Identifying ADGRG1 as a specific marker for tumor-reactive T cells in acute myeloid leukemia.

Besides chemotherapy and hematopoietic stem cell transplantation (HSCT), autologous T cells can also serve as a new treatment approach for AML patients. However, the features of tumor-reactive T cells and their distinctive markers still lack full description. To evaluate the characteristics of tumor-reactive T cells, we collected bone marrow (BM) T cells from newly diagnosed AML patients with RUNX1::RUNX1T1 as examples for paired single-cell RNA sequencing and single-cell V(D)J sequencing. Based on the STARTRAC-like algorithm, we defined bystander T cells and tumor-reactive T cells. Compared with bystander T cells, tumor-reactive T cells presented as senescent-like cytotoxic terminally differentiated T cells (Temra) with upregulated NK-related markers. Additionally, we found ADGRG1 could serve as the specific marker of CD8+ T tumor-reactive T cell and validated it through the Runx1Runx1t1/+; Mx1-Cre mouse model. In chimeric antigen receptor (CAR)-T and target cell system, ADGRG1 was selectively upregulated upon antigen-TCR encounter. Moreover, ADGRG1+CD8+ T cells released a higher level of IFN-γ and showed higher cell-killing ability when exposed to matched AML blasts. Together, our findings depict the single-cell profile of tumor-reactive T cells in AML BM and propose that ADGRG1 can act as an indicator of T cell tumor reactivity in AML, which may be further harnessed for adoptive cell therapy and tumor-reactive TCR enrichment.

Mitochondrial genetic variations in leukemia: a comprehensive overview.

Leukemias are a group of heterogeneous hematological malignancies driven by diverse genetic variations, and the advent of genomic sequencing technologies facilitates the investigation of genetic abnormalities in leukemia. However, these sequencing-based studies mainly focus on nuclear DNAs. Increasing evidence indicates that mitochondrial dysfunction is an important mechanism of leukemia pathogenesis, which is closely related to the mitochondrial genome variations. Here, we provide an overview of current research progress concerning mitochondrial genetic variations in leukemia, encompassing gene mutations and copy number variations. We also summarize currently accessible mitochondrial DNA (mtDNA) sequencing methods. Notably, somatic mtDNA mutations may serve as natural genetic barcodes for lineage tracing and longitudinal assessment of clonal dynamics. Collectively, these findings enhance our understanding of leukemia pathogenesis and foster the identification of novel therapeutic targets and interventions.

COVID-19 transmission and control in land public transport: A literature review.

Land public transport is an important link within and between cities, and how to control the transmission of COVID-19 in land public transport is a critical issue in our daily lives. However, there are still many inconsistent opinions and views about the spread of SARS-CoV-2 in land public transport, which limits our ability to implement effective interventions. The purpose of this review is to overview the literature on transmission characteristics and routes of the epidemic in land public transport, as well as to investigate factors affecting its spread and provide feasible measures to mitigate the infection risk of passengers. We obtained 898 papers by searching the Web of Science, Pubmed, and WHO global COVID database by keywords, and finally selected 45 papers that can address the purpose of this review. Land public transport is a high outbreak area for COVID-19 due to characteristics like crowding, inadequate ventilation, long exposure time, and environmental closure. Different from surface touch transmission and drop spray transmission, aerosol inhalation transmission can occur not only in short distances but also in long distances. Insufficient ventilation is the most important factor influencing long-distance aerosol transmission. Other transmission factors (e.g., interpersonal distance, relative orientation, and ambient conditions) should be noticed as well, which have been summarized in this paper. To address various influencing factors, it is essential to suggest practical and efficient preventive measures. Among these, increased ventilation, particularly the fresh air (i.e., natural ventilation), has proven to effectively reduce indoor infection risk. Many preventive measures are also effective, such as enlarging social distance, avoiding face-to-face orientation, setting up physical partitions, disinfection, avoiding talking, and so on. As research on the epidemic has intensified, people have broken down many perceived barriers, but more comprehensive studies on monitoring systems and prevention measures in land public transport are still needed.

