Analysis of the generation of photon pairs in periodically poled lithium niobate

The process of spontaneous parametric down-conversion (SPDC) in nonlinear crystals makes it fairly easy to generate entangled photon states. It has been known for some time that the conversion efficiency can be improved by employing quasi-phase-matching in periodically poled crystals. Using two single-photon detectors, we have analyzed the photon pairs generated by SPDC in a periodically poled lithium niobate crystal pumped by a femtosecond laser. Several parameters could be varied in our setup, allowing us to obtain data in close agreement with both thermal and Poissonian photon-pair distributions.Comment: 4 pages, 4 figures, uses ws-procs10x7.cls; v2: Sign in equation (5) correcte

Defective function of GABA-containing synaptic vesicles in mice lacking the AP-3B clathrin adaptor

AP-3 is a member of the adaptor protein (AP) complex family that regulates the vesicular transport of cargo proteins in the secretory and endocytic pathways. There are two isoforms of AP-3: the ubiquitously expressed AP-3A and the neuron-specific AP-3B. Although the physiological role of AP-3A has recently been elucidated, that of AP-3B remains unsolved. To address this question, we generated mice lacking μ3B, a subunit of AP-3B. μ3B−/− mice suffered from spontaneous epileptic seizures. Morphological abnormalities were observed at synapses in these mice. Biochemical studies demonstrated the impairment of γ-aminobutyric acid (GABA) release because of, at least in part, the reduction of vesicular GABA transporter in μ3B−/− mice. This facilitated the induction of long-term potentiation in the hippocampus and the abnormal propagation of neuronal excitability via the temporoammonic pathway. Thus, AP-3B plays a critical role in the normal formation and function of a subset of synaptic vesicles. This work adds a new aspect to the pathogenesis of epilepsy

Energetics of Nonthermal Electrons and Protons in Intense Solar Flares

Abstract We analyze Yohkoh gamma-ray energy spectra of X-class solar flares on October 27, 1991 (X6.1), November 6, 1997 (X9.4), July 14, 2000 (X5.7) and November 24, 2000 (X2.3) to study the energy content of nonthermal electrons and protons. The accelerated electron and proton spectra are derived from a spectral analysis of the continuum and lines above 1 MeV. The energy content in >1 MeV and >10 MeV protons are estimated to be 6x10 28 -4x10 30 and 2.5x10 28 -5x10 29 ergs, respectively. We study the flare to flare variation in the energy contents of > 1 MeV electrons and >10 MeV protons. Ratios of > 1 MeV electrons to >10 MeV proton energy contents vary within an order of magnitude

Role of multipotent fibroblasts in the healing colonic mucosa of rabbits. Ultrastructural and immunocytochemical study

Light- and electron microscopy and immunocytochemistry were used to study the healing colonic mucosa of rabbits after experimental excision. Between 3 and 5 days, abundant young fibroblasts which retained many features of mesenchymal cells invaded the growing capillaries into the loose connective tissue of the healing colonic mucosa. Our electron microscopy revealed the transformation of these young fibroblasts into smooth muscle cells, into histiocyte-like cells involved in phagocytotic activity, and into vasoformative cells incorporated into the growing capillaries. The mitotic proliferation of pre-existing smooth muscle cells at the ulcer margin did not seem to be the major reason for re-establishment of the muscular tissue. The present immunocytochemistry revealed an active production of fibronectin in rough endoplasmic reticulum in the young fibroblasts. This may mean that this glycoprotein is involved in the re-establishment of both connective and muscular tissues by enhancement of adhesion and chemoattractant activities of such cells. In addition, the immunoreaction of endothelial celis of the growing capillaries suggests a role of this glycoprotein in the acceleration of the neocapillarization

Hyperplastic cellular components of a hemangiopericytoma. An ultrastructural study

Based on ultrastructural features of cellular components of a hemangiopericytoma, hyperplastic cells are classifiable into fibroblast-like (group 1), endotheloid (group 11) and pericyte-like (group 111) cells. The transformation of the group 1 cells to the group 11, or to the group 111 cells, is pronounced in our electron micrographs and this may imply that the group 1 cell is the principal cell of origin in this neoplasm. The smooth muscle-like (group IV) cells comprising the media of the arteries and veins in this neoplasm may represent modified, possibly de-differentiated smooth muscle cells reacted to the neoplastic proliferation of the surrounding adventitial (group 1) cells

The toxic effects of bis (tributyltin) oxide on the rat thoracic aorta

The toxic effects of bis (tributyltin) oxide (TBTO) on the ultrastructure and permeability of rat thoracic aorta were studied electron microscopically and the accumulation sites of tin were determined with an X-ray microanalyzer. Male Wistar rats received O.O5ml/kg of TBTO as an emulsion in 1 m1 of distilled water througb a stomach tube. After time intervals of 2, 4, 6, 8, 10, 12 h after intubation, thoracic aortae were isolated and prepared for electron microscopy. Marked swelling of mitochondria in the aortic endothelial cells appeared at 4 h after TBTO treatment. By x-ray microanalysis, tin L-a peaks (3.44 keV) were obtained from these swollen mitochondria. Subendothelial edema progressed between 6 and 8 h after TBTO treatment. By tracer experiment, it was seen that large amounts of peroxidase reaction products filled the expanded subendothelial space. At 12 h after TBTO treatment, degenerative changes of the endothelial cells were prominent. These results indicated that orally administered TBTO accumulated in the mitochondria of the endothelial cells of thoracic aorta. The direct toxic effects of TBTO on mitochondria might induce severe damage to the endothelial cells and cause disturbance of the permeability barrier function of the endothelial layer and subendothelial edema