Associations between single and multiple dietary vitamins and the risk of periodontitis: results from NHANES 2009-2014.

Background: Periodontitis is a prevalent inflammatory periodontal disease that has an impact on the overall quality of life. Although several studies have indicated an association between individual vitamin intake and periodontitis risk, the associations of the multivitamins with periodontitis risk remain unclear. Aim: This study aimed to explore the joint effect of multivitamins (including vitamin A, vitamin B1, vitamin B2, vitamin B6, vitamin B12, vitamin C, vitamin D, vitamin E, and vitamin K) on periodontitis. Methods: For this cross-sectional study, data were collected from participants aged ≥ 30 years in the National Health and Nutrition Examination Surveys 2009-2014 (n = 9,820). We employed weighted multivariate logistic regression models to evaluate the single association between individual vitamin intakes and periodontitis, and Bayesian kernel machine regression (BKMR), weighted quantile sum (WQS) regression, and quantile g-computation (qgcomp) models to assess the joint effect of nine vitamins on periodontitis. Results: The overall prevalence of periodontitis was approximately 35.97%. After adjustment of covariates, vitamin B6 [odds ratio (OR) = 0.82, 95% confidence interval (CI): 0.72-0.94] and vitamin E (OR = 0.79, 95%CI: 0.69-0.92) were negatively related to the likelihood of developing periodontitis, respectively. The result of three models indicated that, mixture of vitamin A, vitamin B1, vitamin B2, vitamin B6, vitamin B12, vitamin C, vitamin D, vitamin E, and vitamin K had a significant negative combined effect on the risk of periodontitis. In the BKMR model, when all remaining vitamins were at their median levels, the periodontitis risk decreased with increased concentration levels of vitamin E and vitamin B2. WQS analysis indicated the highest weighted chemical was vitamin E, followed by vitamin B12 and vitamin D. In the qgcomp model, vitamin E received the highest negative weights for the periodontitis risk, followed by vitamin B2 and vitamin D, respectively. Conclusion: Both dietary vitamin B6 and vitamin E were associated with decreased odds of periodontitis. Additionally, the mixture-exposed analyses consistently showed the negative correlations between nine dietary vitamins mixtures and periodontitis.

Epidemiological variations and trends in glaucoma burden in the Belt and Road countries.

BACKGROUND: Analyzing the glaucoma burden in "Belt and Road" (B&R) countries based on age, gender, and risk factors from 1990 to 2019 in order to provide evidence for future prevention strategies. METHODS: We applied global burden of disease(GBD) 2019 to compare glaucoma prevalence and Years lived with disabilities (YLDs) from 1990 to 2019 in the B&R countries. Trends of disease burden between 1990 and 2019 were evaluated using the average annual percent change and the 95% uncertainty interval (UI) were reported. RESULTS: From 1990 to 2019, most B&R countries showed a downward trend in age-standardized prevalence and YLDs (all P < 0.05). Additionally, only the age-standardized YLDs in males of Pakistan has a 0.35% increase (95%CI:0.19,0.50,P < 0.001), and most B&R countries has a decline(all P < 0.05) in age-standardized YLDs in every 5 years age group after 45 years old except for Pakistan(45-79 years and > 85 years), Malaysia(75-84 years), Brunei Darussalam(45-49 years), Afghanistan(70-79 years). Finally, in all Central Asian countries, the age-standardized YLDs due to glaucoma caused by fasting hyperglycemia demonstrated have an increase between 1990 and 2019 (all P < 0.05), but Armenia and Mongolia have a decrease between 2010 and 2019 (all P < 0.05). CONCLUSION: The prevalence of glaucoma continues to pose a significant burden across regions, ages, and genders in countries along the "B&R". It is imperative for the "B&R" nations to enhance health cooperation in order to collaboratively tackle the challenges associated with glaucoma.

MicroRNA-126 (MiR-126): key roles in related diseases.

