Cancer remains a leading cause of death worldwide, despite many advances being made in recent decades. Changes in the tumor microenvironment, including dysregulated immunity, may contribute to carcinogenesis and cancer progression. The cysteinyl leukotriene (CysLT) pathway is involved in several signal pathways, having various functions in different tissues. We summarized major findings of studies about the roles of the CysLT pathway in cancer. Many in vitro studies suggested the roles of CysLTs in cell survival/proliferation via CysLT₁ receptor (CysLT₁R). CysLT₁R antagonism decreased cell vitality and induced cell death in several types of cancer cells, such as colorectal, urological, breast, lung and neurological malignancies. CysLTs were also associated with multidrug resistance of cancer, and CysLT₁R antagonism might reverse chemoresistance. Some animal studies demonstrated the beneficial effects of CysLT₁R antagonist in inhibiting tumorigenesis and progression of some cancer types, particularly colorectal cancer and lung cancer. The expression of CysLT₁R was shown in various cancer tissues, particularly colorectal cancer and urological malignancies, and higher expression was associated with a poorer prognosis. The chemo-preventive effects of CysLT₁R antagonists were demonstrated in two large retrospective cohort studies. In summary, the roles of the CysLT pathway in cancer have been delineated, whereas further studies are still warranted.

An increased incidence of temporomandibular disorders (TMD) among patients with sleep apnea (SA) has been reported. However, the association between TMD and SA has not been demonstrated in a large-scale study. This population-based cohort study with the Taiwan National Health Insurance (NHI) Research Database aimed to understand the association between SA and TMD. We identified adult patients with suspected SA (identified with diagnostic codes) and excluded those diagnosed with TMD prior to SA. Patients with SA diagnosis after polysomnography were also identified as probable SA patients. The index dates were the dates of their initial SA diagnosis. Ten control subjects were matched, by age and sex, to each SA patient, and were assigned the same index dates as the SA patients. In total, 10,408 suspected SA patients (including 4105 probable SA patients) matched to 104,080 control subjects (including 41,050 subjects matched to the probable SA patients) in this study. The TMD incidence rate was significantly higher in the SA patients than in the control subjects (2.8 vs. 1.0 per thousand-patient-year in probable SA patients vs. the corresponding control subjects, with an adjusted incidence rate ratio [95% confidence interval] = 2.5 [2.3–2.7], p < 0.0001). SA patients significantly showed a higher cumulative incidence of TMD than the corresponding control subjects (p < 0.0001). Multivariable Cox regression analysis revealed SA as an independent risk factor for the development of TMD (adjusted hazard ratio = 2.5 [1.7–3.7], p < 0.0001). In summary, this study confirmed an increased TMD incidence in the SA patients. While treating TMD patients, dentists should pay careful attention to the potential underlying SA.

Background: For investigating the host response in Acinetobacter baumannii associated pneumonia, we analyzed the host genetic sequences obtained from metagenomic next-generation sequencing (mNGS). Methods: The samples for mNGS were bronchoalveolar lavage fluid (BALF) collected from the lungs of patients infected with A. baumannii and from patients without bacterial infections. BALF samples from patients with pneumonia were collected from the lungs of patients infected with A. baumannii with New Delhi metallo-β-lactamase (NDM, before treatment), A. baumannii with NDM (post-treatment), A. baumannii without resistant genes, and those without bacterial infection. Partek was used for investigating enriched functions and pathways related to the pulmonary host response to pneumonia caused by A. baumannii with NDM infection and A. baumannii without antimicrobial-resistant genes. The STRING was employed for identifying protein interaction pathways related to the pulmonary host response to pneumonia caused by A. baumannii without antimicrobial-resistant genes. Results: In pulmonary host response to pneumonia caused by A. baumannii with NDM, five immune system-related pathways and five pathways related to signal transduction were identified. No significant differences were observed in the immune system and signal transduction pathways in the pulmonary host response to pneumonia caused by A. baumannii without antimicrobial-resistant genes. However, significant differences were noted in the phagosome, ferroptosis, and regulation of the actin cytoskeleton in cellular processes. Conclusions: mNGS provides information not only on pathogen gene expression but also on host gene expression. In this study, we found that pneumonia with A. baumannii carrying the NDM resistance gene triggers stronger immune responses in the lung, while pneumonia with A. baumannii lacking antimicrobial resistance genes is more linked to iron-related pathways.

Interstitial pneumonia with autoimmune features (IPAF) is a new disease entity proposed in 2015. Numerous questions regarding IPAF require clarification, including diagnostic criteria, standard managements for stable disease and exacerbation, and prognosis. We report a case of a 67-year-old Asian woman who presented with progressive dyspnea. Chest computed tomography (CT) scans revealed nonspecific interstitial pneumonia. Serologic testing indicated positive anti-Jo-1 without presence of extrathoracic manifestations. An IPAF diagnosis was made after a multidisciplinary discussion. The patient experienced a severe exacerbation requiring mechanical ventilation, and she was successfully salvaged with methylprednisolone pulse therapy and single-dose cyclophosphamide. During the one-year follow-up, she reported bilateral leg muscle weakness with noticeably elevated serum creatine kinase, suggesting polymyositis. The development of malignancy was also noted 15 months after the initial presentation, and the patient eventually died. This report demonstrated successful salvage treatment with glucocorticoid pulse therapy for IPAF with acute exacerbation. However, the maintenance therapy failed to control disease progression. The treatment strategies for exacerbation and stable disease in IPAF remain unknown and need further studies. Given the high risk of evolution into a defined connective tissue disease (CTD), regular evaluation of the clinical features and biomarkers of CTDs is essential for patients with IPAF.