L-histidine attenuates NEFA-induced inflammatory responses by suppressing Gab2 expression.

Non-esterified fatty acids (NEFAs), key to energy metabolism, may become pathogenic at elevated levels, potentially eliciting immune reactions. Our laboratory's findings of reduced L-histidine in ketotic states, induced by heightened NEFA concentrations, suggest an interrelation with NEFA metabolism. This observation necessitates further investigation into the mitigating role of L-histidine on the deleterious effects of NEFAs. Our study unveiled that elevated NEFA concentrations hinder the proliferation of Bovine Mammary Epithelial Cells (BMECs) and provoke inflammation in a dose-responsive manner. Delving into L-histidine's influence on BMECs, RNA sequencing revealed 2124 genes differentially expressed between control and L-histidine-treated cells, with notable enrichment in pathways linked to proliferation and immunity, such as cell cycle and TNF signaling pathways. Further analysis showed that L-histidine treatment positively correlated with an increase in EdU-555-positive cell rate and significantly suppressed IL-6 and IL-8 levels (p < 0.05) compared to controls. Crucially, concurrent treatment with high NEFA and L-histidine normalized the number of EdU-555-positive cells and cytokine expression to control levels. Investigating the underlying mechanisms, Gab2 (Grb2-associated binder 2) emerged as a central player; L-histidine notably reduced Gab2 expression, while NEFA had the opposite effect (p < 0.05). Gab2 overexpression escalated nitric oxide (NO) production and IL6 and IL8 expression. However, L-histidine addition to Gab2-overexpressing cells resulted in NO concentrations indistinguishable from controls. Our findings collectively indicate that L-histidine can counteract NEFA-induced inflammation in BMECs by inhibiting Gab2 expression, highlighting its therapeutic potential against NEFA-related metabolic disturbances.

Comparative Metabolomic Profiling of L-Histidine and NEFA Treatments in Bovine Mammary Epithelial Cells.

Non-esterified fatty acids (NEFAs) are pivotal in energy metabolism, yet high concentrations can lead to ketosis, a common metabolic disorder in cattle. Our laboratory observed lower levels of L-histidine in cattle suffering from ketosis, indicating a potential interaction between L-histidine and NEFA metabolism. This relationship prompted us to investigate the metabolomic alterations in bovine mammary epithelial cells (BMECs) induced by elevated NEFA levels and to explore L-histidine's potential mitigating effects. Our untargeted metabolomic analysis revealed 893 and 160 metabolite changes in positive and negative models, respectively, with VIP scores greater than 1 and p-values below 0.05. Notable metabolites like 9,10-epoxy-12-octadecenoic acid were upregulated, while 9-Ethylguanine was downregulated. A pathway analysis suggested disruptions in fatty acid and steroid biosynthesis pathways. Furthermore, L-histidine treatment altered 61 metabolites in the positive model and 34 in the negative model, with implications for similar pathways affected by NEFA. Overlaying differential metabolites from both conditions uncovered a potential key mediator, 1-Linoleoylglycerophosphocholine, which was regulated in opposite directions by NEFA and L-histidine. Our study uncovered that both NEFA L- and histidine metabolomics analyses pinpoint similar lipid biosynthesis pathways, with 1-Linoleoylglycerophosphocholine emerging as a potential key metabolite mediating their interaction, a discovery that may offer insights for therapeutic strategies in metabolic diseases.

Life cycle assessment of carbon footprint in dual-phase automotive strip steel production.

As the demand for automotive materials grows more stringent in environmental considerations, it becomes imperative to conduct thorough environmental impact assessments of dual-phase automotive strip steel (DP steel). However, the absence of detailed and comparable studies has left the carbon footprint of DP steel and its sources largely unknown. This study addresses this gap by establishing a cradle-to-gate life cycle model for DP steel, encompassing on-site production, energy systems, and upstream processes. The analysis identifies and scrutinizes key factors influencing the carbon footprint, with a focus on upstream mining, transportation, and on-site production processes. The results indicate that the carbon footprint of DP steel is 2.721 kgCO2-eq/kgDP, with on-site processes contributing significantly at 88.1%. Sensitivity analysis is employed to assess the impact of changes in resource structure, on-site energy, CO2 emission factors, and byproduct recovery on the carbon footprint. Proposals for mitigating carbon emissions in DP steel production include enhancing process gas recovery, transitioning to cleaner energy sources, and reducing the hot metal-to-steel ratio. These findings offer valuable insights for steering steel production towards environmentally sustainable practices.