In eukaryotes such as humans, some non-coding single-stranded RNAs (ncRNAs) help to regulate the pre- and post-transcriptional expression of certain genes, which in turn control many important physiological processes, such as cell proliferation, distinctions, invasion, angiogenesis, and embryonic development. microRNA-126 is an important member of these miRNAs that can be directly or indirectly involved in the control of angiogenesis. Recently, numerous studies have expounded that microRNA-126 can inhibit or promote angiogenesis as well as attenuate inflammatory responses through complex molecular mechanisms. As such, it serves as a biomarker or potential therapeutic target for the prediction, diagnosis, and treatment of relevant diseases. In this review, we present the advancements in research regarding microRNA-126's role in the diagnosis and treatment of related diseases, aiming to provide innovative therapeutic options for the diagnosis and treatment of clinically relevant diseases.

2,4,6-trinitrotoluene causes mitochondrial toxicity in Caenorhabditis elegans by affecting electron transport.

As a typical energetic compound widely used in military activities, 2,4,6-trinitrotoluene (TNT) has attracted great attention in recent years due to its heavy pollution and wide distribution in and around the training facilities, firing ranges, and demolition sites. However, the subcellular targets and the underlying toxic mechanism of TNT remain largely unknown. In this study, we explored the toxic effects of TNT biological reduction on the mitochondrial function and homeostasis in Caenorhabditis elegans (C. elegans). With short-term exposure of L4 larvae, 10-1000 ng/mL TNT reduced mitochondrial membrane potential and adenosine triphosphate (ATP) content, which was associated with decreased expression of specific mitochondrial complex involving gas-1 and mev-1 genes. Using fluorescence-labeled transgenic nematodes, we found that fluorescence expression of sod-3 (muls84) and gst-4 (dvls19) was increased, suggesting that TNT disrupted the mitochondrial antioxidant defense system. Furthermore, 10 ng/mL TNT exposure increased the expression of the autophagy-related gene pink-1 and activated mitochondrial unfolded protein response (mt UPR), which was indicated by the increased expression of mitochondrial stress activated transcription factor atfs-1, ubiquitin-like protein ubl-5, and homeobox protein dve-1. Our findings demonstrated that TNT biological reduction caused mitochondrial dysfunction and the development of mt UPR protective stress responses, and provided a basis for determining the potential risks of energetic compounds to living organisms.

WTAP-Mediated N6-Methyladenosine of RNAs Facilitate the Pathophysiology of Atopic Dermatitis.

N6-methyladenosine (m6A) is the most abundant dynamic and reversible internal chemical modification of RNA in eukaryotic cells and is essential in multiple pathophysiological processes. However, it has not been reported in atopic dermatitis (AD). We used Arraystar m6A-mRNA epitranscriptomic microarray to screen for differentially expressed genes and their m6A levels and m6A-related enzymes in patients with AD. We confirmed that the m6A RNA methyltransferase WTAP and 2 candidate differentially expressed genes (S100A9 and SERPINB3) were significantly upregulated in keratinocytes in public data and epidermal lesions of patients with AD. In vitro cell experiments confirmed that WTAP influenced the expression of the 2 candidate differentially expressed genes and promoted primary human epidermal keratinocyte proliferation while inhibiting human epidermal keratinocyte differentiation. Furthermore, we showed that WTAP, S100A9, and SERPINB3 expression correlated with AD severity. Our findings revealed that WTAP-mediated m6A modification promoted the expression of S100A9 and SERPINB3 to aggravate human epidermal keratinocyte proliferation and dysdifferentiation contributing to the pathophysiological development of AD.

Comparative analysis of clinical and immunological profiles across Omicron BA.5.2 subvariants using next-generation sequencing in a Chinese cohort.

