Several problems differentiate the treatment of children, especially those with congenital ocular disease, from adults, including the absence of complaints and the complication of systemic diseases. However, the most challenging is the continuing developing anatomical and functional development and immaturity in children. Consequently, the timing of disease onset and treatment can greatly affect the prognosis, and the prognosis cannot be confirmed without long-term follow-up periods.

The prognosis for unilateral congenital cataract is very poor. However, some cases achieved good vision with successful refractive correction and amblyopia therapy, suggesting that long-term parental enthusiasm and adherence are important for the visual prognosis.

Penetrating keratoplasty is rarely performed in children, and outcomes at our hospital have been extremely poor for congenital corneal opacity over the past 28 years. The visual prognosis is also poor for large limbal dermoids approaching the center of the cornea, which did not respond to preoperative amblyopia therapy. Consequently, early excision, lamellar keratoplasty, wearing of hard contact lenses, and amblyopia therapy were considered necessary.

Treatment of pediatric ocular disease should consider the pros and cons, methods, and timing, especially the development of the pediatric eye and the time of onset of the disease.

Neutrophils serve as the frontline defenders in the host's response to infections. However, the available methods for assessing the activated status of neutrophils are still limited. The immature cells that appear during sepsis are large with complex cytoplasmic components and rich nucleic acids, making them diagnosable by cell population data analysis using the automated cell counter. The changes are expressed as increased forward scattered light, side fluorescence light, and side fluorescence distribution width. Additionally, changes in side fluorescence light may indicate the neutrophil extracellular trap formation and can be useful for the diagnosis of sepsis-associated disseminated intravascular coagulation.

Platelets are one of the major targets of SARS-CoV-2. Activated platelets release prothrombotic substances, express adhesion molecules, and activate coagulation, thereby contributing to the thrombotic tendency in COVID-19. However, the antiplatelet therapy is not recommended in the current international guidelines. We think that the initiation timing and the target severity are the causes of the failure in clinical trials. As shown in the clinical studies that examined the effects of anticoagulants, early initiation in moderate severity is necessary for the success of antithrombotic therapy. Future trials are warranted to study the effects of antiplatelets in such conditions.

Disseminated Intravascular Coagulation (DIC) has been a common diagnosis made by health care givers since the dawn of the 20^th century. However, currently, this diagnosis is entertained rarely in clinical settings that can predispose to this complication. The incidence of four common clinical scenarios traditionally associated with DIC, sepsis, trauma, obstetrical disorders, and cancers, are on the increase due to better diagnostics and management strategies, but DIC is rarely diagnosed in these disease categories currently. The authors suggest the rarity of a DIC diagnosis is due to varied understanding of the pathophysiology of this condition. In this perspectives, we would like to present reasons for this change in consideration and encourage caregivers to consider a DIC diagnosis at an early stage based on new criteria to help patients benefit from available treatments.

Defining success in a clinical trial is not necessarily a straightforward task, especially when the target population is critically ill patients where few agents have demonstrated effectiveness. This has been the case for trials of anticoagulation in patients with sepsis-associated disseminated intravascular coagulation (DIC), which have generally examined patients with severe sepsis but not specifically DIC. Limitations of existing studies include inadequate anticoagulant doses and delayed initiation of treatment. Furthermore, 28-day mortality has been adopted as the primary endpoint but is affected by a panoply of factors other than anticoagulant therapies and may not be the most relevant measure. Future trials must address several current limitations in order to improve our understanding of the role of anticoagulation in patients with sepsis-associated DIC.

The hypothalamus maintains homeostasis by controlling various organs and the central nervous system, but analyzing the human hypothalamic nuclei is challenging. Our previous studies applied areal parcellation to high-resolution functional magnetic resonance imaging (fMRI) data to delineate hypothalamic nuclei boundaries. This article presents stereotaxic coordinates of these nuclei for fMRI analyses, offering guidance on defining regions of interest and appropriate spatial smoothing kernel sizes. The provided coordinates aid future research in nuclear level hypothalamus analyses.

Objectives This study presents the multifaceted effects of candidate loci identified by genome-wide association studies on parameters such as educational background and the clinical symptoms of Japanese patients with schizophrenia along with detailed psychological measurements. This study aimed to investigate whether gene mutations that affect cognitive dysfunction are (1) related to the onset of schizophrenia and (2) also affect cognitive dysfunction in patients with schizophrenia.

Design Case-control study.

Methods This study evaluated 12 single-nucleotide polymorphisms (SNPs) (rs10189857, rs2175263, rs9398171, rs12670234, rs6466056, rs11156875, rs2018916, rs11663602, rs11885093, rs9404453, rs2473938, and rs4275659) that are common in Japanese individuals and demonstrated a relationship with schizophrenia and educational attainment in a previous genome-wide study. We included 640 Japanese patients (schizophrenia group) and 640 healthy participants (control group). Both groups were investigated for the relationship between the SNPs and educational attainment as well as psychometric evaluations of cognitive function.

Results The 12 SNPs were not identified as genetic risk factors for schizophrenia. However, rs9404453 was associated with a decline in educational achievement, educational performance, Japanese Adult Reading Test (JART100) score, and Wechsler Adult Intelligence Scale-Revised (WAIS-R) (full-scale intelligence quotient [FSIQ]) score in patients with schizophrenia, SNP rs6466056 was associated with a decline in the WAIS-R (FSIQ) score, and SNP rs11663602 was associated with a decline in the JART100 score.

Conclusion The SNPs rs9404453, rs6466056, and rs11663602 may be associated with academic performance or cognitive decline in patients with schizophrenia, although the overall findings from psychological tests did not show the expected consistency.

Objectives Infants with fetal growth restriction (FGR) are at a risk of developing metabolic syndromes in adulthood. We hypothesized that skeletal muscle degeneration by nutrition-restricted FGR results in abnormal insulin signaling and epigenetic changes.

Material and Methods To develop a protein-restricted FGR model, rats were fed a low-protein diet (7% protein) during the gestational period; rats fed a normal diet (20% protein) were used as controls. At 8 and 12 weeks of age, the pups were subjected to oral glucose tolerance test (OGTT) and insulin tolerance test (ITT) to evaluate insulin resistance. At 12 weeks, the mRNA and protein levels of insulin signaling pathway molecules in the skeletal muscles were examined. DNA methylation of promoters was detected. DNA extracted from skeletal muscles was used as a template for methylation-specific PCR analysis of GLUT4.

Results The body weight of FGR rats from birth to 8 weeks was significantly lower than that of the controls; no significant difference was observed between the groups at 12 weeks. In the OGTT and ITT, the incremental area under the curve (iAUC) was significantly higher in FGR rats than in the controls at 12 weeks. The mRNA and protein levels of Akt2 and GLUT4 in the plantar muscles were significantly lower in FGR rats than in the controls. GLUT4 methylation was comparable between the groups.

Conclusions Protein-restricted FGR rats showed insulin resistance and altered insulin signaling in skeletal muscles after 12 weeks. However, we could not demonstrate the involvement of DNA methylation in this model.