[Value of fractional exhaled nitric oxide combined with impulse oscillometry in the diagnosis of asthma in preschool children]. / å‘¼å‡ºæ°”ä¸€æ°§åŒ–æ°®è”åˆè„‰å†²æŒ¯è¡æ£€æŸ¥åœ¨å­¦é¾„å‰å„¿ç«¥å“®å–˜ä¸­çš„è¯Šæ–­ä»·å€¼ç ”ç©¶.

OBJECTIVES: To evaluate the value of fractional exhaled nitric oxide (FeNO) combined with impulse oscillometry (IOS) in the diagnosis of asthma in preschool children, and to establish the optimal predictive model. METHODS: A retrospective analysis was performed on 156 children with wheezing, aged 3-5 years, who were admitted from September 2019 to December 2020. These children were divided into an asthma group with 52 children and a non-asthma group with 104 children. The two groups were compared in terms of IOS parameters, FeNO, and clinical data. The multivariate logistic regression analysis was used to establish the optimal predictive model. RESULTS: Compared with the non-asthma group, the asthma group had significantly higher total respiratory system impedance at 5 Hz (Z5), resistance of respiratory system at 5 Hz and 20 Hz (R5 and R20, respectively), resonance frequency, reactance area (AX), and FeNO and a significantly lower reactance difference at 5 Hz (P<0.05). The receiver operating characteristic (ROC) curve analysis showed that Z5, R5, R20, and FeNO had a certain value in the diagnosis of asthma (P<0.05). The multivariate logistic regression analysis established the optimal predictive model of R20+AX+FeNO, with an area under the ROC curve of 0.858 (P<0.05), a sensitivity of 78.8%, and a specificity of 76.9%. CONCLUSIONS: FeNO combined with IOS is helpful for the diagnosis of asthma in preschool children, and the model of R20+AX+FeNO has a certain value in the diagnosis of asthma in these children.

Epidemiological characteristics, clinical characteristics, and prognostic factors of children with atopy hospitalised with adenovirus pneumonia.

BACKGROUND: Atopy may be associated with disease severity and a poor prognosis of human adenovirus (HAdV) pneumonia in children. Our aim was to observe the clinical characteristics and pulmonary radiological changes in children with atopy and HAdV pneumonia in China. METHODS: Children hospitalised with HAdV pneumonia from June 2018 to December 2019 were analysed. All children were divided into atopic with HAdV, non-atopic with HAdV, and atopic without HAdV infection group. Each group was further divided into the mild and severe pneumonia groups according to disease severity. Standard treatment was initiated after admission, and regular follow-up evaluations were conducted at 1 month after discharge. Baseline and clinical characteristics and pulmonary radiological changes in children with and without atopy were evaluated. Risk factors associated with small airway lesions in patients with HAdV pneumonia were analysed. RESULTS: The eosinophil count in the atopic group was significantly higher than that in the non-atopic group (P < 0.05). Severe coughing, wheezing, and small airway lesions on chest high-resolution computed tomography (HRCT) upon admission, after discharge and 1 month after discharge were significantly higher in the atopic group (with or without HAdV infection) than in the non-atopic group (P < 0.05). There were significant differences in the number of patients with wheezing and small airway lesions during hospitalisation and after discharge among the three groups (P < 0.05). The risks of small airway lesions in children with a family or personal history of asthma, severe infection, atopy, and HAdV infection were 2.1-, 2.7-, 1.9-, 2.1-, and 1.4-times higher than those in children without these characteristics, respectively. CONCLUSIONS: Children with atopy and HAdV pneumonia may experience severe coughing in mild cases and wheezing in mild and severe cases. Children with atopy are more susceptible to the development of small airway lesions, recurrent wheezing after discharge and slower recovery of small airway lesions as observed on pulmonary imaging than non-atopic children after HAdV infection. A family or personal history of asthma, atopy, severe infection, and HAdV infection are independent risk factors associated with the development of small airway lesion as observed on chest HRCT.

Hyperpolarization-activated cyclic nucleotide-gated (HCN) channels regulate firing of globus pallidus neurons in vivo.