Objective: The Omicron BA.5.2 variant of SARS-CoV-2 has undergone several evolutionary adaptations, leading to multiple subvariants. Rapid and accurate characterization of these subvariants is essential for effective treatment, particularly in critically ill patients. This study leverages Next-Generation Sequencing (NGS) to elucidate the clinical and immunological features across different Omicron BA.5.2 subvariants. Methods: We enrolled 28 patients infected with the Omicron variant, hospitalized in Zhangjiajie People's Hospital, Hunan, China, between January 20, 2023, and March 31, 2023. Throat swabs were collected upon admission for NGS-based identification of Omicron subvariants. Clinical data, including qSOFA scores and key laboratory tests, were collated. A detailed analysis of lymphocyte subsets was conducted to ascertain the extent of immune cell damage and disease severity. Results: Patients were infected with various Omicron subvariants, including BA.5.2.48, BA.5.2.49, BA.5.2.6, BF.7.14, DY.1, DY.2, DY.3, and DY.4. Despite having 43 identical mutation sites, each subvariant exhibited unique marker mutations. Critically ill patients demonstrated significant depletion in total lymphocyte count, T cells, CD4, CD8, B cells, and NK cells (P < 0.05). However, there were no significant differences in clinical and immunological markers across the subvariants. Conclusion: This study reveals that critically ill patients infected with different Omicron BA.5.2 subvariants experience similar levels of cellular immune dysfunction and inflammatory response. Four mutations - ORF1a:K3353R, ORF1a:L3667F, ORF1b:S997P, S:T883I showed correlation with immunological responses although this conclusion suffers from the small sample size. Our findings underscore the utility of NGS in the comprehensive assessment of infectious diseases, contributing to more effective clinical decision-making.

Myofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling.

Obesity and type 2 diabetes (T2D) are the leading causes of the progressive decline in muscle regeneration and fitness in adults. The muscle microenvironment is known to play a key role in controlling muscle stem cell regenerative capacity, yet the underlying mechanism remains elusive. Here, we found that Baf60c expression in skeletal muscle is significantly downregulated in obese and T2D mice and humans. Myofiber-specific ablation of Baf60c in mice impairs muscle regeneration and contraction, accompanied by a robust upregulation of Dkk3, a muscle-enriched secreted protein. Dkk3 inhibits muscle stem cell differentiation and attenuates muscle regeneration in vivo. Conversely, Dkk3 blockade by myofiber-specific Baf60c transgene promotes muscle regeneration and contraction. Baf60c interacts with Six4 to synergistically suppress myocyte Dkk3 expression. While muscle expression and circulation levels of Dkk3 are markedly elevated in obese mice and humans, Dkk3 knockdown improves muscle regeneration in obese mice. This work defines Baf60c in myofiber as a critical regulator of muscle regeneration through Dkk3-mediated paracrine signaling.

A2AR-mediated lymphangiogenesis via VEGFR2 signaling prevents salt-sensitive hypertension.

AIMS: Excess dietary sodium intake and retention lead to hypertension. Impaired dermal lymphangiogenesis and lymphatic dysfunction-mediated sodium and fluid imbalance are pathological mechanisms. The adenosine A2A receptor (A2AR) is expressed in lymphatic endothelial cells (LECs), while the roles and mechanisms of LEC-A2AR in skin lymphangiogenesis during salt-induced hypertension are not clear. METHODS AND RESULTS: The expression of LEC-A2AR correlated with lymphatic vessel density in both high-salt diet (HSD)-induced hypertensive mice and hypertensive patients. Lymphatic endothelial cell-specific A2AR knockout mice fed HSD exhibited 17 ± 2% increase in blood pressure and 17 ± 3% increase in Na+ content associated with decreased lymphatic density (-19 ± 2%) compared with HSD-WT mice. A2AR activation by agonist CGS21680 increased lymphatic capillary density and decreased blood pressure in HSD-WT mice. Furthermore, this A2AR agonist activated MSK1 directly to promote VEGFR2 activation and endocytosis independently of VEGF as assessed by phosphoprotein profiling and immunoprecipitation assays in LECs. VEGFR2 kinase activity inhibitor fruquintinib or VEGFR2 knockout in LECs but not VEGF-neutralizing antibody bevacizumab suppressed A2AR activation-mediated decrease in blood pressure. Immunostaining revealed phosphorylated VEGFR2 and MSK1 expression in the LECs were positively correlated with skin lymphatic vessel density and A2AR level in hypertensive patients. CONCLUSION: The study highlights a novel A2AR-mediated VEGF-independent activation of VEGFR2 signaling in dermal lymphangiogenesis and sodium balance, which might be a potential therapeutic target in salt-sensitive hypertension.

