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SBI PO Training Call letter 2017 for pre exam training is released by SBI. You can now download SBI PO Pre-training call letter 2017 before appearing in the training. State bank of India will take the pre-exam training examination for the SC/ST/ Minority candidates. A large number of people belongs to this category and those all can register for this examination.
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SBI PO Training Call letter 2017
After submission the SBI PO application form now the candidates are waiting for their SBI PO pre-training call letter download 2017 for all reserved category candidates on its official website. Candidates are advised to visit our website and download their SBI PO Training Call letter for an upcoming exam.
State Bank of India Probationary officer call letter is issued for those aspirants who have successfully submit their application form along with SBI PO application fees and those who belong to SC/ST/ Minority category. To download SBI PO Training Call letter, candidates are advised to visit our website and download SBI PO call letter 2017 for all reserved category candidates can download it SBI official website. We also mentioned the direct link to download SBI PO Training Call letter.
SBI PO Pre Exam training call letter 2017
SBI will soon issue SBI PO Training Call letter for all candidates who belong to these categories they all are eagerly waiting for download their SBI PO Pre-exam training call letter 2017 through visit on the same website.
Now the SBI PO pre-training call letter 2017 is available on its official website and you can easily download through the given below link. We will update the link time to time and you are advised to bookmark our website to check the latest updates regarding SBI PO exam 2017 pre-examination training call letter released.
As per the SBI PO notification, they mentioned that the pre-exam training will be conducted for SC/ST/ Minority aspirants. SBI PO exam training call letter contains candidates name, address, exam time & and date, roll number and other important instruction also mentioned in the call letter.
We suggest to all applicants they must carry the SBI PO training call letter 2017 at the time they go for examination because without this call letter you will be not allowed to sit in this exam. In this, we provide some useful instructions for candidates.
How to download SBI PO Training Call letter?
- Go to the official website of SBI.
- Find the link SBI PO Pre exam training call letter 2017 and click on it.
- Fill your registration number and DOB.
- Click on the submit button.
- Admit card will be displayed on the screen.
- Save it and take a printout of it for future use.


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Iqopton toll
(202) 707-3000 or 1-877-476-0778 (toll free) Revised: 28-Oct-2013.Ouray and Silverton toll road Contributor Names. ppmsca 17845 //hdl.loc.gov/loc.pnp/ppmsca.17845 Library of Congress Control Number 2008676345.
Sign In to Investor Connect - Log inIosif Vulcan (n. 31 martie 1841, Holod, Bihor - d. 8 septembrie 1907, Oradea) a fost un publicist şi scriitor român, animator cultural, membru al Academiei Române.
The Aquatic Exercise Association (AEA) is a nonprofit organization committed to the advancement of aquatic fitness, health and wellness worldwide.Ukjent Fødested? Adopterte kan risikere å ikke få reise til USA- Aasne Veberg fikk norsk statsborgerskap i 1971 da hun ble adoptert fra Sør-Korea.
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Forex Mini Lote Vs Micro Lote Diferencia

El riesgo está allí en el comercio de Forex, pero este riesgo puede ser gestionado si el comerciante se.
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Pak shelling kills another soldier on LoC, toll reaches 14
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Toll Road. 10/19, 1989. Image. Retrieved from the Library of Congress, https://www.loc.gov/item/2012642380. (Accessed April 16, 2016.) APA citation style.

subset: commoncrawl


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ChristCare Groups
In a large church like Desert Hills Lutheran, it takes a concerted effort to make simple contacts turn into true connections. These connections are meant to help each of us grow in the Lord whether it is through service, fellowship, Bible study or prayer/worship. We establish these small groups where people become much more than just a contact to each other. ChristCare (a small group ministry) is part of the Stephen's Ministries from St. Louis, MO. ChristCare groups are designed to assist the congregation in meeting its mission of Celebrating Grace, Making Disciples and Making a Difference.
How can ChristCare help us meet this congregational mission? They do so with the four functions listed below.
♦ ChristCare Group functions during each weekly meeting:
Check the church calendar on the home page for current times and meeting places of specific ChristCare groups. If you have been in a ChristCare group in the past, we would enjoy hearing from you.
2150 S. Camino del Sol, Green Valley, AZ 85622


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Have HVAC Questions? Ask an HVAC Expert for Answers
Hello and thanks for using this service, if you have been waiting do not worry or get upset I am just one of the techs on here and I try to get to as many customers as I can and I just picked up your question now. Please give me time to respond sometimes I get your replies late so there may be a significant delay in responses. Please be patient and often I will ask you questions to narrow down the issue to get is diagnosed correctly.
Do you get a flame briefly?
Ok have you tried to clean out the orifices on the burner, they may be plugged up causing the unit not to light. That often happens
Yes take the cover off to get at them. Also you can check if the valve is getting 24 volts when the ignitor is glowing. If so then either you have a gas supply issue, clogged orifices or bad valve.
We are on the honor system for our time, all I ask is please rate my service using the STAR RATING LINK on your page before you leave. If you are not happy with the service please let me know before leaving a negative rating. This is the only way I am paid or credited through the site for my time. This will also allow you to get directly back to me for FREE follow up questions and tips are greatly appreciated! Thanks


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The Argentinean Junta Drives Out Criminals is a Timeline Event that can occur from 1976 to 1979.
While the event is happening, several criminals may disembark every time a ship arrives on the island as criminals flee Argentina to escape the death squads.
La Guerra Sucia (the Dirty War) was a period in Argentine history where the government cracked down on militant and peaceful left-wing forces alike. Death squads used the pretext of hunting for violent guerrillas as cover for assassinating or kidnapping anyone they saw as an ideological enemy, resulting in thousands of disappearances. Argentina now considers the actions of the junta genocidal and holds a public holiday in memory of the victims.


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[Contains BoyxBoy/Yaoi. Don't Like, Don't Read.]
Sasuke Uchiha, one of the last living Nekos. Since his kind is almost extinct he is hunted, chased, and wanted dead by most. Getting into bloody fights, stealing, and even more mischief soon comes to bite him on the tail.
Almost losing his life, he thinks it's all over and that he in fact failed the Uchiha Clan and especially his mother. Well that is until a certain blonde with blue eyes and cat whiskers stumbles onto the bloody Neko.
Naruto Uzumaki, his name is, takes the Raven kitten home and cleans him up. Little did he know that the decision of taking Sasuke back home and having him as his 'pet' would change his life forever.
Disclaimer: I do not own Naruto!
[Also Has slight NaruKiba...]
_-Hikaru-Hitachiin-_ Jun 17
For some reason I thought that said 'cleansed' and I was like... is some weird ritual about to happen... then I reread it like 8 times xD
Deaths_a_fucker_69 Jun 15
Well naruto already has a fox demon so he's a fox neko I guess Idk so I guess sasuke can be a Neko
the_yaoigoddess Nov 03, 2016
I'm actually considering making this ship 'shippable' from my point of view at the sake.... *searches for fanart* *nosebleeds* new ship ;-;
Fujoshi_Otakuz Jun 30, 2016
I thought this was SasuNaru 😢 WHY HAVE YOY BETRAYED ME BOOK COVER?!?
TwilightGrassi Aug 18, 2016
No.... No..No..No!! We all like Sasunaru not whatever Kiba and Naruto's ship name is
AiMila Sep 06, 2016
No! Naru Kiba ain't the one!!! Break up with him this instant mister!!!


