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Android Rooting refers to making the target application perform privileged operations (as root user) by exploiting system vulnerabilities or flashing devices. Some user might root their devices to customize devices or run the Apps that require root privileges. Unfortunately, rooting a device will introduce some serious security risks. Attackers' application can perform malicious actions by requesting root privileges, such as installing malicious application stealthy, stealing user sensitive data and tempering the application. Considering the security risks, Android platform vendor (Google) and some sensitive applications developers don't want the device to be rooted. Consequently, Google developed Root detection mechanisms in platform level. However, the security of these Root detection mechanisms is still unclear. To analyze the evadable ability of their detection by sophisticated Root methods, the reverse engineering techniques were employed to investigate the security of the Root detection mechanism. Analyzing the implementation of some popular Root detection mechanisms, the weakness was found based on the Root technical principle. Some attack experiments were carried out to demonstrate a number of Root detection mechanisms. Results show that, the Root detection mechanism developed by Google possesses a high security risk, and the proposed Root methods can evade the attacks successfully. And this work implies that the security of the current Root detection mechanisms should be further improved. [ABSTRACT FROM AUTHOR]

Objective: To study the association of free immunoglobulin light chain (FLC) with clinical manifestations and lung inflammation in smokers with normal lung function and chronic obstructive pulmonary disease (COPD) patients., Methods: Thirty-two patients with peripheral lung cancer undergoing surgical resection were enrolled from the Department of Thoracic Surgery,Affiliated Hospital of Xuzhou Medical College. They were divided into non-smoking with normal lung function group (non-smoking group, 10 cases), smoking with normal lung function group (smoking group, 12 cases) and smoking with stable COPD group (COPD group, 10 cases). Their preoperative fasting serum and lung tissues away from cancer were used in the study.Enzyme-linked immunesorbent assays (ELISA) were used to detect the levels of FLC-λ and FLC-κ in serum and lung tissue homogenates. The expression of FLC-λ and FLC-κ in the airway epithelium, alveolar wall and blood vessel wall was detected by immunohistochemistry. The correlation between FLC levels and pulmonary functions were analyzed., Results: The serum levels of FLC-λ and FLC-κ in COPD group and smoking group were (35 ± 11),(38 ± 12) and (26 ± 9),(26 ± 8) mg/L, respectively. They were all significantly increased compared with the non-smoking group [(16 ± 7),(16 ± 5) mg/L]. The differences were all statistically significant (q = 3.590-7.482, P < 0.01), and those of the COPD group were significantly higher than those of the smoking group (q = 3.209-4.198, P < 0.05 and P < 0.01). The concentrations of FLC-λ and FLC-κ in lung tissue homogenates of the COPD group and the smoking group were (1.29 ± 0.31),(1.32 ± 0.30) and (0.86 ± 0.42),(0.85 ± 0.37) µg/mg, respectively. They were all significantly increased compared with those of the non-smoking group [(0.45 ± 0.18),(0.42 ± 0.13) µg/mg],(q = 4.178- 9.795, P < 0.05 and P < 0.01). The levels of FLC-λ and FLC-κ in the lung tissue homogenates from the COPD group were significantly higher than those from the smoking group (q = 4.269-4.349, all P < 0.05). The expression of FLC-λ and FLC-κ was detected in airway epithelium, alveolar wall and blood vessel wall. The levels of FLC-λ and FLC-κ in serum and lung tissue homogenates showed a negative correlation with FEV1 percentage of predicted value (r = -0.476 to -0.591, all P < 0.01)., Conclusions: Expressions of FLC were increased in the serum and the lung tissues of COPD patients and smokers with normal lung function, and closely correlated with airflow limitation. The results suggest that FLC plays a proinflammatory role in the pathogenesis of COPD.

