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Oxygen effects on apparent photosynthetic and dark respiratory O2 exchange rates of detached leaves of Elodea canadensis Michx. (Hydrocharitaceae) were determined over a range of conditions which the submersed plant is likely to experience in shallow water. Apparent photosynthesis is inhibited by O2 under all the experimental regimes of light, temperature, CO2 concentration and pH. This inhibition is not caused solely by an accelerated rate of dark respiration, and the observed variations in O2 inhibition are comparable of O2 effects on photosynthesis and photorespiration of terrestrial CO3plants. Percentage inhibition of apparent photosynthesis is enhanced by high O2 and also by low CO2. These results indicate that high O2, high pH and low CO2 conditions could cause major losses in photosynthetic activity under field conditions. This may account for some of the losses in biomass that are observed under still water conditions. [ABSTRACT FROM AUTHOR]

Surface sterilized buds of young cocoa plants (Theobroma cacao L.) taken at particular stages of the flush cycle were placed in Linsmaier and Skoog agar medium supplemented with a range of growth regulators. Only buds taken at the 1-2 (dormant) stage of the flush cycle and treated with gibberellic acid (GA3) alone and GA3, plus kinetin (KN) supplement showed bud opening. In liquid Linsmaier and Skoog medium buds isolated at the I-2 stage also responded to GA3 and KN. In this case addition of KN caused bud opening, while GA3 either initiated bud opening only or opening followed by leaf expansion depending on the concentration of GA3 supplied. Bud development was inhibited when ABA was included in the medium but this was overcome by the presence of GA3 but not KN. Since a hormonal supplement was required for any response from the excised buds, it is suggested that the intermittent growth of the shoot apex in the intact plant may be determined by hormonal stimuli derived from other parts of the plant. The findings also indicate that the bud apices could be maintained in culture for long periods which may provide a basis for the development of a micropropagation procedure for cocoa. [ABSTRACT FROM AUTHOR]

The export and translocation of radioactivity supplied as 14C-auxin or as a 14C-kinin to a donor leaf of cocoa was followed at different stages of the flush cycle to see whether there was any correlation between the pattern of movement of these growth promoters and apical bud activity. The auxin 3-indole (1-14C) acetic acid, (14C-IAA), and the cytokinin, 6-benzyl-amino (8-14C) purine, (14C-BAP), were introduced into the plant by foliar feeding. Export of the radioactivity derived from the 14C-IAA was predominantly basipetal at all stages of the flush cycle. Most of the tracer accumulated in the lower stem but there was a significantly high proportion in the older leaves. It appeared that the largest proportion of the radioactivity derived from 14C-IAA was found in parts of the plant where growth, or possibly carbohydrate accumulation, was active.. It is suggested that the movement of 14C-IAA and its metabolites in cocoa may be largely determined by the direction of flow of the assimilate stream. The identity of the radioactive compounds exported from the donor leaf showed that some 80% of the fed 14C-IAA was metabolized to other indole compounds including indole aldehyde, indole aspartate and indole acetonitrile. When the 14C present in particular plant parts was expressed as a relative radioactivity ratio, this value, for the apical bud, declined throughout the flush cycle, being highest at bud break, indicating that the capacity of the- bud to accumulate radioactivity derived from 14C-IAA was greatest during the stages of leaf production. The distribution of radioactivity from 14C-BAP indicated both acropetal and basipetal transport of cytokinin but accumulation of radioactivity occurred only in actively growing regions. Unlike 14C-IAA, the 14C-BAP exported from the leaf was not extensively metabolized and about 60% of the transported radioactivity was detected as 14C-BAP and the remainder as conjugated 14C-BAP . For this compound the relative radioactivity ratio in the bud was highest at dormacy break (F-1), suggesting that cytokinin movement to the bud was related to the breaking of dormacy. The changes in pattern of transport of auxin and cytokinin throughout the cocoa plant were correlated with the stages of the flush cycle. [ABSTRACT FROM AUTHOR]

The flush leaves of seedling cocoa plants were assessed at each stage of the flush cycle from leaf unfolding to maturity for differences in leaf lamina presentation angle, surface hairs, stomatal number and development and leaf cuticle thickness. Changes in these parameters were then correlated with cuticular and stomatal diffusive resistance of the leaves. It is suggested that perpendicular positioning of the young flush leaves, the presence of surface hairs, the rapid synthesis of the cuticle and the limited stomatal development during the early stages of leaf expansion, restrict water loss from the developing leaves. Maximum rate of water loss from the leaves of a new flush was only attained after leaves were fully expanded, stomata fully developed and the leaves horizontally positioned. It is suggested that the large increase in water loss from the flush leaves following these changes might lead to an internal water deficit in the plant and hence to increased synthesis of abscisic acid in the shoot which, in turn, will maintain dormancy of the shoot apex in at least part of the interflush period. [ABSTRACT FROM AUTHOR]

