Biology subjects

Jahan, N.

Publications and source records attributed to Jahan, N..

9 recordsLinked to original sources

bioRxiv2026

A Low-Resource Machine-Learning Framework for Cold-Stress Early Warning in Aquaculture Nursery Ponds Using Manual Temperature Readings

Cold stress is a recurring risk in tropical and subtropical aquaculture nursery ponds, yet warning tools remain limited where continuous automated sensors are impractical. This study developed a low-resource cold-stress early warning framework using four years (2022-2025) of 6-hourly manual air and pond-water temperature readings from a Nile tilapia (Oreochromis niloticus) nursery pond in Cumilla, Bangladesh. Models were fitted on 2022-2023, validated on 2024 for threshold selection, and tested on 2025 as an independent year. Cold stress (daily mean water temperature <20{degrees}C) occurred on 133 days; heat stress (>35{degrees}C) on only 4 days. Air-water coupling was strong overall (r = 0.976) but weakened in winter (r = 0.776) and further within the 18-22{degrees}C boundary zone where cold-stress classification is most sensitive. Solar radiation only marginally increased boundary-zone classification AUC from 0.782 to 0.789. In 6-hour regression, the same-hour-yesterday baseline (MAE = 1.117{degrees}C) nearly matched Extreme Gradient Boosting (XGBoost) with MAE of 1.116{degrees}C, cold-zone bias +0.36{degrees}C, and train-test gap 0.02{degrees}C; Random Forest (RF) and Long Short-Term Memory (LSTM) had MAEs of 1.195{degrees}C and 1.244{degrees}C, respectively. For cold-stress classification, Multiple Linear Regression (MLR) gave the highest F1 (0.755), while XGBoost provided the more protective operating point, detecting 95 of 108 cold-stress readings at 6-hour lead time (sensitivity = 0.880, F1 = 0.739). XGBoost warning skill extended to 12, 18, and 24-hour lead times, with F1 scores of 0.722, 0.646, and 0.704, respectively. The framework converts routine manual thermometer readings into short-lead cold-stress alerts for nursery management decisions. Multi-pond validation is needed before deployment.

ecology↗

bioRxiv2026

RNA degradation by ribonuclease T2 is required for phosphate homeostasis in S. cerevisiae

Inorganic phosphate (Pi) is a critical building block for key biomolecules including ATP, DNA, RNA, and phospholipids. Consequently, cells monitor phosphate levels and acquire phosphate when intracellular levels become low. Here we demonstrate an unanticipated connection between the enzymatic activity of the S. cerevisiae RNase T2 ortholog, Rny1, and inorganic phosphate availability. Rny1 has been studied for its role in autophagy-linked RNA degradation under starvation conditions. Here we find that in nutrient-rich conditions, cells lacking Rny1 function exhibit phosphate starvation phenotypes and aberrantly activate the PHO signaling pathway despite the presence of high levels of inorganic phosphate in the growth media. This activation is evidenced by increased PHO gene transcript levels and increased nuclear localization of Pho4 in rny1{Delta} strains. Complementation of rny1{Delta} with wild-type RNY1 and human RNase T2 restores PHO transcript levels to those typically observed in exponentially growing cells. This implicates RNase T2-dependent RNA degradation as required for maintaining intracellular phosphate levels, even under phosphate-replete conditions. Furthermore, consistent with its potential role in freeing phosphate from degraded RNA, RNY1 expression is itself further induced under phosphate-limited conditions. These observations suggest that RNase T2-mediated RNA decay is a part of a potentially conserved metabolic recycling pathway that provides Pi to growing cells. These findings reframe RNA as a key metabolic resource and positions RNase T2 enzymes, and their function in RNA degradation, as an unexpected player in phosphate homeostasis. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=151 SRC="FIGDIR/small/739639v1_ufig1.gif" ALT="Figure 1"> View larger version (37K): org.highwire.dtl.DTLVardef@119a9borg.highwire.dtl.DTLVardef@1bd5b13org.highwire.dtl.DTLVardef@a67bdcorg.highwire.dtl.DTLVardef@dcfd4_HPS_FORMAT_FIGEXP M_FIG C_FIG

molecular biology↗

bioRxiv2025

Pre-Human Immunodeficiency Virus (HIV) infection Th17 CD4+ T cells as predictors of early HIV disease progression

