The general phenomenon of shell structure in atomic nuclei has been understood since the pioneering work of Goeppert-Mayer, Haxel, Jensen and Suess.They realized that the experimental evidence for ...nuclear magic numbers could be explained by introducing a strong spin-orbit interaction in the nuclear shell model potential. However, our detailed knowledge of nuclear forces and the mechanisms governing the structure of nuclei, in particular far from stability, is still incomplete. In nuclei with equal neutron and proton numbers (\(N = Z\)), the unique nature of the atomic nucleus as an object composed of two distinct types of fermions can be expressed as enhanced correlations arising between neutrons and protons occupying orbitals with the same quantum numbers. Such correlations have been predicted to favor a new type of nuclear superfluidity; isoscalar neutron-proton pairing, in addition to normal isovector pairing (see Fig. 1). Despite many experimental efforts these predictions have not been confirmed. Here, we report on the first observation of excited states in \(N = Z = 46\) nucleus \(^{92}\)Pd. Gamma rays emitted following the \(^{58}\)Ni(\(^{36}\)Ar,2\(n\))\(^{92}\)Pd fusion-evaporation reaction were identified using a combination of state-of-the-art high-resolution {\gamma}-ray, charged-particle and neutron detector systems. Our results reveal evidence for a spin-aligned, isoscalar neutron-proton coupling scheme, different from the previous prediction. We suggest that this coupling scheme replaces normal superfluidity (characterized by seniority coupling) in the ground and low-lying excited states of the heaviest N = Z nuclei. The strong isoscalar neutron- proton correlations in these \(N = Z\) nuclei are predicted to have a considerable impact on their level structures, and to influence the dynamics of the stellar rapid proton capture nucleosynthesis process.
Many researchers are now focusing on ways in which the renin‐angiotensin system (RAS) and RAS gene polymorphism affect progressive renal damage, hypertension, cardiac complications, and renal ...allograft function. In this study, we investigated the frequency of polymorphism in the genes for angiotensin‐converting enzyme (ACE), angiotensinogen (AGT), angiotensin II type 1 and 2 receptors (AT1 and AT2), and endothelial nitric oxide synthase (ec‐NOS) in Turkish renal transplant recipients. Angiotensin‐converting enzyme insertion/deletion (I/D) polymorphism was assessed in 125 patients. M235T polymorphism of the angiotensinogen gene, 1166 A/C polymorphism of the AT1 receptor gene, and 3123C/A polymorphism of the AT2 receptor gene, and intron 4 VNTR polymorphism in the ec‐NOS gene were assessed in 40 of the patients. The latter list was also investigated in 50 healthy controls from the general Turkish population. DD/ID/II genotypes of the ACE gene were detected in 56%, 34%, and 10% of the kidney recipient group, respectively. In the 40 recipients who were tested for the other polymorphisms, the corresponding figures for the AGT TT/TM/MM genotypes were 0%, 82.5%, and 17.5%, respectively; for the AT1 CC/CA/AA genotypes were 0%, 2.5%, and 97.5%, respectively; for the AT2 AA/CA/CC genotypes were 0%, 0%, and 100%, respectively; and for the ec‐NOS intron 4 aa/ab/bb genotypes were 0%, 12%, and 88%, respectively. The results revealed that Turkish renal transplant recipients exhibit a wide‐range of RAS gene and ec‐NOS polymorphisms.
Chronic allograft dysfunction (CAD) is a complex phenomenon caused by underlying kidney disease and superimposed environmental and genetic factors. We investigated the relationship between ...polymorphism in the gene encoding for angiotensin‐converting enzyme (ACE) and CAD in renal transplant recipients. The study included 125 patients who underwent transplantation over a 5‐year period. The following information was collected for each case: date of transplantation, age and sex of donor and recipient, donor type, cold ischemia time, number of HLA mismatches, number of acute‐rejection episodes, and laboratory findings at discharge from hospital and annual rechecks. Blood pressure was measured at yearly intervals throughout the follow up. DNA isolated from mononuclear cells in peripheral blood was used as a template for amplification of insertion/deletion (I/D) polymorphism in the ACE gene by polymerase chain reaction. The proportions of patients with the different genotypes were DD=54.4%, ID=33.6%, and II=12%. Chronic allograft dysfunction was detected in 36 (52.9%) of the recipients with DD genotype and 15 (26.3%) of those with ID or II genotypes (P<0.003). Analysis of the major risk factors for CAD showed that the serum creatinine level at the time of hospital discharge, the cadaveric donor type, the ACE DD genotype, and the level of proteinuria at 1 year post‐transplantation were associated with poorer renal function (P<0.05). These findings suggest that the DD variant of ACE I/D gene polymorphism is associated with an increased risk of developing CAD.
