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MR

MR vaccine (Mebella)

✓ Approved

Indian Immunologicals · 疫苗 · 疫苗

什么是 MR vaccine？

MR vaccine 是一种疫苗，由Indian Immunologicals研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Subcutaneous Injection。

药物档案

商品名Mebella
公司Indian Immunologicals
药物类别疫苗, 大分子
给药途径Injectable (Others), Subcutaneous Injection
状态Approved
来源： ClinicalTrials.gov, Indian Immunologicals

治疗适应症

MR vaccine 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Infections and infestationsMeasles✓ Approved

相关研究文献

PubMedESC heart failure2026-08-04

Mitral regurgitation and all-cause mortality in acute heart failure; a meta-analysis.

Berrill Max M, Bengisu Meric M, Kipourou Konstantina K, Ken Dror Gie G et al.

Despite previous studies investigating the impact of mitral regurgitation (MR) in acute heart failure (AHF) there are inconsistencies in trial data, and no meta-analyses to date. Our aim was to explore if MR is associated with mortality in AHF. We performed a meta-analysis of AHF patients with MR to investigate any association with all-cause mortality. We identified 27 studies that met our inclusion criteria, encompassing 73,363 patients (age 72.9±4.2years; females 44.4%) with an average follow-up of 1.9 years. Moderate/severe MR was associated with an unadjusted 47% increased mortality risk compared to no/mild MR (OR 1.47 [95% CI 1.30-1.66, p<0.001]). This excess risk of death persisted among studies reporting adjusted data (OR 1.21 [95% CI 1.01-1.45, p=0.038]). Compared to those with no MR, MR severity was associated with increasing risk of death: mild MR OR 1.22 [95% CI 0.98-1.53, p=0.079], moderate MR OR 1.48 [95% CI 1.1-2.01, p=0.011] and severe MR OR 1.60 [95% CI 1.13-2.27, p=0.008]. We observed excess mortality in moderate/severe MR compared to no/mild MR among individuals with a left ventricular ejection fraction (LVEF) <50% (OR 1.26 [95% CI 1.18-1.35, p<0.001]) and LVEF 40-50% (OR 2.00 [95% CI 1.59-2.50, p<0.001]) but not LVEF >50% (OR 1.16 [95% CI 0.91-1.47, p=0.23]. Neither meta-regression nor pre-specified sensitivity analyses affected MR's association with the primary outcome. A substantial degree of heterogeneity was observed across the included studies. We observed that MR during AHF is associated with increased mortality. Although causality cannot be inferred due to the observational design and high heterogeneity of the included studies, MR may represent a phenotype amenable to targeted therapies during decompensated heart failure.

PMID 42549561
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PubMedThe Lancet. Infectious diseases2026-08-04

Efficacy, immunogenicity, and safety of the 9-valent human papillomavirus vaccine in males aged 16-26 years in Japan: a randomised, double-blind, placebo-controlled trial.

Hisamoto Koji K, Yamanaka Masaki M, Nomura Masayasu M, Kanno Nobufumi N et al.

