Biomedical subjects

Yu-Jia Yang

Publications and source records attributed to Yu-Jia Yang.

6 recordsLinked to original sources

PubMed2006

[Effect of hyperbaric oxygenation on neural stem cells and myelin in neonatal rats with hypoxic-ischemic brain damage].

OBJECTIVE: This study investigated the effect of hyperbaric oxygenation (HBO) on neural stem cells (NSCs) and myelin in neonatal rats following hypoxic-ischemic brain damage (HIBD) and aimed to explore the possible mechanism of the protective effect of HBO on HIBD. METHODS: Seven-day-old Sprague-Dawley rat pups were randomly assigned into 4 groups: Normal control, HIBD, hyperbaric air (HBA), and HBO groups (n=30 each). The HIBD model was produced by permanent occlusion of the left common carotid artery and 2 hrs hypoxemia exposure (8% O2 at 37 degrees C). HBA and HBO treatment was administered (2 ATA, once daily for 7 days) in the HBA and HBO groups respectively 1 hr after HIBD. BrdU immunohistochemistry was used to detect the NSCs in the sub-ventricle zone (SVZ) of the lateral ventricle and the dentate gyrus (DG) of the hippocampus. The myelin damage was assessed by myelin basic protein (MBP) immunostaining. RESULTS: The BrdU-positive cells in the SVZ and the DG of the ischemic hemisphere in the HIBD group were dramatically decreased compared with those of the Normal control group at 3 weeks post-HIBD (P < 0.01). The HBO treatment resulted in an increase of BrdU-positive cells in the DG from 153.7 +/- 37.0 to 193.7 +/- 38.8 (P < 0.05). The nestin expression in the HIBD and HBA groups was reduced compared with that in the Normal control group. There was no difference in the nestin expression between the HBO and the Normal control groups. Hypoxia-ischemia (HI) led to marked myelin damage at 1 week post-HIBD. HBO or HBA treatment alleviated the damage. CONCLUSIONS: The HBO treatment can result in the proliferation of BrdU-positive cells and alleviate the myelin damage following HIBD in neonatal rats, thereby offering neuroprotectivity against HI insults.

Animals↗

PubMed2006

[Protective effects of baicalin pretreatment on hypoxic-ischemic brain damage in neonatal rats].

OBJECTIVE: Previous research suggests that dexamethasone (Dex) pretreatment protects neonatal rats against hypoxic-ischemic brain damage (HIBD). Some of the pharmacological effects of baicalin (a traditional Chinese medicine extracted from Scutellaria baicalensis Georgi) are similar to Dex. This study was designed to explore the effect of baicalin on the neuronal apoptosis following HIBD in neonatal rats. METHODS: Six-day-old Sprague-Dawley rats were randomly assigned into Control (without HI), HIBD, Dex-pretreatment and post-treatment, Baicalin-pretreatment and -post-treatment groups. HIBD was induced by ligating the left common carotid artery, followed by exposure to hypoxia. In the pretreatment groups either baicalin (16 mg/kg) or Dex (0.1 mg/kg) was administered to the rats 24 hrs before HIBD; in the post-treatment groups baicalin or Dex was given 30 minutes after HIBD. The rat pups were sacrificed on postnatal day 10, and brain tissues were harvested. Brain water content was determined, morphological changes were observed under a light microscope, and neuronal apoptosis was measured by terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labeling (TUNEL) staining. RESULTS: The brain water content and the number of apoptotic cells were significantly higher in the HIBD group than those of the Control group (P < 0.05). Both baicalin and Dex pretreatment decreased the brain water content from 88.9 +/- 1.7 % (HIBD group) to 87.4 +/- 0.7% (baicalin) or 87.3 +/- 0.6% (Dex) (P < 0.05) and the number of apoptotic cells were reduced from 251 +/- 28 (HIBD group) to 102 +/- 47 (baicalin) or 75 +/- 26 (Dex) (P < 0.05). Baicalin and Dex post-treatment had no effects on the brain water content and the number of apoptotic cells. Loss and degeneration of neurons could be observed in the HIBD group. Baicalin and Dex pretreatment significantly alleviated neuronal injury, but post-treatment did not. CONCLUSIONS: Pretreatment with baicalin, as with Dex, has a protective effect against HIBD in neonatal rats, but baicalin or Dex post-treatment do not reverse the neuronal injuries.

Animals↗

PubMed2006

[Congenital hyperinsulinism: a difficult and complicated case study].

This paper reported a case of congenital hyperinsulinism and reviewed the relevant literatures regarding to the etiology, pathogenesis, clinical and pathological features, diagnosis and treatment of this disorder. The baby (male), with gestational age of 36 weeks and birth weight 4,200 g, was delivered by caesarean section. It presented with hypoglycemia immediately after birth (0.8 mmol/L). Through the course of the disease, the baby's blood sugar manifested with 1.2-2.8 mmol/L although glucocorticoid was administered. 10% glucose solutions were intravenously infused at a speed of 10-17 mg/(kg x min) for this patient to retain a stable blood sugar level. The plasma insulin level was 24.13 U/L and blood sugar level was 1.5 mmol/L on day 30 of his life. The ratio of plasma insulin (U/L) and plasma glucose (mg/dL) was 0.89. These results suggest an inappropriate insulin secretion resulting in persistent hypoglycemia in this baby and so it was definitely diagnosed with congenital hyperinsulinism.

Blood Glucose↗

PubMed2006

[Serologic examination for childhood herpes simplex virus infection].

