Introduction: Bmal1 is an important circadian rhythm gene, and its effect on sepsis has not been entirely elucidated. The aim of this work was to explore the regulatory role and molecular mechanism of BMAL1 in sepsis. Methods: C57BL/6J mice and THP-1 macrophages were used to establish sepsis models in vivo and in vitro, respectively. The peritoneal macrophages (PMs) and liver Kupffer cells (KCs) of mice were extracted, and the expressions of BMAL1 and PGC-1α in various macrophages were detected by Western blotting and RT-qPCR. Overexpression of BMAL1 in macrophages with plasmid. Knocked down the expression of PGC-1α by short hairpin RNAs (shRNA). STL1267 is an inhibitor of BMAL1, was used to inhibit the expression of BMAL1 in mice. Western blotting was used to detected the expression of BMAL1 in macrophages. ELISA was used to detected the levels of imerleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell supernatant and mouse serum, and HE staining was used to detected the pathological changes of organs. In addition, we detected the mutual regulation of BMAL1 and PGC-1α. Results: Both the sepsis models in vivo and in vitro, the protein and mRNA expression of BMAL1 in macrophages were significantly decreased. Overexpression of BMAL1 inhibits LPS-mediated inflammatory response and promotes M2-type polarization of macrophages. Inhibition the expression of BMAL1 by STL1267 further aggravated the inflammatory reaction and multiple organ damage in septic mice. PGC-1α is the downstream factor of BMAL1. After silencing PGC-1α, the inhibitory effect of BMAL1 on inflammatory response of macrophages was significantly weakened. Conclusions: BMAL1 is a key factor in inhibiting macrophage inflammatory response and sepsis, and its molecular mechanism closely related to the regulation of BMAL1 to PGC-1α.

This work conducted a comparative study on DFB lasers based on AlGaInAs/InP heterostructures, and comparatively studied the effects of different trench shapes and different cavity lengths on the laser output characteristics. Based on the vertical trench structure, we obtained a laser output of 90mW at 25°C, Compared with the trenchless laser, the output power was increased to 3.6 times the original, and the threshold current was only 4mA. It allows 8.5nm wavelength tunability within the temperature range of 5-85℃, and still has an edge mode suppression ratio of >45dB at 85℃. After the chip is packaged in a butterfly shape, the relative intensity noise in the 0-40 GHz frequency range is lower than -162.8dB/Hz at the working current of 300mA.

Nucleotide-binding oligomerization domain 2 (NOD2) primarily acts as a cytoplasmic pattern recognition receptor (PRR) recognizing muramyl dipeptide (MDP), the basic unit of bacterial cell wall, playing a key role in the sensing of pathogens. However, accumulating investigations indicate that, in addition to being a PRR, NOD2 also has a wide range of immunomodulatory effects and is involved in the pathogenesis of several inflammatory and infectious diseases, with Crohn’s disease (CD) and leprosy being typical examples. Here, we summarize the MDP dependent and independent activation of NOD2 and the corresponding downstream signaling pathways. In addition to the classic immune response triggered by NOD2, we also review the latest findings of NOD2 regulating immune homeostasis through trained immunity and immune tolerance. Finally, we focus on the diverse roles of NOD2 in defending against mycobacterial infections. A further comprehensive understanding of NOD2 will provide new insights into the treatment of infectious and inflammatory diseases.

A document by Haleema Qayyum Abbasi. Click on the document to view its contents.

A significant foodborne pathogen that causes acute gastroenteritis worldwide is sapovirus (SaV). Currently, SaV genotyping is primarily based on the VP1 gene. The single naming method based on the VP1 region can no longer suit the needs of SaV research due to the emergence of recombinant strains. Therefore, SaV nucleotide sequences with entire VP1 and NS6-7 genes sections were gathered in Genbank, and genetic distance calculations and phylogenetic analyses were carried out to investigate the double nomenclature based on SaV VP1 and NS6-7 genes. They can be further subdivided into genotypes and various genogroups based on the genetic diversity of the entire VP1 region, and 12 genogroups and 30 genotypes were found, including tentative genotypes and genogroups. The work is noteworthy for having discovered a novel genogroup, GNA1. There was an interesting discovery of a class of sequences known as bat-related sequences. The genetic distance between these sequences approached the inter-genogroup genetic distance, which in this study was classified as the bat genogroup. Thirty significant reference sequences are proposed based on the VP1 genotypes. Phylogenetically, twelve P (polymerase)-groups and 29 P-types (Including tentative genotypes and genogroup) were identified based on the genetic diversity of nucleotide sequences in the entire NS6-7 region, and related P-type reference sequences were also suggested. Nine recombinant sequences, comprising six recombinant genotypes (GI.1[P4], GI.2[P1], GII.4[P1], GII.4[PNA1], GII.6[P2], and GV.NA1[P3]), were found as a result of the dual nomenclature of the VP1 and NS6-7 genes. Dual nomenclature based on VP1 and NS6-7 genes can effectively characterize SaV recombination.

