Deletion of Vß3+CD4+ T cells by endogenous mouse mammary tumor virus 3 prevents type 1 diabetes induction by autoreactive CD8+ T cells.

In both humans and NOD mice, type 1 diabetes (T1D) develops from the autoimmune destruction of pancreatic beta cells by T cells. Interactions between both helper CD4+ and cytotoxic CD8+ T cells are essential for T1D development in NOD mice. Previous work has indicated that pathogenic T cells arise from deleterious interactions between relatively common genes which regulate aspects of T cell activation/effector function (Ctla4, Tnfrsf9, Il2/Il21), peptide presentation (H2-A g7, B2m), and T cell receptor (TCR) signaling (Ptpn22). Here, we used a combination of subcongenic mapping and a CRISPR/Cas9 screen to identify the NOD-encoded mammary tumor virus (Mtv)3 provirus as a genetic element affecting CD4+/CD8+ T cell interactions through an additional mechanism, altering the TCR repertoire. Mtv3 encodes a superantigen (SAg) that deletes the majority of Vß3+ thymocytes in NOD mice. Ablating Mtv3 and restoring Vß3+ T cells has no effect on spontaneous T1D development in NOD mice. However, transferring Mtv3 to C57BL/6 (B6) mice congenic for the NOD H2 g7 MHC haplotype (B6.H2 g7) completely blocks their normal susceptibility to T1D mediated by transferred CD8+ T cells transgenically expressing AI4 or NY8.3 TCRs. The entire genetic effect is manifested by Vß3+CD4+ T cells, which unless deleted by Mtv3, accumulate in insulitic lesions triggering in B6 background mice the pathogenic activation of diabetogenic CD8+ T cells. Our findings provide evidence that endogenous Mtv SAgs can influence autoimmune responses. Furthermore, since most common mouse strains have gaps in their TCR Vß repertoire due to Mtvs, it raises questions about the role of Mtvs in other mouse models designed to reflect human immune disorders.

Genome-Wide Analysis and Expression Profiling of Lectin Receptor-like Kinase Genes in Watermelon (Citrullus lanatus).

Watermelon is one of the most important edible plants worldwide. Owing to its special cultivation conditions, watermelon is exposed to many biological and abiotic stresses during its development. Lectin receptor-like kinases (LecRLKs) are plant-specific membrane proteins that play important roles in sensing and responding to environmental stimuli. Although the LecRLK gene family has been identified in a variety of plants, a comprehensive analysis has not yet been undertaken in watermelon. In this study, 61 putative LecRLK genes were identified in watermelon, consisting of 36 G-type, 24 L-type, and 1 C-type LecRLK genes. They were distributed in clusters on chromosomes, and members from the same subfamily were mostly clustered together. The analysis of the phylogenetic tree and conserved motif indicated that there were obvious differences among three ClaLecRLK subfamilies, and there was also rich diversity in the C-terminal within subfamilies. A collinear analysis revealed that the evolution of the ClaLecRLK gene family in different Cucurbitaceae crops was asynchronous. Furthermore, the analysis of the ClaLecRLK protein structure showed that not all proteins contained signal peptides and a single transmembrane domain. A subcellular localization assay confirmed that the number and position of transmembrane domains did not affect ClaLecRLK protein localization in cells. Transcriptome data revealed distinct expression patterns of LecRLK genes of watermelon in various tissues, and their responses to different fungi infection were also significantly different. Finally, the potential binding sites of the ClaLecRLK genes targeted by miRNA were predicted. This study enhances the understanding of the characteristics and functions of the LecRLK gene family in watermelon and opens up the possibility of exploring the roles that LecRLK genes may play in the life cycle of Cucurbitaceae plants.

Autosomal Recessive Cerebellar Ataxia Type 1: Phenotypic and Genetic Correlation in a Cohort of Chinese Patients with SYNE1 Variants.

