To present a recent to increase understanding, diagnosis and treatment of intestinal pneumatosis clinical case, considering the distinctive characteristics of the disease and to expand knowledge about the management of this condition. The case of a female patient aged 65, originally from Bolivia, with a history of osteoarthritis, osteoporosis, asthma and allergies repetition occurs. The patient was admitted to the Department of Surgery No. 1 HNC in November 2015, with an unclear clinical picture. During admission of air bubbles present in the colonic mucosa and tumor lesion is discovered duodenum. Quickly it begins with treatment and adequate support for stabilization. A literature search and an update of the latest updates regarding this disease arises. medical seekers popularity as PUBMED, UP TO DATE, VBS were used. a series of articles about it were selected.
Hyperbaric oxygen protects mandibular condylar chondrocytes from interleukin-1β-induced apoptosis via the PI3K/AKT signaling pathway
Objectives: Mandibular condylar chondrocyte apoptosis is mainly responsible for the development and progression of temporomandibular joint osteoarthritis (TMJ-OA). Interleukin-1β (IL-1β) generally serves an agent that induces chondrocyte apoptosis. Hyperbaric oxygen (HBO) treatment increases proteoglycan synthesis in vivo. We explore the protective effect of HBO on IL-1β-induced mandibular condylar chondrocyte apoptosis in rats and the potential molecular mechanisms. Methods: Chondrocytes were isolated from the TMJ of 3-4-week old Sprague-Dawley rats. The Cell Counting Kit-8 (CCK-8) assay was used to determine cell viability. The phosphorylated phosphoinositide-3 kinase (p-PI3K), phosphorylated AKT (p-Akt), type II collagen (COL2), and aggrecan (AGG) content was detected by immunofluorescence, immunocytochemistry and western blotting. The expression of Pi3k, Akt, Col2 and Agg mRNA was measured using real-time quantitative polymerase chain reaction (RT-qPCR). Results: HBO inhibited the cytotoxicity and apoptosis induced by IL-1β (10 ng/mL) in the mandibular condylar chondrocytes. HBO also decreased the IL-1β activity that decreased p-PI3K and p-AKT levels, and increased COL2 and AGG expression, with the net effect of suppressing extracellular matrix degradation. Conclusions: These data suggest that HBO may protect mandibular condylar chondrocytes against IL-1β-induced apoptosis via the PI3K/AKT signaling pathway, and that it may promote the expression of mandibular condylar chondrocyte extracellular matrix through the PI3K/AKT signaling pathway.
Under the term “osteoarthritis” (OA) is currently meant a clinical syndrome resulting from the combined effect of articular pain and disordered functional activity leading to the deterioration of the quality of life of the patients. The principal objective of rehabilitation of the patients presenting with GA in which all patients with this condition are in need practically after each next aggravation of the pathological process is to relive pain syndrome and restore the functional ability of the joints lost or deteriorated after each exacerbation in order to eventually improve the quality of life of the patients experiencing the constantly progressing degenerative process in the musculoskeletal system.
Hyperbaric oxygen treatment is comparable to acetylsalicylic acid treatment in an animal model of arthritis.
Approximately 1 in 5 adults in the United States are affected by the pain, disability, and decreased quality of life associated with arthritis. The primary focus of treatment is on reducing joint inflammation and pain through a variety of pharmacotherapies, each of which is associated with various side effects. Hyperbaric oxygen therapy is an alternative treatment that has been recommended to treat a variety of inflammatory diseases, ranging from chronic brain injury to exercise induced muscle soreness. The purpose of this set of experiments was to explore the effect of hyperbaric oxygen therapy on joint inflammation and mechanical hyperalgesia in an animal model of arthritis, and compare these effects to treatment with aspirin. Hyperbaric oxygen therapy significantly reduced both joint inflammation and hyperalgesia. As compared with aspirin treatment, hyperbaric treatment was equally as effective in decreasing joint inflammation and hyperalgesia. This article reports that hyperbaric oxygen treatment decreases pain and inflammation in an animal model of arthritis. The effect of hyperbaric oxygen treatment is very similar in magnitude to the effect of acetylsalicylic acid treatment. Potentially, hyperbaric oxygen could be used to treat pain and inflammation in patients with arthritis.
Cu, Zn-SOD values were measured by enzyme immunoassay in the synovial fluid, leukocytes in the synovial fluid, synovial membrane, and leukocytes in blood of the patients with rheumatoid arthritis. SOD activity, lipoperoxide value in serum, ESR, and Lansbury’s index of the patients with rheumatoid arthritis under hyperbaric oxygen (HBO) therapy were also investigated. SOD values of synovial fluid and of leukocytes in synovial fluid from rheumatoid arthritis group were found to be higher than those from osteoarthritis group. No significant difference was found the SOD values in leukocytes of blood and synovial membrane between two groups. In the patients with rheumatoid arthritis under HBO therapy the SOD activity was increased, whereas lipoperoxide values was decreased.