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LEXINGTON, Ky., Oct. 27 (UPI) -- A study using animals found watermelon reduced atherosclerosis -- hardening of the arteries, U.S. researchers say.
Lead investigator Dr. Sibu Saha of the University of Kentucky in Lexington and colleagues said the study used animal mice with diet-induced high cholesterol.
A control group was given water to drink, while the experimental group was given watermelon juice.
By week 8 of the study, the animals given watermelon juice had lower body weight than the control group, due to decrease of fat mass, the researchers said.
The mice experienced no decrease in lean mass and plasma cholesterol concentrations were significantly lower in the experimental group, with modestly reduced intermediate and low-density lipoprotein cholesterol concentrations as compared to the control group, Saha said.
A measurement of atherosclerotic lesion areas revealed that the watermelon juice group also experienced statistically significant reductions in atherosclerotic lesions, as compared to the control group.
"Melons have many health benefits," Saha said in a statement. "This pilot study has found three interesting health benefits in mouse model of atherosclerosis. Our ultimate goal is to identify bioactive compounds that would improve human health."


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Thieves looking to cash in on high metal prices have been walking away with copper downspouts, iron manhole covers, brass mailboxes and even bronze plaques from veterans' graves.
Add to that list: the copper guts of residential central air units.
Police said last week that copper tubing was taken from inside three units on the 6800 block of Walker St. in Tacony on Dec. 1. No one has been arrested in the thefts.
Janice Hall, who has lived on the block for 28 years, was one of the victims. She's not sure what fixing her central air unit will cost her, and she's not going to bother to get the work done right away.
"I don't intend to get it replaced or fixed until the spring because I don't want to get ripped off again."
And then, she said, she's going to make sure the unit is secure enough that someone can't do the same kind of damage again.
For several years, police have been warning residents how vulnerable they are to thieves bold enough to swipe even metals that are attached to houses. Copper downspouts on older homes have proved easy targets, Capt. Frank Bachmayer, then-commander of the 15th Police District, had said earlier this year.
The Northeast Times reported in May that thieves stole, then dumped, four 20-pound bronze markers from veterans' graves. Bronze was fetching $1.70 per pound at that time. The profit the thieves might have realized is easy to calculate. Each 20-pound marker could have sold for $34. Multiply that by four, and the result is $136 — not really a lot of money when the risk of getting arrested is considered.
The thieves who took the copper out of Hall's and her neighbors' central air units probably caused more damage than they gained in profit.
Copper is at $2.80 a pound, said Justin Comerford, office manager at S.D. Richman Sons, a Port Richmond metals dealer. That's not the all-time high for the metal, but it's pretty high, he said, adding there might just be a couple pounds of copper in each central air unit. Again, the arithmetic isn't hard. Each unit might yield $6 to $8 in copper. Multiply that by three, and the top result is $25.
Most other metals are nowhere near as valuable as copper, which means the thieves who swipe iron, for example, are doing a lot of heavy lifting to get little return.
If they worked as hard legitimately, Comerford said, "they'd probably make something of themselves." ••
Reporter John Loftus can be reached at 215-354-3110 or firstname.lastname@example.com
You can reach John Loftus at email@example.com.

subset: commoncrawl


text:
A 'Mass Salon" event at the Texas Nurses Association meeting April 20, 2016
Posted by mariemanthey in Uncategorized.4 comments
Texas has done it again. Last Saturday I introduced Salons to the House of Delegates and for the next two hours, about 170 delegates experienced a Salon conversation at their tables. The same format was used…check in, have a conversation, check out. It is such a simple formula, I am always amazed at what happens at an experiential level. After each table had 'checked out' we had a room wide sharing. And that is where the magic and/or miracle was seen. Among the comments was amazement at how easy and conversation flowed.."like fish moving in a school"…..it seems organic and effortless the way the conversation moved based on the check-in. Another comment was how easy it was despite vast age and experience differences.. "Amazingly energetic". Easy to reach common ground. Nursing has the same values no matter where is it practiced. Found the bedrock of who we are….reached common ground. And finally as always….the word Hope came through. This seems to be an almost universal result of a salon conversation.
The reason I was asked to do this by the TNA is they are encouraging their members to form Salons all over Texas….and the members present were encouraged to become or recruit hosts in their regions. The TNA will provide a website to post information about all meetings, including the opportunity to RSVP right on the website. This is a really important development and will greatly facilitate the success of this movement.
