The disability housing market: opportunity for community development finance as the Americans with Disabilities Act turns 20

Community development

Biocatalytic oxidation of nitrilotriacetate

The specific scope of this work is to study the biological and chemical effects of a single genetic strain of bacteria, Bacillus subtilis #9524, on the specific destruction to innocuous products of sodium nitrilotriacetate (NTA) and sodium tripolyphosphate (STPP). Insofar as the same strain of bacteria was used each time, under limited variability and sterile conditions, the side effects of multiple bacterial strains and their inter-relationships among themselves and the organic substrates are eliminated. This has allowed for excellent replication of results. This is a generalized technique for the evaluation of the biodegradability of a compound. Whereas tests with activated sewage sludge may show results of oxygen consumption, it may be due to multiple variable reasons associated with unknowns for the breakdown of the compound in question. Tests also need to be extensive, in that while tests with lower levels of concentration (1-5ppm) may prove to be somewhat effective, higher concentration levels (10 20ppm) of the compound may prove to possess toxic effects on the bacterial strain in use, due to physical factors of altered solution surface tension and lack of isotonicity. As a result of this study it was found that while there was a minute amount of oxygen consumption at lower levels of NTA, it was not enough to justify saying that NTA was biodegradable. Further experimentation at higher levels of concentration, while having slightly higher levels of oxygen consumption, also showed a trend of increasing toxicity, where an increase in the concentration of the NTA resulted in a lowering of the oxygen demand. Tests on the STPP proved that there was no breakdown, because there was relatively no oxygen consumption, but a known re-entry into the life biochemical processes of the very useful phosphate ion

Organogenesis of kidney and endocrine pancreas: The window opens

Growing new organs in situ by implanting developing animal organ primordia (organogenesis) represents a novel solution to the problem of limited supply for human donor organs that offers advantages relative to transplanting embryonic stem (ES) cells or xenotransplantation of developed organs. Successful transplantation of organ primordia depends on obtaining them at defined windows during embryonic development within which the risk of teratogenicity is eliminated, growth potential is maximized, and immunogenicity is reduced. We and others have shown that renal primordia transplanted into the mesentery undergo differentiation and growth, become vascularized by blood vessels of host origin, exhibit excretory function and support life in otherwise anephric hosts. Renal primordia can be transplanted across isogeneic, allogeneic or xenogeneic barriers. Pancreatic primordia can be transplanted across the same barriers undergo growth, and differentiation of endocrine components only and secrete insulin in a physiological manner following mesenteric placement. Insulin-secreting cells originating from embryonic day (E) 28 (E28) pig pancreatic primordia transplanted into the mesentery of streptozotocin-diabetic (type 1) Lewis rats or ZDF diabetic (type 2) rats or STZ-diabetic rhesus macaques engraft without the need for host immune-suppression. Our findings in diabetic macaques represent the first steps in the opening of a window for a novel treatment of diabetes in humans

Development of a novel xenotransplantation strategy for treatment of diabetes mellitus in rat hosts and translation to non-human primates

Transplantation therapy for diabetes is limited by unavailability of donor organs and outcomes complicated by immunosuppressive drug toxicity. Xenotransplantation is a strategy to overcome supply problems. Implantation of tissue obtained early during embryogenesis is a way to reduce transplant immunogenicity. Insulin-producing cells originating from embryonic pig pancreas obtained very early following pancreatic primordium formation [embryonic day 28 (E28)] engraft long-term in inbred diabetic Lewis or Zucker Diabetic Fatty (ZDF) rats or rhesus macaques. Endocrine cells originating from embryonic pig pancreas transplanted in host mesentery migrate to mesenteric lymph nodes, engraft, normalize glucose tolerance in rats and improve glucose tolerance in rhesus macaques without the need for immune suppression. Engraftment of primordia is permissive for engraftment of an insulin-expressing cell component from porcine islets implanted subsequently without immune suppression. Similarities between findings in inbred rat and non-human primate hosts bode well for successful translation to humans of what could be a novel xenotransplantation strategy for the treatment of diabetes

Tissue engineering the kidney11The guest editor for this paper was Adrian Woolf, London, United Kingdom.

Tissue engineering the kidney. The means by which kidney function can be replaced in humans include dialysis and renal allotransplantation. Dialytic therapies are lifesaving, but often poorly tolerated. Transplantation of human kidneys is limited by the availability of donor organs. During the past decades, a number of different approaches have been applied toward tissue engineering the kidney as a means to replace renal function. The goals of one or another of them included the recapitulation of renal filtration, reabsorptive and secretory functions, and replacement of endocrine/metabolic activities. This review will delineate the progress to date recorded for five approaches: (1) integration of new nephrons into the kidney; (2) growing new kidneys in situ; (3) use of stem cells; (4) generation of histocompatible tissues using nuclear transplantation; and (5) bioengineering of an artificial kidney. All five approaches utilize cellular therapy. The first four employ transplantation as well, and the fifth uses dialysis

Organogenesis of the endocrine pancreas

Organogenesis of the endocrine pancreas. Embryonic pancreatic primordia transplanted into diabetic animal hosts undergo selective endocrine differentiation in situ and normalize glucose tolerance. Pancreatic primordia can be transplanted across isogeneic, allogeneic, and both concordant (rat to mouse) and highly disparate (pig to rodent) xenogeneic barriers. This review explores the therapeutic potential for pancreatic organogenesis posttransplantation of embryonic primordia

Engraftment of Insulin-Producing Cells from Porcine Islets in Non-Immune-Suppressed Rats or Nonhuman Primates Transplanted Previously with Embryonic Pig Pancreas

Transplantation therapy for diabetes is limited by unavailability of donor organs and outcomes complicated by immunosuppressive drug toxicity. Xenotransplantation is a strategy to overcome supply problems. Implantation of tissue obtained early during embryogenesis is a way to reduce transplant immunogenicity. Insulin-producing cells originating from embryonic pig pancreas obtained very early following pancreatic primordium formation (embryonic day 28 (E28)) engraft long-term in non-immune, suppressed diabetic rats or rhesus macaques. Morphologically, similar cells originating from adult porcine islets of Langerhans (islets) engraft in non-immune-suppressed rats or rhesus macaques previously transplanted with E28 pig pancreatic primordia. Our data are consistent with induction of tolerance to an endocrine cell component of porcine islets induced by previous transplantation of embryonic pig pancreas, a novel finding we designate organogenetic tolerance. The potential exists for its use to enable the use of pigs as islet cell donors for humans with no immune suppression requirement