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From: John I Jones <firstname.lastname@example.com>
Harold Peters wrote:
> This is a test of my ability to send an iris photograph. The photo is a view
> of my iris beds taken May 8, 1998. I am still rather new at the internet.
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Published on 13.07.07 in Vol 9, No 3 (2007)
Works citing "Toward a Model for Field-Testing Patient Decision-Support Technologies: A Qualitative Field-Testing Study"
According to Crossref, the following articles are citing this article (DOI 10.2196/jmir.9.3.e21):
(note that this is only a small subset of citations)
- Zhang S, Cabage N. Search Engine Optimization: Comparison of Link Building and Social Sharing. Journal of Computer Information Systems 2017;57(2):148CrossRef
- Baldacchino A, Crocamo C, Humphris G, Neufeind J, Frisher M, Scherbaum N, Carrà G. Decision support in addiction: The development of an e-health tool to assess and prevent risk of fatal overdose. The ORION Project. Computer Methods and Programs in Biomedicine 2016;133:207CrossRef
- Hoffman AS, Llewellyn-Thomas HA, Tosteson ANA, O'Connor AM, Volk RJ, Tomek IM, Andrews SB, Bartels SJ. Launching a virtual decision lab: development and field-testing of a web-based patient decision support research platform. BMC Medical Informatics and Decision Making 2014;14(1)CrossRef
- Abhyankar P, Volk RJ, Blumenthal-Barby J, Bravo P, Buchholz A, Ozanne E, Vidal D, Col N, Stalmeier P. Balancing the presentation of information and options in patient decision aids: an updated review. BMC Medical Informatics and Decision Making 2013;13(Suppl 2):S6CrossRef
- Coulter A, Stilwell D, Kryworuchko J, Mullen P, Ng C, van der Weijden T. A systematic development process for patient decision aids. BMC Medical Informatics and Decision Making 2013;13(Suppl 2):S2CrossRef
- Killoran JB. How to Use Search Engine Optimization Techniques to Increase Website Visibility. IEEE Transactions on Professional Communication 2013;56(1):50CrossRef
- Sivell S, Marsh W, Edwards A, Manstead AS, Clements A, Elwyn G. Theory-based design and field-testing of an intervention to support women choosing surgery for breast cancer: BresDex. Patient Education and Counseling 2012;86(2):179CrossRef
- Durand M, Wegwarth O, Boivin J, Elwyn G. Design and usability of heuristic-based deliberation tools for women facing amniocentesis. Health Expectations 2012;15(1):32CrossRef
- Brunette MF, Ferron JC, Devitt T, Geiger P, Martin WM, Pratt S, Santos M, McHugo GJ. Do smoking cessation websites meet the needs of smokers with severe mental illnesses?. Health Education Research 2012;27(2):183CrossRef
- Elwyn G, Kreuwel I, Durand MA, Sivell S, Joseph-Williams N, Evans R, Edwards A. How to develop web-based decision support interventions for patients: A process map. Patient Education and Counseling 2011;82(2):260CrossRef
- Joseph-Williams N, Evans R, Edwards A, Newcombe RG, Wright P, Grol R, Elwyn G. Supporting Informed Decision Making Online in 20 Minutes: An Observational Web-log Study of a PSA Test Decision Aid. Journal of Medical Internet Research 2010;12(2):e15CrossRef
- Evans R, Joseph-Williams N, Edwards A, Newcombe RG, Wright P, Kinnersley P, Griffiths J, Jones M, Williams J, Grol R, Elwyn G. Supporting Informed Decision Making for Prostate Specific Antigen (PSA) Testing on the Web: An Online Randomized Controlled Trial. Journal of Medical Internet Research 2010;12(3):e27CrossRef
- Guercini S. On Line Media Market and New Advertising Agencies: Analysis of an Italian Case. Journal of Service Science and Management 2009;02(02):117CrossRef
- Elwyn G, Légaré F, Weijden TVD, Edwards A, May C. Arduous implementation: Does the Normalisation Process Model explain why it's so difficult to embed decision support technologies for patients in routine clinical practice. Implementation Science 2008;3(1)CrossRef
According to Crossref, the following books are citing this article (DOI 10.2196/jmir.9.3.e21):
- Kumar RP, Singh AK, Mohan A. Handbook of Research on Modern Cryptographic Solutions for Computer and Cyber Security. 2016. chapter 18:420CrossRef
- Reid P, Laffey D. Encyclopedia of E-Commerce Development, Implementation, and Management. 2016. chapter 78:1102CrossRef


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When my boyfriend of 5 years proposed marriage, I didn't want to break up, so I said yes.
Let me start from the beginning: J and I met when I was 18. Five years my senior, he seemed to my teenage self like a real grown-up. Living on his own and working full time, he was like a contributing member of society -- well, minus the fact that "full time" was at a movie theater and he was a total drug addict. He was still more grown-up then I was at the time, living with my parents and trying to figure out what I wanted to be when I grew up.
J somewhat supported me while I was in college and when I landed my first real job in advertising, I moved in with him. I was 24 years old. Later that year, on Christmas morning, J proposed. I said, "Yeah, OK, sure," because I didn't want to hurt his feelings or break up. When I found out that he had cleared this with my parents and everyone was totally on board, I started to feel in over my head.
My parents and I are pretty tight, and if they weren't opposed to this, then maybe it was for the best, I thought. I tried to be optimistic: "Let's have a long engagement. What's a few years in the grand scheme of things, right?" What I was really doing was stalling, but I wasn't even fully aware of it at the time.
I would be remiss if I didn't mention that this whole period of my life was soaked in beer and Jack Daniel's, under a thick layer of pot smoke and occasionally chemically charged. I basically had no business becoming a life partner to anyone.
Two years after we got engaged, the pressure to get married started. My parents in particular seemed to really push the issue. My mom was so excited; she was basically doing all the planning with very little input from me. I felt like I was on a runaway train and I couldn't get off.
The only time I would insist on something was in an effort to scale back. If it were up to my mom, there would have been 600 people there! In hindsight, I can see that I was trying to keep it small and intimate because I felt like a fraud, and I didn't need 600 witnesses to my mistake (and I certainly didn't want to have to make 600 future apologies).
I don't know why I was scared to speak up. I thought that everyone feels like this before they get hitched, everyone gets cold feet. Regret was forming and I wasn't even married yet.
On the day of my wedding, which went by a blur, one thing stood out. D, the best man and J's best friend for many years, told me I looked beautiful. Lots of people had told me I looked beautiful that day, but when D said it, I remember feeling … well, beautiful. A photo was taken a few moments after he said it, and when I looked back at that photo after the wedding, I felt amazing/terrible feelings of fondness/guilt for thinking what a handsome couple we'd have made, in some bizarro universe where D was the groom and J the best man.
