English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Plus monthly

Global: Zendy Tools annual

Global: Zendy Tools monthly

Global: Zendy Free Plan

IT IS COMMONLY ACCEPTED that many human diseases are due to the action of environmental factors on individuals with increased susceptibility. Differences in individual susceptibilities can be studied in relation with the antigens coded by the HLA region. Those antigens play an important role in self-recognition processes, and many of them are strongly associated with various diseases, as reriewed by Dausset (1977). In contrast, the association with malignant diseases is nonexistent, or at most weak, as in the case of Hodgkin's disease (Oliver, 1977) and nasopharyngeal carcinoma (Simons et al., 1974). As regards primary liver cancer (PLC), weak associations have been reported with A1, by Hammond et al. (1977) in South Africans, with B 12 by Zenvas et al. in Greece (1979). Individual susceptibilities to diseases can also be correlated to genetic markers not coded by the HLA system; Theodoropoulos et al. (1977), for example, have found that the Gc2 gene coding for the corresponding phenotype of the Ge serum glycoprotein was a risk factor for PLC without cirrhosis; various patterns such as serum deficiency, periodicacid-stain-positive and diastase-resistant globules in hepatocytes of another serum protein also produced by the liver (the of -antitrypsin (al-AT)) have been found by some authors to be associated with diseases such as chronic obstructive lung Acceptedl 16 October 1980

M2 alpha-1-antitrypsin phenotype and primary liver cancer