Traumatic brain injuries are extremely common, and although most patients recover from their injuries many TBI patients suffer prolonged symptoms and remain at a higher risk for developing cardiovascular disease and neurodegeneration. Moreover, it remains challenging to identify predictors of poor long-term outcomes. Here, we tested the hypothesis that preexisting cerebrovascular impairment exacerbates metabolic and vascular dysfunction and leads to worse outcomes after TBI. Male mice underwent a mild surgical reduction in cerebral blood flow using a model of bilateral carotid artery stenosis (BCAS) wherein steel microcoils were implanted around the carotid arteries. Then mice underwent a mild-moderate TBI, or a combination of BCAS followed by TBI 30 days post coil implantation. Gene expression profiles, cerebral blood flow, metabolic function, oxidative damage, vascular health and angiogenesis were assessed. Single nuclei RNA sequencing of endothelial cells isolated from mice after TBI showed differential gene expression profiles after TBI and BCAS, that were further altered when mice underwent both challenges. TBI but not BCAS increased mitochondrial oxidative metabolism. Both BCAS and TBI decreased cerebrovascular responses to repeated whisker stimulation. BCAS induced oxidative damage and inflammation in the vasculature as well as loss of vascular density, and reduced the numbers of angiogenic tip cells. Finally, intravascular protein accumulation was increased among mice that experienced both BCAS and TBI. Overall, our findings reveal that a prior vascular impairment significantly alters the profile of vascular health and function of the cerebrovasculature, and when combined with TBI may result in worsened outcomes.

The surface morphology has a significant influence on the fatigue behavior of components. For austenitic stainless steels (ASSs), this issue is even more pronounced due to their metastability. Based on the complex deformation mechanisms of metastable ASSs, which include dislocation slip, deformation twinning, and deformation-induced martensitic phase transformation, the metastable stainless steel AISI 347 was investigated in this study together with the stable AISI 904L as a reference material. 4-point bending fatigue tests with load ratio R = 0.1 and testing frequency f = 10 Hz at ambient temperature were carried out on specimens with 5 technically relevant surfaces morphologies: mechanical polished, milled, micro-shot peened, laser shock-peened, and ultrasonic modified. Systematic material characterizations were carried out to clarify the key influences of these morphologies on the fatigue behavior. Deformation-induced martensite layers were proven to improve the fatigue life in metastable austenitic steels, which open perspectives to extend the lifetime of components.

Abstract. Ferroptosis is a novel non-apoptotic form of cell death characterized by iron-dependent reactive oxygen species (ROS)-mediated lipid peroxidation. In several different cell systems, the tumor suppressor p53 can enhance sensitivity to ferroptotic inducers. At least half of all human cancers show loss of function of p53. Furthermore, many of those tumors express mutant forms of p53 that has lost its wild-type function. Several groups have designed small molecules that can reactivate the wild-type function of these missense p53 mutants. We reasoned that p53 reactivators may also enhances sensitivity of certain cancer cells to ferroptosis stimuli. To test this idea we combined a number of different p53 reactivators with small molecule inducers of ferroptosis. In contrast, we observed that several p53 reactivators protected cells from cell death induced by ferroptotic inducers. Suprisingly, this protection still occurred in p53-null cell lines. We observed that these reactivators were neither free radical scavengers nor ion chelators. One of these p53 reactivator molecules, NSC 59984, reduced expression of GPX4, which is unlikely to explain the ability to reduced sensitivity to ferroptosis. We suggested that these p53 reactivators function via an unknown, p53-independent manner to suppress ferroptosis.

