Survival Mechanism Research Articles

Protective Effect of Biochanin A on Gamma Radiation-Induced Oxidative Stress, Antioxidant Status, Apoptotic, and DNA Repairing Molecules in Swiss Albino Mice.

Radiation therapy is indispensable in medical practice but often causes adverse effects on healthy tissues, necessitating the search for natural radioprotectors. This study investigates the protective effect of Biochanin A (BCA) against gamma radiation-induced oxidative stress and DNA damage in Swiss albino mice. Gamma radiation, a potent ionizing source, generates reactive oxygen species (ROS) that damage cellular biomolecules, including DNA. Antioxidants play a crucial role in neutralizing ROS and preventing oxidative damage. Swiss albino mice were divided into control, BCA control (10 mg/kg body weight), radiation alone (7 Gy), and radiation+ BCA pretreatment groups. BCA, a natural isoflavone with known antioxidant and cytoprotective properties, was administered intraperitoneally before radiation exposure. After irradiation, lipid peroxidation levels, antioxidant enzyme activities/level (superoxide dismutase, catalase, glutathione peroxidase and reduced glutathione), expression levels of DNA repair genes (P53, P21, GADD45α), apoptotic markers (Bax, Bcl-2, Caspase-3, -9 and Cytochrome-C), and inflammatory marker (NF-κB) were analyzed in small intestine tissue. Our findings indicate that gamma radiation significantly elevated lipid peroxidation levels and altered antioxidant enzyme activities, indicating oxidative stress. However, BCA pretreatment mitigated these effects by bolstering antioxidant defences, reducing radiation-induced oxidative damage. Additionally, BCA altered apoptotic markers, NF-κB expression, promoting cell survival mechanisms. At the molecular level, BCA pretreatment upregulated key DNA repair genes (P53, P21, GADD45α), crucial for repairing radiation-induced DNA damage and maintaining genomic stability. These results underscore BCA potential as a radioprotector, suggesting its efficacy in mitigating radiation-induced oxidative stress and preserving cellular integrity. In conclusion, BCA demonstrates promising radioprotective properties by attenuating oxidative stress, enhancing antioxidant defences, modulating apoptotic pathways, and promoting DNA repair mechanisms following gamma radiation exposure. Further research is necessary to elucidate its precise mechanisms of action and explore its potential therapeutic applications in radiation oncology and environmental radioprotection.

Salmonella dry surface biofilm: morphology, single-cell landscape, and sanitization.

In this study, Salmonella Typhimurium dry surface biofilm (DSB) formation was investigated in comparison with wet surface biofilm (WSB) development. Confocal laser scanning microscopic analysis revealed a prominent green cell signal during WSB formation, whereas a red signal predominated during DSB formation. Electron microscopy was also used to compare the features of DSB and WSB. Overall, WSB was unevenly scattered over the surface, whereas DSB was evenly dispersed. In contrast to WSB cells, which have a distinct plasma membrane and outer membrane layer, DSB cells are contained in large capsules and compressed. Next, microbiome single-cell transcriptomics was used to investigate the functional heterogeneity of the Salmonella DSB microbiome, with nine clusters successfully identified. Although over 60% of the dried cells were metabolically inactive, the rest of the Salmonella cells still demonstrated specific antioxidative and virulence capabilities, suggesting a possible concern for low-moisture food (LMF) safety. Finally, because sanitization in LMF industries must be conducted without water, a list of 39 flavonoids was tested for their combined effect with 70% isopropyl alcohol (IPA) against DSB, and morin induced the greatest reduction in the green:red ratio from 3.67 to 0.43. Significantly higher reductions of Salmonella viability in DSB were achieved by 10-, 100-, 1,000-, and 10,000-µg/mL morin (1.69 ± 0.25, 3.21 ± 0.23, 4.32 ± 0.24, and 5.18 ± 0.16 log CFU/sample reductions) than 70% IPA alone (1.55 ± 0.20 log CFU/sample reduction) (P < 0.05), indicating the potential to be formulated as a dry sanitizer for the LMF industry.IMPORTANCEDSB growth of foodborne pathogens in LMF processing environments is associated with food safety, financial loss, and compromised consumer trust. This work is the first comprehensive examination of the characteristics of Salmonella DSB while exploring its underlying survival mechanisms. Furthermore, morin dissolved in 70% IPA was proposed as an efficient dry sanitizer against DSB to provide insights into biofilm control during LMF processing.

