Biology subjects

Gao, Y.

Publications and source records attributed to Gao, Y..

At least 649 records · Page 36Linked to original sources

bioRxiv2019

On the Complexity of Sequence to Graph Alignment

Availability of extensive genetics data across multiple individuals and populations is driving the growing importance of graph based reference representations. Aligning sequences to graphs is a fundamental operation on several types of sequence graphs (variation graphs, assembly graphs, pan-genomes, etc.) and their biological applications. Though research on sequence to graph alignments is nascent, it can draw from related work on pattern matching in hypertext. In this paper, we study sequence to graph alignment problems under Hamming and edit distance models, and linear and affine gap penalty functions, for multiple variants of the problem that allow changes in query alone, graph alone, or in both. We prove that when changes are permitted in graphs either standalone or in conjunction with changes in the query, the sequence to graph alignment problem is [Formula]-complete under both Hamming and edit distance models for alphabets of size [≥] 2. For the case where only changes to the sequence are permitted, we present an O(|V| + m|E|) time algorithm, where m denotes the query size, and V and E denote the vertex and edge sets of the graph, respectively. Our result is generalizable to both linear and affine gap penalty functions, and improves upon the run-time complexity of existing algorithms.

bioinformatics↗

bioRxiv2019

High-quality genome assembly and high-density genetic map of asparagus bean

Asparagus bean (Vigna. unguiculata ssp. sesquipedialis), known for its very long and tender green pods, is an important vegetable crop broadly grown in the developing countries. Despite its agricultural and economic values, asparagus bean does not have a high-quality genome assembly for breeding novel agronomic traits. In this study, we reported a high-quality 632.8 Mb assembly of asparagus bean based on the whole genome shotgun sequencing strategy. We also generated a high-density linkage map for asparagus bean, which helped anchor 94.42% of the scaffolds into 11 pseudo-chromosomes. A total of 42,609 protein-coding genes and 3,579 non-protein-coding genes were predicted from the assembly. Taken together, these genomic resources of asparagus bean will facilitate the investigation of economically valuable traits in a variety of legume species, so that the cultivation of these plants would help combat the protein and energy malnutrition in the developing world.

genomics↗

bioRxiv2019

Quantitative Analysis of Global Protein Stability Rates in Tissues

Protein degradation is an essential mechanism for maintaining homeostasis in response to internal and external perturbations. Disruption of this process is implicated in many human diseases, but quantitation of global stability rates has not yet been achieved in tissues. We have developed QUAD (Quantification of Azidohomoalanine Degradation), a technique to quantitate global protein degradation using mass spectrometry. Azidohomoalanine (AHA) is pulsed into mouse tissues through their diet. The mice are then returned to a normal diet and the decrease of AHA abundance can be quantitated in the proteome. QUAD analysis reveals that protein stability varied within tissues, but discernible trends in the data suggest that cellular environment is a major factor dictating stability. Within a tissue, different organelles, post-translation modifications, and protein functions were enriched with different stability patterns. Surprisingly, subunits of the TRIC molecular chaperonin possessed markedly distinct stability trajectories in the brain. Further investigation revealed that these subunits also possessed different subcellular localization and expression patterns that were uniquely altered with age and in Alzheimers disease transgenic mice, indicating a potential non-canonical chaperonin. Finally, QUAD analysis demonstrated that protein stability is enhanced with age in the brain but not in the liver. Overall, QUAD allows the first global quantitation of protein stability rates in tissues, which may lead to new insights and hypotheses in basic and translational research.\n\nSummaryProtein degradation is an important component of the proteostasis network, but no techniques are available to globally quantitate degradation rates in tissues. In this study, we demonstrate a new method QUAD (Quantification of Azidohomoalanine Degradation) that can accurately quantitate degradation rates in tissues. QUAD analysis of mouse tissues reveal that unique degradation trends can define different tissue proteomes. Within a tissue, specific protein characteristics are correlated with different levels of protein stability. Further investigation of the TRIC chaperonin with strikingly different subunit stabilities suggests a non-canonical chaperonin in brain tissue. Consistent with the theory that the proteostasis network is compromised with age, we discovered that protein stability is globally enhanced in brains of old mice compared to young mice.

cell biology↗

bioRxiv2019

Rice annexin OsANN4 interacting with OsCDPK24, reduces root aerenchyma formation by modulating H2O2 under ABA treatment

