Whole-genome shotgun sequencing unravels the influence of environmental microbial co-infections on the treatment efficacy for severe pediatric infectious diseases.

Background: The microbiome plays a pivotal role in mediating immune deviation during the development of early-life viral infections. Recurrent infections in children are considered a risk factor for disease development. This study delves into the metagenomics of the microbiome in children suffering from severe infections, seeking to identify potential sources of these infections. Aims: The aim of this study was to identify the specific microorganisms and factors that significantly influence the treatment duration in patients suffering from severe infections. We sought to understand how these microbial communities and other variables may affect the treatment duration and the use of antibiotics of these patients with severe infections. Method: Whole-genome shotgun sequencing was conducted on samples collected from children aged 0-14 years with severe infections, admitted to the Pediatrics Department of Xiamen First Hospital. The Kraken2 algorithm was used for taxonomic identification from sequence reads, and linear mixed models were employed to identify significant microorganisms influencing treatment duration. Colwellia, Cryptococcus, and Citrobacter were found to significantly correlate with the duration of clinical treatment. Further analysis using propensity score matching (PSM) and rank-sum test identified clinical indicators significantly associated with the presence of these microorganisms. Results: Using a linear mixed model after removed the outliers, we identified that the abundance of Colwellia, Cryptococcus, and Citrobacter significantly influences the treatment duration. The presence of these microorganisms is associated with a longer treatment duration for patients. Furthermore, these microorganisms were found to impact various clinical measures. Notably, an increase in hospitalization durations and medication costs was observed in patients with these microorganisms. In patients with Colwellia, Cryptococcus, and Citrobacter, we discover significant differences in platelets levels. We also find that in patients with Cryptococcus, white blood cells, hemoglobin, and neutrophils levels are lower. Conclusion: These findings suggest that Colwellia, Cryptococcus, and Citrobacter, particularly Cryptococcus, could potentially contribute to the severity of infections observed in this cohort, possibly as co-infections. These microorganisms warrant further investigation into their pathogenic roles and mechanisms of action, as their presence in combination with disease-causing organisms may have a synergistic effect on disease severity. Understanding the interplay between these microorganisms and pathogenic agents could provide valuable insights into the complex nature of severe pediatric infections and guide the development of targeted therapeutic strategies.

Adenovirus and Mycoplasma pneumoniae co-infection as a risk factor for severe community-acquired pneumonia in children.

Background: To investigate the pathogenic characteristics and risk factors of pediatric severe community-acquired pneumonia (CAP). Methods: We retrospectively analyzed the clinical data of hospitalized children with severe CAP from April 2014 to June 2019 in China. Data of age, sex and pathogenic results were collected: bacterial and fungal cultures, respiratory viruses from sputum or bronchoalveolar lavage fluid (BALF), serum Mycoplasma pneumoniae (MP)-IgM and Chlamydia Pneumoniae-IgM, and BALF or blood (1-3)-ß-D-glucan/galactomannan test. Results: A total of 679 children with severe CAP were included in the analysis. The number of cases infected with MP was higher in males than in females. There were significant differences between the ≤1-year and >1-year groups in terms of pathogen. The top three bacteria cultured were Haemophilus influenzae (57/679, 8.4%), Streptococcus pneumoniae (50/679, 7.4%), and Pseudomonas aeruginosa (25/679, 3.7%). The top three viruses detected were adenovirus (AdV, 124/679, 18.3%), respiratory syncytial virus (24/679, 3.5%), and parainfluenza virus (21/679, 3.1%). AdV and MP were the leading pathogens, detected in 18.3% and 32.6% cases, respectively. MP infection increased the risk of AdV infection (OR 3.77, p < 0.0001). MP infection was a risk factor for severe AdV-infected pneumonia, while sex, age, bacteria, Chlamydia Pneumoniae, fungal, and AdV infections were risk factors for severe MP-infected pneumonia. Conclusions: AdV and MP were dominant pathogens in children with severe CAP. AdV and MP infection predisposed each other to develop severe illness. AdV-MP co-infection may lead to severe pneumonia.

Unveiling the potent effect of vitamin D: harnessing Nrf2/HO-1 signaling pathways as molecular targets to alleviate urban particulate matter-induced asthma inflammation.