Dissecting the dynamics of cell death pathways in Hirschsprung’s disease: a comparative analysis of viable and non-viable cells under proinflammatory conditions

PurposeThe present study explores the dynamics of cell death in Hirschsprung’s disease (HSCR) and control (CO) groups under inflammatory stress conditions.MethodsUsing flow cytometry, we analyzed intestinal colonic organoid cultures derived from the ganglionic segment of the HSCR and CO groups. Our analysis focused on the quantification of RIPK1-independent and RIPK1-dependent apoptosis, as well as necroptosis in both viable and non-viable cells under acute and chronic inflammatory stress.ResultsOur findings indicate that HSCR cells are particularly vulnerable to inflammation during acute proinflammatory stress, as evidenced by an increase in dead cells (Zombie +). Under chronic conditions, adaptive changes are observed in both HSCR and CO groups, indicating survival mechanisms. These adaptations are uniquely altered in HSCR, suggesting an impaired response to chronic inflammation. HSCR cells show significantly decreased RIPK1-dependent apoptosis in acute scenarios compared to chronic ones, unlike the CO group, implying varied responses to different inflammatory stresses. In non-viable cells, considerable changes in RIPK1-dependent apoptosis under chronic conditions in HSCR indicate a heightened inflammatory response compared to CO.ConclusionThis research provides insights into cell death regulation in HSCR under inflammatory stress by using patient-derived organoids, underscoring the complexity of its inflammatory response.

Cytotoxic and Radiosensitizing Effects of European and African Propolis in 3D Lung Carcinoma Cell Cultures.

Natural compounds such as propolis have gained wide popularity in the last decades. While its antibacterial, antiviral, and antifungal properties are well known, the anticancer properties of propolis are just beginning to be appreciated. Herein, we comparatively investigate the cytotoxic and radiosensitizing potential of four different ethanolic propolis extracts originating from three different countries (Germany, Ireland, South Africa) in human lung cancer cell models. Liquid chromatography-mass spectrometry (LC-MS/MS) was applied to characterize the four different propolis extracts. Cytotoxicity and radiation survival were determined by 3D matrix-based clonogenic assays and autophagy was examined by western blotting. We found cytotoxicity in a propolis type-, time- and cell model- dependent manner. In the four ethanolic propolis extracts, Coumaric acid, Caffeic acid phenethyl ester, Pinocembrin and Chrysin presented the major compounds identified. Examining the induction of autophagy using the marker LC3B and autophagy inhibition with chloroquine suggested autophagy to be part of the survival mechanisms upon propolis treatment in a cell model-dependent manner. Combining propolis with X-ray irradiation showed the radiosensitizing potential of propolis in human lung cancer cell models, which clearly presented in a manner dependent on the incubation time of propolis and the cell model treated. Propolis treatment showed cytotoxic and radiosensitizing effects of propolis on human lung cancer cells. Since these effects differ greatly between the four propolis extracts studied and originating from different regions, further studies are urgently needed to differentiate propolis species and their anticancer properties in more detail.

Mechanisms of Staphylococcus aureus survival of trimethoprim-sulfamethoxazole-induced thymineless death.

