Biomedical subjects

Hung-Chih Lin

Publications and source records attributed to Hung-Chih Lin.

21 records · Page 2Linked to original sources

PubMedDate not supplied

No association of urokinase gene 3'-UTR polymorphism with bronchopulmonary dysplasia for ventilated preterm infants.

Pathological findings pertaining to bronchopulmonary dysplasia (BPD) are consistent with a process of prolonged lung inflammation and impaired healing. The balance of the competing activities of coagulation and fibrinolysis may contribute to the premature lung's response to acute injury. We investigated the association of the urokinase gene polymorphism with BPD in ventilated preterm infants whose gestational age was below 30 weeks. BPD is defined as infants remaining dependent upon active respiratory support and/or oxygen supplementation and featuring characteristic radiographic changes in the lung fields on the 28th postnatal day (BPD-28d) and at a corrected age of 36 weeks of gestation (BPD-36w). Two hundred and four ventilated preterm infants were enrolled in the study. The typing of each specific genotype polymorphism was performed by polymerase chain reaction (PCR) and restriction analysis. Perinatal risk factors for BPD, genotype distribution, and allelic frequencies were compared between infants suffering from BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. The genotype proportions of the urokinase 3'-UTR polymorphism for BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD did not differ significantly. There was no difference in allelic frequency for the urokinase 3'-UTR polymorphism between BPD (28-d), BPD (36-w) and their respective ventilated preterm infants who did not develop BPD infants. We concluded that urokinase gene 3'-UTR C/T polymorphism is not a suitable marker for predicting susceptibility and severity to BPD for preterm infants of Taiwanese.

3' Flanking Region↗

PubMedDate not supplied

System-based strategy for the management of meconium aspiration syndrome: 198 consecutive cases observations.

To evaluate whether the system-based strategy for management of meconium aspiration syndrome (MAS) could reduce the morbidity and mortality rate of MAS in our institute, a prospective consecutive clinical observation was conducted. System-based strategy including appropriately trained the relevant medical staff to familiar with neonatal resuscitation program, early surfactant replacement or lavage following with high-frequency ventilator (HFV) and/or inhaled nitric oxide (iNO). Outcome measurements were the morbidity and mortality rates of MAS. All infants of MAS in the study period were included except cases of congenital malformations or cyanotic congenital heart disease (CHD). Oxygen, nasal continuous positive airway pressure (CPAP), and intermittent mandatory ventilation (IMV) were applied as clinically indicated. Surfactant was used as replacement or lavage therapy for MAS infants whose oxygen index (OI) exceeded 20 or value for AaDO2 exceeded 400 within 6 hours of age. High-frequency oscillator ventilation (HFO) was applied for infants of MAS that demonstrated intractable respiratory failure with conventional mechanical ventilation and 100% oxygen. Inhaled nitric oxide (iNO) was used with IMV or HFO for infants of persistent pulmonary hypertension (PPHN) when it was unresponsive to conventional therapy. Dexamethasone was prescribed in infants of severe hypotension that did not respond to dopamine and epinephrine. A series of 198 consecutive infants of MAS born in this hospital during 9 years were analyzed. There was no mortality. Fourteen infants developed PPHN, 11 had pneumothorax, 1 had pulmonary hemorrhage, 2 had neurologic sequelae because of severe asphyxia, and 2 developed bronchopulmonary dysplasia. Our results indicated that appropriately trained relevant medical staff with neonatal resuscitation program to avoid complicated MAS and early surfactant replacement or lavage following with HFO and/or iNO could reduce the morbidity and mortality rate of MAS even without extracorporeal membrane oxygenation (ECMO).

Administration, Inhalation↗

PubMedDate not supplied

No association between TAP1 DpnII polymorphism and bronchopulmonary dysplasia.

The possibility that a family history of asthma may have a role in susceptibility to bronchopulmonary dysplasia (BPD) had been raised in several reports, and there was evidence of a strong association between transporter associated with antigen processing (TAP1) polymorphism and asthma in Taiwanese population. To test whether TAP polymorphism has a role in the BPD, we investigated the association between TAP1 polymorphism and BPD by analyzing the results of genotype distribution. The study included 224 ventilated preterm infants (<30 weeks) who had respiratory distress syndrome (RDS) and needed intermittent mandatory ventilation (IMV) during Jan. 1999 to July 2003. The typing of TAP1 polymorphism was performed by polymerase chain reaction (PCR)-based restriction analysis. The demography between two groups of these ventilated preterm infants was not different. We observed no significant differences in genotype distribution or allele frequency of the TAPI polymorphisms between BPD and their respective control infants. There was also no significant difference in genotype distribution of the TAP1 polymorphism with duration of IMV. Therefor, we conclude that TAP1 polymorphism is not a useful marker for predicting the susceptibility or severity to BPD for Taiwanese.

ATP Binding Cassette Transporter, Subfamily B, Mem↗