During photosynthesis, submersed aquatic plant stands create 'envelopes' of raised pH and dissolved O2 concentrations and depleted dissolved CO2 concentrations. These may extend beyondthe plant stands, suppressing the photosynthetic performance and increasing the photorespiratory stress of adjacent species. In competition between three aquatic macrophytes, Elodea canadensis, Elodea nuttallii and Lagarosiphon major, we hypothesized that a competitive advantage is achieved by those species that have the best stress generation/toleration mechanisms. pH and free CO2 conditions were measured under laboratory conditions at two plant densities and compared with measurements of photosynthesis and respiration at various pH and free CO2 concentrations. L. major raised pH faster andphotosynthesized at a greater rate under the experimental conditionsand may gain competitive advantage at high pH. No clear differences in photosynthetic behaviour were observed between the Elodea spp. andit is concluded that a wider range of factors than those studied here are probably involved in competition between the three species. [ABSTRACT FROM AUTHOR]

In laboratory experiments, the growth characteristics of the submerged species Elodea nuttallii (Planch.) St. John and Potamogeton crispus L. were assessed in the presence and absence of floating mats of Azolla filiculoides Lam. and Lemna minuta Kunth. Light penetration and the development of pH and dissolved oxygen differences were monitored. The growth of P. crispus was suppressed much more than that of E. nuttallii and the effects of A. filiculoides were more severe than those of L. minuta. Findings are related to possible field responses of submerged plants under floating mats, especially their abilities to compensate for the potential suppressive effects of floating mats under natural conditions. [ABSTRACT FROM AUTHOR]

In slow-moving and static eutrophic waters, submerged macrophytes growing in dense stands produce a highly structured environment, with reduced internal water flow. An afternoon lull in the net photosynthesis of such stands has been reported from a number of previous studies. This has been attributed to increased photorespiration caused by anaccumulation of photosynthetically-derived, dissolved oxygen in the surrounding water. Results here demonstrate that even in a water quite rich in dissolved inorganic carbon (2.5 mmol l{sup}-1{end}), limitations on the supply of inorganic carbon will normally be more important in curtailing photosynthesis, with photorespiration playing only aminor role. [ABSTRACT FROM AUTHOR]

Active research-driven approaches that successfully incorporate new technology are known to catalyze student learning. Yet achieving these objectives in neuroscience education is especially challenging due to the prohibitive costs and technical demands of research-grade equipment. Here we describe a method that circumvents these factors by leveraging consumer EEG-based neurogaming technology to create an affordable, scalable, and highly portable teaching laboratory for undergraduate courses in neuroscience. This laboratory is designed to give students hands-on research experience, consolidate their understanding of key neuroscience concepts, and provide a unique real-time window into the working brain. Survey results demonstrate that students found the lab sessions engaging. Students also reported the labs enhanced their knowledge about EEG, their course material, and neuroscience research in general.

Previous studies have demonstrated that a range of stimuli activate neurons, including catecholaminergic neurons, in the ventrolateral medulla. Not all catecholaminergic neurons are activated and other neurochemical content is largely unknown hence whether stimulus specific populations exist is unclear. Here we determine the neurochemistry (using in situ hybridization) of catecholaminergic and noncatecholaminergic neurons which express c-Fos immunoreactivity throughout the rostrocaudal extent of the ventrolateral medulla, in Sprague Dawley rats treated with hydralazine or saline. Distinct neuronal populations containing PPCART, PPPACAP, and PPNPY mRNAs, which were largely catecholaminergic, were activated by hydralazine but not saline. Both catecholaminergic and noncatecholaminergic neurons containing preprotachykinin and prepro-enkephalin (PPE) mRNAs were also activated, with the noncatecholaminergic population located in the rostral C1 region. Few GlyT2 neurons were activated. A subset of these data was then used to compare the neuronal populations activated by 2-deoxyglucose evoked glucoprivation (Brain Structure and Function (2015) 220:117). Hydralazine activated more neurons than 2-deoxyglucose but similar numbers of catecholaminergic neurons. Commonly activated populations expressing PPNPY and PPE mRNAs were defined. These likely include PPNPY expressing catecholaminergic neurons projecting to vasopressinergic and corticotrophin releasing factor neurons in the paraventricular nucleus, which when activated result in elevated plasma vasopressin and corticosterone. Stimulus specific neurons included noncatecholaminergic neurons and a few PPE positive catecholaminergic neuron but neurochemical codes were largely unidentified. Reasons for the lack of identification of stimulus specific neurons, readily detectable using electrophysiology in anaesthetized preparations and for which neural circuits can be defined, are discussed., (© 2017 Wiley Periodicals, Inc.)

