Justice Detained: The Effects of Deportation on Immigrant Families

In November 2002, driven by a growing awareness within the Asian and Pacific Islander immigrant communities that more and more people were getting deported, youth activists at AYPAL, based in Oakland, initiated a campaign to find out what was going on and what they could do about it. AYPAL found that the problem of deportation was much worse than the isolated incidents we had heard about, and it is only growing more severe. In 1996, Congress enacted the Illegal Immigration Reform and Immigrant Responsibility Act (IIRIRA), which made it a lot easier to deport immigrants, including many legal permanent residents who had lived in the United States for many years. They were considered deportable if they had committed any crime involving prison or probation time that added up to one year or more. (See "Overview of IIRIRA" section.)AYPAL's research findings:Hundreds of thousands of people are being deported every year to countries all around the world, and there was a huge increase in deportations from 1996 to 1998, coinciding with IIRIRA being implemented in April 1997.The overwhelming majority of "criminal removals" are for non-violent crimes.Deportations hurt families by potentially leaving hundreds of thousands of children who are left behind in poverty.Despite claims that immigrants are contributing to high crime rates, they are actually less likely than native-born citizens to commit crimes.Immigrants released from jail are less likely than the native born to be repeat offenders.Immigrants are being deported to countries that the US State Department deems too dangerous to travel to.Another reason besides IIRIRA for the huge increase in deportations is that many more people in general (both immigrants and native born) are being sent to prison and for longer sentences because of policy changes like "three strikes" and mandatory minimum sentencing

Both Basic and Acidic Amino Acid Residues of IpTxa Are Involved in Triggering Substate of RyR1

Imperatoxin A (IpTxa) is known to modify the gating of skeletal ryanodine receptor (RyR1). In this paper, the ability of charged aa residues of IpTxa to induce substate of native RyR1 in HSR was examined. Our results show that the basic residues (e.g., Lys19, Lys20, Lys22, Arg23, and Arg24) are important for producing substate of RyR1. In addition, other basic residues (e.g., Lys30, Arg31, and Arg33) near the C-terminus and some acidic residues (e.g., Glu29, Asp13, and Asp2) are also involved in the generation of substate. Residues such as Lys8 and Thr26 may be involved in the self-regulation of substate of RyR1, since alanine substitution of the aa residues led to a drastic conversion to the substate. The modifications of the channel gating by the wild-type and mutant toxins were similar in purified RyR1. Taken together, the specific charge distributions on the surface of IpTxa are essential for regulation of the channel gating of RyR1

Low-Dose Prasugrel in Patients with Resistance to Clopidogrel for the Treatment of Cerebral Aneurysms

Thromboembolism is one of the major complications of stent assisted coiling in treatment of cerebral aneurysm. Clopidogrel resistance is so common and prasugrel is more effective in its rapid and potent effect. We investigated changes in the value of P2Y12 resistance unit (PRU) when prasugrel was administered to patients with clopidogrel resistance. One hundred mg of aspirin and 75 mg of clopidogrel were administered for 5 days before the procedure, and PRU were examined. The resistance to clopidogrel was defined as the inhibition of PRU was less than 20%. PRU was re-examined after loading 20 mg of prasugrel. We treated 98 consecutive patients between January 2018 and July 2018, and 24 patients (24.5%) had resistance to clopidogrel. Nineteen patients were female. The mean PRU value at admission was 238.5±36.9 and the percentage inhibition value was 4.8±6.3%. After the use of prasugrel, the mean PRU and percentage inhibition values were measured as 124.9±49.9 and 48.0±19.24, respectively. All patients except one patient had a PRU inhibition value as a responder. There was no hemorrhage or thromboembolic complication during mean 1.5 months follow-up after embolization procedure. In conclusion, in patients resistant to clopidogrel, the low dose prasugrel seems to be effective in keeping the percentage inhibition value of PRU within the normal range in treatment of cerebral aneurysm. Further study will be needed to determine the optimal dose of prasugrel to enhance prevention effect of thromboembolism and to reduce hemorrhagic complications during stent assisted coiling

