The Relationship Between Prognostic Nutritional Indexes and the Clinical Outcomes of Patients with Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Purpose: Nutritional status is related to the clinical outcomes of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The aim of this study was to investigate the association between nutritional status, measured by the prognostic nutritional index (PNI), and adverse hospitalization outcomes in patients with AECOPD. Methods: Consecutive AECOPD patients admitted to the First Affiliated Hospital of Sun Yat-sen University between January 1, 2015 to October 31, 2021 were enrolled. We collected the clinical characteristics and laboratory data of patients. Multivariable logistic regression models were developed to assess the relationship between the baseline PNI and adverse hospitalization outcomes. A generalized additive model (GAM) was used to identify any non-linear relationship. In addition, we performed a subgroup analysis to tested the robustness of the results. Results: A total of 385 AECOPD patients were involved in this retrospective cohort study. Based on the tertiles of PNI, patients in the lower tertiles of PNI showed more worse outcome incidence (30 [23.6%] versus 17 [13.2%] versus 8 [6.2%]; p < 0.001). Multivariable logistic regression analysis revealed that the PNI were independently associated with adverse hospitalization outcomes after adjustment for confounding factors (Odds ratio [OR] = 0.94, 95% CI: 0.91 to 0.97, P < 0.0001). After adjusting for confounders, smooth curve fitting showed a saturation effect, suggesting that the relationship between the PNI and adverse hospitalization outcomes was nonlinear. Two-piecewise linear regression model suggested that the incidence of adverse hospitalization outcomes significantly decreased with PNI level up to the inflection point (PNI = 42), and PNI was not associated with adverse hospitalization outcome after that point. Conclusion: Decreased PNI levels at admission were determined to be associated with adverse hospitalization outcomes in patients with AECOPD. The results obtained in this study may potentially assist clinicians optimize risk evaluations and clinical management processes.

Association of Red Cell Index and Adverse Hospitalization Outcomes in Chronic Obstructive Pulmonary Disease Patients with Acute Exacerbation: A Retrospective Cohort Study.

Purpose: Previous studies have shown that the red cell index (RCI) can be considered as a simple and useful method to evaluate respiratory function. However, at present its association with adverse hospitalization outcomes in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD) is not fully understood. Our study aimed to examine the relationship between adverse hospitalization outcomes and RCI among AECOPD patients. Patients and Methods: We performed a retrospective analysis of consecutive patients from January 2015 to October 2021. In this study, RCI was the independent variable, measured at baseline, and adverse hospitalization outcome was the dependent variable. According to the RCI median (RCI=2.221), we divided 377 patients into two roughly equal groups (188 and 189, respectively). Next, the association between RCI and adverse hospitalization outcomes was explored using multivariable logistic regression models. To identify any non-linear relationship, a generalized additive model (GAM) was employed. Results: With a total of 377 patients with AECOPD, we divided them into two roughly equal groups to compare the clinical factors and RCI levels. The patients in the higher RCI group showed poorer outcome incidence (18 [9.57%] vs 31 [16.40%]; p = 0.049). After accounting for potential confounders, the results showed that RCI was positively associated with adverse hospitalization outcomes (odds ratio [OR] = 1.15, 95% CI: 1.01-1.32). In addition, a non-linear relationship was detected between RCI and adverse hospitalization outcomes, which had an inflection point of 3.2. There were odds ratios and confidence intervals of 0.8 (0.7-1.0) and 1.3 (1.2-1.4) on the left and right sides of the inflection point, respectively. Conclusion: The RCI and adverse hospitalization outcomes exhibited a non-linear relationship in the AECOPD patients. RCI is strongly positively correlated with adverse hospitalization outcomes when it was greater than 3.2.

Development of a Predictive Model for Mortality in Hospitalized Patients With COVID-19.