Trimethoprim-sulfamethoxazole (SXT) is commonly used to treat diverse Staphylococcus aureus infections, including those associated with cystic fibrosis (CF) pulmonary disease. Studies with Escherichia coli found that SXT impairs tetrahydrofolate production, leading to DNA damage, stress response induction, and accumulation of reactive oxygen species (ROS) in a process known as thymineless death (TLD). TLD survival can occur through the uptake of exogenous thymidine, countering the effects of SXT; however, a growing body of research has implicated central metabolism as another potentially important determinant of bacterial survival of SXT and other antibiotics. Here, we conducted studies to better understand the mechanisms of TLD survival in S. aureus. We found that thymidine abundances in CF sputum were insufficient to prevent TLD of S. aureus, highlighting the importance of alternative survival mechanisms in vivo. In S. aureus cultured in vitro with SXT and low thymidine, we frequently identified adaptive mutations in genes encoding carbohydrate, nucleotide, and amino acid metabolism, supporting reduced metabolism as a common survival mechanism. Although intracellular ROS levels rose with SXT treatment in vitro, survival was not improved in the presence of ROS scavengers, unlike in E. coli. SXT challenge induced the SOS response, which was alleviated by added thymidine. Finally, an inactivating mutation in the phosphotransferase gene ptsI conferred both limitation in cellular ATP and improved survival against TLD. Collectively, these results suggest that alterations in core metabolic functions, particularly those that reduce ATP levels, predominantly confer S. aureus survival and persistence during SXT treatment, potentially identifying novel targets for co-treatment.IMPORTANCEStaphylococcus aureus is a ubiquitous organism and one of the leading causes of human infections, many of which are difficult to treat due to persistence, antibiotic resistance, or antibiotic tolerance. As our arsenal of effective antibiotics dwindles, the need for improved treatments becomes increasingly urgent, necessitating a better understanding of the precise mechanisms by which pathogens evade our most critical antimicrobial agents. Here, we report a systematic characterization of the mechanisms of S. aureus survival to treatment with the first-line antistaphylococcal antibiotic trimethoprim-sulfamethoxazole, identifying pathways and candidate targets for enhancing the efficacy of available antimicrobial agents.

Characterization of thioredoxin-thioredoxin reductase system in Filifactor alocis.

Filifactor alocis is a newly appreciated member of the periodontal community with a strong periodontal disease correlation. Little is known about the survival mechanisms by which F.alocis copes with oxidative stress and establishes the infection within the local inflammatory microenvironment of the periodontal pocket. The aim of this study is to investigate if F.alocis putative peroxiredoxin/AhpC protein FA768 may constitute an alkyl hydroperoxide reductase system utilizing putative thioredoxin reductase protein FA608, and putative thioredoxin/glutaredoxin homolog FA1411/FA455. FA768, FA608, FA1411 and FA455 proteins from F.alocis were expressed and purified from Escherichia coli. Insulin and 5,5-dithio-bis-2-nitrobenzoic acid (DTNB) reduction assays were performed to determine if purified FA1411 and FA455 proteins could be a substrate for FA608. The peroxidase activity of FA768 was examined by measuring its ability to reduce hydrogen peroxide (H2O2) with FA608 and FA1411/FA455 provided as the reducing systems. Further, the hydroperoxide substrate specificity of FA768 was analyzed by monitoring the NADPH oxidation in the presence of different peroxides, including H2O2, cumyl hydroperoxide (CHP), and tert-butyl hydroperoxide (t-BHP). In this study, we have demonstrated the existence of a functioning thioredoxin-dependent alkyl hydroperoxide system in F.alocis. This system is comprised of a thioredoxin reductase (FA608), a thioredoxin/glutaredoxin homolog (FA1411/FA455), and a typical 2-cysteine peroxiredoxin/AhpC (FA768). FA608, together with FA1411/FA455, can function as a thioredoxin reductase system to reduce insulin, DTNB, and FA768. FA455 is a glutaredoxin-like protein with thioredoxin functions in F.alocis. Both the FA768/FA608/FA1411 and FA768/FA608/FA455 reductase systems were NADPH-dependent and exhibited specificity for broad hydroperoxide substrates H2O2, CHP, and t-BHP. This is the first study of a thioredoxin dependent alkyl hydroperoxide system from a periodontal pathogen. This system is proposed to protect F.alocis against oxidative stress due to the likely absence of a catalase or an additional peroxiredoxin homolog.

