Factors associated with left ventricular diastolic dysfunction in patients with septic shock.

PURPOSE: To investigate risk factors associated with left ventricular diastolic dysfunction (LVDD) of patients with septic shock. MATERIALS AND METHODS: Patients with septic shock concomitant with or without LVDD were retrospectively enrolled and divided into the LVDD group (n = 17) and control without LVDD (n = 85). The clinical and ultrasound data were analyzed. RESULTS: A significant (P < 0.05) difference existed between the two groups in serum creatinine, APACHE II score, serum glucose, triglyceride, BUN, FT4, LAVI, mitral E, average e', E/average e', septal e', septal e'/septal s', E/septal e', lateral s', lateral e', and E/lateral e'. LAVI > 37 mL/m2, septal e' < 7 cm/s (OR 11.04, 95% CI 3.38-36.05), septal e'/septal s' < 0.8 (OR 4.09, 95% CI 1.37-12.25), E/septal e' > 15 (OR 22.86, 95% CI 6.09-85.79), lateral e' < 8 cm/s (OR 9.16, 95% CI 2.70-31.07), E/lateral e' > 13 (OR 52, 95% CI 11.99- 225.55), lateral s' < 10 (OR 3.36, 95% CI 1.13-9.99), average e' > 10, E/average e' > 10 (OR 9.53, 95% CI 2.49-36.46), APACHE II score > 16 (OR 3.33, 95% CI 1.00-11.03), SOFA > 5 (or 3.43, 95% CI 1.11-10.60), BUN > 12 mmol/L (OR 3.37, 95% CI 1.15-9.87), serum creatinine > 146 µmol/L (OR 5.08, 95% CI 1.69-15.23), serum glucose > 8 mmol/L (OR 3.36, 95% CI 1.09-10.40), and triglyceride > 1.8 mmol/L were significant (P < 0.05) risk factors for LVDD. LAVI > 37 ml/m2, lateral e' < 8 cm/s, E/lateral e' > 13, and SOFA > 5 were significant (P < 0.05) independent risk factors for LVDD. ROC curve analysis demonstrated that the cut-off value and AUC were 37.09 mL/m2 and 0.85 for LAVI, 8.00 cm/s and 0.89 for lateral e', 12.86 and 0.82 for E/lateral e', and 5.00 and 0.69 for SOFA, respectively. CONCLUSION: Left atrial volume index, mitral lateral e', E/lateral e', and SOFA score are significant independent risk factors for predicting left ventricular diastolic dysfunction in patients with septic shock.

Effects of latanoprost on the expression of TGF-ß1 and Wnt / ß-catenin signaling pathway in the choroid of form-deprivation myopia rats.

In this study, we investigated the effect of latanoprost on the expression of TGF- ß1 and Wnt / ß - Catenin signal pathway in the choroid of form-deprivation myopia model rats. Forty rats were randomly divided into two groups: the control group and the FDM model group. Each group had 20 rats. The FDM model group was established by feeding latanoprost daily for 28 days. 15 rats in each group were used to measure the length of the ocular axis and the level of TGF-ß1 in choroidal tissue; the remaining 5 rats in each group were used for choroidal fibroblast culture. After modeling, the rats were killed, the length of the ocular axis was measured with a vernier caliper, and the level of TGF - ß1 protein and mRNA in the choroidal tissue of each group were measured with RT-PCR method. Results showed that compared with the control group, there was a significant difference in the axial length of the FDM model group (P< 0.05). There was a significant difference in the expression of TGF- ß1 protein and mRNA between the two groups (P<0.05). The cultured cells were identified as choroidal fibroblasts by immunocytochemistry. There was no significant difference (P>0.05) in the comparison of GSK3 ß protein in choroidal fibroblasts of rats in each group. TGF-ß 1 and APC protein in FDM group were significantly lower than those in the control group (P<0.05), while dcl3, p21-gsk3 ß and ß - Catenin proteins were significantly higher (P<0.05), and there was no significant difference (P>0.05) in the ratio of various indexes protein in FDM + ddk1 group and the comparison of TGF - ß1 and APC protein in FDM + ddk1 group and FDM group The expression of dcl3, p21-gsk3 ß and ß - Catenin decreased significantly (P<0.05). There was no significant difference in the expression of GSK3 ß mRNA in the choroidal fibroblasts of each group (P>0.05). The expression of TGF - ß 1 and APC mRNA in FDM group was significantly lower than that in the control group (P<0.05), while the expression of dcl3, p21-gsk3 ß and ß-catenin mRNA in FDM + ddk1 group was significantly higher than that in the control group (P<0.05) >In FDM + ddk1 group, TGF-ß 1 and APC mRNA were significantly lower than those in FDM group (P<0.05), while dcl3, p21-gsk3 ß and ß-Catenin mRNA were significantly higher (P<0.05).