D and I had always had an undeniable connetion. Strangers in bars would ask "Which one is your boyfriend, again?" when the 3 of us were out partying together. D's various girlfriends over the years would often corner me with drunken speculation, if not full out accusations. Truthfully, I would tell them that there was nothing going on. We were just really great friends. And why wouldn't I be great friends with my husband's best friend?
Shortly after we were married, I noticed a difference in J. He became uncharacteristically introverted and started slipping at work. He smoked a lot of pot (like, way too much). We also started to constantly fight about money. His pot habit was putting us in debt. We ended up borrowing a huge loan from my dad and had no way to pay it back. In the meantime, J got grumpier and surlier. He'd start to get high at work and then come home, eat dinner in front of the TV and go straight to bed.
Meanwhile, my life was changing in the opposite direction. I was killing it at work (like a boss) and my job in advertising came with fun industry perks: Parties! Events! Expensive dinners with clients! I would sometimes invite J to come along and more often than not he would decline. When he did come, he would get embarrassingly drunk then spend the next few days miserable under the guise of being "hung over."
I know now that a good wife would have helped her partner out of his funk, but I was too inexperienced, already feeling in over my head and in the prime of my professional life. Instead of pulling him up, my attitude was "I'm not letting you drag me down!"
Instead, as a distraction from my marital issues, I developed a super fun drug addiction. Super fun, but also reckless (as super fun things are wont to be), and of course it contributed further to our problems -- both emotionally and financially.
While J and I grew father apart, D and I grew closer together -- as friends. We both had a penchant for partying. While I was embarrassed to bring J out for nights with my friends, D was down to join us and we always had a great time. D and I would spend countless nights wondering, in a post-party glow, what was wrong with J. He had alienated himself from his friends and we didn't know how to help him.
I'm sure my relationship with D was also concerning to J, but he never let on about that. I didn't think it was a problem because he never brought it up. J and I would fight about drugs and money, but never about D.
After a particularly wild summer of drugs and fighting, it was clear to both J and I that our relationship had run its course. In the messy months that followed our split, his friendship with D was tested when D showed loyalty to me time and time again.
Eventually, D and J just stopped talking and D and I relented and did what everyone suspected we'd do -- or had already done. We fell in love. J, understandably, cut us both out of his life. I'm sure he had suspicions as to how far back my romantic relationship with D went, but he never came asking me for answers. I can confidently say that I never cheated sexually -- but I can't deny that there was always something pulling me to D, even though we didn't act on it until many years later.
In the meantime, a lot of tongues started wagging as D and I got together. We both gave up the drugs around this time -- perhaps now that we were together we didn't need them. Still, there was a lot of gossip and hostility amongst mutual "friends." We had to decide not to let those negative opinions stand in our way. We made a conscious choice not to sacrifice our happiness.
My story is not a sympathetic one, I know, but I made the decision and I stand by it.
Today, D and I co-exist in a single dwelling, happily unmarried. We've built a life together that includes a mortgage, yearly vacations, wine and cheese plates and home cooked meals. We also co-created a life, a 16-month-old little girl who makes me realize every day what life is about. D is an amazing dad and the two of them together make my heart dance.
Every time I come across a quote about life being short and doing what you must be happy, I file it away in my head. Because even though I know I did what I had to for my own personal happiness, I wish I could say that it was a guilt-free decision. The stigma associated with trading in your husband for his best friend can make a gal feel like a callow and thoughtless harlot. But my feelings are true and pure and my family is the proof. When I see that little girl laugh, I know that all the decisions that led me to her were the right decisions for me.


text:
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Human Remains Discovered in Franklin CountyThe Forestry Division of the MDC was cleaning the river access at Chouteau Claim about noon Tuesday when they made a grisly discovery.
Great White Sharks in the Mississippi River?Have two great white sharks managed to survive the trip up the Mississippi River from the Gulf of Mexico?
Missouri Bans Feral Hog Hunting on Conservation LandConservation officials say the ban's goal is to completely eradicate the feral hogs, which multiply rapidly and do extensive damage to land, water and habitat.
Armadillos Migrating from Southwest to the CityArmadillos in St. Louis - not something city dwellers are used to seeing, but the Missouri Department of Conservation says get use to it.
Black Bear Killing Shines Light on Weak Poaching PenaltiesViolation of poaching is considered a Class A misdemeanor, which means the maximum penalty someone could receive for that act is a $1,000 fine and/or up to a year in jail, Zarlenga says.
Black Bear Killed in Eastern Missouri; Citation IssuedBear was found dead Monday in Jefferson County.
Watch: Peregrine Falcon Chicks are HatchingThe female will remain at the nest for the first ten days to keep the chicks warm.
MDC Amps Up Measures to Prevent Spread of CWDThe Missouri Department of Conservation will now require hunters in 29 counties to take deer they have killed to a testing facility.
That's A Record-Setting FishTravis Cardona of Hillsboro, Mo. catches whopper black buffalo
Feral Hog Population Rising in MissouriMost are in southern Missouri, but some have been caught in the St. Louis region.
The Smoke Smell is BackThe Missouri Department of Conservation has advised that the smell is stemming from smoke from natural cover and brush fires in Kansas and southern Missouri.
Ameren Missouri Falcon Cam Soars into Fifth SeasonThe ongoing interest in the lives of these amazing birds is reflected in the number of viewers who watch the live camera feed.


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Barry Libman Inc. Offers Two New Online Home Health Care Medical Coding Courses
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CHICAGO – Put in a dash of crazy, add a dash of funny and you are defining "The Asylum," a catch-all name for a couple of show events in Chicago, playing at The Apollo Theater Studio through February 23rd, 2017. Behind the scenes of these showcases is producer Michael Sanow, a Chicago theater veteran. For "The Asylum" information regarding the "Atypical Musical Comedy Show" (Tuesdays) and "Access Comedy" (Thursdays), click here.
Steve Taylor
Blu-ray Review: 'Blue Like Jazz' Attempts to Reinvigorate Christian FilmmakingSubmitted by mattmovieman on August 13, 2012 - 8:47am
CHICAGO – There's a reason why the terms "Christian" and "filmmaker" don't seem to go together. Pictures that push religious agendas tend to sacrifice complex plots and characters in favor of amplifying its message. These films fail not only as entertainment but as quality storytelling. Whenever an aspiring artist attempts to speak for a group rather than oneself, it's almost always a recipe for tediously preachy dreck.
