Pulmonary lymphoepithelioma-like carcinoma: A case report with emphasis on computed tomography findings.

RATIONALE: Pulmonary lymphoepithelioma-like carcinoma (PLELC) is a rare type of primary malignant lung tumor characterized by Epstein-Barr virus infection, with, to the authors' knowledge, a total of only 500 reported cases during the past 30 years worldwide. Histologically, PLELC is similar to undifferentiated nasopharyngeal carcinoma and poorly differentiated squamous cell carcinoma. However, although PLELC accounts for <1% of all lung cancers, it has a better prognosis and is usually detected in non-smokers and individuals of Asian ancestry. PATIENT CONCERNS: The patient presented with chest distress of no apparent cause, dizziness, headaches, and a feeling of disequilibrium without remission, as well as a pulmonary nodule incidentally detected on contrast-enhanced computed tomography (CT). DIAGNOSIS: PLELC was confirmed histopathologically rather than on preoperative CT; nevertheless, CT findings still contributed to the diagnosis. INTERVENTIONS: The patient underwent thoracoscopic wedge resection of the affected lung. OUTCOMES: The patient recovered after the lung nodule was completely removed, and was discharged. No evidence of recurrence or metastasis was found at the latest follow-up appointment 2 months after the operation. LESSONS: PLELC is a rare bronchogenic carcinoma associated with lymphatic tissue with a favorable prognosis in most cases. With nonspecific clinical symptoms, specific radiological findings may facilitate an early diagnosis in some cases, followed by timely surgical intervention.

Voltage-gated sodium channel 1.7 expression decreases in dorsal root ganglia in a spinal nerve ligation neuropathic pain model.

The role of the voltage-gated sodium channel 1.7 (Nav1.7) is unclear in models of neuropathic pain induced by nerve injury. In the present study, we measured expression levels of Nav1.7 in two distinct neuropathic pain models: spinal nerve ligation (SNL) and chronic constriction injury (CCI). In the SNL model, both mRNA and protein levels of Nav1.7 were markedly lower in the L5 dorsal root ganglia (DRG) but were significantly higher in the L4 DRG. Nav1.7 protein levels were notably higher in both L4 and L5 DRGs under CCI conditions. We found that excessive damage of L5 nerves such as SNL reduced expression levels of Nav1.7 in the injured L5 DRG and activated the adjacent uninjured DRG, resulting in Nav1.7 level increases in the adjacent L4 DRG. We confirmed again that Nav1.7 was closely related to neuropathic pain induced by nerve injury. More importantly, our results suggest that tracing the molecular changes exclusively in the L5 DRG in SNL model may not completely explain the pain mechanism; it is necessary to study the adjacent uninjured L4 DRG.

A semisynthetic Atg3 reveals that acetylation promotes Atg3 membrane binding and Atg8 lipidation.

Acetylation of Atg3 regulates the lipidation of the protein Atg8 in autophagy. The molecular mechanism behind this important biochemical event remains to be elucidated. We describe the first semi-synthesis of homogeneous K19/K48-diacetylated Atg3 through sequential hydrazide-based native chemical ligation. In vitro reconstitution experiments with the semi-synthetic proteins confirm that Atg3 acetylation can promote the lipidation of Atg8. We find that acetylation of Atg3 enhances its binding to phosphatidylethanolamine-containing liposomes and to endoplasmic reticulum, through which it promotes the lipidation process.