Comparative studies are lacking on intimate partner violence (IPV) between urban poor and general populations. The objective of this study is to identify the prevalence and risk factors of physical IPV among the general and poor populations in urban Nepal. A cross-sectional study was conducted by structured questionnaire interview. Participants included 905 ever-married women in Kathmandu aged 15 to 49 years. Of the 905 participants, 680 were randomly selected from general population and 225 were recruited from urban poor population, who lived in purposively selected two communities. The prevalence and association between ever experiencing physical IPV and sociodemographic variables were examined. Results showed that the prevalence of physical IPV was 33.8% among the urban poor population (n = 225) and 19.9% among the general population (n = 680; p < .01). Several factors were significantly associated with physical IPV in both populations: the frequency of the husband's drinking, polygyny, and lower household economic status. However, two factors were associated with physical IPV only among the general population: the husband's lower educational level and early marriage. The conclusions of this study are that compared to the general population, the urban poor population showed a significantly higher prevalence of physical IPV and differences in the associated risk factors. The urban poor population requires focused data collection as well as tailored interventions to reduce IPV.

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Dystrophinopathy is caused by alterations in DMD. Approximately 1% of patients remain genetically undiagnosed because intronic variations are not detected by standard methods. Here, we combined laboratory and in silico analyses to identify disease-causing genomic variants in genetically undiagnosed patients and determine the regulatory mechanisms underlying abnormal DMD transcript generation. DMD transcripts from 20 genetically undiagnosed dystrophinopathy patients in whom no exon variants were identified, despite dystrophin deficiency on muscle biopsy, were analyzed by transcriptome sequencing. Genome sequencing captured intronic variants and their effects were interpreted using in silico tools. Targeted long-read sequencing was applied in cases with suspected structural genomic abnormalities. Abnormal DMD transcripts were detected in all cases analyzed. Exonization of intronic sequences was observed in 15 cases and exon skipping in one case; 13 single nucleotide variants and three structural rearrangements were identified as causal genomic variations. DMD transcripts were aberrantly spliced and polyadenylated in two cases in which chromosome rearrangements were detected. In one case, DMD transcripts were terminated due to nucleotide repeat expansion. Our combined analysis approach successfully identified pathogenic events. Detection of diseasing-causing mechanisms in DMD transcripts could inform the therapeutic options for patients with dystrophinopathy.