Multi-generation reproductive toxicity of RDX and the involved signal pathways in Caenorhabditis elegans.

As one of the most frequently used explosives, hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) can cause persistent pollution in the environment, leading to the potential ecological threat crossing the generations. In this study, we employed Caenorhabditis elegans to explore the toxic effects of RDX on the parental and offspring worms and the involved signaling pathways. Exposure up to 1000 ng/mL of RDX produced a significant increase in reactive oxygen species (ROS) production, germ cell apoptosis, and decrease in eggs laid. Various mutants were used to demonstrate the RDX-induced apoptosis signaling pathway, and the metabolism of RDX in the nematodes was found related to cytochrome P450 and GST through RNA sequencing. Exposure of parental worms to RDX produced significant reproductive toxicity in F1 and F2, but was recovered in F3 and F4. The transgenerational effects were associated with the decreased expression of met-2, spr-5, and set-2. Our findings revealed the signaling pathways related to the reproductive toxicity caused by RDX in C. elegans and their future generations, which provided the basis for further exploration of the ecological risks of energetic compounds in the environment.

Predictive model of chemotherapy-related toxicity in elderly Chinese cancer patients.

Purpose: Older cancer patients are more likely to develop and die from chemotherapy-related toxicity. However, evidence on drug safety and optimal effective doses is relatively limited in this group. The aim of this study was to develop a tool to identify elderly patients vulnerable to chemotherapy toxicity. Patients and methods: Elderly cancer patients ≥60 years old who visited the oncology department of Peking Union Medical College Hospital between 2008 and 2012 were included. Each round of chemotherapy was regarded as a separate case. Clinical factors included age, gender, physical status, chemotherapy regimen and laboratory tests results were recorded. Severe (grade ≥3) chemotherapy-related toxicity of each case was captured according to the National Cancer Institute Common Terminology Criteria for Adverse Events, version 5.0. Univariate analysis was performed by chi-square statistics to determine which factors were significantly associated with severe chemotherapy toxicity. Logistic regression was used to build the predictive model. The prediction model was validated by calculating the area under the curve of receiver operating characteristic (ROC). Results: A total of 253 patients and 1,770 cases were included. The average age of the patients was 68.9 years. The incidence of grade 3-5 adverse events was 24.17%. Cancer type (non-GI cancers), BMI<20 kg/m2, KPS<90%, severe comorbidity, polychemotherapy, standard dose chemotherapy, low white blood cells count, anemia, low platelet cells count, low creatine level and hypoalbuminemia were associated with severe chemotherapy-related toxicity. We used these factors to construct a chemotherapy toxicity prediction model and the area under the ROC curve was 0.723 (95% CI, 0.687-0.759). Risk of toxicity increased with higher risk score (11.98% low, 31.51% medium, 70.83% high risk; p < 0.001). Conclusion: We constructed a predictive model of chemotherapy toxicity in elderly cancer patients based on a Chinese population. The model can be used to guide clinicians to identify vulnerable population and adjust treatment regimens accordingly.

Loss of C3a and C5a receptors promotes adipocyte browning and attenuates diet-induced obesity via activating inosine/A2aR pathway.

Complement activation is thought to underline the pathologic progression of obesity-related metabolic disorders; however, its role in adaptive thermogenesis has scarcely been explored. Here, we identify complement C3a receptor (C3aR) and C5a receptor (C5aR) as critical switches to control adipocyte browning and energy balance in male mice. Loss of C3aR and C5aR in combination, more than individually, increases cold-induced adipocyte browning and attenuates diet-induced obesity in male mice. Mechanistically, loss of C3aR and C5aR increases regulatory T cell (Treg) accumulation in the subcutaneous white adipose tissue during cold exposure or high-fat diet. Activated Tregs produce adenosine, which is converted to inosine by adipocyte-derived adenosine deaminases. Inosine promotes adipocyte browning in a manner dependent on activating adenosine A2a receptor. These data reveal a regulatory mechanism of complement in controlling adaptive thermogenesis and suggest that targeting the C3aR/C5aR pathways may represent a therapeutic strategy in treating obesity-related metabolic diseases.

