Corrigendum: Characterizing the neutrophilic inflammation in chronic rhinosinusitis with nasal polyps.

[This corrects the article DOI: 10.3389/fcell.2021.793073.].

Breviscapine Reduces Sepsis-Induced Acute Lung Injury by Targeting CASP8 to Regulate Neutrophil Apoptosis and Inflammation.

Background: Breviscapine has been demonstrated to have beneficial effects in ameliorating acute lung injury (ALI), yet its potential therapeutic value and molecular mechanisms in sepsis-induced ALI remain unexplored. Methods: We utilized network pharmacology approach to identify the potential targets and mechanisms of breviscapine in treating sepsis-induced ALI. To construct a murine model of sepsis, we performed cecal ligation and puncture (CLP). Hematoxylin and eosin (HE) staining and enzyme-linked immunosorbent assay (ELISA) were employed to respectively determine the pathologic changes and levels of inflammatory factors. Neutrophil count and total protein level in bronchoalveolar lavage fluid (BALF) were detected by corresponding kit. Additionally, we utilized flow cytometry, immunofluorescence, Western blotting, and real-time reverse transcription PCR (qRT-PCR) to detect cell apoptosis, protein expression, and gene expression. Finally, we used ELISA kits to detect the activity of myeloperoxidase (MPO) and caspase-8 (CASP8). Results: Breviscapine was revealed to target 81 potential proteins in the treatment of sepsis-induced ALI, while CASP8 was the most important one as demonstrated by network analysis. In vivo experiments demonstrated that breviscapine effectively reduced the severity of sepsis-induced ALI and inflammation, and significantly suppressed neutrophil infiltration in the lung tissues of CLP mice and promoted neutrophil apoptosis in the peripheral blood. In vitro experiments revealed that lipopolysaccharide (LPS)-induced neutrophil apoptosis was inhibited, and the expression and activity of CASP8 were down-regulated. Breviscapine intervention markedly up-regulated the expression and activity of CASP8, consequently activating neutrophil apoptosis and inhibiting inflammatory response by activating the NF-κB signaling pathway. Conclusion: Breviscapine is remarkably effective in improving sepsis-induced ALI, and its mechanism of action may be to induce neutrophil apoptosis, inhibit inflammatory overreaction and reduce its infiltration in pulmonary tissues by up-regulating the expression and activity of CASP8.

The impact of the doctor-nurse-patient workshop transitional care model on the post-operative quality of life of patients with laryngeal cancer.

OBJECTIVE: The aim of this study is to assess the efficacy of the doctor-nurse-patient workshop transitional care model on post-operative care for patients with laryngeal cancer and its influence on quality of life. METHODS: A total of 68 patients with laryngeal cancer who underwent surgical treatment at the hospital between 2021 and 2022 were included in the study. The patients were divided into two groups, a control group and a research group, each consisting of 34 patients, based on the chronological sequence of their surgeries. Patients in the control group received standard nursing care, while those in the research group received the doctor-nurse-patient workshop transitional care model in addition to standard nursing care. After 2 months of care, levels of albumin (ALB), total protein (TP), hemoglobin (Hb), and quality of life scores (measured using the Quality of Life Instrument for Head and Neck Cancer, QLICP-HN) were compared between the two groups. Additionally, the incidence of adverse events during the recovery period was assessed and compared between the two groups. RESULTS: Following 2 months of care, patients in the research group exhibited elevated ALB, TP, and Hb levels compared to those in the control group. Additionally, the average QLICP-HN scores were higher in the research group, while the incidence of adverse events was lower compared to the control group. CONCLUSION: Implementing the doctor-nurse-patient workshop transitional care model in home care for patients with laryngeal cancer can enhance their nutritional status post-surgery and improve their quality of life during home rehabilitation. This, in turn, leads to a reduction in the incidence of adverse events and complications during the recovery period.

The novel non-classical HLA-G*01:55 identified in a Chinese individual.

The non-classical HLA-G*01:55 allele differs from G*01:01:12 at one position in exon 4.

Precipitation changes alter plant dominant species and functional groups by changing soil salinity in a coastal salt marsh.

