Magnetic particle testing, as an efficient non-destructive testing method, has been widely applied in the field of defect detection for precision components. This study reports a case of occupational ultraviolet cataract caused by prolonged exposure of a magnetic particle testing worker to ultraviolet radiation exceeding standard intensity levels. Insufficient awareness of the potential ocular damage caused by long-wave ultraviolet radiation, inadequate provision of protective goggles, and non-compliant occupational hygiene monitoring and health examinations were identified as the primary contributing factors to this case.

Magnetic particle testing, as an efficient non-destructive testing method, has been widely applied in the field of defect detection for precision components. This study reports a case of occupational ultraviolet cataract caused by prolonged exposure of a magnetic particle testing worker to ultraviolet radiation exceeding standard intensity levels. Insufficient awareness of the potential ocular damage caused by long-wave ultraviolet radiation, inadequate provision of protective goggles, and non-compliant occupational hygiene monitoring and health examinations were identified as the primary contributing factors to this case.

Inflammatory bowel disease （IBD）， mainly including ulcerative colitis （UC） and Crohn's disease （CD）， is a common chronic inflammatory disease of the gastrointestinal tract， with its incidence increasing year by year. Due to its long treatment duration， difficulty in treatment， prolonged remission， and high costs， it has attracted global attention. Exploring safe， effective， and sustainable treatment regimens has become an urgent global issue. The pathogenesis of IBD is complex， involving intestinal mucosal injury，disturbances in the internal environment， and inflammatory responses. In recent years， research has found that ferroptosis is also one of the important pathogenic factors of IBD. Ferroptosis， as a new form of non-apoptotic cell death， is characterized by iron dependence， lipid peroxidation， and imbalance in the redox system. Studies have shown that inhibiting ferroptosis in intestinal epithelial cells can protect the intestinal mucosa. Targeted intervention in ferroptosis may be a new direction for the treatment of IBD. IBD is mainly treated with drugs， including corticosteroids， aminosalicylates， biologics， and immunomodulators， but drug resistance and adverse reactions are common. Traditional Chinese medicine （TCM） has unique advantages such as low cost， low drug resistance， and fewer side effects， and has accumulated rich experience in the treatment of IBD. Scholars have confirmed that TCM can inhibit ferroptosis， and recent studies have shown that TCM can not only inhibit iron-dependent lipid peroxidation in intestinal cells but also enhance the antioxidant and anti-inflammatory abilities of intestinal mucosa， thus playing a role in the treatment of IBD. Increasing evidence suggests that TCM may treat IBD by interfering with ferroptosis. This article explores the relevance of TCM intervention in ferroptosis and the treatment of IBD， discusses the possible mechanisms of ferroptosis in IBD， and aims to provide a basis for the diagnosis and treatment of IBD.

Recently, small nucleolar RNAs (snoRNAs) have transcended the genomic "noise" to emerge as pivotal molecular markers due to their essential roles in tumor progression. Substantial evidence indicates a strong association between snoRNAs and critical clinical features such as tumor pathology and drug resistance. Historically, snoRNA research has concentrated on two classical mechanisms: 2'-O-ribose methylation and pseudouridylation. This review specifically summarizes the novel regulatory mechanisms and functional patterns of snoRNAs in tumors, encompassing transcriptional, post-transcriptional, and post-translational regulation. We further discuss the synergistic effect between snoRNA host genes (SNHGs) and snoRNAs in tumor progression. More importantly, snoRNAs extensively contribute to the development of tumor cell resistance as oncogenes or tumor suppressor genes. Accordingly, we provide a comprehensive review of the clinical diagnosis and treatment associated with snoRNAs and explore their significant potential as novel drug targets.

Recently,small nucleolar RNAs(snoRNAs)have transcended the genomic"noise"to emerge as pivotal molecular markers due to their essential roles in tumor progression.Substantial evidence indicates a strong association between snoRNAs and critical clinical features such as tumor pathology and drug resistance.Historically,snoRNA research has concentrated on two classical mechanisms:2'-O-ribose methylation and pseudouridylation.This review specifically summarizes the novel regulatory mecha-nisms and functional patterns of snoRNAs in tumors,encompassing transcriptional,post-transcriptional,and post-translational regulation.We further discuss the synergistic effect between snoRNA host genes(SNHGs)and snoRNAs in tumor progression.More importantly,snoRNAs extensively contribute to the development of tumor cell resistance as oncogenes or tumor suppressor genes.Accordingly,we provide a comprehensive review of the clinical diagnosis and treatment associated with snoRNAs and explore their significant potential as novel drug targets.