Baicalin Blocks Colon Cancer Cell Cycle and Inhibits Cell Proliferation through miR-139-3p Upregulation by Targeting CDK16.

Baicalin was reported to facilitate the apoptosis of colon cells and inhibit tumor growth in vivo. This study aimed to explore the specific mechanism and function of baicalin on colon cells. Relative mRNA levels were tested via qPCR. Cell proliferation, viability, and cell cycle phases were evaluated using MTT, colony formation, and flow cytometry assays, respectively. The interaction between miR-139-3p and cyclin-dependent kinase 16 (CDK16) was measured via a dual-luciferase reporter assay. Immunohistochemistry was used to count the positivity cells in tumor tissues collected from treated xenografted tumor mice. The results showed that baicalin increased miR-139-3p expression while also decreasing CDK16 levels, blocking the cell cycle, and inhibiting cell proliferation in colon cancer cells. miR-139-3p silencing or CDK16 overexpression abolished the inhibitory effects of baicalin on colon cancer proliferation. miR-139-3p directly targeted and interacted with CDK16 at the cellular level. The protective functions of miR-139-3p knockdown on tumor cells were abrogated by silencing CDK16. The combination of baicalin treatment and CDK16 knockdown further inhibited tumor growth of xenografted tumor mice compared with the groups injected with only sh-CDK16 or baicalin in vivo. In conclusion, baicalin inhibited colon cancer growth by modulating the miR-139-3p/CDK16 axis.

Culture and identification of multipotent stem cells in guinea pig sclera.

BACKGROUND: To investigate whether the sclera of guinea pig contains stem cells with multiple differentiation potentials. METHODS: Scleral tissue from guinea pig was separated from the retina and choroid and digested to release single cells. The cells cultured was identified as stem cells by flow cytometric analysis, semiquantitative RT-PCR. Abilities for multipotent differentiation were analyzed by histochemical staining technique (oil-red-O staining, alcian blue staining and alizarin red staining). Scleral fibroblast cell was treated as control group. RESULTS: The cultured scleral stem cells were positive for CD44 and CD105 (mesenchymal stem cell surface markers) by flow cytometry. The cells cultured expressed stem cell markers ABCG2, Notch1, Six2, and Pax6, and the most important component of sclera type I collagen. The positive staining informed that the cells cultured were able to differentiate to adipogenic, chondrogenic, and osteogenic lineages. Scleral fibroblast cell was stained negative by oil-red-O staining and alizarin red staining. Expression of Sox9 in the cells cultured after chondrogenic differentiation significantly increased compared with scleral fibroblast cell. CONCLUSION: The guinea pig sclera contained stem cells with multiple differentiation potentials. The cells were also related to scleral collagen and cartilage related proteins. The finding may provide a new tool to help clarify mechanisms of sclera related disease in further studies.

The impact of international technical cooperation in new energy industry on carbon emissions: evidence from the top 30 countries in the global innovation index.

International cooperation has become a global consensus to solve environmental problems. This paper selects the top 30 countries in the global innovation index as the research sample, based on Patent Cooperation Treaties (PCT) data jointly applied in the field of new energy, constructs the international technical cooperation network, and uses the fixed effect panel regression model to verify the influence of international technical cooperation of new energy industry on carbon emission intensity. The results show that the USA, Germany, the UK, France, and the Netherlands are at the center of the network. International technological cooperation in new energy industry has a significant negative impact on carbon emission intensity. The convening of the United Nations Climate Change Conference in Copenhagen has accelerated global industrial upgrading, and the effect of international technical cooperation in new energy on carbon emission reduction has been strengthened. In addition, the level of economic development, international trade, and research and development (R&D) are also important factors affecting carbon emission intensity. Countries with high network centrality should give full play to their network influence to promote global cooperation in the field of new energy and achieve carbon mitigation targets by signing more environmental agreements.