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Miami Vice
Miami Vice is a 1980's TV show that starred Don Johnson and Philip Michael Thomas as two vice detectives working undercover in Miami. Their look was characterized by pastel or brightly colored T-shirts under suit jackets. Don't forget to show a few chest hairs to complete the look.
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- Keds Champion Slip-On Canvas Sneakers in White $38
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About the Author
Dr. Mario addict and wannabe weight-lifter.
Related Posts
August 29, 2013 by Tom
Michael Knight
In Knight Rider, Michael Knight (David Hasselhoff) is a police officer who's double-crossed by an informant and nearly killed. After undergoing reconstructive surgery and taking on a new identity, he fights crime as a secret agent for Knight Industries. But all we really care about is KITT, the talking Trans Am.October 12, 2016 by Luca
Dirty Harry
In Dirty Harry, Harold Francis Callahan (Clint Eastwood) is a police detective working the case for a psychopathic serial killer calling himself Scorpio. Dirty Harry doesn't hesitate to cross professional and ethical boundaries, dispensing his own brand of justice with his trademark .44 Magnum.
May 13, 2015 by Tom
"Scarface" Tony Montana
In Scarface, Tony Montana (Al Pacino) is a Cuban refugee who arrives in Miami with nothing in his pockets. Through determination and a strong dose of violence, he rises to become a powerful drug kingpin. Don't forget to accessorize with Tony's "little friend".October 21, 2013 by Tom
Alonzo Harris
In Training Day, Detective Alonzo Harris (Denzel Washington) helps the bright-eyed Jake Hoyt (Ethan Hawke) learn the ropes on his first day as LAPD. But this isn't your typical HR orientation, and what Alonzo puts him through definitely ain't OSHA approved.
October 19, 2013 by Kristina
Thomas Magnum of Magnum P.I.
Tom Selleck played the role of Thomas Magnum in Magnum, P.I. He made life in Hawaii look hard as a private eye by driving around in a Ferrari, donning short shorts and smoking the occasional stogie.November 21, 2013 by Jaime
Dick Tracy's wardrobe is pretty simple in comparison to other hard-hitting superheroes. Although he does manage to stand out among other detectives with his bright yellow trench coat and matching hat. Without these token pieces you may end up looking like you just got home from work.
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We examined the effect of aging on Fas ligand (FasL) function in a mouse model of choroidal neovascularization (CNV).
Young and aged mice were laser treated to induce CNV. Bone marrow chimeras were performed between young and aged mice. FasL protein expression was examined in the eye and soluble FasL (sFasL) was measured in the blood. Young and aged mice were treated with a matrix metalloprotease (MMP) inhibitor and systemic sFasL was neutralized by antibody treatment. Macrophages from young and aged mice were tested for sFasL-mediated cytokine production and migration.
The elevated CNV response observed with aging was dependent on bone marrow–derived cells. FasL expression in the eye was increased with age, but decreased following laser treatment. Aged mice had higher levels of sFasL in the blood compared to young mice. Systemic treatment with an MMP inhibitor decreased bloodborne sFasL, and reduced CNV in young and aged mice. Systemic neutralization of sFasL reduced CNV only in aged mice. sFasL increased cytokine production in aged macrophages and proangiogenic M2 macrophages. Aged M2 macrophages had elevated Fas (CD95) expression and displayed increased migration in response to sFasL compared to M1 macrophages derived from young animals.
Age modulates FasL function where increased MMP cleavage leads to a loss of function in the eye. The released form of FasL (sFasL) preferentially induces the migration of proangiogenic M2 macrophages into the laser lesions and increases proangiogenic cytokines promoting CNV. FasL may be a viable target for therapeutic intervention in aged-related neovascular disease.
Age-related macular degeneration (AMD) is a progressive disease that leads to irreversible visual impairment and blindness in millions of people globally. The neovascular form of AMD, which is characterized by choroidal neovascularization (CNV), is the most aggressive form and accounts for the vast majority of blindness associated with this disease. This makes identifying therapies that can control neovascularization a top priority. However, few treatments are available at this time. Anti-VEGF therapy has proved effective at slowing the progression of neovascular AMD, but this treatment does not permanently prevent the progression to blindness.1,2 Consequently, studies exploring the basic mechanisms of disease that might lead to novel therapeutics are an intense area of study.
Age is a significant risk factor in the development of AMD as a number of age-related changes in the eye are associated with the increased incidence of disease.2–4 Aging effects have been noted in animal models5; however, many animal studies designed to explore the mechanisms of AMD are performed on relatively young animals,6–11 which may not take into account age-related factors that might modulate disease, such as changes in the immune system, which may have a significant role in animal models and human AMD.12–14 The laser-induced mouse model of neovascular AMD, which is influenced by macrophages,7,10,11 also is influenced by aging.15–17 However, the effects of aging on the immune mechanisms in this model have not been examined thoroughly to our knowledge. This is in spite of the fact that aging alters immune responses18,19 and macrophage function.16,20
Recently, we described a complex role for macrophages in regulating CNV in this mouse model by demonstrating that macrophages can be pro- or antiangiogenic depending on the conditions of their activation.7,16 In these studies proinflammatory M1 macrophages were inhibitory to the CNV response, while M2 macrophages promoted neovascularization. Furthermore, eyes of aged mice were enriched for M2 macrophages and this accounted for the age-dependent increase in the neovascular response. Thus, the intensity of the neovascularization was the result of a balance between M1 and M2 macrophages, not the absolute number of these cells in the eye.7,17 It still is not clear, however, why age alters macrophage function and what local factors might favor the functions of macrophage subtypes.
Immune privilege is a term applied to organs that have a unique relationship with the immune response. These sites prohibit the spread of inflammation at the expense of immune effector mechanisms, since even minor episodes can threaten organ integrity.21 An important part of immune privilege is the constitutive expression of the death-inducing ligand CD95L (hereafter FasL) on the parenchymal cells of the eye that inhibits inflammation by inducing apoptosis in invading inflammatory cells expressing the Fas receptor (CD95).22–24 Additional studies have extended this concept to pathogenic neovascularization demonstrating an important role for FasL in controlling neovascular responses of the cornea,25 retina,26 and choroid27; an idea that has been extended to tumor biology.28,29 Importantly, the effect of FasL in controlling neovascularization is influenced strongly by the activity of matrix metalloproteases (MMP), which cleave FasL from the cell surface diminishing its proapoptotic function during angiogenic responses. Inhibition of MMP prevents FasL cleavage, and restores its function in the cornea30 and retina.8 The effect of aging on FasL expression and function in the eye currently is unknown and, since this proapoptotic protein is critical to the integrity of the eye,22,31 we thought a better understanding of the changes in FasL with aging should be pursued. Studies presented here revealed that FasL function changes with age due to the increased activity of MMP, which cleave surface FasL, reducing its ability to limit CNV. This resulted in increased levels of soluble FasL (sFasL) release into the blood where bloodborne sFasL impacts the CNV response significantly through differential effects on macrophage subtypes. Specifically, M2 macrophages that dominate the CNV response in aged mice7,16,21,22 produce high levels of VEGF and display enhanced Fas-mediated migration in response to sFasL. M1 macrophages, the dominate macrophage subtype in younger animals, are much less responsive to sFasL in cytokine induction and migration assays. We concluded that increased release of sFasL from the injured eye promotes proangiogenic macrophage infiltration, accounting for elevated CNV responses with age. This also suggests that sFasL might be a therapeutic target in the treatment of blinding eye disorders.
C57BL/6J (stock number 000664), Fasflox/flox (stock number 007895), and CreLysm (stock number 004781) mice were purchased from the Jackson Laboratories (Bar Harbor, ME). The Fasflox/flox mice were crossed to the CreLysm to generate the conditional knockout of Fas in myeloid cells.32 The conditional knockout line was verified as congenic with the C57BL/6J strain by microsatellite analysis (Research Animal Diagnostic and Investigative Laboratory [RADIL], University of Missouri, Columbia, MO). Aged mice were generated by purchasing retired breeders (7 months) and maintaining them in our animal facility until the desired age. Young animals typically were 6 to 12 weeks, while aged mice were used when older than 60 weeks. Specific ages are indicated in Figures 1 through through6.6. All animal experiments were approved by the Animal Studies Committee at Washington University School of Medicine, and conform to the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research. All experiments contained at least 5 mice per group and were repeated a minimum of 3 times.
CNV was induced by rupture of the RPE and underlying Bruch's membrane with a krypton laser in young or aged mice, as described.7,16,27 Mice were anesthetized using intraperitoneal ketamine hydrochloride (86.9 mg/kg) and xylazine (13.4 mg/kg), and their pupils were dilated. Using a krypton red laser, 4 laser burns were placed around the optic nerve (0.05 seconds, 50 μm, 150 mW). After 7 days, the animals were perfused with 3% FITC-conjugated high-molecular weight dextran (2,000 kDa). Eyes were enucleated immediately and fixed in 4% paraformaldehyde for 1 hour. A dissecting microscope was used to remove the cornea and lens, and gently separate the retina from the underlying choroid and sclera. Microscissors were used to make four radial incisions in the sclera-choroidal eyecup to prepare choroidal flat mounts on glass slides. A drop of gel-mount fixative and a glass coverslip were placed on each slide. The choroidal flat mounts were analyzed for presence of CNV by confocal microscopy. The extent of choroidal neovascularization was quantified by Metamorph Imaging software (Universal Imaging Corporation, Downington, PA) and reported as volume of the fluorescence.
To neutralize MMP, in vivo doxycycline (Sigma-Aldrich Corp., St. Louis, MO) was dissolved in PBS and administered daily starting on the day of laser treatment by intraperitoneal (IP) injection. Doses were administered on a mg/kg basis and are indicated in Figures 1 through through6.6. These doses have been used successfully and without side effects in several mouse models.8,33–36 Anti-CD178 (anti-FasL, LEAF) or control hamster IgG (IgG isotype) was injected on the day of laser treatment (day 0), day 1, and day 2 (100 μg per injection per mouse in 150 μL of PBS.
Bone marrow chimeras were constructed by infusing isolated bone marrow from 6-week young mice into lethally irradiated 60-week aged mice (or vice versa) by established protocols.22,27 In brief, mice received 11 Gy (1 Gy = 100 rads) of radiation before receiving 107 bone marrow cells. Mice were rested for 6 weeks before use in the laser-induced CNV model.
Mice were pre-bled 48 hours before laser treatment. They then were laser treated and injected with PBS or doxycycline. Mice were bled at 48 hours via tail vein. The blood samples were centrifuged at 1800g for 5 minutes, and serum was frozen at −70°C for subsequent sFasL assays. Serum concentrations of sFasL were measured with commercially available ELISA kits (R&D Systems, Minneapolis, MN) according to the manufacturer's instructions. The concentration in serum samples was determined from the standard curve and had a detection limit of 3.6 pg/ml. Levels below the detection limit were coded as 0 pg/mL and were included in the analysis. All assays were conducted in triplicate.
Mice were killed, and eyes were enucleated and dissected. RPE/choroid/sclera complexes were treated with trypsin (2 mg/mL; Life Technologies, Grand Island, NY) for 30 minutes at 37°C, and the RPE cell layer was peeled off gently using fine forceps. RPE cells were homogenized in ice-cold lysis buffer and centrifuged for 10 minutes at 15,000g at 4°C. Supernatant was collected and protein concentration was determined by bicinchoninic acid (BCA) protein assay. A total of 30 μg of protein was mixed with loading buffer (Sigma-Aldrich, Corp.), boiled for 5 minutes, and loaded onto a 10% Bis-Tris Nu-PAGE gel (Life Technologies). For Western blotting, proteins were transferred to nitrocellulose membranes and then blocked with 5% skim milk in tris-buffered saline, 0.1% Tween-20 (TBST) for 1 hour at room temperature. Blots were incubated with primary antibody overnight at 4°C and followed by corresponding secondary horseradish peroxidase-conjugated antibodies (Cell Signaling, Danvers, MA). Immunoreactive bands were determined by exposing the nitrocellulose blots to chemiluminescence solution and exposing to autoradiography film. Actin was used as the loading control.
Macrophages were prepared from bone marrow cultures. Bone marrow was isolated from proximal limb bones as described previously.7 Briefly, all muscle tissue was removed from the bones and the bones were washed in 70% alcohol for 5 seconds before two washes in PBS. The ends of the bones were cut with scissors and the marrow harvested by flushing with RPMI-1640 medium using a syringe and 25-gauge needle. Isolated bone marrow cells (2 × 105/mL) were cultured in RPMI-1640 with 10% FBS along with 1000 U/mL granulocyte macrophage colony-stimulating factor (GM-CSF, for M1 macrophages) or macrophage colony-stimulating factor (M-CSF, for M2 macrophages)37,38 for 10 days in 100 mm petri dishes (final volume 10 mL). On days 3 and 6, an additional 500 U/mL and 1000 U/mL GM-CSF (or M-CSF) were added, respectively. On day 10, the nonadherent cells containing dendritic cells were discarded. The adherent cells were removed and harvested mechanically with a cell scraper. Cells were greater than 90% CD11b+ as determined by flow cytometry. M1 and M2 polarization was verified by assessing cytokine profile following lipopolysaccharide (LPS) stimulation (100 ng/mL). Fas expression was tested examined by flow cytometry before and after LPS stimulation (100 ng/mL) for 24 hours.
Tests were conducted using transwell permeable supports (24 well format; Corning/Costar, Corning, NY) with a 5 μm pore size polycarbonate membrane insert separating the upper and lower chambers. Macrophages (1.5 × 105) were seeded in the upper chambers with varying concentrations of recombinant mouse sFasL (0–1; 1 nM = 18.5 ng), while the chemoattractant recombinant mouse Ccl2 (10 ng/mL) was placed in the lower chamber. Cells only in the upper chamber and medium only in the lower chamber served as a negative control. After incubation at 37°C for 2 hours, the inserts were removed carefully, and cells that had migrated into the lower chamber were allowed to settle at 37°C for another 2 hours. Cell numbers in the lower chambers were counted at 100× magnification and at least 10 randomly chosen fields were counted. Duplicate chambers were run for each experiment that was repeated at least 3 times. Data are expressed as mean ± SE.
Macrophages (young and aged) were treated with varying concentration of sFasL and LPS (200 ng/mL) for 24 hours and the supernatants harvested by centrifugation. In some experiments 2 ng/mL mouse recombinant IFNγ was included. TNFα, IL-10, IL-6, and VEGF were measured by ELISA (R&D Systems) according to the manufacturer's instructions.
Recombinant proteins Ccl2, IL-10, M-CSF, GM-CSF, TNFα, and human sFasL were purchased from Peprotech (Rocky Hill, NJ). Mouse IFNγ was purchased from Thermoscientific (Rockford, IL). Anti-CD178 (LEAF), Control Armenian Hamster IgG (LEAF), Anti-CD11b-PE were purchased from Biolegend (San Diego, CA). Anti-FasL (C178) and anti- actin-HRP for Western blots were purchased from Santa Cruz Biotechnology (Dallas, TX). E. coli LPS O55:B4 was purchased from Sigma-Aldrich, Corp. Anti-Fas–biotin was purchased from Life Technologies, Anti-F4/80 FITC and Anti-CD11b-APC from eBioscience (San Diego CA), and Anti-rabbit HRP from Cell Signaling.
Differences between the control and treatment groups in CNV experiments were evaluated on a pairwise basis using a generalized linear modeling approach, adjusting for correlation between the samples taken from each mouse using a repeated measures method. We report P values for these comparisons, unadjusted for multiple comparisons as the comparisons were established a priori. All statistical analyses were conducted using SAS Proc GLM (SAS 9.1.3; SAS Institute, Cary, NC). P < 0.01 was considered significant and these values are indicated in all Figures by an asterisk (*). Differences in macrophage migration and cytokine responses were evaluated by a Student's t-test. P < 0.05 was considered significant and indicated in all Figures by an asterisk (*).
Previous studies have shown that with increased age the CNV response in the mouse model is elevated following laser treatment,5 and these results are confirmed in Figure 1A, which shows that beginning at 52 weeks of age a consistent and reproducible increase in CNV was observed. That this was related to bone marrow–derived cells was explored by constructing radiation bone marrow chimeras where syngeneic bone marrow cells from young (6 weeks) and mice (60 weeks) aged were transferred to lethally irradiated young (6 weeks) or aged (60 weeks) recipients. Six weeks following bone marrow reconstitution, mice were laser treated and the CNV response was assessed on day 7. Figure 1B shows that when aged mice were reconstituted with young bone marrow CNV responses were similar to what was observed in young animals given young bone marrow. In contrast, when bone marrow from aged mice was present in young or aged mice, CNV responses were elevated consistently. These results suggested that it is age-dependent changes in the bone marrow–derived precursor cells that dictate the effect of aging on CNV.
