c-Jun Polyclonal Antibody
- Known as:
- c-Jun Polyclonal Antibody
- Catalog number:
- a-0470-100
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Epigentek inc
- Gene target:
- c-Jun Polyclonal Antibody
Related products to: c-Jun Polyclonal Antibody
Related articles to: c-Jun Polyclonal Antibody
- - Source: PubMed
Publication date: 2026/06/23
Khatami SomayehGhavidel Yazdi SomayehForouzanfar FatemehBakhshian OmidEghbali ParnianSaburi Ehsan - Dear Editor, The 2026 Bundibugyo Ebolavirus (BDBV) outbreak has once again demonstrated that the threat of emerging diseases remains a major global health challenge. The outbreak, first detected in the Democratic Republic of Congo (DRC) and spread to Uganda, is not only a regional crisis but also a test of the world's preparedness for pathogens with epidemic potential. Unlike Zaire Ebolavirus (EBOV), which has benefited from effective vaccines and treatments in recent years, BDBV still lacks a licensed vaccine or specific treatment[1]. As of June 6, a total of 515 laboratory-confirmed cases and 91 deaths have been reported in DRC, while Uganda has reported 19 laboratory-confirmed cases and two deaths. The occurrence of unexplained deaths among both the community and healthcare workers, along with prior reports of an unidentified hemorrhagic fever, suggest that the outbreak has been likely originated in March 2026 or even earlier. Accordingly, the virus is believed to have spread unnoticed for several weeks before being identified through genomic sequencing in mid-May 2026[2]. The resurgence of Ebola in Africa results from a complex interaction of environmental, social, and political factors. Deforestation, the development of mining activities, the expansion of agriculture, and increased human contact with wildlife have elevated the likelihood of spillovers from wildlife reservoirs, particularly fruit bats, which are considered the most likely natural hosts of ebolaviruses. Moreover, weak disease surveillance systems and limited access to health services have delayed the identification of early cases. The similarity of the initial symptoms of Ebola to other endemic diseases in the region, such as malaria, makes early diagnosis difficult and provides ample opportunity for transmission to spread. Insecurity, misinformation, attacks on healthcare facilities, and armed conflict in the region have also posed serious challenges to the implementation of contact tracing programs and rapid response to the epidemic[3,4]. One of the most critical challenges highlighted by this outbreak is the weakness of diagnostic capacities in the affected areas. The initial 2007 outbreak of BDBV proved that delayed lab confirmation paralyzes public health responses[5]. Now, dealing with a much larger outbreak in 2026, the persistence of this challenge highlights a dangerous failure to invest in diagnostic infrastructure over the last 19 years. Many health facilities do not have access to molecular laboratories, rapid sample transport systems, and biosafety infrastructure[6]. These limitations delay the diagnosis and isolation of patients, thus perpetuating disease transmission. Investment in the development of mobile laboratories, rapid point-of-care diagnostic tests, and digital reporting systems can dramatically reduce the time to diagnosis and response to an outbreak. The BDBV outbreak shows that laboratory preparedness must be considered an essential part of global health security. Furthermore, the early detection of emerging pathogens depends not only on diagnostic technologies but also on the expertise of local scientists who are able to recognize unusual epidemiological and laboratory patterns. During the current outbreak, suspected Ebola cases initially tested negative using common diagnostic tests (designed for Zaire Ebola Virus), which delayed the identification of the BDBV. Specifically, field-based diagnostics in Bunia were calibrated exclusively to detect the EBOV responsible for recent Congolese outbreaks. Consequently, patient samples collected throughout late April and early May yielded negative results, requiring cross-country transport to Kinshasa for genomic confirmation[2]. This experience revealed a major vulnerability in outbreak preparedness: diagnostic tools designed for known threats may be ineffective in detecting less common or unexpected pathogens. Therefore, strengthening local scientific capacities, developing genomic surveillance, and expanding access to flexible and adaptable diagnostic platforms should be considered as a top priority for global health security. The lack of a licensed vaccine for BDBV was one of the most significant challenges of this epidemic. While the rVSV-ZEBOV vaccine has played a significant role in controlling Zaire ebolavirus, there is no licensed vaccine for BDBV. In response to this outbreak, efforts to develop mRNA-based vaccines, adenoviral vectors, rVSV-based vaccines, and multipotent vaccines have been accelerated[7]. However, the experience of this epidemic has shown that the development of medical products for rare diseases continues to face financial and investment constraints. This challenge highlights the need for sustained support from governments and international institutions for research and development of pathogens with epidemic potential. The 2026 Bundibugyo outbreak provides several key lessons for the global community. First, early detection and rapid diagnosis are the most important factors in containing the epidemic. The 19-year interval between the 2007 BDBV outbreak and the 2026 outbreak underscores persistent shortcomings in investment toward decentralized, pan-ebolavirus diagnostic infrastructure, with diagnostic delays hindering timely outbreak identification in both instances. Second, the trust and active participation of local communities are as important as medical interventions. Additionally, the rapid cross-border transmission dynamics between the DRC and Uganda demonstrate that blanket travel restrictions and border closures are impractical. As communities in the Great Lakes region routinely cross national borders for trade and healthcare, coordinated regional surveillance and timely information sharing are likely to be more effective than broad border closures in mitigating disease transmission[8]. Third, the protection of health workers must be a priority in preparedness plans. Fourth, a "One Health" approach is essential for simultaneous monitoring of humans, animals, and the environment. Although BDBV is not a new pathogen, the lack of licensed medical interventions and limited investment in research reflect many of the vulnerabilities associated with the concept of "Disease X."