Megalencephalic leukoencephalopathy with subcortical cysts (MLC, OMIN: 604004) caused by mutations in the MLC1 gene, is an rare autosomal recessive disorder. More patients are with infancy and young children onset, whereas adult cases are rare. Only 2 patients from 1 family have been reported in domestic adult cases. Now a 58-year-old female MLC patient is reported. The clinical manifestations of the patient included large head circumference, slow responses, walking difficulties, seizures and paroxysmal loss of consciousness. The result of whole exome sequencing revealed a homozygous insertion mutation c.920_943dup in the MLC1 gene. The mutation in this patient has not been reported in the Human Gene Mutation Database.

Peptides that are composed of dextrorotary (d)-amino acids have gained increasing attention as a potential therapeutic class. However, our understanding of the in vivo fate of d-peptides is limited. This highlights the need for whole-body, quantitative tracking of d-peptides to better understand how they interact with the living body. Here, we used mouse models to track the movement of a programmed death-ligand 1 (PD-L1)-targeting d-dodecapeptide antagonist (DPA) using positron emission tomography (PET). More specifically, we profiled the metabolic routes of [⁶⁴Cu]DPA and investigated the tumor engagement of [⁶⁴Cu/⁶⁸Ga]DPA in mouse models. Our results revealed that intact [⁶⁴Cu/⁶⁸Ga]DPA was primarily eliminated by the kidneys and had a notable accumulation in tumors. Moreover, a single dose of [⁶⁴Cu]DPA effectively delayed tumor growth and improved the survival of mice. Collectively, these results not only deepen our knowledge of the in vivo fate of d-peptides, but also underscore the utility of d-peptides as radiopharmaceuticals.

Objective::To analyze the temporal trends of maternal mortality ratio (MMR) due to obstetric hemorrhage and its specific causes in Chinese mainland from 2000 to 2019, to identify whether the rate of change has accelerated or slowed down during this period, and to find the prior cause of obstetric hemorrhage that needs to be intervened in the future.Methods::Individual information on maternal deaths and total number of live births from 336 surveillance sites across 31 provinces in Chinese mainland was collected from the National Maternal and Child Health Surveillance System between 2000 and 2019. Maternal death was defined according to the World Health Organization’s criterion. The final underlying cause of death was confirmed by the national review and was coded according to International Classification of Diseases -10. Linear trends for changes in characteristics of maternal deaths were assessed using linear or logistic models with the year treated as a continuous variable. The MMR and 95% confidence intervals ( CI) for regions or causes were estimated by Poisson’s distribution. Joinpoint regression was used to assess the accurate temporal patterns. Results::The national MMR due to obstetric hemorrhage was 18.4 per 100,000 live births (95% CI: 15.0-22.2) in 2000. It peaked in 2001 (22.1 per 100,000 live births, 95% CI: 18.3-26.4) and was lowest in 2019 (1.6 per 100,000 live births, 95% CI: 1.0-2.3). For specific regions, the MMR due to obstetric hemorrhage in rural areas and western regions both experienced a slight rise, followed by a rapid decline, and then a slow decline. For specific causes, no change point was found in joinpoint analysis of the national MMR caused by placenta previa, postpartum uterine atony, and retained placenta (the annual percent change was -12.0%, -10.5%, and -21.0%, respectively). The MMR caused by postpartum hemorrhages (PPH) significantly declined by 8.0% (95% CI: 1.9-13.6) per year from 2000 to 2007. The annual percent change of MMR caused by PPH accelerated further to -25.0% between 2007 and 2011, and then decreased to -7.8% between 2011 and 2019. The proportion of maternal deaths due to antepartum hemorrhages increased from 7.6% (8/105) in 2000 to 14.3% (4/28) in 2019. The changes in the proportion of causes were different for maternal deaths due to PPH. The proportion of postpartum uterine atony increased from 39.0% (41/105) in 2000 to 60.7% (17/28) in 2019, and the proportion of uterine rupture also increased from 12.3% (13/105) in 2000 to 14.3% (4/28) in 2019. However, the proportion of retained placenta decreased from 37.1% (39/105) in 2000 to 7.1% (2/28) in 2019. Conclusion::Over the last 20 years, the intervention practice in China has proved that targeted interventions are beneficial in reducing the MMR due to obstetric hemorrhage. However, the MMR has reached a plateau and is likely to increase for some specific causes such as uterine rupture. China needs to develop more effective interventions to reduce maternal deaths due to obstetric hemorrhage, especially for postpartum uterine atony and uterine rupture.

