Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

Four soluble factors—putrescine, glucosamine, nicotinamide, and signal transducer and activator of transcription 3 (STAT3) inhibitor BP-1-102—were shown to differentiate bone marrow mononucleated cells (BMNCs) into functional insulin-producing cells (IPCs) in vitro. Transplantation of these IPCs improved hyperglycemia in diabetic mice. However, the role of endogenous BMNC regeneration in this effect was unclear. This study aimed to evaluate the effect of these factors on in vivo BMNC differentiation into IPCs in diabetic mice. Mice were orally administered the factors for 5 days, twice at 2-week intervals, and monitored for 45–55 days. Glucose tolerance, glucose-stimulated insulin secretion, and pancreatic insulin content were measured. Chimeric mice harboring BMNCs from insulin promoter luciferase/green fluorescent protein (GFP) transgenic mice were used to track endogenous BMNC fate. These factors lowered blood glucose levels, improved glucose tolerance, and enhanced insulin secretion. Immunostaining confirmed IPCs in the pancreas, showing the potential of these factors to induce β-cell regeneration and improve diabetes treatment.

This study aimed to evaluate the imaging and pathological findings in axillary lymph nodes in patients with breast cancer who received concurrent ipsilateral coronavirus disease 2019 (COVID-19) vaccination. Of the 19 women with breast cancer who received concurrent COVID-19 vaccination shot in the arm ipsilateral to breast cancer, axillary lymphadenopathy was observed in 84.2% (16 of 19) of patients on ultrasound (US) and 71.4% (10 of 14) of patients on magnetic resonance imaging (MRI), and 21.0% (4 of 19) of patients were diagnosed with metastasis. Abnormal US and MRI findings of cortical thickening, effacement of the fatty hilum, round shape, and asymmetry in the number or size relative to the contralateral side were noted in more than half of the non-metastatic and metastatic lymph nodes; however, statistical significance was not noted. Axillary lymphadenopathy is commonly observed in patients with breast cancer who receive concurrent ipsilateral COVID-19 vaccination without specific differential imaging features. Thus, understanding the limitations of axillary imaging and cautious interpretation is necessary to avoid overestimation or underestimation of the axillary disease burden.

Amebic liver abscess (ALA) is the most common extraintestinal manifestation of amebiasis. Amebiasis, a parasitic infection caused by Entamoeba histolytica, used to be a prevalent protozoan disease in Korea, however, with an improving sanitary system, it has been among very uncommon etiology of liver abscess. A recent report suggested that ALA is an emerging parasitic infection in human immunodeficiency virus (HIV)-infected patients even in areas where the disease is not endemic and recommended HIV screening in patients in areas where ALA is not endemic, particularly those without history of travel to a disease-endemic area. We report on two patients who were admitted for treatment of ALA and then diagnosed as HIV infection. We also reviewed the etiology and characteristics of ALA in our hospital during the last 5 years.
Amebiasis ; Diagnosis* ; Entamoeba histolytica ; HIV Infections ; HIV* ; Humans* ; Korea ; Liver Abscess ; Liver Abscess, Amebic* ; Mass Screening

Amebic liver abscess (ALA) is the most common extraintestinal manifestation of amebiasis. Amebiasis, a parasitic infection caused by Entamoeba histolytica, used to be a prevalent protozoan disease in Korea, however, with an improving sanitary system, it has been among very uncommon etiology of liver abscess. A recent report suggested that ALA is an emerging parasitic infection in human immunodeficiency virus (HIV)-infected patients even in areas where the disease is not endemic and recommended HIV screening in patients in areas where ALA is not endemic, particularly those without history of travel to a disease-endemic area. We report on two patients who were admitted for treatment of ALA and then diagnosed as HIV infection. We also reviewed the etiology and characteristics of ALA in our hospital during the last 5 years.
Amebiasis ; Diagnosis ; Entamoeba histolytica ; HIV Infections ; HIV ; Humans ; Korea ; Liver Abscess ; Liver Abscess, Amebic ; Mass Screening

