Wireless pulmonary artery sensor implantation in a unilateral lung transplant recipient.

Patients with lung transplantation can have concomitant left ventricular failure which can either precede the lung transplantation or develop after. Implantable wireless pulmonary artery (PA) pressure monitors to guide hemodynamic management in heart failure such as the CardioMEMS device (Abbott, Sylmar, CA, USA) have been shown to improve outcomes. However, in a lung transplant recipient there are unique physiological and practical considerations when contemplating to implant a PA pressure sensor such as safety of implanting the device, choice of site of implantation, accuracy of wedge tracings to calibrate, and exclusion of vascular stenoses post transplantation. We discuss these considerations in the context of a man in his early 60s with a known left lung transplant two years previously who developed worsening heart failure needing invasive monitoring. Right lung PA sensor placement was considered, but on selective pulmonary angiography the right PA was found to be of small caliber and with significant tortuosity. After careful hemodynamic assessment, the PA sensor was implanted in the PA of the transplanted lung which is the first such case to our knowledge. Learning objective: We report the first documented case of an implantable wireless pulmonary artery pressure monitor (CardioMEMs) into a transplanted lung. Device-related complications, such as pulmonary artery injury, infection, and hemoptysis, must be assessed after placement. Given the changes in pulmonary artery pressures after lung transplantation, recalibration of the CardioMEMs device may need to be considered if placed within first year of transplant.

2-Deoxy-d-ribose induces ferroptosis in renal tubular epithelial cells via ubiquitin-proteasome system-mediated xCT protein degradation.

Ferroptosis is a novel form of cell death triggered by iron-dependent lipid peroxidation. Recent findings suggest that inhibiting system χc-induces ferroptosis by reducing intracellular cystine levels, and that ferroptosis in renal tubular epithelial cells (RTECs) contributes to acute kidney injury (AKI) and diabetic nephropathy. Moreover, 2-deoxy-d-ribose (dRib) has been shown to inhibit cystine uptake through xCT, the functional unit of system χc-, in ß-cells. This study aimed to investigate if dRib induces ferroptosis in RTECs and identify the underlying mechanisms. dRib treatment reduced cystine uptake and glutathione (GSH) content, and increased intracellular levels of malondialdehyde (MDA), 4-hydroxynonenal (4-HNE), lipid reactive oxygen species (ROS), and cell death in both NRK-52E cells and primary cultured RTECs. However, treatment with inhibitors of ferroptosis, such as deferoxamine (DFO), ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1), counteracted the effects of dRib on GSH, MDA, 4-HNE, and lipid ROS levels, as well as cell death. Additionally, 2-mercaptoethanol (2-ME) treatment or xCT gene overexpression protected against dRib-induced changes. Moreover, transmission electron microscopy revealed dRib-induced mitochondrial shrinkage, decrease in cristae number, and outer membrane rupture. Furthermore, dRib treatment upregulated the expression of genes associated with ferroptosis, and downregulated xCT protein expression. The decrease in xCT protein caused by dRib was consistently observed even when treated with the protein synthesis inhibitor cycloheximide. However, treatment with the proteasome inhibitor MG132 reversed the dRib-induced decrease in xCT protein expression. Additionally, dRib increased xCT protein ubiquitination. Overall, dRib induces ferroptosis in RTECs by degrading xCT protein through ubiquitin-proteasome system (UPS), resulting in reduced intracellular cystine uptake. Therefore, targeting the regulation of system χc-through UPS could be a potential therapeutic approach for AKI and diabetic nephropathy.

Invasive Pulmonary Angiogram Performance and Interpretation in the Diagnosis of Pulmonary Thromboembolic Disease.

Invasive or selective pulmonary angiography has historically been used as the gold standard diagnostic test for the evaluation of a wide array of pulmonary arterial conditions, most commonly pulmonary thromboembolic diseases. With the emergence of various noninvasive imaging modalities, the role of invasive pulmonary angiography is shifting to the assistance of advanced pharmacomechanical therapies for such conditions. Components of invasive pulmonary angiography methodology include optimal patient positioning, vascular access, catheter selections, angiographic positioning, contrast settings, and recognition of angiographic patterns of common thromboembolic and nonthromboembolic conditions. We review the pulmonary vascular anatomy, step-by-step performance, and interpretation of invasive pulmonary angiography.