Interferometric detection of prostate specific antigen based on enzyme immunoassay

AbstractInterferometric detection of Prostate-specific antigen (PSA) based on enzyme immunoassay are investigated. Refractive index changes of substrate are measured for PSA detection. Michelson scheme of optical interferometer was used so as to be applicable to a disposable fluidic chip. When interferometer is used for the measurements of refractive index changes, the detection is over 8 times more sensitive than that of absorbance changes for the same amount of target protein

Novel Antidepressant-Like Activity of Caffeic Acid Phenethyl Ester Is Mediated by Enhanced Glucocorticoid Receptor Function in the Hippocampus

Caffeic acid phenethyl ester (CAPE) is an active component of propolis that has a variety of potential pharmacological effects. Although we previously demonstrated that propolis has antidepressant-like activity, the effect of CAPE on this activity remains unknown. The present study assessed whether treatment with CAPE (5, 10, and 20 µmol/kg for 21 days) has an antidepressant-like effect in mice subjected to chronic unpredictable stress via tail suspension (TST) and forced swim (FST) tests. CAPE administration induced behaviors consistent with an antidepressant effect, evidenced by decreased immobility in the TST and FST independent of any effect on serum corticosterone secretion. Western blots, conducted subsequent to behavioral assessment, revealed that CAPE significantly decreased glucocorticoid receptor phosphorylation at S234 (pGR(S234)), resulting in an increased pGR(S220/S234) ratio. We also observed negative correlations between pGR(S220)/(S234) and p38 mitogen-activated protein kinase (p38MAPK) phosphorylation, which was decreased by CAPE treatment. These findings suggest that CAPE treatment exerts an antidepressant-like effect via downregulation of p38MAPK phosphorylation, thereby contributing to enhanced GR function

In vitro antioxidant and anti-adipogenic effects of slendesta, standard potato extracts containing 5% protease inhibitor II

Background: The objective of the present study is to observe the anti-adipogenic effects of Slendesta (SLD), a standard potato protein extracts containing 5% potato protease inhibitor II (PI2) on the 3T3-L1 preadipocytes which are able to differentiate into mature adipocytes and accumulate lipids, as an obesity model with cytotoxicity and antioxidant effects.Materials and Methods: The cytotoxicity of SLD was observed against 3T3-L1 preadipocyte cell line by MTT assay, and also antiadipogenic effects were observed through lipid accumulation assay during 3T3-L1 differentiation as comparing with N-Acetyl-Lcysteine (NAC). In addition, antioxidant effects of SLD were detected by free radical scavenging capacity and superoxide dismutase (SOD)-like activity as comparing with ascorbic acid.Results: The SLD showed obvious cytotoxicity against 3T3-L1 pre-adipocyte cell line at higher concentrations, from 1.5 mg/ml for 72 h treatment, and the cytotoxic IC50 of SLD after 24, 48 and 72 h treatment times were detected as 10.11 ± 0.67, 5.71 ± 0.37 and 5.34 ± 0.21 mg/ml, respectively. The SLD also concentration-dependently inhibited the lipid accumulations formatted during 3T3-L1 cell differentiations. The adipogenic specific genes including PPARγ, C/EBPα, C/EBPβ and leptin were found to be reduced in SLD and NAC-treated cells compared to control cells. Furthermore, the SLD effectively showed DPPH radical scavenging activity (IC50 = 161.98 ± 64.65 μg/ml) and SOD-like effects (IC50 = 284.54 ± 54.47 μg/ml), and the cellular ROS was significantly inhibited in the SLD-treated cells compared to control cells.Conclusion: The results suggest that SLD effectively inhibit the differentiations of 3T3-L1 preadipose cell probably through antioxidant activities and direct cytotoxicity in case of higher concentration, along with satiety effects mediated by increases of circulating cholecystokinin. These findings are considered as direct evidences that SLD may serve as a predictable functional ingredient for obesity as an alternative therapy.Key words: Slendesta, potato protease inhibitor II, 3T3-L1 cell, cytotoxicity, anti-adipogenic effects, antioxidant effects

