Hi stana,
common cold is a typical example of a self-contained disease that goes away in a few days untreated and maybe in a couple of weeks when treated. [;D]
Side effects of various drugs and remedies seem to play the trick.
Increasing temperature could be useful, theoretically, because rhinoviruses are fragile and heat sensitive. In the old days (over 20yrs ago) they recommended to use cotton in your nostrils to increase temperature inside. Who knows.
Cheers,
iko
Get better Neil ![8D]
BTW , my Microbiology teacher says that for rhinoviruses the best cure is to inhale hot air from your range (i`m not sure for this word, I looked in the vocabulary, It`s the place where you cook coffee etc. ) Optimal temperature for them to multuply is 33 C, which is the temperature in your upper respiratory pathways. Thay don`t feel comfortable on 37 C , though.
...with a little help from Rhinology and viruses:
4xC = Cardiff Common Cold Centre... How neat!
(https://www.thenakedscientists.com/forum/proxy.php?request=http%3A%2F%2Fwww.killallanimals.com%2Fkillers%2Frhino.jpg&hash=1b7f5653b169ee4736b8ec22ceb0272f)
http://www.killallanimals.com/killers/rhino.jpg
Acute cooling of the body surface and the common cold.
Eccles R.
Common Cold Centre, Cardiff School of Biosciences, Cardiff University, United Kingdom.
There is a widely held belief that acute viral respiratory infections are the result of a "chill" and that the onset of a respiratory infection such as the common cold is often associated with acute cooling of the body surface, especially as the result of wet clothes and hair. However, experiments involving inoculation of common cold viruses into the nose, and periods of cold exposure, have failed to demonstrate any effect of cold exposure on susceptibility to infection with common cold viruses.
Present scientific opinion dismisses any cause-and-effect relationship between acute cooling of the body surface and common cold.
This review proposes a hypothesis; that acute cooling of the body surface causes reflex vasoconstriction in the nose and upper airways, and that this vasoconstrictor response may inhibit respiratory defence and cause the onset of common cold symptoms by converting an asymptomatic subclinical viral infection into a symptomatic clinical infection.
Rhinology. 2002 Sep;40(3):109-14.
Me ride me bike and take 'cod'
not to catch a 'cold'! [;)]
(https://www.thenakedscientists.com/forum/proxy.php?request=http%3A%2F%2Fwww.motocicliste.net%2Fmoto%2Fbetaalp%2Falp%25202.JPG&hash=da7bea0140ab4ca73ae5be02607891a8)
http://www.motocicliste.net/moto/betaalp/alp%202.JPG
...Holmes and colleagues conducted a trial of cod-liver oil among industrial workers in a factory in the American midwest.
http://www.cabincrittersinc.com/Adj.%20Cod%20Fish%20copy.jpg
...vitamin D3 makes good antimicrobial peptides for you:
The role of cathelicidin and defensins in pulmonary inflammatory diseases.
Herr C, Shaykhiev R, Bals R.
Philipps-University, Department of Internal Medicine, Division for Pulmonary Diseases, Marburg, Germany.
Antimicrobial peptides (AMPs) protect the epithelia of mucosal organs like the respiratory or the gastrointestinal tract from invading microorganisms. As an integral part of the innate immune system they display antimicrobial activity against gram- and gram-negative bacteria as well as against fungi and enveloped and non-enveloped viruses.
Besides their microbicidal effects they have important functions in the regulation of repair and inflammation. AMPs are sometimes referred to as 'alarmins' due to their ability to recruit, modulate and activate components of the immune system. In contrast, some AMPs suppress activation of the immune system. AMPs are also involved in tissue repair, cancer biology and angiogenesis. Based on their antimicrobial and immunomodulatoy functions, AMPs are probably involved in the pathogenesis of infectious and inflammatory diseases of the lung. Inborn or acquired deficiencies contribute to susceptibility to infection and colonisation. The potential pro-inflammatory role of AMPs contributes to the disease processes in inflammatory disorders such as asthma, chronic obstructive pulmonary disease, sepsis or pulmonary fibrosis. This review summarises the knowledge about the functions of AMPs in the pulmonary innate host defence system and their role in respiratory disease.
Expert Opin Biol Ther. 2007 Sep;7(9):1449-61.
(https://www.thenakedscientists.com/forum/proxy.php?request=http%3A%2F%2Fwww2.warwick.ac.uk%2Ffac%2Fsci%2Fmoac%2Fcurrentstudents%2Fpeter_cock%2Fphotos%2Fmarburg%2Fmarburg.jpg&hash=5520f8587426466e21ba6797a2024427)
http://www2.warwick.ac.uk/fac/sci/moac/currentstudents/peter_cock/photos/marburg/marburg.jpg
Cutting edge: vitamin D-mediated human antimicrobial activity
against Mycobacterium tuberculosis is dependent on the induction of cathelicidin.
Liu PT, Stenger S, Tang DH, Modlin RL.
Division of Dermatology, Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Host defense against intracellular pathogens depends upon innate and adaptive antimicrobial effector pathways. TLR2/1-activation of monocytes leads to the vitamin D-dependent production of cathelicidin and, at the same time, an antimicrobial activity against intracellular Mycobacterium tuberculosis. To determine whether induction of cathelicidin was required for the vitamin D-triggered antimicrobial activity, the human monocytic cell line THP-1 was infected with M. tuberculosis H37Ra and then activated with the active vitamin D hormone 1,25-dihydroxyvitamin D(3) (1,25D(3)). 1,25D(3) stimulation resulted in antimicrobial activity against intracellular M. tuberculosis and expression of cathelicidin mRNA and protein. Using small interfering RNA (siRNA) specific for cathelicidin, 1,25D(3)-induced cathelicidin mRNA and protein expressions were efficiently knocked down, whereas a nonspecific siRNA control had little effect. Finally, 1,25D(3)-induced antimicrobial activity was completely inhibited in the presence of siRNA against cathelicidin, instead leading to enhanced intracellular growth of mycobacteria. These data demonstrate that cathelicidin is required for the 1,25D(3)-triggered antimicrobial activity against intracellular M. tuberculosis.
J Immunol. 2007 Aug 15;179(4):2060-3.