Film Review: Pretentious 'Blue Like Jazz' Can't Find the Right GrooveSubmitted by BrianTT on April 12, 2012 - 3:02pm
Rating: 2.5/5.0
CHICAGO – Donald Miller's "Blue Like Jazz" is a beloved book that spent 43 weeks on the New York Times bestseller list and sold over 1.5 million copies. I haven't read it. But I have to believe that it worked on its fans in a way that Steve Taylor's film simply cannot. This is clearly a personal story, one that touched people by relating to issues they've grappled with in their own lives. By taking Taylor's memories and turning them into cinema, the ability to touch has been removed another degree of separation and the resulting film is a misstep, the kind of work that thinks it's saying something important but feels more pretentious than precious.


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Let us know when your receive great advice so we can thank our lawyers and point others with similar questions in the right direction.Got it!
gave tenants 30 day eviction notice for nonpayment of two months rent by personally handing them one, mailing them a copy and mailing them a copy certified mail, they they told me that if I wanted them out I would have to get a sheriff to evict them, Is this something I can go down to the court house and do myself or do I need an attorney for this
It's something that you can do by yourself, but I'd be potentially concerned about the implications of that, as if you mess up even the slightest technicality, you could be hit with having to pay the tenants' attorney fees.
Some areas to be particularly concerned about are the adequacy of your notice. While a 30 day notice for nonpayment of rent can technically be accomplished (i.e., as a 30 day for cause notice), a 30 day no cause notice is almost always a better, safer option, and it can be pursued in tandem with a 72 hour notice for nonpayment of rent.
To limit your own liabilities and to ensure that the process is expedited as much as possible, you should consult with a landlord/tenant attorney in your area.
If you found this answer helpful, please click the "Mark as good answer" button, below. If you'd like to contact me regarding potentially representing you with regards to your legal matter, please click on my profile and give my office a call. My answer to your Avvo question, however, is informational only and is not intended to be legal advice, nor does it form the basis for any attorney-client relationship whatsoever, which can only be formed upon signing an Engagement Agreement and depositing a Retainer Fee into client trust. Further, I am only licensed in Oregon and laws vary from state to state. If you have an Oregon-related issue, feel free to contact me for a consultation. If you are outside of Oregon, please consult an attorney in your area for legal advice.
I agree with Mr. Parks. Oregon's Landlord-Tenant Act is weighted in tenants' favor and there are many technical rules a landlord must follow. Even innocent mistakes in when notice is given, how it is served, and what the notice says can easily cost a landlord additional time and money and sometimes they are even ordered to pay a tenant's attorney's fees. If you aren't experienced in serving tenants notices and going to court to evict them, you need to consult with a landlord-tenant attorney in your county to make sure your notice isn't defective BEFORE you file an eviction.
Even if your notice turns out to have been defective, you may not have lost that much time (or any depending on how much time they have left). The reason is that you can also serve a 72-hour notice for non-payment of rent (again, have a landlord-tenant attorney draft this for you or at least review yours). If it's the first 72-hour notice you've given these tenants, they'll have the opportunity to "cure" it by paying rent within the time specified, but you can always serve them a non-defective 30 day notice WITHOUT cause at the same time so that no matter what, you can file an eviction complaint at the end of the 30-day period.
My responses to posts on AVVO are not legal advice, nor do they create an attorney-client relationship. In order to provide true (and reliable) legal advice, an attorney must be able to ask questions of the person seeking legal advice and to thus gather the appropriate information. In order for an attorney-client relationship to exist, you and I both have to agree the the terms of such an agreement.
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Value of anti-infective chemoprophylaxis in primary systemic vasculitis: what is the evidence?
- Frank Moosig1Email author,
- Julia U Holle1 and
- Wolfgang L Gross1
DOI: 10.1186/ar2826
© BioMed Central Ltd 2009
Published: 28 October 2009
Although infections are a major concern in patients with primary systemic vasculitis, actual knowledge about risk factors and evidence concerning the use of anti-infective prophylaxis from clinical trials are scarce. The use of high dose glucocorticoids and cyclophosphamide pose a definite risk for infections. Bacterial infections are among the most frequent causes of death, with Staphylococcus aureus being the most common isolate. Concerning viral infections, cytomegalovirus and varicella-zoster virus reactivation represent the most frequent complications. The only prophylactic measure that is widely accepted is trimethoprim/sulfamethoxazole to avoid Pneumocystis jiroveci pneumonia in small vessel vasculitis patients with generalised disease receiving therapy for induction of remission.
In patients with small vessel vasculitis (SVV), infectious complications are at least as often the cause of death as uncontrolled disease activity. For example, in the recently published MEPEX-trial about 25% of the patients did not survive the first year, and most of the deaths were attributable to overwhelming infectious complications [1]. Despite the fact that infections substantially contribute to morbidity and mortality in patients with primary systemic vasculitis (PSV), data on risk factors and on the burden of specific infectious agents are scarce. In oncology, recommendations for anti-infective chemoprophylaxis (AIP) are often derived from randomised controlled trials evaluating the effectiveness of the prophylactic intervention itself [2, 3]. Such data are widely missing in PSV.
