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Turning Pathogens into Transmissible Vaccines via Loss-of-Function Research and Interferon Gene Insertion: Trampling Death by Death?
Theodor-Nicolae Carp
Throughout several centuries, infectious pathogenic agents have been used as models for the ongoing efforts of vaccine development, which saved hundreds of millions of lives from life-threatening infectious diseases worldwide. Nonetheless, there has been a missing gap that various polymorphic microbes have been taking advantage of in their evolutionary pathway: the interferon system, which often prevented the timely activation of second and third-line host immunity, leading to chaotic and mismatching immune responses. The phenomenon of increased incubation period of various infectious diseases may be a result of the increased abilities of such microbial agents to directly and indirectly undergo molecular self-camouflaging, which prevents the activation of Type I and Type III Interferon-encoding genes (INGs) in indirect and direct manners respectively, and cleaves the mRNA molecules encoding such interferon glycoproteins, often causing major delays in the process of autocrine and paracrine signalling of Type I and Type III Interferon glycoproteins, which in turn allows an unrestricted, exponential increase of the microbial load/count, giving rise to a statistical probability that the quality of the delayed immune response will be low and contributory to the processes of pathogenesis and pathophysiology. Some microbial proteins as such also inhibit the translation of Interferon-Stimulated Genes, thereby substantially affecting the signalling rates within the cytokine system and often bringing a negative domino effect upon the activation rates of the adaptive immune system. Apprehending the foundational layer of the current problems in evolutionary microbiology, epidemiology and public health studies is most likely crucial for the course of immunological, pharmaceutical and vaccine-related clinical research. In the current case, it is the complex set of molecular capabilities to suppress Type I and Type III Interferon-based signalling displayed by several polymorphic microbes of public health concern, and it may be that the rates of immunopathogenesis induced by such microbes are directly proportional with such pathogenic abilities of induced interferon suppression. Proportional medical responses could include the development of approaches involving low dosages of human recombinant Type I and Type III Interferon glycoprotein and perhaps also of protollin in the nasopharyngeal cavity, potentially bringing an example of putting a novel concept of a “United Immune System” into practice. Furthermore, similar dosages of such interferons could be administered into human immune cells including plasmacytoid dendritic cells, as well as natural and adaptive lymphocytes, to optimise their immune function and integrity against various environmental hazards. Ultimately, clinical researchers may isolate the pathogenic agents, attenuate them through the process of loss-of-function laboratory research, before performing gene editing to insert Type I, Type III and perhaps also Type IV Interferon-encoding, perhaps as well as Pattern Recognition Receptor (PRR) Agonist-encoding genes that specifically match the PRR targeted by the implicated microbes, into their genomic profile and potentially releasing the genetically-modified pathogens back into the environment transmissible factories of Type I and Type III Interferons, perhaps as well as of specific PRR Agonist proteins, which could include outer membrane proteins from the B serogroup of Neisseria meningitidis bacteria. If the microbial genetic activities implicating evasion of the interferon system are too intense and multilateral, at least some of the microbial genes responsible for such activity could be permanently removed in some exchange with the human genes encoding major elements of the interferon system that would be inserted into the microbial genome afterward. It may be important to mention that the process of clinical weakening of the isolated microbes would be aimed at reducing the activity of microbial genes implicated in pathogenesis and pathophysiology, and perhaps not as much microbial genes involved in reproduction and transmission. Such a change may bring various pathogenic agents into a path of evolutionary self-destruction, as they would start producing and sending signals to the proximal, innate immune system as soon as they enter the first host cells, making their same processes of induced innate immune suppression ineffective, and several dilemmas in microbial evolution could ultimately be tackled as a result, possibly even at least attenuating the phenomenon of acquired antibiotic resistance by various pathogenic bacteria. A clinical approach as such is likely based on the model of increasing the accessibility to insulin-based treatment against Diabetes Mellitus via insulin-encoding gene insertion into the genomes of harmless bacteria prior to their administration into human host organisms, which saved millions of lives worldwide. Processes of shrinkage of any level of limitations to potential efficacy would include the manual utilisation of inhalators, oral drops and/or injectable serums containing such modified microbes to ensure that such an immunising effect would be conferred simultaneously with exposure to the artificially-changed genetic version of the microbe. A set of clinical responses involving all such pathways may ultimately bring a promise of a health-related “Golden Age” throughout the world.