Functional links connecting gene transcription and condensin-mediated chromosome condensation have been established in species ranging from prokaryotes to vertebrates. However, the exact nature of these links remains misunderstood. Here we show in fission yeast that the 3' end RNA processing factor Swd2.2, a component of the Cleavage and Polyadenylation Factor (CPF), is a negative regulator of condensin-mediated chromosome condensation. Lack of Swd2.2 does not affect the assembly of the CPF but reduces its association with chromatin. This causes only limited, context-dependent effects on gene expression and transcription termination. However, CPF-associated Swd2.2 is required for the association of Protein Phosphatase 1 PP1(Dis2) with chromatin, through an interaction with Ppn1, a protein that we identify as the fission yeast homologue of vertebrate PNUTS. We demonstrate that Swd2.2, Ppn1 and PP1Dis2 form an independent module within the CPF, which provides an essential function in the absence of the CPF-associated Ssu72 phosphatase. We show that Ppn1 and Ssu72, like Swd2.2, are also negative regulators of condensin-mediated chromosome condensation. We conclude that Swd2.2 opposes condensin-mediated chromosome condensation by facilitating the function of the two CPF-associated phosphatases PP1 and Ssu72.

There has been significant concern that the dental curriculum and system of clinical education, in particular, is not designed to take advantage of the explosion in knowledge in biomedical science and its application to the health of the public. Although there are some examples of innovations in dental education on a global scale that have the capacity to increase the assimilation of basic and clinical knowledge, most of the dental education models are mired in the traditional '2 + 2' approach to education. This can be seen in North America and the European '2 + 3' model or the stomatological '4 + 2' approach. In each of these systems, the basic and behavioural science courses continue to be perceived as hurdles over which students must leap in order to reach the clinical programmes where there is little opportunity to use basic science information to advance patient care and treatment. Examples of issues that are not well represented include: innovations in imaging; diagnosis; bio-materials; science-based approaches to clinical practice; novel approaches to therapeutics; interactions between the oral, dental and craniofacial complex and systemic health and disorders; the role of oral infections and systemic disease; the increasing appreciation of chronic diseases and disorders such as osteoporosis and diabetes that affect oral tissues; the promise of bioengineering, tissue engineering and biomimetics; the potential use of saliva as a diagnostic tool; the understanding of oral complications of cancer treatment; the treatments of HIV/AIDS diseases and hepatitis; the use of dental and dental hygiene staff on health-care teams to deal with issues such as birth defects, orofacial trauma, head and neck cancer, chronic pain management and so on. There seems to be an excessive emphasis on restorative dentistry and, to a lesser extent, on the more biological approaches to diagnosis, prevention and therapeutics. This continued lack of integration of basic and clinical sciences in the curriculum continues to foster a dental workforce that is highly technically competent to provide specific clinical services but poorly equipped to evaluate and implement new biological approaches to diagnosis, therapeutics and intervention. Unfortunately, after many attempts by organized dental symposia aimed at the integration of basic and clinical sciences, there has been little discernible curricular change. It appears that there is an opportunity through this global congress to identify the best practices in the various global curricula that could change this paradigm in dental education and lead us toward the education of a more scientifically orientated practitioner-one who can take advantage of innovations in new and emerging technologies in their application to patient care. It is the challenge of this section to try to ascertain the best method or methods by which dental education promotes research to the dental student and what research represents in terms of critical thinking and evidence-based approaches to dental education and clinical practice.

Objective: This paper maps dentists, primary care physicians, physician assistants, nurse practitioners, and nurse midwives in rural areas and rural areas meeting criteria as underserved for primary health care., Methods: Computer-based mapping was used to localize health care provider groups by five-digit ZIP code. For each rural and each rural primary care health professional shortage area (PC-HPSA) ZIP code, the number of providers in each group was determined. The different combinations of providers were determined., Results: All providers in rural areas were present at levels substantially lower than national averages, particularly in PC-HPSA areas. Dentists were approximately equal in number to primary care physicians in rural areas and the largest group in PC-HPSAs. Approximately 75 percent of rural residents lived in ZIP code areas with dentists available. Over 5.8 million rural residents and over 50 percent of rural PC-HPSA residents had no providers available in their ZIP code areas., Conclusions: Rural areas continue to have a short supply of primary care providers and dentists. Dentists were present in many areas where primary care provider presence was absent or very low. These data, including those relating to provider co-presence, can be used to develop strategies to overcome health care access problems due to provider shortages.