Rates of infections, mortality and infection related mortality in major studies on primary systemic vasculitis
Type of study
Follow up (months)
Reported infections (classified as serious)
Type of serious infections (number of patients)a
Total deaths (%)
Death due to or in conjunction with infection (% of total deaths)
Type of infection leading to death (number of patients) b
Giant cell arteritis
Matteson et al. 1996 [4]
49 (24)
3 (6)
Chevalet et al. 2000 [5]
Oral GC ± initial GC iv pulse
31 (22)
Pneu (20), Sep (1), Abs (1)
5 (3)
Jover et al. 2001 [6]
18 (4)
Pneu (1), TB (1), PN (1), CC (1)
Hoffman et al. 2002 [7]
Pneu (1)
3 (3)
1 (33)
Pneu (1)
Mazlumzadeh et al. 2006 [8]
Oral GC ± initial GC iv pulse
18 (0)
Hoffman et al. 2007 [9]
GC ± Inflix
Histo (1), VZV (1)
Martinez-Taboada et al. 2007 [10]
GC ± Eta
8 (0)
Takayasu arteritis
Hoffman et al. 2004 [11]
GC + Inflix or Eta
Churg-Strauss syndrome/polyarteritis nodosa
Cohen et al. 2007 [12]
GC + 6 pulse CY versus 12 pulse CY
TS recommended
4 (8)
3 (75)
CMV (1), Pneu (1) and NI
Gayraud et al. 1997 [13]
GC + pulse CY versus oral CY
1 (4)
1 (100)
Pneu (1), Sep (1), Asp (1)
Guillevin et al. 1995 [14]
GC + pulse CY ± PE
TB (3), Pneu (3), Sep (2), Sig (1)
11 (17)
2 (18)
Sep (1) and NI
Guillevin et al. 1992 [15]
15 (19)
2 (13)
Sep (1) and NI
Guillevin et al. 1991 [16]
19 (27)
5 (26)
Pneu/Sep (4), TB (1)
Microscopic polyangitis
Nachman et al. 1996 [17]
6 (6)
2 (33)
Sep (2)
Wegener's granulomatosis
Metzler et al. 2007 [18]
GC + Lef or MTX
25 (0)
WGET Research Group 2005 [19]
GC + CY/MTX ± Eta
6 (3.5)
2 (33)
Sep (2)
Schmitt et al. 2004 [20]
Optional TS, optional fungi, optional CMV
Pneu (2), Abs (1), UTI (1), CMV (1), Col (1)
2 (13)
1 (50)
Pneu (1)
Metzler et al. 2004 [21]
GC + Lef
9 (1)
Pneu (1)
Bligny et al. 2004 [22]
Mainly GC + CY
TS or Penta in most patients
PCP (12), Asp (5), VZV (3), CMV (6), Sep (8), Papo (1), TB (4), Abs (1), Toxo (2)
25 (27)
13 (52)
Sep (4), PCP (5), CMV (2), Pneu (3), Asp (3), TB (1), Papo (1)
Reinhold-Keller et al. 2002 [23]
7 (0)
2 (3)
Mahr et al. 2001 [24]
TS in most patients
PCP (19), Pneu (3), Asp (5), CMV (5), TB (2), VZV (2), Papo (1), Sep (2), SA (1)
18 (37)
7 (39)
PCP (5), Sep (1), Pneu (3), Asp (2), Papo (1), CMV (1)
Reinhold-Keller et al. 2000 [25]
Mainly GC + CY followed by MTX or TS
TS in case of CY
Pneu (32), Sep (10), CMV (3), PCP (1)
22 (14)
5 (23)
Sep (4), Pneu (1)
Guillevin et al. 1997 [26]
GC + oral CY versus GC + pulse CY
TS in most patients after high incidence of PCP in the first patients
Pneu (3), Sep (3), SA (1), CMV (4), Papo (1), PCP (10)
19 (38)
9 (47)
PCP (6), Pneu (1), Sep (1), Papo (1)
de Groot et al. 1996 [27]
MTX versus TS ± GC
No additional
Stegeman et al. 1996 [28]
Placebo versus TS
No additional
1 (1.2)
Sneller et al. 1995 [29]
3 (7)
2 (67)
PCP (2), Cryp (1)
ANCA-associated vasculitis
Pagnoux et al. 2008 [30]
GC + MTX versus Aza
TS or Penta
46 (6)
Sep (2)
1 (0.8)
1 (100)
Sep (1)
Walsh et al. 2008 [31]
GC + Campath-1H
Acyc, fungi
31 (21)
Staph (10), CMV (2), PCP (2), Asp (2), Sal (19), Pseu (1), E. coli (1), Acti (1)
31 (44)
12 (39)
Jayne et al. 2007 [1]
GC + oral CY + PE versus iv GC pulse
TS suggested
61 (37)
35 (26)
19 (54)
de et al. Groot 2005 [32]
GC + CY versus MTX
Optional TS
18 (8)
CMV (1), SA (1), Cory (1), Pneu (2), UTI (1)
4 (4)
1 (25)
Booth et al. 2004 [33]
GC + Inflix ± CY
TS, fungi
Pneu (3), Sep (1), Abs (1), Opht (1)
2 (6)
1 (50)
Pneu (1)
Birck et al. 2003 [34]
1 (5)
1 (100)
Jayne et al. 2003 [35]
GC + oral CY followed by GC + oral CY versus Aza
TS recommended
33 (11)
8 (5)
5 (63)
Pneu (2) and NI
Haubitz et al. 1998 [36]
GC + oral CY versus pulse CY
Sep (4), Pneu (5), VZV (1), CMV (1), Endo (1), SD (1)
3 (6)
3 (100)
Sep (3)
de Groot et al. 2009 [37]
GC + oral CY versus pulse CY
51 (17)
Pneu (3), Sep (3), Div (1), PCP (1), HSV (1), Abs (1)
14 (9.4)
6 (43)
Sep (6), PCP (1)
Furthermore, there are great variations in the use of AIP: some trials used routine prophylaxis against Pneumocystis jiroveci pneumonia (PCP; formerly named Pneumocystis carinii), other fungi and cytomegalovirus (CMV), and others did not. Most protocols left the use of AIP optional and in many the actual use was not even recorded, or at least not reported. Finally, the therapeutic intervention is given infrequently in sufficient detail; for example, the cumulative dose of glucocorticoids (GCs) is usually not mentioned.
When thinking about AIP, both the individual risk for the patient and the evidence for the efficiency and safety of the prophylactic intervention must be taken into account.
Factors influencing susceptibility to infections
Because, to date, no PSV trials have used infection as the primary endpoint, information on possible risk factors can only be retrieved from adverse event reporting in cohort studies or therapeutic trials. In Table 1 the rates of infections, serious infections and fatal infections in different entities and under distinct medication are summarised. In conjunction with data from other medical conditions the following conclusions might be drawn.
It is obvious that immunosuppressive medication is a major risk factor for infections [38]. A high GC dose (often defined as more than 30 mg per day prednisolone-equivalent), especially in the form of intravenous methylprednisolone, is a significant risk factor [1, 39]. With respect to common clinical experience, its importance seems to be underestimated in clinical trials because, for example, the cumulative GC dose is not usually stated. In a study on giant cell arteritis (GCA) solely treated with GCs, 86% of the patients experienced severe GC-related adverse events, including severe infections in 31% [40]. Schmidt and colleagues [41] reported a relative risk of severe infections - that is, infections leading to hospitalisation - of 2.44 in the first 6 months of GC treatment in a large GCA trial and increased infection-related mortality. Rising awareness of GC complications, including infections, makes GC sparing an increasingly important aim. According to the European League Against Rheumatism (EULAR) recommendations for conducting clinical trials in PSV, protocols should be designed to reduce patients' total exposure to GCs, which includes recording cumulative GC doses and the use of GC-sparing drugs like methotrexate (MTX) [42].
