Schematic overview of phospholipase-mediated phospholipid hydrolysis and its impact on triacylglycerol (TAG) stability during rice bran storage.

Schematic overview of the two-stage screening approach used to identify NK cell fitness genes. (A) CRISPRa mechanism, showing dCas9-VP64-mediated upregulation of target genes. (B) Whole-genome CRISPRa screening in HER2-CAR-NK92 cells transduced with a CRISPR sgRNA library and transferred into mice bearing HT29 tumours, followed by tumour collection and next-generation sequencing (NGS). (C) Barcoded ORF mini-screen in primary peripheral blood NK (PBNK) cells transduced with HER2-CAR and an ORF library, transferred into HT29 tumour-bearing mice, with subsequent tumour collection and NGS analysis.

Spinal cord injury is a disease with no complete cure. It typically results in loss of motor and sensory functions below the level of the lesion, leading to significant physical and psychological disorders. After spinal cord injury, the microenvironmental balance at the site of injury is disrupted, creating complex conditions that are not conducive to nerve regeneration and recovery of spinal cord function, such as hemorrhage and ischemia, glial scar formation, and nerve demyelination. As our knowledge of the spinal cord microenvironment has expanded, researchers have determined that therapeutic strategies that modulate the microenvironment represent a significant and efficacious avenue of investigation. This review summarizes the characteristics of microenvironmental changes at various stages after spinal cord injury. Additionally, it discusses novel strategies developed recently based on regulating the microenvironment after spinal cord injury to promote recovery. The investigation of a long-acting, targeted, and multitemporal combination therapy strategy to repair spinal cord injuries shows promise in terms of its developmental potential. A schematic overview of changes of microenvironment components after SCI and strategies for reconstructing microenvironment. NISCI Non-traumatic spinal cord injury, SCI Spinal cord injuryTSCI Traumatic spinal cord injury. Created with biorender.com

ABSTRACT Schematic representation and experimental overview of electrocoagulation (EC) treatment of distillery spentwash using aluminum electrodes (Al–Al plain, Al punched, and Al anodized). The setup includes a DC power supply connected to electrodes immersed in wastewater, showing the EC reactor during operation. Insets display electrode types, treated samples with visible color reduction, and sludge formation. Key operating parameters highlighted include voltage, electrode distance, electrolysis time, and anodization thickness. Electrochemical reactions at anode and cathode are illustrated. The graphical abstract emphasizes process optimization leading to high color and COD removal efficiency, with superior performance observed for anodized aluminum electrodes. Electrocoagulation (EC) is a wastewater treatment option, emphasizing its environmental friendliness, dense footprint, quick setup, and versatility. It looks at the key EC operational parameters and how they relate to conventional chemical coagulation, which are essential to comprehending the mechanism of pollutant removal. The study emphasizes the necessity of additional investigation to construct models for industrial-scale application and optimize process parameters. The distillery spentwash underwent a diagnostic description using standard analytical techniques, with treatment outcomes analyzed in terms of chemical oxygen demand (COD) and color removal efficiency. Various operational parameters, viz. voltage, electrode distance, electrolysis time, and anodization thickness, were investigated, and optimization was carried out using the response surface method. pH and stirring speed were maintained at constant levels of 7 and 500 rpm, respectively. The highest removal efficiencies were achieved under optimal conditions: 150-min electrolysis time, 25 V, electrode distance of 2 cm, and anodization thickness of 5 μm. Under these optimized conditions, the responses were estimated as follows 93.025% (color) and 89.896% (COD) removal efficiency in the Al-anodized electrode. Comparison among the three electrodes, namely Al -Al, Al punched, and Al anodized, indicated that the maximum pollutants removal was observed with the Al-anodized electrode.

