Reprogramming of lipid metabolism in the tumor microenvironment: a strategy for tumor immunotherapy.

Lipid metabolism in cancer cells has garnered increasing attention in recent decades. Cancer cells thrive in hypoxic conditions, nutrient deficiency, and oxidative stress and cannot be separated from alterations in lipid metabolism. Therefore, cancer cells exhibit increased lipid metabolism, lipid uptake, lipogenesis and storage to adapt to a progressively challenging environment, which contribute to their rapid growth. Lipids aid cancer cell activation. Cancer cells absorb lipids with the help of transporter and translocase proteins to obtain energy. Abnormal levels of a series of lipid synthases contribute to the over-accumulation of lipids in the tumor microenvironment (TME). Lipid reprogramming plays an essential role in the TME. Lipids are closely linked to several immune cells and their phenotypic transformation. The reprogramming of tumor lipid metabolism further promotes immunosuppression, which leads to immune escape. This event significantly affects the progression, treatment, recurrence, and metastasis of cancer. Therefore, the present review describes alterations in the lipid metabolism of immune cells in the TME and examines the connection between lipid metabolism and immunotherapy.

PCIF1, the only methyltransferase of N6,2-O-dimethyladenosine.

N6-methyladenosine(m6A), is the most abundant post-transcriptional modification of mRNA in biology. When the first nucleotide after the m7G cap is adenosine, it is methylated at the N6 position to form N6,2-O-dimethyladenosine (m6Am). m6Am is a reversible modification located at the first transcribed nucleotide, which is present in about 30% of cellular mRNAs, thus m6Am can have a significant impact on gene expression in the transcriptome. Phosphorylated CTD interaction factor 1(PCIF1), the unique and specific methyltransferase of m6Am, has been shown to affect mRNA stability, transcription, and translation. Several studies have shown that PCIF1 is clearly associated with tumor, viral, and endocrine diseases. Moreover, PCIF1 may be related to the tumor microenvironment, immune cell typing, and programmed cell death protein 1(PD-1) drug resistance. Here, we summarize the mechanism of PCIF1 involvement in mRNA modifications, and outline m6Am modifications and diseases in which PCIF1 is involved. We also summarized the role of PCIF1 in immune and immune checkpoint blockade(ICB) treatment, and predicted the possibility of PCIF1 as a biomarker and therapeutic target.

Quality evaluation of Hawk tea from different months and regions based on quantitative analysis of multiple components with a single marker (QAMS) combined with HPLC fingerprint.

BACKGROUND: Hawk tea, a medicinal and edible plant, has been consumed for thousands of years in Southwest China. To date, no unified food safety standard for Hawk tea has been established, and systematic research on the quality of Hawk tea is lacking. OBJECTIVE: The aim of this study was to develop a comprehensive evaluation method for the quality of Hawk tea based on inclusions content, high-performance liquid chromatography (HPLC) fingerprinting combined with the quantitative analysis of multiple components with a single marker (QAMS) method. METHODS: The contents of total flavonoids, total phenols, total polysaccharides, and total protein were determined using the colorimetric method. An effective comprehensive evaluation method was established to classify the 16 batches of samples based on HPLC fingerprint analysis combined with similarity analysis (SA), hierarchical cluster analysis (HCA), principal component analysis (PCA), partial least-squares discrimination analysis (PLS-DA), and the QAMS method. RESULTS: Flavonoids were the main chemical components of Hawk tea. The accuracy of the QAMS method was verified by comparing the calculated results with those of the external standard method (ESM). No significant differences were found between the two methods. Additionally, the fingerprint of Hawk tea was also established. CONCLUSION: The method established in this study can be used for the comprehensive quality evaluation of Hawk tea and can also provide a reference for the quality evaluation of other herbal medicines.

Genetic and transcriptomic dissection of an artificially induced paired spikelets mutant of wheat (Triticum aestivum L.).

