Global cost of correcting vision impairment from uncorrected refractive error

Objective

To estimate the global cost of establishing and operating the educational and refractive care facilities required to provide care to all individuals who currently have vision impairment resulting from uncorrected refractive error (URE).

Methods

The global cost of correcting URE was estimated using data on the population, the prevalence of URE and the number of existing refractive care practitioners in individual countries, the cost of establishing and operating educational programmes for practitioners and the cost of establishing and operating refractive care facilities. The assumptions made ensured that costs were not underestimated and an upper limit to the costs was derived using the most expensive extreme for each assumption.

Findings

There were an estimated 158 million cases of distance vision impairment and 544 million cases of near vision impairment caused by URE worldwide in 2007. Approximately 47 000 additional full-time functional clinical refractionists and 18 000 ophthalmic dispensers would be required to provide refractive care services for these individuals. The global cost of educating the additional personnel and of establishing, maintaining and operating the refractive care facilities needed was estimated to be around 20 000 million United States dollars (US$) and the upper-limit cost was US$ 28 000 million. The estimated loss in global gross domestic product due to distance vision impairment caused by URE was US$ 202 000 million annually.

Conclusion

The cost of establishing and operating the educational and refractive care facilities required to deal with vision impairment resulting from URE was a small proportion of the global loss in productivity associated with that vision impairment.     

Regression of experimental Burkitt's lymphoma induced by Epstein-Barr virus-immortalized human B cells

Epstein-Barr virus (EBV)-immortalized human B cells survive only transiently when injected subcutaneously into athymic mice, whereas Burkitt's lymphoma cells give rise to progressively growing subcutaneous tumors. In this study, we tested whether these Burkitt's tumors could be induced to regress via a bystander effect induced by EBV-immortalized B cells. Simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in the same subcutaneous site resulted in tumors that regressed with necrosis and scarring. Similarly, simultaneous inoculation of EBV-immortalized B cells and Burkitt's lymphoma cells in separate subcutaneous sites resulted in regression of a proportion of the Burkitt's tumors. Furthermore, most of the established human Burkitt's tumors regressed with necrosis and scarring after intratumor inoculations with EBV-immortalized B cells. The EBV-immortalized B cells continued to exert this antitumor effect even when killed with irradiation. The experimental approach to Burkitt's lymphoma treatment described here exploits the ability of athymic mice to reject EBV-immortalized B cells to target an effective antitumor response to malignant cells normally incapable of eliciting it.     

关于全基因组相关分析的研究--你首先想要什么：好消息,坏消息,或者好消息？

很久以来都认为遗传成分参与2型糖尿病（T2DM）的发病，但是有关遗传学上的发现一直进展缓慢，这是由于遗传成分的复杂性。有关糖尿病相关的各种表型的研究的大量资料提示，所谓的“T2DM”可能是许多疾病的统称，由于它们具有通常相互重叠的多种基本发病机制。因此，对曾抱有期望的T2DM的遗传学基础的寻求已经证明是很艰难的。     

Natural killer cell precursors in the CD44neg/dim T-cell receptor population of mouse bone marrow

Natural killer (NK) cells develop from the nonadherent cell component of NK long-term bone marrow (BM) cultures (NK-LTBMC). Because these nonadherent cells are depleted of mature NK cells and T cells, but appear to enriched for NK precursors, they were used as a starting population to begin to define the NK precursors that function in NK- LTBMC. As the stromal cell component of NK-LTBMC has been shown to support interleukin (IL)-2-induced, CD44 dependent, NK cell development from nonadherent NK precursors, NK-LTBMC stroma was used in a limiting dilution assay (LDA) to quantitate the precursors. NK-LTBMC in 96-well plates were irradiated (20 Gy) to kill hematopoietic cells (including the NK precursors), seeded with limiting dilutions of the cells to be quantitated, cultured with 500 U/mL IL-2 for 13 days and assayed for development of NK activity by adding 51Cr-labeled YAC-1 cells to the wells and evaluating the release of 51Cr after 4 hours. Flow cytometric analysis, sorting, and quantitation of the nonadherent cell component of NK-LTBMC showed that NK precursors were concentrated in the CD44neg/dim subset that comprised 10% of the "lymphoid" gated cells. When the CD44neg/dim subset was sorted from BM of mice treated with 5- fluorouracil (5-FU) day before (-1FUBM), there were about 30% T cells, but no NK-1.1+ cells. When the T cells were removed by sorting and the CD44neg/dim, alphabeta, gammadelta T-cell receptorneg (TCR-) subpopulation was seeded onto irradiated stroma with IL-2, they proliferated, developed NK activity, became NK-1.1+ and CD44bright and remained alphabeta, gammadelta TCR-. The frequency of NK precursors in this population as estimated from the LDA was about 1/500.     

Assembly of contact-phase factors on the surface of the human neutrophil membrane

H-kininogen (HK), a major factor involved in contact-phase activation, was recently immunolocalized on the external surface of human neutrophils. Experiments were, therefore, designed to consider the question of whether the complete assembly of contact factors occurs on the outer surface of the neutrophil membrane. By immunolocalization techniques, and using specific antibodies directed against the various contact factors, we now demonstrate that plasma prekallikrein (PK), factor XI (FXI), and factor XII (FXII) are present on the exterior face of the human neutrophil. Failure to localize HK, PK, or FXI by monoclonal antibodies directed to their reciprocal binding sites, and displacement of PK/FXI by peptide HK31, which mimics the relevant binding site(s) of HK, suggested that prekallikrein and FXI are anchored to the neutrophil membrane through attachment to the kininogen molecule. Probing of the kinin moiety by a specific antibody showed that kininogen molecules bound to the neutrophil cell membrane contain the kinin sequence, which can be released by plasma kallikrein or by tissue kallikrein. Our results led us to the novel conclusion that neutrophils provide a circulating platform for the components of the contact-phase system.     

FS01.3Disperse (yes), orange (yes), 3 (no): what do we test in textile dye dermatitis?

Introduction:  Patients sensitized to para‐phenylenediamine (PPD) have a high degree of patch test reactivity to Disperse Orange 3 (DO3), and a lesser one to Disperse Red 1 and Red 17. Two successive patients positive to PPD, Disperse Red 1 and 17, negative to DO3 were real eye‐openers for our considerations about purity of our current allergen DO3.
Materials and methods:  We realized comparative thin‐layer chromatography (TLC), with DO3 from Chemotechnique®(DO3‐Chem) and Trolab®(both extracted from petrolatum), and "pure" DO3 from two chemical providers. TLC clearly indicated that DO3‐Chem was not DO3. HPLC analysis with pure DO3 from Chemotechnique® and comparison of structures by NMR with samples of DO3, revealed that DO3‐Chem was Disperse Orange 31 (DO31). In addition, signals through the GERDA network allowed the collection of test materials and observations. Among other members, only 2 used DO3‐Chem (from 2 different batches) that was DO31 too, according to TLC Results: According to their data, they observed no or a lower reactivity to DO3 than expected (4 patients DO3‐Chem + among 23 PPD+ e.g.). Finally, the error was proved to be due to the provider of the dye to Chemotechnique®, who likely deleted the 1 of Disperse Orange 31 on his packaging.
Discussion:  Chemical structure of DO31 indicates a possible in vivo hydrolysis into nitroaniline and a second compound, a substituted PPD derivative that clearly does not frequently react in PPD positive patients. Like drugs, patch tests are submitted to post‐commercialization controls. In addition to allergens providers who should enhance their quality controls, dermato‐allergologists have to be vigilant, and must active networks when they observe a rare bird.