Specific mechanisms of precipitation change due to global climate variability on plant communities in coastal salt marsh ecosystems remain unknown. Hence, a field manipulative precipitation experiment was established in 2014 and 5 years of field surveys of vegetation from 2017 to 2021 to explore the effects of precipitation changes on plant community composition. The results showed that changes in plant community composition were driven by dominant species, and that the dominance of key species changed significantly with precipitation gradient and time, and that these changes ultimately altered plant community traits (i.e., community density, height, and species richness). Community height increased but community density decreased with more precipitation averaged five years. Furthermore, changes in precipitation altered dominant species composition and functional groups mainly by influencing soil salinity. Salinity stress caused by decreased precipitation shifted species composition from a dominance of taller perennials and grasses to dwarf annuals and forbs, while the species richness decreased. Conversely, soil desalination caused by increased precipitation increased species richness, especially increasing in the dominance of grasses and perennials. Specifically, Apocynaceae became dominance from rare while Amaranthaceae decreased in response to increased precipitation, but Poaceae was always in a position of dominance. Meanwhile, the dominance of grasses and perennials has the cumulative effect of years and their proportion increased under the increased 60% of ambient precipitation throughout the years. However, the annual forb Suaeda glauca was gradually losing its dominance or even becoming extinct over years. Our study highlights that the differences in plant salinity tolerance are key to the effects of precipitation changes on plant communities in coastal salt marsh. These findings aim to provide a theoretical basis for predicting vegetation dynamics and developing ecological management strategies to adapt to future precipitation changes.

The B-box transcription factor BnBBX22.A07 enhances salt stress tolerance by indirectly activating BnWRKY33.C03.

Salt stress has a detrimental impact on both plant growth and global crop yields. B-box proteins have emerged as pivotal players in plant growth and development regulation. Although the precise role of B-box proteins orchestrating salt stress responses in B. napus (Brassica napus) is not well understood in the current literature, further research and molecular explorations are required. Here, we isolated the B-box protein BnBBX22.A07 from B. napus. The overexpression of BnBBX22.A07 significantly improved the salt tolerance of Arabidopsis (Arabidopsis thaliana) and B. napus. Transcriptomic and histological analysis showed that BnBBX22.A07 enhanced the salt tolerance of B. napus by activating the expression of reactive oxygen species (ROS) scavenging-related genes and decreasing salt-induced superoxide anions and hydrogen peroxide. Moreover, BnBBX22.A07 interacted with BnHY5.C09, which specifically bound to and activated the promoter of BnWRKY33.C03. The presence of BnBBX22.A07 enhanced the activation of BnHY5.C09 on BnWRKY33.C03. Overexpression of BnHY5.C09 and BnWRKY33.C03 improved the salt tolerance of Arabidopsis. Functional analyses revealed that BnBBX22.A07-mediated salt tolerance was partly dependent on WRKY33. Taken together, we demonstrate that BnBBX22.A07 functions positively in salt responses not only by activating ROS scavenging-related genes but also by indirectly activating BnWRKY33.C03. Notably, our study offers a promising avenue for the identification of candidate genes that could be harnessed in breeding endeavours to develop salt-resistant transgenic crops.

Mitochondria Transplantation to Bone Marrow Stromal Cells Promotes Angiogenesis During Bone Repair.

Angiogenesis is crucial for successful bone defect repair. Co-transplanting Bone Marrow Stromal Cells (BMSCs) and Endothelial Cells (ECs) has shown promise for vascular augmentation, but it face challenges in hostile tissue microenvironments, including poor cell survival and limited efficacy. In this study, the mitochondria of human BMSCs are isolated and transplanted to BMSCs from the same batch and passage number (BMSCsmito). The transplanted mitochondria significantly boosted the ability of BMSCsmito-ECs to promote angiogenesis, as assessed by in vitro tube formation and spheroid sprouting assays, as well as in vivo transplantation experiments in balb/c mouse and SD rat models. The Dll4-Notch1 signaling pathway is found to play a key role in BMSCsmito-induced endothelial tube formation. Co-transplanting BMSCsmito with ECs in a rat cranial bone defect significantly improves functional vascular network formation, and improve bone repair outcomes. These findings thus highlight that mitochondrial transplantation, by acting through the DLL4-Notch1 signaling pathway, represents a promising therapeutic strategy for enhancing angiogenesis and improving bone repair. Hence, mitochondrial transplantation to BMSCS as a therapeutic approach for promoting angiogenesis offers valuable insights and holds much promise for innovative regenerative medicine therapies.

MICB*002:06, a novel exonic variant of MICB (MHC class I chain-related gene B).

MICB*002:06 differs from MICB*002:01:01 by one nucleotide change at nucleotide 33 in exon 1 from C to T.

