Differences in Curriculum Structure between High School and University Biology: The Implications for Epistemological Access

Despite doing well in biology at high school, some students struggle with the same subject at university level. This can have implications for epistemological access - access to knowledge that allows students to remain at university. Therefore, it is important to identify factors that may be causing this problem. We propose that one such factor may be differences in the structure of knowledge between the two levels. Therefore, this paper will assess some of the differences in the structuring of knowledge that exist between a high school and a university biology curriculum. To do this, a section of a high school and a university textbook which cover the same topic will be analysed using one aspect of Legitimation Code Theory called Semantics. Our findings suggest that there is a mismatch between the semantic range students are expected to navigate at university and that demanded by high school biology, and that this may pose a stumbling block to students gaining epistemological access to first-year study at university. If this is indeed the case, then pedagogic interventions which explicitly address this may contribute to improving undergraduate student retention and throughput rates at university.     

Insights into plant consciousness from neuroscience,physics and mathematics: A role for quasicrystals?

There is considerable debate over whether plants are conscious and this, indeed, is an important question. Here I look at developments in neuroscience, physics and mathematics that may impact on this question. Two major concomitants of consciousness in animals are microtubule function and electrical gamma wave synchrony. Both these factors may also play a role in plant consciousness. I show that plants possess aperiodic quasicrystal structures composed of ribosomes that may enable quantum computing, which has been suggested to lie at the core of animal consciousness. Finally I look at whether a microtubule fractal suggests that electric current plays a part in conventional neurocomputing processes in plants.     

Specificity of cycloheximide in higher plant systems

Although cycloheximide is extremely inhibitory to protein synthesis in vivo in higher plants, the reported insensitivity of some plant ribosomes suggests that it may not invariably act at the ribosomal level. This suggestion is reinforced by results obtained with red beet storage tissue disks, the respiration of which is stimulated by cycloheximide at 1 microgram per milliliter. Inorganic ion uptake by these disks is inhibited by cycloheximide at 1 microgram per milliliter while the uptake of organic compounds, by comparison, is unaffected. Ion uptake by all nongreen tissues tested is inhibited by cycloheximide, but leaf tissue is unaffected, indicating that the ion absorption mechanism in the leaf may differ fundamentally from that in the root. It is concluded that cycloheximide can affect cellular metabolism other than by inhibiting protein synthesis and that the inhibition of ion uptake may be due to disruption of the energy supply.     

Tumour biology of a breast cancer at least partly reflects the biology of the tissue/epithelial cell of origin at the time of initiation - a hypothesis

A hypothesis is presented suggesting that initiation of breast epithelial cell freezes the cell at least partly according to the development/differention of cell at the time of initiation. Tumour biology will mimic the physiology of normal cell development at the time of initiation and this is preserved at least partly onwards. Also preferentially, tumours will develop from the cell type that is proliferating at the time of initiation. This may explain the overrepresentation of different types of histology in breast cancer in relation to age of the woman. The development of each tumour may follow at least partly a distinct pathway of evolution.     

Importance of autophosphorylation at Ser186 in the A-loop of salt inducible kinase 1 for its sustained kinase activity

Autophosphorylation is an important mechanism by which protein kinases regulate their own biological activities. Salt inducible kinase 1 (SIK1) is a regulator in the feedback cascades of cAMP-mediated gene expression, while its kinase domain also features autophosphorylation activity. We provide evidence that Ser186 in the activation loop is the site of autophosphorylation and essential for the kinase activity. Ser186 is located at the +4 position of the critical Thr residue Thr182, which is phosphorylated by upstream kinases such as LKB1. The relationship between phosphorylation at Ser186 and at Thr182 in COS-7 cells indicates that the former is a prerequisite for the latter. Glycogen synthase kinase-3beta (GSK-3beta) phosphorylates Ser/Thr residues located at the fourth position ahead of the pre-phosphorylated Ser/Thr residues, and inhibitors of GSK-3beta reduce the phosphorylation at Thr182. The results of an in vitro reconstitution assay also indicate that GSK-3beta could be the SIK1 kinase. However, overexpression and knockdown of GSK-3beta in LKB1-defective HeLa cells suggests that GSK-3beta alone may not be able to phosphorylate or activate SIK1, indicating that LKB1 may play a crucial role by phosphorylating SIK1 at Thr182, possibly as an initiator of the autophosphorylation cascade, and GSK-3beta may phosphorylate SIK1 at Thr182 by recognizing the priming-autophosphorylation at Ser186 in cultured cells. This may also be the case for the other isoform SIK2, but not for SIK3.     

