Precise Sm-Nd and U-Pb isotopic dating of the supergiant Shizhuyuan polymetallic deposit and its host granite, SE China

The supergiant Shizhuyuan W-Sn-Bi-Mo deposit is hosted by the Qianlishan granite, a small, highly fractionated granitic pluton (~10 km2) with multiple phases of intrusions within the Early Yanshanian granitoid province of SE China. Strong alteration of skarn and greisen that formed in the contact zone between the first and second phases of granite intrusions and Devonian limestone is responsible for the polymetallic mineralizations. SHRIMP U-Pb zircon analysis indicates that the two early phases of the Qianlishan granite formed contemporaneously at 152 ± 2 Ma. Metasomatic minerals (garnet, fluorite and wolframite) separated from the skarn and greisen yield a Sm-Nd isochron age of 149 ± 2 Ma that is interpreted as the formation age of the Shizhuyuan deposit. Therefore, the mineralization of the supergiant Shizhuyuan polymetallic deposit formed contemporaneously with, or very shortly after, the intrusion of the small, highly fractionated Qianlishan granite. © 2004 Cambridge University Press.published_or_final_versio

Bacteria-Induced Uroplakin Signaling Mediates Bladder Response to Infection

Urinary tract infections are the second most common infectious disease in humans and are predominantly caused by uropathogenic E. coli (UPEC). A majority of UPEC isolates express the type 1 pilus adhesin, FimH, and cell culture and murine studies demonstrate that FimH is involved in invasion and apoptosis of urothelial cells. FimH initiates bladder pathology by binding to the uroplakin receptor complex, but the subsequent events mediating pathogenesis have not been fully characterized. We report a hitherto undiscovered signaling role for the UPIIIa protein, the only major uroplakin with a potential cytoplasmic signaling domain, in bacterial invasion and apoptosis. In response to FimH adhesin binding, the UPIIIa cytoplasmic tail undergoes phosphorylation on a specific threonine residue by casein kinase II, followed by an elevation of intracellular calcium. Pharmacological inhibition of these signaling events abrogates bacterial invasion and urothelial apoptosis in vitro and in vivo. Our studies suggest that bacteria-induced UPIIIa signaling is a critical mediator of bladder responses to insult by uropathogenic E. coli

Determination of boron in serum, plasma and urine by inductively coupled plasma mass spectrometry (ICP-MS). Use of mannitol-ammonia as diluent and for eliminating memory effect

A rapid and accurate method has been developed for the determination of boron in serum, plasma and urine by inductively coupled plasma mass spectrometry. The memory effects of B were examined using different diluents/rinse solutions, including water, nitric acid, Triton X-100, ammonia and mannitol in water, in nitric acid and in ammonia. A combination of ammonia with mannitol, as both diluent and flush solution, gave the best precision, the minimum memory effect and the lowest background. A sample dilution of 20-fold was simply made for serum and plasma and 100-fold for urine for determination with a single calibration curve. Beryllium was employed as the internal standard to control matrix effects and to compensate for possible fluctuation and instrument drift. The isotope B-10(+) was utilised to avoid spectral overlap by the intense C-12(+) isotope. The final solution of blank, standards and samples contained 0.25% w/v mannitol, 0.1 M ammonia and 20 ng ml(-1) of Be. Six samples, including human and horse serum, human and horse plasma, and human urine, were analysed to test the reliability of the method. A limit of detection (3 sigma) of 0.015 ng ml(-1) was obtained and the recoveries of spiked boron (two spiking levels for each matrix) from the selected samples ranged from 98% to 104%. Much higher concentrations of B in urine (approximate to 1 mu g ml(-1)) were found compared to those in serum and plasma samples (32.8-61.1 ng ml(-1))

Freeze-Fracture Replica Immunolabelling Reveals Urothelial Plaques in Cultured Urothelial Cells

