Extended urbanization in small and medium-sized cities: the case of Cirebon Indonesia

Although urbanization in smaller cities is arguably not imperative, the future of urban living is no longer expected to be principally in mega-cities. People increasingly live in intermediate and smaller cities, in line with the proportion of people residing in urban areas, which is also gradually rising. Smaller cities in Indonesia, like other smaller cities in the developing world, are relatively densely populated, and many of them are experiencing extended urbanization, thereby exceeding their administrative boundaries. This paper seeks to explore the factors triggering urban development in these smaller cities, for a case in Indonesia. Urban change in Cirebon Region has accelerated in recent years, very much in line with the decentralization policy in Indonesia. This paper shows how urban change is in!uenced by economic restructuring, which encourages people to live closer to the core of the region, representing a new link between the core and new emerging urban areas in the region. This paper reveals these attributes to identify the characteristics of smaller urban centres, thereby contributing a more nuanced image of small cities in general.

Damaging effects of advanced glycation end product in the murine macrophages cell line J774A.1.

The interaction of reducing sugars, such as aldose, with proteins and the subsequent molecular rearrangements, produces irreversible advanced glycation end-products (AGEs), a heterogeneous class of non-enzymatic glycated proteins or lipids. AGEs form cross-links, trap macromolecules and release reactive oxygen intermediates. AGEs are linked to aging, and increase in several related diseases. The aim of this study was to assess, in a murine macrophage cell line, J774A.1, the effects of 48 h of exposure to glycated serum containing a known amount of pentosidine, a well-known AGE found in the plasma and tissues of diabetic and uremic subjects. Fetal bovine serum was incubated with ribose (50 mm) for 7 days at 37 °C to obtain about 10 nmol/ml of pentosidine. The cytotoxic parameters studied were cell morphology and viability by neutral red uptake, lactate dehydrogenase release and tetrazolium salt test. In the medium and in the intracellular compartment, bound and free pentosidine were evaluated by HPLC, as sensitive and specific glycative markers, and thiobarbituric acid reactive substances (TBARs), as index of the extent of lipid peroxidation. Our results confirm that macrophages are able to take up pentosidine. It is conceivable that bound pentosidine is degraded and free pentosidine is released inside the cell and then into the medium. The AGE increase in the medium was combined with an increase in TBARs, meaning that an oxidative stress occurred; marked cytotoxic effects were observed, and were followed by the release of free pentosidine and TBARs into the culture medium.