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Splicing factor SC35 is an essential component of the spliceosome, the cellular apparatus that removes introns from pre-mRNA to provide alternatively spliced isoforms. Many proteins associated with development of uterine receptivity and embryo implantation are present as isoforms, the tissue-specific expression of which may be regulated through alternative splicing. SC35 was identified as being increased at implantation sites during early pregnancy in mice. However, the present study has demonstrated that SC35 is present in human and rhesus monkey endometrium, that the protein is increased during the secretory phase of the oestrous cycle compared with the proliferative phase in both these primates and that it is present in a distinct pattern within the nucleus of both epithelial and stromal cells, as well as in cells of the vasculature. Both the intensity of immunoreactive protein and the proportion of cells that stain for SC35 alter with the phase of the oestrous cycle. A very precise expression pattern of SC35 (both protein and mRNA) was seen during early placentation in rhesus monkeys. At implantation sites between day 24 and day 35 of early pregnancy, SC35 was expressed strongly in cytotrophoblasts within the trophoblastic shell, in syncytiotrophoblast at the periphery of the cell column and in both cytotrophoblast and syncytiotrophoblast in the floating villi. In the adjacent maternal decidua, expression of SC35 was weak. These results indicate a role for SC35 in preparation of a receptive uterus, in the provision of secreted proteins to support blastocyst development and in trophoblast invasion.

A difference in length or height growth is observed between populations in developing and developed countries and, within a country, between well‐off and poor subpopulations. The aim of this community‐based study was to identify possible risk factors for growth stunting in early life using the infancy‐childhood‐puberty (ICP) growth model. A periurban slum, a village and an urban slum, plus a local control group in Lahore, Pakistan, were investigated. In total, there were 425 infants born from September 1984 to March 1987 in the study. Children were followed from birth to 24 months and anthropometric data were recorded at each examination. A well‐designed questionnaire was used to collect background information to identify risk factors for growth faltering over this period. The age at onset of the childhood component was determined individually using the ICP growth model. A late onset was defined as onset after 12 months. Univariate odds ratio analysis identified 20 significant risk factors for a delayed childhood onset in the total sample. Backward logistical analysis showed that only six variables were significant, i.e. small number of rooms in a household, episode(s) of diarrhoeal diseases, poor house structure, low body mass index, early end of breastfeeding and birth in warm season. Stratified analysis showed that episode(s) of diarrhoeal diseases and birth in warm season were the only significant risk factors in the two poor areas. This study also found that the impact of diarrhoeal diseases on length growth persisted after allowing for birth season. Seasonal variation in length growth was seen in the age at onset of the childhood component. General socioeconomic status was found to be a risk factor for growth faltering in early life. Diarrhoeal diseases and being born in a warm season are particular risk factors for growth faltering in early life.