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<title>International-Journal-of-Biomedical-Investigation-ISSUE VOLUME Volume 9 ISSUE Issue 2</title>
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International-Journal-of-Biomedical-Investigation: VOLUME Volume 9 ISSUE Issue 2, July-Dec 2026
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<title>International-Journal-of-Biomedical-Investigation-ISSUE VOLUME Volume 9 ISSUE Issue 2</title>
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		<title>Visceral-Leishmaniasis-Kala-azar-Epidemiology-Pathogenesis-Diagnosis-and-Emerging-Therapeutic-Strategies-</title>
		<pubDate>01-Aug-2026</pubDate>
<link>http://ijbi.edwiserinternational.com/admin/uploads/92638U.pdf</link>
		<author>Deepak-SK-Fazal-B-Karim-MJ-et-al-</author>
		<comments>{http://www.edwiserinternational.com/contact-us.php}</comments>
		<category>Pharmaceutical Science,Medical Science</category>
		<description>{<![CDATA[Visceral leishmaniasis (VL), commonly known as Kala-azar, is one of the most severe neglected tropical diseases caused primarily by intracellular protozoan parasites belonging to the Leishmania donovani complex. Despite significant advances in disease control, VL continues to pose a major public health challenge, particularly in tropical and subtropical regions of South Asia, East Africa, and South America. The disease is transmitted through the bite of infected female phlebotomine sandflies and is characterized by persistent fever, hepatosplenomegaly, pancytopenia, weight loss, and progressive immune dysfunction. The pathogenesis of VL involves complex interactions between Leishmania parasites and host immune responses, including parasite survival within macrophages, modulation of cytokine networks, oxidative stress regulation, and immune evasion mechanisms. This review provides a comprehensive overview of the epidemiology, transmission dynamics, and global burden of visceral leishmaniasis, while highlighting recent advances in understanding its molecular and cellular pathogenesis. Current diagnostic approaches, including parasitological examination, serological assays, antigen detection methods, and molecular techniques such as polymerase chain reaction (PCR), are critically discussed with emphasis on their sensitivity, specificity, and clinical applicability. Furthermore, conventional therapeutic strategies, including amphotericin B formulations, miltefosine, paromomycin, and combination regimens, are evaluated alongside emerging approaches such as nanotechnology-based drug delivery systems, immunomodulatory therapies, vaccine development, host-directed therapies, and novel antileishmanial compounds. An improved understanding of parasite biology, hostpathogen interactions, and mechanisms of therapeutic resistance is essential for developing safer, more effective, and sustainable interventions. This review emphasizes the need for integrated approaches combining early diagnosis, optimized treatment strategies, surveillance programs, and innovative therapeutic platforms to achieve effective control and eventual elimination of visceral leishmaniasis.]]>}</description>
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		<title>Comprehensive-Review-of-4T1-CT26-AND-MC38-Syngenic-Tumour-Models-in-Preclinical-Cancer-Research-</title>
		<pubDate>16-Aug-2026</pubDate>
<link>http://ijbi.edwiserinternational.com/admin/uploads/8XaYJS.pdf</link>
		<author>Sharma-P-Fazal-B-Kumar-P-et-al-</author>
		<comments>{http://www.edwiserinternational.com/contact-us.php}</comments>
		<category>Pharmaceutical Science,Medical Science</category>
		<description>{<![CDATA[Syngeneic tumour models are indispensable tools in preclinical cancer research because they allow tumour development within an intact immune system, enabling investigation of tumourimmune interactions and evaluation of immunotherapies. This review provides a comprehensive overview of three widely used syngeneic tumour models: 4T1, CT26, and MC38. Their origins, genetic backgrounds, tumour establishment, biological characteristics, immunological profiles, and principal research applications are discussed. The 4T1 model, established in BALB/c mice, is characterized by aggressive tumour growth, spontaneous metastatic potential, and an immunosuppressive tumour microenvironment, making it particularly valuable for investigating metastatic breast cancer and mechanisms of treatment resistance. CT26, a BALB/c-derived colorectal carcinoma model, demonstrates measurable tumour growth and moderate immunogenicity and is widely utilized for studying immune-cell infiltration, cytokine responses, cancer vaccines, and immune checkpoint modulation. MC38, established in C57BL/6 mice, exhibits comparatively high immunogenicity and substantial immune-cell infiltration, making it an important model for investigating immune checkpoint blockade, particularly PD-1/PD-L1-directed therapies. The review further discusses approaches for tumour establishment and characterization, evaluation of therapeutic responses, applications in cancer immunotherapy, and the advantages and limitations of these models. Finally, emerging approaches involving multi-omics, advanced immune profiling, tumour microenvironment modulation, and complementary humanized models are discussed as strategies to improve their translational relevance. Collectively, 4T1, CT26, and MC38 provide complementary and biologically distinct platforms for investigating cancer progression, tumourimmune interactions, therapeutic responses, and the development of novel anticancer and immunotherapeutic strategies.]]>}</description>
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		<title>Decoding-Natures-Disease-Tolerance-Toolkit-Comparative-Immunobiology-of-Large-Mammals-PathogenHost-Interactions-and-Translational-Opportunities-for-Human-Medicine</title>
		<pubDate>18-Aug-2026</pubDate>
<link>http://ijbi.edwiserinternational.com/admin/uploads/7kOF4U.pdf</link>
		<author>Kumar-S-Karim-MJ-Fazal-B-et-al</author>
		<comments>{http://www.edwiserinternational.com/contact-us.php}</comments>
		<category>Pharmaceutical Science,Medical Science</category>
		<description>{<![CDATA[Large mammals represent a valuable yet comparatively underexplored source of biological information for understanding the mechanisms that determine disease resistance, disease tolerance, immune-mediated tissue injury, and survival. Unlike conventional laboratory models, large mammals exhibit distinctive physiological, immunological, metabolic, and evolutionary adaptations that can substantially influence hostpathogen interactions. This review provides a comprehensive comparative perspective on the biological mechanisms underlying lethal disease in large mammals, with particular emphasis on the interaction between pathogen virulence, innate and adaptive immunity, inflammatory signalling, cellular stress, regulated cell death, tissue injury, and systemic organ dysfunction. Major disease models, including bovine leukemia virus, African swine fever, bovine respiratory disease, chronic wasting disease, foot-and-mouth disease, hemorrhagic septicemia, and bovine tuberculosis, are considered to illustrate distinct patterns of persistent infection, acute systemic inflammation, immune evasion, immunosuppression, neurodegeneration, and immunopathology. The review further examines species-specific immune adaptations, highlighting elephants as models of enhanced tumour surveillance, camelids as unique sources of heavy-chain-only antibodies and nanobody technologies, and bats as important models for understanding antiviral resistance and disease tolerance. Particular emphasis is placed on the emerging concept that survival depends not only on pathogen elimination but also on the ability of the host to limit collateral tissue damage during infection. Collectively, comparative immunology of large mammals provides an evolution-inspired framework for discovering mechanisms of disease resistance and tolerance and translating naturally evolved biological solutions into innovative strategies for infectious disease, inflammatory disorders, and cancer research.]]>}</description>
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