Diffusion Kurtosis Imaging for Assessing the Therapeutic Response of Transcatheter Arterial Chemoembolization in Hepatocellular Carcinoma.

Objective: This study aimed to evaluate the therapeutic response of hepatocellular carcinoma (HCC) after transcatheter arterial chemoembolization (TACE) with diffusion kurtosis imaging (DKI). Methods: Forty-three patients with fifty-nine hepatic cancer nodules were recruited for this study. All patients were treated by TACE. Magnetic resonance imaging (MRI) and DKI (b=0, 800, 1,500, 2,000mm2/s) were performed before and one month after initiating TACE. Patients were classified as either progressing groups or non-progressing groups. Mean kurtosis (MK), mean diffusion (MD), and apparent diffusion coefficient (ADC) values of the tumor tissue were analyzed. Results: Twenty-three HCCs were classified as progressing groups, and thirty-six HCCs were non-progressing groups. After TACE, the values of MD and ADC in non-progressing groups (1.92±0.36×10-3mm2/s, 1.36±0.23×10-3mm2/s) were greater than progressing groups (1.44±0.32× 10-3mm2/s, 1.10±0.23×10-3mm2/s), however, the MK values in non-progressing groups (0.47±0.12) were lower than progressing groups (0.72±0.14). The MK values of tumor among non-progressing patients decreased one month after TACE (0.47±0.12) relative to the preoperative values (0.71±0.12) (P<0.05). In the non-progressing groups, the MD and ADC values of tumor after TACE (1.92±0.36×10-3mm2/s, 1.36±0.23×10-3mm2/s) became higher than their preoperative values (1.44±0.35×10-3mm2/s, 1.09±0.22×10-3mm2/s) (P<0.05). In the progressing groups, the MK, MD, and ADC values of tumor after TACE remained similar before TACE (P>0.05). The sensitivity, specificity, and AUC of the ROC curve for the assessment of HCC progress after TACE by MK (85.2%, 97.5%, and 0.95, respectively) were greater than by ADC (78.6%, 66.5%, and 0.75, respectively) and MD (76.2%, 64.3%, and 0.71, respectively). Conclusions: DKI for assessing the therapeutic response of TACE in HCC shows great promise. MK is more advantageous in the assessment of HCC progress after TACE.

Polarization design for ground-to-satellite quantum entanglement distribution.

High-fidelity transmission of polarization encoded qubits plays a key role in long distance quantum communication. By establishing the channel between ground and satellite, the communication distance can even exceed thousands of kilometers. Aimed to achieve the efficient uplink quantum communication, here we describe a high-fidelity polarization design of a transmitting antenna with an average polarization extinction ratio of 887:1 by a local test. We also implement a feasible polarization-compensation scheme for satellite motions with a fidelity exceeding 0.995 ± 0.001. Based on these works, we demonstrate the ground-to-satellite entanglment distribution with a violation of Bell inequality by 2.312±0.096, which is well above the classic limit 2.

Knockdown of lncRNAXLOC_001659 inhibits proliferation and invasion of esophageal squamous cell carcinoma cells.

