Vacuum polarization and Hawking radiation

ix, 109 leaves : ill. ; 29 cmQuantum gravity is one of the interesting fields in contemporary physics which is still in progress. The purpose of quantum gravity is to present a quantum description for spacetime at 10^-33cm or find the `quanta' of gravitational interaction.. At present, the most viable theory to describe gravitational interaction is general relativity which is a classical theory. Semi-classical quantum gravity or quantum field theory in curved spacetime is an approximation to a full quantum theory of gravity. This approximation considers gravity as a classical field and matter fields are quantized. One interesting phenomena in semi-classical quantum gravity is Hawking radiation. Hawking radiation was derived by Stephen Hawking as a thermal emission of particles from the black hole horizon. In this thesis we obtain the spectrum of Hawking radiation using a new method. Vacuum is defined as the possible lowest energy state which is filled with pairs of virtual particle-antiparticle. Vacuum polarization is a consequence of pair creation in the presence of an external field such as an electromagnetic or gravitational field. Vacuum polarization in the vicinity of a black hole horizon can be interpreted as the cause of the emission from black holes known as Hawking radiation. In this thesis we try to obtain the Hawking spectrum using this approach. We re-examine vacuum polarization of a scalar field in a quasi-local volume that includes the horizon. We study the interaction of a scalar field with the background gravitational field of the black hole in the desired quasi-local region. The quasi-local volume is a hollow cylinder enclosed by two membranes, one inside the horizon and one outside the horizon. The net rate of particle emission can be obtained as the difference of the vacuum polarization from the outer boundary and inner boundary of the cylinder. Thus we found a new method to derive Hawking emission which is unitary and well defined in quantum field theory

Rosuvastatin Intervention in Patients with Chronic Hepatitis B (CHB) Expands CD14+ CD16− Classical Monocytes via Aryl Hydrocarbon Receptor (AHR)

Chronic hepatitis B (CHB) poses treatment challenges, with treatment response and disease outcome often determined by the immune response, particularly mononuclear phagocytes. Monocytes can differentiate into various subpopulations influenced by AHR. Statins, known for inflammation modulation, may impact monocyte function via AHR activation. This study explored rosuvastatin (RSV)’s effects on monocyte subtypes, inflammatory markers, and AHR in CHB patients. Fifteen CHB patients were randomly assigned to receive either 20 mg RSV or a placebo daily for three months. Flow cytometry assessed CD14+ CD16− (classical), CD14+ CD16+ (intermediate), and CD14dim CD16+ (patrolling) monocyte subtypes, along with AHR levels in each subset. ELISA quantified cytokines IL-6, IFN-γ, IL-12, IL-10, TNF-α, TGF-β, and IL-1β. RSV expanded CD14+ CD16− classical and reduced CD14+ CD16+ intermediate monocytes in CHB patients while increasing AHR+ cell percentages in all subsets. RSV treatment upregulated key AHR target genes (Cyp1a1, Cyp1b1, and ARNT), indicating robust AHR signaling activation. It also reduced pro-inflammatory cytokine levels (IL-6, IFNγ, IL-12, TNF-α) and elevated anti-inflammatory cytokines (IL-10, TGF-β). Thus, RSV may modulate the immune response by altering monocyte subtypes in CHB patients via AHR activation