Association of triglyceride glucose index and triglyceride glucose-body mass index with sudden cardiac arrest in the general population.

BACKGROUND: Insulin resistance (IR) significantly contributes to cardiovascular disease (CVD) development. Triglyceride glucose (TyG) index and triglyceride glucose-body mass index (TyG-BMI) are recognised as convenient proxies for IR. However, their relationship with sudden cardiac arrest (SCA) remains unclear. METHODS: This prospective cohort analysis included 355,242 UK Biobank participants with available TyG index and TyG-BMI data and no history of CVD. Cox proportional risk models assessed the association between the TyG index, TyG-BMI and SCA risk. Additionally, Accelerated Failure Time (AFT) models were employed to investigate the timing of SCA onset. The impact of dynamic increases in TyG index and TyG-BMI levels on SCA risk was examined using restricted cubic spline. RESULTS: Over a median follow-up period of 165.4 months (interquartile range 156.5-174 months), 1,622 cases of SCA were recorded. Multivariate Cox regression analysis revealed a 9% increase in SCA risk per standard deviation increase in TyG index (adjusted hazard ratio (aHR) = 1.09, 95% confidence interval (CI) 1.04-1.15) and an 14% increase per standard deviation increase in TyG-BMI (aHR 1.14, 95% CI 1.09-1.2). AFT models indicated earlier median times to SCA occurrence with increasing quintiles of TyG index and TyG-BMI compared to the lowest quintile (P for trend < 0.05). SCA risk was linearly (P = 0.54) and non-linearly (P = 0.007) correlated with gradual increases in TyG index and TyG-BMI levels, respectively. Sex-stratified analyses showed stronger associations in women. CONCLUSIONS: Higher TyG index and TyG-BMI levels are associated with an increased SCA risk and earlier onset, particularly in women.

The RTK-RAS signaling pathway is enriched in patients with rare acute myeloid leukemia harboring t(16;21)(p11;q22)/FUS::ERG.

Acute myeloid leukemia (AML) with t(16;21)(p11;q22)/FUS::ERG is a rare AML subtype associated with poor prognosis. However, its clinical and molecular features remain poorly defined. We determined the clinicopathological, genomic, and transcriptomic characteristics and outcomes of patients with AML harboring FUS::ERG at our center. Thirty-six AML patients harboring FUS::ERG were identified, with an incidence rate of 0.3%. These patients were characterized by high lactate dehydrogenase levels (median: 838.5 U/L), elevated bone marrow blast counts (median: 71.5%), and a CD56-positive immunophenotype (94.3%). Notably, we found that RTK-RAS GTPase (RAS) pathway genes, including NRAS (33%) and PTPN11 (24%), were frequently mutated in this subtype. Transcriptome analysis revealed enrichment of the phosphatidylinositol-3-kinase-Akt (PI3K-Akt), mitogen-activated protein kinase (MAPK), and RAS signaling pathways and upregulation of BCL2, the target of venetoclax, in FUS::ERG AML compared to RUNX1::RUNX1T1 AML, a more common AML subtype with good prognosis. The median event-free survival in patients with FUS::ERG AML was 11.9 (95% confidence interval [CI]: 9.0-not available [NA]) months and the median overall survival was 18.2 (95% CI: 12.4-NA) months. Allogeneic hematopoietic stem cell transplantation failed to improve outcomes. Overall, the high incidence of RTK-RAS pathway mutations and high expression of BCL2 may indicate promising therapeutic targets in this high-risk AML subset.

Effects of therapeutic ultrasound in patients with knee osteoarthritis: A systematic review and meta-analysis.

