Gene Expression Research Articles

Biomarkers for tracking metabolic changes pre-post nutritional epigenetics diet/intervention to prevent autism and attention deficit/hyperactivity disorders in children

The prevalence of autism and attention deficit/hyperactivity disorders is increasing worldwide. Recent studies suggest the excessive intake of ultra-processed food plays a role in the inheritance of these disorders via heavy metal exposures and nutritional deficits that impact the expression of genes. In the case of the metallothionein (MT) gene, biomarker studies show dietary zinc (Zn) deficits impact MT protein levels in children with autism and are associated with the bioaccumulation of lead and/or mercury in children exhibiting autism/attention deficit/hyperactivity disorders symptomology. The impact of dietary changes on lead and mercury exposures and MT gene behavior could be determined using a randomized test and control group design. Pregnant women serving in the test-group would participate in a nutritional epigenetics education intervention/course designed to reduce ultra-processed food intake and heavy metal levels in blood while increasing whole food intake and MT and Zn levels. Changes in maternal diet would be measured using data derived from an online diet survey administered to the test and control groups pre-post intervention. Changes in maternal lead, mercury, Zn, and MT levels would be measured via blood sample analyses prior to the intervention and after childbirth via cord blood analyses to determine infant risk factors.

Establishment and characterization of a new human gallbladder cancer cell line, OCUG-2

BACKGROUND Gallbladder cancer (GBC) is a highly aggressive malignant tumor originating from the biliary tract. As one of the most common malignancies in the biliary system, GBC is particularly challenging due to its tendency to remain asymptomatic, which often results in delayed diagnoses even at advanced stages. Combined with its invasive potential and poor response to conventional therapies, GBC has a high mortality rate, highlighting the critical need for innovative therapeutic approaches. Identifying molecular biomarkers for early detection and discovering novel therapeutic targets might be essential to improving outcomes of patients with GBC. AIM To establish a novel GBC cell line to investigate the molecular mechanisms underlying GBC progression and evaluate potential therapeutic targets. METHODS We developed a unique GBC cell line, named OCUG-2, derived from a metastatic peritoneal implant, and verified its authenticity using short tandem repeat (STR) profiling. RT-PCR and RNA sequencing (RNA-seq) were performed to assess gene expression profiles, with functional enrichment analyzed through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The MTT cell proliferation assay and an invasion assay were performed to evaluate response to nine inhibitors. Immunohistochemistry (IHC) was conducted on 34 GBC samples to analyze insulin-like growth factor 1 receptor (IGF1R) expression. RESULTS OCUG-2 cells displayed adhesive growth with dendritic morphology and a 30-hour doubling time. Subcutaneous inoculation of OCUG-2 cells into mice confirmed their tumorigenic potential. STR analysis authenticated the cell line, and there was high mRNA and protein expression of IGF1R in OCUG-2 cells. The IGF1R inhibitor picropodophyllotoxin significantly inhibited OCUG-2 cell proliferation, yielding an IC50 of 0.49 μM. RNA-seq analysis identified gene fusions, and GO/KEGG functional enrichment analyses revealed pathways implicated in cancer progression. IHC analysis showed IGF1R positivity in 18 of 34 GBC cases, with significant association between IGF1R expression and poor prognosis. In invasion assays, an IGF1R inhibitor effectively reduced OCUG-2 cell invasiveness. CONCLUSION IGF1R might be a promising target for GBC. The newly established OCUG-2 cell line serves as a valuable model for investigating the molecular mechanisms of GBC and evaluating therapeutic strategies.

Mitigation Exposed to Acute Cadmium Stress in Nile Tilapia by Dietary Quercetin: Exploring the Growth Performance, Intestinal Health, Stress Biomarkers, and Immune Responses.

