Novel approach of phosphate-reclamation as struvite from sewage sludge by utilising hydrothermal carbonization.

Hydrothermal carbonization (HTC) showed promising performance as an alternative sewage sludge treatment already, as the draining ability of sludge is improved while fuel properties of the yielded hydrochar are superior to native sludge. On the other hand, the sole combustion of sewage sludge and its corresponding hydrochars are a waste in terms of nutrients like phosphorus and nitrogen. Therefore, a combination of HTC and a nutrient recycling strategy via the precipitation of phosphate and nitrogen as struvite (magnesium ammonium phosphate) are introduced in this research. We used an anaerobically digested sewage sludge with high loads of aluminium- and ironsalts. Phosphate release cannot be reached by HTC alone, as phosphate is heavily bound in stable iron- and aluminium-associations. An acid leaching step removes it from the hydrochar (58.5-94.8% P), while the process liquid arising from HTC is used as ammonium source (107-291 mmol l-1NH4). After adjusting pH and addition of a magnesium source, struvite is rapidly precipitated in high purity. Nitric acid is used as a "catalyst" in HTC to improve the degree of carbonization on one hand but also improve the phosphate recovery on the other hand by increasing the amount of ammonium available for struvite formation in the process liquid. The highest total recovery rate of phosphate from sludge was 82.5 wt.% and therefore this approach showed to be a serious alternative to other P-recovery techniques.

The immunosuppressive mechanism of total lymphoid irradiation. I. The effect on IL-2 production and IL-2 receptor expression.

Total lymphoid irradiation is an effective immunosuppressive therapy used to prepare patients for organ transplantation and to treat several autoimmune diseases. We have used the mouse model to investigate the mechanism of TLI-induced immunosuppression. Mice were irradiated with 250-rad daily fractions to a total dose of 3500 rads. Splenocytes from control and TLI-treated mice were analyzed for IL-2 production, IL-2 receptor expression after mitogen stimulation, and percent L3T4 positive cells. At two weeks following the completion of TLI, IL-2 production from whole spleen populations had decreased 90% compared with controls (TLI mean IL-2 units = 25 +/- 9.0, control mean = 277 +/- 104). IL-2 receptor expression on splenocytes following Con A stimulation was decreased 80% compared with controls (TLI mean percentage of IL-2 receptor expressing cells = 16.2 +/- 4.1, control mean = 82.0 +/- 7.5). L3T4+ cells that expressed IL-2 receptor were also decreased following TLI (TLI mean = 4.4 +/- 1.4, control mean = 22.0 +/- 3.8), as were proliferative responses to Con A and PHA. Addition of recombinant mouse IL-2 did not restore IL-2 receptor expression or proliferative responses. Whole TLI-treated splenocytes did not suppress IL-2 production or proliferative responses of normal splenocytes. These immunologic abnormalities recovered over time, and by 8 weeks post TLI IL-2 production, IL-2 receptor expression, L3T4+ cell numbers and proliferative responses had returned toward normal. These results suggest that TLI therapy transiently depletes IL-2 producing, IL-2 receptor expressing, and mitogen responsive lymphocytes. The immunosuppression is not mediated through a suppressor cell and is independent of IL-2 production.

Mechanisms of total lymphoid irradiation-induced immunosuppression. II. Failure of con A-stimulated splenocytes from TLI-treated mice to express IL-2 and IL-2 receptor RNA.

Total lymphoid irradiation is a radiotherapy procedure used as an alternative immunosuppressive regimen in organ transplantation. Following TLI mature lymphocytes are depleted, and splenocytes do not proliferate to mitogens, produce IL-2, or express IL-2 receptors. We now show that mitogen stimulated splenocytes from TLI-treated mice do not secrete IL-2 protein by an IL-2 ELISA assay. Northern blot analysis and RNase protection assays reveal that TLI splenocytes do not make IL-2 RNA or IL-2 receptor RNA following mitogen stimulation. TLI splenocytes produce at least 1000 times less IL-2 RNA after Con A stimulation than normal splenocytes. TLI therapy resembles anti-CD4 therapy and CsA in that each results in an IL-2-"depleted" state.

A model hospital standards and accreditation system for Pakistan.

This article treats the use of a system of hospital standards and accreditation as a means to improve the quality of health care services in Pakistan. In it the author stresses the importance of nationwide standards for accreditation as an educational measure and an incentive to improve, as opposed to a punitive measure. The author outlines a series of recommendations, which followed from the Workshop on Hospital Standards and Accreditation, on the implementation of an accreditation system. These recommendations include the establishment of a National Council, composed of representatives from the government, the private sector and professional organizations, with the authority to oversee the system. The recommendations also stress that the accreditation system should be voluntary, in keeping with the system's educational rather than punitive goal. Finally, the author details a methodology for developing standards in specialized areas through corresponding standards committees.

Blocking of mixed lymphocyte reaction by spleen cells from total lymphoid-irradiated mice involves interruption of the IL-2 pathway.

Treatment with total lymphoid irradiation (TLI) before organ transplantation results in high incidences of donor-specific tolerance. However, the exact mechanism of how TLI induces or maintains tolerance is not known. In many experimental systems of tolerance, lack of IL-2 plays a central role in tolerance induction, as stimulation of immunocompetent cells with Ag in an insufficient IL-2 environment results in tolerance. To examine whether tolerance induction by TLI might involve the IL-2 pathway, we examined how TLI cells affect the ability of immunocompetent cells to produce IL-2 and express IL-2R in the MLR. Responder cells from MLR cultures in which cells from TLI-treated mice were added proliferated 50 to 70% less and produced 68 to 94% less IL-2 bioactivity than responder cells from control cultures. However, coculture of TLI cells into MLR did not alter IL-2R expression on responder cells, as measured by two-color FACS analysis. We found no evidence that TLI cells deleted MLR responder cells. Interestingly, exogenous IL-2 did not restore proliferation of MLR responder cells. These results suggest that TLI may induce tolerance by interrupting the IL-2 pathway in immunocompetent cells. Moreover, that exogenous IL-2 failed to restore immunocompetence suggests that tolerance in the TLI model may be easy to induce and very stable, and provides a rationale for the higher incidences of donor-specific tolerance after TLI treatment.