Adolescent ; Basal Ganglia ; pathology ; Calcinosis ; Child ; Child, Preschool ; Female ; Humans ; Infant ; Male ; Risk Factors ; Stroke ; etiology ; Wounds and Injuries

Adult ; Female ; Humans ; Laryngeal Diseases ; microbiology ; Male ; Middle Aged ; Pharyngeal Diseases ; microbiology ; Pharyngitis ; microbiology ; Syphilis ; Treponema pallidum

Forearm ; innervation ; Ganglion Cysts ; surgery ; Humans ; Male ; Middle Aged ; Muscle, Skeletal ; innervation ; surgery ; Tendons ; surgery ; Ulnar Nerve ; surgery

In November 2018,the American Heart Association(AHA) updated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. The new guideline provided the evidence review and treatment recommendation for antiarrhythmic drug therapy in pediatric shock-refractory ventricular fibrillation/pulseless ventricular tachycardia cardiac arrest. The update was carried out by the Pediatrics Working Group of the International Liaison Committee on Resuscitation(ILCOR)for ongoing clinical evidence review. The update continues with the view of 2015's edition that either lidocaine or amiodarone may be used to treat pediatric patients with shock-refractory ventricular fibrillation or pulseless ventricular tachycardia. The flow chart of cardiac arrest for pediatric advanced life support was slightly adjusted.

This paper reported a new type of amylase (neoamylase) secreted by a Bacillus strain ZX99. The enzyme was a kind of ectoenzyme that could catalyze starch into isomalto-oligosaccharide effectively, but could not act on pullulan as substrate. The strain Bacillus ZX99 was mutated by ultraviolet ray and a mutant strain BS3.232 was screened. The activity of the neoamylase produced from BS3.232 increased by 60% over that from ZX99 under the same conditions. The results of thin-layer chromatography of products from starch and pullulan catalyzed by the enzyme demonstrated that the enzyme was different from neopullulanase and can be used to produce isomaltooligosaccharide from starch, including isomaltose, panose, isomaltotriose, isomaltotetose.

OBJECTIVETo evaluate the diagnostic value of measuring serum C-reactive protein (CRP) and procalcitonin (PCT) levels, within 6 hours after admission to the pediatric intensive care unit (PICU) in children with bloodstream infection (BSI)-associated sepsis and septic infection at other sites.

METHODSA retrospective analysis was performed on 30 children with a confirmed diagnosis of systemic inflammatory response syndrome who were admitted to the Shengjing Hospital of China Medical University between January 2010 and January 2012. Clinical data on serum CRP, PCT and D-dimer levels were collected within 6 hours after admission. The diagnostic values of the indices were determined by comparative analysis.

RESULTSSerum CRP and PCT levels in children with BSI-associated sepsis were significantly higher than in children with septic infection at other sites (P<0.05), but there was no significant difference in serum D-dimer levels between the two groups (P>0.05). Serum PCT level was superior to serum CRP level in distinguishing children with BSI-associated sepsis from those with septic infection at other sites. Serum PCT level could not realistically be used for diagnosing BSI-associated sepsis when it was less than 2 ng/mL (negative predictive value: 100%), but could be reliably used when it was more than 10 ng/mL (positive predictive value: 77%).

CONCLUSIONSSerum PCT level is superior to serum CRP level in distinguishing children with BSI-associated sepsis from those with septic infection at other sites within 6 hours after admission to the PICU. Serum PCT level has a better diagnostic value for BSI-associated sepsis when it is more than 10 ng/mL.

C-Reactive Protein ; analysis ; Calcitonin ; blood ; Calcitonin Gene-Related Peptide ; Child ; Fibrin Fibrinogen Degradation Products ; analysis ; Humans ; Protein Precursors ; blood ; Retrospective Studies ; Sensitivity and Specificity ; Sepsis ; blood ; diagnosis

Cardiomyopathies ; diagnosis ; therapy ; Carnitine ; deficiency ; Female ; Humans ; Hyperammonemia ; diagnosis ; therapy ; Infant ; Muscular Diseases ; diagnosis ; therapy

OBJECTIVETo study the correlation between the blood serum brain natriuretic peptide (BNP) level and the left cardiac function in children with congenital heart disease (CHD).

METHODSThe clinical data of 41 CHD children were retrospectively analyzed. Patients were divided into two groups based on the existence of congestive heart failure (CHF): CHD+CHF (n=21) and CHD alone (n=20). The blood serum BNP level was determined using chemiluminescence immunoassay, and the left ventricular ejection fraction (LVEF) was measured with echocardiogram.

RESULTSThe serum BNP level was 1353 pg/mL (range: 926-2978) in the CHD+CHF group, which was significantly higher than in the CHD alone group[149 pg/mL (range: 75-242)] (P<0.01). The LVEF was 60% (range: 53%-65%) in the CHD+CHF group, which was significantly lower than in the CHD alone group[68% (range: 64%-72%)] (P<0.01). The serum BNP level showed a negative correlation with the LVEF level (r=-0.652, P<0.01).

CONCLUSIONSThe blood serum BNP level is related to the cardiac function. For children with severe CHD+CHF, serum BNP level can be used as a sensitive indicator for evaluating cardiac function damage.