OBJECTIVE: This study was designed to investigate the value of serologic examination in the diagnosis of childhood herpes simplex virus (HSV) infection. METHODS: Serum samples were collected from 2 436 outpatients and inpatients. The samples were divided into two groups. Group 1 consisted of 321 samples which were assayed for HSV-1 IgG, HSV-1 IgM, HSV-2 IgG or HSV-2 IgM antibody using herpes simplex virus antibody kits between January 2003 and November 2005. Group 2 consisted of 2115 samples which were assayed for HSV-2 IgG and IgM antibodies by TORCH testing between October 2004 and November 2005. RESULTS: In Group 1, the total seroprevalence of HSV infection was 44.6%, with 38.9% being HSV-1 positive and 15.9% HSV-2 positive; HSV-IgM positivity was found in 41.1% and 25.5% were HSV-IgG positive; HSV-1 seroprevalence significantly increased with age (P < 0.05). In Group 2 the seroprevalence of HSV-2 infection was 1.9%; all of the samples were HSV-2 IgG positive. CONCLUSIONS: HSV serologic examination is useful in the diagnosis of HSV infection in children.

Adolescent↗

PubMed2005

[Effect of heat shock protein 70 on nuclear factor-KappaB/inhibitor protein-alpha of nuclear factor-KappaB in brain edema induced by infection in rat].

OBJECTIVE: To study the effect of heat shock protein 70 (HSP70) on activation of nuclear factor-KappaB (NF-KappaB) and degradation of inhibitor KappaB-alpha protein (I-Kappa B alpha) in brain edema induced by Pertussis bacilli infection in rats. METHODS: Brain edema was induced by injection of Pertussis bacilli suspension via the left internal carotid artery. Seventy-two Sprague-Dawley rats were divided randomly into brain edema group, pretreatment with heat shock group, and normal saline control group. The rats were sacrificed 4, 8 and 24 hours after injection of Pertussis bacilli and normal saline, respectively. HSP70 expression and the degradation of I-Kappa B alpha were assayed in all animals with Western blot analysis. Electrophoretic mobility shift assay (EMSA) was performed to assess NF-KappaB activation of nuclear extract of neurones. RESULTS: The results showed that HSP70 expression was significantly increased in heat shock group compared with control group and brain edema group. The activity of NF-KappaB started to increase at 2 hours in brain edema group and peaked at 24 hours. The expression of I-Kappa B alpha began to decrease at 2 hours and reached the lowest level at 24 hours. In heat shock group the activity of NF-KappaB complexes was lower than that in brain edema group, and the expression of I-Kappa B alpha higher than that in brain edema group at corresponding time points. CONCLUSION: HSP70 shows a protective effect on development of brain edema as its expression increases. The mechanism might be associated with its inhibitory effect on degradation of I-Kappa B alpha and activation of NF-KappaB.

Animals↗

PubMed2003

Neuroprotective effects of nimodipine and MK-801 on acute infectious brain edema induced by injection of pertussis bacilli to neocortex of rats.

OBJECTIVE: To explore the mechanism and type of acute infectious brain edema induced by injection of pertussis bacilli (PB) in rat neocortex, to study the neuroprotective effect of non-competitive antagonist of N-methl-D-aspartate (NMDA) receptor (MK-801) and antagonist of Ca(2+) channels (nimodipine) on brain edema, and to investigate the relationship between percentage of water content and cytosolic free calcium concentration ([Ca(2+) ](i)) in synaptosomes or content of Evans Blue (EB). METHODS: 95 SD rats were randomly divided into five groups, ie, normal control group, sham-operated control group, PB group, nimodipine treatment group and MK-801 pretreatment group. The acute infectious brain edema was induced by injection of PB into the rats. Quantitative measurements of water content and the concentration of EB were performed. [Ca(2+) ](i) was determined in calcium fluorescent indication Fura-2/AM loaded neuronal synaptosome with a spectrofluorophotometer. To observe the effect of MK-801 and nimodipine, we administered MK-801 48 hours and 24 hours before the injection of PB in MK-801 pretreatment group, and nimodipine after the injection of PB in nimodipine treatment group. The specific binding of NMDA receptor was measured with [(3)H]-MK-801 in the neuronal membrane of cerebral cortex. RESULTS: The levels of water content and EB content of brain tissues, and [Ca(2+) ](i) in the neuronal synaptosomes increased more significantly in the PB-injected cerebral hemisphere in the PB group than those of normal control group and sham-operated control group (P<0.05). The water content and [Ca(2+) ](i) increased with the duration of infectious brain edema. Nimodipine administered after the injection of PB could significantly decrease the water content, EB and [Ca(2+) ](i) (P<0.05). MK-801 could significantly decrease the water content, EB and [Ca(2+) ](i) in 4 h and 24 h groups (P<0.05). The Kd values were 30.5 nmol/L+/-3.0 nmol/L and 42.1 nmol/L+/-4.2 nmol/L in PB group and NS group respectively (P<0.05), and Bmax were 0.606 pmol/mg.pro+/-0.087 pmol/mg.pro and 0.623 pmol/mg.pro+/-0.082 pmol/mg.pro respectively, without statistical significance (P>0.05). CONCLUSIONS: The changes in the permeability of blood-brain barrier (BBB) and Ca(2+)-overload may participate in the pathogenesis of infectious brain edema. Treatment with nimodipine can dramatically reduce the damage of brain edema and demonstrate neuroprotective effect on brain edema by inhibiting the excess of Ca(2+) influx and reducing the permeability of BBB. MK-801 pretreatment may inhibit the delayed Ca(2+) influx into the neurons. The infectious brain edema is not only cytotoxic brain edema (intracellular edema) but also vasogenic brain edema (extracellular edema) followed by earlier BBB breakdown, so infectious brain edema is complicated with brain edema.

Acute Disease↗