A call to consider an aortic stenosis screening program.

Aortic stenosis (AS) is the most common age-related valvular condition with a prevalence of 13.1% in patients older than 75 years of age. Based on the severity of AS and symptoms, current guidelines recommend interval monitoring with transthoracic echocardiogram (TTE). However, no guidelines exist regarding screening asymptomatic persons for AS. Prevalence of AS is comparable to conditions such as colorectal cancer, lung cancer, breast cancer, and abdominal aortic aneurysm where dedicated screening programs are offered resulting in reduction of overall morbidity and mortality. We review recent advancements in treatment options, and we propose an AS screening program for high-risk individuals without known history of AS including all persons over age 75 and persons aged 70 years and older with dialysis dependent end-stage renal disease (ESRD).

Diagnostic Pitfalls of Chylothorax After Dasatinib Treatment of Chronic Myeloid Leukemia.

BACKGROUND Chronic myeloid leukemia (CML) is a myeloproliferative malignancy generally treated with Dasatinib, a tyrosin-kinase inhibitor. Pleural effusions are a known adverse effect, but only 0.8% of patients develop pleural effusions after 6 years of use. Recent case reports have implicated Dasatinib as a rare cause of chylothorax. CASE REPORT We describe a woman in her 30's with a history of chronic myeloid leukemia, who had been taking Dasatinib for 10 years and presented to the Emergency Department after a chest X-ray revealed bilateral pleural effusions in the setting of worsening dyspnea on exertion for 6 months. She had previously received radiotherapy at age 11 prior to an allogenic bone marrow transplant nearly 30 years prior. Thoracentesis removed 900 cc of chylous fluid, and flow cytometry and cultures found no evidence of infection or malignancy. Dasatinib was discontinued, and she was treated with diuretics, steroids, and a low-fat diet. The effusions reaccumulated twice in the following month and required 2 additional thoracenteses and courses of steroids. Months later, the bilateral chylous effusions recurred, and MR lymphangiogram demonstrated 2 thoracic duct tears. CONCLUSIONS While previous reports have indicated that Dasatinib can rarely cause chylous pleural effusions, it is unlikely after 5 years of use, and other etiologies must be considered by clinicians. Initial misattribution to Dasatinib alone can delay further necessary investigations, including lymphangiography. In our patient, it is more likely that other factors contributed to her chylothorax, including her previous radiotherapy 30 years prior, given her recurrence of chylous effusions following cessation of the medication.

Human Borrelia miyamotoi infection: A cause of persistent fever and severe hyperthermia in New England.

An adult male presented to a hospital in southwestern Connecticut with tachypnea, generalized weakness, altered mental status, and relapsing fever with maximum recorded temperature of 106 °F. He required active cooling, antipyretic therapy, broad spectrum antibiotics, and intubation for airway protection after an episode of emesis. Initial laboratory and imaging workup were remarkable for elevated inflammatory markers, acute kidney injury, and bilateral lower lobe infiltrates. Further workup with lumbar puncture and electroencephalography were unrevealing. Extensive testing for causes of relapsing fever including tickborne diseases revealed that the patient was seropositive for Borrelia miyamotoi. Notably, he had no rash, and workup found no evidence of coinfection by other Borrelia, Ehrlichia or Anaplasma species. This case illustrates the need for clinicians to test for tick-borne diseases when evaluating for cases of relapsing fever in New England and is among the first case reports to demonstrate Borrelia miyamotoi as a cause of severe pyrexia.

Identification of osteopontin as a urinary biomarker for autosomal dominant polycystic kidney disease progression.