Objective: To observe the effects of leptin on the expression of Akt, Pho-Akt, Bcl-2, Bax, caspase-3 and the apoptosis of airway smooth muscle cells (ASMCs), and to explore the possible mechanisms., Methods: ASMCs were derived from rat airway tissue and cultured in vitro. The cells were randomly divided into 5 groups including a control group, leptin at concentrations of 50, 100, 200 µg/L groups (group Lep50, Lep100, Lep200), and PI3K specific antagonist with Lep200 group. Then the cells of different groups were incubated for 24 h. An apoptosis detection kit was used for annexin V and PI staining. The expression of Akt, phosphorylation Akt, Bcl-2, Bax, caspase-3 were measured by Western blot., Results: The apoptosis rates of ASMCs in group Lep50, Lep100 and Lep200 were (3.97 ± 0.39)%, (1.88 ± 0.72)% and (0.77 ± 0.11)%, respectively, all significantly lower than that in the control group (7.38 ± 0.49)% (F = 89.57, P < 0.05). Furthermore, the concentration of leptin was negatively related to the apoptosis rate (r = -0.711, P < 0.05). The apoptosis rates of PI3K specific antagonist with Lep200 group (3.29 ± 0.36)% was higher than that of group Lep200 (0.77 ± 0.11)% (F = 89.57, P < 0.01). After the intervention of leptin, the expression of Bcl-2 was upregulated and positively correlated with leptin concentration (r = 0.939, P < 0.05); Bax was downregulated and negatively related to the leptin concentration (r = -0.908, P < 0.05); while the Bcl-2/Bax ratio was raised after leptin treatment (F = 20.56, P < 0.05). Leptin inhibited the activation of caspase-3 in the negative way. (r = -0.961, P < 0.05). The results also showed that leptin significantly increased phosphorylation of Akt that positively related to leptin concentration (r = 0.958, P < 0.05). Compared with group Lep200, the expression of Pho-Akt and Bcl-2 in PI3K specific antagonist with Lep200 group were downregulated (F = 32.93, 19.48, respectively, P < 0.05), while the expression of Bax and caspase-3 was increased (F = 10.10, 29.86, respectively, P < 0.05); the Bcl-2/Bax ratio was lower in group Lep200 as compared to the PI3K specific antagonist with Lep200 group (F = 20.56, P < 0.05)., Conclusion: Leptin can significantly inhibit ASMC apoptosis partially via the PI3K/Akt signaling pathway.

Aim: To explore the relationship between obesity and difficult-to-treat asthma by observing the expressions of leptin receptor (OB-R), interferon regulatory factor-1 (IRF-1) and glucocorticoid receptor-β (GR-β) in airway smooth muscle cells (ASMCs) of obese rats with asthma., Methods: Sixty rats were randomly divided into 4 groups, 2 groups with normal weight: control group (group A), asthmatic group (group B), and 2 groups with obesity: control group (group C), asthmatic group (group D). The trachea smooth muscle was obtained from the rats of each group, and ASMCs were isolated, purified, and cultured in vitro. Then the expression of OB-R mRNA was measured by RT-PCR, and the levels of IRF-1 and GR-β proteins were measured by Western blotting., Results: The expression of OB-R mRNA in airway smooth muscle cells in group B, C and D were higher than that in group A, while it in group D was significantly higher than group B and C. What's more, the levels of IRF-1 and GR-β proteins increased in group B, C and D as compared with group A, and were significantly higher in group D than in group B and C, respectively., Conclusion: The increased expressions of OB-R, IRF-1 and GR-β in ASMCs of obese rats with asthma may play a role in the onset of obese asthma and glucocorticoid resistance.

