2019 novel coronavirus (2019-nCoV) is widespread in China and other countries. The target of 2019-nCoV and severe acute respiratory syndrome coronavirus (SARS-CoV) is angiotensin-converting enzyme 2 (ACE2) positive cells. ACE2 is present in the salivary gland duct epithelium, and thus it could be the target of 2019-nCoV and SARS-CoV. SARS-CoV-related animal model experiments show that it can infect the epithelial cells on the salivary gland duct in Chinese rhesus macaques by targeting ACE2. Clinical studies confirmed that 2019-nCoV and SARS-CoV could be detected in saliva of human patients. We hypothesize that the infection of 2019-nCoV and SARS-CoV will lead to inflammatory pathological lesions in patients' target organs, and possibly inflammatory lesions in salivary glands. 2019-nCoV may cause acute sialoadenitis in the acute phase of infection. After the acute phase, chronic sialoadenitis may be caused by fibrosis repairment. Although there was no direct evidence to prove this, the available indirect evidence indicates a high probability of our hypothesis.

Angioleiomyoma is a benign soft-tissue tumor originating from vascular smooth muscle, and is rare in the head and neck. The present study retrospectively examined a cohort of patients with head and neck angioleiomyoma treated at the West China Hospital of Stomatology, and also subjected archived tissues to modern immunohistochemical analysis. In total, 21 patients were treated for angioleiomyoma between 1978 and 2012 at the West China Hospital of Stomatology, Sichuan University (Chengdu, Sichuan, China). Medical records were examined and paraffin block sections were cut and stained with hematoxylin and eosin, Masson’s trichrome stain and Van Gieson stain, prior to being subjected to immunohistochemical analysis to re-evaluate and confirm the diagnoses. Angioleiomyomas were found to account for only 0.18% of the benign head and neck tumors in the patients presenting to the hospital over the past 34 years. The diagnosis was more common in males (male:female ratio, 1.625:1) and the mean age at diagnosis was 42.5 years. The most common sites were the buccal mucosa, parotid gland and palate. More than half of the tumors (61.9%) were >2 cm in diameter. Five tumors presented with pain and/or tenderness. The histological subtype was reported as solid in five cases, venous in six, cavernous in nine and venous-cavernous in one. Three tumors exhibited nerve neurofibrils. All tumors were excised with no subsequent recurrence. Cytological and imaging examinations were not useful for pre-operative diagnosis. Angioleiomyoma is a benign tumor that causes limited morbidity. Surgical excision is the only effective treatment and recurrence is rare. The present study revealed that nerves were present in a small proportion (14.3%) of tumors. It was hypothesized that the compression of nerves accompanying numerous blood vessels in the tumor may cause pain, particularly in venous- and cavernous-type angioleiomyomas.

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BackgroundCeramides are a class of sphingolipids that form the structural component of the cell membrane and also act as second messengers in cell signaling pathways. Emerging results suggest that ceramide induces growth arrest and apoptosis in various human cancer cells. However, the mechanisms underlying its antitumor activity are yet to be identified. Endoplasmic reticulum stress (ER stress), a cellular adaptive response, is believed to initially compensate for damage but can eventually trigger cell death if the stimulus is severe or prolonged. In this study, we investigated whether ceramide induces cell death in human salivary adenoid cystic carcinoma (ACCs) through activation of the apoptotic ER stress.ResultsRT-PCR, real-time PCR and western blot demonstrated that exogenous ceramide treatment up-regulated GRP78 and p-eIF2α expression and XBP1 splicing. Moreover, the ceramide synthase inhibitor FB1 abolished ceramide-induced ER stress. Up-regulation of the ER stress-associated apoptosis promoting transcription factor CHOP and p-JNK suggested that the antitumor activity of ceramide is owing to activation of apoptotic ER stress. Mechanistically, [Ca2+]ER depletion and SERCA inhibition by ceramide treatment suggested that it induces ER stress by disrupting [Ca2+]ER homeostasis. The chemical chaperone TUDCA inhibited ceramide-induced ER stress and cell death. In addition, the downstream metabolite of ceramide, S1P, cannot activate ER stress.ConclusionsThese results demonstrated that exogenous ceramide induces cancer cell death through a mechanism involving severe ER stress triggered by the disruption of ER Ca2+ homeostasis.