BACKGROUND: Studies have shown that long non-coding RNAs (lncRNAs) play a key role in almost all key physiological and pathological processes, including different types of malignant tumors. Our previous lncRNA microarray results have shown that lncRNA XLOC_001659 is upregulated in esophageal cancer (EC) tissues, with a fold change of 20.9 relative to normal esophageal tissues. But its effect and the molecular biological mechanisms on proliferation and invasion of EC cells remain unclear. AIM: To investigate the effect of lncRNA XLOC_001659 on esophageal squamous cell carcinoma (ESCC) cells and explore the molecular biological mechanisms involved. METHODS: RT-qPCR assay was used to quantify the expression levels of lncRNAXLOC-001659 and miR-490-5p. The proliferative capacity of the cells was determined using CCK8 and colony formation assays, and the effect of lncRNAXLOC-001659 on the invasion of ESCC cells was determined by Transwell assay. Dual-luciferase reporter assay was used to detect the target genes of lncRNAXLOC-001659 and miR-490-5p. RESULTS: The results of RT-qPCR showed that the expression of lncRNAXLOC_001659 was upregulated in ESCC cells. CCK-8 assay showed that knockdown of lncRNAXLOC_001659 significantly inhibited ESCC cell proliferation. Colony formation and Transwell invasion assays showed that knockdown of lncRNAXLOC_001659 or overexpression of miR-490-5p significantly inhibited ESCC cell growth and invasion. Furthermore, lncRNAXLOC_001659 acts as an endogenous sponge by competitively binding to miR-490-5p to downregulate miR-490-5p. Further results confirmed that miR-490-5p targeted PIK3CA, and the recovery of PIK3CA rescued lncRNAXLOC_001659 knockdown or miR-490-5p overexpression-mediated inhibition of cell proliferation and invasion, which suggested the presence of an lncRNAXLOC_001659/miR-490-5p/PIK3CA regulatory axis. CONCLUSION: Knockdown of lncRNA XLOC_001659 inhibits proliferation and invasion of ESCC cells via regulation of miR-490-5p/PIK3CA, suggesting that it may play a role in ESCC tumorigenesis and progression.

Satellite testing of a gravitationally induced quantum decoherence model.

Quantum mechanics and the general theory of relativity are two pillars of modern physics. However, a coherent unified framework of the two theories remains an open problem. Attempts to quantize general relativity have led to many rival models of quantum gravity, which, however, generally lack experimental foundations. We report a quantum optical experimental test of event formalism of quantum fields, a theory that attempts to present a coherent description of quantum fields in exotic spacetimes containing closed timelike curves and ordinary spacetime. We experimentally test a prediction of the theory with the quantum satellite Micius that a pair of time-energy-entangled particles probabilistically decorrelate passing through different regions of the gravitational potential of Earth. Our measurement results are consistent with the standard quantum theory and hence do not support the prediction of event formalism.

Comparison of diffusion kurtosis imaging versus diffusion weighted imaging in predicting the recurrence of early stage single nodules of hepatocellular carcinoma treated by radiofrequency ablation.

OBJECTIVE: This study aimed to compare the diffusion kurtosis imaging (DKI) versus diffusion weighted imaging (DWI) in predicting the recurrence of early stage single nodules of hepatocellular carcinoma (HCC) treated by radiofrequency ablation (RFA). MATERIALS AND METHODS: A retrospective analysis of 107 patients with early stage single nodules of HCC was performed, all patients treated by RFA. Recurrence rate of HCC was recorded after a median follow-up of 36 months. During follow-up, the data of magnetic resonance imaging (MRI), DWI and DKI were obtained in multiple time points. The predictive values of DWI and DKI were analyzed using ROC curves. RESULTS: The overall recurrence rate was 66.3% (71/107). The sensitivity, specificity, and AUC for ADC, MD and MK after RFA (78.6, 73.3% and 0.842; 85.7, 83.3% and 0.839; 85.7, 96.7% and 0.956) were higher than before RFA (44.3, 53.3% and 0.560; 51.2, 56.7% and 0.543; 43.6, 67.3% and 0.489). The sensitivity, specificity, and AUC for MK after RFA were 85.7, 96.7%, and 0.956, respectively, which were significantly greater than those of ADC (78.6, 73.3% and 0.842; P < 0.05) and MD (85.7, 83.3% and 0.839). CONCLUSIONS: The prediction efficacy of DKI for the recurrence of early stage single nodules of HCC was better than that of DWI. And, MK was the most sensitive predictor among the DKI.

