Water-Stress-Induced Ethylene Production in Wheat : A Fact or Artifact?

Effects of water stress on ethylene evolution from excised leaf segments and intact plants of wheat (Triticum aestivum L. cv Katepwa) were studied. Excised leaf segments of 8 day or 6 week old plants were dried until they lost 8% of their fresh weight (water potential about −2.3 megapascals). These and nondried control leaf segments (water potential about −1.0 megapascal) were sealed in glass tubes, and their ethylene production rates were compared by head space analysis via gas-chromatography. The dried leaves of both ages produced significantly more ethylene than the corresponding controls. However, when 6 week old intact plants were water-stressed by withholding water supply, and their ethylene production measured using a continuousflow system, no increase in ethylene was deteceted despite a drop in water potential to −2.9 megapascals over 6 days. Even the leaf segments excised from plants that had been subjected to water stress for 2, 4, or 6 days produced no more ethylene (in sealed tubes) than the leaves from well-watered plants. In fact, the ethylene production by these segments decreased with the increase in the severity of stress experienced by the plants. The results show that the commonly reported overproduction of ethylene by excised leaves subjected to rapid drying represents an artifact, which has little relevance to the water stress responses of intact wheat plants.     

Radiation induced isostaining: fact or fiction?

Two different experiments were set up to induce differential staining in M-1¹ cells or to induce isostaining in M-2 cells after -irradiation of human lymphocytes. Neither of these two unusual staining patterns previously described by Luchnik and Porjadkova (1977) were observed. Possible explanations for this disagreement are discussed.Abbreviations SCE Sister chromatid exchange - IS Isostained regions - S-1, S-2, S-3 and S-4 First, second, third and fourth DNA synthetic periods after addition of 5-bromodeoxyuridine - M-1, M-2, M-3, M-4 and M-5 First, second, third, fourth and fifth mitosis after addition of 5-bromodeoxyuridine - BrdU 5-bromodeoxyuridine - EMEM Eagle's Minimum Essential Medium     

Decline in regeneration during aging: Appropriateness or stochastics?

There is a standpoint according to which the suppression of the ability of cells in a multicellular organism to proliferate, taking place during aging, as well as the corresponding decline in the regenerative capacities of tissues and organs, is caused by the specialized mechanisms having emerged in the evolution that decrease the risk of malignant transformation and, thereby, provide for protection against cancer. At the same time, various macromolecular defects start to accumulate in senescent cells of the body, which, on the contrary, elevate the probability for malignant transformation of these cells. Thus, according to the mentioned concept, the restriction of cell proliferation is a double-edged sword, which, on the one hand, decreases the probability for malignant tumor development in young age and, on the other hand, limits the lifespan due to accumulation of “spoiled” cells in old age. However, it remains unclear why normal human cells placed under in vitro conditions and thus having no mentioned “anticancer” barriers, which function at the body level only, NEVER undergo spontaneous malignant transformation. In addition, it is unclear how the freshwater hydra escapes both aging and cancer, as it under certain conditions contains no postmitotic and senescent cells at all and under these conditions (excluding the need for sexual reproduction) can live almost indefinitely, possessing a tremendous regenerative potential (a new organism can emerge from even 1/100 part of the old one). Presumably, the restriction of cell proliferation in an aging multicellular organism is not the result of a certain special program. Apparently, there is no program of aging at all, the aging being a “byproduct” of the program of development, whose implementation in higher organisms necessarily requires emergence of cell populations with a very low and even zero proliferative activity, which actually determines the limited ability of the corresponding organs and tissues to regenerate. On the other hand, the populations of highly differentiated cells incapable or poorly capable of reproduction (e.g., neurons, cardiomyocytes, and hepatocytes) are the particular factor that determines the normal functioning of higher animals and humans. Even regeneration of such organs with the help of stem cells may interfere with the necessary links in elaborate systems. The reductionism (“everything is determined by adverse changes in individual cells”), which has recently become widespread in experimental gerontological research, has brought about several model systems for studying the aging mechanisms in isolated cells (Hayflick phenomenon, stationary phase aging model, cellular kinetic model for testing of geroprotectors and geropromoters, etc.). However, it currently seems that data obtained using such models are inappropriate for an automatic extrapolation to the situation in the whole body. Presumably, impairments in regulatory processes functioning at the neurohumoral level are the major players in the mechanisms underlying aging of multicellular organisms rather than a mere accumulation of macromolecular damage in individual cells. It cannot be excluded that a disturbance of such regulation is the particular reason for the abnormal INCREASE in proliferation intensity of some cell populations that are frequently observed in old age and that lead to senile acromegaly and development of numerous benign tumors. It looks like the quality of CONTROL over cells, organs, and tissues becomes poorer with age rather than the quality of the cells themselves, which leads to an increase in the death rate.     