BACKGROUND: Asthma is the most common allergic disease characterized by an inflammatory response in the airways. Mechanismly, urban particulate matter (PM) is the most widely air pollutant associated with increased asthma morbidity and airway inflammation. Current research found that vitamin D is an essential vitamin with anti-inflammatory, antioxidant and other medical efficacy. Inadequate or deficient vitamin D often leads to the pathogenesis and stability of asthma. NGF exacerbates airway inflammation in asthma by promoting smooth muscle cell proliferation and inducing the Th2 immune response. Activation of the Nrf2/HO-1 signaling pathway can exert a protective effect on the inflammatory response in bronchial asthma. However, the specific mechanism of this pathway in PM-involved asthmatic airway smooth muscle cells remains unclear. METHODS: Mice were sensitized and challenged with Ovalbumin (OVA) to establish an asthma model. They were then exposed to either PM, vitamin D or a combination of both, and inflammatory responses were observed. Including, acetylcholine stimulation at different concentrations measured airway hyperresponsiveness in mice. Bronchoalveolar lavage fluid (BALF) and serum were collected for TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF) analysis. Additionally, lung tissues underwent histopathological examination to observe alveolar structure and inflammatory cell infiltration. Specific ELISA kits were utilized to determine the levels of the inflammatory factors TNF-α, IL-1ß, IL-6, and Nerve growth factor (NGF). Nrf2/HO-1 signaling pathways were examined by western blot analysis. Meanwhile, we constructed a cell system with low HO-1 expression by lentiviral transfection of airway smooth muscle cells. The changes of Nrf2, HO-1, and NGF were observed after the treatment of OVA, PM, and Vit D were given. RESULTS: The in vivo results showed that vitamin D significantly alleviated pathological changes in lung tissue of PM-exposed mice models. Mechanismly, vitamin D decreased substantial inflammatory cell infiltration in lung tissue, as well as the number of inflammatory cells in BALF. Furthermore, vitamin D reduced the heightened inflammatory factors including of TNF-α, IL-1ß, IL-6, and NGF caused by PM exposure, and triggered the activity of nucleus Nrf2 and HO-1 in PM-exposed asthmatic mice. Notably, knockdown HO-1 weakens the Vitamin D- mediated inhibition to pollution toxicity in asthma. Importantly, in vitro experiments on OVA-stimulated mice airway smooth muscle cells, the results showed that OVA and PM, respectively, reduced Nrf2/HO-1 and increased NGF's expression, while vitamin D reversed the process. And in the HO-1 knockdown cell line of Lenti-si-HO-1 ASMCs, OVA and PM reduced Nrf2's expression, while HO-1 and NGF's expression were unchanged. CONCLUSIONS: The above results demastrate that vitamin D downregulated the inflammatory response and the expression of NGF by regulating the Nrf2/HO-1 signaling pathways in airway smooth muscle cells, thereby showing potent anti-inflammatory activity in asthma.

Etiology and clinical features of children with bronchiectasis in China: A 10-year multicenter retrospective study.

INTRODUCTION: The current study aims to investigate the etiology spectrum and the clinical characteristics of bronchiectasis in Chinese children. METHODS: The study is designed as a multicenter retrospective study. 193 cases were enrolled in 13 centers in China between 2008 and 2017. The inclusive cases must meet the clinical as well as the HRCT criteria. Only if both two radiologists confirmed the diagnosis, the case could be enrolled. The cases that could not provide clinical and imageology data were excluded. The data were entered into the specialized system and then analyzed. RESULTS: One hundred sixty-nine cases (87%) were found to have the underlying etiology. Post-infective (46%), primary immunodeficiency (14%), and PCD (13%) were the common causes. All cases came from 28 provinces in Mainland China. The median age of symptom onset was 5.8 (2.0, 8.9) years. The median age of diagnosis was 8.4 (4.5, 11.6) years. The main symptoms were cough, sputum expectoration, and fever during the exacerbation. Nineteen percent of patients suffered from limited exercise tolerance. Clubbing was found in 17% of cases. Nearly 30% of patients presented growth limitations. On the HRCT findings, 126 cases had diffused bronchiectasis, and bilateral involvement was found in 94 cases. The lower lobes and right middle lobes were most commonly involved. Approximately 30% of cultures of sputum and bronchoalveolar lavage were positive. CONCLUSION: A majority of cases could be found the underlying etiology. Post-infective, primary immunodeficiency, and PCD were the most common causes. Some clinical figures might indicate a specific etiology.

