贵州贞丰县水银洞金矿床成矿特征和金的超常富集机制研究

黔西南地区是我国最重要的卡林型金矿床集中区，在该区卡林型金矿床具有断裂型和层控型两大类。断裂型金矿床产于高角度压扭性断裂中，赋矿层位一般为中、下三叠统地层，容矿岩石主要是泥质粉砂岩和粉砂质泥岩。层控型金矿床主要产于上二叠统地层中，容矿岩石主要是不纯的生物碎屑灰岩，背斜控矿明显。由于目前断裂型金矿一研究程度高，而层控型金矿研究程度低．近年来在层控型金矿床中一些大型和特大型矿床以及富矿体和高拮位矿石的新发现，使层控型金矿床成为黔西南卡林型金矿床的重要和具有特征的类型。因此，作者选择了水银洞金矿床这个大型较富的一卜林型金矿床进行系统研究，对其成矿特征和金的超常富集机制获得以下认识：1．金矿床受构造与有利岩性组合的双重控制。金矿床位于灰家堡背斜核部，矿体产在粘土岩叶灰岩一粘土岩组合之灰岩中，以层状·似层状为主。一些低角度的断层控制了少量的断裂型金矿体。2．金矿床具有低温成矿特征，主成矿期流体包裹体的均一温度2约℃士，出现硅化、白云右化、黄铁矿化和粘土化等围岩蚀变，特征的Au-As-11g-Tl元素组合。矿石中Au主要不均匀分布在富砷环带中。纳米金可能是水银洞金矿床金的主要存在形式，并且快速沉淀在几个微米宽的细小黄铁矿中的砷黄铁矿环带和几一卜微米小的热液毒砂中。成矿条件的骤变和黄铁矿的吸附是重要因素。3．成矿流体具有低温低盐度和较高压力和富挥发份的特点，均一温度在220 ℃士，盐度在6士W七％NoCI、，压力为1．6士0．4Kbal＂s，在Vc，I4＋限川j』包裹体中Cll。含量高达63mole％、N：为18nlole％、C0；为19mole％。高压和富挥发份促使成矿流体从深部迁移至控矿背斜核部，并由于断层的作用挥发份的快速逃逸，压力骤降，促使流体快速卸载，一形成金的快速沉淀，形成微细浸染壮的原生金矿石：4．成矿物质主要来自深部。系卿勺岩矿地球化学研究和同位素示踪显示断，成矿一物质可能是燕山期构造岩浆活动形成的成矿流体（慢源铅）上升溶解地壳铅和混入地壳淋滤错大而形成的壳物质的混合；容矿地层均为正常沉积作用形成，． 没有发现具有特殊意义的沉积层（矿源层）；成矿特征元素Au、As、51。、Tl和伴生的其他热液活动元素来自热液的带入，没有证据显示出地层岩石中有大规模的成矿元素迁出。5．区域＿日也壳的活动性，长时期的热状态，有利于大范围内形成超压成矿流体。而地壳的伸展拉张促使了基底早己有的断裂再度复活，并与成矿期断裂一起切穿地壳，为深部超压成矿流体涌入成矿体系提供了必要的通道和热动力条件，使断裂系统就象抽水泵一样，汇聚成矿流体进入地壳上部成矿体系。由于本地区浅层构造的复杂性，导致成矿现象复杂多样，常形成而状矿化，大区域上呈“金三角”。不象羊国西部地区卡林型金矿产出区，金矿在区域上呈线形分布,众多超大型金矿被发现。

黔滇地区富（含）铊矿床的低温地球化学及其环境效应研究

铊是一种低温元素，可形成富铊矿床。主要呈独立矿物红铊矿、斜硫砷系铊矿、Imhofite等形式存在。在卡林型金矿中Aa-Tl关系密切。流体包裹体、稳定同位素稀土元素地球化学，成矿模拟实验研究表明：富铊矿床的成矿流体主要来自大气降水和地层中的热卤水，成矿物质主要来源于地层，部分可能来自深部。从而建立了富（含）铊矿床形成的三阶段成矿模式。铊的环境地球化学研究表明，富铊矿床的开发利用是导致环境铊污染和地方性锭中毒的原因。