Objective::To analyze the temporal trends of maternal mortality ratio (MMR) due to obstetric hemorrhage and its specific causes in Chinese mainland from 2000 to 2019, to identify whether the rate of change has accelerated or slowed down during this period, and to find the prior cause of obstetric hemorrhage that needs to be intervened in the future.Methods::Individual information on maternal deaths and total number of live births from 336 surveillance sites across 31 provinces in Chinese mainland was collected from the National Maternal and Child Health Surveillance System between 2000 and 2019. Maternal death was defined according to the World Health Organization’s criterion. The final underlying cause of death was confirmed by the national review and was coded according to International Classification of Diseases -10. Linear trends for changes in characteristics of maternal deaths were assessed using linear or logistic models with the year treated as a continuous variable. The MMR and 95% confidence intervals ( CI) for regions or causes were estimated by Poisson’s distribution. Joinpoint regression was used to assess the accurate temporal patterns. Results::The national MMR due to obstetric hemorrhage was 18.4 per 100,000 live births (95% CI: 15.0-22.2) in 2000. It peaked in 2001 (22.1 per 100,000 live births, 95% CI: 18.3-26.4) and was lowest in 2019 (1.6 per 100,000 live births, 95% CI: 1.0-2.3). For specific regions, the MMR due to obstetric hemorrhage in rural areas and western regions both experienced a slight rise, followed by a rapid decline, and then a slow decline. For specific causes, no change point was found in joinpoint analysis of the national MMR caused by placenta previa, postpartum uterine atony, and retained placenta (the annual percent change was -12.0%, -10.5%, and -21.0%, respectively). The MMR caused by postpartum hemorrhages (PPH) significantly declined by 8.0% (95% CI: 1.9-13.6) per year from 2000 to 2007. The annual percent change of MMR caused by PPH accelerated further to -25.0% between 2007 and 2011, and then decreased to -7.8% between 2011 and 2019. The proportion of maternal deaths due to antepartum hemorrhages increased from 7.6% (8/105) in 2000 to 14.3% (4/28) in 2019. The changes in the proportion of causes were different for maternal deaths due to PPH. The proportion of postpartum uterine atony increased from 39.0% (41/105) in 2000 to 60.7% (17/28) in 2019, and the proportion of uterine rupture also increased from 12.3% (13/105) in 2000 to 14.3% (4/28) in 2019. However, the proportion of retained placenta decreased from 37.1% (39/105) in 2000 to 7.1% (2/28) in 2019. Conclusion::Over the last 20 years, the intervention practice in China has proved that targeted interventions are beneficial in reducing the MMR due to obstetric hemorrhage. However, the MMR has reached a plateau and is likely to increase for some specific causes such as uterine rupture. China needs to develop more effective interventions to reduce maternal deaths due to obstetric hemorrhage, especially for postpartum uterine atony and uterine rupture.

Objective:To analyze the clinical phenotype, imaging characteristics and genetic characteristics of a family of early-onset dementia caused by a new mutation in the triggerring receptor expressing on myeloid cells 2 gene (TREM2).Methods:Clinical data were collected from a patient with early-onset dementia. Then whole exome sequencing was performed for the proband, followed by Sanger sequencing for the family members.Results:The clinical manifestations of the proband (a 49-year-old female) was personality changes, mental and behavioral abnormalities, memory loss, ataxia, and seizures. Whole-exon sequencing revealed a novel homozygous mutation in exon 2 of TREM2, namely c.154C>T (p.R52C) heterozygosity in four family members, and one patient with similar clinical manifestations was deceased. The proband′s brain magnetic resonance imaging showed bilateral frontotemporal atrophy, bilateral white matter hyperintensity, thin corpus callosum. No bone cysts of the hands and feet were found by digital radiographic imaging.Conclusions:A homozygous mutation in TREM2 gene was detected in a patient with frontotemporal dementia-like dementia, epilepsy, but without bone cysts. This mutation is probably pathogenic. This research highlights the importance of TREM2 gene mutation screening in early-onset dementia, especially in those with atypical presentations.