The globus pallidus plays a significant role in motor control under both health and pathological states. Recent studies have revealed that hyperpolarization-activated cyclic nucleotide-gated (HCN) channels occupy a critical position in globus pallidus pacemaking activity. Morphological studies have shown the expression of HCN channels in the globus pallidus. To investigate the in vivo effects of HCN channels in the globus pallidus, extracellular recordings and behavioral tests were performed in the present study. In normal rats, micro-pressure ejection of 0.05mM ZD7288, the selective HCN channel blocker, decreased the frequency of spontaneous firing in 21 out of the 40 pallidal neurons. The average decrease was 50.4±5.4%. Interestingly, in another 18 out of the 40 pallidal neurons, ZD7288 increased the firing rate by 137.1±27.6%. Similar bidirectional modulation on the firing rate was observed by a higher concentration of ZD7288 (0.5mM) as well as another HCN channel blocker, CsCl. Furthermore, activation of HCN channels by 8-Br-cAMP increased the firing rate by 63.0±9.3% in 15 out of the 25 pallidal neurons and decreased the firing rate by 46.9±9.4% in another 8 out of the 25 pallidal neurons. Further experiments revealed that modulation of glutamatergic but not GABAergic transmission may be involved in ZD7288-induced increase in firing rate. Consistent with electrophysiological results, further studies revealed that modulation of HCN channels also had bidirectional effects on behavior. Taken together, the present studies suggest that HCN channels may modulate the activity of pallidal neurons by different pathways in vivo.

Direct modulation of firing activity by dopamine D2 like receptors in the globus pallidus of both normal and parkinsonian rats.

The globus pallidus occupies a critical position in the indirect pathway of the basal ganglia circuit, which regulates movement under both normal and pathological conditions. Previous studies have shown that the globus pallidus receives dopaminergic innervation from the axonal collaterals of nigrostriatal fibers. Both dopamine D1 and D2 like receptors are expressed in the globus pallidus. The present study was aimed to investigate the direct in vivo electrophysiological effects of dopamine D2 like receptors in the globus pallidus of both normal and parkinsonian rats. Extracellular recordings of multi-barreled microelectrode were used in the present study. In normal rats, micro-pressure ejection of dopamine D2 like receptor agonist quinpirole induced different effects on the firing rate of globus pallidus neurons. In 24 out of the 61 pallidal neurons, quinpirole significantly increased the firing rate by (62.7 ± 11.2)%. In another 16 neurons, quinpirole decreased the spontaneous firing rate by (37.5 ± 2.9)%. Furthermore, co-application of dopamine D2 like receptor antagonist, sulpride, blocked quinpirole-induced modulation of the firing rate of pallidal neurons. On the 6-hydroxydopamine (6-OHDA) lesioned side of parkinsonian rats, quinpirole increased the firing rate in 25 out of the 47 pallidal neurons by (64.2 ± 10.1)%, while decreased the firing rate in 11 neurons by (51.9 ± 6.2)%. Our findings suggest that activation of pallidal dopamine D2 like receptors may bidirectionally modulate the spontaneous firing of globus pallidus neurons in both normal and parkinsonian rats.

Phylogenetic and recombination analysis of rice black-streaked dwarf virus segment 9 in China.

Rice black-streaked dwarf virus (RBSDV) is an economically important virus that causes maize rough dwarf disease and rice black-streaked dwarf disease in East Asia. To study RBSDV variation and recombination, we examined the segment 9 (S9) sequences of 49 RBSDV isolates from maize and rice in China. Three S9 recombinants were detected in Baoding, Jinan, and Jining, China. Phylogenetic analysis showed that Chinese RBSDV isolates could be classified into two groups based on their S9 sequences, regardless of host or geographical origin. Further analysis suggested that S9 has undergone negative and purifying selection.

Exendin-4 increases the firing activity of hippocampal CA1 neurons through TRPC4/5 channels.

