ABSTRACT
<p><b>OBJECTIVE</b>To evaluate the risk factors for unintentional injury among children in the rural areas of Liling, Hunan Province, China, as a basis for developing prevention and intervention measures for unintentional injury in rural children.</p><p><b>METHODS</b>A total of 3 257 students, aged between 5 and 16 years from 4 middle schools and 2 primary schools in eastern and western rural areas of Liling were recruited in October 2013 by stratified sampling and cluster sampling. The general personal information and data on family backgrounds, living environment, and incidence of unintentional injury were collected from all subjects through a self-designed questionnaire. The risk factors for childhood unintentional injury were assessed by an unconditional multiple logistic regression analysis.</p><p><b>RESULTS</b>Out of the 3 257 subjects, 356 (10.93%) were injured during the 12-month period prior to the study. The univariate analysis showed that unintentional injury in these subjects was related to sex, left-behind status, times of internet surfing in internet bars per week, parent companion or not, age of guardian, degree of harmony of parents' marital relationship, employment status of one or both parents as a migrant worker, storage of fireworks and firecrackers at home or not, violence in residential areas, and participation or not in violence in residential areas. The unconditional multiple logistic regression analysis showed that the major risk factors for unintentional injury in these subjects were male gender (OR=0.751, P=0.013), left-behind status (OR=1.779, P<0.001), storage of fireworks and firecrackers at home (OR=1.337, P=0.028) and violence around residential areas (OR=1.517, P<0.001).</p><p><b>CONCLUSIONS</b>Risk for unintentional injury is multifactorial among children in the rural areas of Liling, Hunan. To reduce the incidence of unintentional injury in children in Liling, particular attention should be paid to boys, left-behind children, children who have home storage of fireworks and firecrackers and children who are living in areas with frequent violence.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Male , Logistic Models , Risk Factors , Rural Population , Wounds and InjuriesABSTRACT
<p><b>OBJECTIVE</b>To study the epidemiology of births in urban China.</p><p><b>METHODS</b>A retrospective study was conducted on neonates born in 2005 in the maternity departments of 72 urban hospitals from 22 provinces in China.</p><p><b>RESULTS</b>A total of 45722 infants born between January 1, 2005 and December 31, 2005 were enrolled. The male to female sex ratio was 1.13:1. Preterm births accounted for 8.1%. The incidence of very low birth weight infants was 0.7%. A total of 99.7% of mothers delivering at term had conceived naturally and 0.3% had experienced assisted reproduction. A total of 98.4% of mothers who delivered preterm had conceived naturally and 1.6% had experienced assisted reproduction. The proportion of vaginal deliveries was 50.8% compared to 49.2% delivered by cesarean sections. Many cesarean sections (38.1%) were due to social factors. Infants with an Apgar score≤7 at 1 minute accounted for 4.8%, and 1.6% of infants had an Apgar score≤7 at 5 minutes. Of all the infants included in the study, 7.14% were admitted to neonatal units for treatment. The death rate of all included infants was 0.74%.</p><p><b>CONCLUSIONS</b>The proportion of preterm births was higher in 2005 than in 2002-2003. The proportion of cesarean section deliveries was much higher in urban China than in most other Asian countries and America.</p>
Subject(s)
Humans , Infant, Newborn , Asphyxia Neonatorum , Epidemiology , Cesarean Section , China , Infant Mortality , Premature Birth , Epidemiology , Retrospective Studies , Risk Factors , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To study the pathological changes in the non-myelin sheath by observing histological damages to the neurofilament protein and apoptosis of neurons in rats with experimental autoimmune encephalomyelitis (EAE).</p><p><b>METHODS</b>Forty-eight Wistar rats were randomly divided into two groups: control and EAE (24 rats in each group). Behavioral changes were observed. Inflammation reactions and demyelination were observed by hematoxylin eosin staining and LOYEZ staining.The level of neurofilament was detected by immunohistochemistry. Apoptosis of the neuron in the spinal cord was detected by TUNEL.</p><p><b>RESULTS</b>Behavioral and histological results confirmed that the model of EAE rats was prepared successfully. In the EAE group, typical morphological features of axonal damage (sparsed axonal density, axonal distortion, axonal transection and even axonal disappearance) were found from the seventh day after immunization and the morphological changes were the most obvious on the fourteenth day. Neurofilament density in the EAE group was significantly lower than in the control group (P<0.01) at 7, 14 and 21 days after immunization. The neuronal apoptosis index in the EAE group at 7, 14 and 21 days after immunization was significantly higher than in the control group (P<0.01).</p><p><b>CONCLUSIONS</b>In addition to inflammatory demyelination, axonal damage and neuronal apoptosis can be observed in the early stage of EAE. Pathological changes may be associated with neurological dysfunction.</p>