Plant annexins are calcium- and lipid-binding proteins that have multiple functions, and a significant amount of research on plant annexins has been reported in recent years. However, the functions of annexins in diverse biological processes in rice are largely unclear. Herein, we report that OsANN4, a calcium-binding rice annexin protein, is a substrate for OsCDPK24, and the OsANN4 phosphorylation site is the 13th serine, which is a key site for phosphorylation. Most strikingly, abscisic acid (ABA) promotes the interaction between OsANN4 and OsCDPK24. Moreover, knocking down OsANN4 by RNA interference resulted in visible and invisible phenotypes with exogenous ABA treatment, such as shorter shoots of seedlings, less lateral roots, earlier root aerenchyma formation and so on. The further analyzed results showed that decreased superoxide dismutase (SOD) and catalase (CAT) activity of the RNAi lines, which control H2O2 accumulation for redox homeostasis, and further promoted earlier aerenchyma formation of the root. These results suggest that a proposed molecular mechanism exists between OsANN4 and H2O2 production to response ABA.\n\nHighlightOsANN4 enhances SOD and CAT activities to scavenge H2O2 to alleviate the formation of aerenchyma under ABA treatment. OsCDPK24 interacts with and phosphorylates OsANN4, this interaction strengthened under ABA treatment.

plant biology↗

bioRxiv2019

Early urinary protein changes in the tumor-forming process of the NuTu-19 lung metastasis

The early detection of cancer is essential for effective intervention. Urine, which lacks homeostatic control, has been used to reflect early systemic changes in subcutaneous cancer models. However, urine has not been used to predict whether tumors will be formed in animal models. In this study, a cancer model was established by the tail-vein injection of 2 million NuTu-19 tumor cells. Approximately half of the rats formed lung metastatic carcinoma tumors. Urine samples were randomly selected from 4 tumor-forming rats and 4 non-tumor-forming rats on day 0/12/27/39/52 and analyzed by label-free proteomic quantitative analysis. Compared to day 0, a total of 180 and 118 urinary proteins in tumor-forming and non-tumor-forming rats, respectively, showed significant changes. Functional enrichment analysis of the differential proteins in tumor-forming rats revealed similar events during cancer metastasis cascades and tumor progression, such as the migration of tumor cell lines, coagulation system, TGF-{beta} signaling, the STAT3 pathway and the adhesion of myeloid cells and alveolar macrophages. The differential proteins in non-tumor-forming rats were associated with agranulocyte/granulocyte adhesion and diapedesis, glutathione biosynthesis, IL-12 signaling and vitamin metabolism. After validation by parallel reaction monitoring (PRM) targeted proteomics quantitative analysis, a total of 22 urinary proteins showed significant changes in the early phase of the lung tumor formation process, 5 of which have been associated with the mechanisms of lung cancer, while 3 have been suggested as lung cancer biomarkers. Another 14 urinary proteins showed significant changes in the early phase in non-tumor-forming rats. Our results indicate that urine proteins could differentiate early tumor-forming and non-tumor-forming status.

cancer biology↗

bioRxiv2019

A device to collect exhaled breath to study biomarkers in small animal models

Biomarkers are measurable changes associated with disease. Exhaled breath provides many signs of bodily changes and has been proposed to be a good early biomarker source because it lacks homeostatic mechanisms. Earlier biomarker detection can provide earlier diagnosis, which can bring about more choices and more time for treatment. The benefit of studying exhaled breath in animal models is that most interfering factors can be avoided, and earlier changes in disease may be found. However, there is currently no device that can effectively collect exhaled breath from small animals. In this study, such a device was designed, constructed, and used for the study of candidate biomarkers from the exhale breaths of a papain-induced pulmonary emphysema rat model.

biochemistry↗

bioRxiv2019

Integration of gut microbiome, host biomarkers, and urine metabolome data reveals networks of interactions associated with distinct clinical phenotypes

