Risk stratification for postoperative pancreatic fistula using the pancreatic surgery registry StuDoQ|Pancreas of the German Society for General and Visceral Surgery

Background

Postoperative pancreatic fistula (POPF) is a major factor for morbidity and mortality after pancreatic resection. Risk stratification for POPF is important for adjustment of treatment, selection of target groups in trials and quality assessment in pancreatic surgery. In this study, we built a risk-prediction model for POPF based on a large number of predictor variables from the German pancreatic surgery registry StuDoQ|Pancreas.

Genetic polymorphism of IgG in the mink. III. Instability of expression and the problem of the genetic control of C gamma-allotypes

Quantitative expression of C gamma-allotype H4 of mink immunoglobulins was studied by enzyme-linked immunosorbent assay. The results presented suggest that production of H4 is under specific regulation. the concentration of H4 varies three orders of magnitude (10-10,000 micrograms/ml) from one mink to another. Fifteen percent of the sera of normal minks have the low H4 concentration, undetectable by the standard procedure of double immunodiffusion routinely used to test mink IgG allotypes. However, expression of these 'minor' allotypes may be significantly enhanced by hyperimmunization. Instability of this kind seems to be the main cause of earlier described deviations from Mendelian inheritance of C gamma-allotypes H2, H3 and H4.     

Changes in the electrical activity of a single node of Ranvier of an isolated nerve fiber due to novocain

Summary A solution of novocain in small concentrations (1·10^–8 and 1·10^–7) does not cause changes of action potential (AP) amplitude and threshold of depolarization (V) in the node of Ranvier of isolated frog's nerve fiber. A novocain concentration of 5·10^–5 causes a reduction of response amplitude and a rise of the depolarization threshold. Responses are graded, i.e., increase with an increase in the strength of its stimulus. Novocain solution in a concentration of 1·10^–4 depresses AP in the node and causes a rise of threshold of depolarization up to 200%. Changes caused by novocain are usually not completely reversible even after long wash-off. Electrical activity, depressed by novocain in the node of Ranvier restored by the action of a direct current anode. If anode voltage is sufficiently large, the AP is completely restored and the threshold of depolarization is at the same level as before. The effect of a direct current cathode is similar to that of novocain. A cathode current causes a sharp fall of AP and a considerable rise of the threshold of depolarization. The possible mechanism of the novocain action and the restorative effect of the direct current anode is discussed.(Presented by Active Member AMN SSSR A. A. Vishnevskii) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 55, No. 8, pp. 24–28, August, 1963     

The Influence of Alpha-fetoprotein on Natural Suppressor Cell Activity and Ehrlich Carcinoma Growth

The influence of alpha-fetoprotein (AFP) on the bone marrow (BM) natural suppressor (NS) cells of intact Ehrlich carcinoma -bearing CBA mice was studied. Bone marrow NS cells were fractionated into three fractions by isopycnic centrifugation on percoll gradients: NS1 (ρ=1.080 g/ml), NS2 (ρ=1.090 g/ml) and NS3 (1.100>ρ>1.090 g/ml). These fractions were highly different in their sensitivity to known NS cell inductors (interleukin (IL)-2, IL-3 or histamine). None of the NS fractions isolated from the intact mice spontaneously produced antiproliferative activity, however, they showed a high level of NS (antiproliferative and natural killer cell inhibitory) activity under the influence of AFP. A single injection of AFP to intact mice led to an increase of spontaneous NS activity and the inhibition of natural killer cell activity. NS activity, especially NS2, was increased in when tumor cells were subcutaneously inoculated three days after AFP injection. In the AFP-treated mice, the tumor mass at 14 days was 60% larger than that in the untreated mice. Our data confirmed that AFP is a tumor marker that can inhibit cancer immunity and plays a role in cancer pathogenesis.