Fatal complications including cerebral edema and neurologic collapse occur during treatment of diabetic ketoacidosis(DKA). A 6-week-old female infant with fever, dehydration and drowsy mental status was diagnosed as DKA and neurologically deteriorated during treatment. The cranial computed tomography scan revealed multifocal brain infarctions of the left caudate nucleus, bilateral frontal periventricular white matter, and right parietal cortex. A moderate amount of hemorrhage was also noted in both lateral ventricles. She recovered rapidly with supportive treatment over time. The clinical course and radiologic findings of this patient emphasize the importance of brain infarction as a cause of persistent neurologic loss in children with DKA.
Brain Edema ; Brain Infarction* ; Brain* ; Caudate Nucleus ; Child ; Dehydration ; Diabetic Ketoacidosis* ; Female ; Fever ; Hemorrhage* ; Humans ; Infant* ; Lateral Ventricles ; Rabeprazole

Paraquat is a bipyridilium nonselective contact herbicide and well-known pulmonary toxicants. Concentrated solution of paraquat may causes severe corrosive injury and multiple system organ failure. It is poorly absorbed from GI tract, but is extremely toxic and so one swallowed mouthful of Gramoxone(about 5ml) will be fatal. We experienced 3 cases of paraquat poisoning through injection and examined pathologic findings, medical records and concentration of paraquat in blood and tissues. We reviewed the mechanism of action of paraquat, pathologic changes of organ system, concentration of compound in the various organ and cause of death in autopsy cases.
Autopsy* ; Cause of Death ; Gastrointestinal Tract ; Medical Records ; Mouth ; Paraquat* ; Poisoning*

OBJECTIVE: Hematologic abnormalities in toxemia mothers and their babies have been documented. The purpose of this study was to explore the hematologic findings in mothers with toxemia and postnatal hematologic findings in their babies. The relationship of hematologic findings between toxemia mothers before delivery and their babies immediately after birth was also examined. METHODS: Forty-six pairs of singleton toxemia mothers and their babies born by C-section with 28 to 35 weeks of gestation from Jan. 1995 to Dec. 1999 were enrolled. Fifty pairs of singleton normotensive mothers and their babies with the same gestational period and delivery method were matched for control group. Blood samples of mothers were performed before delivery, and those of their babies, were done immediately after birth, day 3 and 7 of life. Hemoglobin(Hb) concentration, total white blood cell(WBC) count, absolute neutrophil count(ANC), and platelet count were examined. RESULTS: Toxemia mothers have significantly lower platelet count compared with controls(191,000+/-83,200/mm3 vs. 252,000+/-92,700/mm3, p<0.05). There were no difference between both groups in Hb, WBC and ANC. On the first day of life, Hb was significantly higher(16.97+/-2.36g/dL vs 14.32+/-1.5g/dL, p<0.05), but WBC, ANC and platelet count were significantly lower in babies born to toxemia mothers than those of control group(p<0.05 for all). In babies born to toxemia mothers, Hb was significantly decreased until the seventh day of life(16.97g/dL, 15.48g/dL, 14.61g/dL, p<0.05), however, WBC and platelet count were significantly decreased until the third day of life and then incresed until the seventh day of life(11,832/mm3, 8,334/mm3, 10,104/mm3 for WBC, p<0.05, and 152,220/mm3, 144,720/mm3, 214,090/mm3 for platelet, p<0.05, respectively). CONCLUSION: Hemoglobin concentration was significantly higher, whereas WBC, ANC and platelet were significantly lower in babies of toxemia mothers than those of control group. In babies born to toxemia mothers, Hb was significantly decreased until the seventh day of life, however, WBC and platelet count were significantly decresed until the third day and then increased until the seventh day of life. There was no relationship between hematologic findings of toxemia mothers and their babies.
Blood Platelets ; Humans ; Mothers* ; Neutrophils ; Parturition ; Platelet Count ; Pregnancy ; Toxemia*

