Characterization of cell-mediated immunity in long-term survivors of gastric or colorectal cancer

Cell-mediated immunity was assessed in 12 patients who were long-term survivors of gastric and colorectal adenocarcinomas. A slight decrease in the T-lymphocyte count was accompanied by preserved proliferative reactivity to mitogens (phytohemagglutinin) or alloantigens in 75 percent of the patients. The influence of autologous patient serum on in vitro lymphoproliferative test results was not significant. Selected sera from both study groups showed values of immune complexes that were within the normal range. The colorectal cancer group had antibody-dependent cellular cytotoxicity within the ranges already established for the normal control subjects. Cellular immune mechanisms seem to have been well preserved in long-term survivors of gastric or colorectal carcinoma.     

Abnormalities of chromosome No. 1: Two cases with lymphocytic lymphomas

Two cases of lymphocytic lymphoma with a duplication of part of the long arm of chromosome #1, between bands 1q25 and 1q32, are presented. The coincidence between this finding with others in the literature supports the concept that this specific chromosome segment is related to the proliferative advantage of malignant cells in neoplasia.     

Amenorrhea and edema.

In a 22 year old woman extensive edema developed during evaluation for amenorrhea. It was learned then that she was consuming escessive amounts of a laxative daily. Balance studies were performed which demonstrated that she excreted large amounts of sodium in her liquid stools while taking the dose of laxative she had been using. The presence of increased plasma renin activity and increased urinary aldosterone suggest that in this patient the occurrence of the edema after she discontinued use of the laxative was due to secondary aldosteronism presumably caused by plasma volume depletion.     

Sister chromatid exchange in malignant lymphomas

Sister chromatid exchange (SCE) was evaluated in peripheral lymphocytes from 20 untreated patients with malignant lymphomas: 6 with Hodgkin's disease (HD), 14 with non-Hodgkin lymphoma (NHL), and 5 with lymphadenitis. The mean SCE frequency (+/- SE) was: 11.2 +/- 0.6, 11.0 +/- 0.6, and 7.2 +/- 0.3 for HD, NHL, and lymphadenitis patients, respectively, and 8.7 +/- 0.2 for the control group. No differences in SCE score were observed in HD and NHL. These results allowed us to consider both groups (HD and NHL) as a single neoplastic population (mean +/- SE, 11.0 +/- 0.4). No significant differences were found between the lymphadenitis and control groups. On the other hand, significantly higher SCE scores were seen in neoplastic populations than in the control and lymphadenitis groups (p less than 0.001 and p less than 0.01, respectively). When SCE was compared by chromosome number and group between neoplastic patients and controls, a higher SCE frequency was observed in chromosomes #1, #2, #3, and B, C + X, E, F chromosome groups than in controls. SCE levels were significantly higher in lymphoma patients in all chromosome numbers and groups mentioned than in patients with lymphadenitis. It is suggested that the high SCE rate in the malignant lymphoma population is possibly related to an increased chromosomal instability.     

Irma Weinberg's 1928 paper “on the problem of the determination of heredity prognosis: The risk in the cousins of schizophrenics”

Irma Weinberg, a German-Jewish Neuropsychiatrist/Physician, authored the fourth report from the German Research Institute for Psychiatry in Munich examining the risk for dementia praecox (DP) in particular relatives of DP probands, here first-cousins. She examined 977 cousins of 54 DP probands and found a best-estimate risk of 1.4%. She conducted within-study analyses, showing a much higher risk for DP in the siblings than cousins of DP probands. She studied DP-related personalities showing a familial link between these conditions and risk for DP. She demonstrated that the risk for DP in cousins was impacted substantially by the distribution, in ancestors, of psychosis and personality abnormalities. After completing work on this article, Weinberg worked in private practice in Frankfurt, emigrating to the Netherlands in 1934, where she worked at a Jewish psychiatric hospital. In 1943, German occupiers evacuated the hospital, transporting the patients and staff, either directly to Auschwitz or, like Weinberg, to the Westerbork transit camp. On September 4, 1944, Dr. Weinberg was transported to Theresienstadt and soon thereafter to Auschwitz, where she was murdered at the age of 53. Her history raises painful questions about the relationship between genetic studies of psychiatric illness in prewar Germany and the Holocaust.