Fluvoxamine alleviates bleomycin-induced lung fibrosis via regulating the cGAS-STING pathway.

Idiopathic pulmonary fibrosis (IPF) is a fatal disease with high mortality and limited effective therapy. Herein, we reported that fluvoxamine, a selective serotonin reuptake inhibitor (SSRI), used in depression and anxiety treatment, also exhibited therapeutic activities in IPF. Fluvoxamine inhibited cyclic GMP-AMP synthase (cGAS) and stimulator of interferon genes (STING), restrained the activation of their downstream targets, including PERK/ eIF2α/ c-Myc/ miR-9-5p/ TBPL1 and TBK1/ YAP/ JNK1/2/ Bnip3/ CaMKII/ cofilin signaling, thus attenuated the activation and migration of fibroblasts upon TGF-ß1 challenge. Fluvoxamine dose-dependently improved pulmonary function, decreased the expression of inflammatory factors, reduced excessive production of extracellular matrix, and thus alleviated bleomycin (BLM)-induced lung fibrosis in mice. Moreover, fluvoxamine at a dose of 10 mg/ kg showed similar efficacy as pirfenidone (PFD) at a dose of 30 mg/kg in a mice model of lung fibrosis. In summary, our results suggest that fluvoxamine is an effective anti-fibrotic agent for IPF.

The role and mechanism of 1,25-dihydroxyvitamin D3 in regulating the Rho-kinase signaling pathway in asthmatic rats.

BACKGROUND: Bronchial asthma (referred to as asthma in the present study) is the most common chronic airway inflammatory disease in childhood. The present study aimed to investigate the effect of 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] on VDR expression, which is closely associated with asthmatic airway smooth muscle cells (ASMCs), and explored its role and mechanism in the Rho-kinase signaling pathway. METHODS: The acute asthma model was induced by ovalbumin (OVA) and pertussis bacillus, and ASMCs obtained from asthmatic rats were cultured in vitro. These cells were randomly divided into five groups: control (N) group, TNF-α (TNF) group, 1,25-(OH)2D3 (VD) group, dexamethasone (DXM) group, and 1,25-(OH)2D3 + DXM (L) group. The protein expression levels of VDR, ROCK, MLC20 and P-MLC20 were detected by western blot, and the mRNA expression levels of VDR, ROCK, MLC20 and P-MLC20 were detected by real-time quantitative PCR. RESULTS: The expression of ROCK, MLC20 and P-MLC20 in each treatment group were significantly lower, when compared to the TNF group (P<0.05), but this remained stronger than (P<0.05) or similar to (P>0.05) that in the N group. CONCLUSIONS: The regulation mechanism of 1,25-(OH)2D3 in alleviating asthma should be correlated to its regulation of the expression of related signaling molecules in the Rho-kinase signaling pathway, and this effect may be achieved by regulating the mRNA and protein expression of the VDR gene.

Genetic Blockade of NAAA Cell-specifically Regulates Fatty Acid Ethanolamides (FAEs) Metabolism and Inflammatory Responses.

N-Acylethanolamine acid amidase (NAAA) is a lysosomal enzyme responsible for the hydrolysis of fatty acid ethanolamides (FAEs). However, the role of NAAA in FAEs metabolism and regulation of pain and inflammation remains mostly unknown. Here, we generated NAAA-deficient (NAAA-/-) mice using CRISPR-Cas9 technique, and found that deletion of NAAA increased PEA and AEA levels in bone marrow (BM) and macrophages, and elevated AEA levels in lungs. Unexpectedly, genetic blockade of NAAA caused moderately effective anti-inflammatory effects in lipopolysaccharides (LPS)-induced acute lung injury (ALI), and poor analgesic effects in carrageenan-induced hyperalgesia and sciatic nerve injury (SNI)-induced mechanical allodynia. These data contrasted with acute (single dose) or chronic NAAA inhibition by F96, which produced marked anti-inflammation and analgesia in these models. BM chimera experiments indicated that these phenotypes were associated with the absence of NAAA in non-BM cells, whereas deletion of NAAA in BM or BM-derived cells in rodent models resulted in potent analgesic and anti-inflammatory phenotypes. When combined, current study suggested that genetic blockade of NAAA regulated FAEs metabolism and inflammatory responses in a cell-specifical manner.