Objective: To observe the effects of moxifloxacin at various concentrations on the expression of Caspase-3, the alteration of mitochondria membrane potential (ΔΨm) and the apoptosis of airway smooth muscle cells (ASMCs), and to explore the possible mechanisms., Methods: ASMCs were derived from rat airway tissues and cultured in vitro. The cells were randomly divided into 5 groups including a control group and 4 groups to which moxifloxacin was added at different concentrations (40, 80, 120, 200 mg/L, groups M40, M80, M120 and M200 respectively). Then the cells of different groups were incubated for 48 h. An apoptosis detection kit was used for annexin V and PI staining, and JC-1 probe was employed to measure mitochondrial depolarization in ASMCs, and the protein of Caspase-3 was measured by Western blot., Results: The apoptosis rates of ASMCs in groups M40, M80, M120 and M200 were (2.95 ± 0.21)%, (7.39 ± 0.63)%, (13.39 ± 0.40)% and (21.20 ± 1.42)%, respectively, all of which were higher than that in the control group (0.94 ± 0.05)%, F = 399.77, P < 0.01. Furthermore, the concentration of moxifloxacin was positively related to the apoptosis rate (r = 0.974, P < 0.01). Compared to the control group (the ratio of orange-red fluorescence to green fluorescence was 10.02 ± 0.20), there was a shift from mitochondrial orange-red fluorescence to green fluorescence among groups with the concentrations of moxifloxacin increasing (6.54 ± 0.15, 4.48 ± 0.14, 2.25 ± 0.10 and 1.99 ± 0.12); the difference was significant (F = 1565.12, P < 0.01), and there was a dose-dependent response (r = -0.946, P < 0.01). The results of Western blot indicated that the expression of Caspase-3 increased with the concentrations of moxifloxacin increasing (0.45 ± 0.05, 0.59 ± 0.04, 0.69 ± 0.06 and 0.84 ± 0.04, respectively), and there was a very low expression of Caspase-3 in the control group (0.31 ± 0.03). The expression of Caspase-3 showed a positive correlation with the concentration of moxifloxacin (r = 0.979, P < 0.01). The apoptosis rate of ASMCs in the different groups had a remarkable correlation with the ΔΨm and Caspase-3 (r = -0.887, P < 0.01; r = 0.955, P < 0.01). There was also a remarkable negative correlation between ΔΨm and Caspase-3 (r = -0.951, P < 0.01)., Conclusion: Moxifloxacin was shown to promote ASMC apoptosis by altering ΔΨm.

Aim: To explore the effect of leptin on the proliferation of rat airway smooth muscle cells(ASMCs) and its possible mechanism., Methods: ASMCs were derived from rat airway tissue and cultured in vitro. RT-PCR and Western blot were used to verify the expression of leptin receptors on ASMCs. And then ASMCs were treated with leptin at different concerntrations (0-100 μg/L) for different periods of time (1-72 h), respectively. Cell proliferation was measured by CCK-8 assay. The expression of p-ERK and PI-3K in ASMCs were quantified by Western blot after being treated with leptin at different concentrations., Results: Leptin of various concentrations was used to treat different time could promote the proliferation of ASMCs in dose-dependent manner (r=0.837, P<0.01)and time-dependent manner (r=0.874, P<0.01). Western bot indicated that the expression of p-ERK and PI-3K increased with the increase of leptin concerntrations (P<0.05). The expression of p-ERK and PI-3K was a positive correlation with the concerntrations of leptin (r=0.793, P<0.01; r=0.746, P<0.01)., Conclusion: Leptin can significantly stimulate ASMCs proliferation and its mechanism may be correlated to activation of p-ERK and PI-3K.

Aim: to observe the effect of PolyI:C on the expression of TLR3 and inflammation cytokine in the airway smooth muscle cells ASMCs of rat, to investigate relationship between the expression of Toll-like receptor 3 (TLR3) in the airway smooth muscle cells and airway inflammation., Methods: airway smooth muscle cells were derived from rat airway tissue and were cultured in vitro, ASMCs were divided into 2 groups: control group and PolyI:C group, PolyI:C group was divided into the different time spots. The mRNA expression of TLR3 was measured by RT-PCR. The level of NF-kappaB was measured by Western blot. The concertration of IL-8 and Eotaxin in ASMCs supernatant were determined by ELISA., Results: the expression of TLR3 mRNA and NF-kappaB protein in the ASMCs in PolyI:C group was significantly higher than those in control group(P<0.05), the concentration of IL-8 and Eotaxin in the ASMCs in PolyI:C group was significantly higher compared to control group (P<0.05); and have time dependent manner., Conclusion: poly I:C promoted the expression of TLR3 in ASMCs, activated NF-kappaB, incresead the concentration of IL-8 and Eotaxin, involved in airway inflammation of asthma.