Abstract Influenza remains a significant and recurrent public health burden in temperate regions. Meteorological factors such as temperature, humidity, and rainfall are recognised as associated with influenza transmission patterns, exhibiting complex, nonlinear, temporally lagged, and spatially heterogeneous effects. This study employed a Spatial Bayesian Distributed Lag Non-Linear Model (SB-DLNM) to investigate the associations between meteorological factors and influenza incidence across 15 Local Health Districts, New South Wales, Australiathe short-term meteorological variables on influenza incidence across multiple Local Health Districts within New South Wales, Australia. The method incorporates (i) cross-basis functions to model delayed and non-linear meteorological impacts; (ii) a comparative analysis of case-crossover and time-series designs to distinguish monthly-lag associations from broader temporal trends; and (iii) spatial partial pooling to enhance the stability of estimates, particularly in data-sparse regions. Temperature demonstrated the strongest associations with influenza risk (Relative Risk (RR) range: 1.16–3.90), with elevated risks observed predominantly at cold temperature extremes. While exposure-response curves suggest minimum risk at moderate temperatures ( $$18-22^{\circ }\hbox {C}$$ ), the available data primarily capture cold-related effects; warm-temperature associations remain uncertain due to limited extreme heat observations. Humidity showed marked spatial heterogeneity with variable effects across districts (RR range: 1.32–5.69), while rainfall demonstrated minimal associations (RR typically 1.03–1.42). Exceedance probabilities for RR>1 were moderate across all variables, ranging from 17.5% to 58%, with no extreme hot spots observed. Partial pooling effectively stabilised estimates in sparse datasets, improving the robustness of spatial risk assessment. These findings underscore the importance of cold temperatures in influenza transmission patterns, providing a robust framework for public health surveillance. Our use of monthly aggregated data captures population-level seasonal associations rather than acute exposure-infection dynamics, which represents an important interpretive constraint.Among the meteorological variables, temperature emerged as the strongest predictor of influenza risk, with peak incidence observed within moderate temperature ranges ( $$20-22^{\circ }\hbox {C}$$ ) Graphical Abstract A schematic overview of the workflow from merging meteorological and influenza data, evaluating four modelling approaches (with Model 3 highlighted as the best), to generating spatial risk maps and relative risk estimates for influenza in NSW.

CPAK oversimplifies the complex 3D anatomy of the bony knee: Role of 3D CT for improved analysis - a schematic overview.

Schematic overview of LLM integration in porous materials research, including NLP-based text mining, LLM adaptation, and autonomous laboratory systems.

Abstract On the occasion of the centenary of our friend and colleague Zoltán Király—one of the most influential plant pathologists of the 20th century—we revisit a question inspired by his pioneering work at the Plant Protection Institute of the Hungarian Academy of Sciences: how is the hypersensitive response (HR), a cornerstone of plant immunity and one of Király's, scientific passions, mechanistically linked to one of the most current topics in plant pathology — the role of small RNAs (sRNAs) in plant defence against microbial pathogens? For the past decade, our laboratory at the Justus Liebig Universität Giessen and more recently at the CNRS Strasbourg has investigated RNA-mediated mechanisms underlying plant resistance to pathogenic microorganisms and pests, including aphids, fungi and viruses (Liu et al., 2020). This research coincides with the emergence of the first RNA-based bioprotectants, particularly double-stranded RNA (dsRNA), now commercially available for controlling insect pests (Wenninger et al., 2025). Yet, despite these advances, our understanding of how sRNAs directly influence plant immune responses, including HR, remains limited. In this short letter we give a schematic overview on the current knowledge on the topic.

Preeclampsia is a severe pregnancy complication marked by impaired trophoblast function and abnormal placental development, leading to significant maternal and fetal morbidity. FK506-binding protein-like (FKBPL) has been identified as a potential biomarker as it is significantly downregulated in early pregnancy stages of women who progress to develop preeclampsia. However, editing the Fkbpl gene in trophoblast cells to create a model of preeclampsia using clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (Cas9) technology is challenging due to inefficient delivery, leading to low editing efficiency and reduced cell viability. To address these challenges, we developed a cost-effective and minimally invasive mechanoporation system using micro-engineered filters to deliver CRISPR/Cas9 plasmid DNA (pDNA) targeting the Fkbpl gene into trophoblast cells. This approach successfully generated cell lines with a 38% knockout (K/O) of Fkbpl expression, significantly reducing cell migration (wildtype (WT): 28.77% ± 4.7 vs. 38% K/O: 4.95% ± 0.8, wound closure, **p < 0.01) and proliferation (WT: 1.26 ± 0.06 vs. 38% K/O: 0.81 ± 0.01, ****p < 0.0001). Lower Fkbpl-K/O efficiency of 17% showed a similar reduction in cell proliferation as the 38% K/O clone. Although a full Fkbpl-K/O in the ACH-3P first-trimester trophoblast cell line was not achieved, the partial K/O provided valuable insights into Fkbpl's role in trophoblast function relevant to preeclampsia pathogenesis. Moreover, treatment with mesenchymal stem cell (MSC)-derived small extracellular vesicles (sEVs) or MSC-sEVs did not restore migratory capacity in Fkbpl-deficient cells (p = 0.14). MSC-sEVs increased proliferation in WT ACH-3P cells at 1 µg (p < 0.05) and 2 µg (p < 0.01) doses, however, were not effective in either 17% or 38% Fkbpl-K/O clones, suggesting that FKBPL is an important mechanism of MSC-sEV-mediated therapeutic effect in trophoblasts in the context of preeclampsia. This study advances gene-editing techniques in placental biology and proposes new therapeutic strategies and mechanisms for pregnancy-related complications.A Schematic overview of CRISPR/Cas9 plasmid delivery using microfiltroporation compared to gold standard electroporation and lipofection technologies in trophoblast cells. A CRISPR/Cas9 plasmid targeting Fkbpl was delivered to the first trimester trophoblast cell line, ACH-3P. Cells were sorted according to green fluorescence protein (GFP) expression, expanded and assessed for changes in cell function using proliferation and migration assays. B Actual images of the isopore silicon nitride (SiN) microfilters used in this study and diagram of cell membrane dynamics in response to mechanoporation. This figure was created with Biorender.com. CRISPR clustered regularly interspaced short palindromic repeats, EP electroporation, MFP microfiltroporation.

