Augmentation of respiratory muscle activities in preterm infants with feeding desaturation / 소아과

PURPOSE: Frequent desaturation due to immature incoordination of suck-swallow-breathing in preterm infants can influence multiple organs such as the heart, lungs, and brain, which can then affect growth and development. Most notably in preterm infants, feeding desaturation may even affect pulmonary function during gavage feeding. Because respiratory muscle activities may reflect the work required during respiration, we evaluated the differences in these activities between full-term and preterm infants with feeding desaturation, and investigated the correlations with clinical variables. METHODS: Nineteen preterm infants with feeding desaturation (group 1) and 19 age-matched full-term infants (group 2) were evaluated. Oromotor function was evaluated using video recording. The root-mean-squre (RMS) envelope of the electromyography signal was calculated to quantify the activities of muscles involved in respiration. The differences in RMS between both groups and the correlation with clinical variables including gestational age (GA), birth weight (BW), and Apgar scores (AS) at 1 and 5 minutes after birth were evaluated. RESULTS: The RMS values of the diaphragm (RMS-D) and rectus abdominis (RMS-R) were significantly greater in group 1 compared to group 2, and the 1- and 5-min AS were significantly lower in group 1 compared to group 2. RMS-D and RMS-R were inversely correlated with GA, BW, 1- and 5-min AS in all infants. CONCLUSION: This study showed that respiratory muscle activities were augmented during feeding in preterm infants compared to full-term infants. Additionally, respiratory muscle activities were inversely correlated with all clinical variables.

Neuroprotective effects of erythropoietin against hypoxic injury via modulation of the mitogen-activated protein kinase pathway and apoptosis / 소아과

PURPOSE: Hypoxic-ischemic encephalopathy is a significant cause of neonatal morbidity and mortality. Erythropoietin (EPO) is emerging as a therapeutic candidate for neuroprotection. Therefore, this study was designed to determine the neuroprotective role of recombinant human EPO (rHuEPO) and the possible mechanisms by which mitogen-activated protein kinase (MAPK) signaling pathway including extracellular signal-regulated kinase (ERK1/2), JNK, and p38 MAPK is modulated in cultured cortical neuronal cells and astrocytes. METHODS: Primary neuronal cells and astrocytes were prepared from cortices of ICR mouse embryos and divided into the normoxic, hypoxia (H), and hypoxia-pretreated with EPO (H+EPO) groups. The phosphorylation of MAPK pathway was quantified using western blot, and the apoptosis was assessed by caspase-3 measurement and terminal deoxynucleotidyl transferase dUTP nick end labeling assay. RESULTS: All MAPK pathway signals were activated by hypoxia in the neuronal cells and astrocytes (P<0.05). In the neuronal cells, phosphorylation of ERK-1/-2 and apoptosis were significantly decreased in the H+EPO group at 15 hours after hypoxia (P<0.05). In the astrocytes, phosphorylation of ERK-1/-2, p38 MAPK, and apoptosis was reduced in the H+EPO group at 15 hours after hypoxia (P<0.05). CONCLUSION: Pretreatment with rHuEPO exerts neuroprotective effects against hypoxic injury reducing apoptosis by caspase-dependent mechanisms. Pathologic, persistent ERK activation after hypoxic injury may be attenuateed by pretreatment with EPO supporting that EPO may regulate apoptosis by affecting ERK pathways.

Brain-Derived Neurotrophic Factor (BDNF) Exerts a Protective Effect via an Anti-Apoptotic Mechanism on Hypoxic-Ischemic Injury in the Rat Brain / 대한주산의학회잡지