Objective: To explore the role of Rho kinase-1 (ROCK-1) in airway inflammation of asthma by observing the effects of fasudil, a specific inhibitor of ROCK-1, on the expression of Rho kinase-1 and airway inflammation in a mouse model of asthma., Methods: Twenty-four female BALB/c mice were randomly divided into 3 groups (n = 8 each): a control group, an asthmatic group and a treatment group. Mice in the asthmatic and the treatment groups were sensitized by intraperitoneal injection of OVA (25 microg) precipitated with 1 mg of alum in 200 microl of saline on days 1 and 15, and subsequently challenged by nebulization of 2% OVA on days 22-26. Mice in the control group were sensitized with Al(OH)3 saline and challenged with saline instead of OVA. Mice of the treatment group were injected intraperitoneally with fasudil (10 mg/kg) 1 h before each OVA challenge. All the mice were killed 24 h after the final challenge, and bronchoalveolar lavage fluid (BALF) was collected for counting total inflammatory cells and eosinophils (EOS). Cytokines and chemokines in BALF were measured by ELISA. The lung tissue slides were examined histologically. The protein and mRNA expression of ROCK-1 were measured by immunohistochemistry and RT-PCR respectively., Results: (1) OVA challenge in mice of the asthmatic group caused a marked increase in the number of the total cells and eosinophils in BALF (q = 25.909, 35.002, respectively, all P < 0.01). When fasudil was applied, both the total cell counts and the eosinophil numbers were significantly decreased. The total cell number was decreased from (1.45 +/- 0.12) x 10(9)/L to (0.89 +/- 0.09) x 10(9)/L (q = 16.676, P < 0.01), and the number of eosinophils was decreased from (0.52 +/- 0.06) x 10(9)/L to (0.20 +/- 0.04) x 10(9)/L (q = 21.537, P < 0.01). (2) Compared with the control group, OVA challenge in mice of the asthmatic group induced eotaxin, IL-5 and IL-13 release into BALF (q = 18.246, 23.009, 25.826, respectively, all P < 0.01). The eotaxin, IL-5 and IL-13 levels in BALF after OVA challenge were (45 +/- 8) ng/L, (157 +/- 23) ng/L and (429 +/- 46) ng/L, respectively. Application of fasudil resulted in inhibition of the augmented levels of eotaxin, IL-5 and IL-13 in BALF, decreased to (20 +/- 5) ng/L, (57 +/- 14) ng/L and (254 +/- 28) ng/L, respectively (q = 13.119, 17.503, 8.449, respectively, all P < 0.01). (3) Mice in the control group showed no detectable inflammatory response in the lung, whereas OVA-challenged mice induced infiltration of inflammatory cells around airways and blood vessels. The majority of the infiltrated inflammatory cells were eosinophils. Application of fasudil significantly reduced the infiltration of inflammatory cells in the peribronchial areas compared with the asthmatic mice. (4) The expression levels of ROCK-1 mRNA and protein in mice of the asthmatic group (0.67 +/- 0.05 and 1.09 +/- 0.06) were much higher than those of the control group (0.26 +/- 0.05 and 0.87 +/- 0.09) (q = 25.614, 8.156, all P < 0.01). When fasudil was administered, the expression levels of ROCK-1 mRNA and protein were significantly attenuated to 0.35 +/- 0.04 and 0.98 +/- 0.08, compared with those of the asthmatic group (q = 20.379, 4.135, all P < 0.01). (5) The expression level of ROCK-1 mRNA was positively correlated with the number of eosinophils and the levels of eotaxin, IL-5 and IL-13 in BALF (r = 0.709, 0.600, 0.613, 0.650, all P < 0.01)., Conclusion: Airway inflammation of bronchial asthma was improved by inhibiting expression and activity of ROCK-1 by fasudil, suggesting that ROCK-1 may be involved in asthmatic airway inflammation induced by OVA challenge.