Background: Therapeutic ultrasound (US) is a treatment for knee osteoarthritis (KOA), but its efficacy and safety are unclear. The objective of this study is to quantify the effect of US on pain relief and function recovery in KOA, and to analyze the US treatment duration and parameters on treatment outcome. Methods: We searched PubMed, MEDLINE, EMBASE, Google Scholar, Cochrane databases and ClinicalTrials.gov databases up to April 7, 2023. RCTs that compared the efficacy of therapeutic US with the control in KOA were included in the study, and the methodological quality of the trials was assessed using the Cochrane Risk of Bias tool. Results: Twenty-one RCTs (1315 patients) were included. US had a positive effect on visual analog scale (VAS) (SMD = -0.64, 95 % CI [-0.88, -0.40], I2 = 71 %) and Western Ontario and McMaster Universities (WOMAC) total scale (SMD = -0.45, 95 % CI [-0.69, -0.20]; I2 = 67 %). Pulsed US with an intensity ≤2.5 W/cm2 reduced visual analog scale (VAS), and differed in sessions (24 sessions (SMD = -0.80, 95 % CI [-1.07, -0.53], I2 = 0 %) vs 10 sessions (SMD = -0.71, 95 % CI [-1.09, -0.33], I2 = 68 %)). For pulsed US, a duration of treatment of 4-8 weeks (SMD = -0.69, 95 % CI [-1.13, -0.25], I2 = 73 %) appeared to be superior to ≤4 weeks (SMD = -0.77, 95 % CI [-1.04, -0.49], I2 = 0 %) for reducing visual analog scale (VAS). No US treatment-related adverse events were reported. Conclusion: Therapeutic US may be a safe and effective treatment for patients with KOA. The mode, intensity, frequency, and duration of US may affect the effectiveness of pain relief. Pulsed US with an intensity ≤2.5 W/cm2, 24 sessions, and a treatment duration of ≤4 weeks appears to have better pain relief.

Research Note: Analysis of microbial diversity on the shell surface of eggs collected from geographically distinct farms in China.

Micro-organisms on the eggshell surface of affect the quality of the egg. Sometimes, these microbes even pose a serious threat to the health of the egg's consumer. Bacterial 16S rDNA and fungal internal transcribed spacer region were sequenced to analyze the microbial diversity on the shell surface of the eggs collected from 4 distinct regions of China: Guyuan (GY; 1.5 million hens), Langfang (LF; 0.1 million hens), Beihai (BH; 1.2 million hens), and Dongguan (DG; 0.2 million hens). The results showed a higher bacterial and fungal abundance on the eggs collected from the northern and southern China farms, respectively. The dominant bacterial phylum detected across all egg samples was Firmicutes. In addition, the shell surfaces of the DG and LF samples harbored abundant levels of Proteobacteria. The dominant fungal phyla detected across all egg samples were Ascomycota and Basidiomycota. The bacterial compositions on eggshell surfaces differed significantly across all geographic regions, and the fungal composition differed significantly between samples collected from the southern and northern farms (P < 0.05). The abundance and composition of microbial colonies on the eggshell surface varied based on their geographical location (climate and environment) and farming scale (management). Our findings provide an important reference for optimizing the cleaning and disinfection methods for fresh eggs collected from different sources.

Median nerve electrical stimulation improves traumatic brain injury by reducing TACR1 to inhibit nuclear factor-κB and CCL7 activation in microglia.