Mind-body medicine and altered states of consciousness in Homo

The mind-body relationship has long been a subject of inquiry from both philosophical and scientific perspectives. Ancient Greek philosophers such as Pythagoras and Plato posited dualistic models, where the mind and body are distinct substances. In contrast, modern approaches in Mind-Body Medicine (MBM) offer integrative models that emphasize the interconnectedness of mental and physical states and the proactive role of the patient in their own healing process. This review examines the evolutionary roots of altered states of consciousness (ASC) as a precursor to current MBM techniques. By tracing ASC to early hominins and their cognitive development, it posits that the ability to enter various ASC—such as those used in rituals, meditation, and other mind-body practices—provided evolutionary advantages, influencing both individual fitness and social cohesion. Moreover, this review discusses tonic immobility in animals as a survival mechanism and explores parallels in human and non-human primate behaviors involving ASC. Additionally, neurochemical pathways that govern ASC, such as serotonergic and dopaminergic regulation, are explored for their roles in promoting social behaviors, cognitive flexibility, and emotional regulation. Furthermore, the role of the default mode network is investigated in relation to psychotropic and mood altering substances and altered states of consciousness. This integrated perspective offers new insights into the origins of MBM and underscores the significance of ASC in both evolutionary and contemporary contexts.

Equitable food and nutrition security initiatives for farmers and fisher folks in Masbate, Philippines

Loss of income among Filipino farmers and fisher folks caused by the pandemic resulted to food and nutrition insecurity in their respective households. Their low level of education limited their source of livelihood into small scale farming, fishing, or both thus also limiting their income and opportunity to find additional sources of income. Descriptive statistics was used alongside Smith’s Interpretative Phenomenological Analysis to analyze the data and understand the respondents’ lived experiences. The pandemics negative effect to their source of livelihood prompted them to institute drastic coping mechanisms for survival. Despite the dire situation the respondents still possess a positive outlook in life and have shown their usual resiliency to disasters. Life lessons drawn from them aided in the formulation of personal and organizational development policies in the context of the province of Masbate, Philippines. Finally, the Smart Sirungan Framework for a Food and Nutrition Secure Future was created and presented for possible utilization and further studies.

Metabolic adaptations of Shewanella eurypsychrophilus YLB-09 for survival in the high-pressure environment of the deep sea.

Elucidation of the adaptation mechanisms and survival strategies of deep-sea microorganisms to extreme environments could provide a theoretical basis for the industrial development of extreme enzymes. There is currently a lack of understanding of the metabolic adaptation mechanisms of deep-sea microorganisms to high-pressure environments. The objective of this study was to investigate the metabolic regulatory mechanisms enabling a strain of the deep-sea bacterium Shewanella eurypsychrophilus to thrive under high-pressure conditions. To achieve this, we used nuclear magnetic resonance-based metabolomic and RNA sequencing-based transcriptomic analyses of S. eurypsychrophilus strain YLB-09, which was previously isolated by our research group and shown to be capable of tolerating high pressure levels and low temperatures. We found that high-pressure conditions had pronounced impacts on the metabolic pattern of YLB-09, as evidenced by alterations in energy, amino acid, and glycerolipid metabolism, among other processes. YLB-09 adapted to the high-pressure conditions of the deep sea by switching from aerobic intracellular energy metabolism to trimethylamine N-oxide respiration, altering the amino acid profile, and regulating the composition and the fluidity of cell membrane. The findings of our study demonstrate the capacity of microorganisms to alter their metabolism in response to elevated pressure, thereby establishing a foundation for a more profound understanding of the survival mechanisms of life in high-pressure environments.

Mapping the epigenomic landscape of post-traumatic stress disorder in human cortical neurons.

The study conducted a comprehensive genome-wide analysis of differential 5mC and 5hmC modifications at both CpG and non-CpG sites in postmortem orbitofrontal neurons from 25 PTSD cases and 13 healthy controls. It was observed that PTSD patients exhibit a greater number of differential 5hmC sites compared to 5mC sites. Specifically, individuals with PTSD tend to show hyper-5mC/5hmC at CpG sites, particularly within CpG islands and promoter regions, and hypo-5mC/5hmC at non-CpG sites, especially within intragenic regions. Functional enrichment analysis indicated distinct yet interconnected roles for 5mC and 5hmC in PTSD. The 5mC marks primarily regulate cell-cell adhesion processes, whereas 5hmC marks are involved in embryonic morphogenesis and cell fate commitment. By integrating published PTSD findings from central and peripheral tissues through multi-omics approaches, several biological mechanisms were prioritized, including developmental processes, HPA axis regulation, and immune responses. Based on the consistent enrichment in developmental processes, we hypothesize that if epigenetic changes occur during early developmental stages, they may increase the risk of developing PTSD following trauma exposure. Conversely, if these epigenetic changes occur in adulthood, they may influence neuronal apoptosis and survival mechanisms.

