Coronavirus disease 2019 (COVID-19) is a global pandemic that has caused severe health threats and fatalities in almost all communities. Studies have detected severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in saliva with a viral load that lasts for a long period. However, researchers are yet to establish whether SARS-CoV-2 can directly enter the salivary glands. Therefore, this study aimed to assess the presence of angiotensin-converting enzyme 2 (ACE2)/transmembrane serine proteases 2 (TMPRSS2) expression in salivary glands using publicly available databases. The distribution of ACE2 and TMPRSSs family in salivary gland tissue and other tissues was analyzed. The Genotype-Tissue Expression dataset was employed to explore the ACE2 and TMPRSS2 expression in various body organs and salivary glands in a healthy population. The single-cell sequencing data for salivary gland samples (including submandibular salivary gland and parotid gland) from mice were collected and analyzed. The components and proportions of salivary gland cells expressing the key protease TMPRSSs family were analyzed. Transcriptome data analysis showed that ACE2 and TMPRSS2 were expressed in salivary glands. The expression levels of ACE2 and TMPRSS2 were marginal without significant differences in different age groups or between men and women. Single-cell RNA sequence analysis indicated that TMPRSS2 was mainly expressed in salivary gland epithelial cells. We speculate that SARS-CoV-2 may be entered in salivary glands.

Background: The development of minimally invasive surgery has initiated many changes in the surgical treatment of esophageal cancer (EC) patients. The aim of this study was to compare the short-term outcomes of robotic-assisted minimally invasive esophagectomy (RAMIE), video-assisted minimally invasive esophagectomy (VAMIE), and open esophagectomy (OE). Methods: Our study included patients who had undergone McKeown esophagectomy at Tianjin Medical University Cancer Institute and Hospital between January 2016 and December 2018. We analyzed clinical baseline data, as well as perioperative and pathological outcomes. Results: A total of 312 cases met the inclusion criteria (OE: 77, VAMIE: 144, RAMIE: 91). The OE group had a greater number of late-stage patients as well as those who received the neo-adjuvant therapy, compared with the other two groups (P=0.001). The procedure time in the OE group was also shorter by approximately 20 minutes (P=0.021). Total blood loss was significantly lower in the two MIE groups (P=0.004) than in the OE group. There were no differences in the total number of dissected lymph nodes between the three groups (OE: 24.09±10.77, VAMIE: 23.07±10.18, RAMIE: 22.84±8.37, P=0.680). Both the lymph node number (P=0.155) and achievement rate (P=0.190) in the right recurrent laryngeal nerve (RLN) area were comparable between the three groups. However, in the left RLN area, minimally invasive approaches resulted in a higher number of harvested lymph nodes (P=0.032) and greater achievement rate (P=0.018).Neither MIE procedure increased the incidence of postoperative complications. Conclusions: Minimally invasive surgery could guarantee the quality of bilateral RLN lymphadenectomy without increasing postoperative complications, especially in RAMIE patients. The rational choice of different surgical approaches would improve both safety and oncological outcomes for patients.

In conclusion, ketamine caused neuroapoptosis and impaired brain functions in the developing rat brain which can be effectively attenuated by dexmedetomidine. Dexmedetomidine alone was not neurotoxic to the developing brain.

Farnesoid X receptor (FXR) is a nuclear hormone receptor involved in bile acid synthesis and homeostasis. Dysfunction of FXR is involved in cholestasis and atherosclerosis. FXR is prevalent in liver, gallbladder, and intestine, but it is not yet clear whether it modulates neurobehavior. In the current study, we tested the hypothesis that mouse FXR deficiency affects a specific subset of neurotransmitters and results in an unique behavioral phenotype. The FXR knockout mice showed less depressive-like and anxiety-related behavior, but increased motor activity. They had impaired memory and reduced motor coordination. There were changes of glutamatergic, GABAergic, serotoninergic, and norepinephrinergic neurotransmission in either hippocampus or cerebellum. FXR deletion decreased the amount of the GABA synthesis enzyme GAD65 in hippocampus but increased GABA transporter GAT1 in cerebral cortex. FXR deletion increased serum concentrations of many bile acids, including taurodehydrocholic acid, taurocholic acid, deoxycholic acid (DCA), glycocholic acid (GCA), tauro-α-muricholic acid, tauro-ω-muricholic acid, and hyodeoxycholic acid (HDCA). There were also changes in brain concentrations of taurocholic acid, taurodehydrocholic acid, tauro-ω-muricholic acid, tauro-β-muricholic acid, deoxycholic acid, and lithocholic acid (LCA). Taken together, the results from studies with FXR knockout mice suggest that FXR contributes to the homeostasis of multiple neurotransmitter systems in different brain regions and modulates neurobehavior. The effect appears to be at least partially mediated by bile acids that are known to cross the blood-brain barrier (BBB) inducing potential neurotoxicity.

During tumor development and progression, intrinsic and extrinsic factors trigger endoplasmic reticulum (ER) stress and the unfolded protein response, resulting in the increased expression of molecular chaperones to cope with the stress and maintain tumor cell survival. Heat shock protein (HSP) GRP94, also known as GP96, is an ER paralog of HSP90 and has been shown to promote survival signaling during tumor-induced stress and modulate the immune response through its multiple clients, including TLRs, integrins, LRP6, GARP, IGF, and HER2. Clinically, elevated expression of GRP94 correlates with an aggressive phenotype and poor clinical outcome in a variety of cancers. Thus, GRP94 is a potential molecular marker and therapeutic target in malignancies. In this review, we will undergo deep molecular profiling of GRP94 in tumor development and summarize the individual roles of GRP94 in common cancers, including breast cancer, colon cancer, lung cancer, liver cancer, multiple myeloma, and others. Finally, we will briefly review the therapeutic potential of selectively targeting GRP94 for the treatment of cancers.