INTRODUCTION: Early identification of patients with novel corona virus disease 2019 (COVID-19) who may be at high mortality risk is of great importance. METHODS: In this retrospective study, we included all patients with COVID-19 at Huanggang Central Hospital from January 23 to March 5, 2020. Data on clinical characteristics and outcomes were compared between survivors and nonsurvivors. Univariable and multivariable logistic regression were used to explore risk factors associated with in-hospital death. A nomogram was established based on the risk factors selected by multivariable analysis. RESULTS: A total of 150 patients were enrolled, including 31 nonsurvivors and 119 survivors. The multivariable logistic analysis indicated that increasing the odds of in-hospital death associated with higher Sequential Organ Failure Assessment score (odds ratio [OR], 3.077; 95% confidence interval [CI]: 1.848-5.122; P < 0.001), diabetes (OR, 10.474; 95% CI: 1.554-70.617; P = 0.016), and lactate dehydrogenase greater than 245 U/L (OR, 13.169; 95% CI: 2.934-59.105; P = 0.001) on admission. A nomogram was established based on the results of the multivariable analysis. The AUC of the nomogram was 0.970 (95% CI: 0.947-0.992), showing good accuracy in predicting the risk of in-hospital death. CONCLUSIONS: This finding would facilitate the early identification of patients with COVID-19 who have a high-risk for fatal outcome.

Effect of Community-Acquired Pneumonia on Acute Exacerbation of Chronic Obstructive Pulmonary Disease.

Community-acquired pneumonia (CAP) is a major contributor to hospitalization for acute exacerbations of chronic obstructive pulmonary disease (AECOPD). The clinical manifestations of AECOPD with and without CAP are confusing. The difference in the survival or readmission rate of AECOPD with or without CAP remains controversial. A prospective cohort study was conducted to evaluate the clinical and laboratory characteristics and in-hospital outcomes of patients who were consecutively hospitalized due to AECOPD from May 2015 to December 2019. Grouping was based on chest computed tomography findings. Multivariable logistic regression was used to explore the predictors for early identification between CAP exacerbations and non-CAP exacerbations. Kaplan-Meier analysis was used to compare the cumulative survival rate and readmission rate for a 12-month follow-up between the two groups. A total of 378 patients with AECOPD were enrolled, including 200 patients with CAP and 178 patients without CAP. The presence of pleuritic pain, usage of ICS, and elevated levels of C-reactive protein and procalcitonin on admission were the predictors for the early discrimination between AECOPD with and without CAP. During a 1-year follow-up, the cumulative survival rate was lower in patients with AECOPD with CAP than in those with AECOPD without CAP (13.0% vs. 3.37%; HR: 4.099; 95% CI, 2.049-8.199; p < 0.001), but the readmission rate was similar in both groups. Patients with first-time exacerbation due to CAP were more likely to experience subsequent pneumonic exacerbation. CAP is frequent among patients hospitalized for AECOPD and associated with increased mortality and successive pneumonic exacerbation.

[Interaction between glycogen synthase kinase-3ß and endoplasmic reticulum stress is involved in high glucose-induced injury in human umbilical vein endothelial cells].

OBJECTIVE: To explore the role of the interaction between glycogen synthase kinase-3ß (GSK-3ß) and endoplasmic reticulum stress (ERS) in the high glucose (HG)-induced injury in human umbilical vein endothelial cells (HUVECs). METHODS: HUVECs treated with 40 mmol/L glucose for 24 h were examined for expression levels of GSK-3ß, GRP78, CHOP and cleaved caspase-3 protein using Western blotting. The cell viability was examined using CCK-8 assay and cell apoptosis was detected with Hoechst 33258 nuclear staining and photofluorography. The intracellular level of reactive oxygen species (ROS) was measured with dichlorfluoresein staining and photofluorography. Mitochondrial membrane potential (MMP) was tested by rhodamine 123 (Rh123) staining and photofluorography. RESULTS: Treatment of HUVECs with 40 µmol/L glucose for 3-24 h activated GSK-3ß in a time-dependent manner, leading to significantly down-regulated expression of phosphorylated (p)-GSK-3ß (P<0.05). HG exposure of the cells for 1-24 h induced ERS, evidenced by time-dependently up-regulated expression of GRP78 and CHOP (P<0.05). LiCl, an inhibitor of GSK-3ß, attenuated HG-induced ERS and significantly lowered the expression levels of GRP78 and CHOP (P<0.01). 4-PBA, an inhibitor of ERS, obviously ameliorated the activation of GSK-3ß by HG as shown by the increase in p-GSK-3ß expression level (P<0.01). HG exposure for 24 h induced obvious injuries in HUVECs, which exhibited decreased cell viability, increased cell apoptosis, increased expression of cleaved caspase-3 and ROS generation, and loss of MMP. Pretreatment of the cells with LiCl or 4-PBA for 60 min before HG exposure significantly lessened the cell injuries (P<0.01). CONCLUSION: Interactions between GSK-3ß and ERS occur in HUVECs exposed to HG and participate in HG-induced cell injuries.