The existing report elucidates that median nerve electrical stimulation (MNS) plays a role in treating traumatic brain injury (TBI). Herein, we explored the mechanism of MNS in TBI. A TBI-induced coma model (skull was hit by a cylindrical impact hammer) was established in adult Sprague-Dawley rats. Microglia were isolated from newborn Sprague-Dawley rats and was injured by lipopolysaccharide (LPS; 10 ng/mL). Consciousness was assessed by sensory and motor functions. Brain tissue morphology was detected using hematoxylin-eosin staining assay. Ionized calcium binding adapter molecule 1, NeuN and tachykinin receptor 1 (TACR1) level were detected by immunohistochemical assay. Levels of pro-inflammatory and anti-inflammatory factors were measured by enzyme linked immune sorbent assay (ELISA). Levels of TACR1, C-C motif chemokine 7 (CCL7), phosphorylation (p)-P65 and P65 were assessed by quantitative real time polymerase chain reaction (qRT-PCR) and western blot. M1 markers (inducible nitric oxide synthase and CD86) and M2 markers (arginase-1 (Arg1) and chitinase 3-like 3 (YM1)) of microglia as well as the transfection efficiency of short hairpin TACR1 (shTACR1) were assessed by qRT-PCR. Immunofluorescence and flow cytometry assay were used to detect microglia morphology and neuron apoptosis. MNS reduced neuron injury and microglia activation in the TBI-induced rat coma model. MNS reversed the effects of TBI on levels of inflammation-related factors, M1/M2 microglia markers, TACR1, p-P65/P65 and CCL7 in rats. shTACR1 reversed the effects of LPS on inflammation-related factors, M1/M2 microglia markers, microglia activation, neuron apoptosis, p-P65/P65 value and CCL7 level. Our results revealed that MNS improved TBI by reducing TACR1 to inhibit nuclear factor-κB (NF-κB) and CCL7 activation in microglia.

The Effects of VR-assisted and Overground Gait Adaptation Training on Balance and Walking Ability in Stroke Patients.

OBJECTIVE: This study compared the effects of virtual reality(VR)-assisted gait adaptation training with the overground gait adaptation training on balance and walking in patients with stroke. METHODS: Fifty-four eligible patients were enrolled. All patients were randomly divided into a VR and control group, with 27 patients in each group. The VR group received VR-assisted training on the treadmill, whereas the control group received overground training in a physical therapy room. After the intervention, patients were assessed using walking speed, obstacle avoidance ability, timed up and go (TUG) test, postural stability, and the Barthel Index (BI). RESULTS: Significant improvements in walking speed, obstacle avoidance ability, TUG test and eye-opening center of pressure (COP) speed were observed after the intervention (P < 0.05). No statistically significant differences were found in eye-closing COP speed, tandem COP speed, single-leg COP speed, and BI (P > 0.05). CONCLUSIONS: Stroke patients may benefit from VR-assisted gait adaptation training in improving walking and static balance function and reducing the risk of falls.

Vericiguat protects against cardiac damage in a pig model of ischemia/reperfusion.

BACKGROUND: The purpose of this research was to verify that vericiguat, a soluble guanylate cyclase (sGC) stimulator, reduces myocardial ischemic reperfusion injury (MIRI), and to learn how this reduction happens. METHODS AND RESULTS: To develop an ischaemia/reperfusion (I/R) model, the left anterior descending artery was blocked in minipigs under anesthesia for 90 minutes, followed by 180 minutes of reperfusion. Vericiguat is administered three hours before surgery. Two weeks after receiving therapy, pigs underwent cardiovascular magnetic resonance imaging (MRI) to evaluate the results. The MRI results suggest improvement in the myocardial infarct after vericiguat treatment. Vericiguat treatment for two weeks enhanced vascularity, inhibited pro-inflammatory cells, and decreased collagen deposition in the infarct zone of pigs. Short-term experiments investigating possible explanations have indicated that vericiguat has antiapoptotic effects on cardiomyocytes and increases levels of autophagy. CONCLUSIONS: Vericiguat, an SGC activator, reduces MIRI in pigs by boosting autophagy, preventing apoptosis, and promoting angiogenesis.

A novel subclonal rearrangement of the STRN3::PDGFRB gene in de novo acute myeloid leukemia with NPM1 mutation and its leukemogenic effects.

