Gene Reports最新文献

{"title":"Molecular insight into the photoperiod sensitivity in crop plants","authors":"Kishor U. Tribhuvan ,&nbsp;Shruti Sinha ,&nbsp;N. Mustafa ,&nbsp;Simardeep Kaur ,&nbsp;Binay K. Singh","doi":"10.1016/j.genrep.2025.102190","DOIUrl":"10.1016/j.genrep.2025.102190","url":null,"abstract":"<div><div>The reproductive phase of the plant is critically regulated by various internal and external factors. Among these, photoperiod sensitivity is one of the key factors that counts the day length to sense the upcoming favourable environmental conditions for flowering and post-flowering events. Photoperiod-sensitive plants have an internal photoperiod-sensing mechanism regulated through a cascade of genes. Induction of flowering in plants largely depends upon the expression of the <em>Flowering Locus T</em> (<em>FT</em>), which encodes florigen, a systemic signalling molecule required to trigger flower induction. It is synthesized in leaves and translocated to the shoot meristem through the phloem. Photoperiod sensitivity in crop plants is a big constraint for production. Strong photoperiod requirements of crop plants for flowering restrict their cultivation to specific geographical niches in a single season. Identifying the gene(s)/QTL(s) for photoperiod sensitivity and the development of day-neutral genotypes is a prime area of research. The availability of day-neutral genotypes in crop plants promises wider adaptability under diverse agroecological environments with multi-seasonal cropping in a year. This review takes into account the genes and QTLs discovered in major cereal and pulse crops and elucidates various mechanisms behind their photoperiod responses. Furthermore, it emphasizes the use of genome editing for photoperiod engineering and explores the prospect of using various modern, cutting-edge technologies for photoperiod research in crop plants.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102190"},"PeriodicalIF":1.0,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RORA polymorphisms are associated with ischemic stroke","authors":"Mohammad Samadian ,&nbsp;Fatemeh Sadat Feghahati ,&nbsp;Maryam Sheikhvand ,&nbsp;Arash Safarzadeh ,&nbsp;Arezou Sayad ,&nbsp;Soudeh Ghafouri-Fard","doi":"10.1016/j.genrep.2025.102191","DOIUrl":"10.1016/j.genrep.2025.102191","url":null,"abstract":"<div><h3>Introduction</h3><div><em>RAR Related Orphan Receptor A</em> (<em>RORA</em>) encodes a nuclear hormone receptor that participates in the pathoetiology of several disorders.</div></div><div><h3>Objective</h3><div>We aimed to evaluate association between two <em>RORA</em> variants (rs11639084 and rs4774388) and risk of ischemic stroke among Iranians.</div></div><div><h3>Methods</h3><div>These polymorphisms were genotyped using 4P-ARMS-PCR method.</div></div><div><h3>Results</h3><div>The rs11639084 polymorphism was associated with risk of stroke in all assumed inheritance models. T allele of this polymorphism was identified as the risk allele increasing the risk of ischemic stroke with OR (95 % CI) of 18.64 (13.58–25.57), <em>P</em> &lt; 0.0001 and AIC = 29.4. Notably, the TT genotype was found to increase risk of this condition compared with CC genotype (OR (95 % CI) = 309.6 (142.2–683.2)) and CC + TC genotypes (OR (95 % CI) = 62.37 (30.06–129.4)). Since AIC estimates the quality of each model relative to other models, allelic model seems to be the best model for appraisal of the association between rs11639084 and risk of ischemic stroke. The rs4774388 polymorphism was associated with risk of stroke in all assumed inheritance models, except for over-dominant model. C allele of this polymorphism was reported to be the risk allele increasing the risk of ischemic stroke with OR (95 % CI) of 8.56 (6.4–11.43), <em>P</em> &lt; 0.0001 and AIC = 29.6. Accordingly, the CC genotype increased susceptibility to ischemic stroke compared with TT genotype (OR (95 % CI) = 22.4 (14.6–42.5)), as well as combination of the other two genotypes (OR (95 % CI) = 12.92 (8.18–20.4)). Similar to the other polymorphism, the highest AIC value belonged to the allelic model.</div></div><div><h3>Conclusions</h3><div>In brief, we showed associations between two <em>RORA</em> polymorphisms and susceptibility to ischemic stroke in Iranian population. <em>RORA</em> might be the functional link between abnormality in circadian rhythm and risk of ischemic stroke. Moreover, this gene might explain the shared genetic background between obesity and stroke.