE and MB. Results Amongst NVAF patients, 34% (N = 150 487) met frailty criteria. Apixaban and rivaroxaban were associated with a lower risk of S/SE vs warfarin (apixaban: HR: 0.61, 95% CI: 0.55–0.69; rivaroxaban: HR: 0.79, 95% CI: 0.72–0.87). For MB, apixaban (HR: 0.62, 95% CI: 0.57–0.66) and dabigatran (HR: 0.79, 95% CI: 0.70–0.89) were associated with a lower risk and rivaroxaban (HR: 1.14, 95% CI: 1.08–1.21) was associated with a higher risk vs warfarin. Conclusion Amongst this cohort of frail NVAF patients, NOACs were associated with varying rates of stroke/SE and MB compared with warfarin. Due to the lack of real‐world data regarding OAC treatment in frail patients, these results may inform clinical practice in the treatment of this patient population

    Improving hypertension management through pharmacist prescribing; the rural alberta clinical trial in optimizing hypertension (Rural RxACTION): trial design and methods

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    <p>Abstract</p> <p>Background</p> <p>Patients with hypertension continue to have less than optimal blood pressure control, with nearly one in five Canadian adults having hypertension. Pharmacist prescribing is gaining favor as a potential clinically efficacious and cost-effective means to improve both access and quality of care. With Alberta being the first province in Canada to have independent prescribing by pharmacists, it offers a unique opportunity to evaluate outcomes in patients who are prescribed antihypertensive therapy by pharmacists.</p> <p>Methods</p> <p>The study is a randomized controlled trial of enhanced pharmacist care, with the unit of randomization being the patient. Participants will be randomized to enhanced pharmacist care (patient identification, assessment, education, close follow-up, and prescribing/titration of antihypertensive medications) or usual care. Participants are patients in rural Alberta with undiagnosed/uncontrolled blood pressure, as defined by the Canadian Hypertension Education Program. The primary outcome is the change in systolic blood pressure between baseline and 24 weeks in the enhanced-care versus usual-care arms. There are also three substudies running in conjunction with the project examining different remuneration models, investigating patient knowledge, and assessing health-resource utilization amongst patients in each group.</p> <p>Discussion</p> <p>To date, one-third of the required sample size has been recruited. There are 15 communities and 17 pharmacists actively screening, recruiting, and following patients. This study will provide high-level evidence regarding pharmacist prescribing.</p> <p>Trial Registration</p> <p>Clinicaltrials.gov <a href="http://www.clinicaltrials.gov/ct2/show/NCT00878566">NCT00878566</a>.</p
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