The term MYH9-related disorders indicates a group of autosomal dominant illnesses, formerly known as May-Hegglin anomaly, Sebastian syndrome, Fechtner syndrome and Epstein syndrome, caused by mutations of MYH9, the gene encoding for the heavy chain of non-muscle myosin IIA (NMMHC-IIA). We experienced a family with macrothrombocytopenia without leukocyte inclusion. A 5-year-old girl was found to have macrothrombocytopenia incidentally. Her father also had macrothromtocytopenia, but had been suffering from hearing loss and chronic renal failure. Meticulous search by light and electron microscopy failed to detect leukocyte inclusions. To our knowledge, these cases seem to be the first description of autosomal dominant Epstein giant platelet syndrome in Korea.
Bernard-Soulier Syndrome* ; Child, Preschool ; Fathers ; Female ; Hearing Loss ; Humans ; Kidney Failure, Chronic ; Korea ; Leukocytes ; Microscopy, Electron ; Nonmuscle Myosin Type IIA

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

Acanthamoeba is an opportunistic pathogen that causes Acanthamoeba keratitis, granulomatous amoebic encephalitis, and other cutaneous diseases. The life cycle of Acanthamoeba consists of 2 stages of trophozoites and cysts. Under adverse environmental conditions, Acanthamoeba encysts, while the conditions become favorable for growth, it reverts to the trophozoite form. Acanthamoeba excystation is crucial for its proliferation and can lead to recurrent infections after incomplete treatment. To identify the factors involved in excystation, A. castellanii was subjected to either encystation- or excystation-inducing conditions, and gene expression profiles were compared using mRNA sequencing. A. castellanii samples were collected at 8 h intervals for analysis under both conditions. Differentially expressed gene analysis revealed that 1,214 and 1,163 genes were upregulated and downregulated, respectively, by more than 2-fold during early excystation. Five genes markedly upregulated in early excystation (ACA1_031140, ACA1_032330, ACA1_374400, ACA1_275740, and ACA1_112650) were selected, and their expression levels were confirmed via real-time PCR. Small interfering RNA (siRNA) targeting these 5 genes was transfected into Acanthamoeba and gene knockdown was validated through real-time PCR. The silencing of ACA1_031140, ACA1_032330, ACA1_374400, and ACA1_112650 inhibited excystation and suggested that these genes might be essential for excystation. Our findings provide valuable insights for suppressing Acanthamoeba proliferation and recurrence.

PURPOSE: This study was performed to compare complications and perinatal factors according to the birth weight groups in the infants of diabetic mothers(IDM). METHODS: Three hundred and one singleton diabetic mothers and their babies of more than 30 weeks' gestational age admitted in the department of Pediatrics, Chonnam University Hospital from January 1996 to March 2002 were enrolled. Complications and perinatal factors were compared between large for gestational age(LGA) and appropriated for gestational age(AGA) infants. RESULTS: Hypomagnesemia was observed in 37.5%, jaundice in 21.3%, hypoglycemia in 11.1%, hypocalcemia in 7.0%, and birth injury in 19.6%. Congenital anomaly was noted in 24.9% with cardiovascular anomaly most commonly. In the LGA group, the frequencies of jaundice, hypoglycemia, tachypnea, and birth injuries were higher, and the interventricular septum was thicker than the AGA group. In the LGA group, Cesarean section rate, maternal height, weight before pregnancy, weight gain during pregnancy, and the incidence of unawareness of gestational DM were significant compared with the AGA group. CONCLUSION: In the LGA group, the frequencies of jaundice, hypoglycemia, tachypnea, and birth injuries were higher, and the interventricular septum was thicker than the AGA group. In the LGA group, maternal height, weight before pregnancy and weight gain during pregnancy were larger, and the incidence of unawareness of gestational DM was higher compared with the AGA group. These results suggest that careful examination and management are needed to detect the high risk, pregnant DM mothers with possible LGA babies.
Birth Injuries ; Birth Weight* ; Cesarean Section ; Female ; Gestational Age ; Humans ; Hypocalcemia ; Hypoglycemia ; Incidence ; Infant* ; Jaundice ; Jeollanam-do ; Mothers* ; Parturition* ; Pediatrics ; Pregnancy ; Tachypnea ; Weight Gain