Subject(s)
Animals , Female , Rats , Apoptosis , Axons , Pathology , Encephalomyelitis, Autoimmune, Experimental , Pathology , Psychology , Immunohistochemistry , Myelin Sheath , Pathology , Neurofilament Proteins , Neurons , Pathology , Rats, Wistar , Spinal Cord , PathologyABSTRACT
<p><b>OBJECTIVE</b>To study the therapeutic efficacy of baicalin and its effect on apoptosis of inflammatory cells in spinal cords in Wistar rats with autoimmune encephalomyelitis (EAE).</p><p><b>METHODS</b>Forty-four rats were randomly divided into four groups: normal control group (control, n=10), EAE group (n=12), and two intervention groups with dexamethasone (DXM) or baicalin. Seven days after immunization, the two intervention groups were injected intraperitoneally with DXM (1 mg/kg) and baicalin (200 mg/kg) for 1 week, respectively. The spinal cords were removed 14 days after immunization, and stained with hematoxylin and eosin. MBP expression in spinal cords was detected by immunohistochemistry. The apoptosis of inflammatory cells in spinal cords was detected by TUNEL.</p><p><b>RESULTS</b>The weight gain rate in the untreated EAE and the DXM or baicalin intervention groups were significantly lower than that in the control group (P<0.05). The weight gain rate in the baicalin intervention group was significantly higher than that in the untreated EAE and the DXM intervention groups (P<0.05). The scores of neurological function in the two intervention groups were significantly higher than that in the untreated EAE group (P<0.05). DXM or baicalin treatment significantly increased the MBP expression compared with the untreated EAE group (P<0.05). The apoptosis of inflammatory cells increased more in the DXM and the baicalin intervention groups compared with the untreated EAE groups (P<0.05).</p><p><b>CONCLUSIONS</b>Baicalin has protective effects against EAE in rats. It can promote the apoptosis of inflammatory cells in spinal cords.</p>
Subject(s)
Animals , Female , Rats , Apoptosis , Dexamethasone , Therapeutic Uses , Encephalomyelitis, Autoimmune, Experimental , Drug Therapy , Pathology , Flavonoids , Pharmacology , Therapeutic Uses , In Situ Nick-End Labeling , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>To investigate the birth information of newborn infants from obstetric departments in the Central South Region of China.</p><p><b>METHODS</b>A retrospective investigation was carried out in 15582 newborns from obstetric departments of 23 hospitals in the Central South Region of China between January 1 and December 31 of 2005.</p><p><b>RESULTS</b>The sex ratio (male/female) of neonates was 1.16∶1. The proportion of preterm infants was 8.11%. The very low birth weight infants accounted for 0.73%. The neonates born by spontaneous labor accounted for 57.52%. Cesarean sections accounted for 40.82% (social factor of cesarean section: 29.91%). The incidence of neonatal asphyxia was 3.78%, in which 0.75% of the cases were severe asphyxia. The mortality of newborn infants was 0.55%, in which the mortality of preterm infants was 5.56%.</p><p><b>CONCLUSIONS</b>The proportion of preterm infants and the incidence of neonatal asphyxia is high in the Central South Region of China. The proportion of births delivered by cesarean section is high, and social factors are probably responsible for the high rate.</p>
Subject(s)
Female , Humans , Infant, Newborn , Male , Asphyxia Neonatorum , Epidemiology , Cesarean Section , China , Epidemiology , Infant Mortality , Infant, Premature , Infant, Very Low Birth Weight , Logistic Models , Retrospective StudiesABSTRACT