Objective: To investigate the effects of leptin on airway inflammation and the expression of Th1/Th2 cytokines., Methods: The obesity and acute asthma models were established in 40 female SD rats, which were randomly divided into a normal weight control group (group A), a normal weight asthmatic group (group B), a normal weight intervention group (group C), an obese control group (group D) and an obese asthmatic group (group E). The airway resistance and airway responsiveness were calculated by transpulmonary pressure and gas flow rate. The numbers of leukocytes, eosinophils (EOS) and neutrophils (N) in bronchoalveolar lavage fluid (BALF) were counted. The concentrations of interleukin-4 (IL-4), interferon-gamma (IFN-gamma) and leptin in serum and BALF were determined by ELISA. The protein and mRNA expression of leptin was measured by Western blot and RT-PCR respectively., Results: The airway resistance in group C and E [(0.890 +/- 0.106) cm H2Oxml(-1)xs(-1), (1.024 +/- 0.096) cm H2Oxml(-1)xs(-1), (1.129 +/- 0.107) cm H2Oxml(-1)xs(-1), (0.946 +/- 0.104) cm H2Oxml(-1)xs(-1), (1.124 +/- 0.095) cm H2Oxml(-1)xs(-1), (1.135 +/- 0.105) cm H2Oxml(-1)xs(-1), respectively.] was increased significantly compared to group B [(0.638 +/- 0.128) cm H2Oxml(-1)xs(-1), (0.745 +/- 0.073) cm H2Oxml(-1)xs(-1), (0.773 +/- 0.090) cm H2Oxml(-1)xs(-1)] (q = 7.128, 8.712, 8.318, 11.300, 11.258, 11.447, all P < 0.05). The numbers of leukocyte and neutrophils in group C and E [(91 +/- 9) x 10(4)/ml, (108 +/- 21) x 10(4)/ml, (12.4 +/- 4.0) x 10(4)/ml, (14.2 +/- 5.9) x 10(4)/ml, respectively.] were increased significantly compared to group B [(79 +/- 7) x 10(4)/ml, (2.4 +/- 1.1) x 10(4)/ml] (q = 2.923, 7.063, 8.629, 10.182, all P < 0.05). The concentrations of IFN-gamma were [(42.3 +/- 3.5) ng/L, (45.1 +/- 4.8) ng/L, (19.2 +/- 1.8) ng/L, (20.3 +/- 1.5) ng/L] in group C and E respectively, which were significantly higher than those of group B [(16.5 +/- 1.4) ng/L, (9.3 +/- 1.0) ng/L] (q = 21.607, 23.952, 16.919, 18.799, all P < 0.05). The protein and mRNA expression of leptin in lung tissue in group C and E [(0.40 +/- 0.07) ng/L, (0.44 +/- 0.05) ng/L, (0.34 +/- 0.06) ng/L, (0.38 +/- 0.04) ng/L, respectively.] were remarkably higher than those of group B [(0.31 +/- 0.03) ng/L, (0.21 +/- 0.04) ng/L] (q = 4.648, 6.713, 8.222, 10.752, all P < 0.05)., Conclusion: Leptin could aggravate airway inflammation featured by infiltration of neutrophils and enhancement of Th1 type inflammation.

Aim: To explore the mechanism of asthma, by evaluating the changes of CCR3 and EOS expression in the lung tissues and bone marrow of Guinea pig asthmatic models at different times., Methods: Guinea pigs (GPs) were sensitized and challenged by OVA to establish the asthmatic model (A, B, C, D, E) . The GPs in control (N) were sensitized and exposed to sterile saline. The sensitized GPs in the models were killed at 30 min, 6 h, 12 h, 24 h and 48 h after challenged by OVA; while the GPs in control were killed at 12 h after saline challenge. The slides were prepared from peripheral blood and bone marrow and then stained with Wright's staining .The total number and percentage of EOS were counted and the expression of CCR3 and CD34 in bone marrow was detected by immunohistochemistry. The pathologic samples of lung tissues were stained with HE. The expression of CCR3 and CD34 of lung tissues was detected by immunohistochemistry., Results: (1)The expression of CCR3, CD34 and EOS in the bone marrow and peripheral tissue with allergic asthma was significantly higher than that in the controls. (2)After challenged by OVA , the expression of CCR3, CD34 and EOS was as fallows: it was at normal level in 30 min except the rise of CD34 rise in lung tissues, it rose and reached the peak from 6 h to 12 h, except the descent of CD34 in lungs; then it decreased in 24 h and reached normal level after 48 h. (3)The changes of bone marrow were earlier than peripheral tissue; The expression of CCR3 was earlier than the expression of CD34 and the recruitment of EOS.CCR3 and CD34 had linearity correlation with EOS except in lung tissues., Conclusion: There is a passage between bone marrow and lung tissue, through which CD34(+) stem cells and EOS passes The expression of CCR3 makes the quick recruitment of CD34(+) cells and EOS from bone marrow to lung tissue possible.