The present study planned to assess the effect of dietary quercetin (DQu) on the mitigation of cadmium stress exposed to Nile tilapia (Oreochromis niloticus). Fish with an initial weight of 7.69 ± 0.84 g were allocated to four groups (4 replicates), where fish in the control group had no cadmium (Cd) or dietary quercetin (DQu), while the second group was exposed to (1 mg/L) Cd without DQu. The third group was fed 5 g Qu kg without Cd, while the fourth group was exposed to (1 mg/L) Cd and fed DQu 5 kg for 60 days. Fish fed DQu showed significant increases (P < 0.001) in all growth indices, expressions of the IGF-1 gene, digestive enzymes, and hemato-biochemical parameters, followed by the control, then fish fed DQu, and exposure to acute Cd stress. Data showed that fish fed DQu significantly improved antioxidant and immunological indices compared to the control group and the fish group exposed to acute Cd stress. Fish fed DQu displayed up-regulated expression of the (CAT), SOD, and KEAP1 genes, while fish exposed to acute Cd stress displayed downregulated expressions of these genes. Correspondingly, fish exposed to acute Cd stress revealed up-regulated expression levels of HSP70, IL-8, and IL-1β genes. Conversely, fish fed DQu displayed downregulation in the expression levels of these genes, followed by the control, and fish subjected to acute Cd stress and fed DQu. The results of the histological study revealed that while fish fed DQu had anti-inflammatory effects, fish exposed to Cd stress displayed inflammatory and irregular characteristics. Therefore, this study suggests that adding Qu to the fish diet boosts fish growth performance and health status and reduces the toxicity of waterborne Cd in Nile tilapia, O. niloticus.

GhTOPP4aD and GhRAF36 inversely regulate cotton (Gossypium hirsutum) response to ABA and salt stress through reversible phosphorylation of GhABI1.

The post-translational phosphorylation modification of stress-related proteins regulated by kinases and phosphatases is one of the crucial regulatory mechanisms for plants in response to salt stress. However, the paired kinases and phosphatases of the same substrate that participate in response to salt tolerance in crops, especially in cotton, remain to be elucidated. Here, we identified GhTOPP4aD as a negative regulator of salt-stress response in cotton. GhTOPP4aD interacted with Raf-like kinase 36 (GhRAF36) and ABA Insensitive 1 (GhABI1) respectively, thereby inhibiting the phosphorylation activity of GhRAF36 and directly dephosphorylating GhABI1 to counteract GhRAF36 regulation. The phosphatase activity of GhABI1 was inhibited by GhRAF36-mediated phosphorylation at two unique residues Thr124 and Ser357 in cotton, whereas it was compromised by GhTOPP4aD. GhTOPP4aD thereby limited ABA signal transduction and orchestrated ABA-responsive gene expression. Together, modulation of the phosphorylation dynamics of GhABI1 by GhRAF36 kinase and GhTOPP4aD phosphatase constitutes an essential mechanism for ABA response and salt tolerance in cotton.

Loss of Myostatin Alters Gut Microbiota and Carbohydrate Metabolism to Influence the Gut–Muscle Axis in Cattle

The gut–muscle axis plays a vital role in host metabolism and health. Although the MSTN gene is a well-known negative regulator of muscle growth, its role in intestinal function and metabolism remains unclear. Understanding this connection is crucial for revealing the systemic impact of MSTN gene editing and its potential to improve metabolic efficiency in livestock. In this study, we investigated the influence of MSTN deletion on gut microbiota composition and carbohydrate metabolism in the cecum and colon of cattle. Using integrated metagenomic, metabolomic, serum biochemical, and muscle transcriptomic analyses, we found significant alterations in microbial communities and key metabolic pathways. Hallella and Escherichia in the colon, as well as Alishewanella in the cecum, were closely linked to carbohydrate metabolism. Differential microbes and metabolites influenced key metabolic pathways, including glycolysis/gluconeogenesis and lipopolysaccharide biosynthesis. Functional gene analysis identified Bacteroides as the most critical bacterium affecting glycolysis/gluconeogenesis. Additionally, genes related to carbohydrate esterases were upregulated. These changes correlated with reduced serum glucose and insulin levels while increasing muscle gene expression related to glucose-to-lactose conversion. Overall, MSTN gene editing alters gut microbiota composition and carbohydrate metabolism in the cecum and colon, thereby influencing host glucose metabolism and energy homeostasis.

Positioning of negative feedback loops within immune signaling pathways influences gene expression noise.