Free-space quantum key distribution in urban daylight with the SPGD algorithm control of a deformable mirror.

Free-space quantum key distribution (QKD) is important to realize a global-scale quantum communication network. However, performing QKD in daylight against the strong background light noise is a major challenge. Here, we develop the stochastic parallel gradient descent (SPGD) algorithm with a deformable mirror to improve the signal-to-noise ratio (SNR). We then experimentally demonstrate free-space QKD in the presence of urban daylight. The final secure key rate of the QKD is 98∼419 bps throughout the majority of the daylight hours.

Satellite-Relayed Intercontinental Quantum Network.

We perform decoy-state quantum key distribution between a low-Earth-orbit satellite and multiple ground stations located in Xinglong, Nanshan, and Graz, which establish satellite-to-ground secure keys with ∼kHz rate per passage of the satellite Micius over a ground station. The satellite thus establishes a secure key between itself and, say, Xinglong, and another key between itself and, say, Graz. Then, upon request from the ground command, Micius acts as a trusted relay. It performs bitwise exclusive or operations between the two keys and relays the result to one of the ground stations. That way, a secret key is created between China and Europe at locations separated by 7600 km on Earth. These keys are then used for intercontinental quantum-secured communication. This was, on the one hand, the transmission of images in a one-time pad configuration from China to Austria as well as from Austria to China. Also, a video conference was performed between the Austrian Academy of Sciences and the Chinese Academy of Sciences, which also included a 280 km optical ground connection between Xinglong and Beijing. Our work clearly confirms the Micius satellite as a robust platform for quantum key distribution with different ground stations on Earth, and points towards an efficient solution for an ultralong-distance global quantum network.

Satellite-to-ground quantum key distribution.

Quantum key distribution (QKD) uses individual light quanta in quantum superposition states to guarantee unconditional communication security between distant parties. However, the distance over which QKD is achievable has been limited to a few hundred kilometres, owing to the channel loss that occurs when using optical fibres or terrestrial free space that exponentially reduces the photon transmission rate. Satellite-based QKD has the potential to help to establish a global-scale quantum network, owing to the negligible photon loss and decoherence experienced in empty space. Here we report the development and launch of a low-Earth-orbit satellite for implementing decoy-state QKD-a form of QKD that uses weak coherent pulses at high channel loss and is secure because photon-number-splitting eavesdropping can be detected. We achieve a kilohertz key rate from the satellite to the ground over a distance of up to 1,200 kilometres. This key rate is around 20 orders of magnitudes greater than that expected using an optical fibre of the same length. The establishment of a reliable and efficient space-to-ground link for quantum-state transmission paves the way to global-scale quantum networks.

Experimental free-space quantum key distribution with efficient error correction.

We report a 17-km free-space quantum key distribution (QKD) experiment using an engineering model of the space-bound optical transmitter and a ground station for satellite-ground QKD. The final key rate of ~ 0.5 kbps is achieved in this experiment with the quantum bit error rate (QBER) of ~ 3.4%. An efficient error correction algorithm, Turbo Code, is employed. Compared with the current error correction algorithm of Cascade, a high-efficiency error correction is realized by Turbo Code with only one-time data exchange. For a low QBER, with only one-time data exchange, the final key rates based on Turbo code are similar with Cascade. As the QBER increases, Turbo Code gives higher final key rates than Cascade. Our results experimentally demonstrate the feasibility of satellite-ground QKD and show that the efficient error correction based on Turbo Code is potentially useful for the satellite-ground quantum communication.

Satellite-based entanglement distribution over 1200 kilometers.