Thank You Texas….for once again Thinking Big
A Salon in New Mexico February 12, 2016
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Next week on Feb. 23 There will be a Salon in Albuquerque.……my hope is that someone gets them started both here and in Sante Fe and I also hope that the movement continues to grow, as it does make a difference!
In a way it reminds me of my early experience with Primary Nursing. The growth was organic. From a couple of short articles in the literature (same with salons) to years of talking about it and helping others get it started…(during which time it was unclear what the impact was) to a slow spreading throughout the profession ( including education finally) and throughout the world. Just like Salons (I hope)…Primary Nursing was alsosort of 'under the radar' of officialdom in health care. No nursing organization ever officially endorsed the concept. No financial impact was ever recognized by the system. For years/decades, I was asked 'how widespread is Primary Nursing throughout the country? For which I had no answer. No one ever counted up the implenentations! No national surveys were done. Ever. We still don't know.
The same thing is happening with Nursing Salons….people ask me where are they happening? Sometimes we hear they are happening….but mostly not…it is a happening! Simply a happening. When Salons 'happen' all over the country, change
happens all over the country. Funny, isn't it?
REFLECTION AND RESOLUTION CONTINUED! January 3, 2016
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Here it is the first Sunday in January and I am actually keeping my resolution to post regularly! Sort of squeezing it in a busy day but here it is. The third area of my current interest and energy choice is the Nursing Peer Support Network we recently created in Minnesota. Many of you know that I have been an active member of the larger nursing community for many decades….over 50 years as a nurse. Some of you also know that for 37 of those years I have been in recovery from the disease of alcoholism……in fact, the majority of my 'visible' contributions to nursing have been accomplished during these 37 years.
At no time during this period of my recovery, during which I have been an active participant in a 12 step program …..did I even SEE what generally happens to nurses who become addicted to either drugs or alcoholism. During the past 2-3 years, I have seen this clearly and am frankly appalled. Two issues in particular 'appall' me;
One is the lack of knowledge nurses have of the continuum that exists from taking that first Percocet or Vicodin ….by 'diverting' it from a patients supply…….to a consequence a few years later when up to 15% of them are facing criminal proceedings even perhaps a felony conviction, which essentially means loss of ones license to practice nursing. We are not doing a good job of making this danger clear to nurses.
The second issue is the paradoxical thinking that leads to an enormous issue of profession shame about the stigma of addiction. The paradox that we hold simultaneously in our 'profession's mind set' is that addiction is both a disease and a moral failure.
The ambivalent feelings and attitudes many nurses have about addiction can be attributed to many factors having to do with family issues, as well as experiences caring for addicts. Nevertheless, as a profession we really need to step up in a mature understanding that addiction is a disease from which individuals can recover and return to their profession with full capacity to be highly effective practioners.
Many states have programs to help nurses into safe recovery. Minnesota did not until we established one a little over a year ago. It is called the Nursing Peer Support Network and the website is http://www.npsnetwork-mn.org.
I will periodically be posting more on this topic as recovery from addiction is a process very similar to what we in nursing are doing in recovery from a state of co-decency to our rightful state of full professional status. I have learned so much in this past year and feel deep passion that we need to face the stigma of addiction fully in order to help the 'still suffering addicted nurse'.
Happy New Year….R & R December 27, 2015
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R & R refers to Reflection and Resolution. My goal in writing this is to honor the end 2015 with reflection and with the same post honor the beginning of 2016 with a committed resolve to keep up the post. My track record for keeping the post relevant is not good, and I intend to develop a 'posting habit'. Goodness knows I have enough life experience creating both good and bad habits, that I should be able to be successful in doing this.
My reflection about the past year is based on the three major areas I now choose to spend my time and energy. They are 1) Clinical practice issues, 2) the history of nursing, especially the U of MN School of Nursing and 3) my newest passion, creating a peer support service for nurses in addiction/recovery/reemployment. (upon immediate reflection….this will either be a couple of posts….or one very long one!)
First of all, Clinical Practice issues. The work of the company I founded, Creative Health Care Management, continues to function as Health Care thought leaders through speaking at national conference, publishing thought-provoking professional books, articles and a quarterly journal, and helping care systems provide a healthy culture for people receiving care and those caring for them. (A very tall order!) I have the sheer pleasure of working with colleagues who are value driven, highly experienced change agents. When we get together and talk about our work (twice a year) it is like the best think tank you can imagine. I will try to do a better job of telling you the exciting ideas and realities of this work.
