Background In the past few months, the coronavirus disease (COVID-19) pandemic has caused extensive economic and social damage. Objective The purpose of this study was to assess the impact of COVID-19–related measures on partner relationships and sexual and reproductive health in China. Methods From May 1 to 5, 2020, 3500 young Chinese individuals were recruited through WeChat or Weibo to participate in a survey to obtain information on sexual and reproductive health (eg, sexual desire, frequency of sexual intercourse, sexual satisfaction, etc). The questionnaire also collected demographic data (eg, age, race, education, current financial status, sexual orientation, relationship status, etc). Results In total, 967 participants were included in the sexual health analysis. Due to the COVID-19 pandemic and related containment measures, 22% of participants (n=212) reported a decrease in sexual desire; 41% (n=396) experienced a decrease in the sexual intercourse frequency; 30% (n=291) reported an increase in the frequency of masturbation; 20% (n=192) reported a decrease in alcohol consumption before or during sexual activities, and 31% (n=298) reported a deterioration in partner relationships during the pandemic. The logistic regression analysis indicated that the following influenced partner relationships: accommodations during the pandemic (P=.046; odds ratio [OR] 0.59; 95% CI 0.30-0.86); exclusive relationship status (yes or no) (P<.001; OR 0.44; 95 % CI 0.27-0.73); sexual desire (P=.02; OR 2.01; 95% CI 1.38-2.97); and sexual satisfaction (P<.001; OR 1.92; 95% CI 1.54-2.50). COVID-19 also caused disruptions in reproductive health services such as prenatal and postnatal care, childbirth and abortion services, contraception availability, and the management of sexually transmitted infections. Conclusions Our results show that many young people have wide-ranging issues affecting their sexual and reproductive health due to the COVID-19 pandemic and related containment measures. Strategies and guidelines are needed to safeguard the sexual and reproductive health of young people during this pandemic.
The generation of beta-thalassemia (β-Thal) patient-specific induced pluripotent stem cells (iPSCs), subsequent homologous recombination-based gene correction of disease-causing mutations/deletions in the β-globin gene (HBB), and their derived hematopoietic stem cell (HSC) transplantation offers an ideal therapeutic solution for treating this disease. However, the hematopoietic differentiation efficiency of gene-corrected β-Thal iPSCs has not been well evaluated in the previous studies. In this study, we used the latest gene-editing tool, clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated 9 (Cas9), to correct β-Thal iPSCs; gene-corrected cells exhibit normal karyotypes and full pluripotency as human embryonic stem cells (hESCs) showed no off-targeting effects. Then, we evaluated the differentiation efficiency of the gene-corrected β-Thal iPSCs. We found that during hematopoietic differentiation, gene-corrected β-Thal iPSCs showed an increased embryoid body ratio and various hematopoietic progenitor cell percentages. More importantly, the gene-corrected β-Thal iPSC lines restored HBB expression and reduced reactive oxygen species production compared with the uncorrected group. Our study suggested that hematopoietic differentiation efficiency of β-Thal iPSCs was greatly improved once corrected by the CRISPR/Cas9 system, and the information gained from our study would greatly promote the clinical application of β-Thal iPSC-derived HSCs in transplantation.
Highlights d TAM efficiently modulates four types of splicing in their native genomic context d Genetic modulation of RNA splicing elucidates functions of splicing isoforms d TAM enables both loss-and gain-of-function studies of splicing events d TAM corrects the open reading frame of 99.9% of DMD transcripts in patient iPSCs
-Thalassemia (-Thal) is one of the most common genetic diseases in the world. The generation of patient-specific -Thalinduced pluripotent stem cells (iPSCs), correction of the disease-causing mutations in those cells, and then differentiation into hematopoietic stem cells offers a new therapeutic strategy for this disease. Here, we designed a CRISPR/Cas9 to specifically target the Homo sapiens hemoglobin  (HBB) gene CD41/ 42(؊CTTT) mutation. We demonstrated that the combination of single strand oligodeoxynucleotides with CRISPR/Cas9 was capable of correcting the HBB gene CD41/42 mutation in -Thal iPSCs. After applying a correction-specific PCR assay to purify the corrected clones followed by sequencing to confirm mutation correction, we verified that the purified clones retained full pluripotency and exhibited normal karyotyping. Additionally, whole-exome sequencing showed that the mutation load to the exomes was minimal after CRISPR/Cas9 targeting. Furthermore, the corrected iPSCs were selected for erythroblast differentiation and restored the expression of HBB protein compared with the parental iPSCs. This method provides an efficient and safe strategy to correct the HBB gene mutation in -Thal iPSCs.
Spinocerebellar ataxia type 3 (SCA3) is caused by an abnormal expansion of the cytosine-adenine-guanine (CAG) triplet in ATXN3, which translates into a polyglutamine (polyQ) tract within ataxin-3 (ATXN3) protein. Although the pathogenic mechanisms remain unclear, it is well established that expression of mutant forms of ATXN3 carrying an expanded polyQ domain are involved in SCA3 pathogenesis, and several strategies to suppress mutant ATXN3 have shown promising potential for SCA3 treatment. In this study, we described successful clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated deletion of the expanded polyQ-encoding region of ATXN3 in induced pluripotent stem cells (iPSCs) derived from a SCA3 patient, and these patient-specific iPSCs retained pluripotency and neural differentiation following expanded polyQ deletion. Furthermore, the ubiquitin-binding capacity of ATXN3 was retained in the neural cells differentiated from the corrected iPSCs. For the first time, this work provides preliminary data for gene editing by CRISPR/Cas9 in SCA3, and demonstrates the feasibility of using a single-guide RNA pair to delete the expanded polyQ-encoding region of ATXN3, suggesting the potential efficacy of this method for future therapeutic application.
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