Case-Control Study on Impact of the Telomerase Reverse Transcriptase Gene Polymorphism and Additional Single Nucleotide Polymorphism (SNP)- SNP Interaction on Non-Small Cell Lung Cancers Risk in Chinese Han Population.

AIMS: To investigate the impact of telomerase reverse transcriptase (TERT) gene polymorphism and additional SNP-SNP interaction on non-small cell lung cancer (NSCLC) risk in Chinese population. METHODS: A total of 828 participants (526 males, 302 females), with a mean age of 71.3 ± 15.7 years old, were selected, including 410 NSCLC patients and 418 normal participants. Logistic regression was performed to investigate association between single nucleotide polymorphism (SNP) and NSCLC risk. Generalized multifactor dimensionality reduction (GMDR) was used to analysis the interaction among four SNPs. RESULTS: Non-small cell lung cancer risk was significantly higher in carriers of G allele of the rs2736100 polymorphism than those with TT (TG + GG vs. TT, adjusted OR (95%CI = 1.68 (1.28-2.07). In addition, we also found that NSCLC risk was also significantly higher in carriers of A allele of the rs2736098 polymorphism than those with GG (GA + AA vs. GG, adjusted OR (95%CI) = 1.52 (1.19-1.93). GMDR analysis indicated that there was a significant two-locus model (P = 0.0100) involving rs2736098 and rs2736100, indicating a potential gene-gene interaction between rs2736098 and rs2736100. Overall, the two-locus models had a cross-validation consistency of 10 of 10, and had the testing accuracy of 62.17%. We found that patients with GA or AA of rs2736098 and TG or GG of rs2736100 genotype have the highest NSCLC risk, compared to patients with GG of rs2736098 and TT of rs2736100 genotype, OR (95%CI) was 2.52 (1.68-3.68), after covariates adjustment. CONCLUSIONS: Minor allele of rs2736098 and rs2736100 in TERT gene and interaction between the two SNP were associated with increased risk of NSCLC risk.

Alzheimer's disease treated with combined therapy based on nourishing marrow and reinforcing Qi.

OBJECTIVE: To study the efficacy and safety of combined Traditional Chinese Medicine (TCM) therapy based on nourishing marrow to improve intellect and reinforcing Qi to activate bloodon mild to moderate Alzheimer's disease (AD). METHODS: Sixty-six patients with AD, whose Mini-Mental State Examination (MMSE) score were from 10-24, were randomized equally into an intervention group and a control group. The control group was given Aricept (5 mg, once daily). The intervention group was further divided into Yang-Qi deficiency (n = 18) and of Yin-Qi deficiency (n = 15) subgroups. Patients in the Yang-Qi deficiency group were intravenously administered shenfu injection, 60 mL, and deproteinized calf blood injection (DCBI), 1.2 g, once daily. The Yin-Qi deficiency group was given shenmai injection, 60 mL, and DCBI, 1.2 g, once daily. Each course lasted 21 days. RESULTS: Compared with the control group and with pre-treatment in the same group, MMSE, clinical dementia rating, and activities of daily living scale scores in the intervention group were significantly improved (all P < 0.05). These metrics mildly improved in the control group compared with before treatment (P > 0.05). No adverse effects were observed in any group during treatment. CONCLUSION: We found that combined TCM therapy is effective and safe for managing mild to moderate AD.

The serum glucan level and pathological changes of antifungal treatment for lower respiratory tract infection of Candida albicans.

