[Management of Obstructive Sleep Apnea Syndrome during the Coronavirus Disease 2019 Pandemic].

The coronavirus disease 2019(COVID-19) pandemic poses a severe threat to global health.As an emerging infectious disease mainly attacking the respiratory tract,it has severely challenged the management of chronic non-infectious respiratory diseases including obstructive sleep apnea(OSA) and asthma.This article reviews the impact of OSA on the incidence of COVID-19 and the underlying pathophysiological mechanism,as well as the effects of OSA on the hospitalization risk and the prognosis and outcome of COVID-19 patients,which will provide novel ideas for the management of OSA during the COVID-19 pandemic.

[An Extrapulmonary Manifestation of Coronavirus Disease 2019:Olfactory Dysfunction].

In addition to acute respiratory symptoms,coronavirus disease 2019(COVID-19)could cause olfactory dysfunction,which becomes the only clinical manifestation of COVID-19 in some cases.We review the epidemiological characteristics,pathological mechanism,screening value,treatment and prognosis of olfactory dysfunction in patients with COVID-19,aiming to achieve an in-depth understanding of the early diagnosis,quarantine,scientific treatment and prognosis of COVID-19.

[Roles of microRNAs in allergic airway diseases].

The microRNAs (miRNAs/miRs) are a class of short non-coding RNAs regulating protein translation via mRNAs silencing. Studies have shown that microRNAs play critical roles in allergic diseases, tumors, and infections. The allergic airway diseases are characterized by inflammation and hyperresponsiveness of the respiratory tract. Several miRNAs are found to be involved in a series of pathophysiologic processes in allergic airway diseases including inflammatory cells infiltration, cytokines' expressions, airway hyperresponsiveness, and proliferation and change in phenotype of smooth muscle cells. Therefore, miRNAs may be new therapeutic targets for these allgeric diseases. This article reviews the roles of miRNAs in asthma and allergic rhinitis and their molecular biological mechanisms.

The Mitochondrial tRNAHis G12192A Mutation May Modulate the Clinical Expression of Deafness-Associated tRNAThr G15927A Mutation in a Chinese Pedigree.

BACKGROUND: Mutations in mitochondrial tRNA (mt-tRNA) genes have been found to be associated with both syndromic and non-syndromic hearing impairment. However, the pathophysiology underlying mt-tRNA mutations in clinical expression of hearing loss remains poorly understood. OBJECTIVE: The aim of this study was to explore the potential association between mttRNA mutations and hearing loss. METHODS AND RESULTS: We reported here the molecular features of a pedigree with maternally transmitted non-syndromic hearing loss. Among 12 matrilineal relatives, five of them suffered variable degree of hearing impairment, but none of them had any medical history of using aminoglycosides antibiotics (AmAn). Genetic screening of the complete mitochondrial genomes from the matrilineal relatives identified the coexistence of mt-tRNAHis G12192A and mt-tRNAThr G15927A mutations, together with a set of polymorphisms belonging to human mitochondrial haplogroup B5b1b. Interestingly, the G12192A mutation occurred 2-bp from the 3' end of the TψC loop of mt-tRNAHis, which was evolutionarily conserved from various species. In addition, the well-known G15927A mutation, which disrupted the highly conserved C-G base-pairing at the anticodon stem of mt-tRNAThr, may lead to the failure in mt-tRNA metabolism. Furthermore, a significant decreased in ATP production and an increased ROS generation were observed in polymononuclear leukocytes (PMNs) which were isolated from the deaf patients carrying these mt-tRNA mutations, suggested that the G12192A and G15927A mutations may cause mitochondrial dysfunction that was responsible for deafness. However, the absence of any functional mutations/variants in GJB2, GJB3, GJB6 and TRMU genes suggested that the nuclear genes may not play important roles in the clinical expression of non-syndromic hearing loss in this family. CONCLUSION: Our data indicated that mt-tRNAHis G12192A mutation may increase the penetrance and expressivity of deafness-associated m-tRNAThr G15927A mutation in this family.

Mitochondrial COI/tRNASer(UCN) G7444A mutation may be associated with hearing impairment in a Han Chinese family.

Mutations in mitochondrial genome have been found to be associated with hearing loss. Of these, the mitochondrial 12S rRNA and tRNASer(UCN) are the hot spots for pathogenic mutations associated with deafness. To understand the putative role of mitochondrial DNA (mtDNA) mutations in hearing loss, we recently initiated a mutational screening for the mtDNA mutations in Hangzhou area from Zhejiang Province. In this study, we described a maternally inherited Han Chinese family with high penetrance of hearing loss, notably, the penetrances of hearing loss in this family were 80% and 40%, when the aminoglycoside was included or excluded. Three matrilineal relatives in this pedigree exhibited different levels of hearing loss with different age at onset. In addition, sequence analysis of the complete mitochondrial genome showed the presence of the well-known C1494T mutation in 12S rRNA gene and the G7444A mutation in the COI/tRNASer(UCN). The C1494T mutation had been reported to be a pathogenic mutation associated with aminoglycoside-induced and non-syndromic hearing loss. While the G7444A mutation was considered as a secondary mutation associated with deafness. However, the lack of functional variants in GJB2 and TRMU genes suggested that nuclear modified genes may not play important roles in deafness expression. Thus, the combination of G7444A and C1494T mutations in mitochondrial genome may account for the high penetrance of hearing loss in this Chinese family.

Synovial sarcoma of the neck masquerading as a malignant second branchial cleft cyst.

Synovial sarcoma is an uncommon, aggressive malignant tumor of the soft tissues primarily involving the extremities of young adults. Head and neck synovial sarcoma is rare, and its diagnosis and therapy are still challenging.We report a case of a young patient with synovial sarcoma, clinically masquerading as cystic mass of the neck and malignant second branchial cleft cyst. The pathological diagnosis of the sarcoma was confirmed by a multimodality diagnostic protocol, including histological, immunohistochemical and molecular genetic analysis. The patient underwent complete surgical excision followed by postoperative radiotherapy and recovered well.

Expression of type IV collagen, metalloproteinase-2, metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 in laryngeal squamous cell carcinomas.

OBJECTIVE: To investigate the significance of type IV collagen, metalloproteinase-2 (MMP-2), metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) expression in laryngeal squamous cell carcinomas (LSCCs). METHODS: Expression was quantified in 44 LSCC and 22 adjacent non-cancer normal tissues using a streptavidin-peroxidase conjugated immunohistochemistry and associations between the levels of the four proteins and clinicopathological characteristics in LSCC were analyzed. RESULTS: Significantly different expression of all four proteins was observed in LSCC and adjacent non-cancer normal tissues (P<0.05). Expression of type IV collagen correlated with primary cancer status (P = 0.04), clinical stage (P = 0.04) and histological grade (P = 0.01). Expression of MMP-9 correlated with the location of the tumor (P = 0.04), cervical node metastasis (P = 0.02) and prognosis (P = 0.02). The (MMP-2+MMP-9)/TIMP-1 score was associated with the prognosis of LSCC (P < 0.01). CONCLUSIONS: This study suggests that expression of type IV collagen and its regulators is strongly associated with the development of LSCC. Type IV collagen and MMP-9 may be more valuable than MMP-2 and TIMP-1 for the evaluation of clinical characteristics. Regulation of type IV collagen may contribute to the balance of MMPs and TIMPs in LSCC.