X-ray powder diffraction data for 5,6-dihydro-3-(4-morpholinyl)-1-[4-(2-oxo-1-piperidinyl)phenyl]-2(1H)-pyridinone, C20H25N3O3, are reported [a = 5.989(2), b = 6.669(3), c = 24.605(5)Å, α = 84.466(7)°, β = 89.859(6)°, γ = 69.074(4)°, unit-cell volume V = 913.11 Å3, Z = 2, and space group P−1]. No detectable impurities were observed.

New geochronological data for the Haolibao porphyry Mo–Cu deposit, NE China, yield Permian crystallization zircon U–Pb ages of 278 ± 5 Ma for granite and 267 ± 10 Ma for the granite porphyry that hosts the Mo–Cu mineralization, and four Re–Os molybdenite ages yield an isochron age of 265 ± 3 Ma. These ages disagree with the previous K–Ar age determinations that suggest a correlation of intrusive rocks of the Haolibao area with the Yanshanian intrusive rocks of Cretaceous age. The mineralizations at the Haolibao area may be related to the tectonic–magmatic activity caused by collisional events between the North China Plate and Mongolian terranes during the Permian. The occurrence of the Haolibao plutonic rocks indicates that the Palaeo-Asian-Mongolian Ocean closed during the Permian along the Xilamulun River suture.

The Chehugou granite-hosted molybdenum deposit is typical of the Xilamulun metallogenic belt, which is an important Mo–Ag–Pb–Zn producer in China. A combination of major and trace element, Sr and Nd isotope, and zircon U–Pb isotopic data are reported for the Chehugou batholith to constrain its petrogenesis and Mo mineralization. The zircon SIMS U–Pb dating yields mean ages of 384.7 ± 4.0 Ma and 373.1 ± 5.9 Ma for monzogranite and syenogranite and 265.6 ± 3.5 Ma and 245.1 ± 4.4 Ma for syenogranite porphyry and granite porphyry, respectively. The Devonian granites are calc-alkaline with K2O/Na2O ratios of 0.44–0.52, the Permian granites are alkali-calcic with K2O/Na2O ratios of 1.13–1.25, and the Triassic granites are calc-alkaline and alkali-calcic rocks with K2O/Na2O ratios of 0.78–1.63. They are all enriched in large-ion lithophile elements (LILEs) and depleted in high-field-strength elements (HFSEs) with negative Nb and Ta anomalies in primitive mantle-normalized trace element diagrams. They have relatively high Sr (189–1256 ppm) and low Y (3.87–5.43 ppm) concentrations. The Devonian granites have relatively high initial Sr isotope ratios of 0.7100–0.7126, negative ɛNd(t) values of −12.3 to −12.4 and 206Pb/204Pb ratios of 16.46–17.50. In contrast, the Permian and Triassic granitoids have relatively low initial 87Sr/86Sr ratios (0.7048–0.7074), negative ɛNd(t) values of −10.1 to −13.1 and 206Pb/204Pb ratios of 17.23–17.51. These geochemical features suggest that the Devonian, Permian and Triassic Chehugou granitoids were derived from ancient, garnet-bearing crustal rocks related to subduction of the Palaeo-Asian Ocean and subsequent continent–continent collision between the North China and Siberian plates.

A joule level of XeF(C-A) laser optically pumped by a sectioned surface discharge was developed. The irradiative intensity of pumping source was diagnosed by calculating XeF2 photo-dissociation wave evolvement which was photographed by a framing camera. The photon flux in the wavelength region of 140 to 170nm is about 5 × 1023 photon s−1cm−2, that corresponds to the irradiative brightness temperature of more than 25000 K. The laser experiments were carried out in different conditions. The maximum laser output energy of 2.5 J was obtained with the total conversion efficiency of 0.1%.

This study reports Müller cell and neuronal changes and microglial reaction in streptozotocin-induced diabetic rats. Glial fibrillary acidic protein (GFAP) immunoreactivity was largely confined to astrocytes in the nerve fiber layer (NFL) and ganglion cell layer (GCL) in control rats. In diabetic rats especially those killed after 12 months, GFAP immunostaining could be traced along the entire length of Müller cell processes, extending from the inner to the outer limiting membrane. With the antibody neuronal nuclei, immunopositive cells were located in the GCL and the inner part of the inner nuclear layer (INL) in both diabetic and age-matched control rats. In diabetic rats, labelled cells were reduced in both layers being more marked in the INL. In age-matched control rats, OX42-immunoreactive microglial cells were distributed mainly in the NFL and GCL; some cells were localized in the inner plexiform layer, but rarely in the outer plexiform layer (OPL). Beginning 1 month after diabetes, the microglial cells appeared hypertrophic. Furthermore, microglial number as estimated from cell counts in different layers of the retina was significantly increased, with the occurrence of some cells in the OPL at 4 months. At 14 and 16 months, reactive microglial cells were detected in the outer nuclear layer and photoreceptor layer. Present results suggest that microglial reaction in induced diabetes was elicited by neuronal cell loss in both GCL and INL as well as by some pathologic changes affecting the photoreceptors.

Retinal microglia were selectively and sequentially labelled in different layers of the retina of postnatal rats following a single intravenous injection of the fluorescent dye, rhodamine isothiocyanate (RhIc). The fluorescent cells were doubly immunostained with OX-42 and ED-1 antibodies that recognise complement type 3 (CR3) receptors and macrophage antigen, respectively. RhIc was first detected in the retinal blood vessels 5 min after injection. At 1 h, a variable number of microglia in the inner layers of the retina, namely, the nerve fibre and ganglion cell layers appeared to emit weak fluorescence. Labelled microglial cells in the inner nuclear and outer plexiform layers were not detected until 1 and 2 d had elapsed following RhIc injection. The number of labelled retinal microglia was progressively increased with time, peaking at 4 d after RhIc injection. The frequency of RhIc labelled cells also increased with age, with the largest number of cells occurring in 7-d-old rats but declined thereafter. In 11 d or older rats, RhIc was confined to the retinal blood vessels. It is concluded that when injected into the circulation, RhIc could readily gain access into the retina tissues due to an inefficient blood-retina barrier in early postnatal stages. It became impeded with maturation of the blood-retina barrier, which was established between 11 and 13 d of age. RhIc that inundated the retinal tissues was thoroughly sequestered by the resident microglial cells. It is therefore suggested that the latter could play a protective role against serum-derived substances that may be deleterious to the developing retina.