PubMed · 4906708
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J Sénécal. 1968. [Malnutrition in children].. https://pubmed.ncbi.nlm.nih.gov/4906708/
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Cataract prevalence increases with age. As the world's population ages, cataract-induced visual dysfunction and blindness is on the increase. This is a significant global problem. The challenges are to prevent or delay cataract formation, and treat that which does occur. Genetic and environmental factors contribute to cataract formation. However, reducing ocular exposure to UV-B radiation and stopping smoking are the only interventions that can reduce factors that affect the risk of cataract. The cure for cataract is surgery, but this is not equally available to all, and the surgery which is available does not produce equal outcomes. Readily available surgical services capable of delivering good vision rehabilitation must be acceptable and accessible to all in need, no matter what their circumstances. To establish and sustain these services requires comprehensive strategies that go beyond a narrow focus on surgical technique. There must be changes in government priorities, population education, and an integrated approach to surgical and management training. This approach must include supply of start-up capital equipment, establishment of surgical audit, resupply of consumables, and cost-recovery mechanisms. Considerable innovation is required. Nowhere is this more evident than in the pursuit of secure funding for ongoing services.
The effect of adjuvant tamoxifen treatment on bone mineral density (BMD) and bone turnover markers was studied in postmenopausal breast cancer patients. The relationship of tamoxifen's effect with the genetic polymorphisms of estrogen receptor (ER)-alpha and ER-beta gene was also studied. Twenty-one postmenopausal breast cancer patients were given tamoxifen (20 mg/day) as the adjuvant treatment after the surgery. BMD of the lumbar supine (dual emission X-rays absorptiometry) and bone resorption (deoxypyridinoline, aminoterminal telopeptide of type I collagen, and carboxyterminal telopeptide of type I collagen) and formation (propeptide of type I procollagen, osteocalcin, and bone-specific alkaline phosphatase) markers were examined at baseline (before the surgery), 6 and 12 months after the start of tamoxifen treatment. Genetic polymorphisms analyzed were TA dinucleotide repeats polymorphism in the promoter region and PvuII and XbaI restriction fragment length polymorphism for the ER-alpha gene and the CA dinucleotide repeats polymorphism in the intron 5 for the ER-beta gene. Tamoxifen significantly increased BMD of the lumbar spine at both 6 (P<0.01) and 12 months (P<0.01) after the start of tamoxifen as compared with that at baseline. The mean percent increase in BMD was 3.3% at 6 months and 2.7% at 12 months. All bone resorption and formation markers significantly decreased at both 6 and 12 months. Among the four genetic polymorphisms studied, only ER-beta CA repeat polymorphism was found to be significantly associated with BMD at 12 months, i.e. BMD of the 21 CA repeats allele carriers was significantly higher than that of the non-carriers (P=0.025). These results suggest that tamoxifen increases BMD of the lumbar supine by reducing the bone turnover in postmenopausal breast cancer patients, and this bone restoring effect of tamoxifen is more marked in ER-beta 21 CA repeats allele carriers than non-carriers.
IDDM10 on chromosome 10p11-q11 has been identified as a putative diabetes susceptibility locus through affected sib-pair (ASP) linkage analysis in UK nuclear families [Davies et al., 1994: Nature 371:130-136; Reed et al., 1997: Hum Mol Genet 6:1011-1016; Mein et al., 1998: Nat Genet 19:297-300]. We extended analysis of linkage to type 1 diabetes in this region by typing a total of 61 markers in a maximum of 418 UK sib-pairs (UK418; peak MLS = 3.84). We then stratified the dataset based on analyses performed previously by both our group [Mein et al., 1998: Nat Genet 19:297-300] and others [Paterson et al., 1999: Hum Hered 49:197-204; Paterson and Petronis, 1999a: Am J Med Genet 84:15-19; Paterson and Petronis, 2000a: J Med Genet 37:186-191; Paterson and Petronis, b: Eur J Hum Genet 8:145-148] and used a permutation procedure to assess the significance of the results. We conclude that the results obtained had a high probability of occurring by chance alone. These data highlight the limitations of stratifying small datasets (n < 500) by additional criteria and the recurrent problems of multiple testing in genetic analysis.