Chemoenzymatic Synthesis of DNP-Functionalized FGFR1-Binding Peptides as Novel Peptidomimetic Immunotherapeutics for Treating Lung Cancer.

Receptor-binding peptides are promising candidates for tumor target therapy. However, the inability to occupy "hot spots" on the PPI interface and rapid metabolic instability are significant limitations to their clinical application. We investigated a new strategy in which an FGFR1-binding peptide (Pep1) was site-specifically functionalized with the dinitrophenyl (DNP) hapten at the C-terminus. The resulting Pep1-DNP conjugates retained FGFR1 binding affinity and exhibited a similar potency in inhibiting FGF2-dependent cell proliferation, comparable to that of native Pep1 in vitro. In addition, three conjugates could recruit anti-DNP antibodies onto the surface of cancer cells, thereby mediating the CDC efficacy. In vivo pharmacokinetic studies and antitumor studies demonstrated that optimal conjugate 9 exhibited significantly prolonged half-lives and improved antitumor efficacy without prominent toxicity compared to those of native Pep1. This is a general and cost-effective approach for generating peptidomimetic immunotherapeutics with multiple antitumor mechanisms that may have broad applications in cancer therapy.

[Action mechanism of Huotu Jiji Pellets in the treatment of erectile dysfunction: An exploration based on network pharmacology and molecular docking].

OBJECTIVE: To explore the potential action mechanism of Huotu Jiji Pellets (HJP) in the treatment of erectile dysfunction (ED) based on network pharmacology and molecular docking. METHODS: We identified the main effective compounds and active molecular targets of HJP from the database of Traditional Chinese Medicine Systems Pharmacology (TCMSP) and Integrative Pharmacology-Based Research Platform of Traditional Chinese Medicine (TCMIP) and the therapeutic target genes of ED from the databases of Genecards. Then we obtained the common targets of HJP and ED using the Venny software, constructed a protein-protein interaction (PPI) network of HJP acting on ED, and screened out the core targets with the Cytoscape software. Lastly we performed GO functional enrichment and KEGG pathway enrichment analyses of the core targets followed by molecular docking of HJP and the core targets using Chem3D and AutoDock Tools and QuickVina-W software. RESULTS: A total of 64 effective compounds, 822 drug-related targets, 1 783 disease-related targets and 320 common targets were obtained in this study. PPI network analysis showed that the core targets of HJP for ED included ESR1, HSP90AA1, SRC, and STAT3. GO functional enrichment analysis indicated the involvement of the core targets in such biological processes as response to xenobiotic stimulus, positive regulation of kinase activity, and positive regulation of MAPK cascade. KEGG pathway enrichment analysis suggested that PI3K-Akt, apoptosis, MAPK, HIF-1, VEGF, autophagy and other signaling pathways may be related to the mechanism of HJP acting on ED. Molecular docking prediction exhibited a good docking activity of the key active molecules of HJP with the core targets. CONCLUSION: This study showed that HJP acted on ED through multi-components, multi-targets and multi-pathways, which has provided some evidence and reference for the clinical treatment and subsequent studies of the disease.

Pterostilbene Alleviates Dextran Sodium Sulfate (DSS)-Induced Intestinal Barrier Dysfunction Involving Suppression of a S100A8-TLR-4-NF-κB Signaling Cascade.

Intestinal barrier hemostasis is the key to health. As a resveratrol analogue, pterostilbene (PT) has been reported to prevent dextran sodium sulfate (DSS)-induced intestinal barrier dysfunction mainly associated with the intestinal NF-κB signaling pathway. However, the exact underlying mechanisms are not yet well-defined yet. In this study, we performed RNA-sequencing analysis and unexpectedly found that alarmin S100A8 sensitively responded to DSS-induced intestinal injury. Accordingly, histologic assessments suggested that the high expression of S100A8 was accompanied by increased intestinal infiltration of macrophages, upregulated intestinal epithelial Toll-like receptor 4 (TLR-4), and activated NF-κB signaling pathway. Interestingly, the above phenomena were effectively counteracted upon the addition of PT. Furthermore, by using a coculture system of macrophage THP-1 cells and HT-29 colon cells, we identified macrophage-secreted S100A8 activated intestinal epithelial NF-κB signaling pathway through TLR-4. Taken together, these findings suggested that PT ameliorated DSS-induced intestinal barrier injury through suppression of the macrophage S100A8-intestinal epithelial TLR-4-NF-κB signaling cascade.