<p><b>OBJECTIVE</b>To study the effect of hyperbaric oxygen (HBO) administered at different pressures and different exposure time on the differentiation of neural stem cells (NSCs) in vitro.</p><p><b>METHODS</b>The cerebral cortices from newborn rats (0-3 days old) were sterilely collected, digested, and centrifuged. After removal of the supernatant, the cells were re-suspended with DMEM/F12 medium containing B27, bFGF and EGF. The NSCs of 2-3 passages were randomly divided into seven groups: a control (untreated) and 6 HBO treatment groups that NSCs were subjected to HBO treatment of different pressures (1, 2 or 3 ATA) and different exposure time (30 or 60 minutes). The differentiated NSCs were examined by neuron-specific enolase (NSE) immunocytochemistry 24 hrs later. Percentage of NSE positive cells differentiated from NSCs was assessed by fluorescent microscopy.</p><p><b>RESULTS</b>The percentage of NSE positive cells differentiated from NSCs was the highest in the HBO 2ATA-60 min group (9.17+/-0.50%) (P<0.01), followed by the HBO 3ATA-60 min (7.89+/-0.62%), HBO 2ATA-30 min (6.72+/-0.76%), HBO 3ATA-30 min (6.08+/-0.57%), HBO 1ATA-60 min (5.45+/-0.52%), HBO 1ATA 30 min (3.85+/-0.44%) and control groups (3.72+/-0.88%). In addition to the HBO 1ATA-30 min group, the other HBO treatment groups had increased significantly percentage of NSE positive cells compared with the control group (P<0.01). Under the same pressure, the 60 min treatment groups had increased significantly percentage of NSE positive cells compared with the 30 min treatment groups (P<0.01).</p><p><b>CONCLUSIONS</b>HBO treatment (2 ATA, 60 minutes) produces a best effect in the differentiation of NSCs into neurons.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Cell Differentiation , Hyperbaric Oxygenation , Neurons , Cell Biology , Pressure , Stem Cells , Cell Biology , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To explore the effects of hyperbaric oxygen (HBO) treatment on the migration and differentiation of endogenous neural stem cells (NSCs) in neonatal rats with hypoxic-ischemic brain damage (HIBD).</p><p><b>METHODS</b>Seven-day-old Sprague-Dawley rats were randomly divided into the normal control (CON), the HIBD model and the HBO groups (HBO treatment was administered at 2 ATA, once daily for 7 days within 3 hrs after HIBD). HIBD model was prepared according to the classic Rice-Vannucci method. BrdU/DCX, BrdU/beta-tubulin, BrdU/GFAP and BrdU/O4 immunofluorescence were examined by confocal microscopy in the subventricular zone (SVZ) and the cortex 7, 14 and 28 days after HBO treatment.</p><p><b>RESULTS</b>The BrdU(+)DCX(+) cells in the SVZ (84 +/- 21 cells/mm2) in the HBO group were significantly higher than those in the CON group (39 +/- 14 cells/mm2) (p<0.05) and the HIBD model group (68 +/- 17 cells/mm2) (p<0.05) 7 days after HBO treatment. Fourteen days after HBO treatment, the BrdU(+) DCX(+) cells decreased in the SVZ and more cells were observed in the cortex in the HBO group as compared with the CON group (p<0.01). The BrdU(+) beta-tubulin(+), BrdU(+)GFAP(+) and BrdU(+) O4(+) cells were observed in the cortex, and more BrdU(+)beta-tubulin(+) and BrdU(+) O4(+) cells were observed in the HBO group as compared with the CON and the HIBD model groups (p<0.05) 28 days after HBO treatment.</p><p><b>CONCLUSIONS</b>HBO treatment may promote endogenous NSCs to migrate to the cortex and differentiate into mature neurocytes in neonatal rats with HIBD.</p>
Subject(s)
Animals , Female , Male , Rats , Animals, Newborn , Bromodeoxyuridine , Metabolism , Cell Differentiation , Cell Movement , Cerebral Cortex , Pathology , Hyperbaric Oxygenation , Hypoxia-Ischemia, Brain , Pathology , Therapeutics , Neurons , Cell Biology , Physiology , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>This study examined the expression of Toll-like receptors (TLR) in peripheral blood mononuclear cells (PBMC) and serum levels of IL-6, IL-10 and TNF-alpha in children with recurrent herpes simplex, in order to investigate the role of TLR2 and TLR9 in recurrent herpes simplex.</p><p><b>METHODS</b>The expression of TLR2 and TLR9 in PBMC was examined by flow cytometer, and serum levels of IL-6, IL-10 and TNF-alpha were detected using ELISA in 22 children with recurrent herpes simplex and in 13 age-matched healthy volunteers.</p><p><b>RESULTS</b>The expression of both TLR2 and TLR9 obviously increased in children with recurrent herpes simplex compared with that in healthy controls (p<0.01). Serum levels of IL-6 and IL-10 increased, while serum TNF-alpha levels decreased significantly in children with recurrent herpes simplex compared with those in healthy controls (p<0.01). There were positive correlations between TLR2 and TLR9 expression and serum IL-6 and IL-10 levels in children with recurrent herpes simplex (p<0.01).</p><p><b>CONCLUSIONS</b>TLR2 and TLR9 in PBMC may participate in the recognition of herpes simplex virus and activate the signal pathway of TLR in children with recurrent herpes simplex. The production and release of IL-6 and IL-10 might be mediated by TLR2 and TLR9.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Male , Cytokines , Blood , Herpes Simplex , Allergy and Immunology , Leukocytes, Mononuclear , Chemistry , Recurrence , Toll-Like Receptor 2 , Blood , Toll-Like Receptor 9 , BloodABSTRACT