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102191"},"PeriodicalIF":1.0,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143550769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulated cell death in thyroid follicular cells: Molecular insights into pyroptosis, apoptosis, and necrosis","authors":"Honghao He,&nbsp;Daiwei Zhao","doi":"10.1016/j.genrep.2025.102185","DOIUrl":"10.1016/j.genrep.2025.102185","url":null,"abstract":"<div><div>Programmed cell death (PCD) pathways are crucial for eliminating functionally redundant, infected, or potentially tumorigenic cells. They play significant roles in maintaining homeostasis, defending against pathogens, preventing cancer, and addressing various other pathologies. Multiple PCD pathways, including apoptosis, necroptosis, and pyroptosis, have been well-characterized. Different molecular and cellular functions are included in these pathways, and each of these processes results in different cellular outcomes, including the activation of inflammatory responses. This review aims to investigate the molecular components that regulate apoptosis, pyroptosis, and necroptosis, with a particular emphasis on the interaction pathways between these processes in the context of thyroid follicular cell death. It aims to examine the implications of these pathways for thyroid health and disease, as well as providing an in-depth understanding of the flexible and coordinated nature of PCD pathways in thyroid cells, emphasizing their interconnectedness and the plasticity of their molecular regulation. It underscores the potential of using this flexibility in therapeutic strategies for thyroid-related disorders. Significant plasticity has been observed in the regulation of PCD pathways in recent genetic and biochemical investigations. Apoptosis can be induced by inflammatory caspases, for example, that usually cause pyroptosis, and the stimulus of apoptosis can induce pyroptosis. This flexibility is particularly evident in the cellular response to infections. Understanding the coordinated regulation of different PCD pathways could open new avenues for targeted therapeutic interventions in thyroid diseases, potentially improving treatment outcomes for thyroid-related disorders.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102185"},"PeriodicalIF":1.0,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143563258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biofilm formation, pigment production, and virulence gene profiles in Pseudomonas aeruginosa isolates from respiratory and urinary tract infections","authors":"Mohammad Sarkheili,&nbsp;Farzin Asghari-Sana,&nbsp;Samira Ahmadi Asli,&nbsp;Shabnam Golbouy Daghdari","doi":"10.1016/j.genrep.2025.102184","DOIUrl":"10.1016/j.genrep.2025.102184","url":null,"abstract":"<div><div><em>Pseudomonas aeruginosa</em> is a major opportunistic pathogen, recognized for its antibiotic resistance, biofilm formation, and virulence factors. This study investigated 50 clinical isolates from respiratory and urinary tract infections in hospitals in Urmia, Iran, to explore the correlation between biofilm production, antibiotic resistance, pigment production, and the presence of virulence genes. Pyoverdine was produced by 40 % of the isolates, pyocyanin by 58 %, and 6 % of the strains did not produce any pigments. No significant association was found between pigment production and infection type. Biofilm formation was observed in 86 % of the isolates, with strong biofilm producers exhibiting significantly higher pyoverdine production than pyocyanin (<em>p</em> &lt; 0.001). The highest antibiotic resistance in <em>P. aeruginosa</em> isolates was observed against meropenem (94 %), while the lowest was against aztreonam (26 %). Multidrug resistance was present in 76 % of the isolates, with no significant correlation found between pigment production and antibiotic resistance. The prevalence of virulence genes included <em>algD</em> (86 %), <em>plcH</em> (82 %), <em>plcN</em> (80 %), <em>toxA</em> (72 %), <em>lasB</em> (66 %), and <em>exoS</em> (64 %). Although most genes showed no significant differences between respiratory and urinary isolates, <em>exoS</em> was significantly more prevalent in respiratory isolates (87.5 %, <em>p</em> &lt; 0.001) compared to urinary isolates (42.3 %). Additionally, <em>algD</em> and <em>lasB</em> were co-detected in 72.09 % of biofilm-producing isolates (<em>p</em> &lt; 0.05). In conclusion, the frequent detection of <em>P. aeruginosa</em> in clinical samples, along with its virulence factors, high pigment production, and biofilm formation, enhances its ability to cause persistent infections. These findings suggest that <em>exoS</em> plays a key role in respiratory infections, highlighting the pathogen's adaptability to various infection sites. This information provides a valuable foundation for developing more effective, targeted treatment strategies against this challenging pathogen.