On the evaluation of diffusivities in gels using the diffusion cell technique

Modeling of the gel-immobilized cell system requires accurate measurement of diffusion coefficients. Three methods of the quasi-steady-state (QSS) method, the time-lag (TL) method and a variant quasi-steady-state (VQSS) method were critically assessed and compared for the evaluation of diffusivities using the diffusion cell technique. Experimental data from our laboratory were used for the analysis of the influence of crucial theoretical assumptions not being fulfilled in each method. The results highlighted a risk in obtaining highly variable diffusion coefficients by not validating the QSS and the accuracy of the measurements. In the TL method, the estimation of diffusivities based on the plot intercept that was mostly used in the literature, results in a many fold lower value when compared to that based on the plot slope. The comparison with the QSS and VQSS methods confirmed similar diffusivity obtained by the TL method based on the plot slope. It thus suggested that the correct estimation of diffusivities by the TL method could be based on the plot slope only. Furthermore, the errors associated with the solute mass in the gel, the sample withdrawal and the non-negligible concentration changes in the chambers were also discussed. It is concluded that diffusion cell technique has to be employed cautiously for a correct evaluation of diffusivities. (C) 2001 Elsevier Science B.V. All rights reserved.

Study abroad and complexity, accuracy and fluency (CAF) development: a longitudinal investigation of French and Chinese Learners of L2 English

This longitudinal study tracked third-level French (n=10) and Chinese (n=7) learners of English as a second language (L2) during an eight-month study abroad (SA) period at an Irish university. The investigation sought to determine whether there was a significant relationship between length of stay (LoS) abroad and gains in the learners' oral complexity, accuracy and fluency (CAF), what the relationship was between these three language constructs and whether the two learner groups would experience similar paths to development. Additionally, the study also investigated whether specific reported out-of-class contact with the L2 was implicated in oral CAF gains. Oral data were collected at three equidistant time points; at the beginning of SA (T1), midway through the SA sojourn (T2) and at the end (T3), allowing for a comparison of CAF gains arising during one semester abroad to those arising during a subsequent semester. Data were collected using Sociolinguistic Interviews (Labov, 1984) and adapted versions of the Language Contact Profile (Freed et al., 2004). Overall, the results point to LoS abroad as a highly influential variable in gains to be expected in oral CAF during SA. While one semester in the TL country was not enough to foster statistically significant improvement in any of the CAF measures employed, significant improvement was found during the second semester of SA. Significant differences were also revealed between the two learner groups. Finally, significant correlations, some positive, some negative, were found between gains in CAF and specific usage of the L2. All in all, the disaggregation of the group data clearly illustrates, in line with other recent enquiries (e.g. Wright and Cong, 2014) that each individual learner's path to CAF development was unique and highly individualised, thus providing strong evidence for the recent claim that SLA is "an individualized nonlinear endeavor" (Polat and Kim, 2014: 186).

Expert assessments of retrofitting coal-fired power plants with carbon dioxide capture technologies

A set of 13 US based experts in post-combustion and oxy-fuel combustion CO2 capture systems responded to an extensive questionnaire asking their views on the present status and future expected performance and costs for amine-based, chilled ammonia, and oxy-combustion retrofits of coal-fired power plants. This paper presents the experts' responses for technology maturity, ideal plant characteristics for early adopters, and the extent to which R&D and deployment incentives will impact costs. It also presents the best estimates and 95% confidence limits of the energy penalties associated with amine-based systems. The results show a general consensus that amine-based systems are closer to commercial application, but potential for improving performance and lowering costs is limited; chilled ammonia and oxy-combustion offer greater potential for cost reductions, but not without greater uncertainty regarding scale and technical feasibility. © 2011 Elsevier Ltd.

Unrecognized pretransplant and donor‐derived cryptococcal disease in organ transplant recipients.

BACKGROUND: Cryptococcosis occurring ≤30 days after transplantation is an unusual event, and its characteristics are not known. METHODS: Patients included 175 solid-organ transplant (SOT) recipients with cryptococcosis in a multicenter cohort. Very early-onset and late-onset cryptococcosis were defined as disease occurring ≤30 days or >30 days after transplantation, respectively. RESULTS: Very early-onset disease developed in 9 (5%) of the 175 patients at a mean of 5.7 days after transplantation. Overall, 55.6% (5 of 9) of the patients with very early-onset disease versus 25.9% (43 of 166) of the patients with late-onset disease were liver transplant recipients (P = .05). Very early cases were more likely to present with disease at unusual locations, including transplanted allograft and surgical fossa/site infections (55.6% vs 7.2%; P < .001). Two very early cases with onset on day 1 after transplantation (in a liver transplant recipient with Cryptococcus isolated from the lung and a heart transplant recipient with fungemia) likely were the result of undetected pretransplant disease. An additional 5 cases involving the allograft or surgical sites were likely the result of donor‐acquired infection. CONCLUSIONS: A subset of SOT recipients with cryptococcosis present very early after transplantation with disease that appears to occur preferentially in liver transplant recipients and involves unusual sites, such as the transplanted organ or the surgical site. These patients may have unrecognized pretransplant or donor-derived cryptococcosis.

