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      <title>Wiley: IUBMB Life: Table of Contents</title>
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         <link>https://iubmb.onlinelibrary.wiley.com/doi/10.1002/iub.70118?af=R</link>
         <pubDate>Sun, 07 Jun 2026 21:59:22 -0700</pubDate>
         <dc:date>2026-06-07T09:59:22-07:00</dc:date>
         <source url="https://iubmb.onlinelibrary.wiley.com/journal/15216551?af=R">Wiley: IUBMB Life: Table of Contents</source>
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         <title>Hormesis and the Golden Ratio: Toward a Universal Estimator of Adaptive Capacity</title>
         <description>IUBMB Life, Volume 78, Issue 6, June 2026. </description>
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ABSTRACT
Hormesis represents a universal feature of biological plasticity across species and environmental contaminants. Here I propose that the maximum stimulatory peak converges upon the golden ratio (φ = 1.618), representing a 61.8% increase above baseline, a value embedded within the empirically observed 30%–60% range but offering mathematical precision for a unifying quantitative reference. I further hypothesize that the internal architecture of the hormetic zone may follow the complementary proportion of φ (0.382), with the rising phase occupying the smaller fraction (steep ascent) and the falling phase the larger fraction (gradual decline), reflecting natural selection for rapid threat response followed by sustained benefit. This framework positions the golden ratio as a potential evolutionary optimum, a Pareto‐efficient allocation where further investment yields diminishing returns. While the dose‐width to toxicity remains variable and context‐dependent, the peak magnitude may reveal a fundamental constraint on the adaptive capacity of life. Testing this hypothesis requires systematic meta‐analysis of existing databases and targeted experiments manipulating resource availability, genetic background, and evolutionary history.
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&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;Hormesis represents a universal feature of biological plasticity across species and environmental contaminants. Here I propose that the maximum stimulatory peak converges upon the golden ratio (&lt;i&gt;φ&lt;/i&gt; = 1.618), representing a 61.8% increase above baseline, a value embedded within the empirically observed 30%–60% range but offering mathematical precision for a unifying quantitative reference. I further hypothesize that the internal architecture of the hormetic zone may follow the complementary proportion of &lt;i&gt;φ&lt;/i&gt; (0.382), with the rising phase occupying the smaller fraction (steep ascent) and the falling phase the larger fraction (gradual decline), reflecting natural selection for rapid threat response followed by sustained benefit. This framework positions the golden ratio as a potential evolutionary optimum, a Pareto-efficient allocation where further investment yields diminishing returns. While the dose-width to toxicity remains variable and context-dependent, the peak magnitude may reveal a fundamental constraint on the adaptive capacity of life. Testing this hypothesis requires systematic meta-analysis of existing databases and targeted experiments manipulating resource availability, genetic background, and evolutionary history.&lt;/p&gt;</content:encoded>
         <dc:creator>
Evgenios Agathokleous
</dc:creator>
         <category>WORKING HYPOTHESIS</category>
         <dc:title>Hormesis and the Golden Ratio: Toward a Universal Estimator of Adaptive Capacity</dc:title>
         <dc:identifier>10.1002/iub.70118</dc:identifier>
         <prism:publicationName>IUBMB Life</prism:publicationName>
         <prism:doi>10.1002/iub.70118</prism:doi>
         <prism:url>https://iubmb.onlinelibrary.wiley.com/doi/10.1002/iub.70118?af=R</prism:url>
         <prism:section>WORKING HYPOTHESIS</prism:section>
         <prism:volume>78</prism:volume>
         <prism:number>6</prism:number>
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         <link>https://iubmb.onlinelibrary.wiley.com/doi/10.1002/iub.70117?af=R</link>
         <pubDate>Sat, 30 May 2026 01:21:49 -0700</pubDate>
         <dc:date>2026-05-30T01:21:49-07:00</dc:date>
         <source url="https://iubmb.onlinelibrary.wiley.com/journal/15216551?af=R">Wiley: IUBMB Life: Table of Contents</source>
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         <title>MicroRNAs in HPV‐Associated Carcinogenesis: Potential Biomarkers in Oropharyngeal and Cervical Cancers</title>
         <description>IUBMB Life, Volume 78, Issue 6, June 2026. </description>
         <dc:description>
ABSTRACT
High‐risk human papillomavirus (HPV) infection is a key etiological factor in cervical cancer (CC) and oropharyngeal squamous cell carcinoma (OPSCC). Increasing evidence indicates that host microRNAs (miRNAs) are central regulators in HPV‐induced carcinogenesis and represent promising molecular biomarkers for diagnosis and prognosis. In cervical cancer, deregulated expressions of miRNAs such as miR‐21, miR‐27a, miR‐34a, miR‐155, and miR‐218 have been consistently reported. These miRNAs influence critical pathways controlling apoptosis, cell proliferation, and immune evasion. The oncoproteins E6 and E7 from HPV can disrupt normal miRNA biogenesis, leading to the suppression of tumor‐suppressor genes such as PTEN and PDCD4 and the activation of oncogenic signaling networks. Circulating miRNAs detected in serum and plasma, including miR‐205 and miR‐196a, show potential as non‐invasive biomarkers for early detection and disease monitoring in cervical cancer (CC). In oropharyngeal cancer (OPC), particularly HPV‐positive OPSCC, altered miRNAs such as miR‐21, miR‐31, miR‐375, and miR‐9 have been implicated in tumor initiation and progression. Distinct miRNA profiles have been observed between HPV‐positive and HPV‐negative tumors, suggesting a role for these molecules in differentiating subtypes with different clinical outcomes. Salivary and serum miRNA assays have shown potential for early detection, reflecting tumor‐specific molecular changes in a minimally invasive manner. Overall, miRNA profiling offers a promising approach for stratifying HPV‐associated cervical and OPCs. Integrating miRNA panels with HPV genotyping and epigenetic data may enhance precision in risk assessment and therapeutic targeting. Future longitudinal studies with standardized methodologies are needed to validate these miRNAs as reliable clinical biomarkers.