The CNV response in this model is regulated by the expression of FasL on RPE cells, such that loss of FasL function increases the response,8,27 while FasL overexpression can diminish CNV.9 Consequently, we asked whether FasL expression in RPE cells was diminished with age and if this also might contribute to the elevated CNV response. Using an antibody that identifies the extracellular domain of the protein, elevated FasL protein expression in the RPE was detected in the untreated aged eyes compared to younger animals (Fig. 2A, 37 kDa band). However, when expression in the RPE was examined following laser treatment, a reduction in FasL was observed in aged mice (Fig. 2B). Thus, in spite of the elevated FasL expression with aging, laser injury reduced expression significantly compared to young animals, suggesting other factors related to age may be influencing the expression of this protein on RPE cells.
The expression of FasL on the cell surface is regulated tightly by several factors, including the activity of proteases.8,24,39 In the laser-induced CNV model, FasL is cleaved from the surface of RPE cells by MMP, resulting in the release of a cleavage product (sFasL) that can be detected in the blood maximally at 48 hours post-laser. Neutralizing MMP decreased the blood levels of sFasL, stabilized FasL on the surface of the RPE, and reduced CNV.8 Since increased MMP activity has been linked to AMD and increasing age,40–43 we asked whether the reduction of FasL in the eye following laser treatment of aged mice was the result of cleavage by MMP.8 Initially, we measured the level of bloodborne sFasL in young and aged mice, and found that at 48 hours aged animals had significantly higher levels compared to young animals (Fig. 2C). That elevated sFasL was related to MMP function was demonstrated by treating mice with doxycycline following laser treatment. In young and aged mice doxycycline treatment diminished the level of bloodborne sFasL (Fig. 2C) as well as CNV response (Figs. 2D, D,2E).2E). Thus, increased cleavage of FasL by MMP with age can account for the decrease in RPE-associated FasL and the elevated blood levels observed with age.
The soluble form of FasL (i.e., sFasL) can have potent immunoregulatory properties apart from the induction of apoptosis,31,44–46 including induction of cell migration in macrophages47 and neutrophils.48 Thus, sFasL released from the eye might have similar functions in the laser-induced CNV model. We tested the idea by systemically neutralizing sFasL with an anti-FasL antibody following laser treatment. While anti-FasL treatment had a little effect on CNV in young mice (Fig. 3A), it reduced the CNV response significantly in aged mice (Fig. 3B). Notably, antibody neutralization reduced the response in aged mice, but it did so only to the level of the maximal response observed in young animals. This consistent finding suggested that with aging sFasL may have additional biological properties that were not detectable when the laser model was performed in younger animals.
Macrophages regulate the CNV response based on their subtype, such that intensity of neovascularization is dependent on a balance between antiangiogenic M1 macrophages and proangiogenic M2 macrophages.7,16,17 In young animals, M1 macrophages are the predominant subtype in the laser lesions, but with advancing age the M2 macrophages dominate the response elevating CNV.16 An interesting explanation for our results would be that sFasL, which is elevated in aged mice after laser treatment (Fig. 2), has different effects on macrophages derived from young and aged animals. This also would account for the differential effect of neutralizing sFasL in young and aged animals (Fig. 3). We tested this idea by examining 2 parameters of macrophage function, cytokine production and migration, with the idea that macrophages from young and aged mice would response differently to the presence of sFasL, and this would be indicative of the macrophage subtype present. Macrophages were prepared from bone marrow cultures of young and aged animals, and their ability to produce VEGF, IL-10, and IL-6 were determined. sFasL treatment alone induced substantial VEGF production in aged macrophages without the need for an additional stimulus (Fig. 4A). This effect was reversed when IFNγ, an inflammatory cytokine that promotes M1 macrophage function,7,16 was added. In response to sFasL, neither young nor aged macrophages produced IL-10 (Fig. 4B); however, when stimulated with the TLR4 agonist LPS in conjunction with sFasL significant quantities of IL-10 were detected. In contrast, these two cytokines that are important for elevated CNV in aged animals7,16 were produced in much lower quantities by young macrophages. Production of the cytokine IL-6, which is a major cytokine produced by M1 macrophages, was elevated in response to sFasL (+ LPS) in young macrophages, but to a much greater degree compared to aged macrophages (Fig. 4C).
In addition to regulating cytokine production, locally produced sFasL has been shown to enter the periphery and enable mononuclear cell migration to sites of injury. This sFasL-mediated tissue infiltration resulted in enhanced injury and cellular damage.47 In keeping with the differential cytokine response in young and aged macrophages, we tested whether sFasL might promote preferentially the migration of macrophages depending upon their age. Bone marrow–derived macrophages were prepared from young and aged bone marrow, and tested in a directed migration assay using Ccl2, a chemokine critical to macrophage function in this model.49,50 As shown in Figure 4D, aged macrophages migrate much more robustly toward Ccl2 and this effect was enhanced significantly by the addition of sFasL. Macrophages from young animals showed minimal migration to Ccl2 at the concentration used; however, with the addition of sFasL migration was increased, but not to same extent as observed with aged macrophages. Thus, sFasL has differential effects on cytokine production and migration depending on age of the mice from which the macrophages were obtained.
The dominance of M1 macrophages in young mice and M2 macrophages in aged mice16 suggested that these differences in the macrophage properties demonstrated in Figure 4 reflect the responses of the majority of cells (i.e., M1 macrophages in young mice versus M2 macrophages in aged mice). Thus, to examine directly the migratory capacity of M1 and M2 macrophages, we performed migration assays on specifically polarized cells. We prepared macrophages by culturing bone marrow cells for 10 days in either GM-CSF or M-CSF, as these treatments have been shown to produce M1 and M2 macrophages, respectively.37,38 As shown in Figure 5, macrophages generated by GM-CSF produced elevated TNFα (Fig. 5A) and IL-6 (Fig. 5B) in response to LPS, with minimal production of IL-10 (Fig. 5C), demonstrating that they are of the M1 type. In contrast, M-CSF–cultured macrophages produced very little TNFα or IL-6, but high amounts of IL-10 (Figs. 5A–C) confirming their M2 nature. When these cells were tested in the migration assay (Fig. 5D), M1 macrophages showed little migratory capacity to Ccl2 in the presence of sFasL, while the addition of sFasL to M2 macrophages significantly increased the directed migration of these cells. This is reflected in the expression levels of Ccr2, where both populations of macrophages expressed Ccr2, M2 macrophages expressing higher levels (Fig. 5E). Interestingly, IFNγ, which promotes a proinflammatory antiangiogenic phenotype in macrophages,7,16 inhibited sFasL-induced migration,while IL-10 treatment had no effect (Fig. 5F). We concluded that sFasL has differential effects on macrophage populations where it enhances preferentially the migration of M2 macrophages, and that the effects of sFasL in aged mice reflect the dominance of M2 macrophages in these animals.
Fas (CD95) is the only known receptor for FasL mediating its proapoptotic, cytokine stimulating, and migration promoting properties.44,45,48,51 Macrophages from Fas receptor deficient mice (e.g., in lpr mice) produce copious amounts of proinflammatory cytokines, such as TNFα, IL-12, and IL-1β when stimulated with TLR ligands.32 Thus, without Fas macrophages are more proinflammatory, and polarize toward the M1 subtype and away from the M2 subtype. This also suggests that differential Fas expression might define these macrophage subtypes. We tested this idea by first examining the surface expression of Fas by flow cytometry on polarized M1 and M2 macrophages. Results presented in Figure 6A showed that more F4/80+ M2 macrophages expressed the Fas receptor compared to F4/80+ M1 macrophages, and that this number was enhanced by LPS treatment. In support of the role of Fas in migration M2 macrophages, Fas− macrophages obtained from Fas-deficient Fasf/f x LysM-cre mice did not respond to sFasL in the migration assay (Fig. 6B). Finally, to examine the role of myeloid-derived Fas in the CNV model we tested Fasf/f x LysM-cre mice that are without Fas in the myeloid compartment.32 These results showed that CNV responses were decreased dramatically (Fig. 6C), further implicating the role of Fas expression on myeloid cells in the severity of the CNV lesions. Figure 6D verifies that CD11b+ (which includes the F4/80+ population) from the Fasf/f x LysM-cre mice, expressed minimal Fas receptor.
Age is the single greatest risk factor in the development of the blinding eye disease AMD where the prevalence of disease significantly increases as individuals enter their sixth decade.2,3 In spite of this universal observation, other factors that lead to increased disease incidence remain undefined. Increases in damage from environmental stresses, accumulation of damaged proteins and organelles, and loss of function in important biochemical pathways all have been proposed.3,4,13,52 The immune system is also thought to have a role in disease development12–14,53; however, few studies have addressed how age-related changes in the immune response could be involved. The eye also is an immune privileged organ that can have a strong inhibitory influence on inflammatory and neovascular responses via a number of immunosuppressive mediators.21 How age-dependent changes in the immune system are influenced by immune privilege and how age might alter the function of immune privilege is currently unknown. We have examined the effect of age on an important mediator of immune privilege, FasL, and whether such changes might impact a model of neovascular AMD. Our results showed that, while there is an age-dependent increase in FasL expression on RPE cells, laser injury results in a significant decrease in FasL expression that is due to enhanced MMP activity, which cleaves FasL from the cell surface. Furthermore, increased cleavage of FasL results in significant levels of cleaved FasL (sFasL) in the blood that were enhanced greatly in aged animals. Targeting MMP using an MMP inhibitor reduced CNV and diminished bloodborne sFasL, while neutralizing sFasL systemically inhibited CNV, but only in aged mice. This suggested that sFasL has a role in the age-related increase in CNV. In support of this idea, sFasL had a differential effect of macrophages from young and aged mice where it increased cytokine production and migration of the M2-dominated aged macrophage population, but had little effect on M1-dominated young macrophages. We concluded that with aging the release of sFasL from the injured eye promotes the migration of proangiogenic M2 macrophages that can increase tissue damage and the neovascular response. The source of the macrophages in CNV lesion has been attributed to systemic10,15 and local sources.54 Interplay between local and systemic myeloid derived cells also has been suggested.55 We do not know the precise source of the myeloid-derived cells in the current studies; however, our data showed that the release of sFasL likely is involved in attracting proangiogenic M2 macrophages regardless of their source.
Studies have shown that FasL expression is regulated tightly in lymphoid and nonlymphoid cell populations, thereby preventing unwanted damage to Fas+ cells and tissues throughout the body. Cells that use FasL as a barrier to cellular invasion or as an effector molecule typically do not display the protein on their cell surface. It either is stored in secretory vesicles for rapid mobilization to the cell surface56,57 or produced de novo following cellular activation, stress, or injury.7,58 Originally described as a death-inducing ligand, more recent studies have shown the importance of the Fas/FasL interactions in cytokine production and mononuclear cell migration.44,45,48,51 While the membrane form of FasL is known to mediate its proapoptotic function,51 sFasL, which can be released though the activity of proteases,39,56 mediates many of the nonapoptotic functions of the protein.44,46–48,51 Little is known concerning changes in the function of the Fas/FasL interaction with aging, although it has been reported that the proapoptotic functions of FasL can be diminished with age in certain cell types.59 We reported that age decreases FasL-mediated immune privilege locally though increased cleavage by MMP, suggesting an age-related functional decline in the eye. Further, enhanced cleavage and release of sFasL has adverse effects on immune privilege, particularly in aged mice where it can activate and attract preferentially proangiogenic M2 macrophages. These results are consistent with a recent study on spinal cord injury where sFasL release from damaged tissue recruited monocytes from the periphery increasing tissue damage.47 While the macrophage subtype was not examined in that study it is interesting to speculate that M2 macrophages were involved.
Macrophages originate from the bone marrow and migrate through the blood to body tissues. Under the influence of growth factors, such as M-CSF and GM-CSF, as well as chemokines, such as Ccl2, they can migrate to tissue and take up residence in many areas of the body.60,61 There are networks of myeloid-derived cells lining the uveal tract of the eye,62 in the limbal region of the cornea,63 and in the retina.64 Resident macrophages undergo local activation, and help recruit monocytes and precursors from the bone marrow in response to injury and infection. These cells then accumulate and, under the influence of local factors, can change functional phenotypes based on the local environment. Bone marrow–derived cells are critical to the development of CNV in the laser model7,55 and our studies also showed that the increase in the CNV response observed with aging is dictated by the bone marrow, where young mice infused with aged bone marrow showed elevated CNV. In contrast, replacing the bone marrow of aged mice with bone marrow from young animal reduced the response. The exact nature of the bone marrow cells that regulate CNV with age is not known; however, myeloid cells2,7 and/or mesenchymal cells65 could be involved. Further studies are required to define the critical cell populations to understand eventually many of the aging effects on CNV in the mouse model and ultimately in human exudative AMD.
Many subtypes have been described, but a general classification of classically activated (M1) alternatively activated (M2) has been used.61 While this perhaps is an over simplification, it is useful in understanding how macrophages can influence disease states. M1 macrophages are proinflammatory, secreting cytokines, such as TNFα, IL-6, and IL-12. They also are activated by TLR ligands and IFNγ, acquiring the capacity to kill bacteria as well promote immune responses. Importantly, these cells are antiangiogenic. M2 macrophages, which produce much lower amounts of the proinflammatory cytokines, are best known for their production of IL-10, their ability to be anti-inflammatory and antiangiogenic, and their increase in function in environments rich in IL-4, IL-13, and IL-10.7,16,60,61 While the field of ocular angiogenesis has embraced the idea that macrophages promote neovascular AMD,15,49,66 the field has paid little attention to the functional heterogeneity of these cells, assuming that proinflammatory macrophages promote angiogenesis in the eye.67 However, it is clear from the tumor and atherosclerosis literature,20,60,68,69 as well as our own studies with the laser model of CNV,7,16 that macrophage function is influenced by a number of factors related to the microenvironment. In these studies, alternative activated macrophages (M2) are the culprit, promoting angiogenesis and lesion development. In the laser-induced CNV model, we have shown clearly that it is M2 macrophages that promote neovascularization and are responsible for the increased responses observed with aging.16 Importantly, M1 macrophages are antiangiogenic and can inhibit CNV.7,16 Studies reported here further support this idea, where we showed that proinflammatory cytokines, such as IFNγ, diminish the function of proangiogenic M2 macrophages from aged mice, suggesting that conditions that promote proinflammatory, antiangiogenic M1 macrophage function may diminish neovascularization. Furthermore M2 macrophages have much higher levels of Ccr2 compared to M1 (Fig. 5), suggesting that Ccl2, the major chemokines in the neovascular response, preferentially attracts M2 macrophages. It will be interesting to determine if the reported Ccr2 inhibition by pharmacologic agents70 or the loss of the Ccr2 receptor10 involves diminished recruitment of M2 macrophages.
Finally, the levels of sFasL in blood have been examined in a number of models, including cancer,71 arthritis,72 and thyroid disease.73 A recent study demonstrated a correlation between sFasL and AMD,74 suggesting that increased levels of sFasL in the blood of AMD patients might be a biomarker. Interpreting these result in light of our own findings (see the study of Roychoudhury et al.8 and current studies) suggested that targeting the Fas-FasL pathway alone, or in combination with other treatments may be a viable clinical approach to the treatment of neovascular eye disease.
Supported by National Institutes of Health Grants EY06765, EY015570, EY02687 (Department of Ophthalmology and Visual Science Core Grant), EY019287 (RSA), a Department of Ophthalmology and Visual Science grant from Research to Prevent Blindness (New York, NY), and The BrightFocus Foundation (Clarksburg, MD).
Disclosure: H. Zhao, None; J. Roychoudhury, None; T.A. Doggett, None; R.S. Apte, None; T.A. Ferguson, None
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