Generalist butterflies are characterized by a broad host repertoire that can comprise several families or even different orders of plants. The genetic and physiological mechanisms underlying the use of such a wide host range are still not fully understood. Earlier studies indicate that the consumption of different host plants is associated with host-specific gene expression profiles. It remained, however, unclear if and how larvae can alter these profiles in the case of a changing host environment. Using the polyphagous comma butterfly (Polygonia c-album) we show that larvae can adjust their transcriptional profiles in response to a new host plant. The switch to some of the host plants, however, resulted in a larger transcriptional response and, thus, seems to be more challenging. At a physiological level, no correspondence for these patterns could be found in larval performance. This suggests that a high transcriptional but also phenotypic flexibility are essential for the use of a broad and diverse host range. We furthermore propose that host switch tests in the laboratory followed by transcriptomic investigations can be a valuable tool to examine not only plasticity in host use but also subtle and/or transient trade-offs in the evolution of host plant repertoires. key words: insect-plant association, host plant adaptation, gene expression, phenotypic plasticity

Aims Tick-borne diseases (TBDs) pose a significant and increasing health threat globally. About 45 tick species have been described from Ghana, located in Sub-Saharan Africa, but it is unknown how well-informed local citizens are regarding the risks posed by ticks and TBDs. This research aimed to assess the public knowledge and awareness of TBPs and TBDs in Ghana through questionnaires. The survey underscored the potential veterinary and public health threats of TBDs, emphasizing the importance of awareness creation. Methods Utilizing a cross-sectional design, we collected data from 538 respondents across all 16 regions of Ghana through questionnaires and assessed public knowledge and awareness of TBDs. W used both an electronic survey form and a structured interview questionnaire to assess respondents’ knowledge of ticks and TBDs. Descriptive table statistics were used to tabulate frequencies and percentages of all categorical responses and more closely tested for associations between certain variable pairs. Results Results from the study identified limited public knowledge and awareness among animal owners and non-animal owners in Ghana. Furthermore, the results highlighted the association between domestic animal ownership and increased human-tick encounters. The findings suggest a pressing need for targeted public education on TBDs in Ghana. Conclusions As Ghana imports livestock, the risk of TBD spread demands attention. Overall, the survey contributes essential insights for veterinary and public health interventions, stressing the urgency of raising awareness and understanding among the public regarding the risks associated with ticks and TBDs. The cohabitation of humans with a variety of domestic animals, coupled with varying levels of veterinary service utilization, presents opportunities for targeted public health interventions.

Abstract Background and Purpose: G-protein-coupled receptor (GPR158), an orphan receptor, is highly expressed in the medial prefrontal cortex in (mPFC) and identified as a novel therapeutic target for treating depression. Trilobatin (TLB) is a naturally-occurring food additive with potent neuroprotective properties. However, its pharmacological effects and molecular mechanisms against depression remains unknown. We explored whether TLB alleviates depression by targeting GPR158. Experimental Approach: Chronic unpredictable mild stress (CUMS)-induced depression mice model was used to explore antidepressant-like effect of TLB. GPR158-deficent mice were treated with TLB to determine whether TLB exerts its antidepressant-like effect by targeting GPR158. Key Results: TLB effectively alleviated CUMS-induced depressive-like behavior in mice. Mitophagy was contributed to the antidepressant-like effect of TLB, as evidenced by qRT-PCR array. As anticipated, TLB up-regulated autophagy associated protein expression of PFC in mice and restored mitochondrial dynamic balance, further inhibiting oxidative stress, as reflected by reducing ROS generation and increasing antioxidant enzymes. Mechanistically, GPR158 deficiency also up-regulated autophagy associated proteins expression and rejuvenated mitochondrial dynamic, further attenuating depressive-like behavior in response to CUMS insult. Most importantly, TLB directly bound to GPR158 and decreased its protein expression. Encouragingly, the promotive effect of TLB on mitophagy and its antidepressant-like effect were enhanced in GPR158-deficent mice. Conclusions and Implications: Our findings not only highlight GPR158-mediated mitophagy as a crucial pharmacological target for managing depression, but also reveal a new-found pharmacological property of TLB: serving as a novel naturally-occurring ligand of GPR158 to safeguard depression from oxidative stress by promoting mitophagy.

