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  • Book
    [edited by] Klaus Bohndorf, Mark W. Anderson, Mark Davies, Herwig Imhof, Klaus Woertler.
    Contents:
    Acute trauma and chronic strain : essentials
    Acute trauma and chronic strain (according to regions)
    Infections of the bones, joints and soft-tissues
    Tumors and tumor-like lesions of the bone, the joints and the spine
    Bone marrow
    Necroses of the skeletal system
    Osteochondroses
    Metabolic, hormonal and toxic osteopathies
    Constitutional disorders of bone and joint development
    Rheumatic disorders
    Miscellaneous bone, joint and soft-tissue disorders
    Interventions involving the bone, soft tissues and joints
    Radiology expert advisory reports on the skeleton and the joints.
    Digital Access Thieme-Connect 2016
  • Article
    Schauberger CW, Thies RL, Fischer LJ.
    J Pharmacol Exp Ther. 1977 May;201(2):450-5.
    Pretreatment with n-butanol (10 mmol/kg i.p.) 30 minutes before alloxan (100 mg/kg) protects mice from the permanent hyperglycemic effects (measured at 72 hours) of the diabetogenic agent. This dose of n-butanol caused an elevation of serum glucose at 30 minutes, the time of alloxan administration. Since glucose administration can protect animals from alloxan, the possibility that alcohol-induced hyperglycemia protected mice from alloxan was investigated. Mannoheptulose, an antagonist of glucose action at the pancreatic beta-cell, when given 24 minutes after n-butanol and 6 minutes before alloxan, eliminated the alcohol-induced protection. Fasted mice did not exhibit n-butanol-induced hyperglycemia at 30 minutes and alloxan given at that time produced diabetes. No protection was observed in fed animals when n-butanol was given 5 minutes before alloxan. The high serum levels of butanol and normal serum glucose which were observed at 5 minutes after alcohol administration indicated that the lack of protection was not due to a lack of circulating alcohol but resulted from an absence of hyperglycemia. The results indicate that pretreatment with n-butanol protects mice from alloxan-induced diabetes by the indirect mechanism of producing hyperglycemia at the time of alloxan administration.
    Digital Access Access Options