Effects of Altitude on Fire Smoke Diffusion in Semi-Lateral Smoke Exhaust Highway Tunnels

This paper aims to study the effects of altitude and the size of smoke outlet on fire smoke diffusion and discharge in semi-lateral smoke exhaust highway tunnels. At first, simulations of semi-lateral smoke exhaust highway tunnels were carried out in FDS (Fire Dynamics Simulator), then the distribution laws of temperature, CO concentration, smoke mass flow, and visibility in the tunnel under the conditions of different altitudes and smoke outlet areas were analyzed to figure out the effects of altitude and size of smoke outlet on fire smoke diffusion and discharge in the said tunnels. The results suggest that, in case of the same fire source power, the velocity of smoke diffusion increases with the altitude; for curves of different altitudes, the tunnel roof temperature features are basically the same, that is, the higher the altitude, the higher the temperature at the tunnel roof. When the fire source power is 20 MW, the smoke mass flow at the smoke outlet decreases with the increase of altitude, but the CO concentration grows with it, indicating that the smoke exhaust efficiency is higher in high-altitude areas. When the altitude reaches 4200 m and the fire source power is 20 MW, with the increase of smoke outlet area, the smoke discharge effect of the tunnel shows an upward trend, taking both the smoke discharge effect and economy into consideration; the smoke outlet should take a size of 4 x 3 m

Fas-positive T cells regulate the resolution of airway inflammation in a murine model of asthma

Persistent airway inflammation, mucus production, and airway hyperreactivity are the major contributors to the frequency and severity of asthma. Why lung inflammation persists in asthmatics remains unclear. It has been proposed that Fas-mediated apoptosis of inflammatory cells is a fundamental mechanism involved in the resolution of eosinophilic airway inflammation. Because infiltrating eosinophils are highly sensitive to Fas-mediated apoptosis, it has been presumed that direct ligation of Fas on eosinophils is involved. Here, we utilize adoptive transfers of T cells to demonstrate that the delayed resolution of eosinophilia in Fas-deficient mice is a downstream effect of Fas deficiency on T cells, not eosinophils. Interestingly, the mice that received Fas-deficient T cells, but not the controls, developed a persistent phase of inflammation that failed to resolve even 6 wk after the last challenge. This persistent phase correlated with decreased interferon (IFN)γ production by Fas-deficient T cells and could be reproduced with adoptive transfer of IFNγ-deficient T cells. These data demonstrate that Fas deficiency on T cells is sufficient for the development of long-term allergic airway disease in mice and implies that deregulation of death receptors such as Fas on human T cells could be an important factor in the development and/or chronic nature of asthma

Allergen Exposure in Lymphopenic Fas-Deficient Mice Results in Persistent Eosinophilia Due to Defects in Resolution of Inflammation

Asthma is characterized by chronic airway type-2 inflammation and eosinophilia, yet the mechanisms involved in chronic, non-resolving inflammation remain poorly defined. Previously, our group has found that when Rag-deficient mice were reconstituted with Fas-deficient B6 LPR T cells and sensitized and challenged, the mice developed a prolonged type-2-mediated airway inflammation that continued for more than 6 weeks after the last antigen exposure. Surprisingly, no defect in resolution was found when intact B6 LPR mice or T cell specific Fas-conditional knockout mice were sensitized and challenged. We hypothesize that the homeostatic proliferation induced by adoptive transfer of T cells into Rag-deficient mice may be an important mechanism involved in the lack of resolution. To investigate the role of homeostatic proliferation, we induced lymphopenia in the T cell-specific Fas-conditional knockout mice by non-lethal irradiation and sensitized them when T cells began to repopulate. Interestingly, we found that defective Fas signaling on T cells plus antigen exposure during homeostatic proliferation was sufficient to induce prolonged eosinophilic airway inflammation. In conclusion, our data show that the combination of transient lymphopenia, abnormal Fas-signaling, and antigen exposure leads to the development of a prolonged airway eosinophilic inflammatory phase in our mouse model of experimental asthma

Non-apoptotic Fas (CD95) Signaling on T Cells Regulates the Resolution of Th2-Mediated Inflammation

Fas (CD95/APO-1) and its ligand (FasL/CD95L) promote the resolution of type 2 lung inflammation and eosinophilia. We previously found that Fas-deficiency on T cells, but not eosinophils, delayed resolution of inflammation. However, Fas can signal both cell death and have a positive signaling function that can actually activate cells. In this study, we investigated whether Fas-induced death or Fas-activated signaling pathways promote resolution of allergic lung inflammation. By increasing T cell survival through two Fas-independent pathways, using Bim-deficient T cells or Bcl-xL overexpressing T cells, no differences in resolution of Th2-mediated inflammation was observed. Furthermore, Th2 cells were inherently resistant to Fas-mediated apoptosis and preferentially signaled through non-apoptotic pathways following FasL treatment. Utilizing Fas-mutant mice deficient in apoptotic but sufficient for non-apoptotic Fas signaling pathways, we demonstrate that non-apoptotic Fas signaling in T cells drives resolution of Th2-mediated airway inflammation. Our findings reveal a previously unknown role for non-apoptotic Fas signaling on Th2 cells in the induction of resolution of type 2 inflammation

A Rare Case of Histiocytic Sarcoma Secondary to Gastrointestinal Stromal Tumor in the Stomach: Transdifferentiation or Synchronicity?

Histiocytic sarcoma is a rare malignant histiocytic neoplasm composed of cells with morphologic and immunophenotypic features of mature tissue histiocytes. It occurs anywhere in the body and behaves aggressively. However, its etiology is unknown. Here, we report a 68-year-old female who developed histiocytic sarcoma following chemotherapy with imatinib (Gleevec) for gastrointestinal stromal tumor. Possible mechanisms of transdifferentiation from gastrointestinal stromal tumor to histiocytic sarcoma are discussed based on the features of our case and other two similar cases in the literature

Extracranial Meningioma in the Scalp with Concurrent Steatocystoma

This report documents a rare case of an extracranial meningioma on the posterior scalp without apparent dural connection. Additionally, a sebaceous steatocystoma of the anterior scalp presented alongside the meningioma. A steatocystoma localized to the scalp is also remarkably rare. To our knowledge, this is the first report documenting both an extracranial meningioma and a steatocystoma presenting concurrently on the scalp. A male patient in his thirties presented with a mass lesion on the scalp. A CT scan revealed one posterior scalp mass with no intracranial abnormalities. Post excision histologic examination confirmed an extracranial meningioma (meningothelial variant, WHO Grade I). A second anterior scalp mass, not revealed by CT scan, was discovered during surgery. It was excised and diagnosed as a steatocystoma. Meningiomas predominantly occur intracranially but, in some instances, may present as a standalone extracranial tumor without intracranial abnormalities. Because extracranial meningioma is uncommon, it may be overlooked during clinical diagnosis of scalp masses. We recommend that this neoplasm be routinely considered in the differential diagnosis of extracranial tumors. The discovery of another rare tumor—a steatocystoma located in immediate proximity on the scalp—is further remarkable. We briefly review relevant case reports and etiologies and consider a potential relationship between the two neoplasms. However, it remains more likely that the concurrence of these tumors in our patient was simply coincidental