<p><b>OBJECTIVE</b>To study the protective effects of multiple course hyperbaric oxygen (HBO) treatment against hypoxic-ischemic brain damage (HIBD) in neonatal rats when HBO treatment is delayed (96 hrs after the HIBD event).</p><p><b>METHODS</b>Eighty-eight 7-day-old Sprague-Dawley rat pups were randomly assigned to control, HIBD and HBO groups. The HBO group was subdivided into cohorts receiving treatment 2 h, 48 h and 96 h, respectively, after HIBD was induced. The three subgroups comprising different therapeutic windows were further randomly assigned to receive 1, 2 or 3 courses of HBO treatment ("HBO-1, -2 and -3 sub-groups"). HBO was administered once daily (2 ATA), a course lasting for seven days. There was an interval of three days between the courses. All pups were sacrificed at the end of HBO treatment (31 days after HIBD). TUNEL staining was used for testing neuronal apoptosis in the cortex and the CA1 of the hippocampus, and NSE staining was used to ascertain cortical neuronal population.</p><p><b>RESULTS</b>1.There were significantly more TUNEL positive cells in the HIBD group than in the control group; NSE positive cells were significantly lower than in controls (P<0.01). 2. With the more delayed therapeutic window, the effects of apoptosis inhibition and neuronal protection of a single course of HBO were gradually reduced. 3. With increasing courses of HBO treatment, the effects of apoptosis inhibition and neuronal protection of HBO increased gradually in rats receiving treatment 48 and 96 hrs after HIBD. In the HBO group receiving treatment 2 hrs after HIBD, the number of apoptotic cells and NSE positive cells were close to that of the control group after one course of HBO treatment.</p><p><b>CONCLUSIONS</b>One course of HBO administered within 2 hrs after HIBD can effectively inhibit neuron apoptosis and protect neurons. The effects of apoptosis inhibition and neuron protection of HBO can be increased through increasing the number of HBO treatment courses in neonatal rats with HIBD even if initiation of treatment is delayed after HIBD.</p>
Subject(s)
Animals , Female , Male , Rats , Animals, Newborn , Apoptosis , Hippocampus , Pathology , Hyperbaric Oxygenation , Hypoxia-Ischemia, Brain , Pathology , Therapeutics , Phosphopyruvate Hydratase , Blood , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>To study the effect of intracerebral transplantation of bone marrow stromal cells (BMSCs) on brain white matter of neonatal rats with hypoxic-ischemic brain damage (HIBD).</p><p><b>METHODS</b>Thirty-four 7-day-old neonatal rats were randomly assigned to three groups: normal control (n=10), HIBD (n=12) and HIBD+BMSCs transplantation (n=12). The HIBD and the HIBD+BMSCs transplantation group rats were subjected to left carotid artery ligation, followed by hypoxia exposure for 2 hrs, in order to induce HIBD. The rats in the HIBD+BMSCs transplantation group received transplantation of BMSCs labeled nucleus with Hochest 33324 into the left hippocampus 24 hrs after HIBD induction. Myelin basic protein (MBP) expression in the left corpus callosum and the subcortical white matter and the number of oligodendrocyte precursors positively stained O4 in the left periventricular area and the subcortical white matter were detected by immunohistochemistry at ages of 45 days.</p><p><b>RESULTS</b>The labeled BMSCs survived and were found mainly in the left hemisphere 37 days after transplantation. The positive rate of O4 expressed by the transplanted BMSCs was 3.70+/-1.09%. More hypomyelination in the left corpus callosum and the subcortical white matter, and less number of O4 positive oligodendrocytes in the left periventricular area and the subcortical white matter were found in the HIBD group compared with the normal control group (P<0.01). The HIBD rats receiving BMSCs transplantation had increased O4 positive oligodendrocytes in the left periventricular area and the subcortical white matter and improved MBP immunoreactivity in the left corpus callosum and the subcortical white matter compared with the HIBD group (P<0.01).</p><p><b>CONCLUSIONS</b>Intracerebral transplantation of BMSCs can improve brain white matter damage in neonatal rats with HIBD.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Antigens, Differentiation , Bone Marrow Cells , Physiology , Brain , Pathology , Hypoxia-Ischemia, Brain , Metabolism , Pathology , Therapeutics , Immunohistochemistry , Myelin Basic Protein , Rats, Sprague-Dawley , Stromal Cells , TransplantationABSTRACT