The genesis of snowdrifts and its governing processes are not fully understood. Yet, the assessment of snow redistribution by the wind is essential in snow-affected regions for risk management, water resources and mitigation tactics. Factors such as flow turbulence and snow properties showed to be crucial for the snow-wind interaction on flat terrain. In this work, we add a third component and investigate the drifting mechanisms of snow around complex building structures using numerical Euler-Lagrange simulations. The German Antarctic research station Neumayer III is investigated in particular. Results show that structure-borne snowdrifts are strongly influenced by the wind forcing, precipitation, snow cohesion and fine changes in the obstacle shape. Thus, these factors should be cautiously included in numerical models simulating snow transport at small scales.

Drought conditions caused by soil moisture stress and/or high vapour pressure deficit pose a challenge to many terrestrial ecosystem models (TEMs). The Canadian LAnd Surface Scheme Including biogeochemical Cycles (CLASSIC) employs an empirical approach to link soil moisture stress with stomatal conductance. Such soil moisture-based empirical approaches typically perform poorly during drought. Here, we implemented an explicit plant hydraulics parameterization, i.e., Stomatal Optimization based on Xylem hydraulics (SOX), in CLASSIC, thereby connecting the soil-plant-atmosphere continuum through plant hydraulic traits. Performance of the resulting CLASSIC$_{SOX}$ was evaluated against carbon and water fluxes measured with eddy covariance at eight boreal forest flux tower sites in North America. Compared to CLASSIC, CLASSIC$_{SOX}$ better simulated gross primary productivity (GPP) across all sites, i.e., coefficient of determination (R$^{2}$) increased (0.51 to 0.59), root mean square error (RMSE) and bias decreased (1.85 to 1.54 g C m$^{-2}$ d$^{-1}$) and (-0.99 to -0.58 g C m$^{-2}$ d$^{-1}$), respectively. Under drought conditions, identified using the Palmer drought severity index, GPP simulated with CLASSIC$_{SOX}$ improved compared to CLASSIC, i.e., R$^{2}$ increased (0.51 to 0.60), and RMSE and bias decreased (1.79 to 1.46 g C m$^{-2}$ d$^{-1}$) and (-0.97 to -0.53 g C m$^{-2}$ d$^{-1}$), respectively. In contrast, CLASSIC$_{SOX}$ simulated evapotranspiration worsened, i.e., R$^{2}$ decreased (0.61 to 0.42), RMSE increased (0.54 to 0.62 mm d$^{-1}$), and bias changed direction (0.09 to -0.09 mm d$^{-1}$). As evaporation is a highly parameterized process in CLASSIC, it likely needs to be re-parameterized to account for the SOX transpiration behaviour.

The interrelationality of health and peace is complex, multifactorial, and imbued with political and economic challenges. Peace and health outcomes reflect shared fundamental values related to the achievement of a balanced holistic condition on the individual and collective level. This causal relationship between social inequity and health requires special attention be paid to the impact of political instability and structural violence on undermining health systems in conflict zones. The mutual dependency between peace and health means that peace cannot be achieved without the existence of physical, mental, social, and spiritual health, and holistic health cannot be sustained under violent conditions. The interrelationality of peace and health as mutual conditions shape our understanding of global solidarity in relation to health diplomacy and peace promotion, if addressed equally across all conflict zones This prospective analytical review discusses the complex interplay between peace and health in three global contexts utilizing contextual analysis of the unique interdisciplinary factors at play that contribute to, or hinder the advancement of global health and peace in Palestine, Venezuela, and Ukraine. Peace is a multifaceted phenomenon that necessitates the participation, dedication, and action of all sectors and stakeholders in the global society, including health professionals. Both the “right to health” and the “right to peace” can be realized through two approaches: (1) holding governments accountable for maintaining peace and protecting health systems, and (2) the implementation of policies and actions that promote nonviolence education, intergroup communication, and social justice. Highlights: Countries around the globe are facing multiple, (re)emerging and complex crises and conflicts, aggravated by increasing social, political, and economic pressures that mainly impact people’s health and health systems. The existing global governance structures of peacebuilding for health are powerless, ineffective, and still unclear, thus setting health actors up for failure, when it comes to sustaining long-lasting changes and addressing the root causes of crisis. Crises including political pressures, historic suffering due to coloniality, protracted conflicts, lack of advocacy and firm international laws enforcement, hypocritical standards of intervention, absence of health equity, and an absence of ethical and human rights frameworks, all impede the creation of peaceful societies that promote health and vice versa. Palestine, Ukraine, and Venezuela reflect diverse contexts where clear disparities are present in global solidarity, humanitarian intervention, global interest, advocacy, and willingness to promote the health-peace nexus are reported. Continued impunity, partiality, and injustice undermine health-peace promotion and scale up global health disruptions, and the shared challenges of suboptimal health status should be sufficiently handled based on equal rights, equity, accountability, and transparency regardless of variations in geography, ethnicity, region, political context.

