Research in theoretical nuclear physics. Final report, April 1, 1993--March 31, 1996

This report describes the accomplishments in basic research in nuclear physics carried out by the theoretical nuclear physics group in the Department of Physics at the University of Texas at Austin, during the period of April 1, 1993 to March 31, 1996. The work done covers three separate areas, low energy nuclear reactions, intermediate energy physics, and nuclear structure studies. Although the various subjects are spread among different areas, they are all based on two techniques that they have developed in previous years. These techniques are: (a) a powerful method for continuum-random-phase-approximation (CRPA) calculations of the nuclear response; and, (b) the direct reaction approach to complete and incomplete fusion reactions, which enables them to describe on a single footing all the different types of nuclear reactions, i.e., complete fusion, incomplete fusion and direct reactions, in a systematic way based on a single theoretical framework. In this report, the authors first summarize their achievements in these three areas, and then present final remarks

Can only flavor-nonsinglet H dibaryons be stable against strong decays?

Using the QCD sum rule approach, we show that the flavor-nonsinglet $H$ dibaryon states with J$^{\pi} = 1^+$, J$^{\pi} = 0^+$, I=1 (27plet) are nearly degenerate with the J$^{\pi} = 0^+$, I=0 singlet $H_0$ dibaryon, which has been predicted to be stable against strong decay, but has not been observed. Our calculation, which does not require an instanton correction, suggests that the $H_0$ is slightly heavier than these flavor-nonsinglet $H$s over a wide range of the parameter space. If the singlet $H_0$ mass lies above the $\Lambda \Lambda$ threshold (2231~MeV), then the strong interaction breakup to $\Lambda \Lambda$ would produce a very broad resonance in the $\Lambda \Lambda$ invariant mass spectrum which would be very difficult to observe. On the other hand, if these flavor-nonsinglet J=0 and 1 $H$ dibaryons are also above the $\Lambda \Lambda$ threshold, but below the $\Xi^0n$ breakup threshold (2254 MeV), then because the direct, strong interaction decay to the $\Lambda \Lambda$ channel is forbidden, these flavor-nonsinglet states might be more amenable to experimental observation. The present results allow a possible reconciliation between the reported observation of $\Lambda \Lambda$ hypernuclei, which argue against a stable $H_0$, and the possible existence of $H$ dibaryons in general.Comment: 10 pages, 2 figure

Non-local spin correlation as a signature of Ising anyons trapped in vacancies of the Kitaev spin liquid

In the Kitaev chiral spin liquid, Ising anyons are realized as Majorana zero modes bound in $Z_2$ fluxes, which, however, are thermal excitations with finite decay rates. On the other hand, a lattice vacancy traps a $Z_2$ flux even in the ground state, resulting in the stable realization of a Majorana zero mode in the $Z_2$ flux. We demonstrate that spin-spin correlation functions between two vacancy sites exhibit long-range correlation arising from the fractionalized character of Majorana zero modes, in spite of the strong decay of bulk spin correlations. Remarkably, this non-local spin correlation does not decrease as the distance between two vacancy sites increases, signaling teleportation of Majorana zero modes. Furthermore, we clarify that the non-local correlation can be detected electrically via the measurement of non-local conductance between two vacancy sites, which is also utilized for the readout of Majorana qubits. These findings pave the way to the measurement-based quantum computation with Ising anyons trapped in vacancies of the Kitaev spin liquid.Comment: 6 pages + 4 figures, and a Supplemental Materia

Administration route-dependent induction of antitumor immunity by interferon-alpha gene transfer.