Throughout several centuries, infectious pathogenic agents have been used as models for the ongoing efforts of vaccine development, which saved hundreds of millions of lives from life-threatening infectious diseases worldwide. Nonetheless, there has been a missing gap that various polymorphic microbes have been taking advantage of in their evolutionary pathway: the interferon system, which often prevented the timely activation of second and third-line host immunity, leading to chaotic and mismatching immune responses. The phenomenon of increased incubation period of various infectious diseases may be a result of the increased abilities of such microbial agents to directly and indirectly undergo molecular self-camouflaging, which prevents the activation of Type I and Type III Interferon-encoding genes (INGs) in indirect and direct manners respectively, and cleaves the mRNA molecules encoding such interferon glycoproteins, often causing major delays in the process of autocrine and paracrine signalling of Type I and Type III Interferon glycoproteins, which in turn allows an unrestricted, exponential increase of the microbial load/count, giving rise to a statistical probability that the quality of the delayed immune response will be low and contributory to the processes of pathogenesis and pathophysiology. Some microbial proteins as such also inhibit the translation of Interferon-Stimulated Genes, thereby substantially affecting the signalling rates within the cytokine system and often bringing a negative domino effect upon the activation rates of the adaptive immune system. Apprehending the foundational layer of the current problems in evolutionary microbiology, epidemiology and public health studies is most likely crucial for the course of immunological, pharmaceutical and vaccine-related clinical research. In the current case, it is the complex set of molecular capabilities to suppress Type I and Type III Interferon-based signalling displayed by several polymorphic microbes of public health concern, and it may be that the rates of immunopathogenesis induced by such microbes are directly proportional with such pathogenic abilities of induced interferon suppression. Proportional medical responses could include the development of approaches involving low dosages of human recombinant Type I and Type III Interferon glycoprotein and perhaps also of protollin in the nasopharyngeal cavity, potentially bringing an example of putting a novel concept of a “United Immune System” into practice. Furthermore, similar dosages of such interferons could be administered into human immune cells including plasmacytoid dendritic cells, as well as natural and adaptive lymphocytes, to optimise their immune function and integrity against various environmental hazards. Ultimately, clinical researchers may isolate the pathogenic agents, attenuate them through the process of loss-of-function laboratory research, before performing gene editing to insert Type I, Type III and perhaps also Type IV Interferon-encoding, perhaps as well as Pattern Recognition Receptor (PRR) Agonist-encoding genes that specifically match the PRR targeted by the implicated microbes, into their genomic profile and potentially releasing the genetically-modified pathogens back into the environment transmissible factories of Type I and Type III Interferons, perhaps as well as of specific PRR Agonist proteins, which could include outer membrane proteins from the B serogroup of Neisseria meningitidis bacteria. If the microbial genetic activities implicating evasion of the interferon system are too intense and multilateral, at least some of the microbial genes responsible for such activity could be permanently removed in some exchange with the human genes encoding major elements of the interferon system that would be inserted into the microbial genome afterward. It may be important to mention that the process of clinical weakening of the isolated microbes would be aimed at reducing the activity of microbial genes implicated in pathogenesis and pathophysiology, and perhaps not as much microbial genes involved in reproduction and transmission. Such a change may bring various pathogenic agents into a path of evolutionary self-destruction, as they would start producing and sending signals to the proximal, innate immune system as soon as they enter the first host cells, making their same processes of induced innate immune suppression ineffective, and several dilemmas in microbial evolution could ultimately be tackled as a result, possibly even at least attenuating the phenomenon of acquired antibiotic resistance by various pathogenic bacteria. A clinical approach as such is likely based on the model of increasing the accessibility to insulin-based treatment against Diabetes Mellitus via insulin-encoding gene insertion into the genomes of harmless bacteria prior to their administration into human host organisms, which saved millions of lives worldwide. Processes of shrinkage of any level of limitations to potential efficacy would include the manual utilisation of inhalators, oral drops and/or injectable serums containing such modified microbes to ensure that such an immunising effect would be conferred simultaneously with exposure to the artificially-changed genetic version of the microbe. A set of clinical responses involving all such pathways may ultimately bring a promise of a health-related “Golden Age” throughout the world.
Posted: 13 February 2025
Cloud-Driven Data Analytics for Growing Plants Indoor
Nezha Kharraz,
István Szabó
Posted: 13 February 2025
Effect of Pretreatment Methods on the Sensory and Nutritional Properties of a Yoghurt-Like Product Made from Tiger Nuts (Cyperus esculentus L.)
