Delivery capabilities impact project performance

The aim of this research is to study project delivery capabilities impact project performance. If the companies know the factors that influencing the project’s performance, they will focus on that and can deliver the project successfully. For the factors of project delivery capabilities is a set as independent variable. The factors that have been use in this research are process, organizations, methods, metric and leaderships because these are the top five factors that have impact on project performance. Then, the dependent variable of project performance is time. Sixty respondents from the construction industry in Kuantan, Pahang that are registered under CIDB were surveyed by questionnaire. The questionnaires were distributed using mail, google doc, and face to face. Software SPSS was use to analyse the data to get the results. The objectives of this research are to investigate project delivery capabilities practices in project management and to rank the project delivery capabilities according to priorities in project performance Results show that project delivery capabilities impact project performance and the finding are parallel accordance with previous researches but had different ranking of factors

Beyond the Bayley: Neurocognitive Assessments of Development During Infancy and Toddlerhood

The use of global, standardized instruments is conventional among clinicians and researchers interested in assessing neurocognitive development. Exclusively relying on these tests for evaluating effects may underestimate or miss specific effects on early cognition. The goal of this review is to identify alternative measures for possible inclusion in future clinical trials and interventions evaluating early neurocognitive development. The domains included for consideration are attention, memory, executive function, language and socio-emotional development. Although domain-based tests are limited, as psychometric properties have not yet been well-established, this review includes tasks and paradigms that have been reliably used across various developmental psychology laboratories

Plasticity may change inputs as well as processes, structures, and responses

Significant work has documented neuroplasticity in development, demonstrating that developmental pathways are shaped by experience. Plasticity is often discussed in terms of the results of differences in input; differences in brain structures, processes, or responses reflect differences in experience. In this paper, I discuss how developmental plasticity also effectively changes input into the system. That is, structures and processes change in response to input, and those changed structures and processes influence future inputs. For example, plasticity may change the pattern of eye movements to a stimulus, thereby changing which part of the scene becomes the input. Thus, plasticity is not only seen in the structures and processes that result from differences in experience, but also is seen in the changes in the input as those structures and processes adapt. The systematic study of the nature of experience, and how differences in experience shape learning, can contribute to our understanding of neuroplasticity in general

Prolactin-induced mouse mammary carcinomas model estrogen resistant luminal breast cancer.

INTRODUCTION: Tumors that express estrogen receptor alpha (ERα+) comprise 75% of breast cancers in women. While treatments directed against this receptor have successfully lowered mortality rates, many primary tumors initially or later exhibit resistance. The paucity of murine models of this luminal tumor subtype has hindered studies of factors that promote their pathogenesis and modulate responsiveness to estrogen-directed therapeutics. Since epidemiologic studies closely link prolactin and the development of ERα+ tumors in women, we examined characteristics of the aggressive ERα+ and ERα- carcinomas which develop in response to mammary prolactin in a murine transgenic model (neu-related lipocalin- prolactin (NRL-PRL)). To evaluate their relationship to clinical tumors, we determined phenotypic relationships among these carcinomas, other murine models of breast cancer, and features of luminal tumors in women. METHODS: We examined a panel of prolactin-induced tumors for characteristics relevant to clinical tumors: histotype, ERα/progesterone receptor (PR) expression and estrogen responsiveness, Activating Protein 1 (AP-1) components, and phosphorylation of signal transducer and activator of transcription 5 (Stat5), extracellular signal regulated kinase (ERK) 1/2 and AKT. We compared levels of transcripts in the ERα-associated luminal signature that defines this subtype of tumors in women and transcripts enriched in various mammary epithelial lineages to other well-studied genetically modified murine models of breast cancer. Finally, we used microarray analyses to compare prolactin-induced ERα+ and ERα- tumors, and examined responsiveness to estrogen and the anti-estrogen, Faslodex, in vivo. RESULTS: Prolactin-induced carcinomas were markedly diverse with respect to histotype, ERα/PR expression, and activated signaling cascades. They constituted a heterogeneous, but distinct group of murine mammary tumors, with molecular features of the luminal subtype of human breast cancer. In contrast to morphologically normal and hyperplastic structures in NRL-PRL females, carcinomas were insensitive to ERα-mediated signals. These tumors were distinct from mouse mammary tumor virus (MMTV)-neu tumors, and contained elevated transcripts for factors associated with luminal/alveolar expansion and differentiation, suggesting that they arose from physiologic targets of prolactin. These features were shared by ERα+ and ERα- tumors, suggesting a common origin, although the former exhibited transcript profiles reflecting greater differentiation. CONCLUSIONS: Our studies demonstrate that prolactin can promote diverse carcinomas in mice, many of which resemble luminal breast cancers, providing a novel experimental model to examine the pathogenesis, progression and treatment responsiveness of this tumor subtype

Effect of remote ischaemic conditioning on clinical outcomes in patients with acute myocardial infarction (CONDI-2/ERIC-PPCI): a single-blind randomised controlled trial.