Due to the fact that Candida albicans colonizes in the upper respiratory tracts of healthy people, whether or not its isolation from airway secretions is sufficient to warrant treatment remains controversial. The animal models of immunosuppressive rats with pulmonary candidiasis were established by the intratracheal inoculating suspensions of C. albicans, and the animals were divided into the following three groups: (1) antifungal treatment group, (2) saline control group, and (3) blank control group. We noted the following in our studies: (1) The fungal load of the saline control group gradually increased such that it was higher than those of the antifungal treated group and was significant from the fourth day of treatment (P < 0.01). (2) The serum (1,3)-ß-D-glucan (BG) in the saline control group also gradually increased so that it was significantly higher than found with the treated group by the sixth day of treatment (P < 0.05), and in fact, the rank of pulmonary colony count and BG in the two groups at different time points showed an almost perfect linear correlation. (3) The median survival period of the rats in the antifungal treated group and saline control group was 15 and 8 days respectively, no rats died in the blank control group. (4) The lung lesions from the saline control group gradually became more aggravated than those in the antifungal treated group; no significant pathological changes were found in the blank control group. Antifungal treatment (micafungin) is capable of efficaciously decreasing the lung fungal burden, and continuous monitoring of BG is useful for the evaluation of therapeutic effect of antifungals. Infection of C. albicans with associated pathological damage implies the need for antifungal therapy.

Evaluation of galactomannan enzyme immunoassay and quantitative real-time PCR for the diagnosis of invasive pulmonary aspergillosis in a rat model.

Since there is no consensus about the most reliable assays to detect invasive aspergillosis from samples obtained by minimally invasive or noninvasive methods, we compared the efficacy of an enzyme-linked immunosorbent assay (ELISA) for galactomannan (GM) detection and quantitative real-time PCR assay (qRT-PCR) for the diagnosis of invasive pulmonary aspergillosis. Neutropenic, male Sprague-Dawley rats (specific pathogen free; 8 weeks old; weight, 200 ± 20 g) were immunosuppressed with cyclophosphamide and infected with Aspergillus fumigatus intratracheally. Tissue and whole blood samples were harvested on days 1, 3, 5, and 7 post-infection and examined with GM ELISA and qRT-PCR. The A. fumigatus DNA detection sequence was detected in the following number of samples from 12 immunosuppressed, infected rats examined on the scheduled days: day 1 (0/12), day 3 (0/12), day 5 (6/12), and day 7 (8/12) post-infection. The sensitivity and specificity of the qRT-PCR assay was 29.2% and 100%, respectively. Receiver operating characteristic curve (ROC) analysis indicated a Ct (cycle threshold) cut-off value of 15.35, and the area under the curve (AUC) was 0.627. The GM assay detected antigen in sera obtained on day 1 (5/12), day 3 (9/ 12), day 5 (12/12), and day 7 (12/12) post-infection, and thus had a sensitivity of 79.2% and a specificity of 100%. The ROC of the GM assay indicated that the optimal Ct cut-off value was 1.40 (AUC, 0.919). The GM assay was more sensitive than the qRT-PCR assay in diagnosing invasive pulmonary aspergillosis in rats.

Hydrogen sulfide attenuates doxorubicin-induced cardiotoxicity by inhibition of the p38 MAPK pathway in H9c2 cells.

We previously demonstrated the protective effect of hydrogen sulfide (H2S) against doxorubicin (DOX)-induced cardiotoxicity through inhibition of endoplasmic reticulum stress. The aim of the present study was to explore the role of p38 mitogen-activated protein kinase (MAPK) in DOX-induced cardiotoxicity and ascertain whether exogenous H2S protects DOX-induced injury by inhibiting p38 MAPK in cardiomyoblasts (H9c2). We observed that exposure of H9c2 cells to 5 µM DOX not only markedly induced injuries, including cytotoxicity, apoptosis, overproduction of reactive oxygen species (ROS) and dissipation of mitochondrial membrane potential (MMP), but also enhanced the expression level of phosphorylated (p)-p38 MAPK. The DOX-induced increase in expression of p-p38 MAPK was significantly attenuated by pretreatment of H9c2 cells with either 400 µM sodium hydrogen sulfide (NaHS) (a donor of H2S) or 1,000 µM N-acetyl-L-cysteine (NAC, an ROS scavenger) prior to exposure to DOX. Pretreatment with either 400 µM NaHS or 3 µM SB203580, a selective inhibitor of p38 MAPK, ameliorated DOX-induced cardiomyocyte injuries, as evidenced by an increase in cell viability, and decreases in the number of apoptotic cells, ROS generation as well as dissipation of MMP. In conclusion, the findings of the present study demonstrated that the activation of p38 MAPK contributes to DOX-induced injuries, including cytotoxicity, apoptosis, mitochondrial damage and oxidative stress in H9c2 cells. We also provide novel evidence that exogenous H2S protects H9c2 cells against DOX-induced cardiotoxicity by inhibition of the p38 MAPK pathway.