Heat shock proteins in oncology: Diagnostic biomarkers or therapeutic targets?

Heat shock proteins (HSP) are a family of proteins induced in cells exposed to different insults. This induction of HSPs allows cells to survive stress conditions. Mammalian HSPs have been classified into six families according to their molecular size: HSP100, HSP90, HSP70, HSP60, HSP40 and small HSPs (15 to 30kDa) including HSP27. These proteins act as molecular chaperones either helping in the refolding of misfolded proteins or assisting in their elimination if they become irreversibly damaged. In recent years, proteomic studies have characterized several different HSPs in various tumor types which may be putative clinical biomarkers or molecular targets for cancer therapy. This has led to the development of a series of molecules capable of inhibiting HSPs. Numerous studies speculated that over-expression of HSP is in part responsible for resistance to many anti-tumor agents and chemotherapeutics. Hence, from a pharmacological point of view, the co-administration of HSP inhibitors together with other anti-tumor agents is of major importance in overcoming therapeutic resistance. In this review, we provide an overview of the current status of HSPs in autoimmune, cardiovascular, and neurodegenerative diseases with special emphasis on cancer.     

Shift in Black Rhinoceros Diet in the Presence of Elephant: Evidence for Competition?

In African large herbivore assemblages, megaherbivores dominate the biomass and utilise the greatest share of available resources. Consequently, they are considered a separate trophic guild that structures the food niches of coexisting large herbivores. However, there exists little empirical evidence on how food resources are shared within this guild, and none for direct competition for food between megaherbivores. Using the histological analysis of faeces, we explore this phenomenon for African elephant Loxodonta africana and black rhinoceros Diceros bicornis in the Addo Elephant National Park, South Africa, where the accumulated impacts of elephant have reduced browse availability. Despite being unable to generalise beyond our study sites, our observations support the predictions of competition theory (as opposed to optimality theory) by showing (1) a clear seasonal separation in resource use between these megaherbivores that increased as resource availability declined, and (2) rhinoceros changed their selectivity in the absence of elephant (using an adjacent site) by expanding and shifting their diet along the grass-browse continuum, and in relation to availability. Although black rhinoceros are generally considered strict browsers, the most significant shift in diet occurred as rhinoceros increased their preferences for grasses in the presence of elephant. We speculate that the lack of specialised grazing adaptations may increase foraging costs in rhinoceros, through reduced harvest- and handling-efficiencies of grasses. In the short-term, this may be off-set by an enhanced tolerance for low quality food and by seasonally mobilising fat reserves; however, the long-term fitness consequences require further study. Our data suggest that managing elephant at high densities may compromise the foraging opportunities of coexisting browsers. This may be particularly important in small, fenced areas and overlapping preferred habitats where impacts intensify.     

Heat shock proteins in health and disease: therapeutic targets or therapeutic agents?

For many years, heat shock or stress proteins have been regarded as intracellular molecules that have a range of housekeeping and cytoprotective functions, only being released into the extracellular environment in pathological situations such as necrotic cell death. However, evidence is now accumulating to indicate that, under certain circumstances, these proteins can be released from cells in the absence of cellular necrosis, and that extracellular heat shock proteins have a range of immunoregulatory activities. The capacity of heat shock proteins to induce pro-inflammatory responses, together with the phylogenetic similarity between prokaryotic and eukaryotic heat shock proteins, has led to the proposition that these proteins provide a link between infection and autoimmune disease. Indeed, both elevated levels of antibodies to heat shock proteins and an enhanced immune reactivity to heat shock proteins have been noted in a variety of pathogenic disease states. However, further evaluation of heat shock protein reactivity in autoimmune disease and after transplantation has shown that, rather than promoting disease, reactivity to self-heat shock proteins can downregulate the disease process. It might be that self-reactivity to heat shock proteins is a physiological response that regulates the development and progression of pro-inflammatory immunity to these ubiquitously expressed molecules. The evolving evidence that heat shock proteins are present in the extracellular environment, that reactivity to heat shock proteins does not necessarily reflect adverse, pro-inflammatory responses and that the promotion of reactivity to self-heat shock proteins can downregulate pathogenic processes all suggest a potential role for heat shock proteins as therapeutic agents, rather than as therapeutic targets.     

Assessment of a Syndromic Surveillance System Based on Morbidity Data: Results from the Oscour? Network during a Heat Wave

Background

Syndromic surveillance systems have been developed in recent years and are now increasingly used by stakeholders to quickly answer questions and make important decisions. It is therefore essential to evaluate the quality and utility of such systems. This study was designed to assess a syndromic surveillance system based on emergency departments'' (ED) morbidity rates related to the health effects of heat waves. This study uses data collected during the 2006 heat wave in France.

