The emission factors for indoor straw combustion are a major data gap for estimating the polycyclic aromatic hydrocarbon (PAH) emissions in China. The emission factors for open-fire straw burning were borrowed from our previous study and a rough estimate was developed. As one of the most important emission sources in China, the emission factors for indoor straw combustion needed to be determined and revised accurately. In this study, a representative straw in rural China was collected and burned in similar conditions with those used by countryside families. The smoke produced was sampled and the PAH concentrations were analyzed by gas chromatography-mass selective detection (GC-MSD), and much higher emission factors were found. Based on the newly measured emission factors, the emission amount from indoor straw combustion was updated. In addition, recently published emission factors were compiled in a comprehensive database and some new sources were included. Additionally, the emission inventory was extended to cover the period from 1950 to 2005 and upgraded to a scale resolution of one kilometer. In the updated inventory, the total quantity of 16 PAHs emitted from China was 116,000 tons in 2003, with indoor straw and firewood combustions as the most important sources. Although vehicular emission contributed a relatively small percentage of the total emission, it was still one of the major sources in the urban areas of China. The total PAH emission increased continuously for four decades, starting from 1950, but fluctuated since 1990 due to variations in coke production.

Context The Amur tiger and leopard, once roaming over the Eurasian continent, are now endangered and confined to the Sikhote-Alin Mountains, Russia-a landscape that has been increasingly fragmented due to human activities. The ultimate fate of these big cats depends on whether they can resettle in their previous main historical range in NE China. Recent sightings of these animals along the China-Russia border have aroused new hope, but direct evidence is lacking.Objectives The main objectives of our study were (1) to determine the abundance and spatiotemporal patterns of tigers, leopards, and primary prey; (2) to investigate factors influencing the resettlement of the two big cats; and (3) to propose a landscape-scale conservation plan to secure the long-term sustainability of the Amur tiger and leopard. Methods We monitored the two felids, their prey, and human activities, with 380 camera-trap stations, for a total of 175,127 trap days and over an area of 6000 km 2 in NE China. We used the constraint line method to characterize cattle grazing and human influences on tigers, leopards, and their prey species.Tianming Wang and Limin Feng contributed equally to this work.

Multiple Ca2+ channels confer diverse functions to hair cells of the auditory and vestibular organs in the mammalian inner ear. We used gene-targeting technology to generate a 1D Ca 2+ channel-deficient mice to determine the physiological role of these Ca 2+ channels in hearing and balance. Analyses of auditory-evoked brainstem recordings confirmed that a 1D )/) mice were deaf and revealed that heterozygous (a 1D +/) ) mice have increased hearing thresholds. However, hearing deficits in a 1D +/) mice were manifested mainly by the increase in threshold of low-frequency sounds. In contrast to impaired hearing, a 1D )/) mice have balance performances equivalent to their wild-type littermates. Light and electron microscope analyses of the inner ear revealed outer hair cell loss at the apical cochlea, but no apparent abnormality at the basal cochlea and the vestibule. We determined the mechanisms underlying the auditory function defects and the normal vestibular functions by examining the Ba 2+ currents in cochlear inner and outer hair cells versus utricular hair cells in a 1D +/) mice. Whereas the whole-cell Ba 2+ currents in inner hair cells consist mainly of the nimodipine-sensitive current (85%), the utricular hair cells express only 50% of this channel subtype. Thus, differential expression of a 1D channels in the cochlear and utricular hair cells confers the phenotype of the a 1D null mutant mice. Because vestibular and cochlear hair cells share common features and null deletion of several genes have yielded both deafness and imbalance in mice, a 1D null mutant mice may serve as a model to disentangle vestibular from auditory-specific functions.

The contamination and outflow of atmospheric polycyclic aromatic hydrocarbons (PAHs) in the Chinese Northern Plain, a region with a total area of 300 000 km2 and a high PAH emission density, were investigated. Polyurethane foam (PUF) and PM10 samples were collected at 46 sites located in urban, rural (towns or villages), and control (remote mountain) areas in the winter from November 2005 to February 2006. The observed concentrations of atmospheric PAHs were generally higher than those reported for developed countries and southern Chinese cities. It was found that there was no significant difference in air PAH concentrations between the urban and the rural areas (514 +/- 563 ng/m3 and 610 +/- 645 ng/ m3, respectively), while the PAH concentrations at the control sites (57.1 +/- 12.6 ng/m3) were 1 order of magnitude lower than those at the other sites. The primary reason for the similarity in PAH concentrations between urban and rural areas was the fact that the predominant sources of biomass and domestic coal combustion were widely spread over the study area. The partition constants (K(PM10)) of PAHs were significantly correlated to the corresponding values of subcooled liquid-vapor pressure (pL0). However, the regression slopes of log K(PM10) versus log pL0 were much steeper than -1, indicating adsorption dominated over absorption. Three distinct patterns of outflow from the study area were identified by forward trajectory and cluster analysis.