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102184"},"PeriodicalIF":1.0,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143563257","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"LncRNAs PVT1, HULC, and HOTTIP: A promising biomarker trio for diffuse large B-cell lymphoma","authors":"Milad Shahsavari ,&nbsp;Sedigheh Arbabian ,&nbsp;Farzaneh Hosseini ,&nbsp;Mohamad Reza Razavi","doi":"10.1016/j.genrep.2025.102182","DOIUrl":"10.1016/j.genrep.2025.102182","url":null,"abstract":"<div><h3>Background</h3><div>Diffuse large B-cell lymphoma (DLBCL) is the most common subtype of non-Hodgkin lymphoma (NHL) and is characterized by heterogeneity in morphology, genetics, and behavior. While the standard immunochemotherapy regimen, R-CHOP, can lead to sustained complete remission in most patients, those with relapses and poor prognoses require alternative R2-CHOP therapy.</div></div><div><h3>Methods</h3><div>Experimental and bioinformatic approaches explored the signaling pathways of three critical lncRNAs, PVT1, HULC, and HOTTIP, and their biological functions. The expression of these lncRNAs was quantitatively evaluated using real-time PCR in 100 patients before and after conventional treatment.</div></div><div><h3>Results</h3><div>PVT1, HULC, and HOTTIP expression were significantly elevated by 7.412 ± 2.497, 6.42 ± 3.32, and 4.09 ± 2.38 folds, respectively, compared to normal cases (<em>p</em> &lt; 0.001). The expression levels were significantly higher in DLBCL patients aged &gt;60 than those aged &lt;60. A significant positive correlation was observed between HULC and HOTTIP expression. Post-treatment measurements showed a significant downregulation of PVT1 and HOTTIP (p &lt; 0.001 and <em>p</em> = 0.032, respectively). Overexpression of lncRNA-miRNA interaction network analysis indicated deregulated targets, including hsa-miR-200a-3p, hsa-miR-372-3p, hsa-miR-186-5p, and others.</div></div><div><h3>Conclusions</h3><div>The long non-coding RNAs (lncRNAs) PVT1, HULC, and HOTTIP, which exhibited elevated expression levels in patients with diffuse large B-cell lymphoma (DLBCL) before treatment and decreased to normal levels following treatment, could serve as valuable diagnostic biomarkers or prognostic indicators of treatment response. Their distinct conditional expression patterns across different age demographics further support their potential utility.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102182"},"PeriodicalIF":1.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143529446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HLA Class I and II genes: A key factor for type one diabetes susceptibility","authors":"Gaurang Telang ,&nbsp;Smriti Mishra ,&nbsp;Anurag Sureshbabu ,&nbsp;Sameer Chiloo ,&nbsp;Shantanu Joshi ,&nbsp;Senthil Thyagarajan","doi":"10.1016/j.genrep.2025.102183","DOIUrl":"10.1016/j.genrep.2025.102183","url":null,"abstract":"<div><div>Type 1 diabetes (T1D) is one of the most chronic autoimmune diseases categorized by pancreatic β-cell destruction. The susceptibility towards T1D is determined using a composite interface between numerous genetic and environmental factors. The clinical inception of T1D is led by the presence of autoantibodies in contrast to β-cells. The main genetic mechanism of T1D is associated with the Major histocompatibility complex (MHC) i.e., HLA genes and it has about 50 % inclination of genetic influence located on the short arm of chromosome 6p21 extends around 4000 kb, and holds over 200 genes. These are the key fragments of genetic risk factors of T1D. The genes encrypt HLA Class I and II which mediate the pathogenetically immune mechanism. Their main purpose is intrusion and inflammation in the pancreatic islets known as insulitis. The utmost links between disease and HLA loci are with Class II genes expressed in antigenic presenting cells and also play a great role in β-cell autoimmunity, tolerance, and autoreactive T-cell response. Other non-HLA genes are also involved in this development. T cells play an important role in the recognition of islet autoantigens along with the cytokines. Many in-vivo models also provide the genetic analysis that shows the presence of frequent chromosomal regions susceptible to T1D development. Recent advances in techniques like HLA genotyping, DNA typing, and next-generation sequencing expand the genetic element information with distinct prominence of therapeutic as well as treatment, and diagnosis approaches.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102183"},"PeriodicalIF":1.