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD), one of the most common human monogenic diseases, is characterized by the presence of numerous fluid-filled renal cysts and is a leading cause of end-stage renal disease (ESRD). Urinary biomarkers may be useful for predicting the variable course of ADPKD progression from cyst growth to ESRD. METHODS: To identify candidate urinary biomarkers of ADPKD progression, we used CRISPR/Cas9 genome editing to generate porcine fibroblasts with mono- and biallelic ADPKD gene knockout (PKD2+/- and PKD2-/-, respectively). We then performed RNA-sequencing analysis on these cells. RESULTS: Levels of osteopontin (OPN), which is expressed by renal epithelial tubular cells and excreted into urine, were reduced in PKD2-/- cells but not in PKD2+/- cells. OPN levels were also reduced in the renal cyst cells of ADPKD patients. Next, we investigated whether OPN excretion was decreased in patients with ADPKD via enzyme-linked immunosorbent assay. OPN levels excreted into renal cyst cell culture media and urine from ADPKD patients were decreased. To investigate whether OPN can predict the rate of ADPKD progression, we compared urinary excretion of OPN in ADPKD patients with slow progression and those with rapid progression. Those with rapid progression had an estimated glomerular filtration rate of >60 mL/min/1.73 m2 . Urinary OPN excretion levels were lower in rapid progressors than in slow progressors. CONCLUSION: These findings suggest that OPN is a useful urinary biomarker for predicting ADPKD progression.

Facial Diplegia Variant of Guillain-Barré Syndrome in Pregnancy Following COVID-19 Vaccination: A Case Report.

Serious neurologic complications from coronavirus disease 2019 (COVID-19) vaccination are rare, and only a few cases of Guillain-Barré syndrome (GBS) have been reported after COVID-19 vaccination. We present the first reported case of the facial diplegia variant of GBS after recent COVID-19 vaccination in a pregnant woman. The 30-year-old patient was 27 weeks pregnant at the time she was diagnosed with the facial diplegia variant of GBS. Her symptoms began two weeks after she received the Ad26.COV2.S COVID-19 vaccine. A thorough evaluation for GBS was done, including a lumbar puncture that demonstrated elevated cerebrospinal fluid (CSF) protein and nerve conduction study (NCS) that found evidence of a diffuse sensorimotor demyelinating polyneuropathy. Nasal swab testing for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was negative on two occasions five days apart. All other diagnostic testing was unremarkable or nonexplanatory of the patient's clinical presentation. She was started on intravenous immunoglobulin (IVIG) and had significantly improved dysphasia, dysarthria, and facial strength. The patient recovered to baseline four weeks after presentation.

Haemophilus Parainfluenzae mural endocarditis with large atrial septal defect and peripheral embolization.

Mural endocarditis is a rare subclass of infective endocarditis (IE) associated with intra-cardiac tumors, prosthesis, valvular vegetation's, or structural abnormalities such as ventricular septal defects. Bacteria classified as HACEK (Haemophilus species, Aggregatibacter actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) are rare causes of IE found in only 1.3% to 10% of cases. We describe the second reported case of mural endocarditis involving the left ventricle (LV) caused by a Haemophilus species. A young male with no prior intravenous drug use, valvular heart disease, or recent dental work presented with splenic infarcts. H. para-influenza was identified on blood cultures. Cardiac imaging revealed a 1.5 cm LV mass underneath the posterior leaflet of the mitral valve and a large Atrial Septal Defect (ASD). Awaiting surgery, the patient sustained embolic and hemorrhagic cerebral events. The patient underwent debulking of LV mass, ASD closure, and mitral valve repair complicated by post-pericardiotomy syndrome, and he completed six weeks of ceftriaxone therapy. The patient met modified Duke Criteria, but the diagnosis was challenging due to absence of risk factors, sub-acute symptom onset, delayed blood culture growth, and ambiguous characterization of the mass on imaging. .

Direct current cardioversion-triggered atypical Tako-tsubo cardiomyopathy: a case report and review of literature.

Background: Tako-tsubo stress cardiomyopathy is a clinical syndrome marked by transient reduction of left ventricular function in the setting of emotional or physical stress and in the absence of obstructive coronary artery disease. We describe a case of an atypical variant of Tako-tsubo in a male patient following an elective direct current cardioversion (DCCV). Case summary: A 78-year-old male whose atrial fibrillation persisted after earlier unsuccessful direct current DCCV and radiofrequency ablations presented to the emergency department for acutely worsening dyspnoea and orthopnoea 12 h following his most recent DCCV. Previously, he was known to have non-obstructive coronary artery disease. Evaluation was notable for troponin I 0.019 ng/mL (negative <0.050 ng/mL), pro-brain natriuretic peptide 2321 pg/mL (reference range 0.0-900 pg/mL). There were no acute electrocardiogram abnormalities. He required bilevel positive airway pressure but was weaned off eventually to room air. Transthoracic echocardiogram revealed newly reduced left ventricular ejection fraction of 45-50%, associated with hypokinesis of the basal anteroseptal segment, as well as akinesis of mid-inferoseptal and mid-anteroseptal segments. Apical contractility was preserved. On Day 5 of hospitalization, diagnostic left heart catheterization again revealed benign coronary anatomy, and he was discharged home the following day. Discussion: Only five other cases of cardioversion mediated Tako-tsubo cardiomyopathy have been reported in the literature. To our knowledge, this is the first case of DCCV-induced atypical Tako-tsubo cardiomyopathy. Although overall prognosis is favourable, some have been observed to require advanced support therapy. Given risk for life-threatening complications, patients undergoing cardioversion should be educated on symptoms of congestive cardiomyopathy.

