Roundup disrupts male reproductive functions by triggering calcium-mediated cell death in rat testis and Sertoli cells

Glyphosate is the primary active constituent of the commercial pesticide Roundup. The present results show that acute Roundup exposure at low doses (36 ppm, 0.036 g/L) for 30 min induces oxidative stress and activates multiple stress-response pathways leading to Sertoli cell death in prepubertal rat testis. The pesticide increased intracellular Ca²⁺ concentration by opening L-type voltage-dependent Ca²⁺ channels as well as endoplasmic reticulum IP₃ and ryanodine receptors, leading to Ca²⁺ overload within the cells, which set off oxidative stress and necrotic cell death. Similarly, 30 min incubation of testis with glyphosate alone (36 ppm) also increased ⁴⁵Ca²⁺ uptake. These events were prevented by the antioxidants Trolox and ascorbic acid. Activated protein kinase C, phosphatidylinositol 3-kinase, and the mitogen-activated protein kinases such as ERK1/2 and p38MAPK play a role in eliciting Ca²⁺ influx and cell death. Roundup decreased the levels of reduced glutathione (GSH) and increased the amounts of thiobarbituric acid-reactive species (TBARS) and protein carbonyls. Also, exposure to glyphosate–Roundup stimulated the activity of glutathione peroxidase, glutathione reductase, glutathione S-transferase, γ-glutamyltransferase, catalase, superoxide dismutase, and glucose-6-phosphate dehydrogenase, supporting downregulated GSH levels. Glyphosate has been described as an endocrine disruptor affecting the male reproductive system; however, the molecular basis of its toxicity remains to be clarified. We propose that Roundup toxicity, implicated in Ca²⁺ overload, cell signaling misregulation, stress response of the endoplasmic reticulum, and/or depleted antioxidant defenses, could contribute to Sertoli cell disruption in spermatogenesis that could have an impact on male fertility.     

Biography,Authenticity and Personalised Post-Mortem Practices in Aotearoa/New Zealand

Current thanatology discourse details a new ethos of openness transforming death-related practices, accentuating a shift to personalised rituals, authenticity and expressive grief. Drawing on ethnographic interviews with mourners and funeral professionals, this article explores these putative post-mortem changes and critically assesses the claims and counterclaims concerning funerary arrangements in New Zealand. While underscoring the complexity of mortuary practices, this study explicates the varying notions of authenticity that pervade the funeral discourse. Although funeral professionals emphasised the significance of grief and bereavement processes characterised by a need for honesty and transparency, bereaved participants proffered an alternative interpretation of authenticity that privileged biographical coherence and the need to confer transcendence to the dead. These findings not only emphasise the inadequacies of the aforementioned representations of post-mortem change, but elucidate the context-specific conceptualisations of authenticity and the continuing relationships between the living and the dead in Aotearoa/New Zealand.     

Transgenerational cell fate profiling

The illicit generation of tetraploid cells constitutes a prominent driver of oncogenesis, as it often precedes the development of aneuploidy and genomic instability. In addition, tetraploid (pre-)malignant cells display an elevated resistance against radio- and chemotherapy. Here, we report a strategy to preferentially kill tetraploid tumor cells based on the broad-spectrum kinase inhibitor SP600125. Live videomicroscopy revealed that SP600125 affects the execution of mitosis, impedes proper cell division and/or activates apoptosis in near-to-tetraploid, though less so in parental, cancer cells. We propose a novel graphical model to quantify the differential response of diploid and tetraploid cells to mitotic perturbators, including SP600125, which we baptized “transgenerational cell fate profiling.” We speculate that this representation constitutes a valid alternative to classical “single-cell fate” and “genealogical” profiling and, hence, may facilitate the analysis of cell fate within a heterogeneous population as well as the visual examination of cell cycle alterations.     

Formation of Aerenchyma and the Processes of Plant Ventilation in Relation to Soil Flooding and Submergence

