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The conventional practice of construction site monitoring in Hong Kong relies heavily on in-person site inspection, which is inherently subject to limitations in human resources, health, safety and time. Additionally, given that the advent and application of new digital technologies in the construction industry predominantly occurred after 2010 in Hong Kong, it is more challenging to review/ monitor the changes of a construction site with respect to its historical (pre-2010) status. To overcome these limitations, in this paper, we present the use of the 4D model monitoring method on a case study from the Tung Chung New Town (TCNT) and its extension development in Hong Kong. Nine 3D digital surface models covering a 57-year time period from 1963 to 2020 were built from the historical aerial photographs using the Structure from Motion technique and from the territory-wide airborne LiDAR data. These models were used for monitoring the process of land reclamation, site formation and the subsequent works during the TCNT development. In addition, a preliminary ground model was constructed from approximately 500 Nos. of drillholes to provide an engineering geological background for the study site. It is promising that our innovative 4D digital model and the associated sub-surface rockhead model can be integrated with the Building Information Modelling (BIM) system at a later stage to constituent a Smart Built Environment and to facilitate a smart construction site monitoring practice in near future.

The transient receptor potential vanilloid member 4 (TRPV4) is a non-selective calcium (Ca2+)-permeable channel which is widely expressed in different types of tissues including the lungs, liver, kidneys and salivary gland. TRPV4 has been shown to serve as a cellular sensor where it is involved in processes such as osmoregulation, cell volume regulation and thermoregulation. Emerging evidence suggests that TRPV4 also plays important roles in several aspects of cancer progression. Despite the reported roles of TRPV4 in several forms of cancers, the role of TRPV4 in human colorectal cancer remains largely unexplored. In the present study, we sought to establish the potential role of TRPV4 in colorectal cancer by assessing TRPV4 expression levels and investigating whether TRPV4 pharmacological modulation may alter cell proliferation, cell cycle and cell death in colorectal cancer cells. Quantitative real-time PCR analysis revealed that TRPV4 mRNA levels were significantly lower in HT-29 cells than normal colon CCD-18Co cells. However, TRPV4 mRNA was absent in HCT-116 cells. Pharmacological activation of TRPV4 with GSK1016790A significantly enhanced the proliferation of HT-29 cells while TRPV4 inhibition using RN 1734 decreased their proliferation. Increased proliferation in GSK1016790A-treated HT-29 cells was attenuated by co-treatment with RN 1734. Pharmacological modulation of TRPV4 had no effect on the cell cycle progression but promoted cell death in HT-29 cells. Taken together, these findings suggest differential TRPV4 expression levels in human colorectal cancer cells and that pharmacological modulation of TRPV4 produces distinct effects on the proliferation and induces cell death in HT-29 cells.

This study investigates the reduction of free fatty acids from the problem of used cooking oil in the food industry with bio-waste adsorbents such as banana peels—experimental conditions at the activation temperature of making activated carbon. Adsorption kinetics and temperature of activated effects were studied. Bio-char activated at 600, 650, and 700°C. The used cooking oil and activated carbon were analyzed using Fourier transform infrared spectroscopy, transmission electron microscopy, X-ray energy-dispersive, and BET analysis. Activated carbon has a surface area of 548 m2/g, with an average pore diameter of 35 nm (range of mesophore). As a result, bio-char activated at 700°C is best presented by a linear pseudo-second-order kinetic model suitable for describing the adsorption kinetic. The maximum adsorption capacity was 62 mg/g at 303 K. Carboxylic groups as free fatty acid was removed from used cooking oil used surface of activated carbon. Models best described the experimental data as with the higher values of the correlation coefficient (R2). The results of this study prove that the banana peel bio-waste ingredient, which is food waste, is a potential adsorbent to reduce free fatty acid levels to the standard of 0.3

