Removal of blunt esophageal foreign bodies using Foley catheter under a fluoroscopic guidance is a well-recognized procedure. However, since this procedure is rather cumbersome and uncomfortable to the patient, the authors tried to find an easier and more convenient modified technique. For 10 patients with esophageal foreign body, we tried the method to the patients who is lying in the right lateral decubitus position and 3 assistants hold head. arms, trunk and legs of the patients without tilting the table and without using immobilizer. Foley catheter is inserted through nostril, nasal cavity and pharynx to esophagus. In order to identify the Foley catheter in esophagus, 0.025 inch short wire was inserted in the Foley catheter. The balloon of a Foley catheter was inflated by 10cc of air, and the syringe was kept attached to the Foley catheter during the procedure. After passage of the foreign body through the upper esophageal sphincter, the balloon was deflated immediately and the foreign body was removed through the mouth. We successfully removed in removing all the blunt esophageal foreign body with ease. This modified method is also fast, safe and efficient.
Arm ; Catheters* ; Deception ; Esophageal Sphincter, Upper ; Esophagus ; Foreign Bodies* ; Head ; Humans ; Leg ; Methods* ; Mouth ; Nasal Cavity ; Pharynx ; Syringes

No abstract available.

A 64-year-old male was admitted due to weight loss of 5kg during a month. Chest X-ray showed two large, lobulated masses on both lower lobe. Chest CT showed ill-defined, multilobulated mass on left lower lobe and r-regular, relatively homogenous mass with air-bronchogram on right lower lobe. Left lower lobectomy and right lower lobectomy was performed sequentially with three months intervaL Microscopic findings showed squamous cell carcinoma of both mass. It was thought that this patient had synchronous double primary lung cancer.
Carcinoma, Squamous Cell ; Humans ; Lung Neoplasms ; Lung* ; Male ; Middle Aged ; Thorax ; Tomography, X-Ray Computed ; Weight Loss

BACKGROUND: Cytosolic Ca2+ overload and oxygen derived free radicals may contribute to stunned myocardium. The pnt study was aimed to investigate the effects of nicardipine and sodium nitroprusside (SNP) on the functional recovery of postischemic reperfused myocardium. METHODS: Fifty-seven halothane-anesthetized dogs were subjected to 15 minutes of 1eft anterior descending coronary artery (LAD) occlusion and 3 hours of reperfusion. They were randomly assigned to receive either intracoronary nicardipine (n=11) or SNP (n=10) alone or both (nicardipine plus SNP, n=10). Eleven dogs that received saline i.c. served as the controL Regional myocardial contractility was evaluated by systolic shortening (%SS), the preload recruitable stroke work slope (Mw), and intramyocardial pressure (IMPs). Diastolic function was assessed by time constant of myocardial relaxation (IMP-tau) and postsystolic shortening (%PSS), LAD blood flow was measured by a Doppler flowmeter as well. RESULTS: LAD occlusion produced a significant reduction in systolic as well as diasto1ic functions to similar degrees in all groups. However, %SS was significantly higher in the nicardipine, SNP and nicardipine-SNP groups (67%, 56%, and 68% of baseline values, respectively) than in the controls (20%) at 3 hours of reperfusion. Furthermore, Mw recovered to the baseline with the onset of reperfusian in the three experimental groups. IMP-tau was restored to the baseline during early nperfusion in the SNP-treated groups but was significantly prolonged in the control and nicardipine poups throughout the seperfusion. LAD blood flow during reperfusion was higher in the SNP-treated groups in comparison to the control group. CONCLUSIONS: Treatment with either nicardipine or SNP enhances the recovery of mgional contractile function in the canine model of myocardial stunning. SNP not nicardipine is also beneficial in attenuation of early diastolic dysfunction. Nicardipine combined with SNP improved systolic as well as early diastolic functions more significantly when compared to either nicardipine or SNP alane.
Animals ; Coronary Vessels ; Cytosol ; Dogs* ; Flowmeters ; Free Radicals ; Heart ; Myocardial Stunning* ; Myocardium ; Nicardipine* ; Nitroprusside* ; Oxygen ; Pharmacology ; Relaxation ; Reperfusion ; Sodium* ; Stroke