The activity of the cyclin-dependent kinase 1 (Cdk1), Cdc28, inhibits the transition from anaphase to G1 in budding yeast. CDC28-T18V, Y19F (CDC28-VF), a mutant that lacks inhibitory phosphorylation sites, delays the exit from mitosis and is hypersensitive to perturbations that arrest cells in mitosis. Surprisingly, this behavior is not due to a lack of inhibitory phosphorylation or increased kinase activity, but reflects reduced activity of the anaphase-promoting complex (APC), a defect shared with other mutants that lower Cdc28/Clb activity in mitosis. CDC28-VF has reduced Cdc20- dependent APC activity in mitosis, but normal Hct1- dependent APC activity in the G1 phase of the cell cycle. The defect in Cdc20-dependent APC activity in CDC28-VF correlates with reduced association of Cdc20 with the APC. The defects of CDC28-VF suggest that Cdc28 activity is required to induce the metaphase to anaphase transition and initiate the transition from anaphase to G1 in budding yeast.

The spindle checkpoint delays the metaphase to anaphase transition in response to defects in kinetochore-microtubule interactions in the mitotic apparatus (see [1] [2] [3] [4] for reviews). The Mad and Bub proteins were identified as key components of the spindle checkpoint through budding yeast genetics [5] [6] and are highly conserved [3]. Most of the spindle checkpoint proteins have been localised to kinetochores, yet almost nothing is known about the molecular events which take place there. Mad1p forms a tight complex with Mad2p [7], and has been shown to recruit Mad2p to kinetochores [8]. Similarly, Bub3p binds to Bub1p [9] and may target it to kinetochores [10]. Here, we show that budding yeast Mad1p has a regulated association with Bub1p and Bub3p during a normal cell cycle and that this complex is found at significantly higher levels once the spindle checkpoint is activated. We find that formation of this complex requires Mad2p and Mps1p but not Mad3p or Bub2p. In addition, we identify a conserved motif within Mad1p that is essential for Mad1p-Bub1p-Bub3p complex formation. Mutation of this motif abolishes checkpoint function, indicating that formation of the Mad1p-Bub1p-Bub3p complex is a crucial step in the spindle checkpoint mechanism.

We show that MAD3 encodes a novel 58-kD nuclear protein which is not essential for viability, but is an integral component of the spindle checkpoint in budding yeast. Sequence analysis reveals two regions of Mad3p that are 46 and 47% identical to sequences in the NH(2)-terminal region of the budding yeast Bub1 protein kinase. Bub1p is known to bind Bub3p (Roberts et al. 1994) and we use two-hybrid assays and coimmunoprecipitation experiments to show that Mad3p can also bind to Bub3p. In addition, we find that Mad3p interacts with Mad2p and the cell cycle regulator Cdc20p. We show that the two regions of homology between Mad3p and Bub1p are crucial for these interactions and identify loss of function mutations within each domain of Mad3p. We discuss roles for Mad3p and its interactions with other spindle checkpoint proteins and with Cdc20p, the target of the checkpoint.

Most policy-makers and researchers agree that although the United States is headed for a significant physician surplus, problems of equity in access to care still remain. To help meet this challenge, Title VII of the Public Health Service Act focuses on producing generalist physicians to serve in medically underserved areas (MUAs). This study estimates the impact Title VII support for generalist training has on reducing and eliminating health professional shortage areas (HPSAs) under multiple scenarios that vary either the Title VII funding level or the percentage of Title VII-funded program graduates who practice in MUAs. For each scenario, the number of Title VII-funded residency graduates who initially practice in MUAs and the time it would take to eliminate HPSAs are estimated. Using 1996 rates, the analysis predicts that 1,214 generalist physicians will enter practice in HPSAs annually, leading to elimination of HPSAs in 24 years. In 1997, Title VII-funded programs increased the rate of graduates entering HPSAs, resulting in 1,357 providers and reducing the time for HPSA elimination to 15 years. Doubling the funding for these programs would increase the number of Title VII-funded generalist physicians entering MUAs and could decrease the time for HPSA elimination to as little as 6 years. The study concludes that eliminating HPSAs requires broader Title VII influence and continuous improvement in rates of production of graduates who practice in MUAs. Without Title VII graduates and continuous improvement of Title VII program, MUA rates, the number of HPSAs and the number of Americans with reduced access to essential health care will continue to expand.