Signaling pathways are noisy biological circuits. This noise is caused by random fluctuations in the number of proteins that function within these pathways. To properly respond to external stimuli, the ratio of noise to information needs to be minimized. To regulate noise, biological pathways produce proteins that either reduce (negative feedback) or amplify (positive feedback) signaling following stimulation. Negative feedback loops can shut down signaling by interfering with the first steps of signaling, which entail the detection of stimuli. Conversely, signaling might be left intact, and instead, negative feedback loops might interfere with the last step, which is the production of output. These regulatory differences can affect noise within signaling pathways. Here, we examined this using stochastic (inherently random) models to simulate immune signaling in response to pathogens. We found that negative feedback loops that function at later stages of signaling can decrease noise in the output, while negative feedback loops that act at earlier stages amplify the noise, but this noise can be reduced by the presence of a strong positive feedback loop.

Jund orchestrates cis-regulatory element dynamics to facilitate endothelial-to-hematopoietic transition

The tightly controlled spatiotemporal expression of developmental genes depends on the concerted action of cis-regulatory elements (CREs) and transcription factors (TFs) to ensure cell fate decisions. Endothelial-to-hematopoietic transition (EHT) is a cell fate transition process by which endothelial cells acquire hematopoietic identity and become hemogenic endothelial cells (HECs) and then hematopoietic stem and progenitor cells, but the underlying CRE network dynamics and its regulation by TFs remain unclear. In this study, we characterized the dynamics of CRE activation and TF occupancy during zebrafish EHT, and found that the enhancer-promoter collaboration forms the basis for EHT. Moreover, a ubiquitously expressed TF AP-1 collaborates with diverse lineage-specific TFs to remodel enhancer landscape. Deletion of AP-1 family member Jund impaired hematopoietic specification, resulting from the enhanced endothelial identity in the HEC. Mechanistically, Jund and hematopoietic TF Hoxa9a collectively repress the activity of an endothelial-related dll4 enhancer through tight control of the active histone modification H3K27ac. Our study provides insights into the cooperative function among ubiquitous TFs and cell type-specific TFs in orchestrating cell fate transition.

Primary Bile Acid Shapes Peripheral Immunity in Inflammatory Bowel Disease-associated Primary Sclerosing Cholangitis.

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease often associated with underlying inflammatory bowel disease (IBD). This study investigates how PSC predisposes altered inflammatory immune responses and compared to IBD alone. A case-control study was conducted with a cohort of 75 patients, including 16 with PSC (14 with concomitant IBD), 39 with IBD alone, and 20 controls. Serum bile acid profile, proteomic analysis, and immune-related gene expression in colon tissue were examined. Colonic tissue from PSC patients exhibited upregulation of immune regulation and inflammatory signaling mRNA markers, including LGR5, IL-8, CCL2, COX2, TWIST1, and SNAIL. Additionally, PSC patients displayed a distinct proinflammatory serum proteomic signature and moderate elevation of some bile acids, such as glycochenodeoxycholic acid (GCDCA). Co-incubation of human-derived monocytes with GCDCA partially replicated the inflammatory profile observed in PSC. These findings suggest that circulating bile acids modulate peripheral immune system proinflammatory response, contributing to the unique PSC phenotype.

Differential Expression Characteristics of Two Isoforms nr5a2f and nr5a2m in Gonadal Differentiation of Chinese Giant Salamanders, Andrias davidianus.

Nr5a2 (nuclear receptor subfamily 5, group a, member 2) is involved in gonad development and sex hormone synthesis. In this study, the full length of Nr5a2f and Nr5a2m were obtained by Nr5a2 variable splicing from Andrias davidianus, and the tissue distribution was detected. We identified Nr5a2f of 2455 bp and Nr5a2m of 2150 bp length, encoding 479 and 325 amino, respectively. We first characterized Nr5a2f and Nr5a2m gene expression in developing gonads. Results showed that Nr5a2f had significantly high expression in the ovary and little expression in other tissues, during the sex differentiation and sex reversal, Nr5a2f expression was gradually decreased in the ovary and the expression in the testis was significantly lower than in the ovary from 1 year to 6 year old. Significantly high expression was observed in the ovary and reversal ovary, while low expression was in the testis and reversal testis. While Nr5a2m expression exhibited the opposite profile, high expression was observed in the brain and testis. During sex differentiation and sex reversal, high expression was shown in the testis and low expression in the ovary from one year to six years old and significantly higher expression emerged in testis and reversal testis than in ovary and reversal ovary. In situ hybridization, results showed that Nr5a2f began to express in female undifferentiated gonads and the expression level increased from 48 dpf to 91, while Nr5a2m was expressed in male undifferentiated gonads. Three RNA interference sites were designed and we detected that site 293 exhibited a significant inhibitory effect in ovary cells. After Nr5a2f expression was inhibited by site 293, we observed that female-based gene Nr5a2f, foxl2 and cyp19 expression were decreased, while the male-based gene dmrt1 and cyp17 expression was increased. These results suggested that Nr5a2f and Nr5a2m exhibited different expression patterns in the process of sex differentiation, which provided a foundation for further functional characterizations.