Aim: This study aimed to identify studies that provide comprehensive information on the biological-molecular changes of inflammatory breast cancer (IBC) from January 1, 2000, to the end of November 2021. Materials and Methods: Two researchers independently searched electronic databases using keywords and Boolean operators. Inclusion criteria included studies published in English, peer-reviewed, and with appropriate information on IBC’s biological-molecular changes. Exclusion criteria were studies not in English, those without sufficient information on molecular and biological processes related to cancer, or those including other cancers. Results: From an initial selection of 1639 studies, 11 were selected based on the inclusion and exclusion criteria. The results highlight the importance of rigorous search strategies in identifying relevant studies in the field of cancer research. Conclusion: Understanding the unique traits of inflammatory breast cancer is crucial in determining its aggressive nature. Differential diagnosis of IBC from other types of breast cancer is necessary as genetic and molecular alterations in IBC are also present in non-IBC breast cancer, despite potential differences in treatment.

Hydrology has a long history due to its early origin, but it is still considered young due to lack of a solid scientific foundation as a natural science. To lay a solid foundation of hydrology, field experimentation is crucial for investigating hydrological processes and revealing hydrological mechanisms. Professor Wei-Zu Gu (1932–2022) was an internationally renowned scientist in the field of hydrology and is recognized as the greatest pioneer of experimental hydrology and isotope hydrology in China. He created the Hydrohill experimental catchment, which serves as both a great public works for experimental hydrology and a valuable legacy for future researchers to conduct hydrological experiments. This legacy represents an innovative infrastructure that bridges the gap between natural watershed experiments and artificial physical models. The Hydrohill is an intensively-instrumented experimental catchment, allowing for comprehensive measurement of elements of the hydrologic cycle and their tracing indicators in a sophisticated manner. To provide an in-depth understanding of the Hydrohill, this paper presents its short history, experimental objectives, site description (including location, construction, and instrumentation), site conditions (such as soil, hydrological and meteorological properties), and contributions to hydrologic science. We pay our respects to Professor Gu for his hard work in creating the Hydrohill for experimental hydrology and enhancing our understanding of hydrological processes and mechanisms. Finally, we hope that with healthy operation at Chuzhou Scientific Hydrology Laboratory (CSHL) along with support from Professor Gu’s friends, CSHL will enable the continued growth of the Hydrohill so that it can address some unsolved problems in hydrology.

Purpose: To observe whether the effect of orthokeratology (OK) lenses on myopia control in children with allergic conjunctivitis (AC) after three years of wear differs from that in children without allergic conjunctivitis (nAC) and to identify potential influencing factors. Methods: This was a retrospective case‒control study. Patients aged 8-15 years who were fitted with OK lenses in 2019 and had a spherical equivalent (SE) between -6 and -0.75 dioptres and astigmatism ≥-1.50 D were collected. A three-year follow-up was also conducted, documenting all corneal adverse events (AEs) and the increase in axial length (AL) of the eye after three years of wearing OK lenses. Patients were divided into groups with and without AC based on their medical history and physical signs at the initial fitting. Only the right eye data of patients were used for statistical analysis. Baseline data and AL elongation after three years were compared between the two groups. Results: A total of 309 patients were included in this study, with 47 in the AC group and 262 in the nAC group. There were no statistically significant differences between the two groups in terms of age , sex, SE, AL of the eye and environment. During the three-year follow-up period, 20 patients (42.6%) in the AC group and 75 patients (28.6%) in the nAC group experienced AEs, and these two groups were not significantly different ( P=0.057). After three years of OK lens wear, the AL elongation in the AC group was 0.96±0.45 mm, whereas it was 0.69±0.45 mm in the nAC group (P<0.001). The AL elongation in AC patients was significantly greater than that in nAC patients. AL elongation was not correlated with the occurrence of AEs. In the AC group, AL elongation was correlated only with age, while in the nAC group, axial elongation was related to age, initial SE, and initial AL. Conclusions: In children with AC, the effect of wearing OK lenses on controlling axial elongation is weaker than that in patients without AC. This attenuation is unrelated to the occurrence of corneal AEs.