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of single-nucleotide polymorphisms in opioid receptors genes on opioid use disorder susceptibility among Egyptian population: A case-control study","authors":"Amira A. Abdelnoor ,&nbsp;Mostafa M. Kamel ,&nbsp;Fatma M. Elgazzar ,&nbsp;Afaf M. Elsaid ,&nbsp;Anas M. AboSamak","doi":"10.1016/j.genrep.2025.102180","DOIUrl":"10.1016/j.genrep.2025.102180","url":null,"abstract":"<div><h3>Background</h3><div>Opioid use disorder (OUD) vulnerability, progression, and course are driven by biological, developmental, environmental, and genetic factors. Single nucleotide polymorphisms (SNPs) in opioid receptor (OPR) genes can influence receptor expression, structure, or function, potentially altering OUD susceptibility and impacting treatment response and relapse rates. Delta receptors 1 (OPRD1), kappa receptors 1 (OPRK1), and mu receptors 1 (OPRM1) are commonly studied OUD-related genes. They were examined in different ethnic groups, and their results conflicted. Therefore, this research aimed to determine the impact of sociodemographic and genetic factors on OUD risk in a sample of Egyptians. It fills a crucial gap in understanding the effect of SNPs within OPR genes on OUD among Egyptians.</div></div><div><h3>Methods</h3><div>This case-control study evaluated 50 opioid substance users versus 50 healthy, age- and sex-matched non-substance users. The sociodemographic profiles and opioid use data were collected from medical records and semi-structured interviews. Participants were assessed through the DSM-5 and ICD-11 Symptom Checklist. The SNPs in T921C of OPRD1, G36T of OPRK1, and A118G of OPRM1 genes were adopted. Venous blood samples were collected for DNA extraction and gene SNPs were examined after PCR amplification under an ultraviolet transilluminator.</div></div><div><h3>Results</h3><div>The OUD group exhibited polymorphisms in OPRD1 (2 %), OPRK1 (10 %), and OPRM1 (2 %) with no significant associations between SNPs and OUD. Multivariable regression analysis identified important OUD risk factors, including low education levels and a positive family history of SU. They were associated with an increased likelihood of OUD with 8 and 6 times, respectively.</div></div><div><h3>Conclusion</h3><div>This study provides initial evidence suggesting that OUD susceptibility among Egyptians is mainly related to sociodemographic factors rather than genetic polymorphisms in OPR genes. Pre-university education, including illiterate participants, as well as participants with primary and secondary education, increased OUD susceptibility risk &gt;8 times (<em>P</em> value &lt; 0.001, adjusted odds ratio 8.652 with 95 % confidence interval). A positive family history of SU was linked with increased susceptibility by more than sixfold (<em>P</em> value 0.029, adjusted odds ratio 6.101 with 95 % confidence interval).</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102180"},"PeriodicalIF":1.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527301","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of PCSK9 gene polymorphism on atorvastatin efficacy in Iraqi hyperlipidemic patients","authors":"Khalid Qasim Mohammed ,&nbsp;Mazin H. Ouda ,&nbsp;Suzanne Jubair","doi":"10.1016/j.genrep.2025.102181","DOIUrl":"10.1016/j.genrep.2025.102181","url":null,"abstract":"<div><h3>Background</h3><div>Many clinical observations within the local hyperlipidemic population indicate that many individuals continue to experience elevated cholesterol and low-density lipoprotein (LDL) levels despite being treated with atorvastatin. Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a crucial role in regulating LDL metabolism. This study investigates the impact of the rs28942111; T &gt; A single nucleotide polymorphism (SNP) in PCSK9 gene on the effectiveness of atorvastatin therapy among hyperlipidemic patients in Iraq.</div></div><div><h3>Methodology</h3><div>This cross-sectional study involved 149 Iraqi patients, male and female aged 28 to 85 years, who were diagnosed with primary hyperlipidemia and had been treated with oral atorvastatin (40 mg) for a minimum of six months. The lipid profiles and liver function were evaluated, the genetic analysis to identify the rs28942111 SNP was performed using the allele-specific polymerase chain reaction technique.</div></div><div><h3>Results</h3><div>The distribution of genotypes for the rs28942111; T &gt; A SNP revealed that 128 patients (85.9 %) were TT carriers, while 21 patients (14.1 %) were AA carriers, no heterozygous mutant type was detected. Significant high levels of LDL, total cholesterol (TC), and aspartate transaminase were observed among the AA carriers compared to TT carriers (<em>p</em>-value equals to 0.001).