Design and experiment of Panax notoginseng root orientation transplanting device based on YOLOv5s.

Consistent root orientation is one of the important requirements of Panax notoginseng transplanting agronomy. In this paper, a Panax notoginseng orientation transplanting method based on machine vision technology and negative pressure adsorption principle was proposed. With the cut-main root of Panax notoginseng roots as the detection object, the YOLOv5s was used to establish a root feature detection model. A Panax notoginseng root orientation transplanting device was designed. The orientation control system identifies the root posture according to the detection results and controls the orientation actuator to adjust the root posture. The detection results show that the precision rate of the model was 94.2%, the recall rate was 92.0%, and the average detection precision was 94.9%. The Box-Behnken experiments were performed to investigate the effects of suction plate rotation speed, servo rotation speed and the angle between the camera and the orientation actuator(ACOA) on the orientation qualification rate and root drop rate. Response surface method and objective optimisation algorithm were used to analyse the experimental results. The optimal working parameters were suction plate rotation speed of 5.73 r/min, servo rotation speed of 0.86 r/s and ACOA of 35°. Under this condition, the orientation qualification rate and root drop rate of the actual experiment were 89.87% and 6.57%, respectively, which met the requirements of orientation transplanting for Panax notoginseng roots. The research method of this paper is helpful to solve the problem of orientation transplanting of other root crops.

Neonatal lupus erythematosus as a rare trigger of gastrointestinal involvement in neonates.

Cutaneous and cardiac involvement in neonatal lupus erythematosus (NLE) has been extensively studied; however, gastrointestinal system involvement (GSI) remains unexplored. This study aimed to investigate the clinical features of GSI in patients with NLE with a particular focus on feeding intolerance (FI) and diarrhea. We conducted a retrospective analysis of the clinical data of patients diagnosed with NLE at the Children's Hospital of Soochow University between 2011 and 2022. In this study, of 39 patients diagnosed with NLE, 27 presented with GSI. 9 patients who presented with FI or diarrhea as the primary manifestation were positive for anti-SSA antibody, and 5 were dual positive for anti-SSA and anti-SSB antibodies. Among the mothers of the NLE patients with GSI, 18 had systemic lupus erythematosus, 3 had Sjogren's syndrome, 2 had mixed connective tissue disease, and one each had autoantibody abnormalities and photosensitivity symptoms; 4 mothers denied having any autoimmune disease. In this study, 69.23% of patients with NLE exhibited GSI, which was linked to hypocomplementemia and anti-SSA antibodies. Thus, clinicians should remain vigilant for NLE in neonates, particularly when accompanied with rash and other organ dysfunction and when the high-risk factors of FI and diarrhea have been excluded.

Decomposition of the site-level energy consumption and carbon dioxide emissions of the iron and steel industry.

Identifying the key factors influencing energy consumption and CO2 emissions is necessary for developing effective energy conservation and emission mitigation policies. Previous studies have focused mainly on decomposing changes in energy consumption and CO2 emissions at the national, regional, or sectoral levels, while the perspective of site-level decomposition has been neglected. To narrow this gap in research, a site-level decomposition of energy- and carbon-intensive iron and steel sites is discussed. In this work, the logarithmic mean Divisia index (LMDI) method is used to decompose the changes in the energy consumption and CO2 emissions of iron and steel sites. The results show that the production scale significantly contributes to the increase in both energy consumption and CO2 emissions, with cumulative contributions of 229.63 and 255.36%, respectively. Energy recovery and credit emissions are two key factors decreasing site-level energy consumption and CO2 emissions, with cumulative contributions to the changes in energy consumption and CO2 emissions of -158.30 and -160.45%, respectively. A decrease in energy, flux, and carbon-containing material consumption per ton of steel promotes direct emission reduction, and purchased electricity savings greatly contribute to indirect emission reduction. In addition, site products and byproducts promote an increase in credit emissions and ultimately inhibit an increase in the total CO2 emissions of iron and steel sites.

The TTN p. Tyr4418Ter mutation causes cardiomyopathy in human and mice.

