Nearer my mall to thee: The decline of the Johannesburg Central Business District and the emergence of the neo-apartheid city

African Studies Seminar series. Paper presented 5 October, 1998Many people subscribe to the notion that the Johannesburg central business district, or CBD, has declined substantially in recent years. A closer examination of the available data, however, suggests that the process has in fact been evident for some 40 years (Lauf 1959). By the 1950s, white residential growth had already begun to bulge out to the north (Figure 1), while the 1960s saw the beginnings of a similar movement of office accommodation. Furthermore, some of the major developments that emerged in the downtown area during the 1970s, and that were intended to reinforce the status of the CBD, in fact did much to hasten the decline of downtown retailing. The neo-apartheid city that we see unfolding today has deep historical roots

E-cadherin and loss of heterozygosity at chromosome 16 in breast carcinogenesis: different genetic pathways in ductal and lobular breast cancer?

Loss of heterozygosity at the long arm of chromosome 16 is one of the most frequent genetic events in breast cancer. In the search for tumour suppressor genes that are the target of loss of heterozygosity at 16q, the E-cadherin gene CDH1 was unveiled by the identification of truncating mutations in the retained copy. However, only lobular tumours showed E-cadherin mutations. Whereas investigations are still devoted to finding the target genes in the more frequent ductal breast cancers, other studies suspect the E-cadherin gene to also be the target in this tumour type. The present article discusses the plausibility of those two lines of thought

The cadherin–catenin complex in nasopharyngeal carcinoma

Abnormal Wnt signaling and impaired cell–cell adhesion due to abnormal E-cadherin and β-catenin function have been implicated in many cancers, but have not been fully explored in nasopharyngeal carcinoma. The aim of this study was to analyze β-Catenin cellular location and E-cadherin expression levels in nasopharyngeal carcinoma. E-cadherin expression levels were also correlated with clinical data and underlying pathology. β-Catenin and E-cadherin expression were examined in 18 nasopharyngeal carcinoma and 7 non-tumoral inflammatory pharynx tissues using immunohistochemical methods. Patient clinical data were collected, and histological evaluation was performed by hematoxylin/eosin staining. β-catenin was detected in membrane and cytoplasm in all cases of nasopharyngeal carcinoma, regardless of histological type; in non-tumoral tissues, however, β-catenin was observed only in the membrane. As for E-cadherin expression levels, strong staining was observed in most non-tumoral tissues, but staining was only moderate in nasopharyngeal carcinoma tissues. E-cadherin expression was associated with β-catenin localization, study group, metastatic disease, and patient outcomes. Reduced levels of E-cadherin protein observed in nasopharyngeal carinoma may play an important role in invasion and metastasis. Cytoplasmic β-catenin in nasopharyngeal carcinoma may impair cell–cell adhesion, promoting invasive behavior and a metastatic tumor phenotype

The cadherin–catenin complex in laryngeal squamous cell carcinoma

Abnormal Wnt signaling and impaired cell–cell adhesion due to abnormal E-cadherin and β-catenin function have been implicated in many cancers, but have not been fully explored in laryngeal squamous cell carcinoma. In this study, β-catenin cellular location and E-cadherin expression levels were analyzed in 16 laryngeal squamous cell carcinomas (LSCCs) (9 glottic and 7 supraglottic) and 11 samples of non-tumoral inflammatory larynx tissue, using immunohistochemical methods. All non-tumoral tissues showed equally strong membranous expression of β-catenin, while cytoplasmic expression was found in only 3 of the 11 samples. By contrast, whereas 8/9 glottic LSCCs exhibited only membranous expression of β-catenin, 6/7 supraglottic LSCCs displayed both membranous and cytoplasmic expression (p = 0.003). Strong E-cadherin staining was observed in 9/11 non-tumoral tissues and 7/9 glottic LSCCs, whereas 4/7 supraglottic LSCCs exhibited weak expression. Reduced membrane expression of E-cadherin and cytoplasmic retention of β-catenin in supraglottic LSCC seems to be related with more aggressive biological behavior which has been described in clinical studies. Further research is required to clarify the involvement of β-catenin in the mechanism associated with malignant transformation in laryngeal tissues