Identification of Phenotypes Among COVID-19 Patients in the United States Using Latent Class Analysis.

BACKGROUND: Coronavirus disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 or COVID-19) is a heterogeneous disorder with a complex pathogenesis. Recent studies from Spain and France have indicated that underlying phenotypes may exist among patients admitted to the hospital with COVID-19. Whether those same phenotypes exist in the United States (US) remains unclear. Using latent class analysis (LCA), we sought to determine whether clinical phenotypes exist among patients admitted for COVID-19. METHODS: We reviewed the charts of adult patients who were hospitalized primarily for COVID-19 at Greenwich Hospital and performed LCA using variables based on patient demographics and comorbidities. To further examine the reliability and replicability of the clustering results, we repeated LCA on the cohort of patients who died during hospitalization for COVID-19. RESULTS: Two phenotypes were identified in patients admitted for COVID-19 (N = 483). According to phenotype, patients were designated as cluster 1 (C1) or cluster 2 (C2). C1 (n = 193) consisted of older individuals with more comorbidities and a higher mortality rate (25.4% vs 8.97%, p < 0.001) than patients in C2. C2 (n = 290) consisted of younger individuals who were more likely to be obese, male, and nonwhite, with higher levels of the inflammatory markers C-reactive protein and alanine aminotransferase. When we performed LCA on the cohort of patients who died during hospitalization for COVID-19 (n = 75), we found that the distribution of patient baseline characteristics and comorbidities was similar to that of the entire cohort of patients admitted for COVID-19. CONCLUSION: Using LCA, we identified two clinical phenotypes of patients who were admitted to our hospital for COVID-19. These findings may reflect different pathophysiologic processes that lead to moderate to severe COVID-19 and may be useful for identifying treatment targets and selecting patients with severe COVID-19 disease for future clinical trials.

Non-dissecting large thoracic aortic aneurysm leading to chronic aortic insufficiency presenting as acute heart failure.

Large, non-dissecting thoracic aortic aneurysms (TAA) up to 13 cm in size are typically found in elderly patients with non-specific respiratory symptoms yet must be detected quickly due to their mortality risk. We present a 31-year-old man with exertional dyspnea secondary to aortic insufficiency from a 9.4 cm TAA.

The Challenges of ST-Elevation Myocardial Infarction in COVID-19 Patients.

By July 2021, the United States had over 34.4 million confirmed COVID-19 cases. Various cardiovascular manifestations of COVID-19 have been reported including ST-elevation myocardial infarction (STEMI), and there is concern that SARS-CoV-2 may be associated with a higher thrombus burden. We performed a retrospective chart review of 535 adult patients with COVID-19 admitted at Yale-New Haven Health Greenwich Hospital from February 1, 2020, to May 13, 2020. All admitted patients had undergone testing for serum troponin I and various inflammatory markers, and we identified three patients who were diagnosed with acute STEMI. Data was collected via manual chart review and included patient demographics, comorbidities, laboratory tests, electrocardiogram (ECG) results, echocardiography results, diagnoses during hospitalization, inpatient therapies, and outcomes including length of hospital stay, revascularization results, and mortality. Three of our patients had obstructive coronary artery disease confirmed via angiography. One subject was noted to display vasospasm in addition to coronary atherosclerotic obstruction and refractory thrombus formation. Among our patients with COVID-19 and STEMI, presentations were variable in terms of timing of onset of ECG changes, age, gender, race, comorbidities, symptomology, and outcomes.