OBJECTIVE: To generate a mouse model carrying TTNtv Y4370* simulating the newly discovered human heterozygous nonsense TTNtv c.13254T>G (p.Tyr4418Ter) to supplement and improve the functional evidence of pathogenic mutation TTNtv c.13254T>G on the pathogenic type of dilated cardiomyopathy. METHODS: We generated 4 mice carrying TTNtv p. Y4370* through CRISPR/Cas-mediated genome engineering. Monthly serological detection, bimonthly echocardiography, and histology evaluation were carried out to observe and compare alterations of cardiac structure and function between 4 TTN+/- mice and 4 wild-type (WT) mice. RESULTS: For the two-month-old TTN+/- mice, serum glutamic-oxalacetic transaminase (AST), lactic dehydrogenase (LDH), and creatine kinase (CK) were significantly increased, the diastolic Left Ventricular Systolic Anterior Wall (LVAW), and the LV mass markedly rose, with the left ventricular volume displaying an increasing trend and Ejection Fraction (EF) and Fractional Shortening (FS) showing a decreasing trend. Besides, the histological evaluation showed that cardiac fibrosis level and positive rate of cardiac mast cell of TTN+/- mice were obviously increased compared with WT mice. CONCLUSIONS: TTNtv Y4370* could lead to cardiac structure and function alterations in mice, supplementing the evidence of TTNtv c.13254T>G pathogenicity in human.

miR-425-5p Regulates Proliferation of Bovine Mammary Epithelial Cells by Targeting TOB2.

In recent years, rising temperatures have caused heat stress (HS), which has had a significant impact on livestock production and growth, presenting considerable challenges to the agricultural industry. Research has shown that miR-425-5p regulates cellular proliferation in organisms. However, the specific role of miR-425-5p in bovine mammary epithelial cells (BMECs) remains to be determined. The aim of this study was to investigate the potential of miR-425-5p in alleviating the HS-induced proliferation stagnation in BMECs. The results showed that the expression of miR-425-5p significantly decreased when BMEC were exposed to HS. However, the overexpression of miR-425-5p effectively alleviated the inhibitory effect of HS on BMEC proliferation. Furthermore, RNA sequencing analysis revealed 753 differentially expressed genes (DEGs), comprising 361 upregulated and 392 downregulated genes. Some of these genes were associated with proliferation and thermogenesis through enrichment analyses. Further experimentation revealed that TOB2, which acts as a target gene of miR-425-5p, is involved in the regulatory mechanism of BMEC proliferation. In summary, this study suggests that miR-425-5p can promote the proliferation of BMECs by regulating TOB2. The miR-425-5p/TOB2 axis may represent a potential pathway through which miR-425-5p ameliorates the proliferation stagnation of BMECs induced by HS.

miR-196a Promotes Proliferation of Mammary Epithelial Cells by Targeting CDKN1B.

Heat stress (HS) has become one of the key challenges faced by the dairy industry due to global warming. Studies have reported that miR-196a may exert a role in the organism's response to HS, enhancing cell proliferation and mitigating cellular stress. However, its specific role in bovine mammary epithelial cells (BMECs) remains to be elucidated. In this study, we aimed to investigate whether miR-196a could protect BMECs against proliferation arrest induced by HS and explore its potential underlying mechanism. In this research, we developed an HS model for BMECs and observed a significant suppression of cell proliferation as well as a significant decrease in miR-196a expression when BMECs were exposed to HS. Importantly, when miR-196a was overexpressed, it alleviated the inhibitory effect of HS on cell proliferation. We conducted RNA-seq and identified 105 differentially expressed genes (DEGs). Some of these DEGs were associated with pathways related to thermogenesis and proliferation. Through RT-qPCR, Western blotting, and dual-luciferase reporter assays, we identified CDKN1B as a target gene of miR-196a. In summary, our findings highlight that miR-196a may promote BMEC proliferation by inhibiting CDKN1B and suggest that the miR-196a/CDKN1B axis may be a potential pathway by which miR-196a alleviates heat-stress-induced proliferation arrest in BMECs.

miR-889-3p Facilitates the Browning Process of White Adipocyte Precursors by Targeting the SON Gene.