Heme oxygenase-1 alleviates eosinophilic inflammation by inhibiting STAT3-SOCS3 signaling.

Airway inflammation of eosinophilic asthma (EA) attributes to Th2 response, leaving the role of Th17 response unknown. Signal transducer and activator of transcription 3 (STAT3) induce both suppressors of cytokine signaling 3 (SOCS3) and retinoic acid receptor-related orphan nuclear receptor γ (RORγt) to initiate Th17 cell differentiation which is inhibited by SOCS3, a negative feedback regulator of STAT3. Heme oxygenase-1 (HO-1) is a stress-responsive, cytoprotective, and immunoregulatory molecular. Two other isoforms of the enzyme includes HO-2 and HO-3. Because HO-2 does not exhibit stress-related upregulation and distributes mainly in nervous system and HO-3 shows a low enzymatic activity, we tested a hypothesized anti-inflammatory role for HO-1 in EA by inhibiting STAT3-SOCS3 signaling. Animal model was established with Ovalbumin in wild type Balb/C mice. Hemin or SNPP was intraperitoneally (IP) injected ahead of the animal model to induce or inhibit HO-1 expression. Airway inflammation was evaluated by bronchoalveolar lavage, hematoxyline and eosin staining, enzyme-linked immunosorbent assay, and Western blot analysis. In vivo results showed that HO-1 induction inhibited phosphorylation of STAT3 and expression of SOCS3 and RORγt, decreased Th2 and Th17 immune responses, and alleviated airway inflammation. In vitro results revealed that HO-1 inhibited phosphorylation of STAT3 and expression of SOCS3 in naive CD4+ T cells. These findings identify HO-1 induction as a potential therapeutic strategy for EA treatment by reducing STAT3 phosphorylation, STAT3-SOCS3-mediated Th2/Th17 immune responses, and ultimate allergic airway inflammation.

Fulminant Type 1 Diabetes Mellitus Caused by Drug Reaction With Eosinophilia and Systemic Symptoms (DRESS): A Case Report and Review of the Literature.

Drug reaction with eosinophilia and systemic symptoms (DRESS), also known as drug-induced hypersensitivity syndrome (DIHS) is a rare, severe cutaneous adverse drug reaction characterized by fever, skin rashes, lymphadenopathy, leukocytosis with eosinophilia, and/or atypical lymphocytosis, and multiple visceral organ involvement. Moreover, patients with DRESS are at risk of developing autoimmune diseases including thyroiditis, diabetes mellitus (DM), and systemic lupus erythematosus (SLE), etc. several weeks or months after the initial resolution. We described a 9-month boy who was admitted to our hospital because of severe pneumonia and developed DRESS 3 weeks later. After the withdrawal of suspicious drug and administration of systemic corticosteroids, the patient's condition improved gradually. Nevertheless, hyperglycemia was detected 20 days after the initial onset of DRESS, and subsequent fulminant type 1 diabetes mellitus (F1DM) was diagnosed requiring continuous intravenous insulin infusion. After 13 months of follow-up, the blood glucose levels are now well-controlled. Literature research in PubMed for diabetes mellitus associated with DRESS showed 16 articles and 27 related case reports. Of 27 patients with DM related to DRESS, 11 were male, 16 were female. The mean age was 46 years. The duration from the onset of DRESS to the development of DM was 21 days on average. F1DM was diagnosed in 21 patients, T1DM was confirmed in 5 patients, and T2DM was only defined in 1 patient. Glutamic acid decarboxylase antibodies (GAD) were detected in 4 cases. Of 22 cases in which virus examination was carried out, evidence of virus reactivation was established in 16 cases (72.7%). Of patients with F1DM, 16 (88.9%) cases were evidenced by reactivation of herpes virus. A high frequency of HLA genotype and haplotype were found in 11 cases. DM was concomitant with acute pancreatitis in 3 patients and thyroiditis in 2 patients. No patients died from the disease. This work aims to raise awareness of long-term autoimmune sequelae in patients with DRESS.