Efficacy of the nine-valent human papillomavirus (9vHPV; HPV6, 11, 16, 18, 31, 33, 45, 52, and 58) vaccine was shown in females and inferred for males through immunobridging. We evaluated the efficacy of the 9vHPV vaccine in males aged 16-26 years. This randomised, double-blind, placebo-controlled, efficacy, immunogenicity, and safety phase 3 trial was conducted at 22 clinical research, hospital, medical, or treatment sites in Japan, with masking of investigators, sponsor personnel, and participants. Healthy males aged 16-26 years with no history of human papillomavirus (HPV)-related lesions and no previous HPV vaccination were randomly assigned (1:1) centrally, using permutated blocks (block sizes of four), to receive three intramuscular injections of the 9vHPV vaccine or placebo (saline) at day 1, month 2, and month 6. The primary and secondary efficacy endpoints were the combined incidences of 6-month anogenital persistent infection related to HPV6, 11, 16, and 18 and HPV31, 33, 45, 52, and 58. Anogenital swabs and external genital tissue samples were tested for the presence of HPV DNA. Tissue samples were adjudicated for histopathology diagnosis. The primary and secondary efficacy evaluations were tested for superiority with a margin of 0% in the per-protocol population. Another secondary endpoint was antibody responses to each vaccine-targeted HPV type at month 7; immunogenicity analyses were conducted in the per-protocol immunogenicity population. Safety was assessed in participants who received at least one dose of vaccine or placebo. This study is registered with ClinicalTrials.gov (NCT04635423) and is completed. Between Nov 30, 2020, and Dec 25, 2021, 1059 participants were enrolled and randomly assigned to receive the 9vHPV vaccine (n=529) or placebo (n=530). Vaccine efficacy for the primary and secondary endpoints was 89·3% (95% CI 55·4-98·2; p=0·0002) and 63·5% (2·7-86·0; p=0·023), respectively, in the initial efficacy analysis based on a visit cutoff date of Dec 29, 2023, and 91·6% (67·7-98·6) and 72·9% (38·7-89·3) in the end-of-study efficacy analysis based on a visit cutoff date of July 16, 2024. Seroconversion rates were greater than 98% for each vaccine-targeted HPV type. Injection-site adverse events were reported in 370 (70%) of 529 9vHPV vaccine recipients and 162 (31%) of 530 placebo recipients, and vaccine-related systemic adverse events in 58 (11%) vaccine recipients and 52 (10%) placebo recipients; most cases were mild or moderate. No deaths, vaccine-related serious adverse events, or discontinuations due to adverse events were reported. The 9vHPV vaccine prevents anogenital persistent infection related to vaccine-targeted HPV types in males and has an acceptable safety profile. These findings support the use of the 9vHPV vaccine in males to prevent HPV-related anogenital diseases. Merck Sharp & Dohme. For the Japanese translation of the abstract see Supplementary Material section.

PMID 42546724
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PubMedJournal of cellular and molecular medicine2026-08-04

Multi-Omics Profiling Identifies Novel Therapeutic Targets and Pathobiological Mechanisms in Oral Cancer.

Huang Meishan M, Wang Hongwei H, Mo Xiaoqiang X, Huang Xiong X et al.