</div></div><div><h3>Conclusion</h3><div>The rs28942111 SNP in the PCSK9 gene is significantly associated with higher LDL and TC levels, this suggests that this SNP might play an important role in the therapeutic response to atorvastatin among hyperlipidemic patients in Iraq.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102181"},"PeriodicalIF":1.0,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143518995","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Independent and interactive effect of trace elements imbalance and TNF-α promoter variants as risk modifiers in pediatric asthma","authors":"Shivani Singh ,&nbsp;Anumesh K. Pathak ,&nbsp;Manish Raj Kulshrestha ,&nbsp;Aditi Singh ,&nbsp;Vandana Tiwari ,&nbsp;Shetanshu Srivastava","doi":"10.1016/j.genrep.2025.102179","DOIUrl":"10.1016/j.genrep.2025.102179","url":null,"abstract":"<div><h3>Objective</h3><div>To investigate the association between trace element (TEs) levels (zinc, copper, iron, selenium, and magnesium) and <em>TNF-α-308</em> G/A polymorphism and childhood asthma risk, severity, inflammatory markers (hs-CRP, TNF-α), and cell counts (neutrophils and eosinophils) in an Indian cohort.</div></div><div><h3>Methods</h3><div>This prospective case-control study included 433 children (230 patients with asthma and 203 controls). Serum TEs levels were quantified using inductively coupled plasma mass spectrometry, <em>TNF-α-308</em> G/A polymorphism was analyzed via restriction fragment length polymorphism, and serum TNF-α levels were measured using ELISA. Logistic regression models (adjusted for age, sex, and family history) and correlation analyses were conducted.</div></div><div><h3>Results</h3><div>Asthmatic children had significantly higher copper levels (1650.40 vs. 1274.30 μg/L;<em>p</em> = 0.002) and lower zinc (464.16 vs. 632.43 μg/L) and iron (36.00 vs. 60.00 μg/L; <em>p</em> &lt; 0.0001) levels. The <em>TNF-α-308</em> GG genotype significantly increased the asthma risk by 3.2-fold, and the GA genotype conferred a 2.5-fold increased risk. Low zinc levels combined with variant genotypes (GA + GG) increased the risk by 1.9-fold, while low iron levels with these genotypes amplified the risk by 3.2-fold. High Cu levels with variant genotypes increased the risk by 2.5-fold. Zinc was negatively correlated with TNF-α (<em>r</em> = −0.23), hs-CRP (<em>r</em> = −0.33), and neutrophil counts (<em>r</em> = −0.64), whereas copper was positively correlated with TNF-α (<em>r</em> = 0.36; <em>p</em> &lt; 0.0001) and neutrophil counts (<em>r</em> = 0.68). Elevated hs-CRP and TNF-α levels are associated with reduced lung function (FEV1) and increased asthma severity.</div></div><div><h3>Conclusion</h3><div>The interplay between TEs imbalances, TNF-α polymorphisms, and inflammatory responses significantly influences the risk and severity of childhood asthma.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102179"},"PeriodicalIF":1.0,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HR9 cell-penetrating peptide: An effective delivery approach of gene editing vectors for tumor treatment","authors":"Ali Anvar ,&nbsp;Azam Bolhassani ,&nbsp;Iman Salahshoorifar ,&nbsp;Shiva Irani","doi":"10.1016/j.genrep.2025.102177","DOIUrl":"10.1016/j.genrep.2025.102177","url":null,"abstract":"<div><div>HR9 cell-penetrating peptide is an arginine-rich peptide that can deliver various molecules into the cells. In this study, we assessed the efficacy of HR9 peptide in transporting the modified CRISPR vectors pSpCas9n (BB)-2A-GFP (PX461) and pSpCas9n (BB) (PX460) into HPV16 C3 tumor cells, and explored the impact of their treatment through tumor growth assay, and immunohistochemistry and staining techniques. Herein, the HPV16 E6 and E7 genes were targeted using CRISPR/Cas9 technology. Our findings showed improved transfection rates of HR9 peptide compared to the Lipofectamine 2000 transfection reagent for delivery of the CRISPR/Cas9 vectors into C3 tumor cells. Mice treated with PX460-E7 and PX460-E6 + PX460-E7 showed important therapeutic effects regarding tumor volume reduction and pathological analysis. Our study demonstrated the potent delivery of HR9/CRISPR/Cas9 nanoparticles into C3 tumor cells <em>in vitro</em> and <em>in vivo</em>, and also the high efficiency and specificity of CRISPR/Cas9-mediated genome editing in mice.</div></div>","PeriodicalId":12673,"journal":{"name":"Gene Reports","volume":"39 ","pages":"Article 102177"},"PeriodicalIF":1.0,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143510736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}