<p><b>OBJECTIVE</b>To investigate the protective effects of adenovirus-mediated vascular endothelial growth factor (Ad-VEGF)165 gene transfer against hypoxic-ischemic brain damage (HIBD) in neonatal rats.</p><p><b>METHODS</b>Ad-VEGF recombinant adenovirus was constructed by bacterial homologous recombination technology. Seven-day-old Sprague-Dawley rats were randomly assigned to 4 groups: sham-operated (n=20), HIBD (n=25), buffer-treated (n=20), and Ad-VEGF-treated (n=25). The HIBD model was prepared by permanent occlusion of left common carotid artery, followed by exposure to 8% oxygen for 2 hrs. In the Ad-VEGF-treated and the Buffer-treated groups, 2 microL recombinant adenovirus suspension or buffer was injected into the left sensorimotor cortex of the rat brain 3 days after HIBD. Seven days after transplantation, VEGF165 mRNA expression was detected using RT-PCR. Neuronal apoptosis was detected by the terminal deoxynucleotidyl transferase-mediated biotinylated deoxyuridine triphosphate nickel end labeling (TUNEL). CD34 and VEGF protein were detected using immunohistochemistry. Microvascular density in the cerebral cortex was measured based on CD34 positive cells. A radial arm maze test was performed from 30 postnatal days to evaluate long-term learning and memory functions. At 35 postnatal days, the rats were sacrificed for cerebral histological examinations by hematoxylin and eosin.</p><p><b>RESULTS</b>The expression of VEGF165 mRNA increased in the Ad-VEGF-treated group more than in the untreated HIBD and the buffer-treated groups (p<0.05). The number of apoptotic neurons was less in the Ad-VEGF-treated group compared with that in the untreated HIBD and the buffer-treated groups (p<0.05). Microvascular density and VEGF positive cells increased in the Ad-VEGF-treated group compared with that in the untreated HIBD and the buffer-treated groups (p<0.05). In the radial arm maze test, the Ad-VEGF-treated group had more improved achievements than the HIBD and the buffer groups (p<0.05). Neuronal degeneration and necrosis were lessened in the Ad-VEGF-treated group compared with the HIBD and the buffer groups.</p><p><b>CONCLUSIONS</b>Ad-VEGF gene transfer can increase the expression of VEGF mRNA and VEGF protein, decrease neuronal apoptosis, and increase angiopoiesis in the brain. This attenuates brain damage and improves long-term learning and memory functions in neonatal rats after HIBD.</p>
Subject(s)
Animals , Female , Male , Rats , Adenoviridae , Genetics , Animals, Newborn , Cerebral Cortex , Chemistry , Genetic Therapy , Hypoxia-Ischemia, Brain , Therapeutics , In Situ Nick-End Labeling , Neuroprotective Agents , RNA, Messenger , Rats, Sprague-Dawley , Vascular Endothelial Growth Factor A , GeneticsABSTRACT
OBJECTIVE@#To investigate the effect of brain tissue extracts in neonate rats with hypoxic-ischemic brain damage (HIBD) on the differentiation of bone marrow stromal cells (BMSCs) into neural cells.@*METHODS@#Fifteen 7-day-old neonate rats were induced HIBD by left carotid artery ligation and hypoxia exposure, and another 15-day-old neonate rats were served as normal rats. The left and right brain tissue extracts of the normal and HIBD rats were prepared 24 h after the HIBD (8-day old), 72 h after the HIBD (10-day old), and 7 d after the HIBD (14-day old), respectively (n=5). The rat BMSCs of passage 3-5 were cultured in the medium with or without previous brain tissue extracts. The expressions of neuron specific enolase (NSE), glial fibrillary acidic protein (GFAP) and O(4) marked oligodendrocyte were detected after 3 days by immunocytochemistry.@*RESULTS@#The expressions of NSE, GFAP and O(4) of BMSCs cultured in the medium with left or right brain tissue extracts of different day old normal rats were higher than those of BMSCs cultured without the extracts, respectively (P<0.01), and the expressions of NSE, GFAP and O(4) of BMSCs cultured in the medium with left brain tissue extracts of 8 day old and 10 day old HIBD rats were higher than those of BMSCs cultured with right brain tissue extracts of the same day HIBD rats and BMSCs cultured with left or right brain tissue extracts of the same day normal rats (P<0.01 or P<0.05). The expressions of NSE, GFAP and O(4) of BMSCs cultured in the medium with left brain tissue extracts of 8-day-old HIBD rats were higher than those of BMSCs cultured with left brain tissue extracts of 10-day-old and 14-day-old HIBD rats (P<0.01 or P<0.05).@*CONCLUSION@#The brain tissue extracts of normal and HIBD rats can induce BMSCS into neural cells, and the damaged brain tissue extracts of 8-day-old HIBD rats is the best inductor.