BACKGROUND: Remote ischaemic conditioning with transient ischaemia and reperfusion applied to the arm has been shown to reduce myocardial infarct size in patients with ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). We investigated whether remote ischaemic conditioning could reduce the incidence of cardiac death and hospitalisation for heart failure at 12 months. METHODS: We did an international investigator-initiated, prospective, single-blind, randomised controlled trial (CONDI-2/ERIC-PPCI) at 33 centres across the UK, Denmark, Spain, and Serbia. Patients (age >18 years) with suspected STEMI and who were eligible for PPCI were randomly allocated (1:1, stratified by centre with a permuted block method) to receive standard treatment (including a sham simulated remote ischaemic conditioning intervention at UK sites only) or remote ischaemic conditioning treatment (intermittent ischaemia and reperfusion applied to the arm through four cycles of 5-min inflation and 5-min deflation of an automated cuff device) before PPCI. Investigators responsible for data collection and outcome assessment were masked to treatment allocation. The primary combined endpoint was cardiac death or hospitalisation for heart failure at 12 months in the intention-to-treat population. This trial is registered with ClinicalTrials.gov (NCT02342522) and is completed. FINDINGS: Between Nov 6, 2013, and March 31, 2018, 5401 patients were randomly allocated to either the control group (n=2701) or the remote ischaemic conditioning group (n=2700). After exclusion of patients upon hospital arrival or loss to follow-up, 2569 patients in the control group and 2546 in the intervention group were included in the intention-to-treat analysis. At 12 months post-PPCI, the Kaplan-Meier-estimated frequencies of cardiac death or hospitalisation for heart failure (the primary endpoint) were 220 (8·6%) patients in the control group and 239 (9·4%) in the remote ischaemic conditioning group (hazard ratio 1·10 [95% CI 0·91-1·32], p=0·32 for intervention versus control). No important unexpected adverse events or side effects of remote ischaemic conditioning were observed. INTERPRETATION: Remote ischaemic conditioning does not improve clinical outcomes (cardiac death or hospitalisation for heart failure) at 12 months in patients with STEMI undergoing PPCI. FUNDING: British Heart Foundation, University College London Hospitals/University College London Biomedical Research Centre, Danish Innovation Foundation, Novo Nordisk Foundation, TrygFonden

Plasticity may change inputs as well as processes, structures, and responses.

Significant work has documented neuroplasticity in development, demonstrating that developmental pathways are shaped by experience. Plasticity is often discussed in terms of the results of differences in input; differences in brain structures, processes, or responses reflect differences in experience. In this paper, I discuss how developmental plasticity also effectively changes input into the system. That is, structures and processes change in response to input, and those changed structures and processes influence future inputs. For example, plasticity may change the pattern of eye movements to a stimulus, thereby changing which part of the scene becomes the input. Thus, plasticity is not only seen in the structures and processes that result from differences in experience, but also is seen in the changes in the input as those structures and processes adapt. The systematic study of the nature of experience, and how differences in experience shape learning, can contribute to our understanding of neuroplasticity in general

Sample Size, Statistical Power, and False Conclusions in Infant Looking‐Time Research

Infant research is hard. It is difficult, expensive, and time consuming to identify, recruit and test infants. As a result, ours is a field of small sample sizes. Many studies using infant looking time as a measure have samples of 8 to 12 infants per cell, and studies with more than 24 infants per cell are uncommon. This paper examines the effect of such sample sizes on statistical power and the conclusions drawn from infant looking time research. An examination of the state of the current literature suggests that most published looking time studies have low power, which leads in the long run to an increase in both false positive and false negative results. Three data sets with large samples (>30 infants) were used to simulate experiments with smaller sample sizes; 1000 random subsamples of 8, 12, 16, 20, and 24 infants from the overall samples were selected, making it possible to examine the systematic effect of sample size on the results. This approach revealed that despite clear results with the original large samples, the results with smaller subsamples were highly variable, yielding both false positive and false negative outcomes. Finally, a number of emerging possible solutions are discussed