KEY MESSAGE: Morphological, genetic and transcriptomic characterizations of an EMS-induced wheat paired spikelets (PS) mutant were performed. A novel qualitative locus WPS1 on chromosome 1D was identified. Grain yield of wheat is significantly associated with inflorescence or spike architecture. However, few genes related to wheat spike development have been identified and their underlying mechanisms are largely unknown. In this study, we characterized an ethyl methanesulfonate (EMS)-induced wheat mutant, wheat paired spikelets 1 (wps1). Unlike a single spikelet that usually develops at each node of rachis, a secondary spikelet appeared below the primary spikelet at most of the rachis nodes of wps1. The microscope observation showed that the secondary spikelet initiated later than the primary spikelet. Genetic analysis suggested that the PS of wps1 is controlled by a single dominant nuclear gene, designated WHEAT PAIRED SPIKELETS 1 (WPS1). Further RNA-seq based bulked segregant analysis and molecular marker mapping localized WPS1 in an interval of 208.18-220.92 Mb on the chromosome arm 1DL, which is different to known genes related to spike development in wheat. By using wheat omics data, TraesCS1D02G155200 encoding a HD-ZIP III transcription factor was considered as a strong candidate gene for WPS1. Transcriptomic analysis indicated that PS formation in wps1 is associated with auxin-related pathways and may be regulated by networks involving TB1, Ppd1, FT1, VRN1, etc. This study laid the solid foundation for further validation of the causal gene of WPS1 and explored its regulatory mechanism in PS formation and inflorescence development, which may benefit to kernel yield improvement of wheat based on optimization or design of spike architecture in the future.

Genetic dissection of quantitative trait loci for grain size and weight by high-resolution genetic mapping in bread wheat (Triticum aestivum L.).

KEY MESSAGE: Six major QTLs for wheat grain size and weight were identified on chromosomes 4A, 4B, 5A and 6A across multiple environments, and were validated in different genetic backgrounds. Grain size and weight are crucial components of wheat yield. Dissection of their genetic control is thus essential for the improvement of yield potential in wheat breeding. We used a doubled haploid (DH) population to detect quantitative trait loci (QTLs) for grain width (GW), grain length (GL), and thousand grain weight (TGW) in five environments. Six major QTLs, QGw.cib-4B.2, QGl.cib-4A, QGl.cib-5A.1, QGl.cib-6A, QTgw.cib-4B, and QTgw.cib-5A, were consistently identified in at least three individual environments and in best linear unbiased prediction (BLUP) datasets, and explained 5.65-34.06% of phenotypic variation. QGw.cib-4B.2, QTgw.cib-4B, QGl.cib-5A.1 and QGl.cib-6A had no effect on grain number per spike (GNS). In addition to QGl.cib-4A, the other major QTLs were further validated by using Kompetitive Allele Specific PCR (KASP) markers in different genetic backgrounds. Moreover, significant interactions between the three major GL QTLs and two major TGW QTLs were observed. Comparison analysis showed that QGl.cib-5A.1 and QGl.cib-6A are likely new loci. Notably, QGw.cib-4B.2 and QTgw.cib-4B were co-located on chromosome 4B and improved TGW by increasing only GW, unlike nearby or overlapped loci reported previously. Three genes associated with grain development within the QGw.cib-4B.2/QTgw.cib-4B interval were identified by searches on sequence similarity, spatial expression patterns, and orthologs. The major QTLs and KASP markers reported here will be useful for elucidating the genetic architecture of grain size and weight and for developing new wheat cultivars with high and stable yield.

Epigallocatechin gallate prevents peritoneal fibrosis by inhibiting epithelial-mesenchymal transition in human peritoneal mesothelial cells.

The current study set out to elucidate the function of epigallocatechin gallate (EGCG) against peritoneal fibrosis in peritoneal dialysis (PD) patients. Firstly, human peritoneal mesothelial cells (HPMCs) were pretreated with 0, 12.5, 25, 50 or 100µmol/L EGCG. Epithelial-mesenchymal transition (EMT) models were induced by advanced glycation end products (AGEs). Untreated-cells were regarded as the blank control group. Changes in proliferation and migration were analyzed by MTT assay and scratch test and levels of HPMC epithelial and interstitial molecular marker proteins were measured by Western blot assay and immunofluorescence, while trans-endothelial resistance was assessed using an epithelial trans membrane cell resistance meter. Inhibition rates of HPMCs, migration numbers and the levels of Snail, E-cadherin, CK and ZO-1 were all decreased, while the levels of α-SMA and FSP1 and trans cellular resistance values were increased in treatment groups (P<0.05). With the increase of EGCG concentrations, HPMCs growth inhibition rates and migration numbers, the levels of α-SMA and FSP1 and TER values were decreased and the levels of Snail, E-cadherin, CK and ZO-1 were enhanced (P<0.05). Overall, the current study highlights that EGCG effectively inhibits the proliferation and migration of HPMCs, increases permeability, suppresses EMT and ultimately delays peritoneal fibrosis.