Interleukin-12 and interleukin-2 alone or in combination against the infection in invasive pulmonary aspergillosis mouse model.

Aspergillus fumigatus is an intracellular opportunistic fungus causing invasive pulmonary mycosis, characterised by hyphal invasion and destruction of pulmonary tissue. Th1 cytokines could enhance fungicidal activity. The effects from the combination of interleukin-12 (IL-12) and IL-2 are rarely known in invasive pulmonary aspergillosis infection. To assess the cleaning of A. fumigatus infection in the pulmonary tissues by IL-12 and IL-2, interferon-γ (IFN-γ) was detected in the sera using ELISA, quantification of IFN-γ mRNA using real-time RT-PCR and lung Colony-forming unit was assayed by cultivation. Morphology was analysed by histopathological examination. Our results showed that IL-12 and/or IL-2 could enhance the IFN-γ expression in the pulmonary tissue, reduce the colony load in the pulmonary tissue and increase the survival rate of mouse. The combination of IL-12 and IL-2 could assist in increasing the IFN-γ expression in the pulmonary tissue, but neither reduce colony load in the pulmonary tissue nor increase the survival rate of mouse significantly. It was demonstrated that IL-12 and IL-2 were strong immunomodulatory cytokines as a prerequisite for protecting the host from infectious agents.

Retrospective analysis on the impact of tuberculosis on patients with systemic lupus erythematosus (SLE).

Up to now, there have been few reports concerning changes in lupus activity and immune indices of tuberculosis in patients with systemic lupus erythematosis (SLE). A retrospective investigation was given to survey the case data of SLE patients companied with tuberculosis that were treated in our hospital from 2001 to 2010 and compared with that of sex- and age-matched patients with single SLE. Changes in autoantibodies, lupus activity, inflammatory indices, positive rates of tuberculin (PPD) test and tuberculosis antibody (TB-Ab) of both groups were observed. It was indicated by results that ANA antibody level and positive rates of anti-Sm, anti-SSA and anti-SSB antibodies were significantly lower in the TB group than those in the control group (P < 0.05); C3 and C4 levels were significantly higher in the TB group than those in the control group; damage of hematological system (predominantly platelet) was less severe in the TB group than that in the control group (P < 0.05); no significant differences in IgG, IgM and IgA were noted between two groups (P > 0.05); ESR, C-reactive protein and LDH levels were significantly higher in the TB group than those in the control group (P < 0.05); PPD-IgG were significantly higher in the TB group than those in the control group (P < 0.05). These results suggested that after SLE patients were infected with tuberculosis, immune function was altered and lupus activity was inhibited as well.

Hydrogen sulfide protects PC12 cells against reactive oxygen species and extracellular signal-regulated kinase 1/2-mediated downregulation of glutamate transporter-1 expression induced by chemical hypoxia.

Hypoxia and/or ischemia are implicated in neurodegenerative disorders. In these diseases, hypoxia/ischemia may induce oxidative stress, including production of reactive oxygen species (ROS), which result in a decrease in glutamate transporter expression. Hydrogen sulfide (H2S), as the third gasotransmitter, has neuroprotective effects and potent antioxidant properties. In the present study, we investigated the role of glutamate transporter-1 (GLT-1) in the protection of H2S against chemical hypoxia-induced injury in PC12 cells. We found that cobalt chloride (CoCl2), a chemical hypoxia agent, reduced the expression of GLT-1 in a time-dependent manner. Pretreatment with NaHS (a donor of H2S) reversed the CoCl2-induced downregulation of GLT-1 expression. Pretreatment with DHK (a selective inhibitor of GLT-1) for 30 min prior to NaHS preconditioning significantly inhibited the cytoprotection of H2S against CoCl2-induced injuries, leading to an increase in cytotoxicity and apoptosis as well as to a loss of mitochondrial membrane potential (MMP). In addition, we found that similar to the effect of NaHS, pretreatment with NAC (a ROS scavenger) or U0126 (a MEK1/2 inhibitor) blocked the downregulation of GLT-1 expression induced by CoCl2. Collectively, we demonstrated for the first time that ROS and extracellular signal-regulated kinase 1/2 (ERK1/2)-mediated reduction of GLT-1 expression may be involved in chemical hypoxia-induced neural injury and that H2S attenuates this injury partly by upregulating GLT-1 expression in PC12 cells.

