PURPOSE: The purpose of this study was to identify the influences of recognition on low fertility and views of marriage on childbirth will in university students. METHODS: Participants were 190 university students in Chungchungnamdo province, Korea. The data were collected from May to October 2018 and examined using descriptive statistics, t-test, analysis of variance, Pearson correlation and multiple regression with IBM SPSS Statistics ver. 24.0. RESULTS: Childbirth will was significantly correlated with recognition on low fertility (r=0.20, p=0.002) and views on marriage (r=0.53, p<0.001). Factors associated with childbirth will were views on marriage (β=0.24, p<0.001). CONCLUSION Theses results suggests that views on marriage have important influences on childbirth will in university students. To improve childbirth will, the positive views on marriage need to be formulated in university students.

Ludwig’s angina is a rapidly progressive and gangrenous cellulitis in the submandibular, sublingual spaces, and neck. It is characterized by an elevated tongue and laryngeal edema, resulting in airway compromise and, rarely, in sudden death. The most common cause is an odontogenic infection of a molar tooth. Infection can spread to the superior mediastinum and buccal area through anatomical structures. Herein, we report the sudden death of a 45-year-old male who was not diagnosed with Ludwig’s angina. He died in the emergency room 20 minutes after loss of consciousness. Intubation was impossible owing to severe laryngeal edema. The C-reactive protein level was 33.81 mg/dL. On autopsy, a diffuse light green abscess of the submandibular space was detected, along with severe edema of the epiglottis, aryepiglottic fold, and vocal cords. Subsequently, we confirmed that the airway obstruction was caused by Ludwig’s angina based on a literature review. In conclusion, this report emphasizes the need to identify the infection source and perform a detailed dissection according to the anatomical structure in the autopsy procedure for Ludwig’s angina.

Alexithymia is characterized by impairments in the processing of emotions. Although the disruptions in the white matter (WM) integrity in Major depressive disorder (MDD) has frequently been reported, the underlying relationship with alexithymia remains unclear. In the present study, we investigated WM tracts with Tracts Constrained by UnderLying Anatomy approach to discover potential associations between alexithymia and WM integrity to identify the neural basis of impaired emotional self-awareness in MDD. 101 patients with MDD and 99 healthy sex- and age-matched individuals underwent diffusion-weighted imaging. All participants were assessed with the 20-item Toronto Alexithymia Scale (TAS). TAS scores were significantly higher in MDD patients than in controls. Patients with MDD exhibited significantly lower FA values in the left inferior longitudinal fasciculus and it also showed negative associations with TAS. These results contribute to the neurobiological evidence on the association between MDD and alexithymia. Additionally, they suggest that reduced white matter integrity in the regions constitutes a principal pathophysiology underlying impaired emotional recognition and description in MDD.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.

Enchondromas are common benign bone tumors of the hand and are typically located in the medullary cavity of the metaphysis of the tubular bones. Typical radiological findings reveal cartilage lobules with ring and arc calcifications and entrapped normal medullary fat. The regression of an existing enchondroma, in which the cartilage lobules are replaced by fatty marrow, is considered unusual. Only a few studies have been reported on long tubular bones. Herein, we report an unusual case of a 73-year-old man with an enchondroma in the hand. In this case, a histologic appearance of the enchondroma exhibited loss of matrix mineralization, which corresponded to replacement by marrow fat revealed by magnetic resonance imaging.

Ethylene glycol (EG), commonly used as antifreeze, is frequently ingested accidentally or in suicides, and causes acute renal failure. We report an unusual case of EG poisoning with acute liver injury. After vomiting and loss of consciousness, a 48-year-old male was admitted to the emergency room. Despite prompt conservative treatment for metabolic acidosis, kidney function deteriorated, necessitating the continuous renal replacement therapy. Blood toxicology results, showing EG levels of 510 mg/L, arrived 10 hours after admission. Oral ethyl alcohol therapy commenced 16 hours post-admission. By 36 hours, liver function tests indicated significant liver damage, and the patient died 45 hours upon admission. On autopsy, histological findings were hepatic centrilobular necrosis, cerebral perivascular neutrophilic and lymphocytic infiltration with calcium oxalate deposition, and renal tubular necrosis with calcium oxalate deposition. EG concentrations in the blood and gastric contents were 18.7 mg/L and 45.0 mg/L, respectively. Glycolic acid and oxalic acid, metabolites of EG produced by alcohol dehydrogenase in the liver, cause metabolic acidosis, renal tubular calcium oxalate deposition, and acute renal failure, leading to death. Generally, because fomepizole or ethyl alcohol block alcohol dehydrogenase in the liver, acute liver injury by EG poisoning is rare. To the best of authors’ knowledge, only one relevant report was found in the literature described a case in which EG caused centrilobular necrosis in liver. In the current case, delays in diagnosis and antidote therapy without gastric lavage allowed continued metabolism of EG which led to acute liver injury and acute renal failure.