Long-distance entanglement distribution is essential for both foundational tests of quantum physics and scalable quantum networks. Owing to channel loss, however, the previously achieved distance was limited to ~100 kilometers. Here we demonstrate satellite-based distribution of entangled photon pairs to two locations separated by 1203 kilometers on Earth, through two satellite-to-ground downlinks with a summed length varying from 1600 to 2400 kilometers. We observed a survival of two-photon entanglement and a violation of Bell inequality by 2.37 ± 0.09 under strict Einstein locality conditions. The obtained effective link efficiency is orders of magnitude higher than that of the direct bidirectional transmission of the two photons through telecommunication fibers.

Activation of calpain by renin-angiotensin system in pleural mesothelial cells mediates tuberculous pleural fibrosis.

Pleural fibrosis is defined as an excessive deposition of extracellular matrix (ECM) components that results in destruction of the normal pleural tissue architecture. It can result from diverse inflammatory conditions, especially tuberculous pleurisy. Pleural mesothelial cells (PMCs) play a pivotal role in pleural fibrosis. Calpain is a family of calcium-dependent endopeptidases, which plays an important role in ECM remodeling. However, the role of calpain in pleural fibrosis remains unknown. In the present study, we found that tuberculous pleural effusion (TPE) induced calpain activation in PMCs and that inhibition of calpain prevented TPE-induced collagen-I synthesis and cell proliferation of PMCs. Moreover, our data revealed that the levels of angiotensin (ANG)-converting enzyme (ACE) were significantly higher in pleural fluid of patients with TPE than those with malignant pleural effusion, and ACE-ANG II in TPE resulted in activation of calpain and subsequent triggering of the phosphatidylinositol 3-kinase (PI3K)/Akt/NF-κB signaling pathway in PMCs. Finally, calpain activation in PMCs and collagen depositions were confirmed in pleural biopsy specimens from patients with tuberculous pleurisy. Together, these studies demonstrated that calpain is activated by renin-angiotensin system in pleural fibrosis and mediates TPE-induced collagen-I synthesis and proliferation of PMCs via the PI3K/Akt/NF-κB signaling pathway. Calpain in PMCs might be a novel target for intervention in tuberculous pleural fibrosis.

Crosstalk between calpain activation and TGF-ß1 augments collagen-I synthesis in pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease of unknown cause that typically leads to respiratory failure and death within 3-5years of diagnosis. TGF-ß1 is considered a major profibrotic factor. However, TGF-ß1 is necessary but not sufficient to the pathogenesis of fibrotic lesion of the lungs. Recent observations have revealed that calpain, a calcium dependent protease, plays a pivotal role in tissue remodeling and fibrosis. However, the mechanism of calpain mediating pulmonary fibrosis is not understood. Calpain conditional knockout (ER-Cre(+/-)capns1(flox/flox)) mice and primary human lung fibroblasts (HLFs) were used here to investigate the relationship between calpain and TGF-ß1. Calpain knockout mice were protected from fibrotic effects of bleomycin. Bleomycin induced increases in TGF-ß1 via calpain activation in HLFs. Moreover, TGF-ß1 also activated calpain. This crosstalk between calpain activation and TGF-ß1 triggered the downstream signaling pathway including TGF-ß1 Smad2/3 and non-Smad (Akt) pathways, as well as collagen-I synthesis. Taken together, our data indicate that the crosstalk between calpain activation and TGF-ß1 augments collagen-I synthesis in HLFs and in pulmonary fibrosis. Intervention in the crosstalk between calpain activation and TGF-ß1 is a novel potential strategy to prevent pulmonary fibrosis.

Primary analysis and screening of microRNAs in gastric cancer side population cells.

AIM: To explore the microRNA (miRNA) profiles and to determine the key miRNAs within the side population (SP) cells of the gastric cancer cell line MKN-45. METHODS: We used fluorescence-activated cell sorting and Hoechst 33342 labeling to obtain SP cells from the human gastric carcinoma cell line MKN-45. The miRNA expression profiles of the SP and major population (MP) cells were examined using a miRNA gene chip, and key miRNAs were obtained according to aberrant expression and the miRNAs' possible targets as predicted by bioinformatics. RESULTS: Using a significance criterion of a 1.5-fold or greater difference in expression level, we observed an increase in the expression of 34 miRNAs and a decrease in the expression of 34 miRNAs when comparing SP to MP cells. Using quantitative real-time reverse transcription-polymerase chain reaction to test for differentially expressed miRNAs combined with bioinformatics results, we found that the downregulated miRNAs, such as hsa-miR-3175 and hsa-miR-203, and the upregulated miRNAs, including hsa-miR-130a, hsa-miR-324-5p, hsa-miR-34a, and hsa-miR-25-star, may be important in maintaining and regulating the characteristics of SP cells. CONCLUSION: There are key miRNAs expressed within the SP cells of the gastric cancer cell line MKN-45, and include hsa-miR-3175, hsa-miR-203, hsa-miR-130a, hsa-miR-324-5p, hsa-miR-34a, and hsa-miR-25-star.