CXC ligand (L)12 is a chemokine implicated in the migration, invasion and metastasis of cancer cells via interaction with its receptors CXC chemokine receptor (CXCR)4 and CXCR7. In the present study, CXCL12-mediated Ca2+ signalling was compared with two basal-like breast cancer cell lines, MDA-MB-231 and MDA-MB-468, which demonstrate distinct metastatic potential. CXCL12 treatment induced Ca2+ responses in the more metastatic MDA-MB-231 cells but not in the less metastatic MDA-MB-468 cells. Assessment of mRNA levels of CXCL12 receptors and their potential modulators in both cell lines revealed that CXCR4 and CXCR7 levels were increased in MDA-MB-231 cells compared with MDA-MB-468 cells. Cluster of differentiation (CD)24, the negative regulator of CXCL12 responses, demonstrated increased expression in MDA-MB-468 cells compared with MDA-MB-231 cells, and the two cell lines expressed comparable levels of hypoxia-inducible factor (HIF)2α, a CXCR4 regulator. Induction of epithelial-mesenchymal transition (EMT) by epidermal growth factor exhibited opposite effects on CXCR4 mRNA levels compared with hypoxia-induced EMT. Neither EMT inducer exhibited an effect on CXCR7 expression, however hypoxia increased HIF2α expression levels in MDA-MB-468 cells. Analysis of the gene expression profiles of breast tumours revealed that the highest expression levels of CXCR4 and CXCR7 were in the Claudin-Low molecular subtype, which is markedly associated with EMT features.

The critical role of calcium signalling in processes related to cancer cell proliferation and invasion has seen a focus on pharmacological inhibition of overexpressed ion channels in specific cancer subtypes as a potential therapeutic approach. However, despite the critical role of calcium in cell death pathways, pharmacological activation of overexpressed ion channels has not been extensively evaluated in breast cancer. Here we define the overexpression of transient receptor potential vanilloid 4 (TRPV4) in a subgroup of breast cancers of the basal molecular subtype. We also report that pharmacological activation of TRPV4 with GSK1016790A reduced viability of two basal breast cancer cell lines with pronounced endogenous overexpression of TRPV4, MDA-MB-468 and HCC1569. Pharmacological activation of TRPV4 produced pronounced cell death through two mechanisms: apoptosis and oncosis in MDA-MB-468 cells. Apoptosis was associated with PARP-1 cleavage and oncosis was associated with a rapid decline in intracellular ATP levels, which was a consequence of, rather than the cause of, the intracellular ion increase. TRPV4 activation also resulted in reduced tumour growth in vivo. These studies define a novel therapeutic strategy for breast cancers that overexpress specific calcium permeable plasmalemmal ion channels with available selective pharmacological activators. Refereed/Peer-reviewed