text:
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Your little fairy will love these glittery wings with easy to use chest straps. She will have hours of fun pretending to fly around the house or garden in these sweet Milky dress up wings. Glitter silver or gold with matching chest straps (one size).


text:
This content has been marked as final. Show 6 replies
1. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guide827290 Jan 5, 2011 1:00 PM (in response to 725165)hi
i have same problem
please help
2. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guide297706 Jan 6, 2011 12:04 AM (in response to 827290)BPMWorkflowReassign role is no longer used; any references in documentation are doc bugs and we will address them.
Reassign capability is controlled by visibility rules in Task (that is, in .task file go to access --> actions). Note that this can be used to revoke privileges but not grant additional ones.
If the scenario is that the current assignee's manager should have the Reassign privilege:
a. Need to use the concept of Owner
b. Owner can be dynamically assigned; so assign it to manager of assignee (or if you want to use a group, you can do that as well)
c. If needed, take away the other privileges granted to Owner
d. If needed, take away the reassign privilege from Assignee
Related issue is how to control the list of reassign candidates. This can be done with Java; please see http://blogs.oracle.com/soa_how_to/2010/01/how_does_restricted_task_reassignments_work_in_soa_11g.html.
3. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guide827290 Jan 9, 2011 10:51 AM (in response to 297706)tankyou for your attention
i implemented RestrictedAssignmentCallback class . but only predefined users (like weblogic) and created users with "oracle.security.idm.UserManager" api , show in user list for reassignment in worklistapp.
for exmaple i created user with name 'hamed' in weblogic console and restricted reassignment only to him . but it didnt work .
please help me
4. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guide441803 Jan 10, 2011 6:10 PM (in response to 827290)We can only read off only user store. What is the user directory configured to be used in SOA and when you add user in weblogic, do you know where this is added?
5. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guide827290 Jan 11, 2011 5:55 AM (in response to 441803)one scenario is like this :
1- I created user 'weblogic' when i configured application server(new domain creation) .
2- I added new users with weblogic server console that stores them in embeded LDAP .
in this example : "user1" , "user2" , "user3" .
3- I added new users by "DemoCommunitySeedApp" application .
note : I know that this application uses "oracle.security.idm.IdentityStore" , "oracle.security.idm.User" ,
"oracle.security.idm.UserManager" , ... for creatiing new users and groups and application role .
users like : "jcooper" , "jstein", "wfaulk" , were added .
4- I extended IRestrictedAssignmentCallback for a sample task :
package org.basa.soa.restrictAssign;
import java.util.ArrayList;
import java.util.List;
import java.util.Map;
import oracle.bpel.services.workflow.task.IRestrictedAssignmentCallback;
import oracle.bpel.services.workflow.task.IRestrictedAssignees;
import oracle.bpel.services.workflow.task.ITaskAssignee;
import oracle.bpel.services.workflow.task.impl.TaskAssignee;
import oracle.bpel.services.workflow.task.impl.RestrictedAssignees;
import oracle.bpel.services.workflow.task.model.Task;
import oracle.bpel.services.workflow.IWorkflowConstants;
public class RestrictedAssignmentCallback2 implements
oracle.bpel.services.workflow.task.IRestrictedAssignmentCallback {
public IRestrictedAssignees getPermittedAssignees(Task task,
Map propertyMap,
String currentUser,
String identityContext,
String operation) {
IRestrictedAssignmentCallback.OperationType.REASSIGN.toString())) {
System.out.println("in the re assign condistion");
return new RestrictedAssignees(createReassignTaskAssigneeList(),
return null;
public List getRestrictedOperations(Task task,
Map propertyMap,
String currentUser,
String identityContext) {
List retList = new ArrayList();
return retList;
private ITaskAssignee createTaskAssignee(String name, boolean isGrp) {
return (new TaskAssignee(name, isGrp));
private ITaskAssignee createTaskAssignee(String name, String type) {
return (new TaskAssignee(name, type));
private List createReassignTaskAssigneeList() {
List retList = new ArrayList();
retList.add(createTaskAssignee("jstein", IWorkflowConstants.IDENTITY_TYPE_USER));
retList.add(createTaskAssignee("wfaulk", IWorkflowConstants.IDENTITY_TYPE_USER));
retList.add(createTaskAssignee("user2", IWorkflowConstants.IDENTITY_TYPE_USER));
retList.add(createTaskAssignee("user3", IWorkflowConstants.IDENTITY_TYPE_USER));
return retList;
5- I logined in worklist app with weblogic user and want to reassign sample task to some one else ,
but i saw only these users in the list: "weblogic","jcooper","jstein","wfaulk"
and i didnot see these users : "user1","user2","user2"
plaese help
6. Re: [BPM11g] "BPMWorkflowReassign" role in User's Guidecenkozan Jun 6, 2011 4:13 PM (in response to 827290)Hi,
I have the same problem here. I can not update the task as any user. So I can not Add Comment, delete, ad-hoc route the task. Could you find a solution for this?
Plus I can see a similar explanation in a Document like in the first comment.
"To add or delete a comment, you must have permission to update the task."
Where is that permission being hold?
Edited by: cenkozan on Jun 6, 2011 9:11 AM