The central neuropeptide GLP-1 is synthesized by preproglucagon (PPG) neurons in the brain. GLP-1 receptors are widely distributed in central nervous system. Hippocampus is a key component of the limbic system which is involved in learning, memory, and cognition. Previous studies have shown that overexpression of GLP-1 receptors in the hippocampus could improve the process of learning and memory. However, up to now, the direct electrophysiological effects and possible molecular mechanisms of GLP-1 in hippocampal CAl neurons remain unexplored. The present study aims to evaluate the effects and mechanisms of GLP-1 on the spontaneous firing activity of hippocampal CAl neurons. Employing multibarrel single-unit extracellular recordings, the present study showed that micro-pressure administration of GLP-1 receptor agonist, exendin-4, significantly increased the spontaneous firing rate of hippocampal CA1 neurons in rats. Furthermore, application of the specific GLP-1 receptor antagonist, exendin(9-39), alone significantly decreased the firing rate of CA1 neurons, suggesting that endogenous GLP-1 modulates the firing activity of CA1 neurons. Co-application of exendin(9-39) completely blocked exendin-4-induced excitation of hippocampal CA1 neurons. Finally, the present study demonstrated for the first time that the transient receptor potential canonical 4 (TRPC4)/TRPC5 channels may be involved in exendin-4-induced excitation. The present studies may provide a rationale for further investigation of the modulation of GLP-1 on learning and memory as well as its possible involvement in Alzheimer's disease.

Clinical characteristics and genetic profiles of 44 patients with severe combined immunodeficiency (SCID): report from Shanghai, China (2004-2011).

Severe combined immunodeficiency (SCID), a rare type of genetic associated immune disorder, is poorly characterized in mainland China. We retrospectively reviewed 44 patients with SCID who received treatment from 2004 to 2011 in Shanghai, China, and herein summarize their clinical manifestations and immunological and preliminary genetic features. The male-to-female ratio was 10:1. Twenty five patients presented with X-SCID symptoms. Only one patient was diagnosed before the onset of symptoms due to positive family history. The mean time of delay in the diagnosis of X-SCID was 2.69 months (range, 0.5-8.67). Thirty-seven of the 44 patients died by the end of 2011 with the mean age of death being 7.87 months (range, 1.33-31). Six patients received hematopoietic stem cell transplantation (HSCT); only one of them survived, who was transplanted twice. The time between onset and death was shorter in the HSCT-treated group compared with the untreated group (2.87 ± 1.28 and 3.34 ± 0.59 months, respectively), probably due to active infections during transplantation. Bacillus Calmette-Guérin (BCG) complications occurred in 14 of the 34 patients who received BCG vaccination. Transfusion-induced graft-versus-host disease occurred in 5 patients. Total 20 mutations in interleukin-2 receptor subunit gamma (IL2RG) were identified in 22 patients, including 11 novel mutations. Most patients were misdiagnosed before referred to our SCID Center. Therefore, establishing more diagnostic centers dedicated to the care of PID and accessible by primary immunodeficiency patients will facilitate early, correct diagnosis and better care of SCID in China.

[Protective effect of melatonin on myocardial injury in severely- burned rats].

OBJECTIVE: To investigate the protective effect of melatonin (MLT) on myocardial injury in severely-burned rats and its mechanism. METHODS: A total of 30 Sprague-Dawley (SD) rats were randomly assigned to three groups: sham group, burn group and MLT group, each n=10. The dorsal skin of animal was immersed into boiling water for 15 seconds to induce 30% total body surface area (TBSA) full-thickness burn, or immersed into 37 centigrade water for sham operation. Immediately after burn, the animals in burn group and MLT group were given intraperitoneally vehicle (1% alcohol in normal saline) or MLT (10 mg/kg) respectively. Six hours postburn, the blood from tail vessel was collected for serum preparation. After sacrificed, the myocardial tissues of rats were collected for the determination of malondialdehyde (MDA) and reduced glutathione (GSH) as well as glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) activities. Serum levels of creatine kinase (CK) and lactate dehydrogenase (LDH) were also estimated. RESULTS: Compared with the sham control, burn injury increased MDA by 66.7% (1.55±0.17 nmol/mg vs. 0.93±0.05 nmol/mg) and decreased GSH by 27.8% (13.58±0.33 nmol/mg vs. 18.82±0.55 nmol/mg, both P<0.01) in myocardial tissues, GSH-Px activity was also slightly inhibited (74.04±3.42 nmol×min(-1)×mg(-1) vs. 93.79±3.76 nmol×min(-1)×mg(-1), P<0.05), but MPO level was found to increase to 2.8 folds (9.43±1.15 U/g vs. 3.41±0.27 U/g, P<0.01). These changes indicated the occurrence of oxidative stress in myocardial tissues after severe burn. MLT treatment relieved most of the abnormality with significant statistical significances (MDA: 0.89±0.08 nmol/mg vs. 1.55±0.17 nmol/mg, GSH: 17.23±0.54 nmol/mg vs. 13.58±0.33 nmol/mg, MPO: 6.91±0.51 U/g vs. 9.43±1.15 U/g, P<0.05 or P<0.01). In addition, the serum levels of CK and LDH in burn group increased to 37.8 folds and 7.4 folds respectively (both P<0.01). MLT treatment reduced CK by 32.9% and reduced LDH by 21.2% (P<0.05 and P<0.01). CONCLUSION: MLT treatment exerts the protective effect on myocardial injury in severely-burned rats, which is attributed predominantly to its inhibition on burn-induced oxidative stress injury.