Background Tactical combat casualty care (TCCC) requires a massive effort in initial training, keeping personnel current, and ensuring those skills can be applied correctly when necessary. Unlike medical personnel, tactical personnel do not have access to civilian patient populations to ensure clinical skills remain current. There are still no evidence-based models of skill acquisition and skill decay, no understanding of mediating or mitigating factors, and more importantly no mitigation strategies in (military) medical tasks (e.g. 1 2 ). This presentation describes a methodology to quantify performance in TCCC, specifically understanding and quantifying skill acquisition and skill decay. We also present initial results showing that the currently applied retention intervals (i.e. frequency of refresher training) severely overestimate skill retention. Method The methodology we developed to quantitatively assess skill acquisition and retention comprises a skill-lab training with two objectives (figure 1). First, quantifying the technical performance by analysing the outcome and the details of the performance of the medical skill, respectively through live observation by technical observers (macro analysis) and through retrospective video analysis in ‘The Observer XT’ (Version 16, Noldus Information Technology BV, NL) by a medical expert (micro analysis). Second, quantifying the allostatic load by analysing facial expressions as well as performing a voice stress analysis. Abstract A13 Figure 1 Schematic overview of the methodology and its constituent components Recordings, both audio and video, are made using eight high-quality synchronized cameras and two microphones, integrated through the Viso software (Noldus Information Technology BV, NL). The automated emotion and action unit coding software, FaceReader (Version 10, Noldus Information Technology BV, NL) is used to analyse facial expressions. In addition, our model of Voice Stress Analysis 3 is applied to analyse the voice recordings. This combination of assessments is applied as from initial training, and subsequently in repeated measures design with intervals ranging from one month to one year. Results Initial results show that, even right after training, performance is far from consolidated. We measured the outcome lower than 80% success on certain skills, even for basic ones like tourniquet application (56% execution without critical mistakes). Furthermore, the allostatic load analysis shows we are still in the ‘teaching’ phase and not in the ‘training’ phase, that skills are not automated and still require a high amount of attentional engagement. As a side result, we also showed that the usual quantification of performance through observation by instructors overestimates performance, through conscious and unconscious biases. We show that the first three months after initial training are crucial for consolidation, and that the usual approach of yearly refreshers is not adequate. Conclusion The novel content of this project is to integrate what are usually termed ‘hard’ and ‘soft’ skills. The evaluation methodology allows for a detailed skill acquisition and retention analysis, by coupling the macro-outcome to micro-recordings of performance, coupled to facial expression and voice recordings that offer a unique insight into providers’ performance. Even preliminary results show that our current approach to both initial training and refreshers needs updating. Acknowledgment Funding from the Royal Higher Institute for Defence of the Belgian Defence under grant HFM/19–08 is acknowledged. The authors declare that there are no conflicts of interest related to this study.

Molecular investigation of the progenitors, origin and domestication patterns of diploid Chinese old garden roses.