The primary function of the urothelium is to provide the tightest and most impermeable barrier in the body, i.e. the blood-urine barrier. Urothelial plaques are formed and inserted into the apical plasma membrane during advanced stages of urothelial cell differentiation. Currently, it is supposed that differentiation with the final formation of urothelial plaques is hindered in cultured urothelial cells. With the aid of the high-resolution imaging technique of freeze-fracture replica immunolabelling, we here provide evidence that urothelial cells in vitro form uroplakin-positive urothelial plaques, localized in fusiform-shaped vesicles and apical plasma membranes. With the establishment of such an in vitro model of urothelial cells with fully developed urothelial plaques and functional properties equivalent to normal bladder urothelium, new perspectives have emerged which challenge prevailing concepts of apical plasma membrane biogenesis and blood-urine barrier development. This may hopefully provide a timely impulse for many ongoing studies and open up new questions for future research

Parity-related molecular signatures and breast cancer subtypes by estrogen receptor status

INTRODUCTION: Relationships of parity with breast cancer risk are complex. Parity is associated with decreased risk of postmenopausal hormone receptor–positive breast tumors, but may increase risk for basal-like breast cancers and early-onset tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve understanding of the biological mechanisms underlying this complex pattern of risk. METHODS: We developed a parity signature by analyzing microRNA microarray data from 130 reduction mammoplasty (RM) patients (54 nulliparous and 76 parous). This parity signature, together with published parity signatures, was evaluated in gene expression data from 150 paired tumors and adjacent benign breast tissues from the Polish Breast Cancer Study, both overall and by tumor estrogen receptor (ER) status. RESULTS: We identified 251 genes significantly upregulated by parity status in RM patients (parous versus nulliparous; false discovery rate = 0.008), including genes in immune, inflammation and wound response pathways. This parity signature was significantly enriched in normal and tumor tissues of parous breast cancer patients, specifically in ER-positive tumors. CONCLUSIONS: Our data corroborate epidemiologic data, suggesting that the etiology and pathogenesis of breast cancers vary by ER status, which may have implications for developing prevention strategies for these tumors

Observation of a ppb mass threshoud enhancement in \psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p}) decay

The decay channel $\psi^\prime\to\pi^+\pi^-J/\psi(J/\psi\to\gamma p\bar{p})$ is studied using a sample of $1.06\times 10^8$ $\psi^\prime$ events collected by the BESIII experiment at BEPCII. A strong enhancement at threshold is observed in the $p\bar{p}$ invariant mass spectrum. The enhancement can be fit with an $S$-wave Breit-Wigner resonance function with a resulting peak mass of $M=1861^{+6}_{-13} {\rm (stat)}^{+7}_{-26} {\rm (syst)} {\rm MeV/}c^2$ and a narrow width that is $\Gamma<38 {\rm MeV/}c^2$ at the 90% confidence level. These results are consistent with published BESII results. These mass and width values do not match with those of any known meson resonance.Comment: 5 pages, 3 figures, submitted to Chinese Physics

Parity-related molecular signatures and breast cancer subtypes by estrogen receptor status.

INTRODUCTION:Relationships of parity with breast cancer risk are complex. Parity is associated with decreased risk of postmenopausal hormone receptor-positive breast tumors, but may increase risk for basal-like breast cancers and early-onset tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve understanding of the biological mechanisms underlying this complex pattern of risk. METHODS:We developed a parity signature by analyzing microRNA microarray data from 130 reduction mammoplasty (RM) patients (54 nulliparous and 76 parous). This parity signature, together with published parity signatures, was evaluated in gene expression data from 150 paired tumors and adjacent benign breast tissues from the Polish Breast Cancer Study, both overall and by tumor estrogen receptor (ER) status. RESULTS:We identified 251 genes significantly upregulated by parity status in RM patients (parous versus nulliparous; false discovery rate = 0.008), including genes in immune, inflammation and wound response pathways. This parity signature was significantly enriched in normal and tumor tissues of parous breast cancer patients, specifically in ER-positive tumors. CONCLUSIONS:Our data corroborate epidemiologic data, suggesting that the etiology and pathogenesis of breast cancers vary by ER status, which may have implications for developing prevention strategies for these tumors