Mutations in the synaptic nuclear envelope protein 1 (SYNE1) gene have been reported to cause autosomal recessive cerebellar ataxia (ARCA) type 1 with highly variable clinical phenotypes. The aim of this study was to describe the phenotypic-genetic spectrum of SYNE1-related ARCA1 patients in the Chinese population. We screened 158 unrelated patients with autosomal recessive or sporadic ataxia for variants in SYNE1 using next-generation sequencing. Pathogenicity assessment of SYNE1 variants was interpreted according to the American College of Medical Genetics standards and guidelines. We identified eight truncating variants and two missense variants spreading throughout the SYNE1 gene from six unrelated families, including nine novel variants and one reported variant. Of the six index patients, two patients showed the classical pure cerebellar ataxia, while four patients exhibited non-cerebellar phenotypes, including motor neuron symptoms, cognitive impairment, or mental retardation. The variants associated with motor neuron or cognition involvement tend to be located in the C-terminal region of SYNE1 protein, compared with the variants related to pure cerebellar ataxia. Our data indicating SYNE1 mutation is one of the more common causes of recessive ataxia in the Chinese population. The use of next-generation sequencing has enabled the rapid analysis of recessive ataxia and further expanded our understanding of genotype-phenotype correlation.

[A consensus on the standardization of the next generation sequencing process for the diagnosis of genetic diseases (1) - Procedures prior to genetic testing].

Pre-testing preparation is the basis and starting point of genetic testing. The process includes collection of clinical information, formulation of testing scheme, genetic counseling before testing, and completion of informed consent and testing authorization. To effectively identify genetic diseases in clinics can greatly improve the diagnostic rate of next generation sequencing (NGS), thereby reducing medical cost and improving clinical efficacy. The analysis of NGS results relies, to a large extent, on the understanding of genotype-phenotype correlations, therefore it is particularly important to collect and evaluate clinical phenotypes and describe them in uniform standard terms. Different types of genetic diseases or mutations may require specific testing techniques, which can yield twice the result with half the effort. Pre-testing genetic counseling can help patients and their families to understand the significance of relevant genetic testing, formulate individualized testing strategies, and lay a foundation for follow-up.

[A consensus on the standardization of the next generation sequencing process for the diagnosis of genetic diseases (2) - Sample collection, processing and detection].

With high accuracy and precision, next generation sequencing (NGS) has provided a powerful tool for clinical testing of genetic diseases. To follow a standardized experimental procedure is the prerequisite to obtain stable, reliable, and effective NGS data for the assistance of diagnosis and/or screening of genetic diseases. At a conference of genetic testing industry held in Shanghai, May 2019, physicians engaged in the diagnosis and treatment of genetic diseases, experts engaged in clinical laboratory testing of genetic diseases and experts from third-party genetic testing companies have fully discussed the standardization of NGS procedures for the testing of genetic diseases. Experts from different backgrounds have provided opinions for the operation and implementation of NGS testing procedures including sample collection, reception, preservation, library construction, sequencing and data quality control. Based on the discussion, a consensus on the standardization of the testing procedures in NGS laboratories is developed with the aim to standardize NGS testing and accelerate implementation of NGS in clinical settings across China.

[A consensus on the standardization of the next generation sequencing process for the diagnosis of genetic diseases (3) - Data analysis].

Bioinformatic analysis and variant classification are the key components of high-throughput sequencing-based genetic diagnostic approach. This consensus is part of the effort to develop a standardized process for next generation sequencing (NGS)-based test for germline mutations underlying Mendelian disorders in China. The flow-chart, common software, key parameters of bioinformatics pipeline for data processing, annotation, storage and variant classification are reviewed, which is aimed to help improving and maintaining a high-quality process and obtaining consistent outcomes for NGS-based molecular diagnosis.

[A consensus on the standardization of the next generation sequencing process for the diagnosis of genetic diseases (4) - Report interpretation and genetic counseling].

Clinical genetic testing results are compiled into a standardized report by genetic specialists and provided to clinicians and patients (Should the patient be intellectually disabled or under 18, the report will be provided to his/her parents or legal guardians). The content of genetic testing report should conform to relevant guidelines, industry standards and consensus. The decisions of clinicians will be made based on the report and clinical indications. Genetic counselors should provide post-test counseling to clinicians and patients or their authorized family members. A mechanism of follow-up visit after the genetic testing should be established with informed consent. Data should be shared by clinical institutions and genome sequencing institutions. As findings upon follow-up visit can help with further evaluation of the results, genome sequencing institutions should regularly re-analyze historical and follow-up data, and the updated results should be shared with clinical institutions. All activities involving reporting, genetic counselling, follow-up visiting, and re-analyzing should follow the relevant guidelines and regulations.