Despite the control of the COVID-19 pandemic, it remains one of the main concerns of healthcare systems throughout the world. Inflammation and hyper-reactive immune system play an essential role in developing SARS-CoV-2 infection, particularly in immunocompromised patients. Infliximab, an anti-TNFα antibody that is used in autoimmune disorders, may exert an important role in alleviating inflammation and hyper-reactive immunity. In this systematic review and meta-analysis, we have concluded that Infliximab can significantly decrease the mortality rate in patients with COVID-19. Conversely, it did not have a significant effect on the rate of hospitalization, mechanical ventilation, and adverse events during SARS-CoV-2 infection. More studies on the influence of Infliximab on patients with COVID-19 are warranted.

Secondary histiocytoses are exceedingly rare and knowledge about pathophysiology and treatment is limited. We report the first known case of Philadelphia chromosome -like - B-lymphoblastic leukemia complicated by disseminated juvenile xanthogranuloma in an adolescent salvaged successfully with targeted MEK inhibition.

Five pairs of new orcinol-based merosesquiterpenoid enantiomers, named dauresorcinols A−E (1−5), were isolated from the leaves of Rhododendron dauricum. Their structures were elucidated by comprehensive spectroscopic data analysis, quantum chemical calculations, Rh2(OCOCF3)4-induced ECD, and single-crystal X-ray diffraction analysis. Dauresorcinols A (1) and B (2) possess two unprecedented merosesquiterpene skeletons featuring a novel 6,7-dimethyl-11-oxatetracyclo[8.8.0.02,7.012,17]octadecane and a caged 15-isohexyl-2,10-dioxatetracyclo[7.4.1.111,14.03,8]pentadecane motif, respectively. Plausible biogenetic pathways of 1−5 are proposed involving key oxa-electrocyclization and Wagner−Meerwein rearrangement reactions. (+)/(−)-1 and 3−5 showed potent α-glucosidase inhibitory activity, 3 to 22 times stronger than acarbose, an antidiabetic drug targeting α-glucosidase. Docking results provide a basis to design and develop meroterpenoids as novel α-glycosidase inhibitors.

Heterozygous TCF3-Related Disease Presenting as X-linkedAgammaglobulinemia Mimicry in a Male Toddler withB-cell Aplasia, Agammaglobulinemia, and Severe Neutropenia

Here, we describe two patients with juvenile xanthogranuloma (JXG) manifesting with Langerhans cell histiocytosis-associated neurodegenerative disease (ND)-like radiological findings. One patient showed typical radiological abnormalities at onset, which worsened with progressing central nervous system symptoms 7 years after LCH-oriented chemotherapy. Another showed spontaneous regression of clinical symptoms, with a transient radiological change 1 year after salvage chemotherapy for recurrence of JXG. These data regarding JXG-associated ND will facilitate future investigation of the disease, as well as development of therapeutic interventions.

Title : Evans syndrome in the background of 22q11.2 deletion syndrome

Individuals with low socioeconomic status (SES) are at greater risk of contracting and developing severe disease compared to people with higher SES. Age, sex, host genetics, smoking, and Cytomegalovirus (CMV) serostatus are known to have a major impact on human immune responses and thus susceptibility to infection. However, the impact of SES on immune variability is not well understood or explored. Here, we used data from the Milieu Intérieur project, a study of 1,000 healthy volunteers with extensive demographic and biological data, to examine the effect of SES on immune variability. We developed an Elo-rating system using socioeconomic features such as education, income, and household to objectively rank SES in the 1,000 donors. We observed sex specific SES associations, such as females with a low SES having significantly higher frequency of CMV seropositivity compared to high SES females, and males from a low SES having significantly higher frequency of active smoking compared to high SES males. Using random forest models, we identified specific immune genes which were significantly associated with SES in both baseline and immune challenge conditions. Interestingly, many of the SES associations were sex-stimuli specific, highlighting the complexity of these interactions. Our study provides a new way of computing SES in human populations that can help identify novel SES associations and reinforces biological evidence for SES-dependent susceptibility to infection. This should serve as a basis for further understanding the molecular mechanisms behind socioeconomic status effects on immune responses and ultimately disease.