Self-Paced Endurance Performance and Cerebral Hemodynamics of the Prefrontal Cortex: A Scoping Review of Methodology and Findings.

Recent research has suggested that top-down executive function associated with the prefrontal cortex is key to the decision-making processes and pacing of endurance performance. A small but growing body of literature has investigated the neurological underpinnings of these processes by subjecting the prefrontal cortex to functional near-infrared spectroscopy (fNIRS) measurement during self-paced endurance task performance. Given that fNIRS measurement for these purposes is a relatively recent development, the principal aim of this review was to assess the methodological rigor and findings of this body of research. We performed a systematic literature search to collate research assessing prefrontal cortex oxygenation via fNIRS during self-paced endurance performance. A total of 17 studies met the criteria for inclusion. We then extracted information concerning the methodology and findings from the studies reviewed. Promisingly, most of the reviewed studies reported having adopted commonplace and feasible best practice guidelines. However, a lack of adherence to these guidelines was evident in some areas. For instance, there was little evidence of measures to tackle and remove artifacts from data. Lastly, the reviewed studies provide insight into the significance of cerebral oxygenation to endurance performance and the role of the prefrontal cortex in pacing behavior. Therefore, future research that better follows the guidelines presented will help advance our understanding of the role of the brain in endurance performance and aid in the development of techniques to improve or maintain prefrontal cortex (PFC) oxygenation to help bolster endurance performance

Economists\u27 Publication Patterns

The results presented in this paper give a comprehensive picture of the extent of publishing by economists. While it is obvious that the traditional emphasis on refereed journal articles captures only a part of economists\u27 research output, to date it has been difficult to determine how large a part of that output was not being measured. This note provides the necessary perspective and presents information on the relative productivity of faculty at different institutional types and with different years of experience

Adaphostin toxicity in a sensitive non-small cell lung cancer model is mediated through Nrf2 signaling and heme oxygenase 1

<p>Abstract</p> <p>Background</p> <p>Preclinical toxicity of adaphostin has been related to oxidative stress. This study investigated the regulatory mechanism underlying adaphostin induction of heme oxygenase 1 (HMOX1) which plays a significant role in modulation of drug-induced toxicity in the non-small cell lung cancer cell line model, NCI-H522.</p> <p>Methods</p> <p>The transcriptional response of NCI-H522 to adaphostin prominently involved oxidative stress genes, particularly HMOX1. Reactive oxygen species (ROS) involvement was additionally established by generation of ROS prior to modulation of adaphostin-toxicity with antioxidants. To identify up-stream regulatory elements of HMOX1, immunofluorescence was used to evaluate nuclear translocation of the transcription factor, NF-E2-related factor 2 (Nrf2), in the presence of adaphostin. The PI3-kinase inhibitor, wortmannin, was employed as a pharmacological inhibitor of this process.</p> <p>Results</p> <p>Generation of ROS provided a substantial foundation for the sensitivity of NCI-H522 to adaphostin. However, in contrast to leukemia cell lines, transcriptional response to oxidative stress was associated with induction of HMOX1, which was dependent on nuclear translocation of the transcription factor, Nrf2. Pretreatment of cells with wortmannin inhibited translocation of Nrf2 and induction of HMOX1. Wortmannin pretreatment was also able to diminish adaphostin induction of HMOX1, and as a consequence, enhance the toxicity of adaphostin to NCI-H522.</p> <p>Conclusions</p> <p>Adaphostin-induced oxidative stress in NCI-H522 was mediated through nuclear translocation of Nrf2 leading to upregulation of HMOX1. Inhibition of Nrf2 translocation by wortmannin inhibited this cytoprotective response, and enhanced the toxicity of adaphostin, suggesting that inhibitors of the PI3K pathway, such as wortmannin, might augment the antiproliferative effects of adaphostin in solid tumors that depend on the Nrf2/ARE pathway for protection against oxidative stress.</p

Evaluating conservation strategies for the endangered daisy Schoenia filifolia subsp. subulifolia (Asteraceae): fitness consequences of genetic rescue and hybridisation with a widespread subspecies

Context: To establish translocated populations of threatened plants with the genetic resources to adapt to changing environmental conditions, the source of propagation material is an important consideration. Aim: We investigated the fitness consequences of genetic rescue and admixture for the threatened annual daisy Schoenia filifolia subsp. subulifolia, and the common S. filifolia subsp. filifolia, to inform seed-sourcing strategies for translocations of the threatened subspecies. Methods: We evaluated genetic diversity of two populations of S. filifolia subsp. subulifolia and four populations of S. filifolia subsp. filifolia by using microsatellite markers. We grew seedlings from each study population and cross-pollinated inflorescences within and among populations of the same subspecies, and between subspecies. We evaluated the fitness consequences of each cross by using seed set, seed weight and seed viability. Key results: There was a lower genetic diversity in the small (10 000 plants, Nar = 4.42, He = 0.51) population of S. filifolia subsp. subulifolia, although none of the measures was significantly different, and seed fitness was slightly, although not significantly, reduced in interpopulation crosses compared with the small population. Genetic diversity was similar between the threatened and widespread subspecies; however, the subspecies were genetically divergent (Fst = 0.242–0.294) and cross-pollination between subspecies produced negligible amounts of seeds (<3% seed set). Conclusions: Although genetic rescue or admixture of S. filifolia subsp. subulifolia would not necessarily result in greatly increased levels of genetic diversity or seed fitness, we still consider it a potential option. Negligible seed set in crosses between subspecies indicates that deliberate hybridisation is not a possibility. Implications: Studies of fitness consequences of admixture or genetic rescue are rare yet critical to assessing the benefits of different translocation strategies

Evaluation of the significance of polyamines and their oxidases in the aetiology of human cervical carcinoma.

The risk of cancer of the cervix is linked with sexual behaviour. Although infectious agents such as human papillomaviruses (HPVs) are implicated, these alone may be insufficient to induce the disease. We have investigated the potential role of oxidation products of the polyamines spermine and spermidine and the diamine putrescine in seminal plasma (SP) as co-factors in the development of cervical cancer. These amines are oxidised by polyamine oxidase (PAO) and diamine oxidase (DAO) to generate oxygen radicals and hydrogen peroxide, reactive aldehydes and acrolein, which are likely to exert local mutagenic, cytotoxic and immunosuppressive effects in vivo. Using a chemiluminescence assay, we determined the levels of these amines in 187 samples of SP. Spermine plus spermidine, as substrates for PAO, were present in a range equivalent to 0-4.8 mg ml-1 spermine. Putrescine, as a substrate for DAO, was detectable in only 4 of 40 samples assayed (range 0-168 micrograms ml-1) and constitutes a minor component of the oxidisable content of SP. Cervical mucus (126 samples) was assayed for the presence of PAO and DAO. Both enzymes were present in 14.3% of the samples, PAO only in 21.4%, DAO only in 15.1% and neither enzyme in 49.2%. PAO levels ranged from 0 to 0.828 pmol peroxide generated min-1 mg-1 mucus and DAO levels ranged from 0 to 7.0 pmol peroxide generated min-1 mg-1 mucus. These results suggest that sexual activity in the absence of physical barrier contraception may lead to the generation of mutagenic and immunosuppressive polyamine oxidation products within the female genital tract. We thus propose that women with high levels of PAO and/or DAO in their cervical mucus may be at increased risk of cervical cancer, especially if the male partner's SP shows high polyamine levels. HPV infection may synergise with the effects of polyamine oxidation by suppressing apoptosis in keratinocytes carrying potentially oncogenic mutations, leading to the survival and proliferation of transformed cells in the cervix