Epidemiology of autism spectrum disorders: Global burden of disease 2019 and bibliometric analysis of risk factors.

Background: To explore the geographical pattern and temporal trend of autism spectrum disorders (ASD) epidemiology from 1990 to 2019, and perform a bibliometric analysis of risk factors for ASD. Methods: In this study, ASD epidemiology was estimated with prevalence, incidence, and disability-adjusted life-years (DALYs) of 204 countries and territories by sex, location, and sociodemographic index (SDI). Age-standardized rate (ASR) and estimated annual percentage change (EAPC) were used to quantify ASD temporal trends. Besides, the study performed a bibliometric analysis of ASD risk factors since 1990. Publications published were downloaded from the Web of Science Core Collection database, and were analyzed using CiteSpace. Results: Globally, there were estimated 28.3 million ASD prevalent cases (ASR, 369.4 per 100,000 populations), 603,790 incident cases (ASR, 9.3 per 100,000 populations) and 4.3 million DALYs (ASR, 56.3 per 100,000 populations) in 2019. Increases of autism spectrum disorders were noted in prevalent cases (39.3%), incidence (0.1%), and DALYs (38.7%) from 1990 to 2019. Age-standardized rates and EAPC showed stable trend worldwide over time. A total of 3,991 articles were retrieved from Web of Science, of which 3,590 were obtained for analysis after removing duplicate literatures. "Rehabilitation", "Genetics & Heredity", "Nanoscience & Nanotechnology", "Biochemistry & Molecular biology", "Psychology", "Neurosciences", and "Environmental Sciences" were the hotspots and frontier disciplines of ASD risk factors. Conclusions: Disease burden and risk factors of autism spectrum disorders remain global public health challenge since 1990 according to the GBD epidemiological estimates and bibliometric analysis. The findings help policy makers formulate public health policies concerning prevention targeted for risk factors, early diagnosis and life-long healthcare service of ASD. Increasing knowledge concerning the public awareness of risk factors is also warranted to address global ASD problem.

Repetitive transcranial magnetic stimulation promotes functional recovery and differentiation of human neural stem cells in rats after ischemic stroke.

Stem cells hold great promise as a regenerative therapy for ischemic stroke by improving functional outcomes in animal models. However, there are some limitations regarding the cell transplantation, including low rate of survival and differentiation. Repetitive transcranial magnetic stimulation (rTMS) has been widely used in clinical trials as post-stroke rehabilitation in ischemic stroke and has shown to alleviate functional deficits following stroke. The present study was designed to evaluate the therapeutic effects and mechanisms of combined human neural stem cells (hNSCs) with rTMS in a middle cerebral artery occlusion (MCAO) rat model. The results showed that human embryonic stem cells (hESCs) were successfully differentiated into forebrain hNSCs for transplantation and hNSCs transplantation combined with rTMS could accelerate the functional recovery after ischemic stroke in rats. Furthermore, this combination not only significantly enhanced neurogenesis and the protein levels of brain-derived neurotrophic factor (BDNF), but also rTMS promoted the neural differentiation of hNSCs. Our findings are presented for the first time to evaluate therapeutic benefits of combined hNSCs and rTMS for functional recovery after ischemic stroke, and indicated that the combination of hNSCs with rTMS might be a potential novel therapeutic target for the treatment of stroke.