Although some trials using cyclophosphamide (Cyc) report very low rates of infectious complications [17, 33], Cyc use in SVV is associated with higher rates of infections and fatalities than the use of medium potent immunosuppressants such as MTX, azathioprine or leflunomide [22, 24, 26]. Among the latter no differences concerning rates and types of infections can be derived from the available data. When analysing infectious complications, it has to been taken into account that treatment changes over time. For example, the CYCAZAREM-trial demonstrated that oral Cyc could safely be substituted by azathioprine after achieving remission, leading to much lower cumulative Cyc doses [35]. The use of Campath-1H, a monoclonal antibody to CD52 that leads to lymphocyte depletion and profound neutropenia, was associated with high rates of infectious complications, as was expected from experience with its use in haematology [32]. A clear association of drugs with specific types of infections, as is known for tuberculosis (TB) and anti-TNF-α agents, can not be derived from the still limited data from PSV trials.
Types of vasculitis
As shown in Table 1, there are large differences regarding the forms of PSV and their infection-related mortality. Infections and mortality from infectious complications are much more prevalent in SVV than in large vessel vasculitis. In GCA trials, mortality ranged from 0 to 0.03 deaths per patient year and infections caused 0 to 33% of these deaths [4–11]. In SVV this range was 0 to 0.26 deaths per patient year and infections were involved in 0 to 100% of the fatal events [1, 17–37].
Interestingly, in most published clinical trials in GCA, PCP prophylaxis was not used. Despite the fact that high doses of GCs are a major risk factor for the development of PCP, no case of PCP has been reported within these trials [4–10]. In contrast, patients with antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV), especially those with Wegener's granulomatosis (WG), are at high risk for PCP that can not be attributed only to medication [18–29]. There is evidence that at least some entities within the group of PSV confer an altered function of the immune defence per se. In WG, for instance, the granulomatous inflammation of the upper respiratory tract leads to destruction of the barrier function of the surfaces, possibly allowing for invasion of pathogens [43]. It may also be possible that a primary barrier deficiency not only promotes infections but has a role in the aetiology of the disease itself [44].
Disease stage and phase of therapy
In PSV, and especially in SVV, the therapeutic approach usually consists of an induction of remission and a maintenance phase (for review, see [45]). For induction, more aggressive regimens, including Cyc and higher GC doses, are utilised. Furthermore, in SVV the selection of drugs depends on the stage of the disease: in the localised and early systemic stage - that is, disease without threatened vital organ function - induction of remission is usually attempted with medium potent immunosuppressants such as MTX, whereas in generalised and severe disease - that is, with threatened vital organ function or organ failure, respectively-Cyc is used.
In SVV the induction of the remission period is the most vulnerable phase concerning infections and mortality. From studies assessing only maintenance of remission, published mortality rates ranged from 0 to 0.01 deaths per patient year and infections did not significantly contribute to those fatalities [18, 21, 23, 27, 28, 30]. In contrast, trials on induction of remission in SVV reported mortality rates up to 0.26 per patient year. In those trials infections were responsible for the fatal events in up to 100%, and about 50% of deaths, on average, were due to infections [1, 17, 20, 22, 24, 26, 29, 31–37]. Accordingly, mortality was higher in study populations with more severe disease. The highest reported rate was in SVV patients who presented initially with organ (renal) failure [1]. But even in this population, in which one might expect a higher contribution of uncontrolled disease to the death rate, infections are involved in more than 50% of the fatal outcomes.
Types of infection and options for prophylaxis
Bacterial infections
In PSV trials Staphylococcus aureus is the isolate for which fatal outcome has been reported most frequently. As demonstrated in surgical patients and patients on dialysis, prophylactic topical treatment with mupirocin ointment for nasal carriers of S. aureus leads to a significant reduction in the rate of infections with this agent (relative risk 0.55 according to [46]). Especially in WG, the incidence of nasal colonisation with S. aureus is higher than in controls and chronic carriage is associated with higher relapse rates [47]. In addition, relapses are often anteceded by infection, mainly of the upper respiratory tract [48, 49]. Furthermore, it is well documented that trimethoprim/sulfamethoxazole (T/S) treatment reduces the rate of relapse and is able to induce remission in some WG patients, especially those with localised disease [28, 50]. It is not clear whether this effect is achieved by its antibiotic or its immunomodulatory properties. Although its primary end point was relapse rates, the study by Stegeman and colleagues [28] clearly demonstrated a reduction in respiratory-tract as well as non-respiratory-tract infections using T/S in WG patients in remission. This study can be regarded as the only large scale trial of anti-infective prophylaxis in vasculitis.
As topical mupirocin does not cause serious adverse events [46], it is used in some vasculitis centres during the high risk phase of induction of remission in SVV (seven subsequent days three times daily per month). One concern, however, is that with mupirocin there is an increase in infections other than those due to S. aureus [46]. For reasons of possible development of resistance as well as compliance problems, long-term use should be avoided.
Besides topical treatment, systemic antibiotics are another option for AIP, although they have not been used in PSV remission induction trials so far. From randomised controlled trials using, for example, levofloxacine in patients with malignancies during chemotherapy-induced neutropenia (<500 neutrophils per microlitre), it is known that a reduction in the incidence of neutropenic fever and hospitalisation can be achieved [2, 3]. An effect on mortality has not been demonstrated and there are concerns regarding the long-term outcome of such interventions on microbial resistance in the community. As the treatment of PSV using standard protocols does not usually lead to prolonged neutropenia and the effectiveness of chemoprophylaxis with, for example, levofloxacine with regard to mortality has not been proven in patients treated with more intense chemotherapy, there is no standard setting for which the use of systemic antibacterial prophylaxis can be recommended. Although clear evidence for its use during induction of remission - apart from PCP-prophylaxis - is missing, T/S has proven its ability to reduce bacterial infections in patients with WG [28] and, therefore, might be considered in high-risk patients.
Other antibiotics, such as levofloxacine, might only be considered in refractory heavily pre-treated PSV patients undergoing salvage therapy with drugs known to induce severe neutropenia - for example, campath-1H.
Pneumocystis jiroveci
The risk of PCP is especially high in patients with SVV undergoing induction therapy. Without using prophylaxis the incidence of PCP is up to 20% [26] and many fatalities have been reported in earlier trials [22, 24, 26, 29]. It has to be mentioned, however, that the causes of deaths in those patients were multi-factorial and often due to several infectious agents simultaneously. Furthermore, some of the mentioned studies referred to the same patient population [22, 24, 26]. In a retrospective analysis, Ognibene and colleagues [51] found an estimated PCP incidence of 6% in a cohort of 180 WG patients. PCP occurred during induction of remission. Estimating the risk of PCP during induction of remission is further complicated as therapeutic strategies have changed over time, leading to lower cumulative Cyc doses and less frequent use of high dose intravenous GCs. Simultaneously, T/S use as PCP prophylaxis has gained widespread acceptance. Unlike in HIV infection, where a low CD4 count is the strongest risk factor, such factors are insufficiently defined in PSV patients. There is evidence that older age is an independent risk factor [52]. Patients with WG seem to be at increased risk compared to other AAV or PSV patients in general. In WG a low lymphocyte count before and during therapy is associated with PCP [51, 52]. Generally speaking, prolonged (>1 month) GC use at doses >15 to 20 mg per day is the best defined risk factor [53, 54]. Other immunosuppressants, especially Cyc, also increase the risk of PCP [54].