Aristide Guillaume Silapeux Kamda,
Hans Martial Changam,
Isabelle Sandrine BOUELET NTSAMA,
Gilbert Manga Mbassi,
Abdou Razinkou,
Christine Nyangono,
Roger Ponka,
Mercy BIH ACHU,
Elie Fokou
Posted: 13 February 2025
Sensitive and Specific Detection of African Swine Fever Virus Variants: A Novel Quadplex Real-Time PCR Assay with Internal Control
Lihua Wang,
Yuzhen Li,
Xirui Zhang,
Rachel Madera,
Homer Pantua,
Aidan Craig,
Nina Muro,
Danqin Li,
Jamie Retallick,
Franco Matias Ferreyra
African swine fever (ASF), a highly contagious and lethal viral disease, continues to devastate the global swine industry. The emergence of ASF virus (ASFV) variants with varying genomic deletions poses significant challenges to ASF control. This study presents a novel, sensitive, and reliable quadplex real-time PCR assay for detecting ASFV variants lacking key genes (I177L, EP402R, and MGF360-14L), either individually or in combination. The assay targets conserved regions within these genes, ensuring broad coverage of diverse ASFV genotypes. A porcine beta-actin (ACTB) internal control was incorporated to minimize false-negative results. Optimization and evaluation using spike-in tests demonstrated high sensitivity with a limit of detection (LOD) ranging from 1-10 plasmid copies or 0.1 TCID50 of ASFV isolates per reaction. No cross-reactivity was observed when testing serum samples from pigs infected with other common swine viruses. Further validation across a diverse panel of samples, comprising those from naturally ASFV-infected field pigs (n=54), experimentally ASFV-infected pigs (n=50), PBS-inoculated pigs (n=50), ASFV-free field pigs (n=100), and feral pigs (n=6), confirmed 100% specificity. This robust assay provides a valuable tool for rapid and accurate ASF surveillance and control efforts, facilitating the timely detection and mitigation of outbreaks caused by emerging ASFV variants.
African swine fever (ASF), a highly contagious and lethal viral disease, continues to devastate the global swine industry. The emergence of ASF virus (ASFV) variants with varying genomic deletions poses significant challenges to ASF control. This study presents a novel, sensitive, and reliable quadplex real-time PCR assay for detecting ASFV variants lacking key genes (I177L, EP402R, and MGF360-14L), either individually or in combination. The assay targets conserved regions within these genes, ensuring broad coverage of diverse ASFV genotypes. A porcine beta-actin (ACTB) internal control was incorporated to minimize false-negative results. Optimization and evaluation using spike-in tests demonstrated high sensitivity with a limit of detection (LOD) ranging from 1-10 plasmid copies or 0.1 TCID50 of ASFV isolates per reaction. No cross-reactivity was observed when testing serum samples from pigs infected with other common swine viruses. Further validation across a diverse panel of samples, comprising those from naturally ASFV-infected field pigs (n=54), experimentally ASFV-infected pigs (n=50), PBS-inoculated pigs (n=50), ASFV-free field pigs (n=100), and feral pigs (n=6), confirmed 100% specificity. This robust assay provides a valuable tool for rapid and accurate ASF surveillance and control efforts, facilitating the timely detection and mitigation of outbreaks caused by emerging ASFV variants.
Posted: 13 February 2025
Exercise-Induced Acute Physiological Responses of Velocity, Power and Temperature in Paralympic and Conventional Powerlifting Athletes
Rafael Luiz Mesquita Souza,
Felipe J. Aidar,
Leonardo dos Santos,
Jymmys Lopes Dos Santos,
Lucio Marques Vieira Souza,
André Luiz Gomes Carneiro,
Paulo Francisco de Almeida-Neto,
Breno Guilherme de Araújo Tinoco Cabral,
Anderson Carlos Marçal,
Pantelis T. Nikolaidis
Posted: 13 February 2025
Development of Novel Anti-Rhinoceros Podoplanin Monoclonal Antibodies for Flow Cytometry, Western Blot, and Immunohistochemistry
Hiroyuki Suzuki,
Shiori Fujisawa,
Rena Ubukata,
Tomohiro Tanaka,
Airi Nomura,
Keisuke Shinoda,
Takuya Nakamura,
Hiroyuki Satofuka,
Guanjie Li,
Mika K. Kaneko
Podoplanin (PDPN) is a type I transmembrane protein with a highly glycosylated extracellular domain, a transmembrane domain, and a short intracellular domain. PDPN expression is observed in normal tissue and cells, including lung type I alveolar epithelial cells, kidney podocytes, and lymphatic endothelial cells. Therefore, anti-PDPN monoclonal antibodies (mAbs) in various animal species helped to identify PDPN-positive cells.We have developed anti-PDPN mAbs in more than 20 species. These anti-PDPN mAbs are applicable to flow cytometry, western blot, and immunohistochemistry. In this study, anti-rhinoceros PDPN (rhiPDPN) mAbs, PMab-315 (mouse IgG2a, kappa) and PMab-324 (mouse IgG2b, kappa) were established using the Cell-Based Immunization and Screening (CBIS) method. PMab-315 and PMab-324 strongly recognized the rhiPDPN-overexpressed Chinese hamster ovary K1 (CHO/rhiPDPN) and exhibited the same KD value (4.5 × 10−8 M) for CHO/rhiPDPN by a flow cytometry-based assay. Both mAbs can detect rhiPDPN in western blot and immunohistochemistry. These results suggest the usefulness of PMab-315 and PMab-324 for the pathological analysis of rhinoceros-derived tissues and cells.