Perspectives on the formation of an interdisciplinary research team

As research funding becomes more competitive, it will be imperative for researchers to break the mentality of a single laboratory/single research focus and develop an interdisciplinary research team aimed at addressing real world challenges. Members of this team may be at the same institution, may be found regionally, or may be international. However, all must share the same passion for a topic that is bigger than any individual’s research focus. Moreover, special consideration should be given to the professional development issues of junior faculty participating in interdisciplinary research teams. While participation may be “humbling” at times, the sheer volume of research progress that may be achieved through interdisciplinary collaboration, even in light of a short supply of grant dollars, is remarkable.     

Effects of acronycine on nucleic acid synthesis and population growth in mammalian tumor cell cultures

Acronycine — an alkaloid with antineoplastic activity against a wide range of experimental tumors — at concentrations of 0.5-12 μg/ml rapidly inhibits RNA synthesis in L5178Y mouse lymphoma and IRC rat monocytic leukemia cultures. Culture growth is arrested only at acronycine concentrations which markedly inhibit RNA synthesis. DNA synthesis is inhibited at rather higher concentrations but this is not a prerequisite of the arrest of growth. It is suggested that the arrest of growth may be a consequence of the inhibition of RNA synthesis. In both cultures arrest of growth coincides with the appearance of many cells with two apparently normal nuclei. Cells are not arrested in mitosis. It is shown these binucleated cells very probably arise from an inhibition of cell cleavage. Studies with synchronized cultures show that at low drug concentrations, more than one cell cycle may elapse before growth is arrested and binucleated cells appear, indicating the effect on cytokinesis is not immediate. The results suggest that the arrest of growth may be a result of a slow depletion of a component essential for cell cleavage. The disturbance at division is a major factor in arresting growth at low drug concentrations. At higher acronycine concentrations, when RNA synthesis may be inhibited by 80–90%, the cytotoxic effects appear earlier and are less specifically directed at cytokinesis; DNA synthesis is then also rapidly and markedly inhibited.     

A life-history perspective on short- and long-term consequences of compensatory growth

Compensatory or catch-up growth (CG) is widely observed following periods of resource deprivation. Because of this commonness, it is generally assumed that compensatory growth is adaptive, but most theory to date has explicitly ignored considerations of fitness. Following a period of deprivation, when resources become plentiful again, individuals may not respond at all and continue on a "normal" trajectory from a smaller size at age, may exhibit faster-than-normal growth immediately following the end of the period, or may adopt a growth strategy that involves faster-than-normal growth at some later time. Compensating individuals may also overtake control individuals who have been growing normally throughout. We hypothesize that the key to understanding CG is that growth leads to the accumulation of damage at the cellular level that is expressed (and thus must be modeled) at the level of the organism. We show that a life-history model incorporating the mortality consequences of both size and damage provides a framework for understanding compensatory growth. We use the theory to classify physiological and life-history characteristics for which CG is predicted to be the optimal response to deprivation.     

Hepsin Paradox Reveals Unexpected Complexity of Metastatic Process

The existing models of cancer progression assume that a linear sequence of geneticand epigenetic events occurs during this process. In this representation every new event(either loss of a tumor-suppressor, or activation of a proto-oncogene) makes cells even moremalignant. The result is a “super” cell that can form metastases at the distant sites.Metastatic cells are believed to carry all genetic and epigenetic characteristics that arenecessary for metastasis formation. Recently, we have shown that cell-surface proteasehepsin causes disorganization of the basement membrane and promotes prostate cancerprogression and metastasis. In human prostate cancer hepsin is upregulated in theprecancerous lesions and this upregulation is maintained in the primary tumors. Remarkablyand completely unexpected for a metastasis-promoting gene, hepsin is expressed at lowlevels in metastatic lesions and the message is completely absent in metastasis-derivedprostate cancer cell lines. These results demonstrate that genes that play an important role inmetastatic process may exercise their role only at the specific fragments of cancerprogression pathway (for example, during initial invasion and tissue disorganization in theprimary organ) and may have no role in metastatic lesions. Future treatment of cancerpatients may rely heavily on monitoring of tumor progression, as treatment efficient inattenuation of initial tumor progression may be inefficient or even adverse at the advancestages of disease.     

