Optimal care for children and adolescents with type 1 diabetes is well described in guidelines, such as those of the International Society for Pediatric and Adolescent Diabetes. High‐income countries can usually provide this, but the cost of this care is generally prohibitive for lower‐income countries. Indeed, in most of these countries, very little care is provided by government health systems, resulting in high mortality, and high complications rates in those who do survive. As lower‐income countries work toward establishing guidelines‐based care, it is helpful to describe the levels of care that are potentially affordable, cost‐effective, and result in substantially improved clinical outcomes. We have developed a levels of care concept with three tiers: “minimal care,” “intermediate care,” and “comprehensive (guidelines‐based) care.” Each tier contains levels, which describe insulin and blood glucose monitoring regimens, requirements for hemoglobin A1c (HbA1c) testing, complications screening, diabetes education, and multidisciplinary care. The literature provides various examples at each tier, including from countries where the life for a child and the changing diabetes in children programs have assisted local diabetes centres to introduce intermediate care. Intra‐clinic mean HbA1c levels range from 12.0% to 14.0% (108‐130 mmol/mol) for the most basic level of minimal care, 8.0% to 9.5% (64‐80 mmol/mol) for intermediate care, and 6.9% to 8.5% (52‐69 mmol/mol) for comprehensive care. Countries with sufficient resources should provide comprehensive care, working to ensure that it is accessible by all in need, and that resulting HbA1c levels correspond with international recommendations. All other countries should provide Intermediate care, while working toward the provision of comprehensive care.

As a major component of the extracellular matrix, proteoglycans influence the mechanical properties of connective tissue and play an important role in cell-cell and cell-matrix interactions. Genetic defects of proteoglycan biosynthesis lead to multi-system disorders, often most prominently affecting the skeletal system and skin. Specific deficiencies in the enzymes involved in the biosynthesis of the linkage region between the core of the proteoglycan protein and its glycosaminoglycan side chains are known as linkeropathies. We report on a patient from a second family with a homozygous c.830 G>A (p.Arg277Gln) mutation in the B3GAT3 gene. The clinical features expand the previously reported phenotype of B3GAT3 mutations and of linkeropathies in general. This patient has short stature, facial dysmorphisms, skeletal findings, joint laxity, and cardiac manifestations similar to those previously associated with B3GAT3 mutations. However, he also has developmental delay, a visual refractory defect, dental defects, pectus carinatum, and skin abnormalities that have only been associated with linkeropathies caused by mutations in B4GALT6 and B4GALT7. He has bilateral inguinal hernias and atlanto-axial as well as atlanto-occipital instability that have not been previously associated with B3GAT3 mutations. We provide a detailed clinical report and a comparative overview of the phenotypic features of the linkeropathies caused by mutations in B3GAT3, B4GALT6 and B4GALT7.

To date, large-scale production of Cryptosporidium parvum oocysts has only been achieved by amplification in neonatal calves and sheep. Many laboratories currently depend on supplies from external sources and store oocysts for prolonged periods which results in progressive loss of viability. Six to 8-week-old interferon gamma receptor knockout (IFN gamma R-KO) mice on a C57BL/6 background were inoculated by gavage (2000 oocysts/animal). Fecal pellets were collected daily from 7 days post-infection (p.i.) up to 2 weeks p.i. Intestinal oocyst yield was assessed at days 11, 12 and 14 p.i. by homogenization of intestinal tissues. Ether extraction and one or more NaCl flotations were used to purify oocysts. Total recoveries averaged 2.6 x 10(6) oocysts/mouse from fecal material and 3.8 x 10(7) oocysts/mouse from intestinal tissues. Overall, 2.3 x 10(9) purified oocysts were obtained from 60 mice. Recovered oocysts were capable of sporulation and were shown to be infectious both in vitro and in vivo. Oocyst amplification was achieved in only 11-14 days with minimal expense. The simplicity of this method presents a practical alternative for the routine passage, maintenance and storage of C. parvum in biomedical laboratories.