Indigenous well-being in four countries: An application of the UNDP'S Human Development Index to Indigenous Peoples in Australia, Canada, New Zealand, and the United States

<p>Abstract</p> <p>Background</p> <p>Canada, the United States, Australia, and New Zealand consistently place near the top of the United Nations Development Programme's <it>Human Development Index (HDI) </it>rankings, yet all have minority Indigenous populations with much poorer health and social conditions than non-Indigenous peoples. It is unclear just how the socioeconomic and health status of Indigenous peoples in these countries has changed in recent decades, and it remains generally unknown whether the overall conditions of Indigenous peoples are improving and whether the gaps between Indigenous peoples and other citizens have indeed narrowed. There is unsettling evidence that they may not have. It was the purpose of this study to determine how these gaps have narrowed or widened during the decade 1990 to 2000.</p> <p>Methods</p> <p>Census data and life expectancy estimates from government sources were used to adapt the Human Development Index (HDI) to examine how the broad social, economic, and health status of Indigenous populations in these countries have changed since 1990. Three indices – life expectancy, educational attainment, and income – were combined into a single HDI measure.</p> <p>Results</p> <p>Between 1990 and 2000, the HDI scores of Indigenous peoples in North America and New Zealand improved at a faster rate than the general populations, closing the gap in human development. In Australia, the HDI scores of Indigenous peoples decreased while the general populations improved, widening the gap in human development. While these countries are considered to have high human development according to the UNDP, the Indigenous populations that reside within them have only medium levels of human development.</p> <p>Conclusion</p> <p>The inconsistent progress in the health and well-being of Indigenous populations over time, and relative to non-Indigenous populations, points to the need for further efforts to improve the social, economic, and physical health of Indigenous peoples.</p

New urbanism, crime and the suburbs: a review of the evidence

Sustainability now influences government policy in the UK, Australia and USA and planning policy currently advocates high density, mixed-use residential developments in 'walkable', permeable neighbourhoods, close to public transport, employment and amenities. This clearly demonstrates the growing popularity, influence and application of New Urbanist ideas.This paper reviews the criminological research relating to New Urbanism associated with the three key issues of permeability, rear laneway car parking and mixed-use development. These key issues are discussed from an environmental criminology perspective and challenge New Urbanist assumptions concerning crime. The paper proposes that crime prevention through environmental design (CPTED) and its crime risk assessment model represents a valuable tool for New Urbanists to utilise to reduce opportunities for crime and tackle fear of crime in the community. Recommendations for future research and collaboration are discussed

The mechanisms by which polyamines accelerate tumor spread

Increased polyamine concentrations in the blood and urine of cancer patients reflect the enhanced levels of polyamine synthesis in cancer tissues arising from increased activity of enzymes responsible for polyamine synthesis. In addition to their de novo polyamine synthesis, cells can take up polyamines from extracellular sources, such as cancer tissues, food, and intestinal microbiota. Because polyamines are indispensable for cell growth, increased polyamine availability enhances cell growth. However, the malignant potential of cancer is determined by its capability to invade to surrounding tissues and metastasize to distant organs. The mechanisms by which increased polyamine levels enhance the malignant potential of cancer cells and decrease anti-tumor immunity are reviewed. Cancer cells with a greater capability to synthesize polyamines are associated with increased production of proteinases, such as serine proteinase, matrix metalloproteinases, cathepsins, and plasminogen activator, which can degrade surrounding tissues. Although cancer tissues produce vascular growth factors, their deregulated growth induces hypoxia, which in turn enhances polyamine uptake by cancer cells to further augment cell migration and suppress CD44 expression. Increased polyamine uptake by immune cells also results in reduced cytokine production needed for anti-tumor activities and decreases expression of adhesion molecules involved in anti-tumor immunity, such as CD11a and CD56. Immune cells in an environment with increased polyamine levels lose anti-tumor immune functions, such as lymphokine activated killer activities. Recent investigations revealed that increased polyamine availability enhances the capability of cancer cells to invade and metastasize to new tissues while diminishing immune cells' anti-tumor immune functions