The diet of the dog-whelk, Nucella lapillus (Gastropoda Prosobranchia)

The information at present available suggests that, when adult, Nucella lapillus may prey upon a considerable number of different species, but that the diet of recently hatched dog-whelks is rather more restricted. The food preferences of young Nucella have been investigated and it has been concluded that, while the diet of young and adult animals may differ to some extent, it is probably equally varied at all ages, and that cannibalism may be a frequent occurrence amongst all age groups.
It has been determined that the size of the prey influences the selective predation of Mytilus by Nucella. Dog-whelks show a marked preference for mussels in the 1 to 3 cm size range which may possibly be identified chemotactically.     

Does a dose-response relationship reduce sensitivity to hidden bias?

It is often said that an important consideration in judging whether an association between treatment and response is causal is the presence or absence of a dose-response relationship, that is, larger ostensible treatment effects when doses of treatment are larger. This criterion is widely discussed in textbooks and is often mentioned in empirical papers. At the same time, it is well known through both important examples and elementary theory that a treatment may cause dramatic effects with no dose-response relationship, and hidden biases may produce a dose-response relationship when the treatment is without effect. What does a dose-response relationship say about causality? It is observed here that a dose-response relationship may or may not reduce sensitivity to hidden bias, and whether it has or has not can be determined by a suitable analysis using the data at hand. Moreover, a study without a dose-response relationship may or may not be less sensitive to hidden bias than another study with such a relationship, and this, too, can be determined from the data at hand. An example concerning cytogenetic damage among professional painters is used to illustrate.     

Nutrition and metabolic development

Perinatal changes in metabolic processes owing to a change from a high carbohydrate to a high fat (milk) diet at birth are described. It is pointed out that early changes in food composition may have permanent effects and it is suggested that, in the rat, this may be due to structural alterations in the brain at a time when it is still differentiating. Such changes are irreversible.     

International Commission for Protection Against Environmental Mutagens and Carcinogens. ICPEMC Working Paper No. 2. Diet, mutation and cancer

Experimental research designed to determine the effects of variations in diet on the carcinogenic and mutagenic processes is difficult to conduct and even more difficult to interpret in terms of the likely response that such variations will have on the expression of human cancer and mutation. Although some of these difficulties may be due to a failure to persuade adequate numbers of highly trained nutritionists to enter into this type of research, a more germaine reason may be that the high level of complexity of both diet and the disease processes is such as to confound present efforts at interpretation. It is suggested that a stepwise analysis of the effects of dietary factors on each critical stage in carcinogenesis or mutagenesis may ultimately lead to results that are more easily interpreted in terms of human response. To this end it is proposed that studies of DNA-carcinogen or DNA-mutagen adduct formation, or other DNA damage, DNA replication and relevant DNA repair at the target site may be a useful guide to the effect of nutritional changes on mutation and/or cancer initiation. DNA replication at various stages of carcinogenesis, modification of hormonal levels, modification of immune response, or other factors as influenced by diet may provide markers for cancer development. The integration of this data to give an overall perception of the effects of nutrition is briefly discussed.     

Activation of p56lck through mutation of a regulatory carboxy-terminal tyrosine residue requires intact sites of autophosphorylation and myristylation.

Mutation of the major site of in vivo tyrosine phosphorylation of p56lck (tyrosine 505) to a phenylalanine constitutively enhances the p56lck-associated tyrosine-specific protein kinase activity. The mutant polypeptide is extensively phosphorylated in vivo at the site of in vitro Lck autophosphorylation (tyrosine 394) and is capable of oncogenic transformation of rodent fibroblasts. These observations have suggested that phosphorylation at Tyr-505 down regulates the tyrosine protein kinase activity of p56lck. Herein we have attempted to examine whether other posttranslational modifications may be involved in regulation of the enzymatic function of p56lck. The results indicated that activation of p56lck by mutation of Tyr-505 was prevented by a tyrosine-to-phenylalanine substitution at position 394. Furthermore, activation of p56lck by mutation of the carboxy-terminal tyrosine residue was rendered less efficient by substituting an alanine residue for the amino-terminal glycine. This second mutation prevented p56lck myristylation and stable membrane association and was associated with decreased in vivo phosphorylation at Tyr-394. Taken together, these findings imply that lack of phosphorylation at Tyr-505 may be insufficient for enhancement of the p56lck-associated tyrosine protein kinase activity. Our data suggest that activation of p56lck may be dependent on phosphorylation at Tyr-394 and that this process may be facilitated by myristylation, membrane association, or both.     