Podoplanin (PDPN) is a type I transmembrane protein with a highly glycosylated extracellular domain, a transmembrane domain, and a short intracellular domain. PDPN expression is observed in normal tissue and cells, including lung type I alveolar epithelial cells, kidney podocytes, and lymphatic endothelial cells. Therefore, anti-PDPN monoclonal antibodies (mAbs) in various animal species helped to identify PDPN-positive cells.We have developed anti-PDPN mAbs in more than 20 species. These anti-PDPN mAbs are applicable to flow cytometry, western blot, and immunohistochemistry. In this study, anti-rhinoceros PDPN (rhiPDPN) mAbs, PMab-315 (mouse IgG2a, kappa) and PMab-324 (mouse IgG2b, kappa) were established using the Cell-Based Immunization and Screening (CBIS) method. PMab-315 and PMab-324 strongly recognized the rhiPDPN-overexpressed Chinese hamster ovary K1 (CHO/rhiPDPN) and exhibited the same KD value (4.5 × 10−8 M) for CHO/rhiPDPN by a flow cytometry-based assay. Both mAbs can detect rhiPDPN in western blot and immunohistochemistry. These results suggest the usefulness of PMab-315 and PMab-324 for the pathological analysis of rhinoceros-derived tissues and cells.
Posted: 13 February 2025
Vitamin D, Calcium to Magnesium Ratio, and the Gut Microbiome
Patrick Chambers
The gut microbiome has been the subject of increasing interest as integral to our health. Few realize that the enormous benefits of vitamin D (VD) and magnesium (Mg) are highly dependent on a healthy gut microbiome. Short chain fatty acids, especially butyrate, reflect not only a healthy gut microbiome but also VD status. Suboptimal VD, Mg, or butyrate translates to some degree of gut dysbiosis and vice versa. Mg dependent secondary bile acids, indoles, and tryptophan, all microbial metabolites and longevity agents, are also discussed. Mg is indispensable to not only the synthesis of the active form of VD but also that of 7-dehydrocholesterol (7-DHC) from acetate. 7-DHC is the substrate for solar conversion to D3. The steadily increasing Ca:Mg in the Western diet and its ironic impact on parathormone (PTH) is discussed. Gut dysbiosis further complicates this. Biochemical and physiologic interlinkages are legion and most remain hidden. This limited mini review exposes insight into the tight linkage between 25(OH)D and Ca:Mg, facilitated by the gut microbiome. A model incorporating the physiologically discordant but reinforcing effects on this linkage based on genes, culture, socioeconomic status, and diet that also addresses the seemingly contradictory reports regarding calcium (Ca), Mg, and VD efficacy is proposed. The balance between Ca and Mg is at the heart of the global epidemic of insulin resistance. A reliable method for estimating intracellular Mg++ is also proposed. A primary goal of this paper is to awaken the global public to not only the inadequacy of the RDA for Mg dependent vitamin D but also to that for the RDAs for Mg and Ca. Using generally accepted serum reference ranges, the difference between RBC Mg and plasma Mg, and basic physiology, one can both uncover the serious shortfall involving all three and unequivocally demonstrate the significant health risks linked to an out of range Ca:Mg. Conclusions are observational not experimental.