Abstract: Enhanced development of gas-spaces beyond that due to the partial cell separation normally found in ground parenchymas and their derivatives creates tissue commonly termed "aerenchyma". Aerenchyma can substantially reduce internal impedance to transport of oxygen, nitrogen and various metabolically generated gases such as carbon dioxide and ethylene, especially between roots and shoots. Such transport lessens the risk of asphyxiation under soil flooding or more complete plant submergence, and promotes radial oxygen loss from roots leading to oxidative detoxification of the rhizo-sphere. Aerenchyma can also increase methane loss from waterlogged sediments via plants to the atmosphere. This review of the formation and functioning of aerenchyma particularly emphasises research findings since 1992 and highlights prospects for the future. Regarding formation, attention is drawn to how little is known of the regulation and processes that create schizogenous aerenchyma with its complex cell arrangements and differential cell to cell adhesion. More progress has been made in understanding lysigenous aerenchyma development. The review highlights recent work on the processes that sense oxygen deficiency and ethylene signals, subsequent transduction processes which initiate cell death, and steps in protoplast and wall degeneration that create the intercellular voids. Similarities between the programmed cell death and its causes in animals and the predictable patterns of cell death that create lysigenous aerenchyma are explored. Recent findings concerning function are addressed in terms of the diffusion aeration of roots, rhizosphere oxygenation and sediment biogeochemistry, photosynthesis and ventilation, pressurised gas-flows and greenhouse gas emissions and aspects of ventilation related to secondary thickening.     

A Note on the Application of Martingales in a Problem of Non-Communicable Epidemics

The present paper is a Martingale approach to some non-communicable epidemic problem (e.g. cervical cancer). It is assumed the progress of the disease from pre-cancerous lesions to several grades of dysplasia and ultimately leading to carcinomia in situ and invasive cancer follows by consecutive hittings; and the regression (or the backward movement) from these states to ultimately non cancerous state; may be analogous to consecutive healings. Each hitting and healing thus considered to be a birth and death respectively in the density dependent linear birth and death process. Given that a patient is in some states of dysplasia the problem lies in finding the proportion of patients coming back to noncancerous state and the expected time for the same. Martingales constructed on a linear birth and death process have been employed to answer the problems.     

Proto-pyroptosis: An Ancestral Origin for Mammalian Inflammatory Cell Death Mechanism in Drosophila melanogaster

Pyroptosis has been described in mammalian systems to be a form of programmed cell death that is important in immune function through the subsequent release of cytokines and immune effectors upon cell bursting. This form of cell death has been increasingly well-characterized in mammals and can occur using alternative routes however, across phyla, there has been little evidence for the existence of pyroptosis. Here we provide evidence for an ancient origin of pyroptosis in an in vivo immune scenario in Drosophila melanogaster. Crystal cells, a type of insect blood cell, were recruited to wounds and ruptured subsequently releasing their cytosolic content in a caspase-dependent manner. This inflammatory-based programmed cell death mechanism fits the features of pyroptosis, never before described in an in vivo immune scenario in insects and relies on ancient apoptotic machinery to induce proto-pyroptosis. Further, we unveil key players upstream in the activation of cell death in these cells including the apoptosome which may play an alternative role akin to the inflammasome in proto-pyroptosis. Thus, Drosophila may be a suitable model for studying the functional significance of pyroptosis in the innate immune system.     

Genetic variation in piglet mortality in outdoor organic production systems

Piglet mortality from farrowing to weaning is a major concern, especially in outdoor organic production systems. This issue might impair animal welfare and generate economic losses for the farmer. In particular, it is difficult to apply management tools that are commonly used for indoor pig production systems to organic or outdoor production systems. Genetics and breeding approaches might be used to improve piglet survival. However, knowledge remains limited on the genetic background underlying survival traits in organic pigs that are born and reared outdoors. Here, we investigated the mortality of piglets from farrowing to weaning in an outdoor organic pig population and suggested genetic strategies to reduce piglet mortality in this production system. The experiment included mortality records of piglets from farrowing to weaning (around 69 days of age). Pedigree-based threshold models were used to analyse the mortality traits of piglets at 0–3 days of age, 4–11 days, and 12 days to weaning. Stillborn piglets were included in the group of piglets that died at 0–3 days of age. We found that the mortality rate from farrowing to weaning was, on average, 19.2%. However, most piglet deaths (79.1%) occurred at 0–11 days of age. As the age of piglets increased, the direct heritability of piglet mortality rose from 0 to 0.04, whereas maternal heritability decreased from 0.03 to a non-significant value. Piglets with higher BW had a lower mortality rate. However, the genetic correlations between maternal effects on piglet mortality and piglet BW were not significant; thus, selection for piglets with higher BW at around 10 days of age, through improving maternal genetics, would not reduce piglet mortality. Piglet mortality increased from sows with increasing number of parities. Crossbreeding also reduced piglet mortality. In conclusion, selection focusing on sow genotype, the use of younger sows, and crossbreeding could contribute to maintain piglet mortality at lower levels in outdoor organic pig production systems.