[Changes of pulmonary surfactant protein A in young rats with acute lung injury induced by lipopolysaccharide].

OBJECTIVE: Pulmonary surfactant protein A (SP-A) plays an important role in the maintenance of pulmonary surfactant function and innative immune defence. This study aimed to explore the changes of SP-A concentration in the lungs of young rats with acute lung injury. METHODS: Sprague-Dawley rats were randomly assigned to control and lung injury groups. Acute lung injury was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the lung injury group. The same amount of normal saline was given for the control group. The two groups were subdivided into 6 groups sacrificed at 6, 12, 24, 36, 48 and 72 hrs of injection (n=8 each). Western blot was employed to detect SP-A concentration in the lung tissues. RESULTS: SP-A concentration in the lung injury group was not different from the the control group within 12 hrs after LPS injection. SP-A concentration in the lung injury group was elevated significantly during 24-48 hrs after LPS injection, peaking at 36 hrs (6.94+/-0.80 vs 5.01+/-0.36; P< 0.01), compared with the controls. However, SP-A concentration in the lung injury group was significantly reduced 72 hrs after LPS injection compared with the controls (P< 0.01). CONCLUSIONS: The changes of lung SP-A concentration in rats following acute lung injury were time-dependent. The transient elevation of SP-A concentration in the lungs indicated a strong compensation ability of SP-A in the host defence against acute lung injury.

[Relationship between alveolar epithelial type II cells and pulmonary surfactant protein A levels in young rats with acute lung injury].

OBJECTIVE: This study examined the relationship between the ultrastructural alterations of alveolar epithelial cells type II (AEC-II) and pulmonary surfactant protein A (SP-A) levels in the lung tissue of young rats with acute lung injury (ALI) in order to explore the possible mechanism of ALI. METHODS: Forty-eight young Sprague-Dawley rats were randomly divided into control and ALI groups. The rats in the ALI group were intraperitoneally injected with 4 mg/kg of lipopolysaccharide (LPS) in order to induce ALI. The control subjects were injected with the same volume of normal saline. Rats were sacrificed at 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of the left lung and fixed with 2.5% glutaraldehyde for transmission electron microscope examination and for Western blot test of SP-A. RESULTS: The microvilli of AEC-II disappeared 24 hrs after LPS injection. After 24 and 48 hrs of LPS injection, lamellar body (Lb) increased in number, enlarged in size and reduced in density, and the ring-like arrangement of Lb was present. By 48 hrs after LPS injection, giant Lb with vacuole-like deformity appeared. The contents of lung SP-A in the ALI group 24 hrs (6.52+/-0.62 vs 5.02+/-0.35; P<0.01) and 48 hrs (6.65+/-0.62 vs 5.01+/-0.36; P<0.01) after LPS injection were significantly higher than those in the control group. By 72 hrs after LPS injection, Lbs ruptured and were reduced in number. The shape of the nuclei was irregular and the border was blurred. The content of lung SP-A was greatly reduced in the ALI group 72 hrs after LPS injection compared with that in the control group (3.87+/-0.50 vs 5.22+/-0.36; P<0.01). CONCLUSIONS: The alterations of AEC-II and lung SP-A were time-dependent in young rats with ALI induced by LPS. In the early stage of ALI, the lung SP-A content showed a compensatory increase. With the increasing injury of AEC-II cells, the secretion of SP-A presented with a decompensation and the lung SP-A content decreased. This may be one possible mechanism for the development of ARD.

[Protective effect of melatonin against renal dysfunction following severe burn in rats].