The calcium ion (Ca2+) is a ubiquitous second messenger that controls intracellular signals that trigger various cellular responses including cell proliferation, gene transcription and cell death. Intracellular Ca2+ signalling is tightly regulated by the actions of Ca2+ -transporting proteins including Ca2+ channels, Ca2+ exchangers, Ca2+ -ATPases and their regulators. Evidence suggests that deregulation of Ca2+ signalling is associated with several pathophysiological conditions including cancer. Altered expression and/or activity of some Ca2+ transporters have been demonstrated to occur during cancer development and progression. Thus, Ca2+ transporters represent attractive drug targets for therapeutic intervention. The work in this thesis is centred on identifying proteins implicated in Ca2+ signalling that represent drug targets for breast cancer treatment. This thesis also performed functional assessment of such targets in the regulation of Ca2+ -dependent processes including cell proliferation and cell death in breast cancer cells. The first part of this thesis addressed the utility of high throughput siRNA screening in combination with high content imaging in a human basal-like breast cancer cell line for the identification of potential therapeutic targets which are involved in Ca2+ signalling. Screening of an siRNA-based library against Ca2+ signalling modifying proteins revealed 39 possible hits based on the pronounced effects on human MDA-MB-231 basal-like breast cancer cells compared to nontumorigenic MCF-10A cells. From these hits, eight candidate genes were advanced to target validation based on target druggability, plasma membrane localisation and a lack of previous assessment in breast cancer cells. These specific selected targets were then assessed in basal breast cancer cell lines through the assessment of their mRNA levels and the consequences of their silencing and/or pharmacological modulation on Ca2+ signalling, cell viability and cell death.Of the eight candidate genes, three hits were undetectable by real-time RT-PCR in MDA-MB-231 cells. CD24 was the first selected candidate gene and was characterised in the human basal-like breast cancer cell lines MDA-MB-231 and MDA-MB-468. CD24 mRNA levels were higher (more than 800-fold) in MDA-MB-468 compared to MDA-MB-231 cells. Since CD24 has also been linked to the chemokine receptor CXCR4 in breast cancer, the functional role of CD24 was characterised by examining its effect on CXCL12/CXCR4-mediated Ca2+ signalling. Highly metastatic MDA-MB-231 cells displayed more pronounced Ca2+ responses when stimulated with CXCL12 (CXCR4 receptor ligand) than poorly metastatic MDA-MB-468 cells. CD24 silencing in MDA-MB-468 cells did not alter the nature of ATP-induced Ca2+ transients and did not promote an increase in cytosolic free Ca2+ ([Ca2+]CYT). Real-time RT-PCR showed that CXCR4 expression was higher in MDA-MB-231 than MDA-MB-468 cells. Hence, CXCR4 but not CD24 levels are likely responsible for the differences in CXCL12 responsiveness between these two cell lines. CXCR4 expression was significantly reduced during epidermal growth factor (EGF)-induced epithelial to mesenchymal transition (EMT) in MDA-MB-468 cells, indicating that increased CXCR4 is not associated with the acquisition of a more mesenchymal phenotype.This thesis then explored the functional role of another selected target, the Ca2+ permeable ion channel TRPV4 in human basal-like breast cancer cells. Real-time RT-PCR analysis revealed that TRPV4 was present in both MDA-MB-231 and MDA-MB-468 cells, with higher levels (approximately 30-fold) in MDA-MB-468 cells. The functional activity of TRPV4 channels was then investigated using a known TRPV4 agonist - GSK1016790A. Consistent with the levels of TRPV4 mRNA, TRPV4 activation by GSK1016790A elicited more pronounced increases in [Ca2+]CYT in MDA-MB-468 compared to MDA-MB-231 cells. GSK1016790A concentrationresponse curves revealed a lower EC50 value in MDA-MB-468 cells than MDA-MB-231 cells (3.9 nM and 76 nM, respectively). Silencing of TRPV4 using siRNA significantly reduced GSK1016790A-induced Ca2+ influx in both cell lines, indicating that TRPV4 is a functional Ca2+ entry channel in both MDA-MB-231 and MDA-MB-468 cells.Pharmacological inhibition of TRPV4 channels using the TRPV4 antagonist, RN 1734 had no significant effect on the viable cell number in either MDA-MB-231 or MDA-MB-468 breast cancer cells. However, pharmacological activation of TRPV4 channels using GSK1016790A in MDAMB-468 cells but not in MDA-MB-231 cells led to a concentration-dependent induction of cell death. GSK1016790A-mediated cell death was significantly attenuated in the presence of TRPV4 siRNA. The mechanism of GSK1016790A-induced cell death in MDA-MB-468 cells was independent of caspase, as indicated by the insensitivity to cell death by the caspase inhibitor ZVAD-FMK. The work outlined in this thesis demonstrates the importance of confirmation experiments for targets identified by high throughput siRNA screening. These studies have also identified TRPV4 pharmacological activation as a potential novel mechanism to induce the death of breast cancer cells that overexpress this Ca2+ permeable ion channel.

To achieve both qualitative and quantitative understanding of the decomposition of hardened cement paste (HCP) at elevated temperatures, X-ray diffraction (XRD) tests were conducted on HCP samples after exposure to various peak temperatures from 400 to 800°C. The kinetic equations of C-S-H decomposition at 600, 700 and 800°C are proposed. The quantitative measurement using α-Al2O3 as a reference phase, revealed that the decomposition of C-S-H started at 560°C but became significant only above 600°C. The C-S-H decomposition rate increased dramatically with temperatures above 600°C. The decomposition of C-S-H influenced the strength loss of high-performance concrete (HPC) exposed to temperatures above 600°C but had little or no effect on the occurrence of explosive spalling. This test result confirms the vapour pressure mechanism for explosive spalling of HPC. It is also postulated that the strength loss of concrete exposed to temperatures below 600°C must be mainly caused by the HCP pore-structure coarsening.