PURPOSE: Perinatal hypoxic-ischemic (HI) brain injury remains a common cause of chronic handicapping conditions of cerebral palsy, mental retardation, learning disability, and epilepsy. HI brain injury induces cell death via either necrosis or apoptosis. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family. It plays key roles in survival, differentiation, and maintenance of neurons. This study was to investigate the neuroprotective effects of BDNF via the mechanisms of anti-apoptosis in HI brain injury by using cortical astrocyte and neuronal cell culture. METHODS: Cortical astrocytes culture of 1-day-old Sprague-Dawley (SD) rat pups and embryonic cortical neuronal cell culture of SD rats at 14-day gestation were done. The Normoxia group was prepared in 5% CO2 incubators and the Hypoxia group and Hypoxia+BDNF group (after treatment with BDNF for 24 hours) were placed in 1% O2 incubators (94% N2, 5% CO2) for 6 or 18 hours. The expression of Bcl-2 and Bax were assessed by real-time PCR and western blot. The caspase-3 activation was evaluated by caspase activity assay kit. RESULTS: In astrocyte and neuronal cell, the expressions of Bcl-2 in the hypoxia groups were reduced compared to the normoxia groups, whereas, those in the Hypoxia+BDNF groups were increased compared to the hypoxia groups. However, the expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were revealed reversely. In astrocyte, Hypoxia group for 6 hours was not significantly altered in Bcl-2, Bax expressions. CONCLUSION: BDNF neuroprotective effects on HI brain injury in neonatal rats may occur via anti-apoptotic mechanism.

Bee Venom Exerts Neuroprotective Effects on Neuronal Cells and Astrocytes under Hypoxic Conditions Through MAPK Signaling Pathways

PURPOSE: Hypoxic-ischemic brain injuries influence the mechanisms of signal transduction, including mitogen-activated protein kinase (MAPK) that regulates gene expression through transcription factor activity. Several attempts have been made to use bee venom (BV) to treat neurological diseases. However, limited data are available for brain injuries such as neonatal hypoxic-ischemic encephalopathy (HIE) and neurodegenerative disorders. The purpose of this study was to investigate the neuroprotective effects of BV by determining the expression of activated MAPK pathways. METHODS: We examined activation and cell viability in hypoxia (1% O2, 5% CO2, 94% N2) in low glucose-treated (H+low G) neuronal cells and astrocytes in the presence and absence of BV. After they were subjected to hypoxic conditions and treated with low glucose, the cells were maintained for 0, 6, 15, and 24 h under normoxic conditions. RESULTS: Extracellular-signal-regulated kinases 1/2 (ERK1/2), p38 MAPK, and stress-activated protein kinases (SAPK)/Jun amino-terminal kinases (JNK) were activated in H+low G conditions. Particularly, phosphorylation of ERK1/2 was maximized 6 h after exposure to H+low G condition. BV specifically inhibited the phosphorylation of ERK1/2. However, BV had no effect on p38 MAPK or SAPK/JNK. In addition, BV improved neuronal cell and astrocytes viability following exposure to H+low G. CONCLUSION: ERK inactivation is known to mediate protective effects in hypoxic brain injury. Taken together, these results suggest that treatment with BV may be helpful in reducing hypoxic injury in neonatal HIE through the ERK signaling pathway.

A Case of Congenital Bronchial Defect Resulting in Massive Posterior Pneumomediastinum: First Case Report / 대한주산의학회잡지

Bronchial defects in neonates are known to occur very rarely as a complication of mechanical ventilation or intubation. This causes persistent air leakage that may form massive pneumomediastinum or pneumothorax, leading to cardiac tamponade or cardiorespiratory deterioration. Early diagnosis and treatment of bronchial defects are essential, as they can be accompanied by underlying severe lung parenchymal diseases, especially in preterm infants. We encountered an extremely low birth weight infant with an air cyst cavity in the posterior mediastinum that displaced the heart anteriorly, thereby causing cardiopulmonary deterioration. During exploratory-thoracotomy, after division of the air cyst wall (mediastinal pleura), we found a small bronchial defect in the posterior side of the right main bronchus. The patient had shown respiratory distress syndrome at birth, and she was managed by constant low positive pressure ventilation using a T-piece resuscitator after gentle intubation. As the peak inspiratory pressure was maintained low throughout and because intubation was successful at the first attempt without any difficulty, we think that the cause of the defect was not barotrauma or airway injury during intubation. The fact that the margin of the defect was very clear also suggested a congenital origin. To our knowledge, this is the first case of congenital bronchial defect in English literature.