The spindle checkpoint arrests the cell cycle at metaphase in the presence of defects in the mitotic spindle or in the attachment of chromosomes to the spindle. When spindle assembly is disrupted, the budding yeast mad and bub mutants fail to arrest and rapidly lose viability. We have cloned the MAD2 gene, which encodes a protein of 196 amino acids that remains at a constant level during the cell cycle. Gel filtration and co-immunoprecipitation analyses reveal that Mad2p tightly associates with another spindle checkpoint component, Mad1p. This association is independent of cell cycle stage and the presence or absence of other known checkpoint proteins. In addition, Mad2p binds to all of the different phosphorylated isoforms of Mad1p that can be resolved on SDS-PAGE. Deletion and mutational analysis of both proteins indicate that association of Mad2p with Mad1p is critical for checkpoint function and for hyperphosphorylation of Mad1p.

The spindle checkpoint arrests cells in mitosis in response to defects in the assembly of the mitotic spindle or errors in chromosome alignment. We determined which spindle defects the checkpoint can detect by examining the interaction of mutations that compromise the checkpoint (mad1, mad2, and mad3) with those that damage various structural components of the spindle. Defects in microtubule polymerization, spindle pole body duplication, microtubule motors, and kinetochore components all activate the MAD-dependent checkpoint. In contrast, the cell cycle arrest caused by mutations that induce DNA damage (cdc13), inactivate the cyclin proteolysis machinery (cdc16 and cdc23), or arrest cells in anaphase (cdc15) is independent of the spindle checkpoint.

The spindle checkpoint ensures proper chromosome segregation by delaying anaphase until all chromosomes are correctly attached to the mitotic spindle. We investigated the role of the fission yeast bub1 gene in spindle checkpoint function and in unperturbed mitoses. We find that bub1(+) is essential for the fission yeast spindle checkpoint response to spindle damage and to defects in centromere function. Activation of the checkpoint results in the recruitment of Bub1 to centromeres and a delay in the completion of mitosis. We show that Bub1 also has a crucial role in normal, unperturbed mitoses. Loss of bub1 function causes chromosomes to lag on the anaphase spindle and an increased frequency of chromosome loss. Such genomic instability is even more dramatic in Deltabub1 diploids, leading to massive chromosome missegregation events and loss of the diploid state, demonstrating that bub1(+ )function is essential to maintain correct ploidy through mitosis. As in larger eukaryotes, Bub1 is recruited to kinetochores during the early stages of mitosis. However, unlike its vertebrate counterpart, a pool of Bub1 remains centromere-associated at metaphase and even until telophase. We discuss the possibility of a role for the Bub1 kinase after the metaphase-anaphase transition.

The spindle checkpoint regulates the cell division cycle by keeping cells with defective spindles from leaving mitosis. In the two-hybrid system, three proteins that are components of the checkpoint, Mad1, Mad2, and Mad3, were shown to interact with Cdc20, a protein required for exit from mitosis. Mad2 and Mad3 coprecipitated with Cdc20 at all stages of the cell cycle. The binding of Mad2 depended on Mad1 and that of Mad3 on Mad1 and Mad2. Overexpression of Cdc20 allowed cells with a depolymerized spindle or damaged DNA to leave mitosis but did not overcome the arrest caused by unreplicated DNA. Mutants in Cdc20 that were resistant to the spindle checkpoint no longer bound Mad proteins, suggesting that Cdc20 is the target of the spindle checkpoint.

The spindle assembly checkpoint keeps cells with defective spindles from initiating chromosome segregation. The protein kinase Mps1 phosphorylates the yeast protein Mad1p when this checkpoint is activated, and the overexpression of Mps1p induces modification of Mad1p and arrests wild-type yeast cells in mitosis with morphologically normal spindles. Spindle assembly checkpoint mutants overexpressing Mps1p pass through mitosis without delay and can produce viable progeny, which demonstrates that the arrest of wild-type cells results from inappropriate activation of the checkpoint in cells whose spindle is fully functional. Ectopic activation of cell-cycle checkpoints might be used to exploit the differences in checkpoint status between normal and tumor cells and thus improve the selectivity of chemotherapy.