Methods

Data recorded from 15 EDs in the Ile-de-France (Paris and surrounding area) from June to August, 2006, were transmitted daily via the Internet to the French Institute for Public Health Surveillance. Items collected included diagnosis (ICD10), outcome, and age. Several aspects of the system have been evaluated (data quality, cost, flexibility, stability, and performance). Periods of heat wave are considered the most suitable time to evaluate the system.

Results

Data quality did not vary significantly during the period. Age, gender and outcome were completed in a comprehensive manner. Diagnoses were missing or uninformative for 37.5% of patients. Stability was recorded as being 99.49% for the period overall. The average cost per day over the study period was estimated to be €287. Diagnoses of hyperthermia, malaise, dehydration, hyponatremia were correlated with increased temperatures. Malaise was most sensitive in younger and elderly adults but also the less specific. However, overall syndrome groups were more sensitive with comparable specificity than individual diagnoses.

Conclusion

This system satisfactorily detected the health impact of hot days (observed values were higher than expected on more than 90% of days on which a heat alert was issued). Our findings should reassure stakeholders about the reliability of health impact assessments during or following such an event. These evaluations are essential to establish the validity of the results of syndromic surveillance systems.     

Origin of an insect outbreak: escape in space or time from natural enemies?

Initiation of insect outbreaks is poorly understood, and may involve sporadic events that temporarily release insect populations from predation or parasitism. While studying a declining outbreak of the western tussock moth (Orgyia vetusta) on bush lupine (Lupinus arboreus), we witnessed the onset of a new tussock moth outbreak, separated by 1,000 m in space and 2 months in phenological timing from the original population. This new population underwent explosive growth for 2 years and then collapsed because of a massive die-off of lupines. We tested whether during its growth phase, this new outbreak benefited by escaping in either space or time from the natural enemies attacking the original population. In experimental populations on single bushes, we compared predation and parasitism at the sites of the new and the old outbreak. At the site of the old outbreak, we compared predation and parasitism early and late in the season. Parasitism was significantly lower and population growth significantly higher at the new outbreak site than the old one. Neither seasonal timing, predator exclusion, nor their interaction significantly affected survival at either site. Thus the new outbreak appeared to escape in space from parasitism. These results corroborate our previous experimental findings, which suggest that as predicted by theory, the interaction between the tussock moth and its parasitoids can produce large-scale spatial patterning in population densities.     

Synaptic Plasticity in the Hippocampus: Effects of Estrogen from the Gonads or Hippocampus?

Different effects of estrogen on synaptic plasticity have [corrected] been reported. Here, we summarise effects of low, gonad-derived serum estrogen concentrations, of intermediate concentrations, provided by hippocampal cells, and of pharmacological doses of estrogen on synapses and spines and on the expression of synaptic proteins. No effects of low concentrations were found. To study the effects of hippocampus-derived estradiol, we inhibited hippocampal estrogen synthesis by treatment of hippocampal cell cultures with letrozole, an aromatase inhibitor. Alternatively, we used siRNA against Steroidogenic acute regulatory protein (StAR). Spines, synapses, and synaptic proteins were significantly down regulated in response to letrozole and in siRNA-StAR transfected cells. Application of high pharmacological doses of estradiol promoted only synaptophysin expression, a presynaptic protein, but did not increase the number of boutons. Our results point to an essential role of endogenous hippocampal estrogen in hippocampal synaptic plasticity rather than to a direct influence of estrogens derived from peripheral sources, such as the gonads.     

Regional Abnormality of Grey Matter in Schizophrenia: Effect from the Illness or Treatment?

Both schizophrenia and antipsychotic treatment are known to modulate brain morphology. However, it is difficult to establish whether observed structural brain abnormalities are due to disease or the effects of treatment. The aim of this study was to investigate the effects of illness and antipsychotic treatment on brain structures in antipsychotic-naïve first-episode schizophrenia based on a longitudinal short-term design. Twenty antipsychotic-naïve subjects with first-episode schizophrenia and twenty-four age- and sex-matched healthy controls underwent 3T MRI scans. Voxel-based morphometry (VBM) was used to examine the brain structural abnormality in patients compared to healthy controls. Nine patients were included in the follow-up examination after 8 weeks of treatment. Tensor-based morphometry (TBM) was used to identify longitudinal brain structural changes. We observed significantly reduced grey matter volume in the right superior temporal gyrus in antipsychotic-naïve patients with schizophrenia compared with healthy controls. After 8 weeks of treatment, patients showed significantly increased grey matter volume primarily in the bilateral prefrontal cortex, insula, right thalamus, left superior occipital cortex and the bilateral cerebellum. In addition, a greater enlargement of the prefrontal cortex is associated with the improvement in negative symptoms, and a more enlarged thalamus is associated with greater improvement in positive symptoms. Our results suggest the following: (1) the abnormality in the right superior temporal gyrus is present in the early stages of schizophrenia, possibly representing the core region related to schizophrenia; and (2) atypical antipsychotics could modulate brain morphology involving the thalamus, cortical grey matter and cerebellum. In addition, examination of the prefrontal cortex and thalamus might facilitate an efficient response to atypical antipsychotics in terms of symptom improvement.     