text:
By J.R. Tate
Firefighter Michael McGinnis has a damaged previous. utilizing his bothered youth as suggestion, he is channeled his harsh stories towards operating difficult as a seek and rescue guy with the hearth division. he is no stranger to severe events, yet regardless of his years at the activity, not anything can organize him for aiding Casey, his drug addict brother, whilst a deadly bookie hunts him down for unpaid playing debts.
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Michael idea he was once courageous - yet being dragged into Casey's felony existence makes him moment wager every thing he notion he knew approximately himself and his family.
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text:
Welcome to
Grace United Church
Peterborough Ontario
Who We Are
Welcome to Grace Church
Mission Statement
Our Vision
How to Find Us
Small Groups
Our Board
Our Congregation
Contemporary Worship
Traditional Worship
Childrens Programming
Meet the Band
Meet our music maestros
Listen to the message
Whats Up
Special Events
This Week
Annual Report
To Donate
Ministry Reports
Ministry Near
Ministry of Compassion
Collective Kitchens (PCCHU)
Community Repair Service
Parish Nurses & Health Cabinet
Caring through Listening
United Church Women
19th Grace Scouting
Community programs
Ministry Far
Mission and Service Fund
KIVA loans
Proud to Host
Facilities at Grace
19th Grace Scouting
Collective Kitchens
Breast Cancer Support Group
Other Groups, Special Events
How to Book
The Spiritual Commitment
Our Sanctuary
What Is Baptism?
Congregational Involvement
Information on How
Baptism: Taking the First Steps
Email Us
Annual Report
Our Annual Report is produced in early February of each year. It summarizes the activities of Grace Church and is a handy overview of all that has taken place in a year, with acknowledgements to all those who are involved in the many activities and events. We got together on February 26 this year for our Annual Congregational Meeting to review the Annual Report, set our direction for the coming year and approve our budget.
The Annual Report for 2016 is posted below as a PDF. We invite you to review it - it is a great way to find out about the many ministries at Grace and how we are living the Vision - Beyond Our Limits, Beyond Our Walls.
Click Here for Annual Report
Contact Grace United Church