Vitamin B6 prevents heart failure with preserved ejection fraction through downstream of kinase 3 in a mouse model.

BACKGROUND: There is an urgent need to develop an efficient therapeutic strategy for heart failure with preserved ejection fraction (HFpEF), which is mediated by phenotypic changes in cardiac macrophages. We previously reported that vitamin B6 (VB6) inhibits macrophage-mediated inflammasome activation OBJECTIVE: We sought to examine whether the prophylactic use of VB6 prevents HFpEF METHODS: HFpEF model was elicited by a combination of high fat diet and Nω-nitro-l-arginine methyl ester in mice. Cardiac function was assessed using conventional echocardiography and Doppler imaging. Immunohistochemistry and immunoblotting were used to detect changes in the macrophage phenotype and myocardial remodeling-related molecules RESULTS: Co-administration of VB6 with HFpEF mice mitigated HFpEF phenotypes, including diastolic dysfunction, cardiac macrophage phenotypic shifts, fibrosis, and hypertrophy. Echocardiographic improvements were observed, with the E/E' ratio decreasing from 42.0 to 21.6 and the E/A ratio improving from 2.13 to 1.17. The exercise capacity also increased from 295.3 m to 657.7 m. However, these beneficial effects were negated in downstream of kinase 3 (DOK3)-deficient mice. Mechanistically, VB6 increased DOK3 protein levels and inhibited macrophage phenotypic changes, which were abrogated by an AMP-activated protein kinase inhibitor CONCLUSION: VB6 increases DOK3 signaling to lower the risk of HFpEF by inhibiting phenotypic changes in cardiac macrophages.

Predicting the distribution of potentially suitable habitat in China for Cirsium japonicum Fisch. ex DC. under future climate scenarios based on the R-optimized MaxEnt model.

Cirsium japonicum contains a variety of medicinal components with good clinical efficacy. With the rapid changes in global climate, it is increasingly important to study the distribution of species habitats and the factors influencing their adaptability. Utilizing the MaxEnt model, we forecasted the present and future distribution regions of suitable habitats for C. japonicum under various climate scenarios. The outcome showed that under the current climate, the total suitable area of C. japonicum is 2,303,624 km2 and the highly suitable area is 79,117 km2. The distribution of C. japonicum is significantly influenced by key environmental factors such as temperature annual range, precipitation of the driest month, and precipitation of the wettest month. In light of future climate change, the suitable habitat for C. japonicum is anticipated to progressively relocate toward the western and northern regions, leading to an expansion in the total suitable area. These findings offer valuable insights into the conservation, sustainable utilization, and standardized cultivation of wild C. japonicum resources.

The HD-ZIP II gene PaHAT14 increases cuticle deposition by down-regulating ERF gene PaERF105 in Phalaenopsis.

To analyze the gene involved in orchid floral development, a HD-Zip II gene PaHAT14, which specifically and highly expressed in perianth during early flower development was identified from Phalaenopsis. Transgenic Arabidopsis plants expressing 35S::PaHAT14 and 35S::PaHAT14+SRDX (fused with the repressor motif SRDX) exhibited similar altered phenotypes, including small leaves, early flowering, and bending petals with increased cuticle production. This suggests that PaHAT14 acts as a repressor. In contrast, transgenic Arabidopsis plants expressing 35S::PaHAT14+VP16 (fused with the activation domain VP16) exhibited curled leaves, late flowering, and folded petals with decreased cuticle production within hardly opened flowers. Additionally, the expression of the ERF gene DEWAX2, which negatively regulates cuticular wax biosynthesis, was down-regulated in 35S::PaHAT14 and 35S::PaHAT14+SRDX transgenic Arabidopsis, while it was up-regulated in 35S::PaHAT14+VP16 transgenic Arabidopsis. Furthermore, transient overexpression of PaHAT14 in Phalaenopsis petal/sepal increased cuticle deposition due to the down-regulation of PaERF105, a Phalaenopsis DEWAX2 orthologue. On the other hand, transient overexpression of PaERF105 decreased cuticle deposition, whereas cuticle deposition increased and the rate of epidermal water loss was reduced in PaERF105 VIGS Phalaenopsis flowers. Moreover, ectopic expression of PaERF105 not only produced phenotypes similar to those in 35S::PaHAT14+VP16 Arabidopsis but also compensated for the altered phenotypes observed in 35S::PaHAT14 and 35S::PaHAT14+SRDX Arabidopsis. These results suggest that PaHAT14 promotes cuticle deposition by negatively regulating downstream gene PaERF105 in orchid flowers.