Coombs-negative hemolytic anemia in a male with COVID-19.

This case illustrates the need to consider SARS-CoV-2 infection as a catalyst for Coombs-negative hemolytic anemia as well as the potential for IVIG to serve as an effective treatment for the condition.

Seronegative Goodpasture's syndrome associated with organising pneumonia.

Goodpasture's syndrome is a rare vasculitis associated with anti-glomerular basement membrane (anti-GBM) autoantibodies that target type IV collagen found in the basement membranes of glomeruli and alveoli. We present a case of a 79-year-old man with seronegative Goodpasture's syndrome with predominant respiratory symptoms and mild acute kidney injury that initially improved. Final diagnosis was made by immunofluorescent staining on open lung biopsy which also revealed concomitant organising pneumonia. The patient underwent treatment with corticosteroids, cyclophosphamide, haemodialysis and plasmapheresis. This was an atypical presentation wherein the patient only exhibited pulmonary symptoms early in the course of illness in the setting of negative anti-GBM antibody serum testing, which made diagnosis challenging. With this case, we emphasise that clinicians should have a high suspicion for Goodpasture's syndrome in the setting of unexplained severe pulmonary or renal disease despite negative anti-GBM antibody testing.

Diagnosis and treatment of transthyretin-related amyloidosis cardiomyopathy.

Transthyretin-related amyloidosis (ATTR) is a subgroup of amyloidosis that results from extracellular misassembled and toxic amyloid deposits affecting multiple organ systems, and cardiac tissues in particular. Because ATTR often presents as heart failure with preserved ejection fraction (HFpEF), it has been largely underdiagnosed. Once considered incurable with a grave prognosis, ATTR cardiomyopathy has seen the development of promising alternatives for diagnosis and treatment, with early diagnosis and treatment of ATTR cardiomyopathy highly beneficial due to its high mortality rate. For instance, diagnosing ATTR cardiomyopathy previously required a cardiac biopsy, but new modalities, such as cardiac magnetic resonance imaging and radionuclide bone scans, show promise in accurately diagnosing ATTR cardiomyopathy. Ongoing research and clinical trials have focused on identifying new treatments which primarily target amyloid fiber formation by inhibiting TTR gene expression, stabilizing the TTR tetramer, preventing oligomer aggregation, or affecting degradation of amyloid fibers. In this review, we describe the advances made in the diagnosis and treatment of ATTR in order to increase awareness of the disease and encourage a lower threshold for ATTR workup. Our review also highlights the need for improving the screening, diagnosis, and treatment guidelines for ATTR cardiomyopathy.

System χc- overexpression prevents 2-deoxy-d-ribose-induced ß-cell damage.

Pancreatic ß-cells are vulnerable to oxidative stress, which promotes ß-cell failure in type 2 diabetes. System χc- is a sodium-independent, cystine/glutamate antiporter that mediates the exchange of extracellular l-cystine and intracellular l-glutamate. The import of l-cystine through this transporter is the rate-limiting step in the glutathione (GSH) biosynthesis pathway that plays a significant role in antioxidative defense. Previously, we reported that 2-deoxy-d-ribose (dRib) induces oxidative damage through GSH depletion in pancreatic ß-cells. In the current study, we elucidated the mechanism underlying the oxidative stress-induced ß-cell damage. We measured the intracellular l-[14C]cystine uptake, GSH content, reactive oxygen species (ROS) levels, cytotoxicity, and apoptosis in rat insulinoma cell line, RINm5F. Treatment of dRib decreased the intracellular l-[14C]cystine uptake and GSH content and increased the intracellular ROS levels, cytotoxicity, and apoptosis in a time- and dose-dependent manner. Conversely, 2-mercaptoethanol (2-ME), a cystine uptake enhancer, recovered the dRib-induced decrease in l-[14C]cystine uptake, GSH content, and cell viability in a Na+-independent manner. In the case of isolated islets, dRib dose-dependently decreased the intracellular l-[14C]cystine uptake and cell viability; however, dRib-induced cytotoxicity was completely recovered by adding N-acetyl cysteine (NAC). To confirm that system χc- mediates the oxidative stress-induced ß-cell damage, we overexpressed xCT (the substrate-specific subunit of system χc-) using a lentiviral vector in RINm5F cells. Overexpression of xCT fully recovered the dRib-induced decrease in l-[14C]cystine uptake and GSH content and prevented the dRib-induced increase in ROS levels, cytotoxicity, and apoptosis. The overexpression of xCT showed a protective effect against dRib-induced oxidative damage in RINm5F cells. Our study showed that dRib depletes intracellular GSH content through inhibition of cystine transport via system χc- in ß-cells.