OBJECTIVE: To explore the protective effect of melatonin (MLT) against renal dysfunction in the early stage of burn in rats. METHODS: Seventy SD rats were randomly assigned to three groups: sham control (n=10), burn control (n=30) and MLT group (n=30). The 30% total body surface area (TBSA) full-thickness burn was induced by immersing the dorsal skin into boiling water for 30 seconds, while MLT (10 mg/kg, i.p.) was given immediately postburn, and the same dose was repeated once after 12 hours. The contents of malondialdehyde (MDA) and reduced glutathione (GSH) in renal tissue, as well as plasma creatinine (BCr) and urea nitrogen (BUN) levels were measured at 6, 24 and 72 hours postburn, while the activities of glutathione peroxidase (GSH-Px) and myeloperoxidase (MPO) of renal tissue were measured only at 6 hours postburn. RESULTS: MDA content was significantly increased and GSH content was decreased in renal tissue after a 30 % TBSA full-thickness burn at all time points. Plasma BCr and BUN levels were elevated within 24 hours postburn. All these changes peaked at 6 hours postburn (all P<0.01). Single injection of MLT decreased MDA by 27.8% (P<0.01) but increased GSH by 44.4% (P<0.05). It also inhibited the rise in plasma BCr and BUN levels (P<0.05 and P<0.01). However, repeated MLT injection did not show additional effect on these parameters as single injection of MLT. In addition, single dose of MLT also lowered the MPO level by 30.2% (P<0.05), but did not improve the GSH-Px activity at 6 hours postburn. CONCLUSION: Severe burn may result in obvious oxidative stress (within 72 hours postburn) in the kidney with acute renal dysfunction (within 24 hours postburn). Single injection of MLT partially counteracted these changes, due to its high free radical scavenging capacity as well as its inhibitory effect on neutrophil-mediated tissue injury.

[Changes of inflammation-associated factors in children with Mycoplasma pneomoniaepneumonia and concomitant systemic inflammatory response syndrome].

OBJECTIVE: To study the relationship between the changes of inflammation-associated factors, C-reactive protein (CRP), procalcitonin (PCT), erythrocyte sedimentation rate (ESR), white blood cell (WBC) and neutrophils, and the severity in children with Mycoplasma pneomoniae pneumonia (MPP). METHODS: Ninety-two children with acute MPP consisting of 52 cases with concomitant systemic inflammation response syndrome (SIRS) and 40 cases without SIRS were enrolled in this study. The 52 cases with concomitant SIRS were classified into two groups based on the severity of SIRS: mild SIRS (n=25) and severe SIRS (n=27). CRP, PCT, ESR and WBC count and the percentage of neutrophils (NE%) were detected on admission and one week after anti-inflammation treatment. RESULTS: All of patients showed increased serum CRP contents at admission. The serum CRP contents were the highest in the severe SIRS group, followed by the mild SIRS and non-SIRS groups on admission (P < 0.05 or 0.01). The serum CRP contents were reduced in all of patients after 1-week treatment. The severe SIRS group still demonstrated higher serum CRP contents than the non-SIRS and the mild SIRS groups (P < 0.01). The severe SIRS group had increased serum PCT contents on admission, which were significantly higher than those of the mild SIRS and non-SIRS groups (P < 0.01). After 1-week treatment, the serum PCT contents were reduced in the severe SIRS group but remained higher than in the mild SIRS and non-SIRS groups (P < 0.01). ESR increased significantly in the severe SIRS group than in the mild SIRS and non-SIRS groups on admission (P < 0.01). One-week treatment did not significantly decrease ESR in all three groups. The WBC count and NE% in the mild and severe SIRS groups were significantly higher than in the non-SIRS group and the severe SIRS group had higher WBC count and NE% than the mild SIRS group on admission (P < 0.05). The WBC count and NE% decreased after 1-week treatment in the mild and severe SIRS groups (P < 0.05). One inflammation-associated factor (only CRP) increase was predominant in the non-SIRS group (65%), 2 factors increase in the mild SIRS group (56%), and three or more factors increase in the severe SIRS group (70.4%). CONCLUSIONS: The detection of inflammation-associated factors, CRP, PCT, ESR, WBC and neutrophils, are valuable to the evaluation of severity in MPP.

Effect of dexamethasone on the content of pulmonary surfactant protein D in young rats with acute lung injury induced by lipopolysaccharide.