It is well-established that beige/brown adipose tissue can dissipate stored energy through thermogenesis; hence, the browning of white adipocytes (WAT) has garnered significant interest in contemporary research. Our preceding investigations have identified a marked downregulation of miR-889-3p concurrent with the natural maturation of brown adipose tissue. However, the specific role and underlying molecular mechanisms of miR-889-3p in the browning process of white adipose tissue warrant further elucidation. In this research, we initially delved into the potential role of miR-889-3p in preadipocyte growth via flow cytometry and CCK-8 assay, revealing that miR-889-3p can stimulate preadipocyte growth. To validate the potential contribution of miR-889-3p in the browning process of white adipose tissue, we established an in vitro rabbit white adipocyte browning induction, which exhibited a significant upregulation of miR-889-3p during the browning process. RT-qPCR and Western blot analysis indicated that miR-889-3p overexpression significantly amplified the mRNA levels of UCP1, PRDM16, and CIDEA, as well as UCP1 protein levels. Furthermore, miR-889-3p overexpression fostered intracellular triglyceride accumulation. Conversely, the downregulation of miR-889-3p hindered the browning of rabbit preadipocytes. Subsequently, based on target gene prediction and luciferase reporter gene determination, we demonstrated that miR-889-3p directly targets the 3'-UTR region of SON. Lastly, we observed that inhibiting SON could facilitate the browning of rabbit preadipocytes. In conclusion, our findings suggest that miR-889-3p facilitates the browning process of white adipocyte precursors by specifically targeting the SON gene.

Active polypeptide MDANP protect against necrotizing enterocolitis (NEC) by regulating the PERK-eIF2ɑ-QRICH1 axis.

The effect of MDANP effects on ER stress signalling not well known or elucidated. Endoplasmic reticulum (ER) stress plays a critical role in necrotizing enterocolitis (NEC) pathogenesis through the PERK-eIF2ɑ-QRICH1 axis. The present study aimed to explore the protective effects of MDANP in NEC development. Firstly, a function screening was designed to identify the candidate peptides in human milk, and then the identified peptides were validated in NEC patients. In vivo, NEC was induced in mice pups and divided into four groups: (1) control group, (2) NEC group, (3) MDANP + NEC group, and (4) NS + NEC group. In vitro, lentivirus-mediated QRICH1 silencing, was used to transfect NCM460 cell lines, then stimulated with LPS. After LPS stimulation, cells were treated with chemically synthesized MDANP, and the essential proteins in the QRICH1 signalling pathway in cells were tested and compared. After the small-scale screening, a peptide (SKSKKFRRPDIQYPDATDED) named MDANP was determined as the principal peptide. Its protective effect against NEC through inhibiting the expression of ERS key proteins and impeding the intestinal cells' apoptosis was observed in the animal models. Furthermore, the inhibitive effect of MDANP on apoptosis of intestinal epithelial cells through modulating the PERK-eIF2ɑ-QRICH1 ERS pathway was also confirmed in vitro. Taken together, our data suggest that MDANP effectively ameliorates apoptosis in NEC through attenuating PERK-eIF2ɑ-QRICH1.

lncRNA MSTRG4710 Promotes the Proliferation and Differentiation of Preadipocytes through miR-29b-3p/IGF1 Axis.

Obesity, a major global health issue, is increasingly associated with the integral role of long non-coding RNA (lncRNA) in adipogenesis. Recently, we found that lncRNA-MSTRG4710 was highly expressed in the liver of rabbits fed a high-fat diet, but whether it is involved in lipid metabolism remains unclear. A series of experiments involving CCK-8, EDU, qPCR, and Oil Red O staining demonstrated that the overexpression of MSTRG4710 stimulated the proliferation and differentiation of preadipocytes while its knockdown inhibited these processes. Bioinformatics analysis showed that miR-29b-3p was a potential target gene of MSTRG4710, and IGF1 was a downstream target gene of miR-29b-3p. Luciferase reporter gene analysis and qPCR analysis confirmed that miR-29b-3p was a potential target gene of MSTRG4710, and miR-29b-3p directly targeted the 3'UTR of IGF1. The overexpression of miR-29b-3p was observed to regulate IGF1 protein and mRNA levels negatively. Additionally, a total of 414 known differentially expressed genes between the miR-29b-3p mimic, miR-29b-3p negative control (NC), siMSTRG4710, and siMSTRG4710-NC group were screened via transcriptome sequencing technology. The GO- and KEGG-enriched pathways were found to be related to lipid metabolism. The study also established that miR-29b-3p targets IGF1 to inhibit preadipocyte proliferation and differentiation. Notably, IGF1 knockdown significantly reduced preadipocyte proliferation and differentiation. Furthermore, co-transfection of pcDNA3.1(+)-MSTRG4710 and mimics into rabbit preadipocytes revealed that the mimics reversed the promotional effect of pcDNA3.1(+)-MSTRG4710. In conclusion, these results uncover that MSTRG4710 positively regulated cell proliferation and adipogenesis by the miR-29b-3p/IGF1 axis. Our findings might provide a new target for studying adipogenesis in rabbit preadipocytes and obesity.