text:
AquaGen has worked in co-operation with CIGENE and Affymetrix to develop and implement a new tool that analyses more than 900,000 genetic markers per sample from salmon. This is the worlds largest genetic marker set for fish and is a major advance from the previously used set of 6,000 genetic markers.
Improvement in disease resistance and robustness
This new set will in the first instance be used to find other new genes and genetic markers that are associated with valuable traits in salmon. Making improvements against diseases and parasites will be central; CMS, salmon lice and Amoebic Gill Disease (AGD) have been given the highest immediate priority. This new genetic marker set also makes possible so-called genomic selection which is a further development and optimisation of the marker assisted selection that is used today for PD and IPN resistance.
"We are pleased to have been able to develop this ground-breaking genetic marker set for salmon in such a short time", says Nina Santi, Research and development director at AquaGen. "AquaGen is always looking for new technologies that can meet the increasing demand for cost-effective and sustainable production of seafood.
This high-resolution gene marker set gives us entirely new opportunities for improving disease resistance and quality of farmed salmon. We are especially excited about the prospect of implementing genomic selection in our breeding programme. Marker sets will also make it easier to identify genetic variants that underlie complex traits, such as growth and feed efficiency whilst at the same time contributing greatly to the understanding of salmon biology".
Increased precision and speed of genotyping
The development of genetic marker sets and automatic genotyping of Atlantic salmon is complicated because the salmon genome partly is comprised of four chromosome sets compared to the two we find in humans", says Sigbjørn Lien, a professor at the University of life sciences (UMB) and the Centre for Integrative Genetics (CIGENE) ". The good support from, and expertise of, the Affymetrix team of researchers in bioinformatics helped greatly in tackling these obstacles."
"We are very pleased to have worked in partnership with AquaGen and CIGENE and offer them expertise in automatic genotyping using the Axiom® Genotyping Solution" says Andy Sist, Vice president for business unit for genetic analysis and clinical applications at Affymetrix.
"The Axiom® Genotyping Solution is the only platform that provides breeding companies and researchers with a powerful tool for genotyping and analysis, and cost-effective identification and validation of complex genetic traits. Using the Axiom Genotyping Solution® platform, scientific results can be rapidly developed and commercialised".