Oral cancer (OC) remains a therapeutic challenge due to limited validated targets. Cis-pQTLs from the deCODE cohort (n = 35,559) were harmonized with OC-GWAS (3547 cases and 691,466 controls) meta-data through a two-sample Mendelian randomization (MR) framework. Robust Validation included replication in the UKB-PPP dataset, colocalization analysis, SMR (Summary-based MR), HEIDI (Heterogeneity in Dependent Instruments) tests, and eQTL evidence. Additional analyses encompassed protein-protein interaction (PPI) networks, Kyoto Encyclopedia of Genes and Genomes annotation (KEGG)/Gene Ontology (GO) pathway enrichment, mediation, Druggability and side effects analysis. Oral cancer (OC) remains a therapeutic challenge due to limited validated targets. Cis-pQTLs from the deCODE cohort (n = 35,559) were harmonized with OC-GWAS (3547 cases and 691,466 controls) meta-data through a two-sample Mendelian randomization (MR) framework. Robust Validation included replication in the UKB-PPP dataset, colocalization analysis, SMR (Summary-based MR), HEIDI (Heterogeneity in Dependent Instruments) tests, and eQTL evidence. Additional analyses encompassed protein-protein interaction (PPI) networks, Kyoto Encyclopedia of Genes and Genomes annotation (KEGG)/Gene Ontology (GO) pathway enrichment, mediation, Druggability and side effects analysis. To experimentally corroborate the MR findings, the quantitative real-time PCR (qRT-PCR) was performed to examine the mRNA expression levels of selected genes in oral squamous cell carcinoma (OSCC) cell lines (SCC-9 and SCC-25) and normal human oral epithelial cells (HOEC). Multi-omics MR identified TNFSF8 (p = 2.49 × 10-8, OR = 1.24) as a Tier 1 target. XXYLT1 (p = 1.41 × 10-4, OR = 1.34) and HSD17B14 (p = 0.04, OR = 2.00) achieved Tier 2. eQTLs-pQTLs Relationship revealed XXYLT1 expression explained 24.65% of risk through elevated plasma protein levels, TNFSF8 eQTLs mediated 72.80% via protein upregulation. Mediation analyses on CD4 on HLA DR+ CD4+ T cells (7.18%) contributed to the risk of OC by upregulating plasma HSD17B14, while daily cigarette consumption (20.63%) and CD8+ T cell percentage leukocytes (12.06%) contributed to the risk of OC by upregulating plasma TNFSF8. Drug safety assessments highlighted systemic TNFSF8 inhibition may elevate skin cancer risk. Multi-omics MR prioritizes TNFSF8 as a therapeutic target for oral cancer. Multi-omics MR identified TNFSF8 (p = 2.49 × 10-8, OR = 1.24) as a Tier 1 target. XXYLT1 (p = 1.41 × 10-4, OR = 1.34) and HSD17B14 (p = 0.04, OR = 2.00) achieved Tier 2. eQTLs-pQTLs Relationship revealed XXYLT1 expression explained 24.65% of risk through elevated plasma protein levels, TNFSF8 eQTLs mediated 72.80% via protein upregulation. Mediation analyses on CD4 on HLA DR+ CD4+ T cells (7.18%) contributed to the risk of OC by upregulating plasma HSD17B14, while daily cigarette consumption (20.63%) and CD8+ T cell percentage leukocytes (12.06%) contributed to the risk of OC by upregulating plasma TNFSF8. Drug safety assessments highlighted systemic TNFSF8 inhibition may elevate skin cancer risk. qRT-PCR confirmed significant upregulation of XXYLT1 and HSD17B14 in both SCC-9 and SCC-25 cell lines (p < 0.001), which is consistent with MR predictions. TNFSF8 was not reliably detected in these cancer cells, aligning with its proposed immune-mediated mechanism. Multi-omics MR prioritizes TNFSF8 as a therapeutic target for oral cancer. qPCR validation confirms the dysregulation of XXYLT1 and HSD17B14, while findings regarding TNFSF8 underscore its immune origin. These findings warrant further functional studies.

PMID 42548293
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PubMedZhonghua shao shang yu chuang mian xiu fu za zhi2026-08-04

[Bidirectional two-sample MR analysis of causal relationships between human inflammatory proteins and HS and keloids].

Wang S S SS, Xiao K K, Xiao H T HT, Han D W DW et al.

Objective: To explore the causal relationships between human inflammatory proteins and hypertrophic scars (HS) and keloids. Methods: This study was conducted based on bidirectional two-sample Mendelian randomization (MR) analysis. Data of human inflammatory proteins, HS, and keloids were acquired from genome-wide association study database. The inverse variance weighted (IVW) method was adopted to evaluate the causal relationships between 91 kinds of human inflammatory proteins and HS and keloids, i.e., a forward MR analysis. For the above associations, Cochran's Q test was used to assess heterogeneity, MR-Egger regression and MR-PRESSO outlier tests were performed to evaluate horizontal pleiotropy, and the leave-one-out method was applied to analyze the robustness of the results. The IVW method was also used to evaluate whether there was a reverse causal relationship between HS, keloids and inflammatory proteins screened out by aforementioned forward MR analysis. Results: CD6, leukemia inhibitory factor (LIF), tumor necrosis factor ligand superfamily member 12 (TNFSF12), programmed death-ligand 1 (PD-L1), interleukin-17C (IL-17C), LIF receptor (LIFR), osteoprotegerin (OPG), and fibroblast growth factor 23 (FGF23) had significant causal relationships with HS (with ORs of 1.365, 0.506, 1.567, 1.683, 0.621, 1.375, 0.623, and 0.553, respectively, 95% CIs of 1.100-1.693, 0.289-0.887, 1.081-2.273, 1.090-2.599, 0.408-0.947, 1.025-1.845, 0.402-0.966, and 0.315-0.971, respectively, P<0.05). Among them, CD6, TNFSF12, PD-L1, and LIFR were risk factors for HS, while LIF, IL-17C, OPG, and FGF23 were protective factors for HS. CD5, IL-10 receptor subunit alpha (IL-10RA), IL-5, LIF, and OPG had significant causal relationships with keloids (with ORs of 0.744, 1.303, 0.686, 0.603, and 0.715, respectively, 95% CIs of 0.573-0.965, 1.024-1.660, 0.472-0.996, 0.431-0.842, and 0.553-0.924, respectively, P<0.05). Among them, IL-10RA was a risk factor for keloids, whereas CD5, IL-5, LIF, and OPG were protective factors for keloids. No significant heterogeneity or horizontal pleiotropy was observed in the above associations (P>0.05), and the robustness of the results was not driven by any single nucleotide polymorphism. Significant reverse causal relationships existed between HS and TNFSF12 and LIFR of the 8 inflammatory proteins which had significant causal relationships with HS screened out by aforementioned forward MR analysis (with ORs of 0.972 and 0.968, respectively, 95% CIs of 0.949-0.997 and 0.942-0.994, respectively, P<0.05). No reverse causal relationship was found between keloids and the 5 inflammatory proteins which had significant causal relationships with keloids screened out by aforementioned forward MR analysis (P>0.05). Conclusions: CD6, TNFSF12, PD-L1, and LIFR may increase the risk of HS, while LIF, IL-17C, OPG, and FGF23 may decrease the risk of HS. IL-10RA may increase the risk of keloids, while CD5, IL-5, LIF, and OPG may decrease the risk of keloids.