BackgroundComprehensive analyses of multi-omics data may provide insights into interactions between different biological layers in relation to distinct clinical features. Here we integrated data on the gut microbiota, blood parameters and urine metabolites of treatment-naive individuals presenting a wide range of metabolic disease phenotypes to delineate clinically meaningful associations.\n\nResultsTrans-omics correlation networks revealed that candidate gut microbial biomarkers and urine metabolite features covaried with distinct clinical phenotypes. Integration of the gut microbiome, the urine metabolome and the phenome revealed that variations in one of these three systems correlated with changes in the other two. Of specific note in relation to clinical parameters of liver function, we identified Eubacterium eligens, Faecalibacterium prausnitzii and Ruminococcus lactaris to be associated with a healthy liver function, whereas Clostridium bolteae, Tyzzerella nexills, Ruminococcus gnavus, Blautia hansenii, and Atopobium parvulum were associated with blood biomarkers for liver diseases. Variations in these microbiota features paralleled changes in specific urine metabolites. Network modeling yielded two core clusters including one large gut microbe-urine metabolite close-knit cluster and one triangular cluster composed of a gut microbe-blood-urine network, demonstrating close inter-system crosstalk especially between the gut microbiome and the urine metabolome.\n\nConclusionsDistinct clinical phenotypes are manifested in both the gut microbiome and the urine metabolome, and inter-domain connectivity takes the form of high-dimensional networks. Such networks may further our understanding of complex biological systems, and may provide a basis for identifying biomarkers for diseases.

microbiology↗

bioRxiv2018

Co-allocation Action of Azospirillum brasilense Inoculation and Seed Priming for Improving Germination and Seedling Growth in Aged Grass Seeds

Germination of seeds during the transportation or after prolonged storage naturally and inevitably decreases because of ageing, but germination potential can be partially restored with seed priming treatments. A novel attempt was made to investigate the effects of combined treatments and to optimize the conditions for naturally aged seeds of tall fescue (Festuca arundinacea Schreb.), orchardgrass (Dactylis glomerata L.) and Russian wild rye (Psathyrostachys juncea (Fisch.) Nevski) using an orthogonal activity level experimental design [factor A: Azospirillum brasilense concentration, factor B: three seed priming treatments (H2O, MgSO4 and H2O2) and factor C: different priming times]. Multivariate regression model analysis was applied to determine the interactive effects of pairwise factors (A and C) and to optimize experimental conditions. The results showed that the mixed treatments positively affected seed germination and seedling growth. The three seed priming treatments were the dominant factors for germination promotion, whereas the bacterial concentration had the largest effect on seedling growth, especially root elongation. The combined results of all determined attributes showed that A. brasilense bio-priming with H2O2 priming constituted the optimal combination. The optimal bacterial concentration of A. brasilense and the time of seed priming were 52.3 x 106 colony forming units (CFU) mL-1 and 17.0 h, respectively. We also discussed the physiological mechanisms that could repair aged seeds: the malondialdehyde content and antioxidant enzyme (superoxide dismutase, peroxidase, catalase and ascorbate peroxidase) activities were affected.

plant biology↗

bioRxiv2018

The integrated stress response mediates type I interferon driven necrosis in Mycobacterium tuberculosis granulomas

Necrosis in the tuberculous granuloma is a hallmark of tuberculosis that enables pathogen survival and transmission. Susceptibility to tuberculosis and several other intracellular bacteria is controlled by a mouse genetic locus, sst1, and mice carrying the sst1-suscepible (sst1S) genotype develop necrotic inflammatory lung lesions, similar to human TB granulomas. Our previous work established that increased disease severity in sst1S mice reflects dysfunctional macrophage effector or tolerance mechanisms, but the molecular mechanisms have remained unclear. Here we demonstrate that sst1S macrophages develop aberrant, biphasic responses to TNF characterized by super-induction of stress and type I interferon pathways after prolonged TNF stimulation with this late-stage response being initiated by oxidative stress and Myc activation and driven via a JNK - IFN{beta} - PKR circuit. This circuit leads to induction of the integrated stress response (ISR) mediated by eIF2 phosphorylation and the subsequent hyper-induction of ATF3 and ISR-target genes Chac1, Trib3, Ddit4. The administration of ISRIB, a small molecule inhibitor of the ISR, blocked the development of necrosis in lung granulomas of M. tuberculosis-infected sst1S mice and concomitantly reduced the bacterial burden revealing that induction of the ISR and the locked-in state of escalating stress driven by type I IFN pathway in sst1S macrophages plays a causal role in the development of necrosis. Our data support a generalizable paradigm in intracellular pathogen-host interactions wherein host susceptibility emerges within inflammatory tissue due to imbalanced macrophage responses to growth, differentiation, activation and stress stimuli. Successful pathogens such as M. tuberculosis may exploit this aberrant response in susceptible hosts to induce necrotic lesions that favor long-term pathogen survival and transmission. Interruption of the aberrant stress response with inhibitors such as ISRIB may offer novel therapeutic strategies.