Yeast screens identify the RNA polymerase II CTD and SPT5 as relevant targets of BRCA1 interaction.

BRCA1 has been implicated in numerous DNA repair pathways that maintain genome integrity, however the function responsible for its tumor suppressor activity in breast cancer remains obscure. To identify the most highly conserved of the many BRCA1 functions, we screened the evolutionarily distant eukaryote Saccharomyces cerevisiae for mutants that suppressed the G1 checkpoint arrest and lethality induced following heterologous BRCA1 expression. A genome-wide screen in the diploid deletion collection combined with a screen of ionizing radiation sensitive gene deletions identified mutants that permit growth in the presence of BRCA1. These genes delineate a metabolic mRNA pathway that temporally links transcription elongation (SPT4, SPT5, CTK1, DEF1) to nucleopore-mediated mRNA export (ASM4, MLP1, MLP2, NUP2, NUP53, NUP120, NUP133, NUP170, NUP188, POM34) and cytoplasmic mRNA decay at P-bodies (CCR4, DHH1). Strikingly, BRCA1 interacted with the phosphorylated RNA polymerase II (RNAPII) carboxy terminal domain (P-CTD), phosphorylated in the pattern specified by the CTDK-I kinase, to induce DEF1-dependent cleavage and accumulation of a RNAPII fragment containing the P-CTD. Significantly, breast cancer associated BRCT domain defects in BRCA1 that suppressed P-CTD cleavage and lethality in yeast also suppressed the physical interaction of BRCA1 with human SPT5 in breast epithelial cells, thus confirming SPT5 as a relevant target of BRCA1 interaction. Furthermore, enhanced P-CTD cleavage was observed in both yeast and human breast cells following UV-irradiation indicating a conserved eukaryotic damage response. Moreover, P-CTD cleavage in breast epithelial cells was BRCA1-dependent since damage-induced P-CTD cleavage was only observed in the mutant BRCA1 cell line HCC1937 following ectopic expression of wild type BRCA1. Finally, BRCA1, SPT5 and hyperphosphorylated RPB1 form a complex that was rapidly degraded following MMS treatment in wild type but not BRCA1 mutant breast cells. These results extend the mechanistic links between BRCA1 and transcriptional consequences in response to DNA damage and suggest an important role for RNAPII P-CTD cleavage in BRCA1-mediated cancer suppression.

Spike avalanches exhibit universal dynamics across the sleep-wake cycle.

BACKGROUND: Scale-invariant neuronal avalanches have been observed in cell cultures and slices as well as anesthetized and awake brains, suggesting that the brain operates near criticality, i.e. within a narrow margin between avalanche propagation and extinction. In theory, criticality provides many desirable features for the behaving brain, optimizing computational capabilities, information transmission, sensitivity to sensory stimuli and size of memory repertoires. However, a thorough characterization of neuronal avalanches in freely-behaving (FB) animals is still missing, thus raising doubts about their relevance for brain function. METHODOLOGY/PRINCIPAL FINDINGS: To address this issue, we employed chronically implanted multielectrode arrays (MEA) to record avalanches of action potentials (spikes) from the cerebral cortex and hippocampus of 14 rats, as they spontaneously traversed the wake-sleep cycle, explored novel objects or were subjected to anesthesia (AN). We then modeled spike avalanches to evaluate the impact of sparse MEA sampling on their statistics. We found that the size distribution of spike avalanches are well fit by lognormal distributions in FB animals, and by truncated power laws in the AN group. FB data surrogation markedly decreases the tail of the distribution, i.e. spike shuffling destroys the largest avalanches. The FB data are also characterized by multiple key features compatible with criticality in the temporal domain, such as 1/f spectra and long-term correlations as measured by detrended fluctuation analysis. These signatures are very stable across waking, slow-wave sleep and rapid-eye-movement sleep, but collapse during anesthesia. Likewise, waiting time distributions obey a single scaling function during all natural behavioral states, but not during anesthesia. Results are equivalent for neuronal ensembles recorded from visual and tactile areas of the cerebral cortex, as well as the hippocampus. CONCLUSIONS/SIGNIFICANCE: Altogether, the data provide a comprehensive link between behavior and brain criticality, revealing a unique scale-invariant regime of spike avalanches across all major behaviors.

Expansion of the alpha 2-adrenergic receptor family: cloning and characterization of a human alpha 2-adrenergic receptor subtype, the gene for which is located on chromosome 2.

