The cost of inaction: a global tool to inform nutrition policy and investment decisions on global nutrition targets.

At present, the world is off-track to meet the World Health Assembly global nutrition targets for 2025. Reducing the prevalence of stunting in children, low birthweight, and anaemia in women and increasing breastfeeding are among the prioritized global nutrition targets for all countries. Governments and development partners need evidence-based data to understand the true costs and consequences of policy decisions and investments. Yet there is an evidence gap on the health, human capital, and economic costs of inaction on preventing undernutrition for most countries. The Cost of Inaction tool, and expanded Cost of Not Breastfeeding tool, provide country-specific data to help to address the gaps. Every year undernutrition leads to 1.3 million cases of preventable child and maternal deaths. In children, stunting results in the largest economic burden yearly at US$548 billion (0.7% of GNI), followed by US$507 billion for sub-optimal breastfeeding (0.6% global GNI), US$344 billion (0.3% of GNI) for low birthweight and US$161 billion (0.2% of GNI) for anaemia in children. Anaemia in WRA costs US$113 billion (0.1% of GNI) globally in current income losses. Accounting for overlap in stunting, suboptimal breastfeeding, and low birthweight, the analysis estimates that preventable undernutrition cumulatively costs the world at least US$761 billion per year, or $2.1B per day. The variation in the regional and country-level estimates reflect the contextual drivers of undernutrition. In the lead up to the renewed WHA targets and Sustainable Development Goals to 2030, the data generated from these tools are powerful information for advocates, governments, and development partners to inform policy decisions and investments into high-impact low-cost nutrition interventions. The costs of inaction on undernutrition continue to be substantial, and serious coordinated action on the global nutrition targets is needed to yield the significant positive human capital and economic benefits from investing in nutrition.

Interstitial deletion 8q11.2-q13 with congenital anomalies of CHARGE association.

Specific genetic loci responsible for CHARGE association are currently unknown. Herein, we describe a neonate with clinical manifestations consistent with CHARGE association who has a de novo interstitial deletion involving bands 8q11.2 to 8q13. Genetic mapping and genomic microarray technology have been used to more accurately define the breakpoints of this deletion. Within the deleted region, there are approximately 150 expressed genes, one or more of which may contribute to the manifestations of CHARGE association.

4p terminal deletion and 11p subtelomeric duplication detected by genomic microarray in a patient with Wolf-Hirschhorn syndrome and an atypical phenotype.

We report a de novo cryptic 11p duplication found by genomic microarray with a cytogenetically detected 4p deletion. Terminal 4p deletions cause Wolf-Hirschhorn syndrome, but the phenotype probably was modified by the paternally derived 11p duplication. This emphasizes the clinical utility of genomic microarray.

Multiple abnormalities detected by dye reversal genomic microarrays in prostate cancer: a much greater sensitivity than conventional cytogenetics.

Prostate cancer remains the most common male malignancy in Western countries, yet limited information exists regarding genetic changes and clinical correlations. The advent of comparative genomic hybridization microarray (GM) technology has recently allowed for precise screening of DNAs for genetic copy number changes; this offers an advantage over previous techniques, including conventional cytogenetics. A problem with cytogenetic prostate cancer analysis has been the study of the appropriate cell types because this is a highly heterogeneous tumor. We have performed GM using the Spectral Genomics Inc. dye reversal platform on 20 primary prostate tumors. These tumor samples were from frozen tissue collected over the last 10 years and multiple clinical parameters, including follow-up were collected on these patients; cytogenetic analysis was previously attempted on all patients. Eighty percent (16/20) of specimens showed copy number changes, 65% of which were losses and 35% were gains of genetic material. The most common changes observed were loss of an interstitial region of 2q (8 cases, 40%), followed by loss of interstitial 6q (6 cases, 30%), loss at 8p and 13q (5 cases each, 25%), gain at 3p and loss at 5q, 16q, and Xq (4 cases each, 20%), and gain at 8p (3 cases, 15%). There was evidence of correlation of loss at 5q with a positive node status. Cytogenetic studies on these same patients only detected clonal changes in 40% (8/20) specimens and did not detect the majority of abnormalities seen by the GM technique. We propose this technology for the evaluation of prostate and other heterogeneous cancers as a rapid and efficient way to detect genetic copy number changes.