BACKGROUND: The present study was aimed (1) to assess the effects of nitric oxide (NO) synthesis inhibitor on regional myocardial function and systemic and pulmonary hemodynamics; (2) to determine whether the blockade of the cyclo-oxygenase (COX) pathway modifies these effects on the variables, and (3) to investigate the mechanism of cardiac depression following NO synthesis inhibition in an open-chest canine model. METHODS: Twenty-five dogs of either sex were acutely instrumented under 1.6% ethrane anesthesia to measure aortic, pulmonary arterial and left ventricular pressure, pulmonary (cardiac output) and left circumflex coronary flow, and subendocardial segment length. NG-nitro-L-arginine methyl ester (L- NAME) at doses of 0.3, 1.0, 3.0, or 10.0 mg/kg i.v. was administered alone (control dogs, n = 10) or in the presence of COX inhibitor, indomethacin (10 mg/kg i.v., n = 10). Seven dogs (n = 7) received phenylephrine at doses of 0.1, 0.3, 1.0, or 3.0 microgram/kg/min i.v. to compare its hemodynamic effects with those of L-NAME. The preload recruitable stroke work slope (Mw) and percent systolic shortening (%SS) as an index of regional myocardial contractility, and the maximum segment lengthening rate (dL/dt max) and percent post-systolic shortening (%PSS) as an index of regional diastolic function, were evaluated. RESULTS: L-NAME dose-dependantly attenuated both regional systolic (Mw and %SS) and diastolic functions (dL/dt max and %PSS), whereas it caused an increase of coronary flow. L-NAME dose- dependently increased systemic blood pressure and vascular resistance as well as pulmonary arterial pressure and vascular resistance. L-NAME also reduced cardiac and stroke volume indices. Pretreatment with indomethacin did not affect the regional myocardial and systemic hemodynamic responses to L-NAME, but did blunt the coronary flow and pulmonary pressure responses. The magnitude of decreases in cardiac and stroke volume indices and Mw was greater with L-NAME than with phenylephrine (P <0.05), despite the comparable blood pressure increases. CONCLUSIONS:These results suggest (1) that NO plays a significant role in cardiac function as well as in systemic and pulmonary but not coronary, vasomotor activities, and (2) that COX products are involved in pulmonary hemodynamic responses to NO synthesis inhibition. It is also suggested that the decline in cardiac output following the NO synthesis inhibition results from a direct myocardial depressant effect of the drug.
Anesthesia ; Animals ; Arterial Pressure ; Blood Pressure ; Cardiac Output ; Depression ; Dogs* ; Enflurane ; Hemodynamics* ; Indomethacin ; NG-Nitroarginine Methyl Ester ; Nitric Oxide* ; Phenylephrine ; Prostaglandin-Endoperoxide Synthases ; Stroke ; Stroke Volume ; Vascular Resistance ; Ventricular Pressure

No abstract available.
Child* ; Humans ; Measles*

No abstract available.
Child* ; Humans

Purpose: Overweight (OW)/obese girls tend to have an earlier pubertal onset than girls with normal weight. However, only a few studies have reported the progression of puberty in these girls. This study aimed to identify risk factors for rapid pubertal progression in OW/obese girls presenting with precocious breast development. Methods: This retrospective cohort study reviewed the medical records of 110 OW (body mass index [BMI] ≥85th percentile for age and sex) and 213 nonoverweight (NW, BMI <85th percentile for age and sex) girls who presented with breast budding before 8 years of age. OW girls were divided into 2 subgroups: girls with central puberty progression before 9 years of age (OW-RP) and those without (OW-SP). Results: Progression to central puberty before the age of 9 was more common in NW girls than in OW girls (83.8 % vs. 65.2 % in NW vs. OW group, p<0.001), and progression-free survival for 1, 2, and 3 years was higher in the OW group (p<0.001). In a subgroup analysis of OW girls, the OW-RP subgroup had more advanced bone age (BA) at the first visit (p=0.047) and higher initial luteinizing hormone (LH, p=0.010) levels than the OW-SP subgroup. Being NW (p=0.001) and having more advanced BA (p=0.023) at the initial workup were the risk factors for pubertal progression before age 9. Conclusion Pubertal progression seems to be slower in OW girls than in NW girls presenting with precocious breast development. However, it can progress rapidly in OW girls with particularly pronounced BA advancement and high LH levels at the initial workup.

Familial male-limited precocious puberty (FMPP) is a rare form of gonadotropin-independent precocious puberty that is caused by an activating mutation of the LHCGR gene. Herein, we report a case of FMPP with a mutation of the LHCGR gene in a Korean boy with familial history of precocious puberty through 3 generations. A 16-month-old boy presented with signs of precocious puberty, including pubic hair, acne, and increased growth velocity. The patient's grandfather and father had a history of precocious puberty and profound short stature. On physical examination, the patient had prepubertal testes with pubic hair development appropriate for Tanner stage II. The stretched penile length was 7 cm (>2 standard deviation score), and observed bone age was that of a 4-year-old boy. Laboratory findings showed high serum testosterone (5.74 ng/mL [appropriate for Tanner IV–V]; normal range, <0.05 ng/mL) with suppressed luteinizing hormone (<0.07 mIU/mL) and normal serum level of follicular stimulating hormone (0.56 mIU/mL; normal range, 0.38–1.11 mIU/mL). Genetic testing revealed a pathogenic variant of LHCGR (c.1730 C>T (p.Thr577Ileu)), confirming FMPP. Bicalutamide and anastrozole were administered, and pubertal progression was sufficiently suppressed without any specific side effects. To our knowledge, this is the first case of genetically confirmed FMPP in Korea.

Familial male-limited precocious puberty (FMPP) is a rare form of gonadotropin-independent precocious puberty that is caused by an activating mutation of the LHCGR gene. Herein, we report a case of FMPP with a mutation of the LHCGR gene in a Korean boy with familial history of precocious puberty through 3 generations. A 16-month-old boy presented with signs of precocious puberty, including pubic hair, acne, and increased growth velocity. The patient's grandfather and father had a history of precocious puberty and profound short stature. On physical examination, the patient had prepubertal testes with pubic hair development appropriate for Tanner stage II. The stretched penile length was 7 cm (>2 standard deviation score), and observed bone age was that of a 4-year-old boy. Laboratory findings showed high serum testosterone (5.74 ng/mL [appropriate for Tanner IV–V]; normal range, <0.05 ng/mL) with suppressed luteinizing hormone (<0.07 mIU/mL) and normal serum level of follicular stimulating hormone (0.56 mIU/mL; normal range, 0.38–1.11 mIU/mL). Genetic testing revealed a pathogenic variant of LHCGR (c.1730 C>T (p.Thr577Ileu)), confirming FMPP. Bicalutamide and anastrozole were administered, and pubertal progression was sufficiently suppressed without any specific side effects. To our knowledge, this is the first case of genetically confirmed FMPP in Korea.