Pharmacologic, biochemical, and genetic analyses have demonstrated the existence of multiple alpha 2-adrenergic receptor (alpha 2AR) subtypes. We have cloned a human alpha 2AR by using the polymerase chain reaction with oligonucleotide primers homologous to conserved regions of the previously cloned alpha 2ARs, the genes for which are located on human chromosomes 4 (C4) and 10 (C10). The deduced amino acid sequence encodes a protein of 450 amino acids whose putative topology is similar to that of the family of guanine nucleotide-binding protein-coupled receptors, but whose structure most closely resembles that of the alpha 2ARs. Competition curve analysis of the binding properties of the receptor expressed in COS-7 cells with a variety of adrenergic ligands demonstrates a unique alpha 2AR pharmacology. Hybridization with somatic cell hybrids shows that the gene for this receptor is located on chromosome 2. Northern blot analysis of various rat tissues shows expression in liver and kidney. The unique pharmacology and tissue localization of this receptor suggest that this is an alpha 2AR subtype not previously identified by classical pharmacological or ligand binding approaches.

Chromosomal organization of adrenergic receptor genes.

The adrenergic receptors (ARs) (subtypes alpha 1, alpha 2, beta 1, and beta 2) are a prototypic family of guanine nucleotide binding regulatory protein-coupled receptors that mediate the physiological effects of the hormone epinephrine and the neurotransmitter norepinephrine. We have previously assigned the genes for beta 2- and alpha 2-AR to human chromosomes 5 and 10, respectively. By Southern analysis of somatic cell hybrids and in situ chromosomal hybridization, we have now mapped the alpha 1-AR gene to chromosome 5q32----q34, the same position as beta 2-AR, and the beta 1-AR gene to chromosome 10q24----q26, the region where alpha 2-AR is located. In mouse, both alpha 2- and beta 1-AR genes were assigned to chromosome 19, and the alpha 1-AR locus was localized to chromosome 11. Pulsed field gel electrophoresis has shown that the alpha 1- and beta 2-AR genes in humans are within 300 kilobases (kb) and the distance between the alpha 2- and beta 1-AR genes is less than 225 kb. The proximity of these two pairs of AR genes and the sequence similarity that exists among all the ARs strongly suggest that they are evolutionarily related. Moreover, they likely arose from a common ancestral receptor gene and subsequently diverged through gene duplication and chromosomal duplication to perform their distinctive roles in mediating the physiological effects of catecholamines. The AR genes thus provide a paradigm for understanding the evolution of such structurally conserved yet functionally divergent families of receptor molecules.

Cloning and expression of a human kidney cDNA for an alpha 2-adrenergic receptor subtype.

An alpha 2-adrenergic receptor subtype has been cloned from a human kidney cDNA library using the gene for the human platelet alpha 2-adrenergic receptor as a probe. The deduced amino acid sequence resembles the human platelet alpha 2-adrenergic receptor and is consistent with the structure of other members of the family of guanine nucleotide-binding protein-coupled receptors. The cDNA was expressed in a mammalian cell line (COS-7), and the alpha 2-adrenergic ligand [3H]rauwolscine was bound. Competition curve analysis with a variety of adrenergic ligands suggests that this cDNA clone represents the alpha 2B-adrenergic receptor. The gene for this receptor is on human chromosome 4, whereas the gene for the human platelet alpha 2-adrenergic receptor (alpha 2A) lies on chromosome 10. This ability to express the receptor in mammalian cells, free of other adrenergic receptor subtypes, should help in developing more selective alpha-adrenergic ligands.

cDNA for the human beta 2-adrenergic receptor: a protein with multiple membrane-spanning domains and encoded by a gene whose chromosomal location is shared with that of the receptor for platelet-derived growth factor.

We have isolated and sequenced a cDNA encoding the human beta 2-adrenergic receptor. The deduced amino acid sequence (413 residues) is that of a protein containing seven clusters of hydrophobic amino acids suggestive of membrane-spanning domains. While the protein is 87% identical overall with the previously cloned hamster beta 2-adrenergic receptor, the most highly conserved regions are the putative transmembrane helices (95% identical) and cytoplasmic loops (93% identical), suggesting that these regions of the molecule harbor important functional domains. Several of the transmembrane helices also share lesser degrees of identity with comparable regions of select members of the opsin family of visual pigments. We have localized the gene for the beta 2-adrenergic receptor to q31-q32 on chromosome 5. This is the same position recently determined for the gene encoding the receptor for platelet-derived growth factor and is adjacent to that for the FMS protooncogene, which encodes the receptor for the macrophage colony-stimulating factor.

Bacteria localization and chorion thinning among preterm premature rupture of membranes.