Subject(s)
Animals , Rats , Animals, Newborn , Brain , Metabolism , Cell Differentiation , Cells, Cultured , Hypoxia-Ischemia, Brain , Metabolism , Mesenchymal Stem Cells , Cell Biology , Neurons , Cell Biology , Rats, Sprague-Dawley , Tissue Extracts , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To investigate the immunoregulatory function of bone marrow mesenchymal stem cells (MSCs) on allogeneic B lymphocytes in vitro, and explore its possible mechanisms.</p><p><b>METHODS</b>Human MSCs were isolated from bone marrow and expanded in vitro. The purity of MSCs were identified with the spindle fibroblastic morphology by micro-photograph and the phenotype by flow cytometry. MSCs were irradiated with 20 Gy of gamma ray to abolish proliferative capacity. The change of activated B cells proliferative capability and apoptosis with or without MSCs were examined. The effect of MSCs on activated B cells proliferation was compared between transwell cultures and non-transwell cultures. The IgG, IgA and IgM productions of B cells and the immune molecules expression with or without MSCs were assessed. RESULTS (1) MSCs could not induce the proliferation of B lymphocytes, but could suppress LPS activated B lymphocytes proliferation. (2) With the number of MSCs increased, a dose-dependent inhibitory effect was observed in B cell proliferation. MSCs could not induce B cells apoptosis. The activated B cells proliferation with MSCs in transwell culture was decreased, suggesting that MSCs inhibition of B cells might be mediated both by cell-to-cell contact and soluble factors. (3) MSCs suppressed the IgG, IgA and IgM production of B cells, but not suppressed the immune molecules HLA-DR, CD40, CD80 and CD86 expression.</p><p><b>CONCLUSION</b>Bone marrow MSCs can suppress allogeneic B lymphocytes proliferation and its secretion in vitro.</p>
Subject(s)
Humans , Apoptosis , B-Lymphocytes , Allergy and Immunology , Bone Marrow Cells , Cell Biology , Allergy and Immunology , Cell Communication , Cell Proliferation , Cells, Cultured , Immunophenotyping , Mesenchymal Stem Cells , Cell Biology , Allergy and ImmunologyABSTRACT
<p><b>OBJECTIVE</b>To study the effects of heat shock preconditioning on the expression of heat shock protein-70 (HSP70) and apoptosis of the neuron in experimental autoimmune encephalomyelitis (EAE) rats.</p><p><b>METHODS</b>Thirty-six Wistar rats were randomly divided into control, EAE and heat shock preconditioning groups (n=12 each). The EAE animal model was induced with guinea pig myelin basic protein. Heat shock preconditioning was performed 24 hrs prior to the EAE model inducement. No treatment was done in the control group. The neurological signs were observed after immunization. The spinal cords were removed and stained with hematoxylin and eosin. HSP70 was detected by immunohistochemistry. Apoptosis of the neuron was measured by TUNEL.</p><p><b>RESULTS</b>Heat shock preconditioning significantly alleviated clinical signs and neuronal injury. HSP70 expression in the heat shock preconditioning group was significantly higher than in the untreated EAE group (21.08 +/- 0.87 vs 10.17 +/- 0.51; P < 0.01). Heat shock preconditioning suppressed apoptosis of the neuron compared with the EAE group (apoptosis rate: 21.92 +/- 1.00% vs 58.92 +/- 1.67%; P < 0.01).</p><p><b>CONCLUSIONS</b>Heat shock preconditioning might improve the neurological outcome in EAE rats, possibly through the induction of HSP70 synthesis and the reduction of apoptosis of the neuron in spinal cords.</p>
Subject(s)
Animals , Female , Male , Rats , Apoptosis , Bone Marrow , Pathology , Encephalomyelitis, Autoimmune, Experimental , Pathology , Therapeutics , Guinea Pigs , HSP70 Heat-Shock Proteins , Hot Temperature , Neurons , Pathology , Rats, WistarABSTRACT