Identification and candidate gene mining of HvSS1, a novel qualitative locus on chromosome 6H, regulating the uppermost internode elongation in barley (Hordeum vulgare L.).

KEY MESSAGE: A novel qualitative locus regulating the uppermost internode elongation of barley was identified and mapped on 6H, and the candidate gene mining was performed by employing various barley genomic resources. The stem of grass crops, such as barley and wheat, is composed of several interconnected internodes. The extent of elongation of these internodes determines stem height, and hence lodging, canopy architecture, and grain yield. The uppermost internode (UI) is the last internode to elongate. Its elongation contributes largely to stem height and facilitates spike exsertion, which is crucial for final grain yield. Despite the molecular mechanism underlying regulation of UI elongation was extensively investigated in rice, little is known in barley. In this study, we characterized a barley spontaneous mutant, Sheathed Spike 1 (SS1), showing significantly shortened UI and sheathed spike (SS). The extension of UI parenchyma cell in SS1 was significantly suppressed. Exogenous hormone treatments and RNA-seq analysis indicated that the suppression of UI elongation is possibly related to insufficient content of endogenous bioactive gibberellin. Genetic analysis showed that SS1 is possibly controlled by a qualitative dominant nuclear factor. Bulked segregant analysis and further molecular marker mapping identified a novel major locus, HvSS1, in a recombination cold spot expanding 173.44-396.33 Mb on chromosome 6H. The candidate gene mining was further conducted by analyzing sequence differences, spatiotemporal expression patterns, and variant distributions of genes in the candidate interval by employing various barley genomic resources of worldwide collections of barley accessions. This study made insight into genetic control of UI elongation in barley and laid a solid foundation for further gene cloning and functional characterization. The results obtained here also provided valuable information for similar research in wheat.

Identification and validation of two major QTLs for spike compactness and length in bread wheat (Triticum aestivum L.) showing pleiotropic effects on yield-related traits.

KEY MESSAGE: Two major and stable QTLs for spike compactness and length were detected and validated in multiple genetic backgrounds and environments, and their pleiotropic effects on yield-related traits were analyzed. Spike compactness (SC) and length (SL) are greatly associated with wheat (Triticum aestivum L.) grain yield. To detect quantitative trait loci (QTL) associated with SC and SL, two biparental populations derived from crosses of Chuanmai42/Kechengmai1 and Chuanmai42/Chuannong16 were employed to perform QTL mapping in five environments. A total of 34 QTLs were identified, in which six major QTLs were repeatedly detected in more than four environments and the best linear unbiased prediction datasets, explaining 7.13-33.6% of phenotypic variation. These major QTLs were co-located in two genomic regions on chromosome 5A and 6A, namely QSc/Sl.cib-5A and QSc/Sl.cib-6A, respectively. By developing kompetitive allele-specific PCR (KASP) markers that linked to them, the two loci were validated in different genetic backgrounds, and their interactions were also analyzed. Comparison analysis showed that QSc/Sl.cib-5A was not Vrn-A1 and Q, and QSc/Sl.cib-6A was likely a new locus for SC and SL. Both QSc/Sl.cib-5A and QSc/Sl.cib-6A had pleiotropic effects on other yield-related traits including plant height, thousand grain weight and grain length. Therefore, the two loci combined with the developed KASP markers might be potentially applicable in wheat breeding. Furthermore, based on the spatiotemporal expression patterns, gene annotation, orthologous search and sequence differences, TraesCS5A01G301400 and TraesCS6A01G090300 were considered as potential candidates for QSc/Sl.cib-5A and QSc/Sl.cib-6A, respectively. These results provided valuable information for fine mapping and cloning of the two loci in the future.