Child ; Child, Preschool ; Female ; Heart Defects, Congenital ; blood ; physiopathology ; Humans ; Infant ; Male ; Natriuretic Peptide, Brain ; blood ; Stroke Volume ; Ventricular Function, Left

OBJECTIVEThis study examined the protein and mRNA contents of angiotesin converting enzyme (ACE), angiotensin II (Ang II) and type I collagen and the changes of lung histomorphology in neonatal rats with hyperoxia-induced chronic lung disease (CLD) and investigated the protection of captopril against CLD and the possible mechanism.

METHODSA total of 240 term neonatal Wistar rats were randomly assigned into air, model, normal saline and captopril-treated groups (n=60 each). The air group was exposed to room air (FiO2=0.21) immediately after birth. The other three groups were exposed to hyperoxia (FiO2=0.9) for 21 days to induce lung injury. The captopril-treated group received captopril daily (30 mg/kg) by intragastric administration between the 7th and 21st days of hyperoxia exposure. The normal saline group was administrated with normal saline instead. At each time interval of 1, 3, 7, 14 and 21 days after experiment, six rats of each group were randomly chosen and sacrificed. The protein and mRNA levels of ACE, Ang II and type I collagen were measured by enzyme-linked immunosorbentassay, radio-immunity technique and RT-PCR. The changes of lung histomorphology were observed under a light microscope.

RESULTSThe protein and mRNA expressions of ACE, Ang II and type I collagen increased significantly in the model and normal saline groups on the 14th and peaked on the 21st days of exposure compared with those of the air group (P < 0.05 or 0.01). Captopril treatment reduced significantly the protein and mRNA expressions of ACE, Ang II and type I collagen compared the model and normal saline groups on the 14th and 21st days, although the values were significantly higher than the air group (P < 0.05 ). The histopathologic examination demonstrated broadened lung interstitium and reduced alveolar quantity and lung fibrosis was developed in the model and normal saline groups on the 14th day of exposure. Captopril treatment obviously alleviated the changes of lung histomorphology.

CONCLUSIONSCaptopril can inhibit the protein and mRNA expressions of ACE, Ang II and type I collagen and alleviate lung fibrosis in neonatal rats with hyperoxia-induced lung injury/CLD. This may contribute to one of the possible mechanisms underlying the protective effects of captopril against lung injury/CLD.

Animals ; Animals, Newborn ; Body Weight ; drug effects ; Captopril ; therapeutic use ; Chronic Disease ; Collagen Type I ; analysis ; Hyperoxia ; complications ; Lung ; metabolism ; pathology ; Lung Diseases ; prevention & control ; Peptidyl-Dipeptidase A ; analysis ; genetics ; RNA, Messenger ; analysis ; Rats ; Rats, Wistar

OBJECTIVEIn addition to regulating blood pressure, angiotensin II is involved in lung fibrogenesis. This study aimed to explore the effect of losartan, an angiotensin II type 1 receptor antagonist, on lung fibrosis in neonatal rats with hyperoxia-induced chronic lung disease (CLD) and its possible mechanisms.

METHODSNeonatal Wistar rats were randomly divided into four groups within 24 hrs after birth: room air exposure, hyperoxia exposure (85%-90% O2), hyperoxia exposure + losartan, and hyperoxia exposure + placebo. Losartan (5 mg/kg/d) or placebo was administered beginning on the 6th day after birth. After 7, 14 and 21 days of exposure, 8 rats in each group were sacrificed. Lung histological changes were evaluated by hematoxylin-eosin staining. Levels of hydroxyproline (HYP), superoxide dismutase (SOD) and malondialdehyde (MDA) in lung tissues were determined by spectroscopy.

RESULTSHyperoxia exposure resulted in decreased alveolar septation, enlarged terminal air space, increased collagen deposition, pulmonary hemorrhage, and pulmonary consolidation. In the hyperoxia exposure + losartan group, the alveolar septum became thinner and lung fibrosis was alleviated, but the alveolar space was not obviously deflated and the number of secondary septum was not increased. Hyperoxia exposure increased significantly the HYP contents in lung tissues 14 and 21 days after exposure. Addition of losartan to the hyperoxia exposure resulted in decreased HYP contents (471.46 +/- 30.63 mu g/kg vs 545.15 +/- 34.90 mu g/kg for hypoxia alone; P < 0.01) after 21 days of exposure. SOD activity increased 7 days after hyperoxia exposure and then decreased to levels similar to the air exposure group. MDA levels increased to a peak at 7 days and remained at higher levels through 21 days of exposure when compared with the air exposure group (P < 0.01). Losartan treatment significantly increased SOD activities (82.94 +/- 4.62 U/mg protein vs 67.78 +/-8.02 U/mg protein; P < 0.01) and decreased MDA levels (30.54 +/- 5.89 nmol/mg protein vs 48.75 +/- 8.09 nmol/mg protein, P < 0.01) compared with the hyperoxia exposure group 21 days after exposure.

CONCLUSIONSLosartan attenuated lung fibrosis in neonatal rats with hyperoxia-induced CLD, possibly through an increase of antioxidase enzyme activity and reduction of lipid peroxidation.

Angiotensin II Type 1 Receptor Blockers ; therapeutic use ; Animals ; Animals, Newborn ; Bronchopulmonary Dysplasia ; drug therapy ; metabolism ; pathology ; Humans ; Hydroxyproline ; analysis ; Hyperoxia ; complications ; Infant, Newborn ; Losartan ; therapeutic use ; Lung ; pathology ; Malondialdehyde ; analysis ; Pulmonary Fibrosis ; drug therapy ; pathology ; Rats ; Rats, Wistar ; Superoxide Dismutase ; metabolism