Development of test-based wind-driven rain intrusion model for hurricane-induced building interior and contents damage

Major portion of hurricane-induced economic loss originates from damages to building structures. The damages on building structures are typically grouped into three main categories: exterior, interior, and contents damage. Although the latter two types of damages, in most cases, cause more than 50% of the total loss, little has been done to investigate the physical damage process and unveil the interdependence of interior damage parameters. Building interior and contents damages are mainly due to wind-driven rain (WDR) intrusion through building envelope defects, breaches, and other functional openings. The limitation of research works and subsequent knowledge gaps, are in most part due to the complexity of damage phenomena during hurricanes and lack of established measurement methodologies to quantify rainwater intrusion. This dissertation focuses on devising methodologies for large-scale experimental simulation of tropical cyclone WDR and measurements of rainwater intrusion to acquire benchmark test-based data for the development of hurricane-induced building interior and contents damage model. Target WDR parameters derived from tropical cyclone rainfall data were used to simulate the WDR characteristics at the Wall of Wind (WOW) facility. The proposed WDR simulation methodology presents detailed procedures for selection of type and number of nozzles formulated based on tropical cyclone WDR study. The simulated WDR was later used to experimentally investigate the mechanisms of rainwater deposition/intrusion in buildings. Test-based dataset of two rainwater intrusion parameters that quantify the distribution of direct impinging raindrops and surface runoff rainwater over building surface — rain admittance factor (RAF) and surface runoff coefficient (SRC), respectively —were developed using common shapes of low-rise buildings. The dataset was applied to a newly formulated WDR estimation model to predict the volume of rainwater ingress through envelope openings such as wall and roof deck breaches and window sill cracks. The validation of the new model using experimental data indicated reasonable estimation of rainwater ingress through envelope defects and breaches during tropical cyclones. The WDR estimation model and experimental dataset of WDR parameters developed in this dissertation work can be used to enhance the prediction capabilities of existing interior damage models such as the Florida Public Hurricane Loss Model (FPHLM).^

Effects of architectural features of air-permeable roof cladding materials on wind-induced uplift loading

Widespread damage to roofing materials (such as tiles and shingles) for low-rise buildings, even for weaker hurricanes, has raised concerns regarding design load provisions and construction practices. Currently the building codes used for designing low-rise building roofs are mainly based on testing results from building models which generally do not simulate the architectural features of roofing materials that may significantly influence the wind-induced pressures. Full-scale experimentation was conducted under high winds to investigate the effects of architectural details of high profile roof tiles and asphalt shingles on net pressures that are often responsible for damage to these roofing materials. Effects on the vulnerability of roofing materials were also studied. Different roof models with bare, tiled, and shingled roof decks were tested. Pressures acting on both top and bottom surfaces of the roofing materials were measured to understand their effects on the net uplift loading. The area-averaged peak pressure coefficients obtained from bare, tiled, and shingled roof decks were compared. In addition, a set of wind tunnel tests on a tiled roof deck model were conducted to verify the effects of tiles' cavity internal pressure. Both the full-scale and the wind tunnel test results showed that underside pressure of a roof tile could either aggravate or alleviate wind uplift on the tile based on its orientation on the roof with respect to the wind angle of attack. For shingles, the underside pressure could aggravate wind uplift if the shingle is located near the center of the roof deck. Bare deck modeling to estimate design wind uplift on shingled decks may be acceptable for most locations but not for field locations; it could underestimate the uplift on shingles by 30-60%. In addition, some initial quantification of the effects of roofing materials on wind uplift was performed by studying the wind uplift load ratio for tiled versus bare deck and shingled versus bare deck. Vulnerability curves, with and without considering the effects of tiles' cavity internal pressure, showed significant differences. Aerodynamic load provisions for low-rise buildings' roofs and their vulnerability can thus be more accurately evaluated by considering the effects of the roofing materials.

Reduced Androgen Receptor Expression Accelerates the Onset of ERBB2 Induced Breast Tumors in Female Mice

Androgen receptor (AR) is commonly expressed in both the epithelium of normal mammary glands and in breast cancers. AR expression in breast cancers is independent of estrogen receptor alpha (ERα) status and is frequently associated with overexpression of the ERBB2 oncogene. AR signaling effects on breast cancer progression may depend on ERα and ERBB2 status. Up to 30% of human breast cancers are driven by overactive ERBB2 signaling and it is not clear whether AR expression affects any steps of tumor progression in this cohort of patients. To test this, we generated mammary specific Ar depleted mice (MARKO) by combining the floxed allele of Ar with the MMTV-cre transgene on an MMTV-NeuNT background and compared them to littermate MMTV-NeuNT, Arfl/+ control females. Heterozygous MARKO females displayed reduced levels of AR in mammary glands with mosaic AR expression in ductal epithelium. The loss of AR dramatically accelerated the onset of MMTV-NeuNT tumors in female MARKO mice. In this report we show that accelerated MMTV-NeuNT-dependent tumorigenesis is due specifically to the loss of AR, as hormonal levels, estrogen and progesterone receptors expression, and MMTV-NeuNT expression were similar between MARKO and control groups. MMTV-NeuNT induced tumors in both cohorts displayed distinct loss of AR in addition to ERα, PR, and the pioneer factor FOXA1. Erbb3 mRNA levels were significantly elevated in tumors in comparison to normal mammary glands. Thus the loss of AR in mouse mammary epithelium accelerates malignant transformation rather than the rate of tumorigenesis.