Effects of Dizocilpine (MK-801) via Up-modulation of N-methyl-D-aspartate (NMDA) Receptors on Hypoxic-Ischemic Brain Injury in Neonatal Rats / 대한주산의학회잡지

OBJECTIVE: Several studies have demonstrated the neuroprotective effects of (+)-MK-801 hydrogen maleate (dizocilpine), in various animal models of hypoxic-ischemic (HI) brain injury. However limited data are available on the neonatal model of HI brain injury. The aim of the present study was to investigate the effects of dizocilpine and its mechanisms associated with NMDARs expression in neonatal rat model of HI brain injury. METHODS: In in vivo model, 7d-old rat pups underwent permanent unilateral carotid ligation. The animals were divided into six groups: N, normoxia; H, hypoxia without operation; HS, hypoxia with Sham operation; HO, hypoxia with operation; HV, HO treated with vehicle; HD, HO treated with dizocilpine. Dizocilpine (10 mg/kg) was administered intracerebrally to the rats 30 min before HI brain injury. Rat pups were exposed to hypoxia by placing them for 2 hours in hypoxic incubator (92% N2, 8% O2). In in vitro model, embryonic cortical neuronal cell cultures (from SD rats of embryonic days of 18) were done. The normoxia (N) group was prepared in 5% CO2 incubators. The hypoxia (H), and hypoxia treated with dizocilpine (HD) groups were placed in 1% O2 incubators (94% N2, 5% CO2) for 16 hours. In order to estimation of cell viability and growth, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay was done. The degree of neuronal death was evaluated by morphometric method and the protein expression of each NMDARs was quantified by Real Time-PCR and Western blot. RESULTS: Both in the in vitro and in vivo models, the expressions of NMDAR subunits were lower in the hypoxia group than in the normoxia group, whereas they increased in the hypoxia treated with dizocilpine group compared to the hypoxia group. In vitro model, however, the expressions of NR1, NR2A mRNAs decreased in the H group when compared to the N group, whereas they increased a little in the HD group when compared to the H group. CONCLUSION: Dizocilpine was modulated the degeneration of neuronal cell death in neonatal rat model of HI by preservation of NR expression.

Increased serum surfactant protein-D in the infants with acute respiratory syncytial virus bronchiolitis

PURPOSE: Collectin family is an important component of innate immunity, of which surfactant protein (SP)-D and mannose-binding lectin (MBL) are the most characterized. We examined SP-D and MBL in young children with acute respiratory syncytial virus (RSV) bronchiolitis. METHODS: Sixty-three children (7 days of hospital stay. All children were evaluated if they had recurrent wheezing during follow-up. SP-D and MBL were measured using enzyme-linked immunosorbent assay in serum collected on admission and compared with controls. Their levels were evaluated in relation to the symptom severity during admission and recurrence of wheezing after discharge. RESULTS: Serum SP-D increased significantly in the patients (P<0.01), but MBL showed no difference compared to the controls. SP-D levels were significantly higher in severe group compared with nonsevere group (P<0.05). SP-D levels in the patients with recurrent wheezing after discharge were significantly higher than in those without (P<0.05). MBL showed no difference in relation to the symptom severity or recurrence of wheezing. CONCLUSION: Our study showed that serum SP-D was associated with the severity of RSV bronchiolitis and suggests that it might be a biomarker of lung injury and recurrence of wheezing illnesses in the young children admitted with their first RSV bronchiolitis.

