PURPOSE: Gastroesophgeal reflux (GER) is defined as involuntary movement of gastric contents into esophagus. Relaxation of lower esophageal sphincter caused by immature anatomical development in newborn and young infants produces GER frequently. We wanted to know whether the frequency of GER is influenced by feeding types and position or not. We studied in 16 subjects according to feeding types (breast feeding group: BFG-7, formula feeding group: FFG-9) who admitted to the Soonchunhyang university hospital for recurrent regurgitation with 24 hr esophageal pH monitoring from August 1996 to July 1999. METHODS: We compared two groups by number of reflux episode, reflux rate, longest episode, numbers of episodes lasting >5 minutes, longest episode in upright position and longest episode in supine position. We used Mann-Whitney test for statistical analysis. RESULTS: 1) The subjects were 7 infants in BFG and 9 infants in FFG, 16 in total, and mean age was 2.1, and 2.6 months for BFG and FFG, respectively. 2) The reflux numbers were 244+/-151/day, 275+/-155/day for BFG and FFG, respectively. 3) The reflux rate was 14+/-15% for BFG and 28+/- 22% for FFG. It was lower in BFG. 4) The longest episode was 20+/-28 minutes for BFG and 58+/-66 minutes for FFG. It was significantly longer in FFG. 5) The numbers of episodes lasting>5 minutes were 5+/-6 for BFG and 9+/-3 for FFG. 6) The longest episode in upright position was 10+/-8 minutes for BFG and 40+/-47 minutes for FFG. It was significantly shorter in BFG. 7) The longest episode in supine position was 18+/-29 minutes for BFG and 52+/-66 minutes for FFG. It was significantly shorter in BFG. CONCLUSION: Breast feeding is strongly recommended to reduce the regurgitation in infancy. It is an another benefit of breast feeding.
Breast Feeding ; Dyskinesias ; Esophageal pH Monitoring ; Esophageal Sphincter, Lower ; Esophagus ; Gastroesophageal Reflux* ; Humans ; Infant ; Infant, Newborn ; Relaxation ; Supine Position

Purpose: Although activating thermogenic adipocytes is a promising strategy to reduce the risk of obesity and related metabolic disorders, emerging evidence suggests that it is difficult to induce adipocyte thermogenesis in obesity. Therefore, this study aimed to investigate the regulation of adipocyte thermogenesis in diet-induced obesity. Methods: Adipose progenitor cells were isolated from the white and brown adipose tissues of control diet (CD) or high-fat diet (HFD) fed mice, and fully differentiated white and brown adipocytes were treated with β-agonists or 18-carbon fatty acids for β-adrenergic activation or peroxisome proliferator-activated receptor (PPAR) activation. Results: Compared to the CD-fed mice, the expression of uncoupling protein 1 (Ucp1) was lower in the white adipose tissue of the HFD-fed mice; however, this was not observed in the brown adipose tissue. The expression of peroxisome proliferator-activated receptor gamma (Pparg) was lower in the brown adipose progenitor cells isolated from HFD-fed mice than in those isolated from the CD-fed mice. Norepinephrine (NE) treatment exerted lesser effect on peroxisome proliferator-activated receptor-γ coactivator (Pgc1a) upregulation in white adipocytes derived from HFD-fed mice than those derived from CD-fed mice. Regardless which 18-carbon fatty acids were treated, the expression levels of thermogenic genes including Ucp1, Pgc1a, and positive regulatory domain zinc finger region protein 16 (Prdm16) were higher in the white adipocytes derived from HFD-fed mice. Oleic acid (OLA) and γ-linolenic acid (GLA) upregulated Pgc1a expression in white adipocytes derived from HFDfed mice. Brown adipocytes derived from HFD-fed mice had higher expression levels of Pgc1a and Prdm16 compared to their counterparts. Conclusion These results indicate that diet-induced obesity may downregulate brown adipogenesis and NE-induced thermogenesis in white adipocytes. Also, HFD feeding may induce thermogenic gene expression in white and brown primary adipocytes, and OLA and GLA could augment the expression levels.

Active infective endocarditis, involving native, is often complicated by conduction abnormalities. These conduction disturbances are considered to represent an extension of the infection from the valve to the annulus, and to the surrounding myocardium. We describe a case of a 59-year-old woman who presented with dyspnea due to staphylococcal endocarditis, which was complicated by a complete heart block.
Dyspnea ; Endocarditis ; Endocarditis, Bacterial* ; Female ; Heart Block* ; Heart* ; Humans ; Middle Aged ; Myocardium

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db(DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/ enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db(DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/ enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db(DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/ enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db(DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/ enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.

The short duration and fast onset of action of alfentanil underpins its suitability for use in anesthetic techniques. In these case studies, we have assessed the efficacy, safety and feasibility of alfentanil as an analgesic adjuvant of propofol based general anesthesia. Propofol was titrated to Keep the bispectral index in the 40 50 range. Alfentanil was infused at the effect site concentration of 80 or 160 ng/ml using a computer assisted continuous infusion. Two patients in this pilot study showed stable hemodynamics, smooth emergence and satisfactory postoperative pain control with additional analgesics in PACU.
Alfentanil ; Analgesics ; Anesthesia* ; Anesthesia, General ; Hemodynamics ; Humans ; Pain, Postoperative ; Pilot Projects ; Propofol

Malignant mesenchymomas by definition are composed of two or more cellular types that would ordinarily derive from primitive mesenchyme. They grow rapidly, recur frequently, metastasize, and can be found in a wide variety of locations. Malignant mesenchymomas as primary cardiac tumor are extremely rare with poor prognosis. Only 15 cases of cardiac malignant mesenchymoma were reported in worldwide literature in 1961-1992. We report a case of primary cardiac malignant mesenchymoma in 58 year-old female patient admitted due to hemoptysis and mild exertional dyspnea.
Dyspnea ; Female ; Heart Neoplasms ; Heart* ; Hemoptysis ; Humans ; Mesenchymoma* ; Mesoderm ; Middle Aged ; Prognosis

Ruptured aneurysm of sinus of Valsalva is an uncommon congenital lesion, which was first reported in 1840 by Thurman. Its incidence is representing up to 3.5% of patients undergoing congenital heart disease surgery. Predominant symptoms are dyspnea, palpitation, and chest pain, present above the half. An early diagnosis is helpful because of the favorable surgical prognosis. Echocardiography remains useful in detecting abnormalities, and provides important information prior to cardiac catheterization and surgery. Cardiac catheterization and angiography are necessary for diagnosis of receiving chamber and associated lesions such as ventricular septal defect, aortic regurgitation, and other congenital abnormalities. The effective treatment is surgery. Without operation, cause of death are heart failure or bacterial endocarditis. We report two cases of asymptomatic ruptured aneurysm of sinus of Valsalva, confirmed by transesophageal echocardiography, and cardiac catheterization. The corrective surgery was performed without complication.
Aneurysm, Ruptured* ; Angiography ; Aortic Valve Insufficiency ; Cardiac Catheterization ; Cardiac Catheters ; Cause of Death ; Chest Pain ; Congenital Abnormalities ; Diagnosis ; Dyspnea ; Early Diagnosis ; Echocardiography ; Echocardiography, Transesophageal* ; Endocarditis, Bacterial ; Heart Defects, Congenital ; Heart Failure ; Heart Septal Defects, Ventricular ; Humans ; Incidence ; Prognosis ; Sinus of Valsalva*