The Impact of Deep Brain Stimulation of the Subthalamic Nucleus on Sleep-Wake Function and Circadian Rhythms in Patients with Parkinson's Disease.

Deep brain stimulation (DBS) of the subthalamic nucleus (STN) is a well-established therapy in advanced Parkinson's disease (PD) improving motor and non-motor signs including sleep. The mechanisms of sleep improvement are insufficiently understood. The objective was to identify stimulation-dependent effects on the sleep-wake cycle and circadian clock regulation. Fourteen PD patients who underwent STN DBS (PD-DBS) were assessed before as well as 6 and 12 months post-surgery. As control groups, 18 PD patients under best medical treatment (PD-CON) and 25 healthy controls (H-CON) were also enrolled. Wrist actigraphy to measure sleep and sleep questionnaires, such as the PD Sleep Scale (PDSS), were applied and the expression of clock genes in peripheral blood was measured. Electrode placement in the STN was localized, and the local impact of STN DBS was estimated. STN DBS improved daytime sleepiness 12 months post-surgery (P = 0.006) which was correlated with limbic VTA (r = 0.737, P = 0.006). PDSS scores decreased 6 months post-surgery (P = 0.050) and were positively associated with activation of the motor part of the STN (r = 0.582, P = 0.037). Time in bed increased after surgery and was also positively correlated with the activation of the motor part of the STN (r = 0.941, P = 0.005). There were no changes in clock gene expression between groups and over time (all P ≥ 0.323). Sleep and daytime sleepiness are improved after STN DBS in PD. Different STN sub-proportions contribute to these improvements. The changes in sleep appear not be driven by changes in clock gene expression.

Toxoplasma IMC1 is a central component of the subpellicular network and plays critical roles in parasite morphology, replication, and infectivity.

Parasites in the phylum Apicomplexa maintain their intracellular lifestyle using specialized organelles that mediate the lytic cycle of host cell invasion, intracellular replication, and egress. One of these organelles is the inner membrane complex (IMC), which consists of membrane vesicles supported by a cytoskeletal meshwork formed from proteins called alveolins. This study focuses on the first identified alveolin IMC1 and determines its precise function via expression timing, gene knockout, deletion and mutagenesis, partner identification, and in vivo infection studies. We show that this protein is critical to the ultrastructure of the parasite which is important for every stage of its lytic cycle. We also identify key regions of the protein that are important for localization, function, and interaction with another key alveolin, IMC4.

Mechanism of Circadian Regulation in Ferroptosis of the BMAL1/NRF2 Pathway in Renal Ischemia–Reperfusion

Background: Renal ischemia–reperfusion injury (IRI) is a frequent cause of kidney transplant failure. Recent studies have shown that the extent of injury is closely linked to ferroptosis, and the process of cellular ferroptosis is diurnal and regulated by circadian genes. NRF2, involved in iron–heme metabolism, may be related to ferroptosis. We hypothesize that the pathway plays a role in circadian regulation in ferroptosis in renal IRI. Methods: Using hematoxylin and eosin (H&amp;E) staining, enzyme-linked immunosorbent assay (ELISA), Cell Counting Kit-8 (CCK8), flow cytometry, real-time quantitative reverse transcription PCR (qRT-PCR), and Western blotting, we analyzed renal tubular tissues in vivo and in vitro and compared the groups with IR injury treatment, inhibition of ferroptosis, and inhibition of BMAL1 gene expression at the ZT0 (zeitgeber time 0) and ZT12 (zeitgeber time 12) time points. Results: IR injury treatments caused exacerbation of injury, both in vivo and in vitro, and were more pronounced at the ZT12 time point, which correlates with circadian rhythms. The use of the ferroptosis inhibitor (Fer-I) attenuated IR injury, suggesting that IRI is associated with ferroptosis. In contrast, reduced BMAL1-gene expression exacerbated injury, and NRF2, which is elevated in IR injury, was suppressed. Conclusions: The circadian gene BMAL1 affects the circadian rhythm of ferroptosis in renal IRI through the regulation of NRF2 and its downstream pathway. In this study, renal injury is well ameliorated by the ferroptosis inhibitor, exhibiting potential as a therapeutic agent for use in renal transplantation.