<p><b>OBJECTIVE</b>A recent study has suggested that hyperbaric oxygen (HBO) therapy administered within 3 hrs following hypoxic-ischemic brain damage (HIBD) may alleviate brain white matter damage (WMD) in neonatal rats. However it is unclear whether a delayed HBO therapy (more than 3 hrs following HIBD) has neuroprotective effects in neonatal rats. This study aimed to explore the effect of HBO therapy administered at different time points following HIBD on WMD in neonatal rats.</p><p><b>METHODS</b>The HIBD model was prepared according to the Rice-Vannucci procedure in 7-day-old Sprague-Dawley rats. HBO therapy was administered at 3, 6, 12, 24 or 72 hrs after HIBD, once daily for consecutive 7 days. T-maze test, the foot-fault test and the radial arm maze test were performed after 14 days of HIBD. Myelin basic protein (MBP) in the callositas and corpora striata was examined by immunohistochemical method 28 days after HIBD.</p><p><b>RESULTS</b>The rats receiving HBO therapy at 3, 6 and 12 hrs after HIBD performed significantly better in the T-maze test, the radial arm maze test and the foot-fault test than the untreated HIBD rats. There were no significant differences in the behavioral test results between the HBO-treated groups administered HBO at 24 and 72 hrs after HIBD and the untreated HIBD group. The MBP expression in the HBO-treated groups treated within 12 hrs after HIBD was significantly higher than that in the untreated HIBD group (P < 0.05). When the HBO therapeutic window was delayed to 24 hrs after HIBD, there were no significant differences in the MBP expression between the HBO-treated and the untreated HIBD groups.</p><p><b>CONCLUSIONS</b>HBO therapy administered within 12 hrs following HIBD can alleviate brain WMD in neonatal rats, but the efficacy of HBO therapy administered 24 hrs after HIBD does not appear to be satisfactory.</p>
Subject(s)
Animals , Female , Male , Rats , Animals, Newborn , Brain , Pathology , Hyperbaric Oxygenation , Hypoxia-Ischemia, Brain , Metabolism , Pathology , Psychology , Therapeutics , Immunohistochemistry , Maze Learning , Myelin Basic Protein , Rats, Sprague-Dawley , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>Previous studies suggest that hyperbaric oxygen (HBO) treatment promotes the proliferation of neurocytes in neonatal rats following hypoxic-ischemic brain damage (HIBD). The Wnt signaling pathway is associated with neurogenesis. This study examined whether HBO promoted neural stem cells (NSCs) proliferation after HIBD, and whether that the proliferation correlated with Wnt-3 protein expression.</p><p><b>METHODS</b>Seven-day-old Sprague-Dawley rats were randomly divided into three groups: normal control, hypoxia-ischemia (HI), and HI-HBO. HI was induced by the ligation of left common carotid artery, followed by a 2-hr exposure to 8% O2 in the latter two groups. HBO was administered 3 hrs after HI in the HI-HBO group for continuous 7 days (2 atmospheres absolute, once daily). The proliferating NSCs in the subventricular zone (SVZ) was examined by BrdU/nestin immunofluorescence and the expression of Wnt-3 protein in NSCs was examined by nestin/Wnt-3 immunofluorescence at 6 and 24 hrs and at 3, 7 and 14 days of HI. The cellular expressions of nestin and Wnt-3 protein were analyzed by laser scanning confocal microscopy. The linear regression analysis was used to evaluate the correlation between cellular Wnt-3 and nestin protein. The expressions of nestin and Wnt-3 protein in the ischemic cerebral hemisphere were analyzed with Western blotting.</p><p><b>RESULTS</b>The number of BrdU/nestin positive cells in the SVZ increased 3 hrs after HBO therapy, peaked at 7 days and remained at a higher level until 14 days after HBO therapy in the HI-HBO group compared with the normal control and the HIBD groups. The level of Wnt-3 protein in NSCs increased significantly 3 hrs after HBO therapy, peaked at 3 days and remained at high levels until 14 days after HBO therapy in the HI-HBO group compared with the normal control and the HIBD groups. The level of cellular nestin protein was closely correlated with the level of cellular Wnt-3 protein (r = 0.893, P < 0.05). The Western blotting analysis demonstrated increased Wnt-3 and nestin protein expressions in the ischemic cerebral hemispheres.</p><p><b>CONCLUSIONS</b>HBO treatment promotes the proliferation of NSCs in HIBD neonatal rats, which is correlated with the activation of Wnt signaling.</p>