Because the disease's heterogeneity is ignored, the current diagnosis of myocarditis with advanced heart failure is imprecise, and there are no established criteria for subtyping this type of myocarditis. We analyzed data from 83 consecutive patients with aggressive myocarditis using a deep learning method to categorize them into three prognostically relevant phenogroups (PGs) based on myocardial whole-slide images: PG1, characterized by structural damage; PG2, dominated by autoimmune response; and PG3, driven by infections. Whole-exome sequencing of all patients revealed a significant concentration of mutations in myocardial structure-related genes in PG1, with the titin gene ( TTN) being the most frequently mutated. In contrast, mutations in immune-related genes were more prevalent in PG2 and PG3. RNA sequencing revealed unique molecular signatures: PG1 was associated with apoptosis, fibrosis, and the activation of abnormal metabolic pathways, whereas PG2 and PG3 were linked to cell damage and the activation of divergent immune pathways. Immunohistochemical staining suggested that PG1 and PG2 were characterized by T cell infiltration while PG3 was characterized by macrophage infiltration. In addition, the interleukin-6 signal transducer (IL6ST) was identified as a novel prognostic biomarker for myocarditis. A plasma IL6ST content ≥ 332.45 ng/ml was found to be associated with poor survival from recurrence symptom [hazard ratio (HR) 22.8, 95% confidence interval (CI) 2.3 to 227.2, Log-rank p value < 0.0001]. Finally, we used a decision tree model incorporating four clinical parameters to further validate the effectiveness of these features. This study identified three distinct PGs of aggressive myocarditis with significant differences in pathological manifestations, immunophenotyping, survival outcomes, clinical presentations, and molecular profiles. This approach improves patient selection for novel interventions and thus enables precision medicine. Schematic overview of the study. A myocarditis transplantation cohort was established and a digital pathology platform for myocarditis tissue was developed. An AI model was developed from pathological images to generate prognostic pathologic maps. The cohort was categorized into three subtypes, which were further analyzed based on clinical characteristics and genomics. A decision tree model was then designed to infer the subtype of each patient, providing a clinically relevant method for classification.

BackgroundExtragonadal follicle-stimulating hormone (FSH) receptor (FSHR) expression in various cancers and their endothelial vessel cells has highlighted novel opportunities for targeted FSHR therapy.MethodsWe investigated the specificity/cytotoxicity of Phor21 fusion lytic peptide, conjugated to 12 different FSHβ-chain fragments to ablate FSHR-expressing cancer cells in vitro and in vivo. Additionally, the use of the gonadotropin-releasing hormone (GnRH) antagonist cetrorelix (CTX) alone or with the Phor21-FSHβ33-53 C/S conjugate for anticancer therapy was analyzed.ResultsPhor21 linked to the FSHβ33–53 fragment with cysteine (Cys) replaced by serine (Ser) (Phor21-FSHβ33-53 C/S) demonstrated the highest specific cytotoxicity towards FSHR possessing cancer cells vs. other compounds. Recombinant human FSH treatment significantly decreased the cytotoxicity of Phor21-FSHβ33-53 C/S conjugate in FSHR-positive cancer cells. Phor21-FSHβ33-53 C/S (further addressed as Phor21-FSHβ) treatment in vivo significantly inhibited the growth of FSHR-positive cancer xenografts, resulting in necrosis. The efficacy of the Phor21-FSHβ was enhanced by co-treatment with the gonadotropin-releasing hormone (GnRH) antagonist cetrorelix (CTX). CTX alone exerted pro-apoptotic effects. CTX significantly inhibited the growth of prostate cancer LNCaP cell xenografts. Although FSHR-positive tumor vessel endothelial cells were previously reported in LNCaP cell xenografts, we were unable to reproduce FSHR expression. Consequently, Phor21-FSHβ had no effect on tumor destruction because of the lack of Fshr transcripts in the endothelium of these tumor vessel cells.ConclusionThis novel functional evidence shows that any cancer cell expressing FSHR can be specifically targeted and destroyed by the conjugated lytic peptide Phor21-FSHβ33–53 (Phor21-FSHβ). FSHR expression was not detected in the tumor vessel endothelial cells, which needs further re-evaluation.Graphical Schematic overview of the Phor21-FSHb33-53C/S (Phor21-FSHβ) conjugate or CTX specifically targeted to kill FSHR-positive cancer cells. (Figure created using BioRender.com). Phor21-FSHb33-53C/S conjugate, Phor21 lytic backbone conjugated with a native or modified fragment of the FSHb subunit (FSHb33-53); CTX, GnRH antagonist cetrorelix