Can interferon-inducible gene expression guide treatment? A prospective study in QuantiFERON-positive uveitis with undetermined cause

Abstract PURPOSE: The purpose of this study was to evaluate the utility of baseline interferon (IFN)-inducible gene expression as a prognostic biomarker for Anti-tubercular therapy (ATT) response in patients with undetermined cause of uveitis who tested positive for QuantiFERON-TB Gold (QFT-positive uveitis). METHODS: This prospective cohort study included 17 QFT-positive uveitis patients at a tertiary uveitis center in Indonesia. Baseline and week 2 peripheral blood transcripts were evaluated through real time-quantitative polymerase chain reaction to assess the expression of 10 IFN-inducible genes (IRF7, IFIT2, STAT1, IL1B, MyD88, TLR8, FCGR1B, GBP1, UBE2L6, and SERPING1). Patients were stratified into clusters based on gene expression patterns. The primary outcome was complete resolution of uveitis at 6 months. RESULTS: Hierarchical clustering revealed two distinct groups. Patients with higher baseline expression of IFN genes (Cluster 2) were more likely to achieve complete uveitis resolution after ATT compared to those with lower expression levels (Cluster 1) (80% vs. 43%). Using a previously established IFN gene signature score (IGSS) cutoff (≥5.61), 82% of high-scoring patients showed complete resolution, compared to only 33% in the low-scoring group (P = 0.046). However, week 2 gene expression changes did not correlate with treatment response, indicating limited utility in monitoring disease activity or predicting long-term outcomes. CONCLUSION: Baseline, but not week 2, peripheral blood IFN-inducible gene expression may serve as a prognostic biomarker for stratifying QFT-positive uveitis patients through prediction of their response to treatment. Patients with higher baseline IGSS are more likely to require ATT to achieve uveitis resolution at 6-month follow-up.

Correlation of serum Helios, CD226, tigit, and Foxp3 with tear film osmotic pressure and dry eye disease in patients with rheumatoid arthritis

Objective: This study investigated the correlation between serum Helios, CD226, TIGIT, and Foxp3 levels and tear film osmotic pressure in individuals with rheumatoid arthritis (RA) and dry eye disease.Methods: This case-control study enrolled 100 RA patients with dry eye and 100 healthy controls from May 2021 to June 2022. mRNA expression of target genes was quantified using quantitative real-time PCR (qRT-PCR). Tear film osmolality was measured with a commercial osmometer. Statistical analyses included Pearson correlation and multivariate logistic regression.Results: Compared with controls, RA patients exhibited significantly higher mRNA levels of Helios, CD226, TIGIT, and Foxp3 (P<0.05), along with elevated mean tear osmolarity (312.5±12.3 vs. 295.4±10.8 milliosmoles per liter (mOsm/L), P<0.05). Notably, 68% of RA patients exceeded the 308 mOsm/L diagnostic threshold versus 22% controls (P<0.05). Helios (r=0.62) and Foxp3 (r=0.58) correlated positively with osmotic pressure, while TIGIT showed a negative correlation (r=-0.49, P<0.05). Logistic regression revealed that elevated levels of Helios (OR=2.1, 95% CI: 1.4–3.2), CD226 (OR=1.8, 95% CI: 1.2–2.7), and Foxp3 (OR=1.9, 95% CI: 1.3–2.8) were associated with increased dry eye risk (P<0.05).Conclusion: These immune markers demonstrate significant associations with tear film instability in RA, serving as potential biomarkers for ocular comorbidity monitoring.