MgAl-LDH nanoflowers as a novel sensing material for high-performance humidity sensing.

This work details a novel application of MgAl-LDH nanoflowers, applied in the fabrication of humidity sensors using quartz crystal microbalance (QCM). An oscillating circuit approach has been utilized to thoroughly investigate the humidity detection characteristics of QCM sensors that are fabricated using MgAl-LDH nanoflowers. The examination encompassed various parameters such as the sensors' response, humidity hysteresis, repeatability, and stability. Experimental results clearly indicate that these MgAl-LDH nanoflower-based QCM sensors exhibit a distinct logarithmic frequency response to varying moisture levels. Notably, the sensitivity of the sensors is intricately tied to the amount of MgAl-LDH nanoflowers utilized during the deposition process. Moreover, these sensors maintain remarkable stability across a wide humidity range spanning from 11% to 97% RH. Additionally, the MgAl-LDH nanoflower-based QCM sensors possess minimal humidity hysteresis and display swift dynamic response and recovery periods, further highlighting their potential for humidity detection applications.

Recent and speculative remote myocardial trauma: a case series.

Background: Cardiac blunt trauma clinically presents as a spectrum of injuries of varying severity. However, the diagnosis of complications of remote myocardial trauma is often challenging, especially if the patient forgets to mention a remote history of chest trauma. Case summary: In this study, we present a patient who recently experienced traumatic myocardial dissection and interventricular septal rupture, alongside three patients exhibiting a mimic double-chambered left ventricle, indicative of prior remote myocardial trauma potentially associated with myocardial dissecting tear. Discussion: Patients with recent severe myocardial injury are detectable through cardiac imaging. However, forgotten remote myocardial trauma can lead to adverse myocardial remodelling, heart failure, and arrhythmias. Long-term myocardial remodelling can obscure initial myocardial imaging characteristics, posing challenges in interpretation. Our case series suggests that remote myocardial trauma may be more prevalent than commonly thought of in clinical practice.

Metabolic Labeling and Digital Microfluidic Single-Cell Sequencing for Single Bacterial Genotypic-Phenotypic Analysis.

Accurate assessment of phenotypic and genotypic characteristics of bacteria can facilitate comprehensive cataloguing of all the resistance factors for better understanding of antibiotic resistance. However, current methods primarily focus on individual phenotypic or genotypic profiles across different colonies. Here, a Digital microfluidic-based automated assay for whole-genome sequencing of single-antibiotic-resistant bacteria is reported, enabling Genotypic and Phenotypic Analysis of antibiotic-resistant strains (Digital-GPA). Digital-GPA can efficiently isolate and sequence antibiotic-resistant bacteria illuminated by fluorescent D-amino acid (FDAA)-labeling, producing high-quality single-cell amplified genomes (SAGs). This enables identifications of both minor and major mutations, pinpointing substrains with distinctive resistance mechanisms. Digital-GPA can directly process clinical samples to detect and sequence resistant pathogens without bacterial culture, subsequently provide genetic profiles of antibiotic susceptibility, promising to expedite the analysis of hard-to-culture or slow-growing bacteria. Overall, Digital-GPA opens a new avenue for antibiotic resistance analysis by providing accurate and comprehensive molecular profiles of antibiotic resistance at single-cell resolution.

Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues.