OBJECTIVE: Bacterial colonization of the fetal membranes and its role in pathogenesis of membrane rupture is poorly understood. Prior retrospective work revealed chorion layer thinning in preterm premature rupture of membranes (PPROM) subjects. Our objective was to prospectively examine fetal membrane chorion thinning and to correlate to bacterial presence in PPROM, preterm, and term subjects. STUDY DESIGN: Paired membrane samples (membrane rupture and membrane distant) were prospectively collected from: PPROM = 14, preterm labor (PTL = 8), preterm no labor (PTNL = 8), term labor (TL = 10), and term no labor (TNL = 8), subjects. Sections were probed with cytokeratin to identify fetal trophoblast layer of the chorion using immunohistochemistry. Fluorescence in situ hybridization was performed using broad range 16 s ribosomal RNA probe. Images were evaluated, chorion and choriodecidua were measured, and bacterial fluorescence scored. Chorion thinning and bacterial presence were compared among and between groups using Student's t-test, linear mixed effect model, and Poisson regression model (SAS Cary, NC). RESULTS: In all groups, the fetal chorion cellular layer was thinner at rupture compared to distant site (147.2 vs. 253.7 µm, p<0.0001). Further, chorion thinning was greatest among PPROM subjects compared to all other groups combined, regardless of site sampled [PPROM(114.9) vs. PTL(246.0) vs. PTNL(200.8) vs. TL(217.9) vs. TNL(246.5)]. Bacteria counts were highest among PPROM subjects compared to all other groups regardless of site sampled or histologic infection [PPROM(31) vs. PTL(9) vs. PTNL(7) vs. TL(7) vs. TNL(6)]. Among all subjects at both sites, bacterial counts were inversely correlated with chorion thinning, even excluding histologic chorioamnionitis (p<0.0001 and p = 0.05). CONCLUSIONS: Fetal chorion was uniformly thinner at rupture site compared to distant sites. In PPROM fetal chorion, we demonstrated pronounced global thinning. Although cause or consequence is uncertain, bacterial presence is greatest and inversely correlated with chorion thinning among PPROM subjects.

Energy recovery in individuals with knee osteoarthritis.

OBJECTIVE: Pathological gaits have been shown to limit transfer between potential (PE) and kinetic (KE) energy during walking, which can increase locomotor costs. The purpose of this study was to examine whether energy exchange would be limited in people with knee osteoarthritis (OA). METHODS: Ground reaction forces during walking were collected from 93 subjects with symptomatic knee OA (self-selected and fast speeds) and 13 healthy controls (self-selected speed) and used to calculate their center of mass (COM) movements, PE and KE relationships, and energy recovery during a stride. Correlations and linear regressions examined the impact of energy fluctuation phase and amplitude, walking velocity, body mass, self-reported pain, and radiographic severity on recovery. Paired t-tests were run to compare energy recovery between cohorts. RESULTS: Symptomatic knee OA subjects displayed lower energetic recovery during self-selected walking speeds than healthy controls (P = 0.0018). PE and KE phase relationships explained the majority (66%) of variance in recovery. Recovery had a complex relationship with velocity and its change across speeds was significantly influenced by the self-selected walking speed of each subject. Neither radiographic OA scores nor subject self-reported measures demonstrated any relationship with energy recovery. CONCLUSIONS: Knee OA reduces effective exchange of PE and KE, potentially increasing the muscular work required to control movements of the COM. Gait retraining may return subjects to more normal patterns of energy exchange and allow them to reduce fatigue.

HIV-1 envelope gp41 antibodies can originate from terminal ileum B cells that share cross-reactivity with commensal bacteria.

Monoclonal antibodies derived from blood plasma cells of acute HIV-1-infected individuals are predominantly targeted to the HIV Env gp41 and cross-reactive with commensal bacteria. To understand this phenomenon, we examined anti-HIV responses in ileum B cells using recombinant antibody technology and probed their relationship to commensal bacteria. The dominant ileum B cell response was to Env gp41. Remarkably, a majority (82%) of the ileum anti-gp41 antibodies cross-reacted with commensal bacteria, and of those, 43% showed non-HIV-1 antigen polyreactivity. Pyrosequencing revealed shared HIV-1 antibody clonal lineages between ileum and blood. Mutated immunoglobulin G antibodies cross-reactive with both Env gp41 and microbiota could also be isolated from the ileum of HIV-1 uninfected individuals. Thus, the gp41 commensal bacterial antigen cross-reactive antibodies originate in the intestine, and the gp41 Env response in HIV-1 infection can be derived from a preinfection memory B cell pool triggered by commensal bacteria that cross-react with Env.