A patient with acquired hemophilia A induced by clopidogrel / 대한혈액학회지

Acquired hemophilia A (AHA) is a rare bleeding disorder caused by autoantibodies against factor VIII (FVIII). Treatment with clopidogrel is a cause of AHA, but its clinical course is unknown. Recently, we treated a 65-year-old man who was hospitalized for cerebellar infarction and had a prolonged activated partial thromboplastin time (aPTT) with soft tissue oozing after 3 weeks of clopidogrel use. We terminated clopidogrel administration and transfused the patient with fresh frozen plasma. However, the aPTT increased up to 98.8 seconds, and the FVIII and FVIII inhibitor levels were <1% and 5.4 Bethesda units/mL, respectively. Clopidogrel-associated AHA was considered, and we began steroid treatment. Two months later, FVIII, FVIII inhibitor, and aPTT values were normalized. No further bleeding or aPTT prolongation has been reported during the 2-year follow-up period. AHA should be considered in patients taking clopidogrel and experiencing bleeding, unless the platelet count and coagulation screen are normal.

Clinical Characteristics of Tuberculosis in School-Age Children and Adolescents at a Single Institution / 소아알레르기및호흡기학회지

PURPOSE: In the present study, we investigated the clinical characteristics of tuberculosis in school-age children and adolescents, which is important as a reservoir for future disease burden. METHODS: Ninety patients, aged from 6 to 18 years, who were diagnosed and treated with tuberculosis during the period from January 2005 to July 2011, were enrolled. We retrospectively analyzed the medical records and investigated clinical characteristics of the patients. RESULTS: Eight patients were 6 to 12 (9%) and 82 were over 13 years of age (91%). There was a significantly higher percentage of males than females in the latter age group (P<0.01). Route of infection was not confirmed in 74 patients, and 16 patients were diagnosed through the school or military medical examinations with no clinical symptoms. Seventy patients (78%) were presented with pulmonary tuberculosis. Chronic persistent coughing was the most common presenting symptom, and both upper lobes were most frequently involved. Nineteen patients over 13 years of age had adult-type cavitary tuberculosis. The positive results for acid-fast smears or cultures were not high, and the rate of positive tuberculin skin test was 88%. The most frequent adverse effects of anti-tuberculosis treatment were hepatotoxicity, hyperuricemia, and gastrointestinal disorders. The duration of the treatment was much prolonged in 8 patients who had drug-resistant tuberculosis. CONCLUSION: Our study showed that pulmonary tuberculosis should be suspected in the adolescents who have prolonged respiratory symptoms. It also indicates that pulmonary tuberculosis in adolescents has similar characteristics to tuberculosis in adults, which suggests the potential important role of adolescent tuberculosis in community disease transmission.

Increased Nasal Interleukin-33 in the Infants with Acute Respiratory Syncytial Virus Bronchiolitis / 소아알레르기및호흡기학회지

PURPOSE: Interleukin (IL)-33, a member of the IL-1 cytokine family, is considered to be important for innate-type mucosal immunity of the lung and also has been suggested to induce Th2-type immune responses. We aimed to investigate if IL-33 is involved in airway inflammation due to respiratory syncytial virus (RSV) infection in young children. METHODS: Thirty-eight infants ( or =2 of the following clinical findings: hypoxemia (7 days of hospital stay. The levels of IL-33 and the IL-33 receptor (sST2) were measured using enzyme-linked immunosorbent assay in nasal secretion samples collected from the patients on admission and compared with 20 age-matched controls. We also investigated the levels of IL-33 and sST2 in relation to the atopic status and symptom severity of the patients. RESULTS: Nasal IL-33 levels in the patients with acute RSV bronchiolitis were significantly increased (P<0.05), but sST2 showed no difference compared to the controls. Neither IL-33 nor sST2 showed significant difference in relation to the atopic status or severity of symptoms. CONCLUSION: Our study showed significantly increased IL-33 in the nasal secretions of the young infants admitted with acute RSV bronchiolitis and suggests that IL-33 is involved in the pathogenesis of RSV-induced airway inflammation.