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Durable Automotive Angle Sensors
Designed for automotive and other mobile applications
Southborough, MA… Novotechnik, U.S. introduces the new RSC3200 Series of angle sensors that feature shaft connectivity options and provide absolute, rotary position measurement. Analog outputs are 0.25 to 4.75 V or 0.5 to 4.5 V.
Built-In coupling accepts D-Shaft with shaft customization available. The sensors are sealed to IP 67 or IP 69k depending on version. RSC3200 Series sensors are extremely durable with MTTF of 285 years for each of the two channels.
Designed for automotive and other mobile applications, RSC3200 Series of non-contacting sensors are fully redundant, measure angles up to 360° and have an operating temperature range of -40 to +125°C. Repeatability is 0.5°, resolution is 12-bit and absolute linearity is within ±1.0% FS at 360°.
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With the SLS, SOS, and STO functionalities, the SCHUNK EGN gripping system certified in accordance with DIN EN ISO 13849 enables safe human/machine collaboration. If the production process is interrupted by an emergency shut-off, the SCHUNK EGN goes into either a safely limited speed mode or a safe stop mode depending on the activated protection zone. In contrast to other solutions available on the market, the SCHUNK safety gripping system is continuously powered even in the safe operating stop so that the gripped parts are reliably held even without mechanical maintenance of gripping force. As soon as the protection zone is released, the gripper immediately switches back to the regular operating mode without the system having to be restarted.


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Accident, illness or loss of a loved one is awful enough without the added pressure of dealing with a claim for compensation.
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Winners of the Point to Point competitions revealed
Following fiercesome competition in our tent at the Aldington Point to Point on Easter Monday, the winner and two runners up in the childrens' colouring competition have been picked. The winning entries and photographs from the da… | Read more


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Last weekend we went with the Youth of the church for the second year in a row to clean up the park area near to our church. You can see the pictures and read about this initiative from last year in our blog post Ta Pastrojmë Gjakovën – Clean Up Gjakovë. Last year we collected 8 sacks of rubbish from a small area just across the road from our church and this year we collected 7 so there is perhaps a gradual improvement taking place.
Urime Vitin e Ri – Happy New Year! We hope that everyone reading this had a wonderful Christmas and is being blessed so far in 2017. It seems like 2016 went so quickly, especially the last month which was jam packed full of church activities, family commitments and challenges. Continue reading "Happy New Year! It's been a while…"
Every now and again it's good to take the church outside the building and spend time in fellowship somewhere different. The Youth Ministry is no exception and, because some of the boys were occupied with the inter-church football tournament the number of young people was diminished. Helen went with Drita (another church leader who is responsible for the Youth Ministry) and eight of the young people to the local shopping centre for an hour of bowling. Continue reading "Youth ministry doesn't just happen in the church"
Back in June we wrote about a national campaign to clean up Kosova (Please see Ta Pastrojmë Kosovën – Clean Up Kosova) when we spent a day clearing rubbish from Brekoc, a village we often support with food parcels (Please see Food, and more…). Today, as part of the Youth Ministry of our Church, Rebirth of Kosova, we worked with the Youth to clean up Gjakovë. Continue reading "Ta Pastrojmë Gjakovën – Clean Up Gjakova"
Please click below to read our latest Prayer Letter which has news, updates and prayer requests from the last few months.
We took over leading one of the Youth Cell Groups at church at the end of February and we asked for prayers to bond well with the group and for them to grow in confidence speaking English with us, using and building on what they have already learned at school and in private courses. Continue reading "Youth Cell Group and Kosovapoly"
After the busy Easter weekend there was no time to rest for Ilir who went with six other young guys from the church to play in a special football tournament organised by Scripture Union and held in the capital, Prishtina. Continue reading "Easter Monday Football Tournament"
Today we finished a two week study on the life of Joseph (Genesis 37-50) with our youth cell group. Continue reading "Youth Cell Group – The life of Joseph"
We were involved in running a Youth Camp this summer for all the youth that attend meetings and groups at the church. This video gives an overview of the activities.


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NEW YORK, Feb 6 (Reuters) - A former partner at Grant Thornton was arrested on Wednesday on charges that he stole nearly $4 million in client payments meant for the global accounting firm.
Craig Haber, 59, diverted the money to his own bank accounts from 2004 to 2012, according to a criminal complaint filed in U.S. District Court in New York.
"Fraud is always serious, but it is especially alarming when, as alleged here, it is committed by professionals who are supposed to be gatekeepers responsible for ensuring financial rectitude," Manhattan U.S. Attorney Preet Bharara said in a statement.
The complaint did not identify Grant Thornton by name. But a spokesman for Grant Thornton confirmed its identity, adding that it has been cooperating in the investigation.
The accounting firm, which had $4.2 billion in revenues globally at the end of its September fiscal year, terminated him in July, the complaint said.
"Grant Thornton disclosed this former partner's conduct to the authorities promptly after discovering possible financial improprieties, which resulted in his separation from the firm," Tim Blair, a spokesman for Grant, said in an email.
A lawyer for Haber, Michael Bachner, declined comment.
Haber worked at the accounting firm since 1990, making partner in 1993, the complaint said. He worked out of its New York offices, primarily providing tax advisory services related to investment partnerships, the document said.
Beginning in 2004, Haber on multiple occasions told clients to mail checks directly to his office, rather than routing them through its Chicago headquarters as normal, the complaint said.
Haber then deposited the checks into a bank account with a name similar to his firm's, the charging documents said. He then transferred the money into two personal bank accounts, the complaint said.
The money was used to pay for, among other things, the mortgage on his apartment, a gym membership, child support and a brokerage account, the complaint said.
The case is United States v. Haber, U.S. District Court, Southern District of New York, 13-0329. (Reporting By Nate Raymond and Dena Aubin in New York; editing by Andrew Hay)


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I recently had the privilege of attending the annual American Academy of Ophthalmology conference in Chicago, IL. While there, I took notice of the (self-proclaimed) 'talk' of the meeting. He seemed to be an individual with a rather dry sense of humour and went by the name 'Mr. Hyperosmolarity.' Upon first glance, it was clear that the man had a special affinity for all things dry and salty. Being that I suffer from moderate dry eye myself, I took immediate notice of Mr. … [Read more...]
The Heart of the Problem in Dry Eye Disease: 'Mr. Hyperosmolarity'
Menopause and Dry Eye Symptoms: A Clear Connection
As if irritability, insomnia and fatigue weren't enough, research has shown that dry eye disease can also stem from the hormonal changes that occur during menopause. Actually, Dr. Henrik Sjögren first established a connection between hormones and dry eye symptoms as far back as the 1930's! And thanks to Dr. Sjögren and other researchers like him, we now have an even better understanding on the hormone-ocular surface connection. Most people think of moodiness, hot … [Read more...]
Treating Dry Eye Disease and Sjögren's Syndrome with One Amazing Oil
Most dry eye sufferers have tried every drop, oil, compress and nutritional supplement on the market in search of some relief from the itchy, burning sensation of Dry Eye Disease. Though some find successful treatment via a combination of artificial tears and nutritional supplements, for example, others seem to be treatment resistant when it comes to easing persistent dry eye symptoms. Indeed, thousands of individuals are 'itching' for a permanent cure to Dry Eye … [Read more...]
9 Houseplants for Improving Sick Building Syndrome & Indoor Air Quality for Dry Eyes
Home is where the heart is. It's that old saying that usually rings true; until you consider that the air we breathe indoors is often more polluted than the air outside. The fact is downright scary, especially since the average American spends about 90% of their time inside inhaling stealth pollutants like xylene, formaldehyde, benzene and polychlorinated biphenyl. To make matters worse, these harsh chemicals come from everyday items like cleaning agents, sealants, … [Read more...]