Au Nanoparticles Attenuate RANKL-Induced Osteoclastogenesis by Suppressing Pre-Osteoclast Fusion.

Osteoclasts are multinucleated terminal cells that originate from a hematopoietic monocyte/macrophage lineage. Excessive osteoclast formation in vivo can lead to bone metabolic diseases such as postmenopausal osteoporosis, multiple myeloma, rheumatoid arthritis, and lytic bone metastases of cancer cells. Au nanoparticles (AuNPs) are inorganic nanoparticles with outstanding biocompatibility. We assessed their effect on osteoclastogenesis and found that pre-osteoclast fusion induced by receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colonystimulating factor (M-CSF) was suppressed by AuNPs. Cell migration and actin ring formation were also significantly inhibited. Finally, AuNPs reduced osteoclast bone absorption function. Interestingly, we observed altered fusogenic gene expression in treated pre-osteoclasts. Our results suggest that AuNPs have potential as a therapeutic agent for osteoclast-related bone metabolism diseases.

Highly Dispersed Fullerenols Hamper Osteoclast Ruffled Border Formation by Perturbing Ca2+ Bundles.

Osteoporosis, a common and serious bone disorder affecting aged people and postmenopausal women, is characterized by osteoclast overactivity. One therapeutic strategy is suppressing the bone resorption function of hyperactive osteoclasts, but there is no effective drug in clinical practice so far. Herein, it is demonstrated that fullerenols suppress the bone resorption of osteoclasts by inhibiting ruffled borders (RBs) formation. The RBs formation, which is supported by well-aligned actin bundles (B-actins), is a critical event for osteoclast bone resorption. To facilitate this function, osteoclast RBs dynamics is regulated by variable microenvironments to bundle F-actins, protrude cell membrane, and so on. B-actin perturbation by fullerenols is determined here, offering an opportunity to regulate osteoclast function by destroying RBs. In vivo, the therapeutic effect of fullerenols on overactive osteoclasts is confirmed in a mouse model of lipopolysaccharide-induced bone erosion. Collectively, the findings suggest that fullerenols adhere to F-actin surfaces and inhibit RBs formation in osteoclasts, mainly through hampering Ca2+ from bundling F-actins, and this is likely due to the stereo-hindrance effect caused by adherent fullerenols.

Tight Junction Protein Occludin Is a Porcine Epidemic Diarrhea Virus Entry Factor.

Porcine epidemic diarrhea virus (PEDV), the causative agent of porcine epidemic diarrhea, has caused huge economic losses in pig-producing countries. Although PEDV was long believed to replicate in the intestinal epithelium by using aminopeptidase N as a receptor, the mechanisms of PEDV infection are not fully characterized. In this study, we found that PEDV infection of epithelial cells results in disruption of the tight junctional distribution of occludin to its intracellular location. Overexpression of occludin in target cells makes them more susceptible to PEDV infection, whereas ablation of occludin expression by use of small interfering RNA (siRNA) in target cells significantly reduces their susceptibility to virus infection. However, the results observed with occludin siRNA indicate that occludin is not required for virus attachment. We conclude that occludin plays an essential role in PEDV infection at the postbinding stages. Furthermore, we observed that macropinocytosis inhibitors blocked occludin internalization and virus entry, indicating that virus entry and occludin internalization are closely coupled. However, the macropinocytosis inhibitors could not impede virus replication once the virus had entered host cells. This suggests that occludin internalization by macropinocytosis or a macropinocytosis-like process is involved in the virus entry events. Immunofluorescence confocal microscopy showed that PEDV was trapped at cellular junctional regions upon macropinocytosis inhibitor treatment, indicating that occludin may serve as a scaffold in the vicinity of virus entry. Collectively, these data show that occludin plays an essential role in PEDV infection during late entry events. Our observation may provide novel insights into PEDV infection and related pathogenesis.IMPORTANCE Tight junctions are highly specialized membrane domains whose main function is to attach adjacent cells to each other, thereby forming intercellular seals. Here we investigate, for the first time, the role of the tight junction protein occludin in PEDV infection. We observed that PEDV infection induced the internalization of occludin. By using genetic modification methods, we demonstrate that occludin plays an essential role in PEDV infection. Moreover, PEDV entry and occludin internalization seem to be closely coupled. Our findings reveal a new mechanism of PEDV infection.