A Rare Case of Pericardial Actinomycosis

Actinomycosis is a common chronic suppurative and granulomatous infection caused by anaerobic or microphilic bacteria primarily from the genus Actinomyces. However, Actinomyces is a rare cause of pericarditis. We experienced a rare case of pericardial actinomycosis. A previously healthy 44-year-old man presented with 3 days of fever, chest pain, and clinical signs of congestive heart failure. Chest computed tomography showed pericardial effusion, pericardial thickening, and bilateral pleural effusion. A subxiphoidpericardiotomy was performed, and a histological specimen was taken from the pericardium. A histological section of the pericardium showed an actinomycotic granule (sulfur granule). His symptoms and signs improved after administration of piperacillin/tazobactam and steroids. He was uneventfully discharged on oral amoxicillin/clavulanate. He recovered fully with no recurrence after six months of follow-up.

Clinical Characteristics of 2009 Pandemic Influenza A (H1N1) Pneumonia in Atopic versus Non-atopic Children / 소아알레르기및호흡기학회지

PURPOSE: Bronchial asthma was reported to be an important risk factor of severe respiratory symptoms due to pandemic H1N1 influenza infection. In this study, we investigated if there was any difference in the clinical features of children with H1N1 pneumonia according to their atopic or asthma status. METHODS: Eighty-eight children admitted with pneumonia due to reverse transcriptase-polymerase chain reaction-confirmed H1N1 influenza infection during the period from September 2009 to January 2010 were enrolled. These patients were divided into atopic (n=42) and non-atopic (n=46) groups. The atopic group consisted of 23 asthmatic children and 19 non-asthmatic children with allergic rhinitis or atopic dermatitis. We retrospectively analyzed the medical records of the patients to investigate if there was any difference in the clinical features according to their atopic or asthma status. RESULTS: There was no age difference between atopic and non-atopic patients. Male preponderance was observed only in the atopic group.(P<0.05) The occurrence of wheezing, severity of respiratory symptoms, and number of emergency-room visits were significantly higher in atopic than non-atopic patients.(P<0.05) However, those variables showed no difference between asthmatic and non-asthmatic patients within the atopic group. Twelve patients in the atopic, non-asthmatic group were followed for 1 year after discharge, and 5 patients were diagnosed to have asthma with recurrence of wheezing and/or positive results to methacholine challenge tests. CONCLUSION: Our study shows that H1N1 influenza infection may cause more severe respiratory symptoms in atopic patients than in non-atopic patients, regardless of their asthma status. allergic rhinitis.(R=0.195, P=0.002). About 17% of the parents who care the allergic rhinitis children experienced the work absence due to their child's illness.

The Neuroprotective Effects of 6-cyano-7-nitroquinoxalin-2,3-dione (CNQX) Via Mediation of Nitric Oxide Synthase on Hypoxic-ischemic Brain Injury in Neonatal Rats

PURPOSE: Current studies have demonstrated the neuroprotective effects of 6-cyano-7-nitroquinoxalin-2,3-dione (CNQX) in many animal models of brain injury, including hypoxic-ischemic (HI) encephlopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether CNQX can protect the developing rat brain from HI injury via mediation of nitric oxide synthase. METHODS: In an in vivo model, left carotid artery ligation was done in 7-day-old Sprague-Dawley (SD) rat pups. The animals were divided into six groups; normoxia (N), hypoxia (H), hypoxia with sham-operation (HS), hypoxia with operation (HO), HO treated with vehicle (HV), and HO treated with CNQX at a dose of 10 mg/kg (HC). Hypoxia was made by exposure to a 2 hr period in the hypoxic chamber (92% N2, 8% O2). In an in vitro model, embryonic cortical neuronal cell culture of SD rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia (N), hypoxia (H), and hypoxia treated with CNQX (HC). The N group was prepared in 5% CO2 incubators and the other groups were placed in 1% O2 incubators (94% N2, 5% CO2) for 16 hr. RESULTS: In the in vitvo and in vivo models, the expressions of iNOS and eNOS were reduced in the hypoxia group when compared to the normoxia group, whereas they were increased in the CNQX-treated group compared to the hypoxia group. In contrast, the expression of nNOS was showed reversely. CONCLUSION: CNQX has neuroprotective property over perinatal HI brain injury via mediation of nitric oxide synthase.