Bleomycin induced epithelial-mesenchymal transition (EMT) in pleural mesothelial cells.

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease characterized by the development of subpleural foci of myofibroblasts that contribute to the exuberant fibrosis. Recent studies revealed that pleural mesothelial cells (PMCs) undergo epithelial-mesenchymal transition (EMT) and play a pivotal role in IPF. In animal model, bleomycin induces pulmonary fibrosis exhibiting subpleural fibrosis similar to what is seen in human IPF. It is not known yet whether bleomycin induces EMT in PMCs. In the present study, PMCs were cultured and treated with bleomycin. The protein levels of collagen-I, mesenchymal phenotypic markers (vimentin and α-smooth muscle actin), and epithelial phenotypic markers (cytokeratin-8 and E-cadherin) were measured by Western blot. PMC migration was evaluated using wound-healing assay of culture PMCs in vitro, and in vivo by monitoring the localization of PMC marker, calretinin, in the lung sections of bleomycin-induced lung fibrosis. The results showed that bleomycin induced increases in collagen-I synthesis in PMC. Bleomycin induced significant increases in mesenchymal phenotypic markers and decreases in epithelial phenotypic markers in PMC, and promoted PMC migration in vitro and in vivo. Moreover, TGF-ß1-Smad2/3 signaling pathway involved in the EMT of PMC was demonstrated. Taken together, our results indicate that bleomycin induces characteristic changes of EMT in PMC and the latter contributes to subpleural fibrosis.

Ischemic postconditioning decreases matrix metalloproteinase-2 expression during ischemia-reperfusion of myocardium in a rabbit model: A preliminary report.

OBJECTIVE: To investigate the effect of ischemic postconditioning on the expression of matrix metalloproteinase (MMP)-2 during ischemia-reperfusion of myocardium in a rabbit model. METHODS: Thirty-six male New Zealand white rabbits were randomly divided into sham, ischemia-reperfusion and ischemic postconditioning groups. Myocardial ischemia-reperfusion was created by ligating the left anterior descending coronary artery for 30 min followed by 3 h of reperfusion. Myocardial infarction sizes were determined by dual staining with triphenyltetrazolium chloride and trypan blue. Plasma levels of MMP-2 were measured using ELISA. Myocardial MMP-2 messenger RNA was analyzed by reverse transcription polymerase chain reaction. RESULTS: The mean (± SD) infarct size in the ischemic postconditioning group was significantly smaller compared with the ischemia-reperfusion group (37.1±3.8% versus 57.5±1.9%; P=0.02). The incidence of ventricular tachycardia in the ischemic postconditioning group was also lower than in the ischemia-reperfusion group (8.5% versus 75%; P=0.003). MMP-2 messenger RNA expression in the ischemic postconditioning group was significantly lower compared with the ischemia-reperfusion group (0.4944±0.0476 versus 0.6989±0.0694; P=0.02). CONCLUSION: Ischemic postconditioning reduces myocardial ischemia-reperfusion injury, possibly by inhibiting the expression of MMP-2.

Characterization of cancer stem-like cells in the side population cells of human gastric cancer cell line MKN-45.