The gut microbiome has been the subject of increasing interest as integral to our health. Few realize that the enormous benefits of vitamin D (VD) and magnesium (Mg) are highly dependent on a healthy gut microbiome. Short chain fatty acids, especially butyrate, reflect not only a healthy gut microbiome but also VD status. Suboptimal VD, Mg, or butyrate translates to some degree of gut dysbiosis and vice versa. Mg dependent secondary bile acids, indoles, and tryptophan, all microbial metabolites and longevity agents, are also discussed. Mg is indispensable to not only the synthesis of the active form of VD but also that of 7-dehydrocholesterol (7-DHC) from acetate. 7-DHC is the substrate for solar conversion to D3. The steadily increasing Ca:Mg in the Western diet and its ironic impact on parathormone (PTH) is discussed. Gut dysbiosis further complicates this. Biochemical and physiologic interlinkages are legion and most remain hidden. This limited mini review exposes insight into the tight linkage between 25(OH)D and Ca:Mg, facilitated by the gut microbiome. A model incorporating the physiologically discordant but reinforcing effects on this linkage based on genes, culture, socioeconomic status, and diet that also addresses the seemingly contradictory reports regarding calcium (Ca), Mg, and VD efficacy is proposed. The balance between Ca and Mg is at the heart of the global epidemic of insulin resistance. A reliable method for estimating intracellular Mg++ is also proposed. A primary goal of this paper is to awaken the global public to not only the inadequacy of the RDA for Mg dependent vitamin D but also to that for the RDAs for Mg and Ca. Using generally accepted serum reference ranges, the difference between RBC Mg and plasma Mg, and basic physiology, one can both uncover the serious shortfall involving all three and unequivocally demonstrate the significant health risks linked to an out of range Ca:Mg. Conclusions are observational not experimental.
Posted: 13 February 2025
FRET Visualization of High Mechanosensation of von Willebrand Factor to Hydrodynamic Force
Mingxing Ouyang,
Yao Gao,
Binqian Zhou,
Jia Guo,
Lei Lei,
Yingxiao Wang,
Linhong Deng
von Willebrand factor (vWF) is a large glycoprotein in circulation system, which senses hydrodynamic force at vascular injuries and then recruits platelets in assembling clots. How vWF mechanosenses shear flow for molecular unfolding is an important topic. Here, Förster resonance energy transfer (FRET) biosensor was developed to monitor vWF conformation change to hydrodynamic force. The full-length vWF-based biosensor is anchored on cell surface, in which A2 domain is flanked with FRET pair. With 293T cells seeded into microfluidic channels, 2.8 dyn/cm2 shear force induced remarkable FRET change (~60%) in 30 min. Gradient micro-shear below 2.8 dyn/cm2 demonstrated FRET responses positively related to flow magnitudes with 0.14 dyn/cm2 inducing obvious change (~16%). The FRET increases indicate closer positioning of A2’s two termini in vWF, supported with high FRET of A2 only-based biosensor, which probably resulted from flow-induced A2 dissociation from vWF intramolecular binding. Interestingly, gradual increase of flow from 2.8 to 28 dyn/cm2 led to decreasing FRET changes, suggesting the second-level unfolding in A2 domain. LOCK-vWF biosensor with bridged A2 two termini or A2 only biosensor couldn’t sense the shear, indicating structure-flexible A2 and large vWF molecules important in the mechanosensation. In conclusion, the developed vWF-based biosensor demonstrated high mechanosensation of vWF with two-level unfolding to shear force: the dissociation of A2 domain from vWF intramolecular binding under micro shear, and then unfolding of A2 in vWF under higher shear. This study provides new insights on vWF mechanosensitive feature for its physiological functions and implicated disorders.
von Willebrand factor (vWF) is a large glycoprotein in circulation system, which senses hydrodynamic force at vascular injuries and then recruits platelets in assembling clots. How vWF mechanosenses shear flow for molecular unfolding is an important topic. Here, Förster resonance energy transfer (FRET) biosensor was developed to monitor vWF conformation change to hydrodynamic force. The full-length vWF-based biosensor is anchored on cell surface, in which A2 domain is flanked with FRET pair. With 293T cells seeded into microfluidic channels, 2.8 dyn/cm2 shear force induced remarkable FRET change (~60%) in 30 min. Gradient micro-shear below 2.8 dyn/cm2 demonstrated FRET responses positively related to flow magnitudes with 0.14 dyn/cm2 inducing obvious change (~16%). The FRET increases indicate closer positioning of A2’s two termini in vWF, supported with high FRET of A2 only-based biosensor, which probably resulted from flow-induced A2 dissociation from vWF intramolecular binding. Interestingly, gradual increase of flow from 2.8 to 28 dyn/cm2 led to decreasing FRET changes, suggesting the second-level unfolding in A2 domain. LOCK-vWF biosensor with bridged A2 two termini or A2 only biosensor couldn’t sense the shear, indicating structure-flexible A2 and large vWF molecules important in the mechanosensation. In conclusion, the developed vWF-based biosensor demonstrated high mechanosensation of vWF with two-level unfolding to shear force: the dissociation of A2 domain from vWF intramolecular binding under micro shear, and then unfolding of A2 in vWF under higher shear. This study provides new insights on vWF mechanosensitive feature for its physiological functions and implicated disorders.