Although, as for all other potential indications for AIP, there are no clinical trial data on PCP prophylaxis in PSV patients, there is some evidence for its use in SVV (level B to C): infection rates were much higher in trials not using prophylaxis than in those recommending it [22, 26]. Mahr and colleagues [24] introduced T/S prophylaxis during an ongoing protocol as a reaction to high rates of PCP and reported effectiveness. In their analysis, Chung and colleagues [55] concluded that PCP prophylaxis is cost-effective in WG patients unless the annual incidence of PCP fell below 0.2%. According to the EULAR recommendations, T/S prophylaxis is encouraged in all patients being treated with Cyc [56]. The British Society for Rheumatology (BSR) formally recommends PCP prophylaxis at a dose of 960 mg T/S thrice weekly or of 300 mg inhaled pentamidine in all AAV patients treated with GCs and Cyc [57].
Even though PCP is rare in large vessel vasculitis, the use of T/S prophylaxis in all PSV patients receiving GCs >15 mg per day and a GC-sparing immunosuppressant (for example, MTX) might be considered. As severe adverse event rates with T/S are generally low and cessation of the medication is reported in only about 3% of non-HIV-infected patients [58], generous use seems to be appropriate considering the still severe prognosis of PCP in this patient population [59]. However, the potential interaction of MTX and T/S has to be taken into account and strict folate substitution is mandatory. Furthermore, it has to be stressed that there is only little evidence from trials to support T/S prophylaxis in patients receiving medium potency immunosuppression. Its use should be discussed individually according to local praxis.
It is not clear for how long PCP prophylaxis should be given. In some centres one criterion to stop PCP prophylaxis is a GC dose tapered below 15 mg per day and/or the cessation of Cyc therapy. This praxis is based on the observation that PCP in non-HIV patients under GC medication occurred mainly with doses above 15 mg per day [54]. In analogy to experiences in HIV patients, it has been suggested to measure CD4 cell counts and to stop prophylaxis when this value is above 200 per cubic millimetre [60]. However, other risk factors such as impaired cell functions are underestimated by this approach.
CMV is a herpesvirus that leads to latent infection. Its prevalence ranges between 60 and 100%, depending on the geographic area [61]. CMV reactivation leads to a high burden of morbidity and mortality in immunocompromised persons, an interrelation best studied in transplantation medicine [62]. The spectrum of manifestations ranges from non-symptomatic infection to life-threatening disease, for example, pneumonitis. The scale of this problem in rheumatology and especially in PSV patients is insufficiently defined but appears to be less severe in most cases. In vasculitis patients leucopenia is the most frequent manifestation. However, in clinical trials some cases of CMV illness have been described with a relatively high proportion of fatal outcomes [20, 22, 25]. Large scale underreporting must be assumed, since until recent years reliable detection methods have been missing and the awareness of this problem appears to be still low. Mori and colleagues [63] found a high incidence of CMV reactivation in CMV-seropositive patients with connective tissue disease undergoing immuno-suppressive therapy. A recent study by Takizawa and colleagues [39] suggests that GC use, especially in the form of pulsed methylprednisolone as well as other immuno-suppressants, primarily Cyc, are the major risks factors for CMV reactivation in rheumatic diseases. In PSV, and especially in WG, CMV reactivation is an important differential diagnosis if neutropenia occurs.
In solid organ transplant recipients prophylaxis with, for example, ganciclovir or valganciclovir reduces CMV disease [64]. If CMV disease occurs in severely compromised patients with rheumatic diseases, anti-viral therapy might be without benefit as reported by Takizawa and colleagues [39] in a cohort of 85 patients. As CMV itself leads to further immunosuppression, fatal co-infections are promoted [39]. Taken together, these are arguments in favour of anti-viral prophylaxis in CMV-seropositive PSV patients undergoing intense immunosuppression. However, as data from clinical trials are missing, no evidence-based recommendation as to which patients should be introduced to prophylaxis can be given. In praxi prophylaxis (valganaciclovir 900 mg once daily) might be considered only in severely ill PSV patients who need high dose methylprednisolone pulses or Cyc, especially if they had experienced earlier CMV reactivations. An alternative to this, as well as for other latently infected patients who need intense immunosuppression, is the preemptive approach, which also has been proven to be effective in organ-transplant recipients [65]. This requires quantitative monitoring of CMV - for example, by measurement of early antigen (pp65)-positive cells. Takizawa and colleagues [39] suggested a threshold of 5.6 pp65 positive cells per 105 polymorphonuclear cells. Measurement of early antigen is increasingly replaced by quantitative CMV-PCR, which is currently the method of first choice.
Varicella zoster virus
Varicella zoster virus (VZV) reactivation leads to herpes zoster (HZ). Whereas age is the most important risk factor for the development of HZ [66], autoimmune diseases and especially immunosuppressive therapy with Cyc and GCs further increases the probability of reactivation [67]. Several PSV trials report relatively high numbers of VZV reactivation and HZ [28]. However, underreporting of this usually non-life-threatening condition is likely. HZ causes substantial morbidity, especially when post-herpetic neuralgia develops, which is the case in up to 20% of the elderly population [68].
Despite these facts, no trial in PSV has included VZV prophylaxis to our knowledge, although it is feasible and effective at least in patients receiving haematopoietic stem cell transplantation using, for example, aciclovir (2 × 800 mg per day) or valaciclovir [69]. The reason for not administering VZV prophylaxis in PSV may be the high potential for drug interactions and adverse events, especially in patients with renal impairment and the non-life- or organ-threatening nature of HZ in this population. In general, VZV prophylaxis is not recommended in PSV patients. It might be considered only in selected patients who have experienced several VZV reactivations and have an ongoing need for intense immunosuppression. More importantly, patients should be trained to recognise the early signs and symptoms of HZ to enable the immediate start of anti-viral therapy in the case of possible HZ.
Vaccination to avoid HZ is available and effective [70]. In the US it is recommended by the Advisory Committee on Immunization Practices for all persons older than 60 years [70] but it is not recommended in patients under immuno-suppressive medication [71]. Whether patients in remission from PSV under mild immunosuppression may benefit from vaccination warrants further investigation.