Divergent synthesis of dual 1,4-dihydropyridines with different substituted patterns from enaminones and aldehydes through domino reactions.

A concise and efficient protocol for the regioselective synthesis of dual 1,4-dihydropyridines with several substituted patterns has been developed from a cascade cyclization of enaminones and aldehydes in different media (EtOH/CH3CN). The one-pot cascade reaction involves at least five reactive sites and generates multiple C-C and C-N bonds. The established protocol explores the chemistry of enaminones by employing their three reactive sites. The method has several advantages including mild conditions, operational simplicity, and high bond-forming efficiency. It may offer promise in a variety of biochemical applications.

[Clinical features and treatment of refractory Mycoplasma pneumoniae pneumonia unresponded to conventional dose methylprednisolone in children].

OBJECTIVE: To analyze the clinical manifestations of refractory Mycoplasma pneumoniae pneumonia (RMPP) which unresponded to methylprednisolone in the dosage of 2 mg/(kg·d) for 3 days. METHOD: Retrospective analysis was performed on the clinical data of 110 children (64 boys and 46 girls) with RMPP. The patients were divided into "effective group" and "ineffective group" according to initial effect of 2 mg/(kg·d) methylprednisolone. The clinical manifestations, laboratory examination, radiological features and bronchofibroscopic findings of the children were compared. In order to seek the reference indexes which indicate nonresponsive to 2 mg/(kg·d) methylprednisolone, an ROC curve was made, of which the diagnostic cut-off was five independent correlation factors while grouping was made according to patients' different response to glucocorticosteroid. RESULT: The effective group had 86 (86/110, 78.2%) children while ineffective group had 24 (24/110, 21.8%). The ineffective group children had the following performance: 16 children (16/24, 66.7%) in ineffective group had ultrahyperpyrexia (T ≥ 40 °C), which was significantly more severe compared to those in effective group (32/86, 37.3%, P < 0.01); the levels of white blood cell (WBC) count, percentage of neutrophils count (N), C-reactive protein (CRP), serum ferritin (SF), alanine transaminase (ALT), lactic dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB) and fibrinogen (Fib) in ineffective group were significantly higher than those in effective group(P < 0.01); while percentage of lymphocyte count (L) was lower than that in effective group(P < 0.01). Proportion of mixed infection in ineffective group was higher than that in effective group (33.3% vs. 4.7%). Radiological manifestations: It was more frequently seen in ineffective group that chest CT scan indicated high density consolidation in no less than a whole pulmonary lobe and pulmonary necrosis (41.7% vs. 0%). Abundant secretions blockage (45.0% vs. 16.9%) and mucosal necrosis (37.5% vs. 8.1%) on bronchofibroscopy were more frequently seen in ineffective group. The critical values of the five independent correlation factors were CRP 110 mg/L, SF 328 mg/L, LDH 478 IU/L, N 0.78, L 0.13. CONCLUSION: Treatment with 2 mg/(kg·d) methylprednisolone can improve clinical symptoms and radiological manifestations of most children with RMPP quickly, but it may be ineffective in some situations such as lasting high fever or ultrahyperpyrexia for more than 7 days, CRP ≥ 110 mg/L, N ≥ 0.78, L ≤ 0.13, serum LDH ≥ 478 IU/L, SF ≥ 328 µg/L, chest CT scan indicating high density consolidation in more than a whole pulmonary lobe involved and moderate-abundant pleural effusion.

Nerve growth factor exacerbates allergic lung inflammation and airway remodeling in a rat model of chronic asthma.