My love of history started with Primary Nursing. I hated history as a student and therefore knew little about it. Something about Primary Nursing spoke to me about the past so I started reading old AJN's. Amazing! Shortly I was hooked on history, fell in love with Nightingale's story and continued paying attention to history for a couple of decades. In retirement (!) I joined the Heritage committee of the U of MN SON and became chair of the committee several years ago. This committee is made of six people who are passionate about understanding history and who delight in making the connection between the past and the future. We are one of the most hard-working committees of the Alumni Society and our engagement is such that we spend many hours on our subject in addition to the six hours/month in our committee meetings. Faculty and students, with great leadership from Dean Connie White Delaney, have come alive with interest in history and it is being incorporated into curriculum with increasing frequency.
In my next post, I will continue this year end reflection by sharing a newly developed passion for helping nurses who are dealing with addiction, recovery and re-entry into the profession.
Thanks to all who read this. Please dialog with me and with each other. Back soon.
NURSES IN RECOVERY….. September 1, 2014
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Substance use is a serious problem in society and even more serious in the nursing profession.
Nursing is the largest single licensed group within health care. Nurses spend the most time of any health professional in close contact with highly addictive drugs. Historically, chemical dependency and alcoholism have long been identified as significant issues for the profession. Addiction continues to be a major problem….and yet, no nurse enters the field expecting to succumb to a hidden trap that will jeopardize his or her own life and/or license and which may in fact cause harm to vulnerable people entrusted to their care.
The sacred, trusting covenant the nursing profession has with the public is ripped apart by the disease of addiction. Statistically, at least one in ten nurses will acquire a Substance Use Disorder (SUD) within his or her lifetime.
SUD identification often results in an intervention that brings the individual into a place of treatment. Regardless of how that identification is triggered, two actions ensue….the regulation of practice to protect patients and treatment of the disorder. Both the regulation by the Board of Nursing and the reality of treatment and recovery are major life consequences that are challenging and life changing. The need for peer support groups is well understood and already established for most other health professional groups, including physicians, pharmacists and dentists, but there is no such support group for nurses in Minnesota.
UNTIL NOW. A new organizatin is being formed called the Nursing Peer Support Network. Contact me for further information until our website is up. Meanwhile….this is a draft of our eventual goal statement.
To create within the nursing profession a commitment to value every single nurse….especially those on the road to recovery from SUD. This commitment is manifested by 'return to work strategies' that permeate every level and type of employment opportunity throughout healthcare. Nurses will become literate about SUD and recovery and be able to help others in places of employment better understand how to reduce the risks of employing in recovery…..even those with felony convictions. Various strategies and educational opportunities will be created to achieve this goal.
We need you help and support. Feel free to contact me via blog directly to my email or call me at 612-827-1611
A Labor Day reflection: CHOICE AT WORK! September 1, 2014
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I am one of the lucky ones….I knew nearly all my life that I wanted to be a nurse. When I was 5 years old, I was hospitalized for a month during which time I truly felt abandoned by my parents and worse yet, when they did come, a very painful procedure was performed on me. During this time, a nurse named Florence Marie Fisher colored in my coloring book. For reasons only known to God, that meant to me that she cared for me….in the fullest sense of that word care.
I knew from then on that being able to do that for another person was exactly what I wanted my life to be about…..and I've never looked back!
What made it full of wonder is that I have been able to learn so much about how to live from my work. A beautiful framework for living came through my work when I was involved in the original development of Primary Nursing. The framework links the concepts of responsibility authority and accountability in a dynamic relationship that can serve to correctly inform the proper relationship among people….the proper structure for an organization….the proper content of a job description. When each of those three elements….responsibility, authority and accountability are viewed in their proper sequence….when responsibility is legitimately allocated and authority commensurately delegated and accountability mechanisms are designed for recognition and education (and not for punishment)….then all aspects of an activity can be functional….and personal relationships can be healthy. But the most important thing I finally learned (sometime in my mid-forties) is that these same elements are at work in my life. The moment I call my epiphany occurred with a blinding flash of insight…..during which I instantly saw that as long as I blame someone else for whatever is wrong in my life, I am not accepting responsibility for myself. I decided to learn how to change that, and I have never found it necessary to feel victimized by any person or situation or institution again.