OBJECTIVE: Side population (SP) cells may play a crucial role in tumorigenesis and the recurrence of cancer. Many kinds of cell lines and tissues have demonstrated the presence of SP cells, including several gastric cancer cell lines. This study is aimed to identify the cancer stem-like cells in the SP of gastric cancer cell line MKN-45. METHODS: We used fluorescence activated cell sorting (FACS) to sort SP cells in the human gastric carcinoma cell line MKN-45 (cells labeled with Hoechst 33342) and then characterized the cancer stem-like properties of SP cells. RESULTS: This study found that the SP cells had higher clone formation efficiency than major population (MP) cells. Five stemness-related gene expression profiles, including OCT-4, SOX-2, NANOG, CD44, and adenosine triphosphate (ATP)-binding cassette transporters gene ABCG2, were tested in SP and MP cells using quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). Western blot was used to show the difference of protein expression between SP and MP cells. Both results show that there was significantly higher protein expression in SP cells than in MP cells. When inoculated into non-obese diabetic/severe combined immunodeficiency (NOD/SCID) mice, SP cells show higher tumorigenesis tendency than MP cells. CONCLUSIONS: These results indicate that SP cells possess cancer stem cell properties and prove that SP cells from MKN-45 are gastric cancer stem-like cells.

[Immune complex may play an important role in freezing injury of frostbite rats].

AIM: To explore the role of humoral immunity in the pathophysiological process of freezing injury and the possible immune interference in the preventation and treatment of frostbite. METHODS: Severe experimental freezing injury model was made in Wistar rats( n = 20). The concentration of three types of immunoglobulin (IgG, IgA and IgM), two types of complement components (C3 and C4), and circulating immune complex (CIC) were measured respectively before and at 4h, 1d, 3d, and 5d after frostbite. At the same time, the tissue immune complex (TIC) in skeletal muscle and the contents of the red blood cell immune complex (RBC-IC) were also observed and then was the red blood cell immune adherence activity (RCIA). RESULTS: Serum IgG concentration decreased rapidly to the lowest level at 4 h after frostbite IgA concentration dropped to the nadir on 1 day after freezing. Decreases of both immunoglobulins were maintained during the 5 days after frostbite. The fate of both C3 and C4 were the same as those immunoglobulins. Freezing had rather less effect on IgM level. CIC concentration in serum, expressed as the percent of prefreezing increased rapidly and to the zenith on the 3 days post-freezing. By immunofluorescence microscopy, thin continuous linear pattern (IgG) was demonstrated along the SM on the first day post-freezing. Granular and nodular deposits (IgG) appeared along the SM as the time proceeded after frostbite. RBC-IC contents, expressed as the erythrocyte IC rosette rate, increased significantly and to the zenith on the 3 d post-freezing, while RCIA depressed to the nadir at the same time. CONCLUSION: The freezing frostbite is an immune complex related disease which have not been reported by others before.

[Association between the functional monoamine oxidase A gene polymorphism and aggressively driving behavior].

OBJECTIVE: This study is purposed to explore the relationship between aggressively driving behavior and functional polymorphism in the promoter region of the monoamine oxidase-A (MAOA) gene. METHODS: A total of 348 automobile drivers were investigated with Deffenbacher's driver anger scale, driving vengeance questionnaire (DVQ) and driver aggression behavior questionnaire. Eighty-eight drivers were selected as more, medium and less aggressive group, each. Polymerase chain reaction (PCR) and 2.5% agarose gel electrophoresisi were adopted to detect the polymorphism of functional 30 bp-uVNTR in the promoter region of the X-chromosomal MAOA gene and their frequencies of varied genotypes were estimated. RESULTS: Two alleles with 3 and 4 repeats of 30 bp-uVNTR were detected in the drivers. Among the more aggressive group, number of the allele with 3 repeats of 30 bp-uVNTR (63/88) was significantly more than that with 4 repeats (25/88) (chi(2) = 10.21, P < 0.01), and number of the allele with 4 repeats of 30 bp-uVNTR was more in the less aggressive group, indicating that persons with allele of 3 repeats of 30 bp VNTR were more aggressive in their driving than those with 4 repeats. CONCLUSIONS: Aggressively driving behavior in drivers possibly related to their functional MAOA-uVNTR polymorphism. Effect of the gene on aggressively driving behavior should be further studied.