Chromosome translocations in the 5q31-33 region are associated with a range of hematologic malignancies, some of which involve the platelet-derived growth factor receptor beta (PDGFRB) gene. We report a case of acute myeloid leukemia (AML) with a mutation in the NPM1 gene (NPM1-mut AML) and a subclonal gene rearrangement involving the PDGFRB gene. We identified a novel fusion gene, STRN3::PDGFRB, resulting from t(5;14) (q32;q12) chromosomal rearrangement. Sequential FISH confirmed that ~15% of leukemic cells carried the PDGFRB gene rearrangement, which suggests that STRN3::PDGFRB is a previously unreported fusion gene in a subclone. Reverse transcription PCR (RT-PCR) and Sanger sequencing confirmed that the fusion gene consisted of STRN3 exon 7 fused to PDGFRB exon 11, resulting in a chimeric protein containing the coiled-coil domain of striatin-3 and the transmembrane and intracellular tyrosine kinase domains of the PDGFRB. The new protein exhibited distinct cytoplasmic localization and had leukemogenic effects, as demonstrated by its ability to transform Ba/F3 cells to growth factor independence and cause a fatal myelodysplastic/myeloproliferative neoplasm (MDS/MPN)-like disease in mice, which then transformant to T-cell lymphoblastic lymphoma in secondary recipients. Ba/F3 cells expressing STRN3::PDGFRB or ETV6::PDGFRB were sensitive to tyrosine kinase inhibitors (TKIs) and selinexor, but in vitro experiments showed that the combination of imatinib and selinexor had a marked synergistic effect, although only the imatinib alone group could prolong the survival of T-cell blast transformation recipient mice. Our findings demonstrate the leukemogenic effects of the novel fusion gene and provide insights into the clone evolution of AML, which can be influenced by therapy selection. Furthermore, our results provide insight into the potential therapeutic options for patients with this type of mutation, as well as the need for careful consideration of treatment selection to prevent undesirable side effects.

Case report: Application of morphology in the diagnosis of siderosis in a patient with tuberculosis infection.

A 49-year-old male who had been working in welding for more than 30 years was admitted to the hospital for a medical checkup that revealed a lung shadow without specific symptoms such as coughing and sputum. Imaging studies showed diffuse ground-glass changes in both lungs, wall cavities with wall nodules, multiple peripheral nodules, and some nodules with calcification. The patient has been engaged in welding work for more than 30 years and exposed to iron dust. Lung tissue biopsy, routine morphological and pathological fluid basis examination of alveolar lavage fluid, can be considered as pulmonary iron particles, which can be regarded as iron dust lung. Acid-fast bacilli were detected in both fibrobronchoscopic brush extract and alveolar lavage fluid acid-fast staining. As the pathological examination revealed granulomatous inflammation showed caseation necrosis, the patient was judged to have concomitant pulmonary TB. After the diagnosis was made, the patient was no longer exposed to dust and was treated with appropriate anti- tuberculosis (TB) therapy. Lung lesions caused by welding have been reported, but the simultaneous finding of siderosis with pulmonary TB is specific to the case presented here. By describing the imaging features, combining different staining methods of alveolar lavage fluid and pathological examination of lung tissue, we showed various morphological manifestations of this case, aiming at improving the morphological diagnosis level of laboratory physicians and enabling patients to be diagnosed and treated early.

Malaria-derived exosomes exacerbate liver injury during blood stage of Plasmodium berghei infection.