Nature and role of accessory chromosomes in silver-gray foxes. IV. The behavior of accessory chromosomes in meiosis

Comparison of chromosome number at somatic and spermatogonial mitoses has demonstrated the increase in the number of additional chromosomes in cells of germinal tissue. This may evidence a mechanism of B-chromosomes accumulation in foxes. B-chromosomes may lag as univalents, may form bivalent associations, or occasionally form trivalents at the stage of diakinesis-metaphase I, and they may associate with macrobivalents (A-chromosome bivalents). The analysis of metaphase II has shown that the distribution of B-chromosomes in the second metaphase is random resulting in gametes with various numbers of B-chromosomes.     

Dimerization of Toc-GTPases at the chloroplast protein import machinery

Import of chloroplast precursor proteins is controlled by the coordinate action of two homologous GTPases, Toc159 and Toc33, located at the cytosol-outer membrane interface. Recent studies in Arabidopsis showed that the cytosolic form of the precursor binding protein Toc159 is targeted to its receptor at the import machinery, Toc33, via heterodimerization of their GTP-binding domains. Toc33 may also form GDP-bound homodimers, as suggested by the crystal structure of its pea ortholog. Moreover, the structural data suggested that arginine 130 (Arg130) of Arabidopsis Toc33 may function as a GTPase-activating "arginine-finger" at the other monomer in the Toc33 dimer. Here, we demonstrate that Arg130 of Toc33 does not function as an Arginine-finger. A mutant, Toc33-R130A, binds and hydrolyzes GTP like the wild type. However, we demonstrate that Arg130 is involved in both homodimerization of Toc33 and in heterodimerization with the GTP-binding domain of Toc159. The dependence of Toc33 homodimerization on Arg130 is mutual, requiring the presence of Arg130 at both monomers. As the GTPase is not activated by dimerization, it may be activated independently at either monomer, possibly even before dimerization. Independent regulation of GTPase activity may serve to coordinate the interactions of the GTPases during the import of proteins into the chloroplast.     

The influence of increased line-fishing mortality on the sex ratio and age of sex reversal of the venus tusk fish

The age of sex reversal of the venus tusk fish Choerodon venustus , caught by line fishing at various locations on the southern Great Barrier Reef, indicated that C. venustus is capable of modifying its life cycle in response to increased mortality. The evidence suggests Masthead Reef fish, which experience the highest mortality, underwent sex reversal at a smaller size and younger age than at the other sites. The largest female fish, sexually transitional fish and males were smaller at Masthead Reef than at the Swains Reefs or One Tree Reef at Masthead Reef. There was also considerable overlap in the size of males and females within the exploited populations indicating that sex reversal is not initiated at a particular length but may have a social cause. The sex ratio of fish was essentially the same for fish fully susceptible to line fishing in the Swains and Masthead samples. Circumstantial evidence suggested that the absence of large males in a population may initiate sex reversal, indicating the maintenance of a constant sex ratio may have a social basis.     

Loss of MHC and neutral variation in Peary caribou: genetic drift is not mitigated by balancing selection or exacerbated by MHC allele distributions

Theory and empirical results suggest that the rate of loss of variation at Mhc and neutral microsatellite loci may differ because selection influences Mhc genes, and because a high proportion of rare alleles at Mhc loci may result in high rates of loss via drift. Most published studies compare Mhc and microsatellite variation in various contemporary populations to infer the effects of population size on genetic variation, even though different populations are likely to have different demographic histories that may also affect contemporary genetic variation. We directly compared loss of variation at Mhc and microsatellite loci in Peary caribou by comparing historical and contemporary samples. We observed that similar proportions of genetic variation were lost over time at each type of marker despite strong evidence for selection at Mhc genes. These results suggest that microsatellites can be used to estimate genome-wide levels of variation, but also that adaptive potential is likely to be lost following population bottlenecks. However, gene conversion and recombination at Mhc loci may act to increase variation following bottlenecks.     

Field and laboratory observations on the foraging and feeding techniques of blue tits (Parus caeruleus) and coal tits (P. ater) in relation to their habitats

I have tried to show (a) that results in the literature suggest that blue tits and coal tits survive better in their usual habitats of broad-leaved and conifer woods respectively; (b) that the higher mortality in the ‘wrong’ habitat may be attributed at least in part to an inability to acquire an adequate supply of food; (c) from my own and other people's field observations, that wild coal tits and blue tits use different feeding techniques; (d) from my own laboratory experiments, that each species is ‘best’ at the feeding techniques which it in general uses in the wild, and also that each species prefers to use the feeding techniques at which it is ‘best’; (e) that the feeding techniques of coal tits may be adapted to exploit the type of food supply found in conifers, while those of blue tits may be adapted for feeding in broad-leaved trees.