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As the use of mobile phone devices is now highly prevalent, many studies have sought to evaluate the effects of the radiofrequency-electromagnetic radiation (RF-EMR) on both human health and biology. While several such studies have shown RF-EMR is capable of inducing cellular stress, the physicobiological origin of this stress remains largely unresolved. To explore the effect of RF-EMR on the male reproductive system, we exposed cultured mouse spermatogonial GC1 and spermatocyte GC2 cell lines, as well as cauda epididymal spermatozoa to a waveguide generating continuous wave RF-EMR (1.8 GHz, 0.15 and 1.5 W/kg). This study demonstrated that a 4 h exposure is capable of inducing the generation of mitochondrial reactive oxygen species (ROS) in populations of GC1 (7 vs. 18%; p < 0.001) and GC2 cells (11.5 vs. 16 %; p < 0.01), identifying Complex III of the electron transport chain (ETC) as the potential source of electrons producing ROS. Assessing the generation of ROS in the presence of an antioxidant, penicillamine, as well as measuring lipid peroxidation via 4-hydroxynonenal levels, indicated that the elevated incidence of ROS generation observed under our exposure conditions did not necessarily induce an overt cellular oxidative stress response. However, exposure to RF-EMR at 0.15 W/kg for 3 h did induce significant DNA fragmentation in spermatozoa (that was no longer significant after 4 h), assessed by the alkaline comet assay (p < 0.05). Furthermore, this fragmentation was accompanied by an induction of oxidative DNA damage in the form of 8-hydroxy-2′-deoxyguanosine, which was significant (p < 0.05) after spermatozoa were exposed to RF-EMR for 4 h. At this exposure time point, a decline in sperm motility (p < 0.05) was also observed. This study contributes new evidence toward elucidating a mechanism to account for the effects of RF-EMR on biological systems, proposing Complex III of the mitochondrial ETC as the key target of this radiation.

The testicular spermatozoa of all mammalian species are considered functionally immature owing to their inability to swim in a progressive manner and engage in productive interactions with the cumulus–oocyte complex. The ability to express these key functional attributes develops progressively during the cells’ descent through the epididymis, a highly specialized ductal system that forms an integral part of the male reproductive tract. The functional maturation of the spermatozoon is achieved via continuous interactions with the epididymal luminal microenvironment and remarkably, occurs in the complete absence of de novo gene transcription or protein translation. Compositional analysis of the luminal fluids collected from the epididymis of a variety of species has revealed the complexity of this milieu, with a diversity of inorganic ions, proteins, and small non-coding RNA transcripts having been identified to date. Notably, both the quantitative and qualitative profile of each of these different luminal elements display substantial segment-to-segment variation, which in turn contribute to the regionalized functionality of this long tubule. Thus, spermatozoa acquire functional maturity in the proximal segments before being stored in a quiescent state in the distal segment in preparation for ejaculation. Such marked division of labor is achieved via the combined secretory and absorptive activity of the epithelial cells lining each segment. Here, we review our current understanding of the molecular mechanisms that exert influence over the unique intraluminal environment of the epididymis, with a particular focus on vesicle-dependent mechanisms that facilitate intercellular communication between the epididymal soma and maturing sperm cell population.

An album of photographs in the Kansas University Natural History Museum found together with the Patagonian fossils collected by Handel T. Martin in 1904 was assumed in a recent publication to have been assembled by Martin. It comprises 193 numbered pages and 580 photographs of prepared fossil vertebrate specimens, some labeled as from the Museo de La Plata and others, without labels, which were assumed as having been in F. Ameghino’s private fossil collection. However, archival evidence in the Yale Peabody Museum indicates that the album is most likely the original copy of the photographic album assembled by William B. Scott during his visit to Argentina in 1901 to examine fossil specimens from Patagonia in the museums of La Plata and Buenos Aires, and in Ameghino’s collection. It represents an important record of the specimens present at these institutions and in possession of Ameghino near the turn of the last century, a period during which those fossils aroused considerable scientific interest and were in very high demand among researchers and academic institutions, but marked as well by severe conflicts between F. Ameghino and the Director of the Museo de La Plata, F.P. Moreno. As a consequence the collections were subjected to considerable turmoil and many important specimens can no longer be located. The album provides visual references for these specimens and facilitates systematic and taxonomic research by helping to evaluate which specimens were used to erect numerous taxa and which were analyzed by other researchers who published on such remains.

One of the major causes of defective sperm function is oxidative stress, which not only disrupts the integrity of sperm DNA but also limits the fertilizing potential of these cells as a result of collateral damage to proteins and lipids in the sperm plasma membrane. The origins of such oxidative stress appear to involve the sperm mitochondria, which have a tendency to generate high levels of superoxide anion as a prelude to entering the intrinsic apoptotic cascade. Unfortunately, these cells have very little capacity to respond to such an attack because they only possess the first enzyme in the base excision repair (BER) pathway, 8-oxoguanine glycosylase 1 (OGG1). The latter successfully creates an abasic site, but the spermatozoa cannot process the oxidative lesion further because they lack the downstream proteins (APE1, XRCC1) needed to complete the repair process. It is the responsibility of the oocyte to continue the BER pathway prior to initiation of S-phase of the first mitotic division. If a mistake is made by the oocyte at this stage of development, a mutation will be created that will be represented in every cell in the body. Such mechanisms may explain the increase in childhood cancers and other diseases observed in the offspring of males who have suffered oxidative stress in their germ line as a consequence of age, environmental or lifestyle factors. The high prevalence of oxidative DNA damage in the spermatozoa of male infertility patients may have implications for the health of children conceivedin vitro and serves as a driver for current research into the origins of free radical generation in the germ line.