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&lt;h2&gt;ABSTRACT&lt;/h2&gt;
&lt;p&gt;High-risk human papillomavirus (HPV) infection is a key etiological factor in cervical cancer (CC) and oropharyngeal squamous cell carcinoma (OPSCC). Increasing evidence indicates that host microRNAs (miRNAs) are central regulators in HPV-induced carcinogenesis and represent promising molecular biomarkers for diagnosis and prognosis. In cervical cancer, deregulated expressions of miRNAs such as miR-21, miR-27a, miR-34a, miR-155, and miR-218 have been consistently reported. These miRNAs influence critical pathways controlling apoptosis, cell proliferation, and immune evasion. The oncoproteins E6 and E7 from HPV can disrupt normal miRNA biogenesis, leading to the suppression of tumor-suppressor genes such as PTEN and PDCD4 and the activation of oncogenic signaling networks. Circulating miRNAs detected in serum and plasma, including miR-205 and miR-196a, show potential as non-invasive biomarkers for early detection and disease monitoring in cervical cancer (CC). In oropharyngeal cancer (OPC), particularly HPV-positive OPSCC, altered miRNAs such as miR-21, miR-31, miR-375, and miR-9 have been implicated in tumor initiation and progression. Distinct miRNA profiles have been observed between HPV-positive and HPV-negative tumors, suggesting a role for these molecules in differentiating subtypes with different clinical outcomes. Salivary and serum miRNA assays have shown potential for early detection, reflecting tumor-specific molecular changes in a minimally invasive manner. Overall, miRNA profiling offers a promising approach for stratifying HPV-associated cervical and OPCs. Integrating miRNA panels with HPV genotyping and epigenetic data may enhance precision in risk assessment and therapeutic targeting. Future longitudinal studies with standardized methodologies are needed to validate these miRNAs as reliable clinical biomarkers.&lt;/p&gt;</content:encoded>
         <dc:creator>
Rabab S. Hamad, 
Ahmed S. Doghish, 
Sherif S. Abdel Mageed, 
Nehal I. Rizk, 
Osama A. Mohammed, 
Khaled M. Alam‐Eldein, 
Khaled Abuelhaded, 
Haidy Adel Fahmy, 
Heba A. Saad, 
Gehad Elhadad, 
Asmaa M. Farahat, 
Reda M. Mansour
</dc:creator>
         <category>CRITICAL REVIEW</category>
         <dc:title>MicroRNAs in HPV‐Associated Carcinogenesis: Potential Biomarkers in Oropharyngeal and Cervical Cancers</dc:title>
         <dc:identifier>10.1002/iub.70117</dc:identifier>
         <prism:publicationName>IUBMB Life</prism:publicationName>
         <prism:doi>10.1002/iub.70117</prism:doi>
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         <prism:section>CRITICAL REVIEW</prism:section>
         <prism:volume>78</prism:volume>
         <prism:number>6</prism:number>
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         <link>https://iubmb.onlinelibrary.wiley.com/doi/10.1002/iub.70110?af=R</link>
         <pubDate>Sat, 30 May 2026 00:14:54 -0700</pubDate>
         <dc:date>2026-05-30T12:14:54-07:00</dc:date>
         <source url="https://iubmb.onlinelibrary.wiley.com/journal/15216551?af=R">Wiley: IUBMB Life: Table of Contents</source>
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         <title>Issue Information</title>
         <description>IUBMB Life, Volume 78, Issue 6, June 2026. </description>
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         <category>ISSUE INFORMATION</category>
         <dc:title>Issue Information</dc:title>
         <dc:identifier>10.1002/iub.70110</dc:identifier>
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         <prism:doi>10.1002/iub.70110</prism:doi>
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         <prism:section>ISSUE INFORMATION</prism:section>
         <prism:volume>78</prism:volume>
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