Chronic disease, mental health symptoms and poor social relations are reported common causes for poor self-rated health in older people. To assess the co-occurrence rate of chronic diseases, poor mental health and poor social relationships in older people, and determine their association with self-rated health. 6,551 older people in Zhongshan, China, participated a large health surveillance program were randomly selected and questioned about their SRH, chronic conditions, mental health symptoms and social relationships. The association between self-rated health and chronic conditions, poor mental health, social relationships, and their co-occurrence were analyzed. 56.4% of participants reported poor self-rated health. 39.1% experienced at least one chronic disease. 29.0% experienced one or more mental health symptoms; 19.5% experienced at least one poor social relationship. 7.8% had co-occurrence of chronic diseases, mental health problems, and poor social relationships. Logistic regressions showed that poor self-rated health was associated with chronic diseases, poor mental health, poor social relationships and their co-occurrence. The findings indicate the importance of managing chronic disease, poor mental health and poor social relationships for older people.

The 4-bp deletion (-CTTT) at codon 41/42 (CD41/42) of the human beta-globin gene represents one of the most common beta-thalassemia mutations in East Asia and Southeast Asia, which is historically afflicted with endemic malaria, thus hypothetically evolving under natural selection by malaria infection. To understand the evolutionary process of generating the beta(CD41/42) allele and its maintenance, including the effect of natural selection on the pattern of linkage disequilibrium (LD), we sequenced a 15.933-kb region spanning 20.693 kb of the beta-globin cluster surrounding the 4-bp deletion using a sample from a Chinese population consisting of 24 normal individuals and 16 heterozygotes for the deletion. Forty-nine polymorphic sites were found. Analysis of the data, using a variety of methods including formal population genetics analysis and visual approaches, suggests that the spread of the CD41/42 (-CTTT) deletion is most likely mediated by interallelic gene conversion, although independent deletions in different lineages are also possible. The neutrality test resulted in a significant positive Tajima's D for the beta-globin locus, which is consistent with the existence of balancing selection. This suggests that the 4-bp deletion that occurred at this locus may be an event that is subject to natural selection, due to malaria, which leads to the heterozygote advantage, spread widely with further help by conversion and migration. The evolutionary process of this mutant through gene conversion that could conceivably take place between the 4-bp deletion and the normal sequence in the respective region is discussed in detail.

Class III malocclusion is a common dentofacial deformity. The underlying genetic alteration is largely unclear. In this study, we sought to determine the genetic etiology for Class III malocclusion. A four‐generation pedigree of Class III malocclusion was recruited for exome sequencing analyses. The likely causative gene was verified via Sanger sequencing in an additional 90 unrelated sporadic Class III malocclusion patients. We identified a rare heterozygous variant in endoplasmic reticulum lectin 1 (ERLEC1; NM_015701.4(ERLEC1_v001):c.1237C>T, p.(His413Tyr), designated as ERLEC1‐m in this article) that cosegregated with the deformity in pedigree members and three additional rare missense heterozygous variants (c.419C>G, p.(Thr140Ser), c.419C>T, p.(Thr140Ile), and c.1448A>G, p.(Asn483Ser)) in 3 of 90 unrelated sporadic subjects. Our results showed that ERLEC1 is highly expressed in mouse jaw osteoblasts and inhibits osteoblast proliferation. ERLEC1‐m significantly enhanced this inhibitory effect of osteoblast proliferation. Our results also showed that the proper level of ERLEC1 expression is crucial for proper osteogenic differentiation. The ERLEC1 variant identified in this study is likely a causal mutation of Class III malocclusion. Our study reveals the genetic basis of Class III malocclusion and provides insights into the novel target for clinical management of Class III malocclusion, in addition to orthodontic treatment and orthodontic surgery.