Fast and non-destructive discriminating the geographical origin of Hangbaiju by hyperspectral imaging combined with chemometrics.

Hangbaiju is highly appreciated flower tea for its health benefits, and its quality and price are affected by geographical origin. Fast and accurate identification of the geographical origin of Hangbaiju is very significant for producers, consumers and market regulators. In this work, hyperspectral imaging combined with chemometrics, was used, for the first time, to explore and implement the geographical origin classification of Hangbaiju. The hyperspectral images in the spectral range of 410-2500 nm for 75 samples of five different origins were collected. As a versatile chemometrics tool, bagging classification tree-radial basis function (BAGCT-RBFN), compared with classification tree (CT), radial basis function network (RBFN), was applied to discriminate Hangbaiju samples from different origins. The results showed that BAGCT-RBFN based on optimal wavelengths yielded superior classification performances to CT and RBFN with full wavelengths. The recognition rates (RR) of the training and prediction sets by BAGCT-RBFN were 96.0 % and 92.0 %, respectively. Hyperspectral imaging combined with chemometric can be considered as a powerful, feasible and convenient tool for the classification of Hangbaiju samples from different origins. It promises to be a potential way for origin discriminant analysis and quality monitor in food fields.

The protocol of CUT&Tag for metabolic tissue cells.

Cleavage under target and tagment (CUT&Tag) is a technology that utilizes the fusion protein of Tn5 transposase and protein A/G which can guide Tn5 enzyme to the antibody bound to target protein and cleave the chromatin regions adjacent to target protein. Chromatin libraries are then tagged and sequenced by the high-throughput sequencing to obtain chromatin information at specific sites or protein binding locations. CUT&Tag technology plays an important role in the research of DNA and protein interactions. It can be used to understand the modifications of histone and the bindings of transcription factors. Compared with the traditional chromatin immunoprecipitation-sequencing (ChIP-seq) technology, the CUT&Tag has the strengths of high signal-to-noise ratio, good repeatability, short experimental period, and low cell input. It shows great advantages in early embryonic development, stem cells, cancer, epigenetics and other research fields. In this article, we described the protocol of CUT&Tag for metabolic tissue cells (mouse primary islet cells), to provide an epigenetic method for studying metabolic cells.

Research on traceability strategy of food supply chain considering delay effect.

The traceability system has significantly contributed to ensure food safety and quality. However, the biggest difficulty in food traceability is the numerous links from field to table, and there is no stable strategic partnership between supply chain members and the lack of social responsibility of some practitioners. Thus, this study aims to seek the best traceability strategy for companies in centralized model and decentralized model, respectively. Therefore, we have constructed a differential game model based on the delay effect to determine the optimal traceability level and traceable goodwill and compare the profits of the food supply chain (FSC). The results show that the delay time is positively related to the level of traceability effort and has a high impact on the traceable goodwill. Companies in the FSC can formulate optimal traceability strategies based on delay time and foster improvement in food safety and quality.

Dietary intervention preserves ß cell function in mice through CTCF-mediated transcriptional reprogramming.

Pancreatic ß cell plasticity is the primary determinant of disease progression and remission of type 2 diabetes (T2D). However, the dynamic nature of ß cell adaptation remains elusive. Here, we establish a mouse model exhibiting the compensation-to-decompensation adaptation of ß cell function in response to increasing duration of high-fat diet (HFD) feeding. Comprehensive islet functional and transcriptome analyses reveal a dynamic orchestration of transcriptional networks featuring temporal alteration of chromatin remodeling. Interestingly, prediabetic dietary intervention completely rescues ß cell dysfunction, accompanied by a remarkable reversal of HFD-induced reprogramming of islet chromatin accessibility and transcriptome. Mechanistically, ATAC-based motif analysis identifies CTCF as the top candidate driving dietary intervention-induced preservation of ß cell function. CTCF expression is markedly decreased in ß cells from obese and diabetic mice and humans. Both dietary intervention and AAV-mediated restoration of CTCF expression ameliorate ß cell dysfunction ex vivo and in vivo, through transducing the lipid toxicity and inflammatory signals to transcriptional reprogramming of genes critical for ß cell glucose metabolism and stress response.