Genetic and molecular characterization of determinant of six-rowed spike of barley carrying vrs1.a4.

KEY MESSAGE: Decisive role of reduced vrs1 transcript abundance in six-rowed spike of barley carrying vrs1.a4 was genetically proved and its potential causes were preliminarily analyzed. Six-rowed spike 1 (vrs1) is the major determinant of the six-rowed spike phenotype of barley (Hordeum vulgare L.). Alleles of Vrs1 have been extensively investigated. Allele vrs1.a4 in six-rowed barley is unique in that it has the same coding sequence as Vrs1.b4 in two-rowed barley. The determinant of row-type in vrs1.a4 carriers has not been experimentally identified. Here, we identified Vrs1.b4 in two-rowed accessions and vrs1.a4 in six-rowed accessions from the Qinghai-Tibet Plateau at high frequency. Genetic analyses revealed a single nuclear gene accounting for row-type alteration in these accessions. Physical mapping identified a 0.08-cM (~ 554-kb) target interval on chromosome 2H, wherein Vrs1 was the most likely candidate gene. Further analysis of Vrs1 expression in offspring of the mapping populations or different Vrs1.b4 and vrs1.a4 lines confirmed that downregulated expression of vrs1.a4 causes six-rowed spike. Regulatory sequence analysis found a single 'TA' dinucleotide deletion in vrs1.a4 carriers within a 'TA' tandem-repeat-enriched region ~ 1 kb upstream of the coding region. DNA methylation levels did not correspond to the expression difference and therefore did not affect Vrs1 expression. More evidence is needed to verify the causal link between the 'TA' deletion and the downregulated Vrs1 expression and hence the six-rowed spike phenotype.

[From Passive Application to Active Design -Restructuring and Reshaping of Core Specialty Knowledge Systems of Biomedical Engineering (Biomedical Materials Track) Undergraduate Education].

Biomedical engineering (BME) (biomedical materials track) is a typical field of interdisciplinary integration. Its specialty education simultaneously undertakes the duo reformation responsibilities for the new engineering education and the new medical education due to its unique strengths in interdisciplinary nature, comprehensive scope of knowledge, and status of being on the cutting edge of technology. We made an analysis, in this paper, of the opportunities and challenges faced by BME (biomedical materials track) specialty education on the basis of the trends and frontiers of development in biomedical materials in the world. From the perspective of new requirements raised by major national strategies and industrial development for the qualifications and competence of professionals specializing in biomedical materials, thorough reflections were made on the specialized education of BME (biomedical materials track) under the background of the new engineering education and the new medical education. Furthermore, we proposed herein to reconstruct the specialized core knowledge system according to the main line of the reactions and the responses between the biomedical materials and human bodies at different levels and set up a series of courses of biomedical materials science centered on Materiobiology as the core. We also proposed to establish a diversified integrated reform model of the training system incorporating production, learning, research and application for highly competent BME (biomedical materials track) professionals. This paper attempts to contribute to the solution of the major issue of how to train the innovative talents and leaders who will pioneer a new round of diagnosis and treatment technology revolution and the development of the medical device industry.

Targeting KRASG12D mutation in non-small cell lung cancer: molecular mechanisms and therapeutic potential.

Lung malignant tumors are a type of cancer with high incidence and mortality rates worldwide. Non-small cell lung cancer (NSCLC) accounts for over 80% of all lung malignant tumors, and most patients are diagnosed at advanced stages, leading to poor prognosis. Over the past decades, various oncogenic driver alterations associated with lung cancer have been identified, each of which can potentially serve as a therapeutic target. Rat sarcoma (RAS) genes are the most commonly mutated oncogenes in human cancers, with Kirsten rat sarcoma (KRAS) being the most common subtype. The role of KRAS oncogene in NSCLC is still not fully understood, and its impact on prognosis remains controversial. Despite the significant advancements in targeted therapy and immune checkpoint inhibitors (ICI) that have transformed the treatment landscape of advanced NSCLC in recent years, targeting KRAS (both directly and indirectly) remains challenging and is still under intensive research. In recent years, significant progress has been made in the development of targeted drugs targeting the NSCLC KRASG12C mutant subtype. However, research progress on target drugs for the more common KRASG12D subtype has been slow, and currently, no specific drugs have been approved for clinical use, and many questions remain to be answered, such as the mechanisms of resistance in this subtype of NSCLC, how to better utilize combination strategies with multiple treatment modalities, and whether KRASG12D inhibitors offer substantial efficacy in the treatment of advanced NSCLC patients.