Nerve growth factor (NGF) is critical in the pathogenesis of allergic airway inflammation in vivo and induces proliferation of airway smooth muscle cells and matrix metalloproteinase-9 (MMP-9) expression in vitro. However, the effects of NGF on chronic pulmonary diseases of allergic origin remain unknown. To investigate the effects of NGF on lung inflammation and airway remodeling, 32 Wistar rats were randomly divided into four groups: control, NGF, ovalbumin (OVA) and anti-rat-ß-NGF antibody (anti-NGF). Aerosolized OVA was administered to the rats in the NGF, OVA and anti-NGF groups to generate the asthmatic rat model, and NGF or anti-NGF was administered 3 h prior to OVA inhalation every two days. On day 70, bronchial responsiveness tests, bronchoalveolar lavage (BAL) and cell counting were conducted. The levels of serum OVA-specific immunoglobulin E (IgE) and of T-helper cell type-2 (Th2) cytokines [interleukin (IL)-4 and IL-13] in the BAL fluid were measured by enzyme-linked immunosorbent assay. The expression levels of NGF protein and MMP-9 mRNA, and the activity of MMP-9 in the lungs were detected by western blot analysis, quantitative polymerase chain reaction and gelatin zymography analysis, respectively. Our results showed that NGF significantly increased eosinophilic airway inflammation, persistent airway hyperresponsiveness (AHR), the serum levels of OVA-specific IgE and the levels of Th2 cytokines in the BAL fluid, and also increased the expression levels and activity of MMP-9. However, anti-NGF treatment significantly inhibited eosinophilic airway inflammation, persistent AHR and airway remodeling. The results showed that NGF may have exacerbated the development of airway inflammation, AHR and airway remodeling through a Th2 pathway and by increasing the level of MMP-9 expression. Therefore, anti-NGF is potentially beneficial for preventing and treating patients with asthma.

The effect of substance P on asthmatic rat airway smooth muscle cell proliferation, migration, and cytoplasmic calcium concentration in vitro.

Airway remodeling and airway hyper-responsiveness are prominent features of asthma. Neurogenic inflammation participates in the development of asthma. Neurokinin substance P acts by binding to neurokinin-1 receptor (NK-1R). Airway smooth muscle cells (ASMC) are important effector cells in asthma. Increases in ASMC proliferation, migration, and cytoplasmic Ca2+ concentration are critical to airway remodeling and hyper-responsiveness. The effects of substance P on ASMC were investigated in Wistar rats challenged with a previously described asthmatic rat model. To exclude possible influences from other factors, the role of substance P was also investigated in primary cultured rat ASMC. Substance P and WIN62577-induced changes in cytoplasmic Ca2+ concentration were observed by fluorescence microscopy, and expression of Ca2+ homeostasis-regulating genes was assessed with real-time PCR. We found that cytoplasmic Ca2+ concentration increased in normal rat ASMC treated with substance P, but decreased in asthmatic rat ASMC treated with WIN62577, an antagonist of NK-1R. Real-time PCR analysis revealed increased Serca2 mRNA expression but decreased Ip3r mRNA expression after WIN62577 treatment in asthmatic rat ASMC. Flow cytometric analysis (FCM) revealed that most asthmatic rat ASMC stayed at G1 phase after combined treatment with WIN62577 and IL-13 in vitro. Transwell analysis suggested that ASMC migration was reduced after WIN62577 treatment. Therefore, we conclude that NK-1R is related to asthma mechanisms and a NK-1R antagonist downregulates calcium concentration in asthmatic ASMC by increasing Serca2 mRNA and decreasing Ip3r mRNA expression. The NK-1R antagonist WIN62577 inhibited ASMC IL-13-induced proliferation and ASMC migration in vitro and therefore may be a new therapeutic option in asthma.

[Diagnostic study on children's diaphragmatic fatigue].