Epigenetic DNA Methylation in Radiation Biology: On the Field or on the Sidelines?

DNA methylation has been studied with regard to chemotherapeutics for a number of years. The radiation field has just begun to look at this in the context of radiotherapy or radiation exposure. So far, the data suggest that radiation induces epigenetic reprogramming which indicates a purposeful response that influences the cell fate or alters the response to future exposure. Further studies may result in discovery of biomarkers for radiotherapy outcome or prediction of the degree of radiation resistance. Past and ongoing development of DNMT1 inhibitors that lead to DNA hypomethylation appear to sensitize many tumor types to radiation and may be an area with long term clinical implications. J. Cell. Biochem. 116: 212–217, 2015. © 2014 Wiley Periodicals, Inc.     

Changes in molluscan neurosecretory cells during reproductive cessation: cause or effect?

The pond snail Lymnaea stagnalis has a maximum life span of about 22 months. At the age of about 250 days animals start to decrease egg laying activity and at about 500 days most animals ceased egg laying activity. At the age of cessation of egg laying the neurosecretory caudodorsal cells (CDCs) which control egg laying in Lymnaea exhibit reduced branching patterns. At this stage the cells still exhibit their physiological properties. CDCs still contain biologically active peptides and in the isolated CNS they still exhibit an afterdischarge upon electrical stimulation. Probably in the intact animal cessation of egg laying occurs because the CDCs are not activated anymore by natural egg laying inducing stimuli. In very old animals CDCs exhibit signs of degeneration indicating that cell death occur. After an extended period of no egg laying of Lymnaea physiological changes occur in the CDCs. CDCs from animals after an extended period of no egg laying failed to exhibit an afterdischarge. In such CDCs chemical and electrical coupling among the CDCs are reduced. Morphologically reduced CDCs predominantly fail to exhibit an afterdischarge. However, there are minimally branched CDCs that still could give an afterdischarge. Probably morphological reduction is not the only factor that defines afterdischarge failure. At present we suggest the following sequence of changes. 1. Morphological reduction of CDC branching patterns. 2. Cessation of egg laying. 3. Physiological changes in the CDCs resulting in afterdischarge failure. 4. Further morphological and physiological deterioration of CDCs.     

DNA Concentration-Dependent Dissociation of EcoRI: Direct Transfer or?Reaction during Hopping

Direct transfer of proteins between DNA helices is a recognized important feature of the recognition site search process. Direct transfer is characterized by a dissociation rate that depends on total DNA concentration. This is taken as evidence for the formation of an intermediate DNA-protein-DNA ternary complex. We find that the dissociation rate of EcoRI-DNA-specific complexes at 80 mM NaCl depends on the concentration of competitor oligonucleotide suggesting that direct transfer contributes to EcoRI dissociation. This dependence on competitor DNA concentration is not seen at 180 mM salt. A careful examination of the salt concentration dependence of the dissociation rate, however, shows that the predictions for the formation of a ternary complex are not observed experimentally. The findings can be rationalized by considering that just after dissociating from a DNA fragment the protein remains in close proximity to that fragment, can reassociate with it, and diffuse back to the recognition site rather than bind to an oligonucleotide in solution, a hopping excursion. The probability that a protein will bind to an oligonucleotide during a hop can be approximately calculated and shown to explain the data. A dependence of the dissociation rate of a DNA-protein complex on competitor DNA concentration does not necessarily mean direct transfer.     

Teaching of microbiology in Brazil: progress or stagnation?

There is a severe shortage of trained microbiologists in Brazil which is hampering the development and expansion of microbiology/biotechnology research, the development of the biotechnology industries and environmental control agencies. Even some medical areas are affected. The reason for this situation lies in the deficient teaching of microbiology, where undergraduate courses in the biological sciences contain little or no microbiology, and in the low number of professionals that are produced. There are a few post-graduates courses in microbiology but these have high costs and little capacity for expansion. There is a need for incentives for the establishment of more undergraduate university courses, more practical training in specific areas, courses for retraining or updating of professionals already at work and specific programmes by the funding agencies.The objective of this article is to encourage discussion about the present state and the future of the teaching of Microbiology in Brazil. It may also be useful for other countries in the same situation.J.R. Jardim Freire is with the Department of Soil Science, Federal University of Rio Grande do Sul, Av. Bento Gonçalves 7712, 91540-000 Porto Alegre, RS, Brazil; W. Gambale is with the Department of Microbiology, Institute of Biomedical Science, University of São Paulo, Av. Lineu Prestes 1374, 05508-900, São Paulo, SP, Brazil.