Failure to Thrive—An Analysis of 83 Cases

The case histories of 83 children admitted to the hospital with a diagnosis only of failure to thrive were examined. In twenty-six cases there was evidence of maternal deprivation as a factor. Forty patients were found to have significant organic diseases as a possible or probable cause or contributing influence.Twenty-six were found to have some degree of mental retardation, either documented or suspected, but in nearly all of them there were associated factors presumably responsible, at least in part, for failure to thrive.Several children had birth weight less than 2,500 grams, but no child was thought to grow poorly because of prematurity alone. Congenital anomalies such as cleft palate and other problems leading to feeding difficulties were not unusual.In any case of persistent failure of an infant to gain adequately in weight and length, in which the cause is not evident, the child should be admitted to a hospital to determine response in a new environment. Also an adequate social history should be sought and siblings more closely evaluated; and careful study should be made of the renal, gastro-intestinal, cardiac, pulmonary and central nervous systems, even if there are no symptoms or signs referable to these systems.     

Studien über die UV-Mutabilität verschiedener Stämme von Serratia und über die Natur der Färbungsmutationen

Ohne ZusammenfassungHerrn Prof. Dr. Dr. h. c. B. Rajewsky zum 65. Geburtstag gewidmet.     

Properties of current influenza A (H1N1) virus strains and the characteristics of the epidemics they induce

Three epidemics of influenza A (H1N1) occurring in 1977, 1979 and 1981 were studied. These epidemics were found to be gradually dying down, which was manifested by progressively decreasing morbidity rate, the frequency and intensity of seroconversions, as well as by a decrease in the duration of the epidemic period. Changes in the biological properties of influenza A (H1N1) virus were accompanied by changes in its antigenic properties. The drift of neuraminidase in the influenza A (H1N1) virus of 1981 towards increased relationship with neuraminidase in the virus of 1952 was observed, while hemagglutinin in the strains of each of these two groups retained its individual character.     

Differential diagnosis of emotional disorders that cause weight loss.

Recently, anorexia nervosa has received much attention in the scientific and lay press. As a result there is a danger that the other emotional disorders that can present with weight loss and vomiting will be overlooked. Case examples are presented for anorexia nervosa, conversion disorder, schizophrenia and depression. The presentation and treatment of these four disorders are compared.     

Purification and characterization of an inducible Escherichia coli DNA polymerase capable of insertion and bypass at abasic lesions in DNA

We have investigated the ability of DNA polymerases from SOS-induced and uninduced Escherichia coli to incorporate nucleotides at a well-defined abasic (apurinic/apyrimidinic) DNA template site and to extend these chains from this unpaired 3' terminus. A DNA polymerase activity has been purified from E. coli, deleted for DNA polymerase I, that appears to be induced 7-fold in cells following treatment with nalidixic acid. Induction of this polymerase (designated DNA polymerase X) appears to be part of the SOS response of E. coli since it cannot be induced in strains containing a noncleavable form of the LexA repressor (Ind-). The enzyme is able to incorporate nucleotides efficiently opposite the abasic template lesion and to continue DNA synthesis. Although we observe an approximate 2-fold induction of DNA polymerase III in cells treated with nalidixic acid, several lines of evidence argue that DNA polymerase X is unrelated to DNA polymerase III (pol III). In contrast to pol X, pol III shows almost no detectable ability to incorporate at or extend beyond the abasic site; incorporation efficiency at the abasic lesion is at least 100-fold larger for pol X compared to pol III holoenzyme, pol III core, or pol III* (the polymerase III holoenzyme subassembly lacking the beta subunit). Pol X does not cross-react with polyclonal antibody directed against pol III holoenzyme complex or with monoclonal antibody prepared to the alpha subunit of pol III. Despite these structural and biochemical differences, pol X appears to interact specifically with the beta subunit of the pol III holoenzyme in the presence of single-stranded binding protein. Pol X has a molecular mass of 84 kDa. Our results indicate that this novel activity is likely to be identical to DNA polymerase II of E. coli.