immunology↗

bioRxiv2018

Collateral development and arteriogenesis in hindlimbs of domestic swine after ligation of arterial inflow

IntroductionThe development of collateral vasculature is a key mechanism compensating for arterial occlusions in patients with peripheral artery disease (PAD). We aimed to examine the development of collateral pathways after ligation of native vessels in a porcine model of PAD. MethodsRight hindlimb Ischemia was induced in domestic swine (N=11, male, kg) using two different versions of arterial ligation. Version 1 (N=6) consisted of ligation/division of the right external iliac, profunda femoral (RPFA) and superficial femoral arteries (RSFA). Version 2 (N=5) consisted of the ligation of Version 1 with additional ligation/division of the right internal iliac artery (RIIA). Development of collateral pathways was evaluated with standard angiography at baseline (prior to arterial ligation) and at termination (4-8 weeks later). Relative luminal diameter of the arteries supplying the ischemic right hindlimb were determined by 2D angiography, as percent of the size of the distal aortic diameter. ResultsThe dominant collateral pathway that developed after version 1 ligation connected the RIIA to the RPFA and RSFA/popliteal artery. Mean luminal diameter ({+/-} standard error) of the RIIA at termination increased by 38% (P<0.05) compared to baseline. Two co-dominant collateral pathways developed in version: (i) from the common internal iliac trunk and left internal iliac artery to the reconstituted RIIA, which then supplied the RPFA and RSFA/popliteal arteries; and (ii) from left profunda artery to the reconstituted RPFA. Mean diameter of the common internal iliac trunk and left profunda artery both increased at termination in the range of 20% (p < 0.05). ConclusionTwo versions of hindlimb ischemia induction (right ilio-femoral artery ligation with and without right internal iliac artery ligation in swine produced differing collateral pathways, along with changes to the diameter of the inflow vessels (i.e., arteriogenesis). Radiographic and anatomical data of the collateral formation in this porcine model should have value in investigation of the pathophysiology of hindlimb ischemia, and assessment of angiogenic therapies as potential treatments for PAD.

physiology↗

bioRxiv2018

Enrichment of short mutant cell-free DNA fragments enhanced detection of pancreatic cancer

Analysis of cell-free DNA (cfDNA) is promising for broad applications in clinical settings, but with significant bias towards late-stage cancers. Although recent studies have discussed the diverse and degraded nature of cfDNA molecules, little is known about its impact on the practice of cfDNA analysis. Here we reported a new targeted sequencing by combining single-strand library preparation and target capture (SLHC-seq). By applying the new technology in plasma cfDNA from pancreatic cancer patients, we achieved higher efficiency in analysis of mutations than previously reported using other detection assays. SLHC-seq rescued short or damaged cfDNA fragments along to increase the sensitivity and accuracy of circulating-tumor DNA detection. Most importantly, we found that the small mutant fragments are prevalent in early-stage patients, which provides strong evidence for fragment size-based early detection of pancreatic cancer. Collectively, the new pipeline enhanced our understanding of cfDNA biology and provide new insights for liquid biopsy.

cancer biology↗

bioRxiv2018

Dynamic urinary proteomic analysis in a Walker 256 intracerebral tumor model

Patients with primary and metastatic brain cancer have an extremely poor prognosis, mostly due to the late diagnosis of disease. Urine, which lacks homeostatic mechanisms, is an ideal biomarker source that accumulates early and highly sensitive changes to provides information about the early stage of disease. A rat model mimicking the local tumor growth process in the brain was established with intracerebral Walker 256 (W256) cell injection. Urine samples were collected on days 3, 5 and 8 after injection and then analyzed by LC-MS/MS. In the intracerebral W256 model, no obvious clinical manifestations changes or abnormal MRI signals were found on days 3 and 5; at these time points, nine proteins were changed significantly in the urine of all 8 tumor rats. On day 8, when tumors were detected by MRI, twenty-five differential proteins were identified, including 10 proteins that have been reported to be closely related to tumor metastasis or brain tumors. The differential urinary proteomes were compared with those from the subcutaneous W256 model and the intracerebral C6 model. Few differential proteins overlapped. Specific differential protein patterns were observed among the three models, indicating that the urinary proteome can reflect the difference when tumor cells with different growth characteristics are inoculated into the brain and when identical tumor cells are inoculated into different areas, specifically, the subcutis and the brain.