Invasive fungal infections (other than PCP) are rare in PSV. Risk factors for the development of pulmonary Aspergillus sp. infections are prolonged episodes of neutropenia and prolonged use of high-dose GCs [72]. Few cases of invasive Aspergillus infections and fatalities in PSV have been reported [13, 22, 24].
There is generally no indication for the prophylactic use of systemic anti-mycotics in PSV but aspergillosis should be considered as a differential diagnosis in patients if fever of unknown origin does not resolve under a calculated antibiotic therapy.
In contrast to invasive aspergillosis, Candida infections of mucosal membranes are a frequent complication of GC treatment, although leading to invasive candidiasis only very rarely. Nonetheless, oral candidiasis or candida esophagitis are painful and might hinder oral nutrition. In critically ill patients and solid organ transplant recipients prophylaxis using fluconazole is effective in avoiding invasive candidiasis [73, 74]. Using topical non-absorbable antifungal prophylaxis in immunocompetent critically ill patients leads also to a significant reduction in fungal (mainly non-invasive) infections [75]. According to the BSR, prophylaxis with nystatin, amphotericin or fluconazole should be considered in all AAV patients receiving high-dose immunosuppressive therapy [57].
In praxi amphotericin suspension in all patients under long term GC medication with a dose of >15 mg prednisolone per day can be recommended because it is effective, non-absorbable and associated, therefore, with very few side effects. According to a meta-analysis, the non-absorbable nystatin is not more effective in avoiding fungal colonisation than placebo and can not be recommended [76]. Additionally, all patients should be instructed to perform daily self-inspections of the mouth in order to detect mucosal candidiasis early.
Mycobacterium tuberculosis
Only a few cases of TB have been reported in PSV trials, although some of these have been fatal [16]. PSV studies using TNF-α blocking agents included TB screening as a reaction to TB reactivations in early rheumatoid arthritis trials. Therefore, TB reactivation has not been seen in those studies [9, 10, 19]. While a general prophylaxis is clearly not indicated, screening for latent TB should be part of the work-up in PSV patients. For this purpose a full history, physical examination and a chest X-ray is recommended by the BSR guidelines [57], procedures that can be considered to be part of routine care. If latent TB is detected in a patient planned to start induction therapy for PVS, we recommend TB prophylaxis. According to a recent study, rifampin over 4 months might be safer and associated with better adherence than standard 9-month isoniazid [77]. As long as further trials are unavailable, we consider isoniazid plus vitamin B supplementation to be the standard of care, with rifampin being a good alternative in case of incompatibility.
In some PSV, especially in WG, infliximab is used as salvage therapy. In such cases screening and prophylaxis for TB should be performed as recommended for the use of infliximab in rheumatoid arthritis [78].
Possible use of anti-infective chemoprophylaxis in primary systemic vasculitis patients
Infectious agent
Prophylactic measure
Appropriate clinical situation
Level of evidence
Pneumocystis jiroveci
Trimethoprim/sulfamethoxazole 960 mg thrice weekly. Alternative: monthly aerolized pentamidine (300 mg)
Should be given to all patients receiving long term glucocorticoid >15 mg/day and additional intense immunosuppression
B to C
S. aureus
Nasal mupirocin ointment three times daily for 7 consecutive days per month
Might be given to patients with generalized SVV who are S. aureus carriers during induction of remission
Mycobacterium tuberculosis
Isoniazid 5 mg/kg per day up to 300 mg plus pyridoxin (vitamin B6). Alternative: rifampin 10 mg/kg per day up to 600 mg
If latent tuberculosis is detected and immunosuppression necessary, especially when infliximab is used
Varicella-zoster virus
Aciclovir 2 × 800 mg per day
Generally not recommended, but might be considered in very selected cases with several reactivations and ongoing need for intense immunosuppression
Zoster vaccine
Not recommended
Valganaciclovir 1 × 900 mg per day
Not generally recommended, but might be considered in selected severe cases with earlier reactivations and ongoing need for intense immunosuppression
Aspergillus sp.
For example, posaconazole
Not recommended
Candida sp.
Oral amphotericin B suspension, 4 × 1 ml (= 100 mg) per day
Should be considered in patients with long term glucocorticoid therapy >15 mg/day
ANCA associated vasculitis
anti-infective prophylaxis
antineutrophil cytoplasmic antibody
British Society for Rheumatology
- Cyc:
European League Against Rheumatism
giant cell arteritis
herpes zoster
Pneumocystis jiroveci pneumonia
primary systemic vasculitis
small vessel vasculitis
tumour necrosis factor
varicella-zoster virus
Wegener's granulomatosis.
This work was supported by "Deutsche Forschungsgemeinschaft" KFO 170.
Authors' Affiliations
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text:
Courteney Cox and David Arquette are still officially separated, despite co-starring in the just-released "Scream 4" and taking family trips to Disney World with their daughter, Coco.
On Wednesday's "Late Show with David Letterman," Cox talked candidly about the separation and her reaction to Arquette's drunken blathering to Howard Stern about details of their sex life.
Cox did give Arquette credit for having more than 100 days of sobriety, but did say that she was uncomfortable with Arquette's admission to Stern that he'd tried to hit on Cox on the Disney trip and been shot down.
But, since the cat is already out of the bag, Cox confirmed the story to Letterman, saying, "He did try to hit on me. He hit on me pretty hard and I said no more fast pass right now. Not that ride."


text:
This is your resource to discuss support topics with your peers, and learn from each other.
05-01-2013 10:05 AM - edited 05-01-2013 10:08 AM
Hi BB Community,
We have just migrated some users from Lotus Notes to Microsoft Exchange 2010 SP2 RU4, we run BES 5.0.4 for Exchange. Users who were previously migrated (eg a few weeks ago are working fine still, SRP is connected fine, CAL's are fine, I completely wiped the blackberry's and then reset to factory (to remove old BES keys) and installed the latest ROM. However when I go to activate any of them it just sits on the Contacting Server... Users get the ETP.dat sitting in their Exchange mailboxes but it never gets cleared out by the BES server.
Looking through the logs i believe my problem is due to the following error.
[30041] (05/01 23:34:53.960):{0x4CC} Starting handheld for User1
[30463] (05/01 23:34:53.960):{0x4CC} User User1 can not be started, ServerDN not defined, user may restart after ScanGAL
[20154] (05/01 23:34:53.960):{0x4CC} User User1 not started
I have checked the ServerName field for the respective user in the MSAddresses table and I can see the entry does not exist for these new users. I did a rebuild of the Exchange offline address book, gave it a while and then have tried multiple times to execute the "Refresh available user list from company directory" from the new user section and also the Blackberry Solution Topology > Blackberry Domain > Component View > Email
The following article describes my exact problem. Unfortunately these users will want their blackberry's back in about 8 hours so i am really hoping someone can point me in the direction to force the ServerName field to update and or it magically happens in less than the "24 hour" period.