Manipulating the tumour immune microenvironment by N6-methyladenosine RNA modification.

N6-methyladenosine (m6A), a posttranscriptional regulatory mechanism, is the most common epigenetic modification in mammalian mRNA. M6A modifications play a crucial role in the developmental network of immune cells. The expression of m6A-related regulators often affects carcinogenesis and tumour suppression networks. In the tumour microenvironment, m6A-modified enzymes can affect the occurrence and progression of tumours by regulating the activation and invasion of tumour-associated immune cells. Immunotherapy, which utilises immune cells, has been demonstrated to be a powerful weapon in tumour treatment and is increasingly being used in the clinic. Here, we provide an updated and comprehensive overview of how m6A modifications affect invasive immune cells and their potential role in immune regulation. In addition, we summarise the regulation of epigenetic regulators associated with m6A modifications in tumour cells on the antitumour response of immune cells in the tumour immune microenvironment. These findings provide new insights into the role of m6A modifications in the immune response and tumour development, leading to the development of novel immunotherapies for cancer treatment.

Delayed infected hematoma in retrosternal area following total thyroidectomy: a case report.

Introduction and Importance: Postoperative neck hematoma (PNH), a rare complication following thyroidectomy, occurs in only 1.1-3.15% of cases and can lead to life-threatening outcomes. More rarely, delayed PNHs with atypical clinical manifestations and positions have not yet been reported. Early identification and immediate medical intervention are of utmost importance in such cases. Case Presentation: The authors represented a patient with thyroid cancer adherent to the trachea, who underwent post-thyroidectomy, experienced delayed PNH in the retrosternal region and was infected by respiratory pathogens. Meanwhile, the patient developed recurrent laryngeal nerve (RLN) paralysis after surgery. PNH was not identified in the clinical manifestations; instead, it was detected only through successive cervical ultrasound examinations. Clinical Discussion: Although rare, PNH can lead to serious complications, especially delayed complications or those in atypical positions, without neck swelling. When simultaneously with RLN paralysis, the hematoma may be neglected. Therefore, early diagnosis and treatment are crucial. Conclusion: Clinicians should be vigilant of atypical PNH because neck swelling may be absent. Cervical ultrasonography is essential for diagnosis and can be performed multiple times. Cervical CT scans should be part of the routine procedure, while contrast-enhanced ultrasound can help detect active bleeding. Early postoperative antibiotics are recommended if the tumor is closely attached to the trachea.

RNA N6-methyladenosine (m6A) modification in HNSCC: molecular mechanism and therapeutic potential.

Head and neck squamous cell carcinoma ranks seventh in incidence of malignant tumours in the world. Although there are treatments including surgery, radiotherapy and chemotherapy, targeted therapy and immunotherapy, drug resistance to treatment is caused by various reasons, and the survival rate of patients remains frustrating. To overcome the bottleneck of treatment at this stage, it is urgent to identify possible diagnostic and prognostic markers. N6-methyladenosine is a methylation modification on the sixth N atom of adenine which is the most abundant epitope transcriptome modification in mammalian genes. N6-methyladenosine modification is reversible and results from the interaction among writers, erasers and readers. A large number of studies have proven that N6-methyladenosine modification has important significance in promoting the progression and treatment of tumours and have made great progress in research. In this review, we introduce how N6-methyladenosine modification promotes the occurrence and development of tumours, the mechanism of drug resistance, and new findings of N6-methyladenosine modification in radiotherapy and chemotherapy, immunotherapy, and targeted therapy. N6-methyladenosine modification provides more possibilities for improving the overall survival rate and prognosis of patients.

Targeting Neutrophil Extracellular Traps: A Novel Antitumor Strategy.