Defects and countermeasures in laboratory diagnosis of rare IgE multiple myeloma.

BACKGROUND: IgE multiple myeloma (MM) is a rare subtype of MM that is easily misdiagnosed. We report a rare case of IgE-MM and investigate the application of the SLiM-CRAB criteria to screen for high-risk smoldering MM (SMM) patients, so as to summarize the causes and methods used to prevent missed diagnosis or misdiagnosis in IgE-MM. METHODS: The serum monoclonal protein (M-protein) classification and IgE quantification was performed and sent to several individual institutions. The results were collected and the causes of IgE detection defects were analyzed. RESULTS: Upon admission to our hospital, the patient's serum free kappa light chain was 1069.9 mg/L, free lambda light chain was 9.2 mg/L, and free kappa/lambda ratio was 115.9, which met the SLiM criteria, but without CRAB features. Immunofixation electrophoresis (IF) showed "M-like protein aggregation bands" in all lanes. After pretreatment with 1% ß-mercaptoethanol to depolymerize the aggregation of monoclonal protein, the "M-like protein aggregation bands disappeared. The other five institutions did not provide the correct typing results. The quantification of serum IgE was as high as 2.06 × 107 IU/mL, whereas 7 other testing institutions reported IgE levels ranging from 1.0 to 1100 IU/mL. CONCLUSION: High-risk biomarkers in SLiM criteria can achieve good therapeutic effects in rare IgE-MM patients. Serum immunofixation performed without antisera against IgE, insufficient identification of the lytic bands produced by high macromolecule aggregation in IF, and the absence of a prozone effect avoidance procedure during IgE quantitative detection are the primary causes of missed diagnosis or misdiagnosis in patients with IgE-MM.

Simultaneous degradation of p-nitrophenol and reduction of Cr(VI) in one step using microwave atmospheric pressure plasma.

Different physicochemical properties between Cr(VI) and phenolic compounds pose serious challenges for the effective treatment of co-contamination. This study developed an electrodeless high-flow microwave atmospheric plasma jet for the single-step simultaneous degradation of p-nitrophenol (PNP) and reduction of Cr(VI). Following a 15 min treatment with microwave atmospheric pressure plasma, the removal efficiency of Cr(VI) and PNP reached 97.5% and 93.6%, respectively, whereas that of total organic carbon reached 30.2%. Adding PNP to the solution significantly improved Cr(VI) reduction, whereas PNP degradation increased slightly with Cr(VI). The results indicate that the PNP intermediates significantly affected Cr(VI) reduction. Additionally, long-lived H2O2 and short-lived ·H aided the reduction of Cr(VI) during plasma treatment. The addition of hydroxyl scavengers during treatment implied that ·OH was largely responsible for PNP oxidation. High-performance liquid chromatography-mass spectroscopy (HPLC-MS) revealed that PNP intermediates, including p-nitrocatechol and 5-nitrobenzene-1,2,3-triol, function as Cr(VI) reductants. On the basis of the examined intermediate products, the potential PNP degradation pathway was investigated. The factors that could influence simultaneous dehgradation and reduction, including solution pH, gas velocity, and distance between the plasma outlet and the water surface were researched. Low pH supports Cr(VI) reduction, and the promotion of PNP for Cr(VI) reduction applies to all pH values. The degradation of PNP is insensitive to pH values with or without Cr(VI). The optimal gas velocity for PNP degradation and Cr(VI) reduction was revealed to be 6 L/min. The simultaneous removal of PNP and Cr(VI) benefits from a shorter distance between the plasma outlet and the water's surface.