Interleukin-17-producing T helper (Th17) CD4+ T cells are highly susceptible to HIV infection and are depleted early in people living with HIV. Here, we investigated whether systemic Th17 cell levels prior to HIV infection are associated with subsequent HIV disease progression. We analyzed archived cryopreserved peripheral blood mononuclear cells (PBMCs) collected within one year prior to HIV acquisition from participants enrolled in a South African cohort (HIV Vaccine Trials Network [HVTN] 503; n = 35) and an East African cohort (Partners Pre-exposure Prophylaxis/Couples Observational Study [PP/COS]; n = 32). Th17 cell frequencies were quantified by flow cytometry. In HVTN 503, higher pre-HIV IL-17+ CD4+ T cell frequencies were inversely correlated with CD4/CD8 ratio measured both within 180 days (Spearman rank R = -0.42, p = 0.012) and beyond 180 days (R = -0.55, p = 0.001) after HIV infection, and were associated with faster CD4+ T cells decline (adjusted hazard ratio [aHR] = 3.5, 95% CI: 1.2-9.9, p = 0.020). In contrast, no significant association with CD4 decline was observed in the PP/COS cohort (HR = 1.2, 95% CI: 0.4-3.4, p = 0.795). Sex-stratified analyses in HVTN 503 indicated a more pronounced association between pre-HIV IL-17+ CD4+ T cells and faster CD4 decline in males than females. In analyses combining all cohorts, higher pre-HIV IL-17+ CD4+ T cell frequencies remained associated with faster CD4 decline, particularly among younger participants (HR = 3.5; 95% CI: 1.35-9.22, p = 0.010). Pre-HIV IL-17+ CD4+ T cell frequencies were not associated with peak or set-point viral load in either cohort. Together, these findings suggest that pre-HIV Th17 cells abundance may influence subsequent HIV disease progression independently of early viral replication. Author SummaryHIV infection leads to progressive damage of the immune system, but the rate at which this damage occurs varies widely between individuals. Understanding the factors that influence HIV disease progression is essential for improving prevention and treatment strategies. Previous studies have suggested that immune characteristics present before infection may shape disease outcomes after HIV acquisition. In this study, we examined whether the abundance of IL-17-producing CD4+ T cells, known as Th17 cells, measured prior to HIV acquisition, were associated with markers of disease progression after infection. We analyzed blood samples from individuals who were HIV-negative at the time of sampling and later acquired HIV during follow-up. We found that individuals with higher pre-infection levels of Th17 cells experienced faster immune decline after HIV infection, including more rapid loss of CD4+ T cells and lower CD4/CD8 ratios. These associations were observed independently of viral load and varied by cohort, age and sex. Our findings indicate that immune conditions present before HIV infection can influence subsequent disease progression and suggest that Th17 cells may serve as biomarkers to identify individuals at higher risk of rapid HIV-related immune damage.

immunology↗

bioRxiv2024

Targeting fatty acid synthase suppresses tumor development in NF2/CDKN2A-deficient malignant pleural mesothelioma

Malignant pleural mesothelioma (MPM) is an uncommon yet deadly cancer linked to asbestos exposure. The lack of effective early diagnosis and treatment leads to reduced life expectancy among patients with MPM. This study is aimed to identify a novel molecular target inhibitor to develop more effective therapeutics for MPM. Our drug screening assay showed that the fatty acid synthase (FASN) inhibitor cerulenin demonstrates strong and selective anti-proliferative properties against NF2/CDKN2A(p16)-deficient MPM cells, surpassing the effects of cisplatin or pemetrexed. FASN protein is frequently detected in NF2/p16-deficient MPM tumor-derived tissues (15/15, 100%), but rarely in NF2/p16-intact MPM tumors (8/25, 32%). Notably, cerulenin administration successfully reduced the growth of NF2/p16-deficient MPM tumors in xenografted mice. Cerulenin inhibits mitochondrial fission by targeting dynamin-related protein 1 (DRP1) in NF2/p16-deficient cells. Moreover, the disruption of the FASN gene leads to increased ubiquitination of DRP1. These findings suggest that FASN might play a role in the tumorigenesis of MPM cells through the regulation of mitochondrial dynamics. This research offers a novel perspective on the potential development of precision medicine for MPM.

cancer biology↗

bioRxiv2024

Sex differences in change-of-mind neuroeconomic decision-making is modulated by LINC00473 in medial prefrontal cortex

Changing ones mind involves re-appraisals between past-costs versus future-value and may be altered in psychopathology. Long intergenic non-coding RNA LINC00473 in medial prefrontal cortex (mPFC) can induce stress-resilience in a sex-dependent manner, but its role in cognition is unknown. We characterized decision-making behavior in male and female mice in the neuroeconomic paradigm Restaurant Row following virus-mediated expression of LINC00473 in mPFC. Mice foraged for food among varying temporal-costs and subjective-value while on a limited time-budget. Without affecting primary deliberative decisions, LINC00473 selectively influenced re-evaluative choices in a sex-dependent manner. This included changing how mice (i) cached value with the passage of time and (ii) weighed prior mistakes, which underlie the computational bases of sensitivity to sunk costs and regret. These findings suggest a common value function is shared between these neuroeconomic processes and reveal a bridge between molecular drivers of stress-resilience and psychological mechanisms underlying sex-specific proclivities in negative rumination.

neuroscience↗

bioRxiv2021

Expansion of tissue-resident CD8+ T cells and CD4+ Th17 cells in the nasal mucosa following mRNA COVID-19 vaccination