Increased expression of heat shock protein 90 under chemical hypoxic conditions protects cardiomyocytes against injury induced by serum and glucose deprivation.

Heat shock proteins (HSPs) are critical for adaptation to hypoxia and/or ischemia. Previously, we demonstrated that cobalt chloride (CoCl2), a well-known hypoxia mimetic agent, is an inducer of HSP90. In the present study, we tested the hypothesis that CoCl2-induced upregulation of HSP90 is able to provide cardioprotection in serum and glucose-deprived H9c2 cardiomyocytes (H9c2 cells). Cell viability was detected using a CCK-8 assay, while HSP90 expression was detected via western blotting. The findings of this study showed that serum and glucose deprivation (SGD) induced significant cytotoxicity, overproduction of reactive oxygen species (ROS) and a loss of mitochondrial membrane potential (MMP) in H9c2 cells. In addition, SGD downregulated the expression of HSP90 in a time-dependent manner. The selective inhibitor of HSP90 17-allylamino-17-demethoxygeldanamycin (17-AAG) aggravated SGD-induced cytotoxicity. CoCl2 at 100 µM time-dependently enhanced the expression of HSP90. Treatment with CoCl2 from 50 to 200 µM significantly attenuated cytotoxicity and the downregulation of HSP90 expression induced by SGD for 24 h, respectively. Notably, pretreatment of H9c2 cells with 17-AAG at 2 µM for 60 min before exposure to both CoCl2 (100 µM) and SGD significantly blocked the CoCl2-induced cardioprotective effect, demonstrated by decreased cell viability and MMP loss, as well as increased ROS generation. Taken together, these results suggest that HSP90 may be one of the endogenous defensive mechanisms for resisting ischemia-like injury in H9c2 cells, and that HSP90 plays an important role in chemical hypoxia-induced cardioprotection against SGD-induced injury by its antioxidation and preservation of mitochondrial function.

Combined APACH II score and arterial blood lactate clearance rate to predict the prognosis of ARDS patients.

OBJECTIVE: To explore the easily applicable indicators of practical value to evaluate the prognosis of acute respiratory distress syndrome (ARDS). METHODS: Blood and biochemical tests and blood-gas analyses were performed upon entry into the ICUs, 12 h, 24 h, 48 h and 72 h after that in 72 ARDS patients (who were admitted to the ICUs of our hospital from January 2000 to December 2009). Then APACHE II scores were achieved by combining relevant physiological parameters and laboratory results. RESULTS: There was a statistical difference between the death group and survival group at different time points upon entering the ICUs in terms of APACHE II score, alveolar-arterial oxygen difference and arterial blood lactate clearance rate. PaO(2)/FiO(2) values were recorded to be statistically different between the death group and survival group 24 h, 48 h and 72 h, respectively after entry into the ICUs. In addition, registered linear regression existed between APACHE II score, alveolar-arterial oxygen difference or PaO(2)/FiO(2) value and time. APACHE II score 24 h and 72 h after entering ICUs predicted mortality with an area under the ROC curve (AUC) standing respectively at 0.919 and 0.955. Arterial blood lactate clearance rate 12 h, 24 h, 48 h and 72 h after entering ICUs predicted mortality with an area under the ROC curve (AUC) at 0.918, 0.918, 0.909 and 0.991, respectively. CONCLUSIONS: APACHE II score applied in combination with arterial blood lactate clearance rate is of clinical significance in assessing the prognosis of ARDS patients.