The clinical efficacy of surgery, radiotherapy, and chemotherapy for cancer is usually limited by the deterioration of tumor microenvironment (TME). Neutrophil extracellular traps (NETs) are decondensed chromatin extruded by neutrophils and are widely distributed among various cancers, such as pancreatic cancer, breast cancer, and hepatocellular carcinoma. In the TME, NETs interact with stromal components, immune cells and cancer cells, which allows for the reshaping of the matrix and the extracellular environment that favors the initiation, progression, and metastasis of cancer. In addition, NETs impair the proliferation and activation of T cells and NK cells, thus producing a suppressive TME that restricts the effect of immunotherapy. A better understanding of the function of NETs in the TME will provide new opportunities for the prevention of cancer metastasis and the discovery of novel therapy strategies.

PYGL-mediated glucose metabolism reprogramming promotes EMT phenotype and metastasis of pancreatic cancer.

Epithelial-mesenchymal transition (EMT) is closely associated with tumor invasion and metastasis. However, key regulators of EMT in pancreatic ductal adenocarcinoma (PDAC) need to be further studied. Bioinformatics analyses of pancreatic cancer public datasets showed that glycogen phosphorylase L (PYGL) expression is elevated in quasimesenchymal PDAC (QM-PDAC) and positively associated with EMT. In vitro cellular experiments further confirm PYGL as a crucial EMT regulator in PDAC cells. Functionally, PYGL overexpression promotes cell migration and invasion in vitro and facilitates liver metastasis in vivo, while PYGL knockdown has opposite effects. Mechanically, hypoxia induces PYGL expression in a hypoxia inducible factor 1α (HIF1α)-dependent manner and promotes glycogen accumulation. Elevated PYGL mobilizes accumulated glycogen to fuel glycolysis via its activity as a glycogen phosphorylase, thus inducing the EMT process, which could be suppressed by the glycolysis inhibitor 2-deoxy-D-glucose (2-DG). Clinically, PYGL expression is upregulated in PDAC and correlates with its malignant features and poor prognosis. Collectively, the data from our study reveal that the hypoxia/PYGL/glycolysis-induced EMT promotes PDAC metastasis, which establishes the rational for targeting hypoxia/PYGL/glycolysis/EMT signaling pathway against PDAC.

Mechanisms of N6­methyladenosine modification in tumor development and potential therapeutic strategies (Review).

N6­methyladenosine (m6A) modification, as the most common and abundant type of RNA modification in mammalian cells, participates in the processes of mRNA transcription, translation, splicing and degradation, serving to regulate RNA stability. In recent years, a large number of studies have indicated that m6A modification is able to affect tumor progression, participate in tumor metabolism, regulate tumor cell ferroptosis and change the tumor immune microenvironment, thereby affecting tumor immunotherapy. In the current review, the main features of m6A­associated proteins are presented with a focus on the mechanisms underpinning their roles in tumor progression, metabolism, ferroptosis and immunotherapy, also emphasizing the potential of targeting m6A­associated proteins as a promising strategy for the treatment of cancer.

m6A methylation modification and immune cell infiltration: implications for targeting the catalytic subunit m6A-METTL complex in gastrointestinal cancer immunotherapy.

N6-methyladenosine (m6A) methylation modification is a ubiquitous RNA modification involved in the regulation of various cellular processes, including regulation of RNA stability, metabolism, splicing and translation. Gastrointestinal (GI) cancers are some of the world's most common and fatal cancers. Emerging evidence has shown that m6A modification is dynamically regulated by a complex network of enzymes and that the catalytic subunit m6A-METTL complex (MAC)-METTL3/14, a core component of m6A methyltransferases, participates in the development and progression of GI cancers. Furthermore, it has been shown that METTL3/14 modulates immune cell infiltration in an m6A-dependent manner in TIME (Tumor immune microenvironment), thereby altering the response of cancer cells to ICIs (Immune checkpoint inhibitors). Immunotherapy has emerged as a promising approach for treating GI cancers. Moreover, targeting the expression of METTL3/14 and its downstream genes may improve patient response to immunotherapy. Therefore, understanding the role of MAC in the pathogenesis of GI cancers and its impact on immune cell infiltration may provide new insights into the development of effective therapeutic strategies for GI cancers.