PMID 42547441
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PubMedClinics in geriatric medicine2026-08-04

Vaccine-Preventable Diseases in Older Adults.

Al-Jabri Maha M, Rosero Christian C, Saade Elie A EA

Older adults are at an increased risk of vaccine-preventable diseases partly because of physiologic changes in the immune and other body systems related to age and/or accumulating comorbidities that increase the vulnerability to infections and decrease the response to vaccines. Strategies to improve the response to vaccines include using a higher antigenic dose (such as in the high-dose inactivated influenza vaccines) as well as adding adjuvants (such as MF59 in the adjuvanted inactivated influenza vaccine).

PMID 42547175
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PubMedJournal of applied clinical medical physics2026-08-04

Synthetic CT artifacts in MR-only brain radiotherapy: Clinical implementation experience.

Lee Hyeri H, Ayan Ahmet S AS, Beyer Sasha S, Blakaj Dukagjin D et al.

Magnetic resonance imaging (MRI) provides superior soft tissue contrast compared with CT and is essential for delineation of targets and organs at risk in brain radiotherapy. Because CT is traditionally required for dose calculation in radiation therapy, synthetic CT (sCT) generation from MRI has enabled the development of MR-only workflows. Prior studies have primarily focused on dosimetric equivalence between CT- and sCT-based treatment plans, with limited emphasis on practical implementation challenges encountered during clinical use. This study aimed to share clinical experience implementing an MR-only brain radiotherapy workflow, with a focus on practical challenges encountered. Twenty-eight patients underwent a dedicated MR simulation protocol for sCT generation in addition to standard-of-care planning CT simulation. MRI acquisition was performed using an immobilization mask with a dedicated head coil positioned over the mask. The sCT protocol consisted of four sequences: T1 VIBE Dixon, T2 SPACE, PETRA, and TOF-MRA. Clinical treatment plans generated using the planning CT (pCT) for photon therapy were recalculated on the corresponding sCT datasets. Twenty-eight patients were scanned, and 25 synthetic CT datasets were successfully generated. Nine sCT datasets required rigid re-registration because of inter-sequence patient motion. Findings were categorized into workflow-related sCT challenges, including inter-sequence motion, suboptimal coil placement, and external localization marker interference, and algorithm-related imaging artifacts, including HU misclassification at tissue/bone/air interfaces and sCT degradation in post-operative anatomy with surgical meshes. Clinical implementation of a brain MR-only workflow identified two major categories of challenge: workflow-related sCT perturbations and algorithm-related imaging artifacts. This distinction has important implications for mitigation strategies. Case-specific sCT review, structured eligibility screening, and prospective site commissioning are essential for safe clinical deployment. Practical commissioning and per-patient QA checklists are provided as supplementary materials.

PMID 42547918
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