cancer biology↗

bioRxiv2018

CDK12 loss in cancer cells affects DNA damage response genes through premature cleavage and polyadenylation

The cyclin-dependent kinase 12 (CDK12) modulates transcription elongation by phosphorylating the carboxy-terminal domain of RNA polymerase II and appears to selectively affect the expression of DNA damage response (DDR) and mRNA processing genes. Yet, the mechanism(s) by which it achieves this selectivity remains unclear. Using a highly selective CDK12/13 inhibitor, THZ531, and nascent RNA sequencing, we show that CDK12 inhibition results in gene length-dependent elongation defects, leading to premature cleavage and polyadenylation (PCPA) as well as loss of expression of long (>45 kb) genes, a substantial proportion of which participate in the DDR. This early termination phenotype correlated with an increased proportion of intronic polyadenylation sites, a feature that was especially prominent among DDR genes. Finally, phosphoproteomic analysis indicated that pre-mRNA processing factors, including those involved in PCPA, are direct phosphotargets of CDKs 12 and 13. These results support a model in which DDR genes are uniquely susceptible to CDK12 inhibition due primarily to their relatively longer lengths and lower ratios of U1 snRNP binding to intronic polyadenylation sites.

cancer biology↗

bioRxiv2018

Noninvasive prenatal detection of fetal trisomy and single gene disease by shotgun sequencing of placenta originated exosome DNA: a proof-of-concept validation

BackgroundDuring human pregnancy, Placental trophectoderm cells can release exosomes into maternal circulation. Trophoblast cells also give rise to cell-free DNA (cfDNA) and has been used for noninvasive prenatal screening for chromosomal aneuploidy. We intended to prove the existence of exosomal DNA (exoDNA) in the exosomes of maternal blood and compared exoDNA with plasma cfDNA in terms of genome distribution, fragment length, and the possibility of detecting genetic diseases.\n\nMethodsMaternal blood from 20 euploid pregnancies, 9 T21 pregnancies, 3 T18 pregnancies, 1 T13 pregnancy and 2 pregnancies with FGFR3 mutations were obtained. Exosomes enriched from maternal plasma were confirmed by transmission electronic microscopy (TEM), western blotting and flow cytometry. ExoDNA was extracted and its fetal origin was confirmed by realtime fluorescence quantitative PCR(Q-PCR). Besides, exoDNA content was uncovered by Q-PCR. To characterize exoDNA and compare with cfDNA, pair-end whole genome sequencing was performed. Lastly, the fetal risk of genetic diseases was analyzed using the exoDNA sequencing data.\n\nResultsExoDNA span on all 23 pairs of chromosomes and mitochondria, sharing a similar distribution pattern and higher GC content comparing with cfDNA. ExoDNA showed shorter fragments yet lower fetal fraction than cfDNA. ExoDNA could be used to determine fetal gender correctly, and all trisomies as well as de novo FGFR3 mutations.\n\nConclusionsWe proved that fetal exoDNA could be identified in the exosomes extracted from maternal plasma. ExoDNA shared some similar features to cfDNA and could potentially be used to detect genetic diseases in fetus.

genetics↗

bioRxiv2018

The WT1-BASP1 complex is required to maintain the differentiated state of taste receptor cells

The WT1-BASP1 complex is a transcriptional repressor that is involved in cell differentiation; however, the mechanisms underlying its effects are not well-characterized in vivo. In the peripheral taste system which endogenously expresses these proteins, BASP1 co-expression with WT1 begins at the end of development, suggesting a role for the WT1-BASP1 complex in terminal cell differentiation within this system. Using a conditional BASP1 mouse, we demonstrate that BASP1 is critical to maintain the differentiated state of adult cells by inhibiting the activation of WT1-dependent target genes. Our results uncover a central role for the WT1-BASP1 complex in maintaining cell differentiation.

cell biology↗

bioRxiv2018

CSTDB: A Crop Stress-tolerance Gene and Protein Database Integrated by Convolutional Neural Networks