Pleural mesothelioma (PM) is a rare disease, which is going to be a global medical concern in the 21st century, because of its aggressiveness, late diagnosis, and insufficient therapies. This review seeks to enhance the comprehension of medical professionals regarding the risk factors and environmental influences that contribute to the development of the disease, as well as its underlying mechanisms. In addition, we aim to provide a schematic yet thorough overview of diagnostic techniques in PM, emphasizing the significance of the immunohistochemical markers BAP1 and MTAP, with the latter serving as an almost ideal surrogate for the gold-standard diagnostic approach, FISH p16/CDKN2A deletion. The scientific world is grappling with BAP1, MTAP, and the tumour inflammatory microenvironment, because they are the key for personalized treatments and palliative care in this disease. Considering that the survival rate for patients with PM seldom surpasses five years, every moment is significant. Therefore, our article also highlights recent advancements in clinical assessments related to prognostic scoring and treatment options. PM is a complex disease, with gradual progression over decades, which requires further investigation covering the prevention, mutations, diagnosis and treatment.

The increasing demand for sustainable alternatives to fossil-based materials has driven research towards biofabrication approaches. Textile and fashion industry is one of the most polluting industrial sectors in the world, responsible for high greenhouse gas emissions and global wastewater. For that reason, the fashion industry is facing growing pressure to reduce its environmental impact. Among the major environmental issues associated with this sector are the unsustainable cultivation of fibres, the extensive use of non-renewable and non-biodegradable materials and highly polluting production processes. One of these non-eco-friendly processes is leather tanning, which consumes large amounts of water and energy while potentially releasing heavy metals and toxic compounds into the environment. Conversely, plastic-based leathers, have a lower carbon footprint than animal leather during their production, but they are dependent on fossil resources and have negative environmental effects (microplastic accumulation). In this contribution a review on possible sustainable alternatives to synthetic leather is presented, focusing on innovative mycelium-based materials. Particular attention is given to production methods involving liquid-state surface fermentation, highlighting the potential for reducing environmental impact while maintaining desirable material properties. Filamentous fungi and their potential to create leather-like biomaterials through controlled fermentation processes are critically discussed. Important parameters like fungi species selection, nutrient composition, growth conditions and treatment techniques are analysed. A schematic overview of the process is provided in the figure. Moreover, different types of treatments that could enhance mechanical performance, durability and water resistance are explored. Comparisons with real and synthetic leather are analysed, highlighting the advantages that the mycelium-leather has in respect to biodegradability and energy efficiency. Current challenges such as scalability, production cost and the need for standardization are critically considered, as they still limit widespread industrial adoption. Ultimately, current advancements in mycelium biotechnology, bioengineering strategies and material optimization are explored, highlighting the potential of mycelium-based materials as a sustainable alternative to conventional leather.

BackgroundCrosstalk between pancreatic cancer cells and tumor-associated macrophages (TAMs) is a critical driver of malignant progression, and plays an important role in the low response rate to immunotherapy in patients with for pancreatic cancer. Although it is known that cancer cells induce TAM infiltration and M2 polarization, the underlying mechanisms remain elusive. Herein, we identified matrix metalloproteinase 28 (MMP28), a highly expressed protein, as a key regulator of this process.MethodsImmunohistochemical staining and qRT-PCR were used to validate MMP28 as a potential marker for the prognosis of patients with pancreatic cancer. We evaluated the tumor-promoting effect of MMP28 in vitro with CCK-8, Transwell, and EdU assay and Western blotting and explored the potential mechanism of MMP28-induced M2 polarization of TAMs with a coculture system, immunofluorescence staining and flow cytometry. A subcutaneous graft tumor model was constructed to assess the tumor-promoting effect of MMP28 and its ability to induce M2 TAM infiltration.ResultsThe relevant results of this study revealed a strong correlation between MMP28 expression and TAM infiltration, with a predominance of M2-polarized TAMs in pancreatic cancer tissues. Mechanistic investigations demonstrated that MMP28 promotes the secretion of multiple cytokines, including IL-8 and VEGFA through the activation of the MAPK/JNK signaling pathway. These cytokines act as potent chemoattractants and polarizing factors for TAMs. Additionally, we discovered an interaction between MMP28 and ANXA2, which contributes to the regulation of TAM recruitment and polarization. In vivo studies confirmed the critical role of MMP28 in tumor growth and TAM infiltration. Depletion of macrophages, inhibition of JNK, or neutralization of IL-8 and VEGFA significantly suppressed tumor progression. Transcriptomic analysis suggested that IL-8 and VEGFA induce M2 TAM polarization by modulating TAM amino acid metabolism.ConclusionsCollectively, our findings elucidate a novel mechanism by which pancreatic cancer cells manipulate the tumor microenvironment through MMP28-dependent cytokine secretion, promoting TAM infiltration and M2 polarization. These results highlight MMP28 as a promising therapeutic target for pancreatic cancer.Graphical Schematic overview of the mechanisms by which MMP28 promotes the migration and polarization of TAMs. High levels of MMP28 promote the secretion of IL-8 and VEGFA by cancer cells by mediating the phosphorylation of the MAPK/JNK signalling pathway and then recruiting TAMs. IL-8 and VEGFA subsequently induce amino acid metabolism alterations in TAMs by binding to relevant receptors on TAMs, which ultimately promote the polarization of TAMs to the M2 phenotype. In addition, ANXA2 increases MMP28-mediated M2 TAM infiltration by interacting with MMP28.