Figure 1Derivation and characterization of cloned piglets from piPSCs. (A) Preimplantation and post-implantation development of the cloned embryos from piPSCs. Embryos at two-cell (a), four-cell (b), eight-cell (c), blastocyst stages (d, e) and two 36 day-old cloned fetuses (f) are shown. Scale bars are 100 μm. (B) The morphology and fluorescence of the hooves (left), tails (middle) and fibroblasts (right) of the 36 day-old embryos. Scale bars are 100 μm. (C) The morphology, fluorescence and hematoxylin/eosin-stained sections of tissues from piglet 00536-3#. Scale bars are 100 μm. (D) Cloned piglets. 00507-4# from differentiated iPF4-2 cell, 4 days old; 227-1#, 2#, 3# from undifferentiated iPF4-2, 2 days old. (E) Porcine ear fibroblasts (PEFs) from 00507-4#, EGFP positive. Scale bars are 100 μm. (F) PCR demonstrating genomic integration of Oct4, Sox2, and EGFP using tissues of the cloned fetuses and piglets. PEF, the original fibroblasts used to create iPF4-2. 00518, 00536, 00507, 227, foster mothers. 00518-1#, 00518-2#, the cloned fetuses derived from differentiated iPF4-2 cells. 00536-3# , 00507-4#, the cloned piglets derived from iPF4-2-differentiated cells. 227-1#~4#, the HMC piglets derived from iPF4-2. (G) Microsatellite analysis of the donor piPSC line iPF4-2, cloned fetuses and piglets. 00518, 00536, 00507, 227, foster mothers; 00518-1# and 00518-2#, cloned fetuses; 00536-3# and 00507-4#, the cloned piglets from differentiated iPF4-2 cells; 227-1#~4#, the cloned piglets derived from the Scriptaid-treated NT embryos from iPF4-2 cells.www.cell-research.com | Cell Research Nana Fan et al. 165npg

No abstract

NMDA receptor dysfunction may be involved in the pathophysiology of schizophrenia. Based on this hypothesis, we screened 48 Japanese patients with schizophrenia for mutations in the coding region of the NMDAR2B subunit gene (GRIN2B). An association study between the identified DNA sequence variants and schizophrenia was performed in 268 Japanese patients with schizophrenia and 337 Japanese control subjects. Eight single nucleotide polymorphisms were detected, all of which were synonymous. The association sample showed statistically significant excesses of homozygosity for the polymorphisms in the 3' region of the last exon in the patients with schizophrenia (P = 0.004) and higher frequency of the G allele of the 366C/G polymorphism (corrected P = 0.04) in the patients than in the controls. Although we did not detect NMDAR2B protein variants, our findings support the possibility that the GRIN2B gene or a locus in linkage disequilibrium with it may confer susceptibility to schizophrenia. Replication studies in independent samples are warranted. Molecular Psychiatry (2001) 6, 211-216.The glutamate dysfunction hypothesis is one of the main explanatory hypotheses for the pathophysiology of schizophrenia. It originated from the observation that phencyclidine (PCP) intoxication closely mimics schizophrenia. 1 At serum levels that produce schizophrenic symptoms, PCP acts as a noncompetitive antagonist of the N-methyl-d-aspartate (NMDA) receptors. 2 Ketamine and MK-801, two additional noncompetitive antagonists of NMDA receptors, also produce schizophrenic symptoms and exacerbate symptoms in patients with schizophrenia. [3][4][5] NMDA receptors, together with alpha-amino-3-hydroxy-5-methyl-4-isozaxole propionic acid (AMPA) and kainate receptors, comprise the known ionotropic glutamate receptors. 6 Functional NMDA receptors are composed of a common NMDAR1 subunit and one of four NMDAR2 subunits (NMDAR2A-NMDAR2D) combined in an undetermined ratio to make the heteromeric receptor complex. 7,8 Knockout mice lacking each of the known NMDA receptor subunits have been generated. 9-15 Mice lacking NMDAR1 or NMDAR2B protein die perinatally, 9,10,14 knockdown mice expressing only 5% of normal levels of the essential NMDAR1 subunit survive to adulthood but display behavioral abnormalities including increased motor activity and stereotypy and deficits in social and sexual interactions. These behavioral alterations are similar to those observed in pharmacologically induced animal models of schizophrenia and can be ameliorated by treatment with haloperidol or clozapine. These findings support a model in which reduced NMDA receptor activity results in schizophrenic-like behavior. 16 NMDAR2B mRNA is found throughout the entire embryonic brain in mice, but its expression becomes restricted to the forebrain postnatally. 17,18 There is a high degree of regional specialization with respect to specific NMDA receptors within the basal ganglia, and NMDAR2B is abundant in the striatum. 19 NMDAR2B mRNA expression is regulated by cortico-striata...

Prior studies have shown that kreisler mutants display early inner ear defects that are related to abnormal hindbrain development and signaling. These defects in kreisler mice have been linked to mutation of the kr/mafB gene. To investigate potential relevance of kr/mafB and abnormal hindbrain development in inner ear patterning, we analyzed the ear morphogenesis in kreisler mice using a paint-fill technique. We also examined the expression patterns of a battery of genes important for normal inner ear patterning and development. Our results indicate that the loss of dorsal otic structures such as the endolymphatic duct and sac is attributable to the downregulation of Gbx2, Dlx5 and Wnt2b in the dorsal region of the otocyst. In contrast, the expanded expression domain of Otx2 in the ventral otic region likely contributes to the cochlear phenotype seen in kreisler mutants. Sensory organ development is also markedly disrupted in kreisler mutants. This pattern of defects and gene expression changes is remarkably similar to that observed in Gbx2 mutants. Taken together, the data show an important role for hindbrain cues, and indirectly, kr/mafB, in guiding inner ear morphogenesis. The data also identify Gbx2, Dlx5, Wnt2b and Otx2 as key otic genes ultimately affected by perturbation of the kr/mafB-hindbrain pathway.