Transplantation of adipose-derived mesenchymal stem cells into a murine model of passive chronic immune thrombocytopenia.

BACKGROUND: Immune thrombocytopenia (ITP) is a bleeding disorder characterized by antibody-opsonized platelets (PLTs) being prematurely destroyed by macrophages in the reticuloendothelial system. T helper (Th) cells and different Th cytokines play an important role in the pathophysiology of ITP. As immunomodulators, adipose-derived mesenchymal stem cells (ADSCs) regulate Th cells and show therapeutic effects in autoimmune diseases. However, it is not clear how ADSCs affect ITP. In this study, we explored the specific effects of ADSCs on ITP in mice. STUDY DESIGN AND METHODS: BALB/c mice were randomly divided into three groups: normal controls, ITP controls, and ITP with ADSC transplantation. PLT levels were monitored by an automatic blood cell counter, and the cytokines interferon-γ (IFN-γ); interleukin (IL)-2, -4, -10, and -17; and transforming growth factor-ß1 (TGF-ß1) were analyzed by enzyme-linked immunosorbent assays. RESULTS: Compared to the untreated ITP mice, the PLT level of the ITP mice significantly increased after ADSC treatment. In the ADSC group, IFN-γ, IL-2, and IL-17 significantly decreased, while IL-4, IL-10, and TGF-ß1 increased. CONCLUSION: These findings constitute the first experimental evidence that ADSCs are efficacious in improving PLT levels and reducing the related Th cytokines mediating proinflammatory response in ITP mice, which may provide a scientific basis for using ADSCs as a new therapy for ITP.

[Analysis of the risk factors of pulmonary fungal infections related to mechanical ventilation and prognosis of the patients].

OBJECTIVE: To investigate the risk factors of pulmonary fungal infections related to mechanical ventilation and the prognosis of patients. METHODS: A retrospective case-controlled study was conducted to analyze the culture results of the pulmonary secretions in patients with pulmonary fungal and nonfungal infections in association with mechanical ventilations. The risk factors of pulmonary fungal infections related to mechanical ventilation were identified and their impact on the clinical outcome of the patients was evaluated. RESULTS: Of the 127 patients included in this study, 81 (63.78%) were positive and 46 (36.22%) negative for pulmonary fungal infections according to the diagnostic criteria of ventilator-associated pneumonia (VAP). The mortality of the patients with fungal infection was 82.7%, significantly higher than that of patients with non-fungal infection (67.39%, chi2=3.910, P<0.05). Univariate analysis and multivariate logistic regression showed that such factors as old age, duration of mechanical ventilation, tracheal intubation or incision for over 7 days, diabetes, blood glucose over 6.1 mmol/L, multi-organ dysfunction, combined use of antibiotics, at least 3-time changes antibiotics, administration of glucocorticosteroid for over 7 days, and immunodepressant use were all the independence risk factors of pulmonary fungal infection related to mechanical ventilation. Old age, multi-organ dysfunction, blood glucose over 6.1 mmol/L, glucocorticosteroid use for over 7 days, anesthetic use for over 3 days and high APACHE III scores were the risk factors for mortality in patients with the infections. CONCLUSIONS: Pulmonary fungal infection associated to mechanical ventilation is often the results of presence of multiple risk factors, and early identification of these factors for timely antifungal treatment may improve the prognostics of the patients and help reduce the mortality rate.

[An experimental study of the therapeutic effect of interleukin-2 and interleukin-12 with and without amphotericin B on pulmonary fungal infection].

OBJECTIVE: To study the therapeutic effect of interleukin-2 (IL-2) and interleukin-12 (IL-12) with and without amphotericin B on pulmonary fungal infection of mice. METHODS: A mouse model of pulmonary invasive aspergillus fumigatus (IPA) infection was established and the mice were divided into different groups, treated with IL-2 and IL-12 with and without amphotericin B. The survival number of mice in 15 days and the colony count of lung tissue in the different groups were observed. RESULTS: IL-2, IL-12 and amphotericin B showed synergistic effect in prolonging the survival of the infected mice and reducing the colony count in the lung tissue. CONCLUSION: IL-2 and IL-12 are effective adjuvant therapeutic agents in the immunosuppressed hosts.