OBJECTIVE: In the recent twenty years, the diaphragmatic contraction, relaxation functions and electric activity have been explored through electromyography (EMG) and transdiaphragmatic pressure (Pdi) determination. But these techniques required some complex and expensive instruments, so the diagnosis and treatment of children's diaphragmatic fatigue have not been well evaluated. The present study explored the diagnosis of children's diaphragmatic fatigue through measuring ribcage-abdomen motion and analyzed its asynchrony. METHODS: Fifty-three children (male 37, female 16, and age rage from 1 months to 9 years) with respiratory rate > 30 breaths/min, heart rate > 110 beats/min, and respiratory dysfunction had asynchronized ribcage-abdomen motion showed by impedance respirograph (IRG). The authors observed whether ribcage-abdomen motion was synchronic and calculated M levels (staggered peak time/total duration of the breathing cycle). The ribcage and abdomen outputs were displayed on vertical (for rib cage) and horizontal (for abdomen) axes of X-Y instrument. In addition, the change of respiratory frequency and heart rate was observed and arterial blood-gas analysis was also performed. RESULTS: (1) M levels in one-dimensional IRG were positively correlated with alpha angle in two-dimensional IRG (r = 0.956, P < 0.001). Asynchronized respiratory motions could be divided into three types. type I showed completely contra-directional movements of respiration, M levels for (48.1 +/- 4.4)%, an irregularly clockwise loop in the two dimensional IRG, and alpha angle for (138.3 +/- 15.0) degrees. In type II, one dimensional IRG showed displaced peak of the chest and abdomen motion curves, M levels were (16.5 +/- 4.7)%, two dimensional IRG was displaced in a counterclockwise direction, and alpha angle was (55.3 +/- 10.8) degrees. In type III, abdominal motion curve of one dimensional IRG had double peaks, M levels were 0, two dimensional IRG was presented as 8-shaped double circles, alpha angle was (41.3 +/- 3.8) degrees; (2) pH levels in the patients with type I and type II diaphragmatic fatigue were significantly lower, and PCO(2) levels were significantly higher than those with type III or in the normal subjects (P < 0.001 for all), but there was no statistically significant difference between type III and the normal subjects (P > 0.05); (3) Both of respiratory rate and heart rate in type I, type II and type III were higher than those in the normal subjects (all P < 0.001), and the differences among the three types were significant (P < 0.001 for all); (4) Both M levels and alpha angle were negatively correlated with pH levels (r = -0.514, P < 0.001 and r = -0.497, P < 0.001), while positively correlated with PCO(2) levels (r = 0.672, P < 0.001 and r = 0.625, P = 0.01). CONCLUSIONS: (1) IRG can be reliably used to diagnose children's diaphragmatic fatigue. This technique is simple and easy to perform and non-invasive. It is therefore worthy of recommending for further clinical investigations. (2) According to the characteristics of IRG, diaphragmatic fatigue can be divided into three types. (3) The development of children's diaphragmatic fatigue has a series of characteristic changes. (4) To avoid the patients suffering from respiratory failure, it is the key time to adopt the policies of prevention and treatment when IRG shows signs of type III diaphragmatic fatigue.

[Design and clinical application of a three-dimensional biomechanical traction appliance for protrusion of intervertebral disc].

A three-dimensional biomechanical tracting appliance is introduced in the article, which is used to treat the protrusion of intervertebral disc. The appliance is light, practical, adjustable 3D biomechanic, simple and with multiple functions and convenient operation.

[Effect of shenmai injection on diaphragmatic fatigue in children with respiratory failure].

OBJECTIVE: To study the effect of Shenmai injection (SMI) on diaphragmatic fatigue in children with respiratory failure. METHODS: Thirty-five cases of children respiratory failure with diaphragmatic fatigue were divided into two groups. The control group was treated with comprehensive therapy including anti-infection, oxygen inhalation and parenteral nutrition, etc. The SMI group was treated with SMI intravenously, besides the comprehensive therapy as in the control group. Taking electrical impedance respirogram (IRG) as criterion of therapeutic effect, the effective cases after 30 min medication, time for diaphragmatic fatigue disappearance, as well as arterial blood gas analysis before and after treatment were analyzed. RESULTS: (1) In 30 min after medication, the effective cases in the SMI group (15/18) were more than that in the control group (4/17, P < 0.01); (2) Blood pH increased and PaCO2 decreased in both groups after treatment, but the decrease of PaCO2 was more significant in the SMI group (P < 0.05); (3) Time of diaphragmatic fatigue disappearance in the SMI group was shorter than that in the control group (P < 0.01). CONCLUSION: SMI is an effective drug for treatment of diaphragmatic fatigue in children with less adverse effect, and worthwhile for spreading in clinical practice.