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1.35 acres in Taylor County, Kentucky
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4 Stories Up is a fictional, serial story that follows a talented, sexy female drummer as she seeks fame and fortune with a band. Tory is a woman making her her way in a male-dominated world of heavy metal. She is passionate in life and music and she plays for keeps. Her feisty nature often gets her in trouble but she fights on towards perfection in her love, her music and her life. – Find past chapters here.
—– —– —– —– —–
The next several days were difficult for the band as they waited for an answer from Thundering Mountains as to who would be opening for them. Every day, the band would look at Phillip with high hopes and expectations and every day he would just shake his head in silence. It was so frustrating knowing they were on the cusp of playing in an arena with Thundering Mountains and Still Fire!
Finally, almost a week after they had their recording session, Phillip came into the garage and announced, "So, I heard from Thundering Mountains." His expression gave nothing away.
"And?" Doug prompted.
"And, while they liked what they heard…"
Tory bit her bottom lip, anticipating bad news. Her fists clenched and she held her breath.
"They want to hear more of us in person at the arena! We're in!"
"Shut the fuck up!" Doug yelled, jumping into the air.
The band hugged each other, all yelling at once. They were just a mass of arms and legs and laughter.
Just then, Mandy walked in and looked in utter amazement at the group of celebrating together. "Umm," she interrupted, "what's going on?"
Jake broke away from the group and was smiling from ear to ear. "We got the gig," he informed her quietly.
"Jake! That's awesome!" Mandy said quietly back to him with a smile.
"Oh, hi," Tory said to Mandy as she realized suddenly that their group hug was one short. "I didn't hear you come in!"
"I see why!" Mandy laughed, her large hazel eyes glimmering.
"Mandy," Phillip said, his smile now gone. "What can I do for you?"
"I asked her over, dad," Jake said, continuing to smile at her.
"It's practice time, Jake. We have a lot of work to do," Phillip said coldly.
"I thought she could listen," Jake said, frowning. He knew his dad was not happy but he wasn't sure why. "She can help us out with our new songs, let us know if we're on the right track."
"I'm pretty sure that's my job, Jake," Phillip replied.
"I think it was a good idea, Jake," Doug said as he glanced at Mandy and Phillip nervously. "Umm, maybe just a little premature buddy?"
"Having her here will dampen my creative flow," Chris said peevishly.
"Oh for the love of…" Tory shook her head and rolled her eyes. "Mandy, it would be great to have your opinion. Never mind these, these…men. We just may not be ready for anyone else to hear what we have yet, that's all."
"Oh, sure," Mandy said, her cheeks bright red. "I didn't mean to interrupt the, umm, creative flow…"
"Yah," Doug agreed readily. "You totally get what I'm saying, Tory."
"Okay," Mandy said quietly, still very uncomfortable. "I'll leave you guys to create. I'll see you later."
Jake said nothing but kept his eyes to the floor as she left the garage, shutting the door quietly.
"I thought she'd never leave," Chris sniffed. "Okay, let's start."
"I don't want to," Jake said in a whisper.
"Don't get pouty," Phillip admonished his son. "You should have asked before you invited her over."
"Ok dad, sorry," Jake muttered as he picked up his guitar and headed into the house.
"Jake," Phillip called behind him. He put his head in his hands and moaned as the door shut.
"Phillip," Doug started.
"I know, I know," Phillip acknowledged. "I couldn't have handled that worse if I tried."
"What do you mean?" Chris asked, genuinely confused. "You told her how it had to be."
"I was angry that she kept my son out late and made me worry," Phillip corrected him.
"Wait, you mean you didn't kick her out for me?"
"You are truly amazing," Tory said while shaking her head. "You have no idea that there are other people with feelings that matter in this band, do you?"
Chris went back to writing lyrics in a huff.
"Guess I should go apologize," Phillip sighed. He headed towards the door leading into the house.
"Uhm, Phillip?" Doug interjected.
"Mandy went that way." Doug pointed to the door of the garage leading outside.
"I know."
"I'm just saying."
Phillip closed his eyes and prayed for patience with this new complication in his relationship with his son. Sighing again, Phillip went to find Mandy and talk to her.
As he blinked in the warm sunshine, he saw a car in the driveway and Mandy was sitting in the driver's seat with her head on the steering wheel. He walked over and gently knocked on the window. Despite the gentle tap, Mandy jumped and looked up nervously. Her cheeks were wet from tears. Phillip immediately felt ashamed at himself.
"Mandy," he said as she rolled the window down, "could we talk?"
"I, I guess," she said as she rapidly wiped at her cheeks and cleared her throat.
"Look," he said as she opened the door and gingerly got out of her car. "You probably know that I'm Jake's dad."
"He told me," she stated flatly.
"What he may not have told you is that he, well, he hasn't had much of an interest in socializing much."
"Because of his Asperger's. He told me that too."
"Oh, he did. Oh, well, it's just…"
"He told me about his mother and how you are the most important person in his life."
"He told you a lot."
"We were together for quite a while."
"Yah, well, I'm just very protective of him and I don't want to see him get hurt."
"You think I will hurt him."
"I, I don't know…"
Now Mandy started getting angry. "No, you don't know. You don't know me at all so how could you?"
The shame flooded over Phillip again. "I deserve that. No, I don't know you. That's part of why I'm feeling so protective. Jake is acting completely different lately and I think you're part of the reason for that. I'm not sure what to make of all of it."
Mandy's expression softened as she saw the struggle of a single dad who loved his son very much. "Well, I would like to get to know you."
Phillip smiled at her. "Let's start over," he suggested. "Would you like to stay for supper? I'd love to hear more about how you got in the music industry."
"I would love to," she smiled back nervously.
—– —– —– —– —–
Get the latest on Tory and the band between chapters at their official Facebook page!
This is a work of fiction. Names, characters, places and incidents either are products of the author's imagination or are used fictitiously. Any resemblance to actual events or locales or persons, living or dead, is entirely coincidental.
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NEW YORK (TheStreet) -- Shares of Viacom (VIAB) are advancing 1.76% to $67.25 in Wednesday's early morning trading session as analysts at Credit Suisse initiated coverage of the company with an "outperform" rating and a price target of $85.
The firm pointed out that the entertainment content company has been at the epicenter of investor debate about the future of the bundle, which has caused significant multiple compression. However, analysts see recovery potential and believe the risks of near-term disruption to the company's business are modest.
While the core cable networks face some structural challenges, which are now well-known, ratings could stabilize in the second half of 2015, analysts noted.
Additionally, their forecasts include successful cost savings realization with limited topline impact from the announced restructuring program.
Separately, TheStreet Ratings team rates VIACOM INC as a Hold with a ratings score of C. TheStreet Ratings Team has this to say about their recommendation:
"We rate VIACOM INC (VIAB) a HOLD. The primary factors that have impacted our rating are mixed, some indicating strength, some showing weaknesses, with little evidence to justify the expectation of either a positive or negative performance for this stock relative to most other stocks. The company's strengths can be seen in multiple areas, such as its notable return on equity, good cash flow from operations and expanding profit margins. However, as a counter to these strengths, we also find weaknesses including deteriorating net income, generally higher debt management risk and a generally disappointing performance in the stock itself."


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When you peer into your mouth, we'll bet you see many things that are familiar to you. The tongue, tonsils, and uvula all tend to ring a bell with most people. Most of us are also familiar with the epiglottis, whose job it is to prevent the inhalation of food into the windpipe. But, what's that thing called that attaches our tongue to the bottom of our mouth? Well, dear student, that's called the lingual frenulum. And, sometimes, it needs to be snipped. Let's find out why.
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