PURPOSE: To summarize and review the methodological quality of the evidence from trials examining the effectiveness of physical exercise in patients undergoing allogeneic hematopoietic stem cell transplantation (Allo-HSCT). METHODS: Six randomized clinical trials (RCTs) were identified, reviewed for substantive results, and assessed for methodological quality. RESULTS: Six trials met all methodological criteria on the modified Jadad score above 3 out of 5 points. Failure to blind the outcome assessor, and failure to describe the method of blinding of outcome assessor appropriately were the most prevalent methodological shortcomings. Various exercise modalities have been applied, differing in content, frequency, intensity, and duration. Positive results have been observed in part for a diverse set of outcomes, including physical and psychological performance. CONCLUSION: The trials reviewed in this study were of moderate methodological quality. They suggest that exercise in patients undergoing Allo-HSCT may be safe and feasible, and in part patients benefit from increased physical performance both during and after transplantation. Future RCTs should use larger samples, appropriate comparison groups, and a standard of outcome measures, and examine what kind of exercise intervention (aerobic vs. resistance vs. combined) is the most effective for Allo-HSCT patients. It would be necessary to define contraindication for exercise to guarantee its safety.
Exercise ; Exercise Therapy ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells ; Humans ; Outcome Assessment (Health Care) ; Quality of Life ; Transplants

PURPOSE: This study aimed to examine the necessity for research ethics and learning objectives in ethics education at the undergraduate level. METHODS: A total of 393 fourth-year students, selected from nine medical schools, participated in a survey about learning achievement and the necessity for it. RESULTS: It was found that the students had very few chances to receive systematic education in research ethics and that they assumed that research ethics education was provided during graduate school or residency programs. Moreover, the students showed a relatively high learning performance in life ethics, while learning achievement was low in research ethics. CONCLUSION: Medical school students revealed low interest in and expectations of research ethics in general; therefore, it is necessary to develop guidelines for research ethics in the present situation, in which medical education mainly focuses on life ethics.
*Achievement ; *Curriculum ; *Education, Medical, Undergraduate ; Ethics, Medical/*education ; Ethics, Research/*education ; Goals ; Humans ; *Learning ; Schools, Medical ; Students, Medical ; Surveys and Questionnaires

Ischemia/reperfusion-induced myocardial injury is the main cause of acute myocardial infarction. Dendropanax morbifera Léveille has been used in traditional medicines for the treatment of various diseases such as headache, infectious diseases, and general debility. However, the effect of extract from D. morbifera (EDM) on myocardial ischemic injury is still unknown. In this study, the effects of EDM on neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R) injury were investigated. The viability of cardiomyocytes with H (30 min)/R (1 h) decreased; however, treatment with EDM significantly inhibited H/R injury-induced cardiomyocyte death. Further, we observed that reactive oxygen species (ROS) generation and intracellular calcium concentration (Ca²⁺ᵢ) were significantly reduced in EDM-treated cardiomyocytes compared with that in H/R-injured positive control. In addition, western blotting results showed that EDM attenuated abnormal changes of RyR2 and SERCA2a genes in hypoxic cardiomyocytes. These results suggest that EDM ameliorates ROS generation and Ca²⁺ᵢ homeostasis to prevent dysregulation of calcium regulatory proteins in the heart, thereby exerting cardioprotective effects and reducing hypoxia-induced cardiomyocyte damage, which verifies the potential use of EDM as a new therapeutic agent for the treatment of myocardial ischemic injury.
Animals ; Blotting, Western ; Calcium ; Communicable Diseases ; Headache ; Heart ; Homeostasis ; Myocardial Infarction ; Myocytes, Cardiac ; Rats ; Reactive Oxygen Species ; Ryanodine Receptor Calcium Release Channel

Purpose: The objective of this study was to identify the significance of 24-hour postreduction ultrasonography (US) in pediatric patients with intussusception. Methods: A total of 229 patients with intussusception who were treated with saline reduction at Severance Children’s Hospital between January 2014 and September 2020 were retrospectively reviewed. The 229 patients with successful saline reduction were divided into two groups: a recurrence at 24 hours group (R, n=41) and a non-recurrence group (NR, n=188). The full patient sample was divided into two groups: follow-up US (FU) or no followup US (NFU); the recurrence group was divided into follow-up (R-FU) and non-follow-up (R-NFU) subgroups, and stratified analyses were performed. Results: There were no significant differences in age, sex, laboratory findings, symptoms, and sonographic findings between the NR and R groups. In the R group, 24 patients underwent follow-up US, and 17 patients did not. Specific sonographic findings were statistically significant in the R-FU group compared to the R-NFU group (p=0.002). The R-FU group had fewer admissions (p=0.012) and longer mean hospitalization times (p<0.001) than the R-NFU group. The NFU group had a 12.2% recurrence rate, while the R-FU group recurrence rate was 25.8% (p=0.0099), suggesting that the omission of some recurrent events and follow-up US was a significant variable in the recurrence of intussusception. The median time to recurrence was 21 hours which supports the 24-hour follow-up protocol. Conclusion Twenty-four-hour follow-up US was shown to be valuable for detecting early recurrence of intussusception.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