A Preliminary Study of the Potential Molecular Mechanisms of Individual Growth and Rumen Development in Calves with Different Feeding Patterns.

At present, it is common to feed calves with "Concentrate", "Concentrate + hay" and TMR "Total Mixed Rations" feeding patterns in China, which achieved well feeding efficiency, but the three feeding patterns molecular regulation mechanism in actual production is still unclear. The study aimed to explore the most suitable feeding pattern for Chinese Holstein calves to improve the rumen fermentation function and growth performance of calves. In this regard, the interactions between rumen microorganisms and host metabolism were investigated. The rumen volume and weight of calves in the GF group were significantly higher than those in the GFF and TMR groups (p < 0.05), and the rumen pH of calves in the GF group was 6.47~6.79. Metagenomics analysis revealed that the rumen microbiome of GF and GFF calves had higher relative abundances of Methanobrevibacter, Methanosphaera, and Methanolacinia (p < 0.05). Prevotella multisaccharivorax was significantly more abundant in the rumen of GF calves (p < 0.05), indicating that GF group calves had a stronger ability to ferment sugars. Notably, in the pyruvate metabolic pathway, phosphoenolpyruvate carboxylase was significantly up-regulated in GF calves compared with the TMR group, and pyruvate-phosphate dikinase was significantly down-regulated. Metabolomic results showed that Ursodeoxycholic acid was significantly up-regulated in GF calves, and most of the differential metabolites were enriched in Bile secretion pathways. The association analysis study found that the microorganisms of Prevotella and Ruminococcaceae might cooperate with the host, which was helpful for the digestion and absorption of lipids and made the calves have better growth. The three feeding modes had similar effects, but the 'GF' feeding pattern was more beneficial to the individual growth and ruminal development regarding ruminal morphology, contents physiology and microorganisms. Furthermore, the synergistic effect of rumen microorganisms and the host could more effectively hydrolyze lipid substances and promote the absorption of lipids, which was of great significance to the growth of calves.

miR-383-5p Regulates Preadipocyte Proliferation and Differentiation by Targeting RAD51AP1.

Obesity has become a major health problem worldwide, and increasing evidence supports the importance of microRNAs (miRNAs) in its pathogenesis. Recently, we found that miR-383-5p_1 is highly expressed in the perirenal fat of high-fat-fed rabbits, but it is not yet known whether miR-383-5p is involved in lipid metabolism. Here, we used transcriptome sequencing technology to screen 1642 known differentially expressed genes between miR-383-5p mimic groups and miR-383-5p negative control groups. Gene Ontology Resource (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were enriched in the pathway related to lipid metabolism, and glycine biosynthesis, the NOD receptor signal pathway and nonalcoholic fatty liver were significantly enriched. Afterwards, our research results indicated that miR-383-5p can promote the proliferation and differentiation of rabbit preadipocytes, and there is a direct targeting relationship with RAD51AP1. Mechanistically, miR-383-5p directly interacts with the lipid metabolism and participates in adipogenesis and lipid accumulation by targeting RAD51AP1. In conclusion, our data highlight a physiological role for miRNA in lipid metabolism and suggest the miR-383-5p/RAD51AP1 axis may represent a potential mechanism for controlling lipid accumulation in obesity.

The effects of differential feeding on ileum development, digestive ability and health status of newborn calves.