Exploring the Role of CACNA1C, ZNF804A and SLC6A4 in Schizophrenia through Epigenomics and Bioinformatics

Schizophrenia (SCZ) is a complex neuropsychiatric condition in which genetic vulnerability interacts with environmental exposures to influence disease risk and clinical outcomes. Emerging non-genetic causes include early-life stress, substance use and urban living environments, which have been found to interact with inherent genetic predisposition. Recent advances in epigenomics and bioinformatics have illuminated the mechanisms through which these environmental insults may alter gene expression, particularly via DNA methylation, chromatin remodeling and transcription factor binding. Genes such as CACNA1C, ZNF804A and SLC6A4 exemplify loci where regulatory changes may mediate gene-environment interactions. Bioinformatics tools like GTEx, ENCODE, 3DSNP, and methylation datasets from epigenome-wide association studies (EWAS) now provide special perspectives into these molecular processes. This review highlights key epigenetic mechanisms linking environmental exposures to SCZ pathogenesis and explores how integrative computational analyses are enhancing our understanding of this complex disorder. A deeper appreciation of gene- environment interactions may ultimately inform personalized interventions and risk stratification in SCZ care.

Inherited Genetic Variation in Parkinson's Disease: Convergence on Impaired Autophagosome-Lysosome Fusion Through the Altered Expression of mRNA Isoforms.

Parkinson's disease (PD) pathogenesis involves complex interactions between genetic factors. We employed two-sample Mendelian randomization (MR) integrating tissue-specific gene regulatory networks to identify causal genes and regulatory elements modulating PD risk. Two-sample MR analysis identified 79 putative causal genes for PD. A subset of the 79 causal genes was enriched within chr17q21.31 and chr16p11.2 cytobands that have been previously linked to neurodevelopmental disorders. Functional enrichment analysis of the 79 genes revealed autophagosome-lysosome fusion as a key process. Ten genes (ELOVL7, HSD3B7, PLEKHM1, PRSS53, SNCA, STX1B, STX4, ZSWIM7, LINC02210, and RP11-1072 A3.3) showed causal associations with tissue-specific expression patterns driving risk or protection for PD. Further investigation into their tissue-specific isoform expression profile revealed isoform-specific contributions to disease risk (or protection). These findings highlight the critical role of isoform-specific expression of causal genes in modulating PD risk, particularly relating to autophagosome-lysosome fusion. While our findings provide new insights into PD susceptibility, we acknowledge that the observed isoform-specific changes may, in part, reflect sample selection bias. Therefore, further experimental verification is needed to confirm the importance of incorporating tissue-specific gene isoform profiles in understanding PD causal mechanisms.

Phosphodiesterase 3 inhibitors boost bone outgrowth.

C-type natriuretic peptide (CNP) stimulates skeletal growth by acting on the growth plates of long bones, and a CNP variant is clinically used for achondroplasia treatment. We previously reported that CNP stimulates the autonomic Ca2+ influx mediated by TRPM7 channels in growth plate chondrocytes to facilitate extracellular matrix synthesis for bone growth. In this study, we attempted to stimulate CNP signalling using phosphodiesterase (PDE) inhibitors. Based on gene expression data, we focused on the role of PDE3B in growth plates. We performed imaging, biochemical and histological analyses in growth plate chondrocytes and ex vivo and in vivo analyses on bone and skeletal growth to address the pharmacological effects of PDE3 inhibitors. The representative PDE3 inhibitors cilostazol and milrinone elevated cGMP levels and activated cell-surface K+ channels probably due to protein kinase G-mediated phosphorylation in growth plate chondrocytes. The resulting hyperpolarization likely facilitated TRPM7-mediated Ca2+ influx by increasing the Ca2+-driving force. Moreover, cilostazol stimulated the elongation of cultured bones and enlarged the body size of juvenile mice. Several PDE3 inhibitors have been used for clinical treatment of thrombosis, heart failure and asthma, while our observations suggest that the repositioning of PDE3 inhibitors would provide novel medications for skeletal diseases characterized by short stature.

Investigating the enhancement of neural differentiation of adipose-derived mesenchymal stem cell with Foeniculum vulgare nanoemulsions: An in vitro research.

Investigating the enhancement of neural differentiation of adipose-derived mesenchymal stem cell with Foeniculum vulgare nanoemulsions: An in vitro research.

Toll-like receptors and inflammatory cytokines in the skin of Acanthamoeba spp. infected immunocompetent and immunosuppressed mice.

Toll-like receptors and inflammatory cytokines in the skin of Acanthamoeba spp. infected immunocompetent and immunosuppressed mice.

Titanium nanostructure mitigating doxorubicin-induced testicular toxicity in rats via regulating major autophagy signaling pathways.

Titanium nanostructure mitigating doxorubicin-induced testicular toxicity in rats via regulating major autophagy signaling pathways.