OBJECTIVE: Pulmonary surfactant protein-D (SP-D) is regarded as a valuable biomarker in acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). This study was to explore the changes of SP-D content in lung tissue following ALI and the effect of dexamethasone (Dex) on the SP-D content in young rats. METHODS: One hundred and forty-four 21-day-old Sprague-Dawley rats were randomly assigned into control, ALI and Dex-treated groups. ALI was induced by intraperitoneal injection of lipopolysaccharide (LPS) (4 mg/kg) in the rats from the ALI and Dex-treated groups. Normal saline was given for the control group. Dex (5 mg/kg) was administered 1 hr after LPS injection in the Dex-treated group. At each time interval of 6, 12, 24, 36, 48 and 72 hrs after LPS injection, eight rats of each group were randomly chosen and sacrificed. Western blot was employed to detect the content of SP-D in lung tissues. RESULTS: The pulmonary SP-D content decreased significantly at 36, 48 and 72 hrs after LPS administration in the ALI group, and reduced to a nadir (0.92 +/-0.11 vs 3.27 +/- 0.52) at 48 hrs compared with that of the control group (P < 0.01). The SP-D content in the Dex-treated group increased significantly at 36,48 and 72 hrs after LPS administration when compared with the ALI group (P < 0.01). A significant difference in the SP-D content between the Dex-treated and the control group was noted only at 72 hrs after LPS administration (P < 0.05). CONCLUSIONS: The SP-D content in lung tissue was reduced following ALI in young rats at the early stage. Early administration of Dex can significantly increase the pulmonary SP-D content.

Effects of dexamethasone on the ultrastructure of alveolar type II cells in young rats with lipopolysaccharide-induced acute lung injury.

OBJECTIVE: Alveolar type II (AT II) cells play a crucial role in the maintenance of pulmonary surfactant homeostasis and pulmonary immunity. The effects of dexamethasone (Dex) on the ultrastructure of AT II cells after acute lung injury remain unknown. This study focused on the ultrastructural changes caused by acute lung injury and on the effects of Dex administration on these ultrastructural changes in young rats. METHODS: Seventy-two 21-day-old Sprague-Dawley rats were randomly divided into control, acute lung injury and Dex-treated groups. Rats in the lung injury group were intraperitoneally injected with 4 mg/kg lipopolysaccharide (LPS) in order to induce acute lung injury, while the control rats were injected with the same amount of normal saline (NS). The Dex-treated group was injected first with LPS followed 1 hr later by Dex (5 mg/kg) injection. Eight rats in each group were sacrificed 24, 48 and 72 hrs after LPS or NS injection. Lung samples were obtained from the lower parts of left lungs and fixed with 2.5% glutaraldehyde for transmission electron microscope examination. RESULTS: Microvilli of AT II cells disappeared and the number of lamellar bodies (LBs) increased in the lung injury group 24 hrs after LPS injection. The ring-like arrangement of LBs around nuclei was present until 48 hrs after LPS injection. By 48 hrs after LPS injection, giant LBs with vacuole-like abnormalities appeared. The shape of nuclei became irregular and the border of the nuclei became blurred. By 72 hrs after LPS injection, the number of LBs was obviously reduced; nucleoli disappeared; and karyolysis occurred in some of the nuclei. In contrast, in the Dex-treated group, LBs crowded on one side of AT II cells and exocytosis appeared on the same side by 24 hrs after LPS injection. By 48 hrs, the number of LBs was reduced. The number of mitochondria increased, and some of them became swollen and enlarged. However, by 72 hrs, the number of LBs increased and the ring-like arrangement of LBs around the nucleus again appeared. CONCLUSIONS: Ultrastructural changes of AT II cells following lung injury induced by LPS were time-dependent in young rats. Dex may ameliorate AT II cell injury and promote functional restoration of AT II cells in LPS-induced acute lung injury.

Adenosine A2A Receptor Modulates the Activity of Globus Pallidus Neurons in Rats.