A comprehensive review on integrated photo rechargeable batteries- supercapacitors, and their techno-economic feasibility

This image illustrates the effects of different APOE isoforms (ApoE-ε3 and ApoE-ε4) on blood-brain barrier (BBB) integrity, focusing on the molecular interactions between astrocytes and endothelial cells. This figure emphasizes the detrimental effects of ApoE-ε4 on BBB integrity via fibronectin accumulation and altered signaling pathways. The top section provides a schematic overview of the blood-brain barrier, highlighting astrocytes, endothelial cells, and their interface. The left panel represents the ApoE-ε3 condition: Normal fibronectin (FN1) levels support healthy interactions between astrocytes and endothelial cells. Growth factors, including VEGFA, HBEGF, and IGF1, maintain BBB integrity through their respective receptors (VEGFR and EGFR). Green arrows indicate activation of these signaling pathways. The right panel depicts the ApoE-ε4 condition: Elevated fibronectin (FN1) disrupts astrocyte-endothelium interactions. FN1 binds integrins and activates focal adhesion kinase (FAK), inhibiting VEGFA, which is required for endothelial HBEGF that in turn activates IGF1 signaling. Red symbols indicate inhibition of HBEGF, VEGFA, and IGF1 pathways, leading to BBB dysfunction. APOE-ε4 drives fibronectin deposition in Alzheimer's, disrupting astrocyte-endothelia interactions. APOE-ε4 and fibronectin co-localize, forming aggregates at blood-brain barrier (BBB). Fibronectin alters the signaling between VEGF, IGF1, and HBEGF impairing BBB function. Reducing fibronectin restores BBB integrity and offsets APOE-ε4 pathology.

Since the establishment of the iSLK-BAC16 cell culture system, iSLK-BAC16 cells and their derivatives have been widely used for Kaposi's sarcoma-associated herpesvirus (KSHV) studies. However, iSLK-BAC16 cells can be difficult to work with, in part due to the lack of standardized protocols and conflicting troubleshooting suggestions. Here, we describe the protocol for general iSLK-BAC16 cell culture and reactivation, which induces lytic KSHV replication and virion production. This protocol achieves robust levels of KSHV reactivation in our hands and can be readily used for studies of KSHV lytic infection mechanisms. Key features • This protocol describes methods for culturing and antibiotically selecting iSLK-BAC16 cells for robust KSHV reactivation. • Use of flow cytometry to quantify KSHV reactivation rates. • Innovative use of automated plate readers to assess KSHV reactivation. Graphical overview Schematic overview of the procedures used for general iSLK-BAC16 cell culture and Kaposi's sarcoma-associated herpesvirus (KSHV) reactivation of iSLK-BAC16 cells. A typical timeline of iSLK-BAC16 cell culture, antibiotic selection, KSHV reactivation, flow cytometry quantification, and plate reader assessment of KSHV lytic replication. Corresponding media requirements are denoted under the respective procedures. iSLK-BAC16 = doxycycline-inducible endothelial cells harboring the KSHV genome on an artificial bacterial chromosome; Dox = doxycycline; NaBu = sodium butyrate.

Schematic overview of biomass-based aerogels.