Type I interferon (IFN) protein is a cytokine with pleiotropic biological functions that include induction of apoptosis, inhibition of angiogenesis, and immunomodulation. We have demonstrated that intratumoral injection of an IFN-α-expressing adenovirus effectively induces cell death of cancer cells and elicits a systemic tumor-specific immunity in several animal models. On the other hand, reports demonstrated that an elevation of IFN in the serum following an intramuscular delivery of a vector is able to activate antitumor immunity. In this study, we compared the intratumoral and systemic routes of IFN gene transfer with regard to the effect and safety of the treatment. Intratumoral injection of an IFN-α adenovirus effectively activated tumor-responsive lymphocytes and caused tumor suppression not only in the gene-transduced tumors but also in distant tumors, which was more effective than the intravenous administration of the same vector. The expression of co-stimulatory molecules on CD11c+ cells isolated from regional lymph nodes was enhanced by IFN gene transfer into the tumors. Systemic toxicity such as an elevation of hepatic enzymes was much lower in mice treated by intratumoral gene transfer than in those treated by systemic gene transfer. Our data suggest that the intratumoral route of the IFN vector is superior to intravenous administration, due to the effective induction of antitumor immunity and the lower toxicity. © 2010 Japanese Cancer Association

Osteogenic Factor Runx2 Marks a Subset of Leptin Receptor-Positive Cells that Sit Atop the Bone Marrow Stromal Cell Hierarchy

Bone marrow mesenchymal stem and progenitor cells (BM-MSPCs) maintain homeostasis of bone tissue by providing osteoblasts. Although several markers have been identified for labeling of MSPCs, these labeled cells still contain non-BM-MSPC populations. Studies have suggested that MSPCs are observed as leptin receptor (LepR)-positive cells, whereas osteoblasts can be classified as positive for Runx2, a master regulator for osteoblastogenesis. Here, we demonstrate, using Runx2-GFP reporter mice,that the LepR-labeled population contains Runx2-GFPlow sub-population, which possesses higher fibroblastic colony-forming units (CFUs) and mesensphere capacity, criteria for assessing stem cell activity, than the Runx2-GFP− population. In response to parathyroid hormone (PTH), a bone anabolic hormone, LepR+Runx2-GFPlow cells increase Runx2 expression and form multilayered structures near the bone surface. Subsequently, the multilayered cells express Osterix and Type I collagen α, resulting in generation of mature osteoblasts. Therefore, our results indicate that Runx2 is weakly expressed in the LepR+ population without osteoblastic commitment, and the LepR+Runx2-GFPlow stromal cells sit atop the BM stromal hierarchy

Hyperglycemia Induces Skin Barrier Dysfunctions with Impairment of Epidermal Integrity in Non-Wounded Skin of Type 1 Diabetic Mice.

Diabetes causes skin complications, including xerosis and foot ulcers. Ulcers complicated by infections exacerbate skin conditions, and in severe cases, limb/toe amputations are required to prevent the development of sepsis. Here, we hypothesize that hyperglycemia induces skin barrier dysfunction with alterations of epidermal integrity. The effects of hyperglycemia on the epidermis were examined in streptozotocin-induced diabetic mice with/without insulin therapy. The results showed that dye leakages were prominent, and transepidermal water loss after tape stripping was exacerbated in diabetic mice. These data indicate that hyperglycemia impaired skin barrier functions. Additionally, the distribution of the protein associated with the tight junction structure, tight junction protein-1 (ZO-1), was characterized by diffuse and significantly wider expression in the diabetic mice compared to that in the control mice. In turn, epidermal cell number was significantly reduced and basal cells were irregularly aligned with ultrastructural alterations in diabetic mice. In contrast, the number of corneocytes, namely, denucleated and terminally differentiated keratinocytes significantly increased, while their sensitivity to mechanical stress was enhanced in the diabetic mice. We found that cell proliferation was significantly decreased, while apoptotic cells were comparable in the skin of diabetic mice, compared to those in the control mice. In the epidermis, Keratin 5 and keratin 14 expressions were reduced, while keratin 10 and loricrin were ectopically induced in diabetic mice. These data suggest that hyperglycemia altered keratinocyte proliferation/differentiation. Finally, these phenotypes observed in diabetic mice were mitigated by insulin treatment. Reduction in basal cell number and perturbation of the proliferation/differentiation process could be the underlying mechanisms for impaired skin barrier functions in diabetic mice