Vaccines against SARS-CoV-2 have shown high efficacy in clinical trials, yet a full immunologic characterization of these vaccines, particularly within the upper respiratory tract, remains lacking. We enumerated and phenotyped T cells in nasal mucosa and blood before and after vaccination with the Pfizer-BioNTech COVID-19 vaccine (n =21). Tissue-resident memory (Trm) CD8+ T cells expressing CD69+CD103+ expanded [~]12 days following the first and second doses, by 0.31 and 0.43 log10 cells per swab respectively (p=0.058 and p=0.009 in adjusted linear mixed models). CD69+CD103+CD8+ T cells in the blood decreased post-vaccination. Similar increases in nasal CD8+CD69+CD103-T cells were observed, particularly following the second dose. CD4+ Th17 cells were also increased in abundance following both doses. Following stimulation with SARS-CoV-2 spike peptides, CD8+ T cells increased expression of CD107a and CD154. These data suggest that nasal T cells may be induced and contribute to the protective immunity afforded by this vaccine.

immunology↗

bioRxiv2021

Endocervical regulatory T cells are associated with decreased genital inflammation and lower HIV target cell abundance

Regulatory T cells (Tregs) play important roles in tissue homeostasis, but few studies have investigated tissue Tregs in the context of genital inflammation, HIV target cell density, and vaginal microbiota in humans. In women from Nairobi (n=64), the proportion of CD4+ CD25+ CD127low Tregs in the endocervix correlated with those in blood (r=0.31, p=0.01), with a higher Treg frequency observed in the endocervix (median 3.8 vs 2.0%, p<0.0001). Most Tregs expressed FoxP3 in both compartments, and CTLA-4 expression was higher on endocervical Tregs compared to blood (median 50.8 vs 6.0%, p<0.0001). More than half (34/62, 55%) of participants displayed a non-Lactobacillus dominant vaginal microbiota, which was not associated with endocervical Tregs or CD4+ T cell abundance. In a multivariable linear regression, endocervical Treg proportions were inversely associated with the number of elevated pro-inflammatory cytokines (p=0.03). Inverse Treg associations were also observed for specific cytokines including IL-1{beta}, G-CSF, Eotaxin, IL-1RA, IL-8, and MIP-1 {beta}. Higher endocervical Treg proportions were associated with lower abundance of endocervical CD4+ T cells (0.30 log10 CD4+ T cells per log10 Treg, p=0.00028), with a similar trend for Th17 cells (p=0.09). Selectively increasing endocervical Tregs may represent a pathway to reduce genital tract inflammation in women.

immunology↗

bioRxiv2019

Blood-brain barrier dysfunction in aging induces hyper-activation of TGF-beta signaling and chronic yet reversible neural dysfunction

Aging involves a decline in neural function that contributes to cognitive impairment and disease. However, the mechanisms underlying the transition from a young-and-healthy to aged-and-dysfunctional brain are not well understood. Here, we report breakdown of the vascular blood-brain barrier (BBB) in aging humans and rodents, which begins as early as middle age and progresses to the end of the lifespan. Gain-of-function and loss-of-function manipulations show that this BBB dysfunction triggers hyperactivation of transforming growth factor {beta} (TGF{beta}) signaling in astrocytes, which is necessary and sufficient to cause neural dysfunction and age-related pathology. Specifically, infusion of the serum protein albumin into the young brain (mimicking BBB leakiness) induced astrocytic TGF{beta} signaling and an aged brain phenotype including aberrant electrocorticographic activity, vulnerability to seizures, and cognitive impairment. Furthermore, conditional genetic knockdown of astrocytic TGF{beta} receptors, or pharmacological inhibition of TGF{beta} signaling, reversed these symptomatic outcomes in aged mice. Finally, we found that this same signaling pathway is activated in aging human subjects with BBB dysfunction. Our study identifies dysfunction in the neurovascular unit as one of the earliest triggers of neurological aging, and demonstrates that the aging brain may retain considerable latent capacity which can be revitalized by therapeutic inhibition of TGF{beta} signaling.

neuroscience↗

bioRxiv2018

Maternal immunity and antibodies to dengue promote Zika virus-induced microcephaly in fetuses

Zika virus (ZIKV), a recently emerged flaviviral pathogen, has been linked to microcephaly in neonates1. Yet, it is not understood why some fetuses develop severe microcephaly due to maternal ZIKV infection while others do not. The risk for ZIKV-induced microcephaly is greatest during the first trimester of pregnancy in humans2,3, yet this alone cannot account for the varied presentation of microcephaly observed. Given the antigenic similarity between ZIKV and closely related dengue virus (DENV)4, combined with the substantial immunity to DENV in ZIKV target populations in recent outbreaks, we hypothesized that maternal antibodies against DENV could promote ZIKV-induced microcephaly. Here, using immune-competent mice, we show that maternal to fetal transmission of ZIKV occurs, leading to fetal infection and disproportionate microcephaly. DENV-specific antibodies in pregnant female mice enhance vertical transmission of infection and result in a severe microcephaly like-syndrome during ZIKV infection. Furthermore, fetal infection was promoted by the neonatal Fc receptor (FcRN). Our results identify a novel immune-mediated mechanism of vertical transmission of viral infection and raise caution since ZIKV epidemic regions are also endemic to DENV.

immunology↗