The Effects of Resveratrol via Mediation of Nitric Oxide Synthase (NOS) on Hypoxic Retinal Injury in Neonatal Rats / 대한주산의학회잡지

PURPOSE: Retinopathy of prematurity (ROP) is one of the leading causes of blindness, with retinal detachment occurring due to oxygen toxicity in preterm infants. After premature delivery, oxygen levels are significantly increased compared to those in utero and oxygen therapy further increases oxygen levels in the developing retina. This hyperoxia results in reducing vascular endothelial growth factor (VEGF) level. After the cessation of oxygen therapy and the return to normal oxygen levels, the nonperfused portions of the retina become hypoxic. Retinal hypoxia stimulates VEGF which causes retinal neovascularization and retinal proliferation. Further inhibition of VEGF decreases retinal neovascularization. Recently, resveratrol was found to protect the spinal cord, kidney, and heart from ischemia-reperfusion injury through upregulation of nitric oxide (NO). Resveratrol has been reported to either suppress or enhance NO production. Resveratrol inhibits nitric oxide synthase (NOS) activity and modifies inducible nitric oxide synthase (iNOS) expression. In the present study, we aimed to determine whether or not resveratrol exhibits protective effects via mediation of NOS after a hypoxic retinal insult. METHODS: In the in vitro hypoxic retinal injury, primary retinal cell culture was performed using P0-2 Sprague-Dawley (SD) rats. Hypoxia insults were induced through 1% O2 exposure for sixteen hours. Western blotting and real-time PCR using iNOS, endothelia nitric oxide synthase (eNOS), neuronal nitric oxide synthase (nNOS) antibodies and mRNAs were performed. RESULTS: The expressions of iNOS antibody and mRNA were reduced after a hypoxic insult, whereas it was recovered after treatment with resveratrol. In contrast, those of eNOS and nNOS showed reversely. CONCLUSION: Resveratrol appeared to exert retinal protective effects via mediation of NOS on hypoxic retinal injury in neonatal rats.

Neuroprotective Effects of Dizocilpine (MK-801) Via Mediation of Nitric Oxide Synthase on Hypoxic-ischemic Brain Injury in Neonatal Rats / 대한주산의학회잡지

PURPOSE: Current studies have demonstrated the neuroprotective effects of dizocilpine (MK-801) in many animal models of brain injury, including hypoxic-ischemic (HI) encephalopathy, trauma and excitotoxicity, but limited data are available for those during the neonatal periods. Here we investigated whether dizocilpine can protect the developing rat brain from HI injury via mediation of nitric oxide synthase. METHODS: In an in vivo model, left carotid artery ligation was done in 7-day-old Sprague-Dawley (SD) rat pups. The animals were divided into three groups; normoxia, hypoxia with operation (HO), and HO treated with dizocilpine at a dose of 10 mg/kg. Hypoxia was made by exposure to a 2 hours period of hypoxic incubator (92% N2, 8% O2). In an in vitro model, embryonic cortical neuronal cell culture of SD rats at 18-day gestation was done. The cultured cells were divided into three groups: normoxia, hypoxia, and hypoxia treated with dizocilpine. The N group was prepared in 5% CO2 incubators and the other groups were placed in 1% O2 incubators (94% N2, 5% CO2) for 16 hours. RESULTS: Dizocilpin treatment significantly reduced the size of brain infarct in the neonatal rat model of HI. Both in the animal and in vitro experiments, expression of iNOS and eNOS were lower in the hypoxia group than in the normoxia group. Meanwhile, the nNOS expression was greater in the hypoxia group. Dizocilpine treatment attenuated these aberrant expressions of NOSs following hypoxic injury. CONCLUSION: Dizocilpine has neuroprotective property over perinatal HI brain injury via mediation of nitric oxide synthase.

