Human studies of brain stimulation have demonstrated modulatory effects on the perception of pain. However, whether the primary somatosensory cortical activity is associated with antinociceptive responses remains unknown. Therefore, we examined the antinociceptive effects of neuronal activity evoked by optogenetic stimulation of primary somatosensory cortex. Optogenetic transgenic mice were subjected to continuous or pulse-train optogenetic stimulation of the primary somatosensory cortex at frequencies of 15, 30, and 40 Hz, during a tail clip test. Reaction time was measured using a digital high-speed video camera. Pulse-train optogenetic stimulation of primary somatosensory cortex showed a delayed pain response with respect to a tail clip, whereas no significant change in reaction time was observed with continuous stimulation. In response to the pulse-train stimulation, video monitoring and local field potential recording revealed associated paw movement and sensorimotor rhythms, respectively. Our results show that optogenetic stimulation of primary somatosensory cortex at beta and gamma frequencies blocks transmission of pain signals in tail clip test.
Animals ; Brain ; Humans ; Mice ; Mice, Transgenic ; Neurons ; Optogenetics ; Pain Perception* ; Reaction Time ; Somatosensory Cortex* ; Tail*

BACKGROUND: We reviewed a series of 188 resected pulmonary mucinous adenocarcinomas (MAs) to clarify the prognostic significance of lepidic and non-lepidic patterns. METHODS: Non-lepidic patterns were divided into bland, non-distorted acini with uncertain invasiveness (pattern 1), unequivocal invasion into stroma (pattern 2), or invasion into alveolar spaces (pattern 3). RESULTS: The mean proportion of invasive patterns (patterns 2 and 3) was lowest in small (≤ 3 cm) tumors, and gradually increased in intermediate (> 3 cm and ≤ 7 cm) and large (> 7 cm) tumors (8.4%, 34.3%, and 50.1%, respectively). Adjusted T (aT) stage, as determined by the size of invasive patterns, was positively correlated with adverse histologic and clinical features including older age, male sex, and ever smokers. aTis tumors, which were exclusively composed of lepidic pattern (n = 9), or a mixture of lepidic and pattern 1 (n = 40) without any invasive patterns, showed 100% disease- free survival (DFS). The aT1mi tumors, with minimal (≤ 5 mm) invasive patterns (n = 63), showed a 95.2% 5-year DFS, with recurrences (n = 2) limited to tumors greater than 3 cm in total size (n = 23). Both T and aT stage were significantly associated with DFS; however, survival within the separate T-stage subgroups was stratified according to the aT stage, most notably in the intermediatestage subgroups. In multivariate analysis, the size of invasive patterns (p = .020), pleural invasion (p < .001), and vascular invasion (p = .048) were independent predictors of recurrence, whereas total size failed to achieve statistical significance (p = .121). CONCLUSIONS: This study provides a rationale for histologic risk stratification in pulmonary MA based on the extent of invasive growth patterns with refined criteria for invasion.
Adenocarcinoma in Situ ; Adenocarcinoma, Mucinous* ; Disease-Free Survival ; Humans ; Lung ; Male ; Mucins* ; Multivariate Analysis ; Recurrence*

The complement system is a part of the innate immune system that potentiates the ability of antibodies and phagocytic cells to clear microbes and damaged cells. The complement system consists of a number of proteins circulating as inactive precursors. It is stimulated mainly by three pathways: the classical pathway, the alternative pathway, and the lectin pathway. There are many genetic polymorphisms in this system, which can over-activate the immune system. In this study, we collected the polymorphisms reported to over-activate complement cascades that affect the immune system and induce autoimmune diseases.
Antibodies ; Autoimmune Diseases ; Complement System Proteins* ; Immune System ; Phagocytes ; Polymorphism, Genetic*

BACKGROUND: Using analysis of air samples from the workplace, we report on one case of pneumoconiosis in an individual who has been working in a polytetrafluoroethylene (PTFE) spraying process for 28 years. CASE PRESENTATION: The patient was diagnosed with granulomatous lung disease caused by PTFE using computed tomography (CT), lung biopsy and electron microscopy. To assess the qualitative and quantitative exposure to PTFE in workplace, Fourier transform infrared spectroscopy (FT-IR), energy-dispersive X-ray spectroscopy (EDX) and thermogravimetric analysis (TGA) were performed on air samples from the workplace. The presence of PTFE particles was confirmed, and the airborne concentration of PTFE was estimated to be 0.75 mg/m3. CONCLUSIONS: This case demonstrates that long-term exposure to PTFE spraying can cause granulomatous lung lesions such as pneumoconiosis; such lesions appear to be caused not by the degradation products of PTFE from high temperatures but by spraying the particles of PTFE. Along with air-sampling analysis, we suggest monitoring the concentration of airborne PTFE particles related to chronic lung disease.
Biopsy ; Humans ; Hygiene ; Lung ; Lung Diseases ; Microscopy, Electron ; Occupational Diseases ; Pneumoconiosis ; Polytetrafluoroethylene ; Spectroscopy, Fourier Transform Infrared ; Spectrum Analysis

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) is a positive-sense singlestranded RNA (+ssRNA) that causes coronavirus disease 2019 (COVID-19). The viral genome encodes twelve genes for viral replication and infection. The third open reading frame is the spike (S) gene that encodes for the spike glycoprotein interacting with specific cell surface receptor – angiotensin converting enzyme 2 (ACE2) – on the host cell membrane. Most recent studies identified a single point mutation in S gene. A single point mutation in S gene leading to an amino acid substitution at codon 614 from an aspartic acid 614 into glycine (D614G) resulted in greater infectivity compared to the wild type SARS-CoV2. We were interested in investigating the mutation region of S gene of SARS-CoV2 from Korean COVID-19 patients. New mutation sites were found in the critical receptor binding domain (RBD) of S gene, which is adjacent to the aforementioned D614G mutation residue. This specific sequence data demonstrated the active progression of SARS-CoV2 by mutations in the RBD of S gene.The sequence information of new mutations is critical to the development of recombinant SARS-CoV2 spike antigens, which may be required to improve and advance the strategy against a wide range of possible SARS-CoV2 mutations.