Mechanisms of Lung Endothelial Cell Injury and Survival in Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is a progressive, chronic, and incurable inflammatory pulmonary vascular disease characterized by significant sex bias and largely unexplored microbial-associated molecular mechanisms that may influence its development and sex prevalence across various subgroups. PAH can be subclassified as idiopathic, heritable, or associated with conditions such as connective tissue diseases, congenital heart defects, liver disease, infections, and chronic exposure to drugs or toxins. During PAH progression, lung vascular endothelial cells (ECs) undergo dramatic morphofunctional transformations in response to acute and chronic inflammation. These transformations include the appearance and expansion of abnormal vascular cell phenotypes such as those derived from apoptosis-resistant cell growth and endothelial-to-mesenchymal transition (EndoMT). Compelling evidence indicates that these endothelial phenotypes seem to be triggered by chronic lung vascular injury and dysfunction, often characterized by reduced secretion of vasoactive molecules like nitric oxide (NO) and exacerbated response to vasoconstrictors such as Endothelin-1 (ET-1); both long-term known contributors of PAH pathogenesis. This review sheds light on the mechanisms of EC dysfunction, apoptosis, and EndoMT in PAH, aiming to unravel the intricate interactions between ECs, pathogens, and other cell types that drive the onset and progression of this devastating disease. Ultimately, we hope to provide an overview of the complex functions of lung vascular ECs in PAH, inspiring novel therapeutic strategies that target these dysfunctional cells to improve the treatment landscape for PAH, particularly in the face of current and emerging global pathogenic threats.

Exploring controls on the timing of the phytoplankton bloom in western Baffin Bay, Canadian Arctic

In the Arctic Ocean the peak of the phytoplankton bloom occurs around the period of sea ice break-up. Climate change is likely to impact the bloom phenology and its crucial contribution to the production dynamics of Arctic marine ecosystems. Here we explore and quantify controls on the timing of the spring bloom using a one-dimensional biogeochemical/ecosystem model configured for coastal western Baffin Bay. The model reproduces the observations made on the phenology and the assemblage of the phytoplankton community from an ice camp in the region. Using sensitivity experiments, we found that two essential controls on the timing of the spring bloom were the biomass of phytoplankton before bloom initiation and the light under sea ice before sea ice break-up. The level of nitrate before bloom initiation was less important. The bloom peak was delayed up to 20 days if the overwintering phytoplankton biomass was too low. This result highlights the importance of phytoplankton survival mechanisms during polar winter to the pelagic ecosystem of the Arctic Ocean and the spring bloom dynamics.

Carotenoids dispersed in gypsum rock as a result of algae adaptation to the extreme conditions of the Atacama Desert

The high-altitude pre-Andean region of the Atacama Desert is characterized by its stark volcanic rock formations and unique hydrothermal gypsum outcrops (gypcrete) that it hosts. This study delves into the biomolecular composition of the endolithic phototrophic microbes that thrive within these gypcretes. Using advanced Raman spectroscopy techniques, including Raman imaging (complemented by microscopic and 3D microscopic observations), herein we unveil new insights into the adaptive strategies of these gypsum-inhabiting algae. Our Raman imaging results provide a detailed chemical map of carotenoids associated with microbial colonization. This map reveals a significant gradient in pigment content, highlighting a critical survival mechanism for algae and cyanobacteria in this polyextreme environment. Intriguingly, we detected signals for carotenoids not only in the algae-colonized layer, but also deeper within the gypsum matrix - indicating pigment migration following cell disruption. In addition, we conducted an in-depth analysis of individual algal cells from the Trebouxiaceae family, noting their color variations from green to orange, plus describing the spectral differences in detail. This investigation identified in-vivo pigments (carotenoids, chlorophyll) and lipids at the cellular level, offering a comprehensive view of the molecular adaptations enabling life in one of the Earth’s most extreme habitats.

