No abstract available.
Humans ; Positive-Pressure Respiration*

This article expounds the types, applicable diseases and medical departments of noninvasive positive pressure mechanical ventilators and the problems we should pay attention to while using them.
Humans ; Positive-Pressure Respiration

No abstract available.
Laparoscopy ; Positive-Pressure Respiration

No abstract available.
Positive-Pressure Respiration, Intrinsic*

No abstract available.
Positive-Pressure Respiration

No abstract available.
Gram-Positive Cocci*

No abstract available.
Positive-Pressure Respiration*

No abstract available.
Positive-Pressure Respiration*

CD88, which stands for "Cluster of Differentiation 88," is also known as C5aR, which stands for "Complement 5a receptor." This complement receptor has 7 transmembrane domains and is found on various cell types, including monocytes, macrophages, dendritic cells, epithelial cells, adipocytes, and endothelial cells. Atherosclerosis is a condition associated with chronic inflammation of the arterial walls. It's marked by lipid retention and building, monocyte and T lymphocyte recruitment into the intima, foam cell generation, smooth muscle cell proliferation, and collagen and protein accumulation. C5a has been found in a wide range of atherosclerotic lesions, from fatty streaks to advanced plaques. The expression of CD88 has been linked to both proatherogenic and antiatherogenic effects in atherosclerosis. Initial activities of C5a in atherosclerosis include chemotaxis, oxidative burst, and vascular adhesion molecule activation. CD88 expression has also been linked to the formation of atherosclerosis plaques via adaptive immune cell activation. Regulation and effector functions require ligand-receptor binding (C5a-C5aR) in the pathogenesis of atherosclerosis. CD88 expression has been linked to all stages of atherosclerosis. Myeloid cells have been identified to express CD88, which is responsible for many of C5a's biological properties. During atherogenesis, macrophages and dendritic cells are two important antigen presentation cells (APCs) that carry and display the CD88 surface marker. The proliferation and division of CD4+ T helper cells are controlled by macrophages, dendritic cells, and mast cells, which are also responsible for the release of both proatherogenic and antiatherogenic cytokines. However, there is no evidence that naive CD4+ T helper cells express CD88 from any of the research that has been done. Since CD88 is expressed by a wide variety of immune cells in atherosclerotic plaques, including macrophages, dendritic cells, T lymphocytes, and B lymphocytes, this review will focus on the influence of CD88 expressing immune cells in atherosclerosis formation.
CD4-Positive T-Lymphocytes

No abstract available.
Gram-Positive Bacterial Infections* ; Teicoplanin*