Subject(s)
Animals , Female , Male , Rats , Animals, Newborn , Blotting, Western , Bromodeoxyuridine , Metabolism , Cell Proliferation , Fluorescent Antibody Technique , Hyperbaric Oxygenation , Hypoxia-Ischemia, Brain , Metabolism , Pathology , Therapeutics , Intermediate Filament Proteins , Nerve Tissue Proteins , Nestin , Neurons , Cell Biology , Stem Cells , Cell Biology , Wnt Proteins , Wnt3 ProteinABSTRACT
OBJECTIVE@#To explore the effect of hepatocyte growth factor (HGF) on the proliferation, apoptosis and function of hyperoxia exposed Type II alveolar epithelial cells (AEC II) isolated from premature rat lungs, and to explore the mechanism of the protective effect of HGF on hyperoxia-induced lung injury.@*METHODS@#Type II alveolar epithelial cells from fetal rat lungs were cultured. After being purified, AEC II was randomly divided to 4 groups: air group (Air), hyperoxia group (HO), air plus hepatocyte growth factor group (Air+HGF), hyperoxia plus hepatocyte growth factor group (HO+HGF) . The mRNA levels of surfactant associated protein, SPs (including SPA, SPB, SPC) were measured by RT-PCR. The proliferation and apoptosis of AEC II were analyzed with flow cytometric assay and Western blot.@*RESULTS@#(1) Compared with Air group, the apoptosis rate increased significantly in the HO group, while G(2)/M phase percentage and the protein expression levels of proliferating cell nuclear antigen (PCNA) decreased significantly (P<0.01); the S phase percentage and the protein expression levels of PCNA increased significantly in the Air+HGF group. (2) In the HO +HGF group, the apoptosis rate was not significantly different, G0/G1 phase percentage decreased significantly, S phase, G(2)/M phase percentage and the protein expression levels of PCNA increased significantly compared with the HO group. (3) SPs mRNA levels significantly decreased in the HO group compared with those in the Air group. After HGF was added, SPs mRNA levels increased in the HO +HGF group and the Air+HGF group compared with the HO group.@*CONCLUSION@#Hyperoxia can inhibit the proliferation, increase the apoptosis rate and decrease SPs mRNAs levels of AEC II in vitro in premature rats, while HGF can partly inhibit the changes of SPs mRNAs levels and cell proliferation of AEC II resulted from hyperoxia, and HGF may play a protective role in hyperoxia-induced lung injury.
Subject(s)
Animals , Female , Male , Pregnancy , Rats , Animals, Newborn , Apoptosis , Cell Proliferation , Cells, Cultured , Epithelial Cells , Metabolism , Hepatocyte Growth Factor , Pharmacology , Hyperoxia , Metabolism , Pathology , Proliferating Cell Nuclear Antigen , Metabolism , Pulmonary Alveoli , Cell Biology , Pulmonary Surfactant-Associated Proteins , Metabolism , Rats, Sprague-DawleyABSTRACT
<p><b>OBJECTIVE</b>This study was designed to investigate the value of serologic examination in the diagnosis of childhood herpes simplex virus (HSV) infection.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>HSV serologic examination is useful in the diagnosis of HSV infection in children.</p>
Subject(s)
Adolescent , Child , Child, Preschool , Female , Humans , Infant , Infant, Newborn , Male , Antibodies, Viral , Blood , Herpes Simplex , Diagnosis , Allergy and Immunology , Immunoglobulin G , Blood , Immunoglobulin M , Blood , Retrospective Studies , Serologic Tests , Simplexvirus , Allergy and ImmunologyABSTRACT
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.
Subject(s)
Humans , Infant, Newborn , Male , Blood Glucose , Diagnosis, Differential , Hyperinsulinism , Diagnosis , Therapeutics , Insulin , Bodily Secretions , PrognosisABSTRACT
<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>