The globus pallidus is a central nucleus in the basal ganglia motor control circuit. Morphological studies have revealed the expression of adenosine A2A receptors in the globus pallidus. To determine the modulation of adenosine A2A receptors on the activity of pallidal neurons in both normal and parkinsonian rats, in vivo electrophysiological and behavioral tests were performed in the present study. The extracellular single unit recordings showed that micro-pressure administration of adenosine A2A receptor agonist, CGS21680, regulated the pallidal firing activity. GABAergic neurotransmission was involved in CGS21680-induced modulation of pallidal neurons via a PKA pathway. Furthermore, application of two adenosine A2A receptor antagonists, KW6002 or SCH442416, mainly increased the spontaneous firing of pallidal neurons, suggesting that endogenous adenosine system modulates the activity of pallidal neurons through adenosine A2A receptors. Finally, elevated body swing test (EBST) showed that intrapallidal microinjection of adenosine A2A receptor agonist/antagonist induced ipsilateral/contralateral-biased swing, respectively. In addition, the electrophysiological and behavioral findings also revealed that activation of dopamine D2 receptors by quinpirole strengthened KW6002/SCH442416-induced excitation of pallidal activity. Co-application of quinpirole with KW6002 or SCH442416 alleviated biased swing in hemi-parkinsonian rats. Based on the present findings, we concluded that pallidal adenosine A2A receptors may be potentially useful in the treatment of Parkinson's disease.

Effects of methylprednisolone or immunoglobulin when added to standard treatment with intravenous azithromycin for refractory Mycoplasma pneumoniae pneumonia in children.

BACKGROUND: The prevalence of Mycoplasma pneumoniae pneumonia has increased considerably in recent years. To evaluate the efficacy of combined treatment of azithromycin with intravenous immunoglo-bulin (IVIG) or methylprednisolone in children with refractory Mycoplasma pneumoniae pneumonia (RMPP). METHODS: Children with RMPP were randomly allocated to group A [intravenous azithromycin (IA)+ methylprednisolone], group B (IA+IVIG) or group C (IA alone). Following a 7-day treatment, group C patients were randomly separated into two sub-groups: group C1 (IA+methylprednisolone) and group C2 (IA+IVIG). Temperature, respiratory symptoms and signs were examined. The average febrile period after treatment (F2), average total febrile period (F3), infiltration absorption, atelectasis resolution, pleural effusion disappearance were determined. The levels of C-reactive protein (CRP), D-dimer, and lactate dehydrogenase (LDH) were measured. RESULTS: Seven days after enrollment, the average F2 after treatment of group A was the shortest. Compared with the control group C, the combined treatment group A and B showed higher rates of infiltration absorption, atelectasis resolution and pleural effusion disappearance, while lower levels of serum CRP, D-dimer and LDH. Fourteen days after enrollment, all children with combined therapy clinically improved, and presented better laboratory results. Group C1 showed shorter F3 and lower levels of CRP and LDH than those of group C2. Overall, group A showed the shortest F3, also has the lowest CRP and LDH. CONCLUSIONS: Azithromycin with IVIG or methylprednisolone was better treatment for children with RMPP than azithromycin alone. IVIG treatment may be beneficial, especially when the efficacy of corticosteroids is insecure, thus could be considered as an alternative of primary therapeutic approaches.

Electroacupuncture Ameliorates Learning and Memory and Improves Synaptic Plasticity via Activation of the PKA/CREB Signaling Pathway in Cerebral Hypoperfusion.

Electroacupuncture (EA) has shown protective effects on cognitive decline. However, the underlying molecular mechanisms are ill-understood. The present study was undertaken to determine whether the cognitive function was ameliorated in cerebral hypoperfusion rats following EA and to investigate the role of PKA/CREB pathway. We used a rat 2-vessel occlusion (2VO) model and delivered EA at Baihui (GV20) and Dazhui (GV14) acupoints. Morris water maze (MWM) task, electrophysiological recording, Golgi silver stain, Nissl stain, Western blot, and real-time PCR were employed. EA significantly (1) ameliorated the spatial learning and memory deficits, (2) alleviated long-term potentiation (LTP) impairment and the reduction of dendritic spine density, (3) suppressed the decline of phospho-CREB (pCREB) protein, brain-derived neurotrophic factor (BDNF) protein, and microRNA132 (miR132), and (4) reduced the increase of p250GAP protein of 2VO rats. These changes were partially blocked by a selective protein kinase A (PKA) inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H89), suggesting that the PKA/CREB pathway is potentially involved in the effects of EA. Moreover, any significant damage to the pyramidal cell layer of CA1 subregion was absent. These results demonstrated that EA could ameliorate learning and memory deficits and alleviate hippocampal synaptic plasticity impairment of cerebral hypoperfusion rats, potentially mediated by PKA/CREB signaling pathway.