[9]. Unlike Zaire Ebola Virus, for which licensed vaccines and monoclonal antibody therapies are available, BDBV forces public health responses to rely almost entirely on non-pharmaceutical interventions such as isolation and infection control[10]. This gap reflects the structural inequity in global health research and development funding, with pathogens affecting resource-limited regions receiving insufficient attention until they spark an international emergency[2]. The BDBV outbreak proves that global epidemic preparedness cannot be pathogen-selective; it requires proactive investment in broad-spectrum countermeasures and resilient frontline health systems[8]. In conclusion, the 2026 BDBV outbreak is a serious wake-up call for the global health system. The epidemic revealed that gaps in surveillance systems, diagnostic capacities, vaccine development, and preparedness for emerging diseases persist. Investing in health infrastructure, developing Pan-Ebolavirus vaccines, strengthening laboratories, expanding the One-Health approach, and supporting research on emerging zoonotic pathogens must be at the top of global health security priorities. Otherwise, the BDBV outbreak may be just a prelude to larger crises to come. - Source: PubMed
Publication date: 2026/06/28
Jalali TahminehPouriayevali Mohammad HasanSalehi-Vaziri Mostafa - Hypoxia (pO2 < 5-10 mmHg) is a critical feature of the tumor environment that causes genetic and epigenetic changes. This study aimed to evaluate the effect of hypoxia on the expression of immune checkpoint genes (CD39, CD47, and PD-L1) and their regulatory microRNAs (miRNAs; miR-155, miR-424, miR-133, miR-142) in the gastric cancer cell line MKN-45. - Source: PubMed
Publication date: 2026/06/21
Samemaleki SaharOrooji NiloufarKazemi TohidSolgi Ghasem - The flavor of meat is closely associated with its metabolic profile, which varies significantly among different breeds. This study utilized HS-GC-MS (headspace gas chromatography-mass spectrometry) to explore the metabolic differences in breast muscle among six chicken breeds, namely Cobb broiler (KB), Heishui Phoenix Chicken (FW), Qiangshan Cloud Chicken (YD), Daheng Black-bone Chicken (DHW), Daheng Yellow Chicken (DHH), and Daheng Partridge Chicken (DHS). Firstly, the slaughter performance and breast meat quality traits were evaluated. In comparison with the KB, local breeds exhibited lower breast muscle, drip loss, and cooking loss, while showing higher leg muscle rate, shear force, and fat content. In addition, local breeds displayed significantly different meat color, characterized by higher L*, higher a*, and lower b* values. The results showed that a clear separation was achieved between local breeds and Cobb broiler, indicating distinct metabolic differences. Specifically, comparisons of FW vs. KB, YD vs. KB, DHW vs. KB, DHH vs. KB, and DHS vs. KB revealed 17, 12, 28, 17, and 15 significantly altered metabolites, respectively. These differential metabolites were mainly categorized into amino acids, fatty acids, and their derivatives. Correlation analysis identified diverse positive and negative links among these metabolites, constituting a complex metabolic regulatory network. KEGG pathway enrichment analysis revealed that the differential metabolites were primarily enriched in synthesis and degradation of ketone bodies, lipoic acid metabolism, butanoate metabolism, propanoate metabolism, fatty acid biosynthesis, and phenylalanine metabolism. These pathways are pivotal to the nutrient composition and flavor development of breast muscle in chicken. This study reveals metabolic characteristics and differences in breast muscle among diverse chicken breeds, laying a theoretical foundation for optimizing chicken breeding, improving meat quality, regulating flavor traits, and exploring the molecular mechanisms underlying metabolic regulation in chicken breast muscle. - Source: PubMed
Publication date: 2026/06/16
Yu ChunlinLi FucanZhang ZengrongWang JiangxianQiu MohanHu ChenmingChen JialeiYang LiXia BoXiong XiaSong XiaoyanPeng HanZhu ShiliangDu LonghuanZhao JiayiZhang YueyingFan HuaWu JinboYang Chaowu - The virome plays a significant role in maintaining the gut health of the host. Fecal virome transplantation (FVT), a burgeoning therapeutic strategy, holds promise in regulating intestinal microecology and treating associated diseases. However, the presence of eukaryotic viruses in FVT poses potential risks, which may compromise its safety and efficacy. This study leverages the key distinction between bacteriophages and eukaryotic viruses-namely, the presence or absence of an envelope-to reduce the burden of eukaryotic viruses in samples via solvent/detergent (S/D) treatment, while preserving the biologically active phageome. To this end, fecal samples were collected from healthy AA broilers, and the virome was isolated and subjected to S/D treatment. Subsequent DNA virome sequencing analysis was conducted to evaluate the impact of this treatment. The results indicated that S/D treatment tended to decrease the relative abundance of eukaryotic viral families (e.g., Adenoviridae, Parvoviridae), while bacteriophages remained the dominant viral component. α-diversity analysis revealed no significant differences in overall viral diversity post-treatment. However, β-diversity analysis indicated shifts in viral community composition. Further differential virus analysis revealed a significant increase in the relative abundance of specific bacteriophages following treatment. Finally, functional analysis of the virome revealed a diverse array of genes involved in DNA metabolism and host cell wall remodeling. Notably, the primary functional distinction between FVT0 and FVT1 was the attenuated response to eukaryotic viruses in FVT1. Collectively, this study suggests that S/D treatment may reduce the abundance of eukaryotic viruses in FVT, thereby enhancing clinical safety. These findings provide a theoretical basis and methodological support for the safe application of FVT in the treatment of animal diseases, paving the way for more secure and effective viral therapies. - Source: PubMed
Publication date: 2026/06/02
Li HuiminButtimer ColinZeng YujuanLi XinglongJia YiminPang MaodaLi YueZhang HuiZhou YanWang RanBao Hongduo