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Trends in Viet Nams infant and child mortality in the prewar period (before 1965) the war period (1965-75) and the postwar period (1976 and later) were examined. Data were obtained on >13000 live births and 737 deaths of children >6 years from the first 1988 Viet Nam Demographic and Health Survey of reproductive health and behavior. Regions were designated as north and south and levels of war activity were assigned to the following provinces: high Nghe Tinh Binh Tri Tien) intermediate (Hanoi Ha Bac Ha Nan Ninh Phu Khahn) and low (Tien Giang Dong Nai Hai Hung Cao Bang Hau Giang Ho Chi Minh City). The stratified analysis and logistic regressions included confounding factors such as material age infants sex mothers education and birth orders. There was clearly a decreasing mortality rate between the prewar and postwar periods. The relative risk (RR) ratios were 1.3 and 1.8. Decreases were particularly prominent for postneonatal mortality. There was little or no decline between wartime and postwartime mortality (RRs of .9 to 1.0). Mortality risk was increased at all ages for males children born to mothers 21 years old children of less educated mothers and children of birth order 5 or higher. When these factors were adjusted for mortality was higher in the prewar period and declined during the war and remained stable. The south showed a greater reduction of mortality than the north particularly for infant mortality. Analysis of level of war activity showed low and intermediate war level provinces had declines in mortality. High war areas had lower prewar rates (RRs of .6 to .9) and infant mortality declined to levels 30% lower than wartime rates. THus the wartime effect on mortality was most intense in provinces with high levels of war activity. A data limitation affecting the conclusions was the availability of data only on longterm survivors of the war; mortality among orphans was excluded. Another limitation was data pertained to residence at the time of the survey and not at the time of the birth. Estimates may not be very accurate for the war period. The suggestion was that in a rural economy not relying on infrastructure such as manufacturing and transportation provision of essentials is decentralized and less harmful to survival. Caution is urged in applying the findings to other wars or other indices of child health.

PurposeTo identify the molecular basis for autosomal recessively inherited congenital non-syndromic pulverulent cataracts in a consanguineous family with four affected children.MethodsAn autozygosity mapping strategy using high density SNP microarrays and microsatellite markers was employed to detect regions of homozygosity. Subsequently good candidate genes were screened for mutations by direct sequencing.ResultsThe SNP microarray data demonstrated a 24.96 Mb region of homozygosity at 22q11.21-22q13.2 which was confirmed by microsatellite marker analysis. The candidate target region contained the beta-crystallin gene cluster and direct sequencing in affected family members revealed a novel mutation in CRYBB1 (c.2T>A; p.Met1Lys).ConclusionsTo our knowledge this is the first case of an initiation codon mutation in a human crystallin gene, and only the second report of a CRYBB1 mutation associated with autosomal recessive congenital cataracts. In addition, although a number of genetic causes of autosomal dominant pulverulent cataracts have been identified (including CRYBB1) this is the first gene to have been implicated in autosomal recessive nuclear pulverulent cataract.

Human uteroglobin (hUG) or Clara cell 10-kD protein (cc10 kDa) is a steroid-dependent, immunomodulatory, cytokine-like protein, It is secreted by mucosal epithelial cells of all vertebrates studied, The cDNA encoding hUG and the 5' promoter region of the gene have been characterized previously, Here, we report that the structure of the entire hUG gene is virtually identical to those of rabbit, rat, and mouse, It is localized on human chromosome 11q12.3-13.1, a region in which several important candidate disease genes have been mapped by linkage analyses, Our data indicate that candidate genes for atopic (allergic) asthma and Best's vitelliform macular dystrophy are in closest proximity to the hUG gene, To determine whether hUG gene mutation may be involved in the pathogenesis of these diseases, we studied two isolated groups of patients, each afflicted with either atopy or Best's disease, respectively, We detected a single base-pair change in the hUG gene in Best's disease patients and normal controls but no such change was detected in atopy patients, This alteration in hUG gene-sequence in Best disease family appears to be a polymorphism, Although the results of our investigation did not uncover mutations in hUG gene that could be causally related to the pathogenesis of either of these diseases, its conservation throughout vertebrate phyla implies that this gene is of physiological importance, Moreover, the close proximity of this gene to several candidate disease genes makes it an important chromosomal marker in cloning and characterization of those genes.

Bardet–Biedl syndrome (BBS, MIM 209900) is a heterogeneous autosomal recessive disorder characterized by obesity, pigmentary retinopathy, polydactyly, renal malformations, mental retardation, and hypogenitalism1,2,3,4. The disorder is also associated with diabetes mellitus, hypertension, and congenital heart disease4,5,6. Six distinct BBS loci map to 11q13 (BBS1), 16q21 (BBS2), 3p13–p12 (BBS3), 15q22.3–q23 (BBS4), 2q31 (BBS5), and 20p12 (BBS6)7,8,9,10,11,12,13. Although BBS is rare in the general population (