OBJECTIVES: The purposes of this study were to develop the Korean version of Wahler Physical Symptom Inventory (WPSI), to examine the reliability and validity of it, and to investigate usefulness for diagnosing somatization. METHODS: The normal group was composed of 242 persons consist of middle and high school students, university students, and adults living in Seoul, Puchon, and Suwon. The two clinical groups consisted of 33 persons with somatic symptoms and 38 diabetic patients. RESULTS: Internal consistency (Cronbach alpha=.91) was very high. Test-retest reliability was calculated from 46 university group, and it's correlations was also high (.87). And the total score of K-WPSI was significantly and positively correlated with subscales of SCL-90-R. There was significant difference between the normal, psychiatry group, and diabetic group of K-WPSI (F=15.48, p<.001). Especially, K-WPSI was very useful to differentiate between the somatization group and diabetic group. CONCLUSION: K-WPSI was found to be a reliable and valid instrument for diagnosing somatization, and for differentiating somatization and diabetic groups. K-WPSI is a brief and economical questionnaire, which may curtail medical expenses of patients. It is also expectated that K-WPSI can be used for identifying somatization and providing information which may contribute to ascertain diagnosis. The limitation of this study is the small normative data, and not distinguishing sex differences. This limitation should be supplemented by future studies.
Adult ; Diagnosis ; Gyeonggi-do ; Humans ; Surveys and Questionnaires ; Reproducibility of Results ; Seoul ; Sex Characteristics

In recent years, as the aging population grows, aging-induced cognitive impairments including dementia and Alzheimer's disease (AD) have become the biggest challenges for global public health and social care. Therefore, the development of potential therapeutic drugs for aging-associated cognitive impairment is essential. Metabolic dysregulation has been considered to be a key factor that affects aging and dementia. Adenosine monophosphate (AMP)-activated protein kinase (AMPK) is a primary sensor of cellular energy states and regulates cellular energy metabolism. Metformin (1,1-dimethylbiguanide hydrochloride) is a well-known AMPK activator and has been widely prescribed for type 2 diabetes mellitus (T2DM). Since the incidence of T2DM and dementia increases with aging, metformin has been considered to be one of the most promising drugs to target dementia and its related disorders. To that end, here, we tested the efficacy of metformin and HL271, a novel metformin derivative, in aging-induced cognitive decline. Water (control), metformin (100 mg/kg) or HL271 (50 mg/kg) were orally administered to aged mice for two months; then, the mice were subjected to behavioral tests to measure their cognitive function, particularly their contextual, spatial and working memory. AMPK phosphorylation was also measured in the drug-treated mouse brains. Our results show that oral treatment with HL271 (50 mg/kg) but not metformin (100 mg/kg) improved cognitive decline in aged mice. AMPK activation was correlated with behavior recovery after aging-induced cognitive decline. Taken together, these results suggest that the newly synthesized AMPK activator, HL271, could be a potential therapeutic agent to treat age-related cognitive decline.
Adenosine Monophosphate ; Aging ; Alzheimer Disease ; AMP-Activated Protein Kinases ; Animals ; Behavior Rating Scale ; Brain ; Cognition ; Cognition Disorders ; Dementia ; Diabetes Mellitus ; Diabetes Mellitus, Type 2 ; Energy Metabolism ; Incidence ; Memory, Short-Term ; Metformin ; Mice ; Phosphorylation ; Protein Kinases ; Public Health ; Water

Eosinophils are derived from hematopoietic stem cells. Peripheral blood eosinophilia is defined as an absolute eosinophil count of > or =0.5x10(9)/L. Eosinophilia is classified into primary or clonal eosinophilia, secondary eosinophilia, and idiopathic categories including idiopathic hypereosinophilic syndrome. Both hematopoietic and solid neoplasms may be associated with peripheral blood eosinophilia, but multiple myeloma is rarely associated with eosinophilia. We now report the case of a 31-year-old man with multiple myeloma associated with marked eosinophilia who developed multiple organ dysfunction with infiltration of eosinophils. He recovered after treatment with chemotherapy followed by autologous stem cell transplantation.
Adult ; Eosinophilia ; Eosinophils ; Hematopoietic Stem Cells ; Humans ; Hypereosinophilic Syndrome ; Multiple Myeloma ; Stem Cell Transplantation ; Stem Cells ; Transplantation, Autologous

Eosinophils are derived from hematopoietic stem cells. Peripheral blood eosinophilia is defined as an absolute eosinophil count of > or =0.5x10(9)/L. Eosinophilia is classified into primary or clonal eosinophilia, secondary eosinophilia, and idiopathic categories including idiopathic hypereosinophilic syndrome. Both hematopoietic and solid neoplasms may be associated with peripheral blood eosinophilia, but multiple myeloma is rarely associated with eosinophilia. We now report the case of a 31-year-old man with multiple myeloma associated with marked eosinophilia who developed multiple organ dysfunction with infiltration of eosinophils. He recovered after treatment with chemotherapy followed by autologous stem cell transplantation.
Adult ; Eosinophilia ; Eosinophils ; Hematopoietic Stem Cells ; Humans ; Hypereosinophilic Syndrome ; Multiple Myeloma ; Stem Cell Transplantation ; Stem Cells ; Transplantation, Autologous

