Parotid metastasis of rare lung adenocarcinoma: A case report.

BACKGROUND: Lung cancer (LC) is the leading cause of malignancy-related deaths worldwide. The most common sites of metastasis include the nervous system, bone, liver, respiratory system, and adrenal glands. LC metastasis in the parotid gland is very rare, and its diagnosis presents a challenge. Here, we report a case of parotid metastasis in primary LC. CASE SUMMARY: The patient was a 74-year-old male who was discovered to have bilateral facial asymmetry inadvertently two years ago. The right earlobe was slightly swollen and without pain or numbness. Computed tomography (CT) examination showed bilateral lung space-occupying lesions. Pulmonary biopsy was performed and revealed adenocarcinoma (right-upper-lung nodule tissue). Positron emission tomography-CT examination showed: (1) Two hypermetabolic nodules in the right upper lobe of the lung, enlarged hypermetabolic lymph nodes in the right hilar and mediastinum, and malignant space-occupying lesion in the right upper lobe of the lung and possible metastasis to the right hilar and mediastinal lymph nodes; and (2) multiple hypermetabolic nodules in bilateral parotid glands. Parotid puncture biopsy was performed considering lung adenocarcinoma metastasis. Gene detection of lung biopsy specimens revealed an EGFR gene 21 exon L858R mutation. CONCLUSION: This case report highlights the challenging diagnosis of parotid metastasis in LC given its rare nature. Such lesions should be differentiated from primary tumors of the parotid gland. Simple radiological imaging is unreliable, and puncture biopsy is needed for final diagnosis of this condition.

CM3-SII polysaccharide obtained from Cordyceps militaris ameliorates hyperlipidemia in heterozygous LDLR-deficient hamsters by modulating gut microbiota and NPC1L1 and PPARα levels.

Accumulating evidence has demonstrated that polysaccharides derived from edible fungi have lipid-lowering effects in mice. However, the lipid metabolism mechanisms in mice and humans are different. We have previously elucidated the structural characteristics of the alkali-extracted polysaccharide CM3-SII obtained from Cordyceps militaris. This study aimed to investigate whether CM3-SII could ameliorate hyperlipidemia in a heterozygous low-density lipoprotein receptor (LDLR)-deficient hamster model of hyperlipidemia. Our data demonstrated that CM3-SII significantly decreased total plasma cholesterol, non-high-density lipoprotein cholesterol, and triglyceride levels in heterozygous LDLR-deficient hamsters. Unlike ezetimibe, CM3-SII could enhance the concentration of plasma apolipoprotein A1 and the expression of liver X receptor α/ATP-binding cassette transporter G8 mRNA pathway and suppress the expression of Niemann-Pick C1-like 1, which help to reduce cholesterol levels further. Moreover, the results of molecular docking analysis demonstrated that CM3-SII could directly bind to Niemann-Pick C1-like 1 with high affinity. The triglyceride-lowering mechanisms of CM3-SII were related to its downregulation of sterol regulatory element-binding protein 1c and upregulation of peroxisome proliferator-activated receptor α. Importantly, CM3-SII increased the abundance of Actinobacteria and Faecalibaculum and the ratio of Bacteroidetes/Firmicutes. Thus, CM3-SII attenuated hyperlipidemia by modulating the expression of multiple molecules involved in lipid metabolism and the gut microbiota.

Macrophage Plasticity and Atherosclerosis Therapy.

Atherosclerosis is a chronic disease starting with the entry of monocytes into the subendothelium and the subsequent differentiation into macrophages. Macrophages are the major immune cells in atherosclerotic plaques and are involved in the dynamic progression of atherosclerotic plaques. The biological properties of atherosclerotic plaque macrophages determine lesion size, composition, and stability. The heterogenicity and plasticity of atherosclerotic macrophages have been a hotspot in recent years. Studies demonstrated that lipids, cytokines, chemokines, and other molecules in the atherosclerotic plaque microenvironment regulate macrophage phenotype, contributing to the switch of macrophages toward a pro- or anti-atherosclerosis state. Of note, M1/M2 classification is oversimplified and only represent two extreme states of macrophages. Moreover, M2 macrophages in atherosclerosis are not always protective. Understanding the phenotypic diversity and functions of macrophages can disclose their roles in atherosclerotic plaques. Given that lipid-lowering therapy cannot completely retard the progression of atherosclerosis, macrophages with high heterogeneity and plasticity raise the hope for atherosclerosis regression. This review will focus on the macrophage phenotypic diversity, its role in the progression of the dynamic atherosclerotic plaque, and finally discuss the possibility of treating atherosclerosis by targeting macrophage microenvironment.

Association between microRNA-196a2 rs11614913, microRNA-146a rs2910164, and microRNA-423 rs6505162 polymorphisms and esophageal cancer risk: A meta-analysis.

Many observational studies have found that microRNA-196a2 rs11614913, microRNA-146a rs2910164, and microRNA-423 rs6505162 are associated with esophageal cancer risk. However, the results were mixed and inconsistent among these studies. We conducted a meta-analysis to assess the relationship between the polymorphisms of three microRNAs and esophageal cancer susceptibility. We systematically searched the PubMed and EMBASE databases to screen relevant studies. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to compute the risk of esophageal cancer. Because of the differences in ethnicities, sources of controls, and genotyping methods, the meta-analysis was conducted using a random-effect model regardless of heterogeneity. To further explore potential heterogeneity, we performed subgroup and sensitivity analyses, and publication bias was also evaluated. A total of 6 case-control studies on microRNA-196a2 rs11614913, 4 studies on microRNA-146a rs2910164, and 4 studies on microRNA-423 rs6505162 were considered eligible in the meta-analysis. No statistical association was found between microRNA-196a2 rs11614913, microRNA-146a rs2910164, and microRNA-423 rs6505162 polymorphisms and esophageal cancer susceptibility in any genetic model. Subgroup and sensitivity analyses showed similar results. In summary, based on the currently limited proof, no association exists between microRNA-196a2 rs11614913, microRNA-146a rs2910164, and microRNA-423 rs6505162 polymorphism and esophageal cancer risk. However, the result should be cautiously interpreted because of the heterogeneity among studies. Large, high quality clinical trials are required to verify our findings.