Bibliometric Analysis of Bronchopulmonary Dysplasia in Extremely Premature Infants in the Web of Science Database Using CiteSpace Software.

Objectives: To review the literature related to bronchopulmonary dysplasia in extremely pre-mature infants, summarize research direction, and report trends. Methods: CiteSpace is a Java application which supports visual exploration with knowledge discovery in bibliographic databases. Relevant articles from 2008 to 2020 were retrieved from the Web of Science Core Collection database, and we extracted the following data: title, abstract, year, keywords, author, organization, journal and cited literature. We downloaded the data into CiteSpace (version 5.7.R3) to summarize countries, institutions, journals, and authors. We visualized the data with a knowledge map, collaborative network analysis, cluster analysis, and burst keyword analysis. Results: We identified 610 articles on bronchopulmonary dysplasia in extremely pre-mature infants. The United States had the most articles on this topic (302 articles), followed by Canada (49 articles) and Germany (44 articles). The top three institutions, high-yield journals, and authors were all from the United States. The most common keywords were neurodevelopmental disorders, active perinatal care, mechanical ventilation, inflammation, pulmonary hypertension, low-dose hydrocortisone, development, and patent ductus arteriosus. Conclusions: This study illustrates the trends and frontiers in the study of bronchopulmonary dysplasia in extremely pre-mature infants. The current research direction is to identify the risk factors in developing bronchopulmonary dysplasia in extremely pre-mature infants.

Decreased purinergic inhibition of synaptic activity in a mouse model of Niemann-Pick disease type C.

Niemann-Pick disease type C (NPC) is a progressive neurodegenerative disorder characterized by accumulation of free cholesterol in lysosomes, mainly due to a mutation in the NPC1 gene. The pathophysiological basis of the neural disorders in NPC, however, is not well understood. We found that the hippocampal field excitatory postsynaptic potential (fEPSP) was enhanced in NPC1 mutant mice. A1-receptor antagonist or adenosine degrading enzyme enhanced the fEPSP in both types of mice, but had a much weaker effect in the mutant mice, suggesting less tonic inhibition of synaptic transmission by endogenous adenosine in the mutant. Further evidence showed impaired hippocampal long term potentiation (LTP) in mutant mice. Supplement of A1 agonist N6-Cyclopentyladenosine (CPA) partially rescued the impaired LTP in mutant mice. Moreover, adenosine release from hippocampal slices was significantly decreased in the mutant. The enhanced excitatory synaptic transmission and the decreased synaptic plasticity due to the decreased adenosine release in NPC brain may partially contribute to the neural disorders of NPC disease, such as seizures, neurodegeneration, and dementia.

Effects of GSM 1800 MHz on dendritic development of cultured hippocampal neurons.

AIM: To evaluate the effects of global system for mobile communications (GSM) 1800 MHz microwaves on dendritic filopodia, dendritic arborization, and spine maturation during development in cultured hippocampal neurons in rats. METHODS: The cultured hippocampal neurons were exposed to GSM 1800 MHz microwaves with 2.4 and 0.8 W/kg, respectively, for 15 min each day from 6 days in vitro (DIV6) to DIV14. The subtle structures of dendrites were displayed by transfection with farnesylated enhanced green fluorescent protein (F-GFP) and GFP-actin on DIV5 into the hippocampal neurons. RESULTS: There was a significant decrease in the density and mobility of dendritic filopodia at DIV8 and in the density of mature spines at DIV14 in the neurons exposed to GSM 1800 MHz microwaves with 2.4 W/kg. In addition, the average length of dendrites per neuron at DIV10 and DIV14 was decreased, while the dendritic arborization was unaltered in these neurons. However, there were no significant changes found in the neurons exposed to the GSM 1800 MHz microwaves with 0.8 W/kg. CONCLUSION: These data indicate that the chronic exposure to 2.4 W/kg GSM 1800 MHz microwaves during the early developmental stage may affect dendritic development and the formation of excitatory synapses of hippocampal neurons in culture.

Interleukin-2 inhibits NMDA receptor-mediated currents directly and may differentially affect subtypes.

Using whole-cell patch-clamp recordings, this study investigated the effects of interleukin-2 (IL-2) on N-methyl-d-aspartate (NMDA) receptor-mediated currents (I(NMDA)) in rat cultured hippocampal neurons and human embryonic kidney (HEK) 293 cells expressing recombinant NMDA receptors. We found that IL-2 (0.01-1ng/ml) immediately and significantly decreased peak I(NMDA) in cultured neurons. Interestingly, the peak I(NMDA) induced in HEK 293 cells was also inhibited by IL-2. We also found that IL-2 differentially decreased the peak amplitudes of NR2A- and NR2B-containing NMDA receptor-mediated currents (I(NR2A) and I(NR2B)) by 54+/-5% and 30+/-4%, respectively. These results provide new evidence that IL-2 induces rapid inhibition of peak currents of NMDA receptor-mediated responses with possible NR1/NR2A and NR1/NR2B subtype-differentiation, and suggest that the inhibition is mediated by direct interaction between IL-2 and NMDA receptors.

[Cardiovascular response caused by intracerebroventricular microinjection of interleukin-2].

