Definition and prevention of upper respiratory infections
Upper respiratory infections (URTI) are diseases caused by nose, nose, throat, throat or acute bacterial infections. The immediate local inoculation response to the virus and bacterial infections in the upper nose respiratory skin involves non-specific responses to polynucleo-white cells and lymphocytes. Consumable white cells continue to pass through the upper skin of the nose and carry particulate matter such as viruses and bacteria. Nasal slime is usually transparent and colourless, but when it is infected, large movements of white cells enter the nose and airways through the upper skin, and as the concentration of white cells increases in the slime, the colour of the nosy slime changes from transparency to yellow and then to green (44). Non-specific reactions include osmosis, the generation of viruses and fungicide hyperoxidants, the generation of remedial factors, and the production of chemical media such as slow thallium and adrenaline, which play an active role in local defence. As with all biological processes that rely on metabolic activity, local immune responses to upper-respiratory skins slow down due to lower temperatures. The entry of cold air into the nasal airways may damage local immunosuppressive defences in the saloon gland tissue, which slows the oscillation of viruses and bacteria and makes them susceptible to infection. The glands and nasals have also proved to be a refuge for respiratory viruses during the cold winter season, transforming subclinical infections into clinically symptomatic URLs. Acute earitis is a common complication of upper respiratory infections. The majority of acute ear inflammations are complications of viral upper respiratory infections (URI). viral upper-respiratory infections increase the risk of bacterial acute ear inflammation by contributing to increased bacterial reproduction and inflammation in the nasal and osteoporosis drums, thereby facilitating the entry of bacteria into the middle ear. Respiratory viruses can co-infect the center ear with bacterial AOM pathogens and have been identified as the only AOM pathogens. Recent studies have shown that vitamin D affects various components of the immune system. For example, antibacterium LL-37 is considered to be important for congenital immunisation, which is produced by antibacterial beryllium, which is circumcised by protein enzyme 3, and has high levels of antibacterial and antiviral activity. Vitamin D in humans originates from the synthesis of skin exposure to UV and the ingestion of foods containing vitamin D2 or vitamin D3, such as fish, dairy products and mushrooms. Vitamin D synthesized or ingestion is converted to 25-Oxyl Vitamin D (16), mainly in the liver, by hydroxylization. 25-HYVD is combined with vitamin D protein and is circular in blood flow. Subsequently, 25-HVD transferred to the kidneys was re-hydrated in cells, forming 1 α, 25 (OH) 2 Vitamin D (17, 18). 1 α, 25 (OH) 2 Vitamin D is an active form of Vitamin D, working through a combination of organs, tissues and immunoactive cells expressing vitamin D receptors. There is reportedly a correlation between serum 25-HYVD and saliva immunoglobin A (sIGA), which can be adjusted upwards to increase the body’s immunity. Numerous studies have shown that moderate-intensity motion enhances immunisation, while excessive long-term and high-intensity motion can lead to high numbers of lymphocytes in blood count and low lymphocytes, impaired osmosis and neutral particle function, reduced oxidation activity, natural lethal cell solubility (NKCA) and mucous membrane immune protein levels. Intensive training can also enhance the release of inflammatory cytogens, such as alpha, white cell media-1b (IL-1b) and IL-6, thus reducing immunity and increasing the risk of infection. Due attention is therefore paid to heating, vitamin D supplementation, and appropriate exercise can to some extent reduce the incidence of upper respiratory infections.