Barley RNA viromes in six different geographical regions in Korea.

Barley is a kind of cereal grass belonging to the family Poaceae. To examine viruses infecting winter barley in Korea, we carried out a comprehensive study of barley RNA viromes using next-generation sequencing (NGS). A total of 110 barley leaf samples from 17 geographical locations were collected. NGS followed by extensive bioinformatics analyses revealed six different barley viromes: Barley yellow mosaic virus (BaYMV), Barley mild mosaic virus (BaMMV), Barley yellow dwarf virus (BYDV), Hordeum vulgare endornavirus (HvEV), and Barley virus G (BVG). BaYMV and HvEV were identified in all libraries, while other viruses were identified in some specific library. Based on the number of virus-associated reads, BaYMV was a dominant virus infecting winter barley in Korea causing yellow disease symptoms. We obtained nearly complete genomes of six BaYMV isolates and two BaMMV isolates. Phylogenetic analyses indicate that BaYMV and BaMMV were largely grouped based on geographical regions such as Asia and Europe. Single nucleotide polymorphisms analyses suggested that most BaYMV and BaMMV showed strong genetic variations; however, BaYMV isolate Jeonju and BaMMV isolate Gunsan exhibited a few and no SNPs, respectively, suggesting low level of genetic variation. Taken together, this is the first study of barley RNA viromes in Korea.

Complete genome sequence of rice virus A, a new member of the family Tombusviridae.

An evaluation of the virus population in rice plants using next-generation sequencing technologies resulted in the discovery of a new RNA virus, tentatively named rice virus A (RVA). The complete RVA genome sequence was determined and analyzed, revealing a genome organization resembling that of viruses classified in the genera Aureusvirus, Tombusvirus and Zeavirus within the family Tombusviridae. With 4,832 nucleotides, the RVA genome may be the largest monopartite genome sequenced to date in the family Tombusviridae. The 453-amino acid RVA coat protein shares the highest identity with the gp3 protein of an unclassified carascovirus, SF1 (GenBank accession no. KF510027) isolated from San Francisco wastewater, rather than the coat protein of any known member of the family Tombusviridae. These novel characteristics represent a significant divergence from the genomes of viruses belonging to the sixteen existing genera of the family Tombusviridae, demonstrating that RVA is likely a new family member.

P2X7 receptor and NLRP3 inflammasome activation in head and neck cancer.

In this study, we investigated purinergic receptor P2X7 and NACHT, LRR and PYD domains-containing protein 3 (NLRP3) inflammasome expressions, and their role in head and neck cancer. We found upregulation of purinergic receptor P2X7 and all NLRP3 inflammasome components in biopsied head and neck squamous cell carcinoma tissues. Similarly, the expression of purinergic receptor P2X7, apoptosis-associated speck-like protein containing CARD, and pro-form caspase 1 in A253 cells derived from epidermoid carcinoma were highly upregulated in comparison to normal Human Salivary Gland cell line. Active caspase-1 and its final product, active interleukin-1ß, both increased in primed A253 cells stimulated with purinergic receptor P2X7 agonists, while this elevated NLRP3 inflammasome activity was suppressed by purinergic receptor P2X7 antagonists. However, we observed none of these effects in Human Salivary Gland cells. Inhibition of both NLRP3 inflammasome and purinergic receptor P2X7 led to the significant cell death of primed A253 cells, but had no effect on the viability of primed HSG cells or the primary cultured human fibroblast cells. Furthermore, inhibition of either purinergic receptor P2X7 or NLRP3 inflammasome decreased invasiveness of A253, and this effect became more evident when both purinergic receptor P2X7 and NLRP3 inflammasome were simultaneously blocked. Therefore, it is concluded that the purinergic receptor P2X7 and the activation of NLRP3 inflammasome play important roles in the survival and invasiveness of head and neck squamous cell carcinoma in humans.