Between Life and Death: Sea Urchin Embryos Undergo Peculiar DNA Fragmentation after Exposure to Vanadium, Cadmium, Gadolinium, and Selenium.

Exogenous DNA damage represents one of the most harmful outcomes produced by environmental, physical, or chemical agents. Here, a comparative analysis of DNA fragmentation was carried out on Paracentrotus lividus sea urchin embryos exposed to four common pollutants of the marine environment: vanadium, cadmium, gadolinium and selenium. Using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, fragmented DNA was quantified and localized in apoptotic cells mapping whole-mount embryos. This is the first study reporting how different chemicals are able to activate distinctive apoptotic features in sea urchin embryos, categorized as follows: (i) cell-selective apoptosis, showing DNA fragmentation restricted to a subset of extremely damaged cells, acting as an embryo survival mechanism; or (ii) total apoptosis, with fragmented DNA widespread throughout the cells of the entire embryo, leading to its death. Also, this is the first report of the effects of Se exposure on P. lividus sea urchin embryos. These data confirm the TUNEL assay as the most suitable test to study DNA fragmentation in the sea urchin embryo model system. Taken together, this research highlights embryos' ability to find alternative pathways and set physiological limits for development under stress conditions.

Helicobacter pylori and Gastric Cancer: Microbiological Insights and Clinical Implications

Helicobacter pylori is a gram-negative bacterium that is a major factor in a number of gastrointestinal diseases including gastritis, peptic ulcer disease, and gastric cancer. We reviewed the biology of H. pylori, including its microbiological characteristics, pathogenic mechanisms and its key role in gastric carcinogenesis. Here, we discuss the bacterium’s mechanisms of survival and virulence factors, such as CagA and VacA, which together induce chronic inflammation and drive malignant transformation. The current status of clinical manifestations and diagnostic approaches are reviewed, emphasizing the need for accurate detection and effective treatment. Future directions stress the need for novel therapeutic strategies as well as vaccine development, host-pathogen understanding, biomarker discovery and personal medicine to improve patient outcome and reduce the global burden of H. pylori associated diseases.

Structure of Extracellular Vesicles and Their Effect on Bacterial Biofilms Change with the Development of Antibiotic Resistance in the Probiotic Strain Lactiplantibacillus plantarum 8p-a3.

Significant changes in lactobacillus-derived extracellular membrane vesicles, which transfer lipids, polysaccharides, proteins, and nucleic acids, were for the first time observed to accompany the development of resistance to antibiotics (amoxicillin and clarithromycin) in vitro in the probiotic strain Lactiplantibacillus plantarum 8p-a3. The changes occur together with large-scale genome rearrangements, changes in the profile of phenotypic sensitivity to antimicrobials of various groups, and evolution of virulence. Changes in vesicles affected their structure, composition, and activity against biofilms of opportunistic bacteria. The data provide for a better understanding of the molecular mechanisms of microbial survival under selective pressure of antimicrobials, the functional potential of probiotic vesicles, and probiotic safety assessments.

Application of XBP1s Decoy Oligodeoxynucleotide Attenuates Cancerous Phenotype in Huh-7 Hepatocellular Carcinoma Cells.

The spliced form of X-box binding protein 1 (XBP1s) is a key transcription factor in the unfolded protein response (UPR), an adaptive mechanism for cell survival. Many studies demonstrated the induced expression of XBP1s in various cancers, including hepatocellular carcinoma (HCC). Such upregulated expression is linked to an enhancement of cell proliferation, migration, and improvement of the survival rate. In this study, we aimed to assess the therapeutic potential of targeting XBP1s, by specific decoy oligodeoxynucleotide (ODN) and evaluated the cancerous phenotypes in Huh-7 cells. In this experimental study, we transfected Huh-7 cells with XBP1s decoy oligonucleotide (ODN). Subsequently, we assess some cellular features, including viability, migration capacity, proliferation potential, and apoptosis. Therefore, various techniques included wound healing test, BrdU, and annexin/PI assays. Additionally, the colony formation capacity was evaluated. The mRNA expression levels of BAX, BCL-2, c-MYC, CCND1, MMP-9, CDH1, and CD133 were quantified by the reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Transfection of Huh-7 cells by XBP1s decoy ODN led to significant down-regulation of c-Myc, CCND1, MMP-9, BCL-2 and CD133 and up-regulation of CDH1 and BAX transcriptional expressions in comparison with the vehicle group. Our results also demonstrated that transfection of XBP1s-decoy reduced HCC cell viability, proliferation, migration capacity as well as colonization ability in comparison with the vehicle group. These findings proposed the potential application of XBP1s-decoy ODN to reduce cancerous phenotypes such as cell proliferation, cell migration and apoptosis induction in the Huh-7 cell line. More experiments on other cell lines and primary cells could validate our results.