Numerous studies have shown that many genes and proteins in plants are involved in the regulation of plant resistance to abiotic and biotic stresses. The researches on the stress tolerance of crops are also the focus of many researchers. To provides a reliable platform for collecting and retrieving genetic and protein information related to stress tolerance found in crops, we constructed CSTDB(Crops Stress-tolerance Database), an integrated database that includes stress-tolerance genes and proteins for many crop species. The database was developed based on convolutional neural network technology. It is a web-accessible database that contains detailed information on the stress-tolerance genes and proteins of major crop species. Currently, the database records four major crops containing 1,371 abiotic stress-tolerance genes or proteins, and 207 genes or proteins associated with biotic stress. Each gene and protein has detailed functional information and sequence information, such as stress types, Genbank ID, Pubmed ID, Protein ID, 3D model picture and FASTA files. As a user-friendly browsing tool, this database provides search functions, BALST functions and file download functions. CSTDB can be a valuable resource, which is designed to meet the broad needs of researchers working on crops stress-tolerance experiments. Database URL: http://pcsb.ahau.edu.cn:8080/CSTDB

bioinformatics↗

bioRxiv2018

Transcriptome profiling of pathogen-specific CD4 T cells identifies T-cell-intrinsic caspase-1 as an important regulator of Th17 differentiation

One sentence summaryOur study revealed that DCs shape distinct pathogen-specific CD4 T cell transcriptome and from which, we discovered an unexpected role for T-cell-intrinsic caspase-1 in promoting Th17 differentiation.\n\nABSTRACTDendritic cells (DCs) are critical for priming and differentiation of pathogen-specific CD4 T cells. However, to what extent innate cues from DCs dictate transcriptional changes in T cells leading to effector heterogeneity remains elusive. Here we have used an in vitro approach to prime naive CD4 T cells by DCs stimulated with distinct pathogens. We have found that such pathogen-primed CD4 T cells express unique transcriptional profiles dictated by the nature of the priming pathogen. In contrast to cytokine-polarized Th17 cells that display signatures of terminal differentiation, pathogen-primed Th17 cells maintain a high degree of heterogeneity and plasticity. Further analysis identified caspase-1 as one of the genes upregulated only in pathogen-primed Th17 cells but not in cytokine-polarized Th17 cells. T-cell-intrinsic caspase-1, independent of its function in inflammasome, is critical for inducing optimal pathogen-driven Th17 responses. More importantly, T cells lacking caspase-1 fail to induce colitis following transfer into RAG-deficient mice, further demonstrating the importance of caspase-1 for the development of pathogenic Th17 cells in vivo. This study underlines the importance of DC-mediated priming in identifying novel regulators of T cell differentiation.

immunology↗

bioRxiv2018

Unilateral relapse of Behcet’s disease-associated uveitis does not appear to cause asymmetric tear protein profiles

Purpose: To explore whether unilateral relapse of Bechets disease uveitis (BDU) causes differences in the tear proteome between the diseased and the contralateral quiescent eye.\n\nExperimental design: To minimize interindividual variations, bilateral tear samples were collected from the same patient (n=15) with unilateral relapse of BDU. A data-independent acquisition (DIA) strategy was used to identify proteins that differed between active and quiescent eyes.\n\nResults: A total of 1,797 confident proteins were identified in the tear samples, of which 371 are also highly expressed in various tissues and organs. Sixty-two (3.5%) proteins differed in terms of expression between tears in active and quiescent eyes, similar to the number of differentially expressed proteins (74, 4.1%) identified in a randomized grouping strategy. Furthermore, the intrapair trend of the differentially expressed proteins was not consistent and none of the proteins showed the same trend in more than 9 pairs of eyes.\n\nConclusions and clinical relevance: Unilateral relapse of BDU does not appear to cause asymmetric changes in the tear proteome between active and contralateral quiescent eyes. Tear fluid is a valuable source for biomarker studies of systemic diseases.\n\nStatement of clinical relevanceTears are an easily, noninvasively accessible body fluid that is a valuable source of biomarkers for various diseases. Behcets disease uveitis (BDU) has high potential to cause blindness and represents the leading cause of morbidity in BD patients, especially in frequently relapsing cases. Here, we adopted a method combining a \"dry\" method for tear preservation and nano-LC-DIA-MS/MS system to explore whether unilateral relapse of BDU causes differences in the tear proteome between the diseased and the contralateral quiescent eye, with the aim of evaluating tear fluid as a source for biomarker studies of uveitis relapse.

molecular biology↗