Carrier fluidifying agent (CFA) was developed to maintain the workability of high-strength concrete (HSC). It retained the workability of HSC for a period of up to about 90 min. In the present study, the permeation characteristics, carbonation, and chloride diffusion of HSC incorporating CFA were studied. The experimental results showed that the use of CFA can maintain or slightly improve the permeation characteristics of HSC and its resistance to carbonation and chloride diffusion.

One of the methods of producing high strength concrete (HSC) is by reducing the water/cement (w/c) ratio to achieve a compressive cylinder strength of over 41 N/mm2 as defined by the American Concrete Institute or over 60 N/mm2 as stipulated by FIP/CEB. The consequent low workability is then overcome by adding superplasticizer to achieve a specified workability, preferably without segregation, set retardation or excessive air entrainment. For a given workability, the lower the w/c ratio, the higher is the superplasticizer dosage requirement. However, there is a practical upper limit on the dosage of superplasticizer because of its cost, the reduced plasticizing efficiency above an optimum dosage level, and the risk of loss of strength caused by segregation and heavy air entrainment, as well as possible retardation in setting and hardening. For superplasticized concrete, the rapid loss of workability presents a major technical problem for in situ construction using conventional pumping and casting methods. The present1y adopted repeated dosing method imposes manpower, quality control and cost penalties as well as the risk of superplasticizer over-dosing. This paper studies the slump loss behaviour of HSC incorporating a variety of superplasticizers. To retain the workability of HSC, a recently developed and patented admixture, carrier fluidifying agent (CFA) was used in a series of concrete mixes. It was found that CFA maintained the workability of HSC mixes for a period of up to 2 hours. The effects of CFA on the setting, hardening, air content and compressive strength development of the concrete were also studied and no adverse effect was observed. Laboratory trials using a repeated dosing method were also carried out, and apart from being labour intensive, this method was found to be less effective and more expensive.

An admission cohort of 296 Australian methadone maintenance patients was followed over 15 years. The relative risks of death in and out of maintenance were calculated for two age groups, 20-29 and 30-39 years. Heroin addicts in both age groups were one-quarter as likely to die while receiving methadone maintenance as addicts not in treatment. This is because they were significantly less likely to die by heroin overdose or suicide while in maintenance. Methadone maintenance had no measurable effect on the risk of death through nonheroin overdose, violence or trauma, or natural causes. A meta-analysis showed the reduction in overall mortality was consistent with the results of cohort studies conducted in the United States, Sweden, and Germany. The combined results of the five studies again indicated that methadone maintenance reduced addicts' risk of death to a quarter, RR 0.25 (95% CI 0.19 to 0.33).

Datos SOBRE los cálculos del uréter.—De una comunicación á la sociedad francesa de urología, del Dr. E. Jeanbrau, tomamos lo siguiente:—Los cálculos se localizan de preferencia en los puntos extremos de los uréteres, como puede verse por las cifras que anotamos: en la porción lumbar de estos conductos un 22 por 100, en el uréter pelviano el 5.1 por 100 de los casos; un 3.6 por 100 en la porción intra-vesical y solamente un 7 por io» en su trayecto ilíaco. Como se ve, esta predilección de los extremos del conducto para la retención de las piedras, sólo se debe á la mayor estrechez que tiene el uréter en estos puntos, relativamente al resto de su extensión. Son por lo general solitarios, y rara vez se observa la presencia de cálculos en ambos conductos; su forma es la de un hueso de aceituna, por lo regular, siendo muy importante distinguir sus contornos y configuración exterior, ya por su naturaleza y composición diversa, como por las más ó menos graves consecuencias á que dan lugar. Unas veces su superficie es lisa y otras llenas de rugosidades, espinas, protuberancias, &; los primeros deslizan fácilmente y pueden ser expulsados sin inconvenientes, hallándose formados por uratos y fosfatos; los últimos, formados de ácido úrico o de oxalatos, se enquistan y engastan en las paredes, erosionando la mucosa y dando lugar á hematurias frecuentes. Cuenca Serie II, número 4 (febrero 1910)

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