Embryonic dormancy in Aedes aegypti and Aedes albopictus (Diptera: Culicidae): a survival and dispersal mechanism

Aedes aegypti and Aedes albopictus are the main vectors of arboviruses such as dengue, Zika virus, and chikungunya. Ae. aegypti is a widely spread mosquito in tropical and subtropical regions, whereas Ae. albopictus is a culicid of Asian origin that shows exophilic behavior and can be found in subtropical and temperate areas. Climatic factors could influence the distribution of both species, making them use genetic and environmental resources to adapt to the environment, activating survival mechanisms (embryonic dormancy) that increase the developmental period and keep their offspring in the environment. From this perspective, this review aimed to compare the different physiological mechanisms of embryonic dormancy between Ae. aegypti and Ae. albopictus and their impact on the development and environmental adaptability of these two species. A total of 62 articles were identified in the PubMed, Scopus, and Web of Science databases corresponding to the period from 1981 to 2021. In diapause, the results mentioned above are indirectly linked to temperature and directly linked to photoperiod variations. With regard to quiescence, temperature and humidity are directly related to the activation of this mechanism. In conclusion, it is essential to highlight the expansion of arboviruses such as dengue, chikungunya, yellow fever, and Zika virus and their relationship with embryonic dormancy, diapause and quiescence, extremely important strategies for Ae. aegypti and Ae. albopictus to keep their offspring in the environment under adverse conditions.

THE CONSUMPTION EFFECT OF 2007–2008 FINANCIAL CRISIS: EVIDENCE FROM COMMONWEALTH OF INDEPENDENT STATES

To analyze the demand shock effect, we concentrated on the 2008 Financial Crisis, relying on the data from the European Bank for Reconstruction and Development’s “Life in Transition Survey” conducted in 2010. This survey offers detailed information on how households reacted two years after the crisis. Regression models were developed to analyze the measures that households took during the economic decline and their implications for consumption. Such measures entailed alterations in spending patterns, saving practices, and other mechanisms of survival. The empirical investigation of the paper gives an understanding of the effects of demand shock such as the 2008 Financial Crisis on households’ consumption behavior and their ability to cope with the shocks. The results show that Financial Crisis affect negatively the labor market, which had a negative impact on consumption. Moreover, we explored how government tried to help households, what they used, etc.

Exploring Autophagy in Cancer: Therapeutic Perspectives

Autophagy is a catabolic mechanism crucial for sustaining cellular homeostasis, and in this process, encapsulated degraded inside repurposed to facilitate metabolic processes. In cancer, autophagy has a dual role: it acts as a tumor suppressor by preventing the buildup of damaged cellular components, but also as a survival mechanism, that supports tumor growth under stress. Cancer cells often trigger autophagy to manage the increased metabolic demands of rapid growth. This stress tolerance allows tumor cells to maintain energy production, contributing to both tumor progression and resistance to treatment. Preclinical studies have shown that autophagy inhibition reinstates chemotherapeutic sensitivity and increases tumor cell mortality. These findings indicate that targeting autophagy may represent a viable therapeutic approach, with early-phase clinical trials exploring the use of hydroxychloroquine alongside chemotherapy or targeted treatments. As comprehension of autophagy in oncology advances, there is an increasing interest in creating more targeted and efficacious autophagy inhibitors for therapeutic applications.