Posted: 13 February 2025
Effects of Forage-to-Concentrate Ratio on Abnormal Stereotypic Behavior in Lambs and Goat Kids
Cemil Tölü
Posted: 13 February 2025
Exploring Dendroflora Diversity and Ecology in an Urban Park from Western Romania: The Role of Plant Life-Form and Plant Family in Urban Woody Phytocoenosis
Madalina Iordache,
Laurentiu Zamfir,
Alexandra Becherescu,
Codruta Chis
Posted: 13 February 2025
Tools to Dissect Lipid Droplet Regulation, Players, and Mechanisms
Jinmin Liu,
Yimon Aye
Posted: 13 February 2025
Molecular Responses to Abiotic Stress in Key Woody Perennial Fruit Crops: Genetic, Epigenetic and Microbiota Insights for Crop Resilience and Sustainability in Times of Climate Change
Aliki Kapazoglou,
Eleni Tani,
Vasileios Papasotiropoulos,
Sophia Letsiou,
Maria Gerakari,
Eleni Abraham,
Penelope J. Bebeli
Posted: 13 February 2025
Ultra- and Nano-Filtered Colostrum-Based Products Combined with Egg Yolk Extract, Nicotinamide Mononucleotide, and Natural Products Enhance the Cytotoxic Activity of Human Natural Killer (NK) Cells In Vivo
Sergei Boichuk,
Aigul Galembikova,
David Vollmer
Posted: 12 February 2025
Epigenetic Mechanisms in Chronic Obstructive Pulmonary Disease (COPD): A Systematic Review
Rosetta Ragusa,
Pasquale Bufano,
Alessandro Tognetti,
Marco Laurino,
Chiara Caselli
Posted: 12 February 2025
Study on Molecular Mechanism of Cysticercus Cellulosae TPx Protein Regulating Th1/Th2 Cell Imbalance Through JAK/STAT Signaling Pathway
Qianqian Mu,
Haojun Cai,
Haiting Xiong,
Biying Zhou
Posted: 12 February 2025
Clinical Significance of LINC00261 in the pathogenesis of Pancreatic, Colorectal, Hepatocellular, and Gallbladder Cancer
Sanjana Bana,
Sia Daffara,
Aastha Dagar,
Ashutosh Kumar Tiwari,
Kanupriya Medhi,
Sagarika Mukherjee,
Vivek Uttam,
Md Rizwan Ansari,
Hardeep Singh Tuli,
Vikas Yadav
Posted: 12 February 2025
Efficacy of Nano and Conventional Zinc and Silicon Fertilizers for Nutrient Use Efficiency and Yield Benefits in Maize Under Saline Field Conditions
Abbas Shoukat,
Uswah Maryam,
Britta Pitann,
Muhammad Mubashar Zafar,
Allah Nawaz,
Waseem Hassan,
Khalid M Elhindi,
Zulfiqar Ahmad Saqib,
Karl H Muehling
Posted: 12 February 2025
Molluscs as Experimental Models for the Study of Mucomics
Donatella Mentino,
Carlotta De Blasi,
Daniela Semeraro,
Maria Mastrodonato,
Marco Vito Guglielmi
Posted: 12 February 2025
Impact of Pesticide Exposure on High-Frequency Auditory Thresholds and Cochlear Function in Young People Residing Near Agricultural Areas
Felipe Munoz,
Cristian Aedo-Sanchez,
Felipe Paredes-Aravena,
Enzo Aguilar-Vidal,
Pedro Jilberto-Vergara,
Gonzalo Terreros
Posted: 12 February 2025
Organic Food Pricing in Jordan: Does Affordability Hinder Growth?
Johnson Eniola,
Adeyemi Enoch
Posted: 12 February 2025
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