Objective: Autophagy is a major intracellular catabolic pathway governed by the sequential actions of proteins encoded by autophagy-related genes (Atg). ATG9, the only transmembrane protein involved in this process, regulates phospholipid translocation to autophagosomes during the early phases of autophagy. In mammals, two Atg9 isoforms have been reported: Atg9a and Atg9b. In this study, we examined whether the molecular and cellular characteristics of these two isoforms differed in mice. Methods: Whole uteri were collected on days 1, 4, and 8 of pregnancy and from ovariectomized mice injected with vehicle, progesterone, or 17β-estradiol. Cells from reproductive tissues, such as granulosa cells, uterine epithelial cells (UECs), uterine stromal cells (USCs), and oocytes were collected. Two human uterine cell lines were also used in this analysis. Reverse transcription-polymerase chain reaction tests, Western blotting, and immunofluorescence staining were performed. Serum starvation conditions were used to induce autophagy in primary cells. Results: Atg9a and Atg9b were expressed in multiple mouse tissues and reproductive cells. Neither Atg9A nor Atg9B significantly changed in response to steroid hormones. Immunofluorescence staining of the UECs and USCs showed that ATG9A was distributed in a punctate-like pattern, whereas ATG9B exhibited a pattern of elongated tubular shapes in the cytoplasm. In human cancer cell lines, ATG9B was undetectable, whereas ATG9A was found in all cell types examined. Conclusion The Atg9 isoforms exhibited distinct subcellular localizations in UECs and may play different roles in autophagy. Notably, human uterine cells exhibited reduced ATG9B expression, suggesting that this suppression may be due to epigenetic regulation.

OBJECTIVE: Tributyltin (TBT), an endocrine disrupting chemical, has been reported to decrease ovarian function by causing apoptosis in the ovary, but the mechanism is not fully understood. Therefore, we examined whether TBT increases the expression of adipogenesis-related genes in the ovary and the increased expression of these genes is associated with apoptosis induction. METHODS: Three-week-old Sprague-Dawley rats were orally administered TBT (1 or 10 mg/kg body weight) or sesame oil as a control for 7 days. The ovaries were obtained and weighed on day 8, and then they were fixed for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or frozen for RNA extraction. Using the total RNA of the ovaries, adipogenesis- and apoptosis-related genes were analyzed by real-time polymerase chain reaction (PCR). RESULTS: The ovarian weight was significantly decreased in rats administered 10 mg/kg TBT compared to that in control rats. As determined by the TUNEL assay, the number of apoptotic follicles in ovary was significantly increased in rats administered 10 mg/kg TBT. The real-time PCR results showed that the expression of adipogenesis-related genes such as PPARgamma, aP2, CD36, and PEPCK was increased after TBT administration. In addition, apoptosis-related genes such as TNFalpha and TNFR1 were expressed more in the TBT-administered rats compared with the control rats. CONCLUSION: The present study demonstrates that TBT induces the expression of adipogenesis- and apoptosis-related genes in the ovary leading to apoptosis in the ovarian follicles. These results suggest that the increased expression of adipogenesis-related genes in the ovary by TBT exposure might induce apoptosis resulting in a loss of ovarian function.
Adipogenesis ; Animals ; Apoptosis ; DNA Nucleotidylexotransferase ; Female ; In Situ Nick-End Labeling ; Ovarian Follicle ; Ovary ; PPAR gamma ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptors, Tumor Necrosis Factor, Type I ; RNA ; Sesame Oil ; Trialkyltin Compounds ; Tumor Necrosis Factor-alpha

OBJECTIVE: Tributyltin (TBT), an endocrine disrupting chemical, has been reported to decrease ovarian function by causing apoptosis in the ovary, but the mechanism is not fully understood. Therefore, we examined whether TBT increases the expression of adipogenesis-related genes in the ovary and the increased expression of these genes is associated with apoptosis induction. METHODS: Three-week-old Sprague-Dawley rats were orally administered TBT (1 or 10 mg/kg body weight) or sesame oil as a control for 7 days. The ovaries were obtained and weighed on day 8, and then they were fixed for terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) or frozen for RNA extraction. Using the total RNA of the ovaries, adipogenesis- and apoptosis-related genes were analyzed by real-time polymerase chain reaction (PCR). RESULTS: The ovarian weight was significantly decreased in rats administered 10 mg/kg TBT compared to that in control rats. As determined by the TUNEL assay, the number of apoptotic follicles in ovary was significantly increased in rats administered 10 mg/kg TBT. The real-time PCR results showed that the expression of adipogenesis-related genes such as PPARgamma, aP2, CD36, and PEPCK was increased after TBT administration. In addition, apoptosis-related genes such as TNFalpha and TNFR1 were expressed more in the TBT-administered rats compared with the control rats. CONCLUSION: The present study demonstrates that TBT induces the expression of adipogenesis- and apoptosis-related genes in the ovary leading to apoptosis in the ovarian follicles. These results suggest that the increased expression of adipogenesis-related genes in the ovary by TBT exposure might induce apoptosis resulting in a loss of ovarian function.
Adipogenesis ; Animals ; Apoptosis ; DNA Nucleotidylexotransferase ; Female ; In Situ Nick-End Labeling ; Ovarian Follicle ; Ovary ; PPAR gamma ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Receptors, Tumor Necrosis Factor, Type I ; RNA ; Sesame Oil ; Trialkyltin Compounds ; Tumor Necrosis Factor-alpha

Elbow snapping by annular ligament is rare and may be difficult to diagnose, when this condition is not familiar. We report a case of elbow snapping by annular ligament diagnosed by ultrasonography, which was confirmed by arthroscopic observation. The ultrasonographic findings were thickening of the annular ligament and snapping in and out of the radiocapitellar joint during elbow flexion and extension on dynamic ultrasonography.
Diagnosis* ; Elbow Joint ; Elbow* ; Joints ; Ligaments* ; Ultrasonography