AIM: To investigate the cardiovascular response caused by intracerebroventricular (ICV) microinjection of interleukin-2 (IL-2) and explore the underlying mechanism. METHODS: Male Sprague-Dawley rats were anesthetized with intraperitoneal urethane( 1.2 g/ kg). The changes of mean arterial blood pressure (MAP) and heart rate (HR) were observed during ICV microinjection of IL-2 with or without pretreatment of naloxone or atropine or phentolamine. RESULTS: There were no significant effects on cardiovascular response after ICV injection of IL-2 at 500 IU/3 microl and 1 000 IU/3 microl, but IL-2 at 1 500 IU/3 microl could elevate MAP and HR. The responses of MAP and HR reached their maximum levels at 10 min (MAP: 10 +/- 1.8 mmHg, HR: 25 +/- 2 b/min, P < 0.05) after the injection and lasted 15 or 10 minutes respectively. Pretreatment with naloxone (10 microg/10 microl) or atropine (1.5 microg/10 microl) could block the cardiovascular response of ICV injection of IL-2. Pretreatment with phentolamine (10 microg/10 microl) failed to block the cardiovascular responses by IL-2. CONCLUSION: ICV microinjection of interleukin-2 (IL-2) can elevate the MAP and HR, which may be mediated by central opioid and cholinergic system. The alpha-adrenergic system may be not involved in the cardiovascular response of IL-2.

[The regulation of area postrema in cardiovascular function in rabbit].

AIM: To determine the role of area postrema (AP) of rabbit in the regulation of cardiovascular function. METHODS: The rabbits were anesthetized with intravenous injection of 10% urethane and 1% chloralose, and were artificially ventilated. The changes of mean arterial pressure (MAP) and heart rate (HR) were observed when AP was electrically stimulated with different frequency (10 Hz -80 Hz) and after chemical lesion of CVLM or RVLM, respectively. RESULTS: Electrical stimulation of AP with low frequency (10 Hz, 20 Hz) decreased MAP and HR. Stimulation with high frequency(60 Hz, 80 Hz) increased MAP but decreased HR. The changes in MAP and HR were significantly lower (P < 0.01) after CVLM was destroyed when electrical stimulation of AP with 20 Hz, and both changes of MAP and HR were disappeared (P < 0.01) after RVLM was destroyed when electrical stimulation with 20 and 80 Hz. CONCLUSION: Electrical stimulation of AP with low frequency decreases MAP and HR, stimulation with high frequency induces an increase in MAP and decreases in HR. The former is probably related to excitation of CVLM, the cardiovascular effects induced by different frequency of electrical stimulation are all resulted from the activation of RVLM.

[Role of area postrema of medulla in regulation of rat cardiovascular activity].

OBJECTIVE: To explore the role of area postrema (AP) of medulla in control of cardiovascular functions in rat. METHODS: (1) Sprague Dawley rats were anaesthetized with urethane and pentobarbital and the AP was stimulated by electrical stimulus with intensity of 0.1 mA and frequencies ranged 10 approximate, equals 80 Hz. (2) Excitatory amino acid L-glutamate (L- Glu, 0.1 approximate, equals 0.5 mol/L) was microinjected into AP in urethane anaesthetized rats and the changes of mean arterial pressure (MAP) and heart rate (HR) were recorded. RESULT: (1) When the frequencies of 10 Hz, 20 Hz and 40 Hz were used, the electrical stimulation of AP caused decrease of MAP and HR (P<0.001),while the electrical stimulation with the frequencies of 60 Hz and 80 Hz caused an increase of MAP (P<0.05) but a decrease of HR (P<0.001). (2) Microinjection of L-Glu at 0.1 mol/L had no effect on MAP and HR (P>0.05), but it decreased MAP and HR at 0.15 mol/L (P<0.001, P<0.05). The MAP was increased (P<0.001) but HR (P<0.05) was decreased at the concentrations of 0.2 mol/L and 0.5 mol/L, respectively. CONCLUSION: Alterations of MAP and HR induced by electrical or chemical stimulation on AP of medulla are related to the frequency of electrical stimulation or concentration of L-Glu.

[Interaction between opioid receptor and adrenoceptor signaling in ischemia reperfusion of the isolated rat heart].

OBJECTIVE: To investigate the interaction between opioid receptor (OR) stimulation and adrenergic receptor (AR) stimulation in the isolated ischaemia/reperfusion (I-R) rat heart. METHODS: Male Sprague-Dawley rats were used for Langendoff isolated heart perfusion. Myocardial ischemia for 20 min was followed by 30 min of reperfusion, during which the kappa-OR agonist U50488h and beta(1)-AR agonist norepinephrine (NE) were administered. RESULTS: (1) 50488h antagonized the effect of NE in rising left ventricular systolic pressure (LVSP) in the early phase of myocardial ischemia at 10, 20, 30 min of reperfusion. (2) Arrhythmia scores in the I-R+NE+U50488h group were markedly lower than those in the I-R group during the 10 - 20 min reperfusion period. No significant differences in arrhythmia scores were found in either I-R+U50488h or I-R+NE group when compared with I-R group. (3) Compared with the I-R group, U50488h alone or plus NE decreased reperfusion heart rates after myocardial ischemia while NE alone showed no effect. CONCLUSION: It is suggested that the interaction in the signaling pathway between kappa-OR and beta(1)-AR occurred during myocardial I-R of rat heart.