Generalized inverse matrix-exterior penalty function (GIM-EPF) algorithm for data processing of multi-wavelength pyrometer (MWP).

The unknown emissivity of materials is a huge obstacle in multi-wavelength pyrometry (MWP). It leads to a set of ill-posed equations that cannot be directly inverted to obtain the true temperature from a set of multi-wavelength measurements. Constraint optimization algorithms such as the gradient projection (GP) and internal penalty function (IPF) algorithms provide solutions without any emissivity model assumptions but require a narrow fixed emissivity range and an appropriate initial emissivity input value, otherwise, accuracy and computational efficiency are greatly affected. Here, we propose a generalized inverse matrix-exterior penalty function (GIM-EPF) algorithm to realize an efficient and accurate inversion without limiting the emissivity range in advance. First, a set of emissivities is obtained by the generalized inverse matrix method; these emissivities are used as initial values in the exterior penalty function iteration algorithm, from which temperature and spectral emissivity are obtained. Simulation results show that the GIM-EPF algorithm provides results superior to IPF, especially in computational efficiency. The proposed GIM-EPF method is 8 times faster than the IPF method with a 0.56% relative error at the 1800 K true temperature. The GIM-EPF method also allows near real-time diagnosis of rocket exhaust flame temperature. Rocket nozzle temperature experiment results show that the temperatures derived by the GIM-EPF algorithm agree well with the theoretical design temperature and the IPF inversion temperature.

Identification of a Splicing Mutation in ITPR1 via WES in a Chinese Early-Onset Spinocerebellar Ataxia Family.

Mutations in the inositol 1,4,5-triphosphate receptor type 1 gene (ITPR1) lead to SCA15, SCA16, and SCA29. To date, only a few families with SCA29 have been reported. A three-generation Chinese family including four affected persons and two unaffected persons were enrolled in this study. We conducted whole-exome sequencing (WES) of the proband DNA initially to find the causal gene. We ascertained the family with autosomal dominant type of congenital nonprogressive cerebellar ataxia (CNPCA) associated with delayed motor and cognitive impairment. WES study was performed with two patients and identified c.1207-2A-T transition, in exon 14 of ITPR1, which was a splicing mutation. Sanger sequencing showed that four patients within this family carried the mutation and two unaffected members did not carry it. The results showed that the novel splicing mutation of ITPR1 was the causative gene for SCA29. In conclusion, we identified a novel SCA29 causative splicing mutation of ITPR1 in a Chinese family. We suggest ITPR1 gene analysis shall be a priority for diagnosis of patients with early-onset CNPCA. Our study demonstrated that whole-exome sequencing might rapidly improve the diagnosis of genetic ataxias.

The antihyperlipidemic effects of fullerenol nanoparticles via adjusting the gut microbiota in vivo.

BACKGROUND: Nanoparticles (NPs) administered orally will meet the gut microbiota, but their impacts on microbiota homeostasis and the consequent physiological relevance remain largely unknown. Here, we describe the modulatory effects and the consequent pharmacological outputs of two orally administered fullerenols NPs (Fol1 C60(OH)7(O)8 and Fol113 C60(OH)11(O)6) on gut microbiota. RESULTS: Administration of Fol1 and Fol113 NPs for 4 weeks largely shifted the overall structure of gut microbiota in mice. The bacteria belonging to putative short-chain fatty acids (SCFAs)-producing genera were markedly increased by both NPs, especially Fol1. Dynamic analysis showed that major SCFAs-producers and key butyrate-producing gene were significantly enriched after treatment for 7-28 days. The fecal contents of SCFAs were consequently increased, which was accompanied by significant decreases of triglycerides and total cholesterol levels in the blood and liver, with Fol1 superior to Fol113. Under cultivation in vitro, fullerenols NPs can be degraded by gut flora and exhibited a similar capacity of inulin to promote SCFA-producing genera. The differential effects of Fol1 and Fol113 NPs on the microbiome may be attributable to their subtly varied surface structures. CONCLUSIONS: The two fullerenol NPs remarkably modulate the gut microbiota and selectively enrich SCFA-producing bacteria, which may be an important reason for their anti-hyperlipidemic effect in mice.

Small size fullerenol nanoparticles suppress lung metastasis of breast cancer cell by disrupting actin dynamics.

