Tribeca Tower Foundation System

This paper describes the construction of the foundation system for a 52-story apartment building between Duane Street and Thomas Street (the Tribeca Tower) in the City of New York and the design and implementation of a protection program for a 130-year old designated landmark building founded on a stone rubble wall foundation adjacent to the Tribeca Tower

Correspondence

Presents letters to the editor referencing articles and topics discussed in previous issues. "Let Them Eat Stocks," which suggested that laid-off workers be given stock options in lieu of severance pay in the U.S.; "Huddled Excesses," which argued that immigration restriction laid the groundwork for labor's gains in 1920 to 1960 in the U.S.; "Econ 2," which offered views on the issue of minimum wage increase

Finite-difference model for one-dimensional electro-osmotic consolidation

Abstract not availableYadong Zhou, An Deng, Can Wan

Shear Strength Parameters of Improved Peat by Chemical Stabilizer.

The present research aimed to discuss the applicability of cationic grouts in geotechnical engineering. The effects of several cationic stabilizers such as monovalent (sodium silicate), divalent (calcium oxide and calcium chloride), and trivalent (aluminum hydroxide) were investigated on shear strength improvement of tropical peat samples. The unconfined compressive strength (UCS) tests were performed after the time frame of 7, 21, and 30 days as curing time, respectively. Apart from the physicochemical characteristics of the stabilized peat, scanning electron microscopy and energy-dispersive X-ray spectroscopy tests were also carried out to study the ongoing microstructural changes. It is to be noted that the shear strength values for peat samples rose to 8, 6, 6, and 4 % of sodium silicate, calcium oxide, calcium chloride, and aluminum hydroxide, respectively. The highest observed UCS outcome is the one taken from the calcium oxide where the UCS of treated peat after 30-day curing time increased to 76 kPa. The strength changes resulted from the various cationic stabilizers can best be explained via the consideration within the mineralogical composition as well as those physicochemical changes happening in the peat

G1 checkpoint protein and p53 abnormalities occur in most invasive transitional cell carcinomas of the urinary bladder

The G1 cell cycle checkpoint regulates entry into S phase for normal cells. Components of the G1 checkpoint, including retinoblastoma (Rb) protein, cyclin D1 and p16INK4a, are commonly altered in human malignancies, abrogating cell cycle control. Using immunohistochemistry, we examined 79 invasive transitional cell carcinomas of the urinary bladder treated by cystectomy, for loss of Rb or p16INK4a protein and for cyclin D1 overexpression. As p53 is also involved in cell cycle control, its expression was studied as well. Rb protein loss occurred in 23/79 cases (29%); it was inversely correlated with loss of p16INK4a, which occurred in 15/79 cases (19%). One biphenotypic case, with Rb+p16– and Rb-p16+ areas, was identified as well. Cyclin D1 was overexpressed in 21/79 carcinomas (27%), all of which retained Rb protein. Fifty of 79 tumours (63%) showed aberrant accumulation of p53 protein; p53 staining did not correlate with Rb, p16INK4a, or cyclin D1 status. Overall, 70% of bladder carcinomas showed abnormalities in one or more of the intrinsic proteins of the G1 checkpoint (Rb, p16INK4a and cyclin D1). Only 15% of all bladder carcinomas (12/79) showed a normal phenotype for all four proteins. In a multivariate survival analysis, cyclin D1 overexpression was linked to less aggressive disease and relatively favourable outcome. In our series, Rb, p16INK4a and p53 status did not reach statistical significance as prognostic factors. In conclusion, G1 restriction point defects can be identified in the majority of bladder carcinomas. Our findings support the hypothesis that cyclin D1 and p16INK4a can cooperate to dysregulate the cell cycle, but that loss of Rb protein abolishes the G1 checkpoint completely, removing any selective advantage for cells that alter additional cell cycle proteins. © 1999 Cancer Research Campaig