When a heavy atomic nucleus splits (fission), the resulting fragments are observed to emerge spinning 1 ; this phenomenon has been a mystery in nuclear physics for over 40 years 2,3 . The internal generation of six or seven units of angular momentum in each fragment is particularly puzzling for systems that start with zero, or almost zero, spin. There are currently no experimental observations that enable decisive discrimination between the many competing theories for the mechanism that generates the angular momentum [4][5][6][7][8][9][10][11][12] . Nevertheless, the consensus is that excitation of collective vibrational modes generates the intrinsic spin before the nucleus splits (pre-scission). Here we show that there is no significant correlation between the spins of the fragment partners, which leads us to conclude that angular momentum in fission is actually generated after the nucleus splits (post-scission). We present comprehensive data showing that the average spin is strongly mass-dependent, varying in saw-tooth distributions. We observe no notable dependence of fragment spin on the mass or charge of the partner nucleus, confirming the uncorrelated post-scission nature of the spin mechanism. To explain these observations, we propose that the collective motion of nucleons in the ruptured neck of the fissioning system generates two independent torques, analogous to the snapping of an elastic band. A parameterization based on occupation of angular momentum states according to statistical theory describes the full range of experimental data well. This insight into the role of spin in nuclear fission is not only important for the fundamental understanding and theoretical description of fission, but also has consequences for the γ-ray heating problem in nuclear reactors 13,14 , for the study of the structure of neutron-rich isotopes 15,16 , and for the synthesis and stability of super-heavy elements 17,18 .

Large-scale meta-analyses of genome-wide association studies have recently confirmed that the rs340874 single-nucleotide polymorphism in PROX1 gene is associated with fasting glycemia and type 2 diabetes mellitus; however, the mechanism of this link was not well established. The aim of our study was to evaluate the functional/phenotypic differences related to rs340874 PROX1 variants. The study group comprised 945 subjects of Polish origin (including 634 with BMI > 25) without previously known dysglycemia. We analyzed behavioral patterns (diet, physical activity), body fat distribution and glucose/fat metabolism after standardized meals and during the oral glucose tolerance test. We found that the carriers of the rs340874 PROX1 CC genotype had higher nonesterified fatty acids levels after high-fat meal (p = 0.035) and lower glucose oxidation (p = 0.014) after high-carbohydrate meal in comparison with subjects with other PROX1 genotypes. Moreover, in subjects with CC variant, we found higher accumulation of visceral fat (p < 0.02), but surprisingly lower daily food consumption (p < 0.001). We hypothesize that lipid metabolism alterations in subjects with the PROX1 CC genotype may be a primary cause of higher glucose levels after glucose load, since the fatty acids can inhibit insulin-stimulated glucose uptake by decreasing carbohydrate oxidation. Our observations suggest that the PROX1 variants have pleiotropic effect on disease pathways and it seem to be a very interesting goal of research on prevention of obesity and type 2 diabetes mellitus. The study may help to understand the mechanisms of visceral obesity and type 2 diabetes mellitus risk development.

Excited states in 133 Sn were investigated through the β decay of 133 In at the ISOLDE facility. The ISOLDE Resonance Ionization Laser Ion Source (RILIS) provided isomer-selective ionization for 133 In, allowing us to study separately, and in detail, the β-decay branch of 133 In J π = (9/2 +) ground state and its J π = (1/2 −) isomer.

Obesity, influencing the increase of incidence of type 2 diabetes, cardiovascular complications and cancer is a growing medical problem worldwide. The feelings of hunger and satiety are stimulated by the “gut-brain axis”, where a crucial role is played by gastrointestinal hormones: glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, pancreatic polypeptide, peptide YY, oxyntomodulin, cholecystokinin and ghrelin. These hormones affect not only the functioning of the digestive tract, but also might have effects on insulin secretion and are mediators which affect brain areas involved in the regulation of food intake. The effect of their actions can be antagonistic as well as an additive or synergistic, and their secretion is dependent on many factors, such as dietary nutrients or the energy state of the body. Changes in circulating gut hormones concentrations result in activation of various pathways primarily within the hypothalamus and brain stem areas, which modulate feeding behaviour and a number of metabolic processes.

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