Risk Factors for Contralateral Occult Papillary Thyroid Carcinoma in Patients with Clinical Unilateral Papillary Thyroid Carcinoma: A Case-Control Study.

Introduction: Papillary thyroid cancer (PTC) is one of the most prevalent endocrine malignancies that has increased in recent decades around the world. Although the indicator for navigating the surgical extent in PTC patients is still in debate, a key issue is how to predict that there are undetected preoperative tumors in the contralateral thyroid lobe. This study aims to find risk factors for contralateral occult papillary thyroid cancer (COPTC) to facilitate more accurate surgical decisions made for patients with PTC. Materials and Methods: In our study, we included 229 patients who underwent total thyroidectomy plus central and ipsilateral lateral lymph nodes dissection from January 1, 2019, to September 1, 2021. Univariate and multivariate logistic regression analyses were conducted to assess the association between COPTC and clinical-pathological characteristics, as well as the relation between the diameter of the occult lesions and predictors. The forest plot was plotted to visualize the prediction factors from the output of the multivariate regression analysis. A ROC curve was used to evaluate the combining potency of all the risk factors. Results: Of the 229 patients included in our study, 46 with COPTC were assigned to the case group, representing 20.1% in this study. Multifocality in one lobe (OR = 2.21, P=0.03), intact capsule (OR = 2.54, P=0.01), central lymph node metastasis (OR = 3.00, P=0.02), and Hashimoto's thyroiditis (OR = 2.08, P = 0.04) are more prone to present contralateral occult papillary thyroid carcinoma. The ROC curve of the aggregate potency of the risk factors presents AUC = 0.701 (P < 0.001), and the best cutoff value was 2.02, with a sensitivity of 78.3% and specificity of 55.2%. Furthermore, there was no statistical correlation between the diameter of the occult tumor and the four obtained variables. Conclusion: Patients with multifocality in one lobe, intact capsule, central lymph node metastasis, and HT may harbor contralateral papillary thyroid carcinoma. It is essential to be prudent to make a surgical or follow-up decision on these patients. In addition, more clinical rather than postoperative pathological indicators need to be revealed in the future.

[Atmospheric VOCs Pollution Characteristics and Health Risk Assessment of Large-scale Integrated Industrial Area and Surrounding Areas in Southwest China].

To investigate the characteristics of atmospheric volatile organic compound (VOCs) pollution and promote VOCs pollution prevention and control in industrial areas, in December 2020, VOCs samples collected using Summa Canisters at three observation sites were used to study the characteristics of VOCs pollution and source apportionment and to conduct a health risk assessment in large integrated industrial areas and surrounding urban areas in southwest China. The results showed that the mean φ(TVOCs) at site A and site B in an industrial area and at a third urban site were 105.25×10-9, 222.92×10-9, and 82.87×10-9, respectively. Monochloromethane, dichloromethane, acetone, ethanol, and ethane were the species with higher volume fractions at the three sites. Aromatic hydrocarbons and OVOCs had a large contribution to the ozone formation potential (OFP), with a cumulative contribution of more than 50%, and the main reactive species were methyl methacrylate, toluene, p-xylene, and o-xylene; the secondary organic aerosol formation potential (SOAP) of aromatic hydrocarbons contributed more than 80%, with the main active species being toluene, p-xylene, and o-xylene. The results of PMF source analysis showed six main sources of VOCs, in the descending order of the petrochemical industry (21.83%), industrial waste incineration (18.6%), pharmaceutical manufacturing (16.99%), fossil fuel combustion (16.03%), motor vehicle exhaust (14.23%), and chemical manufacturing (12.32%). The mean values of the hazard index (HI) of site A and site B in the industrial area and in the urban site were 0.55, 0.68, and 0.41, respectively, and the mean lifetime cancer risk (LCR) values were 6.71×10-6, 6.72×10-6, and 6.58×10-6, respectively. Both HI and LCR in industrial areas were larger than those in urban areas. The quantitative assessment of risk sources showed that motor vehicle exhaust and fossil fuel combustion contributed relatively high carcinogenic risks.