Pre-weaning is the most important period for the growth and development of calves. Intestinal morphology, microbial community and immunity are initially constructed at this stage, and even have a lifelong impact on calves. Early feeding patterns have a significant impact on gastrointestinal development and microbial communities. This study mainly analyzed the effects of three feeding methods on the gastrointestinal development of calves, and provided a theoretical basis for further improving the feeding mode of calves. it is very important to develop a suitable feeding mode. In this study, we selected nine newborn healthy Holstein bull calves were randomly selected and divided into three groups (n = 3), which were fed with starter + hay + milk (SH group), starter + milk (SF group), total mixed ration + milk (TMR group). After 80 days of feeding Feeding to 80 days of age after, the ileum contents and blood samples were collected, and the differences were compared and analyzed by metagenomic analysis and serum metabolomics analysis. Results show that compared with the other two groups, the intestinal epithelium of the SH group was more complete and the goblet cells developed better. The feeding method of SH group was more conducive to the development of calves, with higher daily gain and no pathological inflammatory reaction. The intestinal microbial community was more conducive to digestion and absorption, and the immunity was stronger. These findings are helpful for us to explore better calf feeding patterns. In the next step, we will set up more biological replicates to study the deep-seated reasons for the differences in the development of pre-weaning calves. At the same time, the new discoveries of neuro microbiology broaden our horizons and are the focus of our future attention.

A Structure Variation in qPH8.2 Detrimentally Affects Plant Architecture and Yield in Rice.

Plant height is an important agronomic trait associated with plant architecture and grain yield in rice (Oryza sativa L.). In this study, we report the identification of quantitative trait loci (QTL) for plant height using a chromosomal segment substitution line (CSSL) population with substituted segments from japonica variety Nipponbare (NIP) in the background of the indica variety 9311. Eight stable QTLs for plant height were identified in three environments. Among them, six loci were co-localized with known genes such as semidwarf-1 (sd1) and Grain Number per Panicle1 (GNP1) involved in gibberellin biosynthesis. A minor QTL qPH8.2 on chromosome 8 was verified and fine-mapped to a 74 kb region. Sequence comparison of the genomic region revealed the presence/absence of a 42 kb insertion between NIP and 9311. This insertion occurred predominantly in temperate japonica rice. Comparisons on the near-isogenic lines showed that the qPH8.2 allele from NIP exhibits pleiotropic effects on plant growth, including reduced plant height, leaf length, photosynthetic capacity, delayed heading date, decreased yield, and increased tiller angle. These results indicate that qPH8.2 from temperate japonica triggers adverse effects on plant growth and yield when introduced into the indica rice, highlighting the importance of the inter-subspecies crossing breeding programs.

Isoform-specific disruption of the TP73 gene reveals a critical role for TAp73γ in tumorigenesis via leptin.

TP73, a member of the p53 family, is expressed as TAp73 and ΔNp73 along with multiple C-terminal isoforms (α-η). ΔNp73 is primarily expressed in neuronal cells and necessary for neuronal development. Interestingly, while TAp73α is a tumor suppressor and predominantly expressed in normal cells, TAp73 is found to be frequently altered in human cancers, suggesting a role of TAp73 C-terminal isoforms in tumorigenesis. To test this, the TCGA SpliceSeq database was searched and showed that exon 11 (E11) exclusion occurs frequently in several human cancers. We also found that p73α to p73γ isoform switch resulting from E11 skipping occurs frequently in human prostate cancers and dog lymphomas. To determine whether p73α to p73γ isoform switch plays a role in tumorigenesis, CRISPR technology was used to generate multiple cancer cell lines and a mouse model in that Trp73 E11 is deleted. Surprisingly, we found that in E11-deificient cells, p73γ becomes the predominant isoform and exerts oncogenic activities by promoting cell proliferation and migration. In line with this, E11-deficient mice were more prone to obesity and B-cell lymphomas, indicating a unique role of p73γ in lipid metabolism and tumorigenesis. Additionally, we found that E11-deficient mice phenocopies Trp73-deficient mice with short lifespan, infertility, and chronic inflammation. Mechanistically, we showed that Leptin, a pleiotropic adipocytokine involved in energy metabolism and oncogenesis, was highly induced by p73γ,necessary for p73γ-mediated oncogenic activity, and associated with p73α to γ isoform switch in human prostate cancer and dog lymphoma. Finally, we showed that E11-knockout promoted, whereas knockdown of p73γ or Leptin suppressed, xenograft growth in mice. Our study indicates that the p73γ-Leptin pathway promotes tumorigenesis and alters lipid metabolism, which may be targeted for cancer management.