PURPOSE: The AT-rich interactive domain 1A (ARID1A) gene encodes BRG1-associated factor 250a, a component of the SWItch/Sucrose NonFermentable chromatin remodeling complex, which is considered a tumor suppressor in many tumors. We aimed to investigate the prognostic significance of ARID1A expression in gastric cancers and explore its relationship with clinicopathologic parameters such as mismatch repair protein expression. MATERIALS AND METHODS: Four tissue microarrays were constructed from 191 resected specimens obtained at Soonchunhyang University Cheonan Hospital from 2006 to 2008. Nuclear expression of ARID1A was semiquantitatively assessed and binarized into retained and lost expression. RESULTS: Loss of ARID1A expression was observed in 62 cases (32.5%). This was associated with more frequent vascular invasion (P=0.019) and location in the upper third of the stomach (P=0.001), and trended toward more poorly differentiated subtypes (P=0.054). ARID1A loss was significantly associated with the mismatch repair-deficient phenotype (P=0.003). ARID1A loss showed a statistically significant correlation with loss of MLH1 (P=0.001) but not MSH2 expression (P=1.000). Kaplan-Meier survival analysis showed no statistically significant difference in overall survival; however, patients with retained ARID1A expression tended to have better overall survival than those with loss of ARID1A expression (P=0.053). In both mismatch repair-deficient and mismatch repair-proficient groups, survival analysis showed no differences related to ARID1A expression status. CONCLUSIONS: Our results demonstrated that loss of ARID1A expression is closely associated with the mismatch repair-deficient phenotype, especially in sporadic microsatellite instability-high gastric cancers.
Chromatin Assembly and Disassembly ; Chungcheongnam-do ; DNA Mismatch Repair* ; Humans ; Microsatellite Instability ; Microsatellite Repeats ; Phenotype ; Stomach ; Stomach Neoplasms*

BACKGROUND: The molecular profile of peritumoral non-neoplastic liver parenchyma (PNLP) has recently been suggested as predictive factor of early and late recurrence of hepatocellular carcinoma (HCC). However, there is no definite cut-off point for tumor-free PNLP in terms of either histological or molecular changes. Therefore, our aim is to determine the numerical cut-off point for separating adjacent PNLP and remote PNLP in histopathologic perspective. METHODS: Peritumoral tissues from 20 resected HCC patients were sampled from 0 to 40 mm distance from the tumor border (divided into 5-mm columns). Histopathologic parameters such as necroinflammatory activity, fibrosis, bile ductular reaction, hepatic venulitis, peliosis, and steatosis were compared between each column. RESULTS: The morphologic changes just adjacent to the tumor were notably severe and faded with distance. The parenchyma within 10 mm of the tumor showed significantly severe inflammation, fibrosis, peliosis and hepatic venulitis compared with those from farther areas. The histopathologic changes of the parenchyma became stable beyond 20 mm. CONCLUSIONS: Results of this study revealed that the parenchyma within 10 mm distance from the tumor, or adjacent PNLP, has histopathologic changes that are directly affected by the tumor, and the parenchyma beyond 20 mm as the remote PNLP without tumor effect.
Bile ; Carcinoma, Hepatocellular ; Fibrosis ; Hepatitis B, Chronic ; Hepatitis, Chronic ; Humans ; Inflammation ; Liver ; Recurrence

BACKGROUND AND OBJECTIVES: Turner syndrome (TS) is known to be caused by a total or partial deletion of one X-chromosome. Besides short stature and failure to enter puberty due to ovarian dysgenesis, auricular malformations, middle ear diseases and hearing impairment are also other clinical features of Turner syndrome. The goal of this study is to report otologic and audiologic characteristics in a group of children with Turner syndrome and correlate with these findings to karyotype. SUBJECTS AND METHOD: We retrospectively reviewed the outpatient charts of those who visited at our department for otologic and audiologic screening test between 2008 and 2011. All 23 TS children (46 ears) were enrolled under regular control of their pediatric endocrinologist for treatment with growth hormon and Estrogen. The mean age was 12.6 years (6-24 years). All children were evaluated by otologic history taking, otoscopy, pure tone audiometry and karyotyping. Furthermore, 16 children undertook auditory brain stem response (ABR) test and 10 children temporal bone computed tomography (CT). RESULTS: Abnormal otoscopic findings were found in 48% (22 ears), abnormal otologic history in 70% (16 children), and abnormal audiologic findings in 70% (32 ears). According to karyotyping, the total p-arm deletion group (74%) showed unfavorable audiologic results. ABR test and temporal bone CT did not show any unique findings, except five poor pneumatization of mastoid. CONCLUSION: Hearing impairment can be present at early age in Turner syndrome. Careful follow up during childhood is necessary to detect early ear and hearing problems for active intervention. Karyotype may be used as a predictor for future hearing impairment.
Audiology ; Audiometry ; Child ; Ear ; Ear Diseases ; Ear, Middle ; Estrogens ; Evoked Potentials, Auditory, Brain Stem ; Hearing ; Hearing Loss ; Humans ; Karyotype ; Karyotyping ; Mass Screening ; Otoscopy ; Outpatients ; Puberty ; Retrospective Studies ; Temporal Bone ; Turner Syndrome