Eutectic Mixture of Local Anesthesia Cream Can Reduce Both the Radial Pain and Sympathetic Response During Transradial Coronary Angiography

BACKGROUND AND OBJECTIVES: adial artery spasm is one of the most common complications of transradial coronary angiography (TRA): the radial artery is prone to cathecholamine-induced contraction and radial pain during TRA could increase the sympathetic tone. The object of this study was to evaluate whether the eutectic mixture of local anesthesia (EMLA) cream, in addition to lidocaine infiltration, could reduce the sympathetic response by reducing radial pain during TRA. SUBJECTS AND METHODS: Seventy-six patients were randomized 1 : 1 to either EMLA or control groups. Radial pain was measured by the visual analogue scale (VAS) and the verbal rating scale (VRS-4). Sympathetic response, including systolic (SBP) and diastolic blood pressure (DBP), pulse rate (PR), stroke volume (SV) and total peripheral resistance (TPR), was measured by photoplethysmography. RESULTS: Radial pain measured during lidocaine infiltration was significantly lower in the EMLA group (VAS: 3.1 vs. 4.0, p=0.04; VRS-4: 2.0 vs. 2.2, p=0.03) and the sympathetic response was significantly blunted in the EMLA group from baseline to lidocaine infiltration (DeltaSBP, mm Hg: 5 vs. 13, p<0.01; DeltaDBP, mm Hg: 2 vs. 7, p=0.03; DeltaPR, beat/min: 2 vs. 8, p<0.01, DeltaSV, mL: 3 vs. 21, p<0.01; DeltaTPR, mm Hg . L/min: 1.0 vs. 5.9, p<0.01). CONCLUSION: In patients undergoing TRA, the EMLA cream, in addition to lidocaine infiltration, effectively reduces the radial pain and thereby the sympathetic response, during lidocaine infiltration.

Clinical Characteristics of Post-Infectious Bronchiolitis Obliterans / 소아알레르기및호흡기학회지

PURPOSE: Bronchiolitis obliterans (BO), an uncommon chronic obstructive lung disease in children, is most often seen following a severe lower respiratory tract infection (LRTI). We investigated the clinical characteristics, etiology, possible risk factors, radiological findings, and response to treatment in children diagnosed with post-infectious BO. METHODS: A retrospective study was performed on 62 patients diagnosed with post-infectious BO based on clinical and high-resolution computed tomography (HRCT) findings from 2005 to 2010. Forty-eight age-matched children who were admitted with the first episode of LRTI and did not subsequently develop BO were also studied as control subjects. RESULTS: Median ages at diagnosis and initial insult were 28 and 17 months, respectively. The median duration from initial LRTI until diagnosis was 5 months. Children who developed BO showed more respiratory compromise during their acute episodes of LRTI than those who did not. Symptom severity score decreased significantly after adequate treatment, which was significantly greater in patients treated with pulse steroid therapy than those treated with other controllers. CONCLUSION: The results suggest that the development of post-infectious BO should be suspected in the children showing persistent respiratory symptoms after severe LRTIs. They also suggest that adequate treatment including pulse steroid therapy may improve clinical status and the prognosis of these patients.

The neuroprotective effect of recombinant human erythropoietin via an antiapoptotic mechanism on hypoxic-ischemic brain injury in neonatal rats / 소아과

PURPOSE: The neuroprotective effects of erythropoietin (EPO) have been recently shown in many animal models of brain injury, including hypoxic-ischemic (HI) encephalopathy, trauma, and excitotoxicity; however, limited data are available for such effects during the neonatal periods. Therefore, we investigated whether recombinant human EPO (rHuEPO) can protect against perinatal HI brain injury via an antiapoptotic mechanism. METHODS: The left carotid artery was ligated in 7-day-old Sprague-Dawley (SD) rat pups (in vivo model). The animals were divided into 6 groups: normoxia control (NC), normoxia sham-operated (NS), hypoxia only (H), hypoxia+vehicle (HV), hypoxia+rHuEPO before a hypoxic insult (HE-B), and hypoxia+rHuEPO after a hypoxic insult (HE-A). Embryonic cortical neuronal cell culture of SD rats at 18 days gestation (in vitro model) was performed. The cultured cells were divided into 5 groups: normoxia (N), hypoxia (H), and 1, 10, and 100 IU/mL rHuEPO-treated groups. RESULTS: In the in vivo model, Bcl-2 expressions in the H and HV groups were lower than those in the NC and NS groups, whereas those in the HE-A and HE-B groups were greater than those of the H and HV groups. The expressions of Bax and caspase-3 and the ratio of Bax/Bcl-2 were in contrast to those of Bcl-2. In the in vitro model, the patterns of Bcl-2, Bax, and caspase-3 expression and Bax/Bcl-2 ratio were similar to the results obtained in the in vivo model. CONCLUSION: rHuEPO exerts neuroprotective effect against perinatal HI brain injury via an antiapoptotic mechanism.