Systemic aging influences various physiological processes and contributes to structural and functional decline in cardiac tissue. These alterations include an increased incidence of left ventricular hypertrophy, a decline in left ventricular diastolic function, left atrial dilation, atrial fibrillation, myocardial fibrosis and cardiac amyloidosis, elevating susceptibility to chronic heart failure (HF) in the elderly. Age-related cardiac dysfunction stems from prolonged exposure to genomic, epigenetic, oxidative, autophagic, inflammatory and regenerative stresses, along with the accumulation of senescent cells. Concurrently, age-related structural and functional changes in the vascular system, attributed to endothelial dysfunction, arterial stiffness, impaired angiogenesis, oxidative stress and inflammation, impose additional strain on the heart. Dysregulated mechanosignalling and impaired nitric oxide signalling play critical roles in the age-related vascular dysfunction associated with HF. Metabolic aging drives intricate shifts in glucose and lipid metabolism, leading to insulin resistance, mitochondrial dysfunction and lipid accumulation within cardiomyocytes. These alterations contribute to cardiac hypertrophy, fibrosis and impaired contractility, ultimately propelling HF. Systemic low-grade chronic inflammation, in conjunction with the senescence-associated secretory phenotype, aggravates cardiac dysfunction with age by promoting immune cell infiltration into the myocardium, fostering HF. This is further exacerbated by age-related comorbidities like coronary artery disease (CAD), atherosclerosis, hypertension, obesity, diabetes and chronic kidney disease (CKD). CAD and atherosclerosis induce myocardial ischaemia and adverse remodelling, while hypertension contributes to cardiac hypertrophy and fibrosis. Obesity-associated insulin resistance, inflammation and dyslipidaemia create a profibrotic cardiac environment, whereas diabetes-related metabolic disturbances further impair cardiac function. CKD-related fluid overload, electrolyte imbalances and uraemic toxins exacerbate HF through systemic inflammation and neurohormonal renin-angiotensin-aldosterone system (RAAS) activation. Recognizing aging as a modifiable process has opened avenues to target systemic aging in HF through both lifestyle interventions and therapeutics. Exercise, known for its antioxidant effects, can partly reverse pathological cardiac remodelling in the elderly by countering processes linked to age-related chronic HF, such as mitochondrial dysfunction, inflammation, senescence and declining cardiomyocyte regeneration. Dietary interventions such as plant-based and ketogenic diets, caloric restriction and macronutrient supplementation are instrumental in maintaining energy balance, reducing adiposity and addressing micronutrient and macronutrient imbalances associated with age-related HF. Therapeutic advancements targeting systemic aging in HF are underway. Key approaches include senomorphics and senolytics to limit senescence, antioxidants targeting mitochondrial stress, anti-inflammatory drugs like interleukin (IL)-1ß inhibitors, metabolic rejuvenators such as nicotinamide riboside, resveratrol and sirtuin (SIRT) activators and autophagy enhancers like metformin and sodium-glucose cotransporter 2 (SGLT2) inhibitors, all of which offer potential for preserving cardiac function and alleviating the age-related HF burden.

Evaluating genomic inbreeding of two Chinese yak (Bos grunniens) populations.

BACKGROUND: Yaks are a vital livestock in the Qinghai-Tibetan Plateau area for providing food products, maintaining sustainable ecosystems, and promoting cultural heritage. Because of uncontrolled mating, it is impossible to estimate inbreeding level of yak populations using the pedigree-based approaches. With the aims to accurately evaluate inbreeding level of two Chinese yak populations (Maiwa and Jiulong), we obtained genome-wide single nucleotide polymorphisms (SNPs) by DNA sequencing and calculated five SNP-by-SNP estimators ([Formula: see text], [Formula: see text], [Formula: see text], [Formula: see text], and [Formula: see text]), as well as two segment-based estimators of runs of homozygosity (ROH, [Formula: see text]) and homozygous-by-descent (HBD, [Formula: see text]). Functional implications were analyzed for the positional candidate genes located within the related genomic regions. RESULTS: A total of 151,675 and 190,955 high-quality SNPs were obtained from 71 Maiwa and 30 Jiulong yaks, respectively. Jiulong had greater genetic diversity than Maiwa in terms of allele frequency and nucleotide diversity. The two populations could be genetically distinguished by principal component analysis, with the mean differentiation index (Fst) of 0.0054. The greater genomic inbreeding levels of Maiwa yaks were consistently supported by all five SNP-by-SNP estimators. Based on simple proportion of homozygous SNPs ([Formula: see text]), a lower inbreeding level was indicated by three successfully sequenced old leather samples that may represent historical Maiwa yaks about five generations ago. There were 3304 ROH detected among all samples, with mean and median length of 1.97 Mb and 1.0 Mb, respectively. A total of 94 HBD segments were found among all samples, whereas 92 of them belonged to the shortest class with the mean length of 10.9 Kb. Based on the estimates of [Formula: see text] and [Formula: see text], however, there was no difference in inbreeding level between Maiwa and Jiulong yaks. Within the genomic regions with the significant Fst or enriched by ROH, we found several candidate genes and pathways that have been reported to be related to diverse production traits in farm animals. CONCLUSIONS: We successfully evaluated the genomic inbreeding level of two Chinese yak populations. Although different estimators resulted in inconsistent conclusions on their genomic inbreeding levels, our results may be helpful to implement the genetic conservation and utilization programs for the two yak populations.