BACKGROUND: Tumor metastasis is the primary cause of mortality in cancer patients. Migratory breast cancer cells in lymphatic and blood vessels seek new sites and form metastatic colonies in the lung and bone, and then these cancer cells often wreak considerable havoc. With advances in nanotechnology, nanomaterials and nanotechnologies are widely applied in tumor therapy. In this paper, small size fullerenol nanoparticles, which are separated by isoelectric focusing electrophoresis (IFE) for discrepancy of isoelectric point (pI), are used in the study of tumor metastasis. RESULTS: In this study, the commendable inhibition of tumor metastasis was uncovered by intravenous injection of purified fullerenol fraction with special surface charge and functional groups, which was separated by IFE for discrepancy of pI. By investigating the actin dynamics in several cancer cell lines, we found these small size fullerenol nanoparticles disturbed actin dynamics. Young's modulus detection and cell migration assays revealed that fullerenol lowered stiffness and restrained migration of breast cancer cells. Filopodia, the main supporting structures of actin bundles, are important for cell motility and adhesion. Scanning electron microscopy showed that fullerenol reduced the number and length of filopodia. Simultaneously, the inhibition of integrin to form clusters on filopodias, which was likely induced by reorganizing of actin cytoskeleton, impacted cancer cell adhesion and motility. CONCLUSIONS: With intravenous injection of these fullerenol nanoparticles, tumor metastasis is well inhibited in vivo. The underlying mechanism most likely to be attributed to the effect of fullerenol nanoparticles on disturbing actin dynamics. With the disordered actin fiber, cell function is varied, including decreased cell stiffness, reduced filopodia formation, and inactivated integrin.

Impact of Titanium Dioxide and Fullerenol Nanoparticles on Caco-2 Gut Epithelial Cells.

The application of nano-products in the food industry increases the risk of people exposed to nanoparticles. Titanium dioxide nanoparticles (T-NPs) are typically and widely used in food field, while fullerenol nanoparticles (F-NPs) have great promise to be used as food additives. Therefore, it is necessary and important to understand the safety of T-NPs and F-NPs in foods. In the present study, Caco-2 gut epithelial cell line was selected as a model to investigate the impact of T-NPs and F-NPs. The viability and proliferation of Caco-2 gut epithelial cells incubated with different concentrations of T-NPs and F-NPs were observed. The results showed that the two kinds of nanoparticles did not induce cell death even lasting for 48 h. The results of apoptosis and DNA damages in the cells indicated that both T-NPs with 50 and 100 µg/mL caused Caco-2 gut epithelial cell apoptosis, but didn't cause significantly DNA damages. F-NPs with 200 and 500 µg/mL concentrations also can induce cell apoptosis but no DNA damage.

Small size fullerenol nanoparticles inhibit thrombosis and blood coagulation through inhibiting activities of thrombin and FXa.

Thrombus is one of main causes of death in the world and also a vital trouble of biomaterials application in vivo. Recently, effect of fullerenol nanomaterials on anticoagulation was found in our research through extension of bleeding times in treated Sprague-Dawley rats via intravenous injection. Inhibiting of fullerenols on thrombosis was ascertained further by thromboembolism model. Effects of fullerenols on intrinsic and extrinsic pathway were distinct in prolonging activated partial thromboplastin time and prothrombin time, which supported that fullerenols induced defects in both pathways. Inhibited activities of activated coagulation factor X (FXa) and thrombin were verified by experiments in vitro and AutoDock Vina. The results suggest that fullerenols depending on small size and certainly surface property occupied the active domain of FXa and thrombin to block their activity; further, thrombosis was inhibited. This putative mechanism offers an insight into how fullerenol NPs were utilized further in biomedical applications.

Effects of Fullerenol Nanoparticles on Rat Oocyte Meiosis Resumption.