Risk Factors of Massive Pulmonary Hemorrhage in Newborn Infants / 대한주산의학회잡지

OBJECTIVES: Massive pulmonary hemorrhage (MPH) is a lethal disease, that large amount of blood is spouted from lung with clinical exacerbation, leading to death in newborn infants. Many of its causes were proved but debated. The purpose of this study is to determine the risk factors of Massive pulmonary hemorrhage of the newborn infants. We defined Mild pulmonary hemorrhage (mPH) as small amount of bleeding from lung with no changes in patient's clinical status. METHODS: Risk factors of MPH were estimated by retrospective multivariable analysis among newborn infants with pulmonary hemorrhage in neonatal intensive care unit of Catholic University Hospital of Daegu from January 2001 to December 2007. RESULTS: Pulmonary hemorrhage was developed in 73 neonates (6.3% of total infants admitted to NICU during the study period) and MPH occurred in 25 neonates (34.2%). Gestational age and Birth weights were lower in neonate with MPH than those with mPH. Thrombocytopenia and hypotension were statistically higher in those with MPH than mPH. There were no different significances between MPH and mPH in mean Bomsel grades of respiratory distress syndrome (RDS), Asphyxia, sepsis, disseminated intravascular coagulopathy (DIC), persistent ductus arteriosus (PDA), and intraventricular hemorrhage (IVH). CONCLUSION: The risk factors for massive pulmonary hemorrhage in newborn infants might be thrombocytopenia, and hypotension.

Retinal Protective Effects of Minocycline via Anti-apoptosis on Oxygen-induced Retinopathy in Neonatal Rats / 대한주산의학회잡지

PURPOSE: Retinopathy of prematurity (ROP) is a leading cause of blindness with retinal detachment due to oxygen toxicity in preterm infants. Recently advances in neonatal care had to led improved survival rates in premature infants and ROP re-emerged as a significant clinical problem. In the present study, we aimed to determine the protective abilities of minocycline in a animal model of ROP and a primary retinal cell cultures of neonatal rat via anti-apoptotic actions using Western blotting and real-time PCR with Bcl-2, Bax and caspase-3 antibodies and mRNAs. METHODS: In the in vivo oxygen-induced retinopathy (OIR), the cyclic hyperoxia was performed that 80% O2 for 1 day and 21% O2 for 1 day from P1-14 of newborn rats. Minocycline was injected intravitreously for 7 days and sacrificed at P21. In the in vitro OIR, primary retinal cell culture was done using P0-P2 SD rats. Hyperoxia injury was done for 100% O2 exposure for 6 hours. Western blotting and real-time PCR using Bcl-2, Bax and caspase-3 antibody and primer were done in the rat model of ROP and the dispersed retinal cell culture. To identify photoreceptors of retinal cells the immunofluorescence assay photoreceptor marker, IRBP, was used. RESULTS: In the in vivo OIR, the expression of Bcl-2 antibody and mRNA was increased and those of Bax and caspase-3 were reduced in the minocycline-treated group. In the in vitro OIR, the result was the same as above. CONCLUSION: In conclusion, minocycline was suggested to have retinal protective effects for hyperoxic injury via anti-apoptotic mechanism.