Acute pancreatitis rarely occurs in the postpartum period. Furthermore, there are very few reports of it after cesarean section delivery. A 35-year-old woman presented with dyspnea and abdominal distension on the third day after cesarean section delivery. Under a suspicion of acute pancreatitis, she was initially managed with conservative treatment. However, she developed intra-abdominal fluid collections and gastric bleeding, which were managed with percutaneous drainage, endoscopic hemostasis, and angiographic embolization. She was discharged with good clinical recovery. Postpartum pancreatitis, especially after cesarean section, is rare; however, its management is not different from that for usual pancreatitis.
Adult ; Cesarean Section* ; Drainage ; Dyspnea ; Esophageal and Gastric Varices ; Female ; Hemorrhage ; Hemostasis, Endoscopic ; Humans ; Pancreatitis* ; Postpartum Period ; Pregnancy ; Stomach Ulcer

OBJECTIVE: To investigate the mechanisms involved in the mRNA expressions of hCG, LH/CG receptor and in hormone secretion in the trophoblast of normal and abnormal early pregnancy. METHODS: hCG, free Beta-hCG, and progesterone concentrations were measured in serum and the mRNA expressions of alpha,Beta-hCG and LH/CG receptor were measured in the placental trophoblast of 22 spontaneous abortion patients (spontaneous abortion group), 20 normal pregnancy women (normal pregnancy group) and 6 hydatidiform mole patients (hydatidiform mole group). RESULTS: 1. Mean values of serum hCG and free Beta-hCG concentrations were the lowest in spontaneous abortion group (46343.63+/-40404.18 mIU/ml, p<0.001; 31.34+/-61.57 mIU/ml, p<0.01 respectively) among the three groups. Mean progesterone concentration was the lowest in spontaneous abortion group (11.84+/-7.60 ng/ml, p<0.01), too.2. The expression levels of alpha,Beta-hCG were the highest in spontaneous abortion group (4.64+/-5.47, p=0.015; 4.57+/-4.42 p=0.002 respectively). The expression levels of LH/CG receptor were not different statistically among the three groups and they were high at the 5th week of gestation, reaching nadir at the 10th week of gestation when the concentrations of serum hCG showed peak values in normal pregnancy group.3. The correlations between serum hCG and progesterone concentrations were positive in both spontaneous abortion (r=0.827, p<0.001) and normal pregnancy (r=0.438, p=0.054) group. Though they were not significant statistically, the correlations between progesterone concentrations and the levels of alpha,Beta-hCG expressions were negative in both spontaneous abortion (r=-0.237, p=0.289; r=-0.211, p=0.347) and normal pregnancy (r=-0.270, p=0.250; r=-0.235, p=0.318) group. In hydatidiform mole group, the correlation between progesterone concentrations and the levels of Beta-hCG expression was positive (r=0.968, p=0.002). CONCLUSION: Our results suggest that the mechanisms involved in the secretion of hCG, progesterone and the expression of alpha,Beta-hCG, LH/CG receptor be normal in spontaneous abortion as in normal pregnancy and in the both groups, hCG stimulate the secretion of progesterone by autocrine function and control the secretion of itself, through the suppression of the expressions of alpha,Beta-hCG and LH/CG receptors. So the cause of spontaneous abortion in early pregnancy may be not placental dysfunction but the defect of embryo itself with poor placental growth.
Abortion, Spontaneous* ; Embryonic Structures ; Female ; Humans ; Hydatidiform Mole ; Pregnancy ; Progesterone ; RNA, Messenger* ; Trophoblasts*

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.

Background: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease that culminates in respiratory failure and death due to irreversible scarring of the distal lung. While initially considered a chronic inflammatory disorder, the aberrant function of the alveolar epithelium is now acknowledged as playing a central role in the pathophysiology of IPF. This study aimed to investigate the regenerative capacity of alveolar type 2 (AT2) cells using IPF-derived alveolar organoids and to examine the effects of disease progression on this capacity. Methods: Lung tissues from three pneumothorax patients and six IPF patients (early and advanced stages) were obtained through video-assisted thoracoscopic surgery and lung transplantation. HTII-280+ cells were isolated from CD31-CD45-epithelial cell adhesion molecule (EpCAM)+ cells in the distal lungs of IPF and pneumothorax patients using fluorescence-activated cell sorting (FACS) and resuspended in 48-well plates to establish IPF-derived alveolar organoids. Immunostaining was used to verify the presence of AT2 cells. Results: FACS sorting yielded approximately 1% of AT2 cells in early IPF tissue, and the number decreased as the disease progressed, in contrast to 2.7% in pneumothorax. Additionally, the cultured organoids in the IPF groups were smaller and less numerous compared to those from pneumothorax patients. The colony forming efficiency decreased as the disease advanced. Immunostaining results showed that the IPF organoids expressed less surfactant protein C (SFTPC) compared to the pneumothorax group and contained keratin 5+ (KRT5+) cells. Conclusion This study confirmed that the regenerative capacity of AT2 cells in IPF decreases as the disease progresses, with IPF-derived AT2 cells inherently exhibiting functional abnormalities and altered differentiation plasticity.