Endoplasmic Reticulum Stress Induces MUC5AC and MUC5B Expression in Human Nasal Airway Epithelial Cells

Objectives Endoplasmic reticulum (ER) stress is known to be associated with inflammatory airway diseases, and three major transmembrane receptors: double-stranded RNA-activated protein kinase-like ER kinase, inositol requiring enzyme 1, and activating transcription factor 6 (ATF6) play important roles in ER stress-related proinflammatory signaling. However, the effects of ER stress and these three major signaling pathways on the regulation of the production of airway mucins in human nasal airway epithelial cells have not been elucidated. Methods In primary human nasal epithelial cells, the effect of tunicamycin (an ER stress inducer) and 4-phenylbutyric acid (4-PBA, ER stress inhibitor) on the expression of MUC5AC and MUC5B was investigated by reverse transcriptasepolymerase chain reaction, real-time polymerase chain reaction, enzyme immunoassay, and immunoblot analysis. Small interfering RNA (siRNA) transfection was used to identify the mechanisms involved. Results Tunicamycin increased the expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules, including spliced X-box binding protein 1 (XBP-1), transcription factor CCAAT-enhancer-binding protein homologous protein (CHOP), and ATF6. In addition, 4-PBA attenuated the tunicamycin-induced expressions of MUC5AC and MUC5B and the mRNA expressions of ER stress-related signaling molecules. Furthermore, siRNA knockdowns of XBP-1, CHOP, and ATF6 blocked the tunicamycin-induced mRNA expressions and glycoprotein productions of MUC5AC and MUC5B. Conclusion. These results demonstrate that ER stress plays an important role in the regulation of MUC5AC and MUC5B via the activations of XBP-1, CHOP, and ATF6 in human nasal airway epithelial cells

Magnolin targeting of ERK1/2 inhibits cell proliferation and colony growth by induction of cellular senescence in ovarian cancer cells

Ras/Raf/MEKs/ERKs and PI3 K/Akt/mTOR signaling pathways have key roles in cancer development and growth processes, as well as in cancer malignance and chemoresistance. In this study, we screened the therapeutic potential of magnolin using 15 human cancer cell lines and combined magnolin sensitivity with the CCLE mutaome analysis for relevant mutation information. The results showed that magnolin efficacy on cell proliferation inhibition were lower in TOV‐112D ovarian cancer cells than that in SKOV3 cells by G1 and G2/M cell cycle phase accumulation. Notably, magnolin suppressed colony growth of TOV‐112D cells in soft agar, whereas colony growth of SKOV3 cells in soft agar was not affected by magnolin treatment. Interestingly, phospho‐protein profiles in the MAPK and PI3 K signaling pathways indicated that SKOV3 cells showed marked increase of Akt phosphorylation at Thr308 and Ser473 and very weak ERK1/2 phosphorylation levels by EGF stimulation. The phospho‐protein profiles in TOV‐112D cells were the opposite of those of SKOV3 cells. Importantly, magnolin treatment suppressed phosphorylation of RSKs in TOV‐112D, but not in SKOV3 cells. Moreover, magnolin increased SA‐β‐galactosidase‐positive cells in a dose‐dependent manner in TOV‐112D cells, but not in SKOV3 cells. Notably, oral administration of Shin‐Yi fraction 1, which contained magnolin approximately 53%, suppressed TOV‐112D cell growth in athymic nude mice by induction of p16Ink4a and p27Kip1. Taken together, targeting of ERK1 and ERK2 is suitable for the treatment of ovarian cancer cells that do not harbor the constitutive active P13 K mutation and the loss‐of‐function mutations of the p16 and/or p53 tumor suppressor proteins