We connected youth of the Mushkegowuk Territory (specifically Fort Albany First Nation) with environmental science and technology mentors in an outreach program contextualized to subarctic Ontario that addressed some of the environmental concerns identified by members of Fort Albany First Nation. Most activities were community-based centering on the general theme of understanding a changing environment (e.g., long range transport of contaminants, global warming, and postglacial isostatic rebound); however, our initiative also included an annual trip for Grade 8 students to the Ontario Science Centre and the Royal Ontario Museum in Toronto, Ontario, to expose students to science in an interactive, fun setting. We found that informal educational settings, resources that relied on spatial/visual cues, group activities, and hands-on and experiential teaching were effective in engaging the schoolchildren. Our hope is that some of the students that attend our community-based camp will pursue a postsecondary education in the environmental sciences. (Contains 1 table and 1 figure.)

Mutations in the type III receptor tyrosine kinase FLT3 are frequent in patients with acute myeloid leukemia (AML) and are associated with a poor prognosis. AML is characterized by the overproduction of reactive oxygen species (ROS), which can induce cysteine oxidation in redox-sensitive signaling proteins. Here, we sought to characterize the specific pathways affected by ROS in AML by assessing oncogenic signaling in primary AML samples. The oxidation or phosphorylation of signaling proteins that mediate growth and proliferation was increased in samples from patient subtypes with FLT3 mutations. These samples also showed increases in the oxidation of proteins in the ROS-producing Rac/NADPH oxidase-2 (NOX2) complex. Inhibition of NOX2 increased the apoptosis of FLT3-mutant AML cells in response to FLT3 inhibitors. NOX2 inhibition also reduced the phosphorylation and cysteine oxidation of FLT3 in patient-derived xenograft mouse models, suggesting that decreased oxidative stress reduces the oncogenic signaling of FLT3. In mice grafted with FLT3 mutant AML cells, treatment with a NOX2 inhibitor reduced the number of circulating cancer cells, and combining FLT3 and NOX2 inhibitors increased survival to a greater extent than either treatment alone. Together, these data raise the possibility that combining NOX2 and FLT3 inhibitors could improve the treatment of FLT3 mutant AML. Blocking NOX2 bolsters AML precision therapy: Internal tandem duplication of Fms-like tyrosine kinase 3 (FLT3-ITD) is a common activating mutation in acute myeloid leukemia (AML) and leads to the increased production of reactive oxygen species (ROS). AML patients on FLT3-targeting therapies have a high rate of relapse. By performing a proteome-wide analysis of cysteine oxidation and phosphorylation of AML blast cells from patients harboring FLT3 mutations, Germon et al. identified the Rac-NOX2 complex as a driver of ROS production in AML cells. Inhibition of NOX2 promoted apoptosis of AML cells carrying the FLT3-ITD mutation and increased the survival of mice grafted with FLT3-ITD AML cells and treated with FLT3 inhibitors. Thus, targeting NOX2 may increase the effectiveness of precision therapy targeting AML. —AB [ABSTRACT FROM AUTHOR]

To prevent air pollution and achieve air quality regulations, it is essential to develop analytical techniques that can determine the concentration of metals in aerosol particles, both in the gas phase and after collection onto filters. Total reflection X-ray fluorescence spectroscopy (TXRF) and laser-induced breakdown spectroscopy (LIBS) are emerging as complementary techniques for determining the elemental composition of aerosol particles. The accuracy of their results relies on calibration methods based on aerosol and multi-element filters representative of the on-line measurement conditions and particulate collection for off-line measurement, respectively. In this paper we propose a novel methodology for characterizing nebulization generated aerosol particles dispersion and deposition by means of TXRF to assess the use of an aerosol generator to produce calibration samples for LIBS and TXRF analysis. Particles concentration and size distribution of the aerosol produced by nebulizing a Cu salt aqueous solution are measured inside a glove box modifying the production parameters and collecting the corresponding particulate deposited on reflectors. The most stable conditions are observed at average flow rate and selected for studying the aerosol spatial distribution. The Cu mass collected on reflectors positioned at a fixed distance and radial geometry with respect to the nozzle exit is measured by TXRF and increases linearly with time. Results suggest that this experimental configuration could be used to realize calibration samples for TXRF analysis representative of particulate deposition. The use of these aerosols as LIBS calibration samples could lead to significant errors due to the observed flow asymmetry. Copyright © 2022 American Association for Aerosol Research [ABSTRACT FROM AUTHOR]