The excellent biocompatibility and biological effects of fullerenol and its derivatives make their biomedical application promising. The potential effects of fullerenol in mammals have been extensively studied, but little is known about its effects on female reproduction. Using canonical oocyte-granulosa cell complexes (OGCs) in vitro maturation culture model, we investigated the effect of fullerenol on the first oocyte meiotic resumption. In the surrounding granulosa cells, fullerenol nanoparticles occluded the extracellular domain of the epidermal growth factor receptor (EGFR) to reduce EGFR-ligand binding and subsequent extracellular signal-regulated kinase 1 and 2 (ERK1/2) activation, which involved the regulation of connexin 43 (CX43) expression and internalization. Downregulation of CX43 expression and the retraction of transzonal projections (TZPs) interrupted the gap junction channel and TZPs based mass transportation. This effect decreased cyclic adenosine monophosphate (cAMP) levels in the oocyte and thereby accelerated rat oocyte meiosis resumption. Moreover, perinuclear distribution of CX43 and EGFR was observed in granulosa cells, which could further exacerbate the effects. Fullerenol nanoparticles interfered with the strict process of oocyte meiosis resumption, which likely reduced the oocyte quality.

Nanoparticles with High-Surface Negative-Charge Density Disturb the Metabolism of Low-Density Lipoprotein in Cells.

Endocytosis is an important pathway to regulate the metabolism of low-density lipoprotein (LDL) in cells. At the same time, engineering nanoparticles (ENPs) enter the cell through endocytosis in biomedical applications. Therefore, a crucial question is whether the nanoparticles involved in endocytosis could impact the natural metabolism of LDL in cells. In this study, we fabricated a series of gold nanoparticles (AuNPs) (13.00 ± 0.69 nm) with varied surface charge densities. The internalized AuNPs with high-surface negative-charge densities (HSNCD) significantly reduced LDL uptake in HepG-2, HeLa, and SMMC-7721 cells compared with those cells in control group. Notably, the significant reduction of LDL uptake in cells correlates with the reduction of LDL receptors (LDL-R) on the cell surface, but there is no change in protein and mRNA of LDL-Rs. The cyclic utilization of LDL-R in cells is a crucial pathway to maintain the homoeostasis of LDL uptake. The release of LDL-Rs from LDL/LDL-R complexes in endosomes depended on reduction of the pH in the lumen. AuNPs with HSNCD hampered vacuolar-type H⁺-ATPase V1 (ATPaseV1) and ATPaseV0 binding on the endosome membrane, blocking protons to enter the endosome by the pump. Hence, fewer freed LDL-Rs were transported into recycling endosomes (REs) to be returned to cell surface for reuse, reducing the LDL uptake of cells by receptor-mediated endocytosis. The restrained LDL-Rs in the LDL/LDL-R complex were degraded in lysosomes.

[Discussion on the standard of clinical genetic testing report and the consensus of gene testing industry].

The widespread application of next generation sequencing (NGS) in clinical settings has enabled testing, diagnosis, treatment and prevention of genetic diseases. However, many issues have arisen in the meanwhile. One of the most pressing issues is the lack of standards for reporting genetic test results across different service providers. The First Forum on Standards and Specifications for Clinical Genetic Testing was held to address the issue in Shenzhen, China, on October 28, 2017. Participants, including geneticists, clinicians, and representatives of genetic testing service providers, discussed problems of clinical genetic testing services across in China and shared opinions on principles, challenges, and standards for reporting clinical genetic test results. Here we summarize expert opinions presented at the seminar and report the consensus, which will serve as a basis for the development of standards and guidelines for reporting of clinical genetic testing results, in order to promote the standardization and regulation of genetic testing services in China.

Directly data processing algorithm for multi-wavelength pyrometer (MWP).

Data processing of multi-wavelength pyrometer (MWP) is a difficult problem because unknown emissivity. So far some solutions developed generally assumed particular mathematical relations for emissivity versus wavelength or emissivity versus temperature. Due to the deviation between the hypothesis and actual situation, the inversion results can be seriously affected. So directly data processing algorithm of MWP that does not need to assume the spectral emissivity model in advance is main aim of the study. Two new data processing algorithms of MWP, Gradient Projection (GP) algorithm and Internal Penalty Function (IPF) algorithm, each of which does not require to fix emissivity model in advance, are proposed. The novelty core idea is that data processing problem of MWP is transformed into constraint optimization problem, then it can be solved by GP or IPF algorithms. By comparison of simulation results for some typical spectral emissivity models, it is found that IPF algorithm is superior to GP algorithm in terms of accuracy and efficiency. Rocket nozzle temperature experiment results show that true temperature inversion results from IPF algorithm agree well with the theoretical design temperature as well. So the proposed combination IPF algorithm with MWP is expected to be a directly data processing algorithm to clear up the unknown emissivity obstacle for MWP.