Liver injury is a common clinical feature of Plasmodium spp. infection and contributes to multi-organ failure of severe malaria. Malaria-derived exosomes (MD-Exos) have recently engaged as key mediators in parasite-host interactions, modulating the subsequent pathogenic process. However, the role of MD-Exos in malaria-related liver injury and the underlying mechanisms remain unclear. Herein, exosomes from C57BL/6 mice infected with or without P. berghei ANKA serum (namely inf-Exos or un-Exos) were isolated and characterized by transmission electron microscopy, western blotting, and nanoparticle tracking analysis. The miRNAs profiling between inf-Exos and un-Exos were generated using RNA-seq and qPCR. The functions of inf-Exos on liver injury were investigated after two types of exosomes injected into mice intravenously (i.v.), by examining histopathological and apoptotic changes, macrophage polarization, and pro-inflammatory response. The infected red blood cells-stimulated mouse Raw264.7 macrophage cells targeted by inf-Exos or un-Exos were cultured for further study and verification the potential mechanisms. We found that both inf-Exos and un-Exos displayed a typical cup-shaped structure with a diameter of 60-200 nm, and had a positive expression of exosomal markers (e.g., CD9, CD63, and CD81). Compared with infected control mice, the treatment of inf-Exos but not un-Exos dramatically enhanced peripheral blood parasitemia and ECM incidence, exacerbated liver histopathological damage, elevated numbers of liver apoptotic cells, CD68+and CD86+ macrophages. The CD68+-TREM-1+ macrophages in liver tissues and the mRNA levels of pro-inflammatory cytokines (e.g., iNOS, TNF-α, IL-1ß, and IL-6) were increased by inf-Exos treatment in vivo. Meanwhile, the treatment of inf-Exos resulted in a substantial increase of the mRNA levels of CD86, iNOS, TNF-α, IL-1ß, and IL-6, but led to a remarkable decrease of Bcl-6 and SOCS-1 in Raw264.7 cells stimulated with iRBC in vitro. Notably, compared to un-Exos, five types of miRNAs (including miR-10a-5p, miR-10b-5p, miR-155-5p, miR-205-5p, and miR-21a-5p), that were previously reported to target Bcl-6 or SOCS-1, present higher abundance on inf-Exos, as demonstrated by RNA-seq and qPCR. Collectively, our data suggest that inf-Exos exacerbate malaria-induced liver pathology via triggering excessive pro-inflammatory response and promoting macrophage M1 polarization. Our findings will provide new insights into the roles of inf-Exos in malaria parasite-host interaction and pathogenesis of liver injury.

Clinical and genetic characterization of Epstein-Barr virus-associated T/NK-cell lymphoproliferative diseases.

BACKGROUND: Epstein-Barr virus (EBV)-associated T-/natural killer (T/NK)-cell lymphoproliferative diseases clinically take on various forms, ranging from an indolent course to an aggressive condition. OBJECTIVE: Clinically, failure to establish precise diagnosis and provide proper treatment makes it difficult to help patients. We sought to better understand the underlying pathogenesis and to identify genetic prognostic factors to achieve better treatment efficacy. METHODS: In this study, 119 cases of EBV-associated lymphoproliferative diseases, including EBV-associated hemophagocytic lymphohistiocytosis (n = 46) and chronic active EBV disease of T/NK cell type (n = 73), were retrospectively examined. RESULTS: Adults aged >20 years at onset accounted for 71.4% of our cohort. About 54.6% patients with unfavorable overall survival developed hemophagocytic lymphohistiocytosis and had higher plasma EBV load. Allogenic hematopoietic stem-cell transplantation was the sole independent favorable factor. We systematically screened germline and somatic aberrations by whole-exome and targeted sequencing. Among 372 antiviral immunity genes, germline variants of 8 genes were significantly enriched. From a panel of 24 driver genes, somatic mutations were frequently identified in dominant EBV-infected T/NK cells. Patients carrying any germline/somatic aberrations in epigenetic modifiers and RIG-I-like receptor (RLR) pathway had worse overall survival than those without 2 type aberrations. Importantly, patients with IFIH1 and/or DDX3X aberrations in the RLR pathway had higher plasma and NK-cell EBV load. Knockdown of DDX3X in NKYS cells downregulated RLR signaling activities and elevated the expression of EBV-encoded oncogenes such as LMP1 and EBNA1. CONCLUSION: Genetic defects were prevalent in adult EBV-associated hemophagocytic lymphohistiocytosis patients and patients with chronic active EBV disease of T/NK cell type; these defects were associated with unfavorable prognosis. These findings can help clinicians work out more precise staging of the condition and provide new insights into these EBV-associated diseases.

Genetic predisposition in patients with severe COVID-19.