Thanks in advance
Hello LeighMo,
Thank you for your question regarding the ServerName field not updating.
The following article will show you how to manually "Refresh available user list from company directory" - http://www.blackberry.com/btsc/KB17400
If this process does not work you may need to check the BlackBerry Enterprise Server logs located at C:\Program Files(x86)\Research In Motion\BlackBerry Enterprise Server\Logs\<Today's Date>. If you look at the MAST log it will show an attempt to update and will show any changes or fails at the bottom of the file.
We hope this helps.
Come follow your BlackBerry Technical Team on Twitter! @BlackBerryHelp
Click "Accept as a Solution" for posts that have solved your issue(s)!
Hello LeighMo,
Normally the ScanGal will start after 12 minutes; this can be forced by the "Refresh from company directory" feature in BAS. If forcing the update and all things being equal with no issues in communication in the environment, the BES should retrieve the updated Global Catalog or GC fairly quickly, although this can depend on the size of the user base.
If you have confirmed the above I suggest contacting BlackBerry Support for further assistance.
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Thanks for the reply smoothrider, I have tried all of your suggestions and I am still having the same problems. I am not sure if the fact these users are mail-enabled (AD user as a contact, no mailbox on exchange) to start with and then because we are migrating them over to be full mailbox enabled users something weird is happening. But that ServerName field still has not updated after trying all of the above suggestions, also tried rebuilding the GAL thought that could have been part of the cause as it would have had them as a contact, yet now they are mailbox enabled.
Either way our last migration is this weekend so looks like its going to remain unresolved, but thanks for the assistance Fozzie and SmoothRider


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text:
I have found the issue with Sunbird 0.5 but I've reproduce it also with Mozilla/5.0 (Windows; U; Windows NT 5.1; en-US; rv:22.214.171.124pre) Gecko/20070813 Calendar/0.7pre. Couldn't find any similar bugs.
After creating a four hour event I moved it to Sunday. Start time of modified event was on Sunday and end time on Monday following week. Then I clicked on it and moved to earlier hour. The shadow showed wrong duration i.e. one hour.
Steps to reproduce:
1) Switch to week view (Monday is first day of the week)
2) Create an event "meeting" (Wednesday 20:00-23:00)
3) Drag and drop it to Sunday ( new start time is 23:00)
4) Click on it and move to earlier hour---> look at the shadow
Shadow shows wrong duration
Confirmed with Mozilla/5.0 (Windows; U; Windows NT 5.1; en-US; rv:22.214.171.124pre) Gecko/20070813 Calendar/0.7pre.
Decathlon, since you were working on that other dragging bug, maybe this one interests you too?
Created attachment 408446 [details] [diff] [review]
[checked in] patch
This patch should fix this issue and another one that actually I don't understand if it's a bug or a wanted behavior because the code has been written to work in this way: when you drag an event in the same day, you can't move it backward over 0:00 i.e. it's impossible to move the start time in the previous day. I don't know if there is a reason for this behavior, I haven't found a bug related to it, but I've changed it because working on this bug, the required changes are minimal and, if I don't miss something, it seems working without problems.
Comment on attachment 408446 [details] [diff] [review]
[checked in] patch
Looks good. The other issue you mention is indeed a bug, thanks for fixing it.
Now all we need is that the shadow automatically spans multiple days when moving an event past midnight. Do we have a followup bug for that?
>+ // don't let mouse position go outside the window edges
>+ if (mousePos < 0) {
>+ mousePos = 0;
>+ }
>+ let pos = mousePos - dragState.mouseOffset;
This could be:
let pos = Math.max(0, mousePos) - dragState.mouseOffset;
>+ if (dragState.endMin > 1440) {
>+ dragState.endMin = 1440;
>+ }
>+ if (dragState.startMin < 0) {
>+ dragState.startMin = 0;
>+ }
Same here:
dragState.endMin = Math.min(1440, dragState.endMin);
dragState.startMin = Math.max(0, dragState.startMin);
I'll change this before checkin.
Pushed to comm-central <http://hg.mozilla.org/comm-central/rev/3d6970158465>
and comm-1.9.1 <http://hg.mozilla.org/releases/comm-1.9.1/rev/f9d0d59c03f5>
Reopened because there are a pair of issues in particular cases.
1. Events with start time at 0:00 and end time the day after or more days after:
dragging the event from the first day and move it to later hours, the shadow doesn't follow the movement like should do (since the event starts at 0:00).
2. Events with duration greater than 24 hours spanning over three or more days
(i.e. that have at least a full day):
dragging the event from the full day and move it to earlier hour, the shadow has incorrect length because doesn't keep in count the event part after the full day.
Both issues are caused by the end minute used to figure out the shadow length.
I have a patch but I want testing a bit before attaching it.
(In reply to comment #4)
> Now all we need is that the shadow automatically spans multiple days when
> moving an event past midnight. Do we have a followup bug for that?
The shadow should also cover the whole event to show the right position when dragging events that spanning more days, but actually it covers only the event part in the day where drag session has started.
I haven't found a bug about this issue, I will file a new one.
Created attachment 410660 [details] [diff] [review]
fix for issues in comment #6
The problem was the end date used to calculate the shadow size. With the real end date and the real start date of the occurrence that spans multiple days, it seems everything fine.
I've also reverted the behavior of the snap (the movement with 15 minutes rounded jump) like the previous code: always to the start side (even if it is in the other day where, for now, the shadow doesn't span).
Comment on attachment 410660 [details] [diff] [review]
fix for issues in comment #6
Looks good, r=philipp
Pushed to comm-central <http://hg.mozilla.org/comm-central/rev/e00dce0f3aaf>
and comm-1.9.1 <http://hg.mozilla.org/releases/comm-1.9.1/rev/779297b4cf98>
Verified with Mozilla/5.0 (Windows; U; Windows NT 6.1; pl; rv:126.96.36.199) Gecko/20091112 Lightning/1.0pre Thunderbird/3.0
(In reply to comment #4)
> Now all we need is that the shadow automatically spans multiple days when
> moving an event past midnight. Do we have a followup bug for that?
If it isn't a duplicate, I've just filed Bug 533414.
These bugs are likely targeted at Lightning 1.0b1, not Lightning 1.0. If this change was done in error, please adjust the target milestone to its correct value. To filter on this bugspam, you can use "lightning-10-target-move".