The coronavirus disease 2019 (COVID-19) is a global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. COVID-19 has a variety of clinical manifestations, ranging from asymptomatic infection or mild symptoms to severe symptoms. Severe COVID-19 patients experience cytokine storm, resulting in multi-organ failure and even death. Male gender, old age, and pre-existing comorbidities (such as hypertension and diabetes ) are risk factors for COVID-19 severity. Recently, a series of studies suggested that genetic defects might also be related to disease severity and the cytokine storm occurence. Genetic variants in key viral immune genes, such as TLR7 and UNC13D, have been identified in severe COVID-19 patients from previous reports. In this review, we summarize the mechanisms underlying immune responses against SARS-CoV-2 and genetic variants that associated with the severity of COVID-19. The study of genetic basis of COVID-19 will be of great benefit for early disease detection and intervention.

Flexible and transparent broadband microwave metasurface absorber based on multipolar interference engineering.

Electromagnetic multipoles enable rich electromagnetic interactions in a metasurface and offer another degree of freedom to control electromagnetic responses. In this work, we design and experimentally demonstrate an optically transparent, flexible and broadband microwave metasurface absorber based on multipolar interference engineering. Different from previous works, the designed metasurface simultaneously supports fundamental electric dipole and high-order electric quadrupole mode, whose interference satisfies the back-scattering suppression condition based on the generalized Kerker effect and thus high absorption. The measurement results indicate that the fabricated metasurface exhibits a high average absorption of 89% in the microwave band from 4 GHz to 18 GHz, together with a good optical transparency. Our study offers an alternative approach for designing broadband microwave metasurface absorber, which is potentially applicable in electromagnetic shielding, radar stealth and energy harvesting.

Prediction and control of aerosol transmission of SARS-CoV-2 in ventilated context: from source to receptor.

Global spread of COVID-19 has seriously threatened human life and health. The aerosol transmission route of SARS-CoV-2 is observed often associated with infection clusters under poorly ventilated environment. In the context of COVID-19 pandemic, significant transformation and optimization of traditional ventilation systems are needed. This paper is aimed to offer better understanding and insights into effective ventilation design to maximize its ability in airborne risk control, for particularly the COVID-19. Comprehensive reviews of each phase of aerosol transmission of SARS-CoV-2 from source to receptor are conducted, so as to provide a theoretical basis for risk prediction and control. Infection risk models and their key parameters for risk assessment of SARS-CoV-2 are analyzed. Special focus is given on the efficacy of different ventilation strategies in mitigating airborne transmission. Ventilation interventions are found mainly impacting on the dispersion and inhalation phases of aerosol transmission. The airflow patterns become a key factor in controlling the aerosol diffusion and distribution. Novel and personalized ventilation design, effective integration with other environmental control techniques and resilient HVAC system design to adapt both common and epidemic conditions are still remaining challenging, which need to be solved with the aid of multidisciplinary research and intelligent technologies.

Close interactions between lncRNAs, lipid metabolism and ferroptosis in cancer.

Abnormal lipid metabolism including synthesis, uptake, modification, degradation and transport has been considered a hallmark of malignant tumors and contributes to the supply of substances and energy for rapid cell growth. Meanwhile, abnormal lipid metabolism is also associated with lipid peroxidation, which plays an important role in a newly discovered type of regulated cell death termed ferroptosis. Long noncoding RNAs (lncRNAs) have been proven to be associated with the occurrence and progression of cancer. Growing evidence indicates that lncRNAs are key regulators of abnormal lipid metabolism and ferroptosis in cancer. In this review, we mainly summarized the mechanism by which lncRNAs regulate aberrant lipid metabolism in cancer, illustrated that lipid metabolism can also influence the expression of lncRNAs, and discussed the mechanism by which lncRNAs affect ferroptosis. A comprehensive understanding of the interactions between lncRNAs, lipid metabolism and ferroptosis could help us to develop novel strategies for precise cancer treatment in the future.