What does all this have to do with work? I believe we all have choices every day about all aspects of our work …..and that the choices we consciously (and unconsciously)make have the power to either expand our spirit….or to destroy it. I am continually amazed at how many people tolerate working in dysfunctional systems …..or in toxic workplace cultures, of for mean-spirited power hungry immature bosses. I know there are many factors operating that may reduce ones awareness or perception of choices. Nevertheless, I have come to believe that even in the most oppressive environments….consciousness of choice instead of consciousness of victimization is the key to being able to grow spiritually.
Ultimately, I think the real lesson to be learned is that we have a choice to manage ourselves…..or not. Self management means being aware of the importance of healthy interpersonal relationships. Open communication (no back-biting) functional trust and mutual respect are the three key ingredients to healthy interpersonal relationships. Open communication means taking the time to learn the tactful way to talk about difficult issues with co-workers….it is a skill we can choose to learn. Trust is a choice we need to be willing to risk giving…..because withholding it breeds only more mistrust….and mutual respect requires the judgment to see everyone (at all levels of status and education) as being of equal importance to the overall workplace morale. And I learned that morale influences the quality of the product more that any other single or combination of factors. In my world that means that the morale of a nursing unit staff will have more impact on the quality of care patients receive than does any other single or combination of factors. And morale is solely determined by the way staff members treat each other in the context of workplace realities….including the reality of more work to do than time available.
These incredibly valuable lessons came to me from my work experience…..and they dovetail completely with what I have learned in recovery.
Consciousness of choice ….of how to respond to my co-workers….of how to be present in my work…. of my values of integrity and authenticity…all of these and more are the opportunities of learning and growth I have received through my work. And I know that all of this came about because Florence Marie Fisher colored in my coloring book when I was five years old. She created a caring relationship with me…..and permanently influenced my life.
She never knew that. I published a book about Primary Nursing in 1979, and dedicated it to her. The publishers tried to find her, but where unable to. Recently I came across those onion-skin copies of the publisher's letters to a couple of State Boards of Nursing trying to find her and remembered that they were unsuccessful in locating my Florence Marie Fisher. But I thought to myself that afternoon few months ago……Google! And so I googled her and found her obituary….which also listed her survivors. I have since had the pleasure of meeting her son and grandchildren and telling them about the impact she had….not only on my life…but also on my work, which has in turn influenced the experience of nurses and patients throughout the United States….and now also internationally. Of course they had no idea…..her simple act at work of coloring in my coloring book was a sublime act of co-creation. As nurses we can all find ways to choose to color in a coloring book. It is a choice we have to make, individually, and repeatedly. It is a choice that will not be documented….cannot be charged for….and that has a major impact on the lives of at least two people, the patients we care for and on ourselves. The choice to 'be with' the patient, instead of just 'doing for' changes the nursing experience for each individual who experiences this choice.
MinnPost Article on Nursing and Addiction May 29, 2014
Posted by mariemanthey in Uncategorized.2 comments
I was honored to be asked to talk with MinnPost reporter Sarah T. Williams about the problem of nursing and addiction. I'm really happy with how this turned out.To read the article, click here.
Gratitude breeds gratitude;discontent breeds discontent April 26, 2014
Posted by mariemanthey in Uncategorized.1 comment so far
Everyone is free every day to choose how they want to experience the day. As Dr. Phil says, ….we get to choose to contaminate or contribute…..every single day. Often, the stress and workload in bedside nursing and in most hospital managerial roles can obscure this truth. It can seem like everyone else has more impact on our experience than we do. '
However, we can opt to contribute by intentionally reflecting on the aspects of our lives and work that we are grateful for…..and we can intentionally refuse to spread discontent by not engaging in it….even when we are invited to do so by a colleague.
It is time for each of us to take back the power we have to manage our own lives. Choices have consequences. Let us be clear about that and aware daily that we own our life experience.
NURSE MANAGERS: DO YOU EVER HAVE FUN AT WORK? WHAT GIVES YOU JOY…..AT WORK? January 16, 2014
Posted by mariemanthey in Uncategorized.3 comments
Many years ago I had a NM role, and looking back on it I remember it as a very positive experience. Lots of times I knew we had done a great job and our work was appreciated by both patients and physicians and even our bosses. I wonder how often today there is any recognition for excellence in nursing practice. I don't mean just the HCAPS scores…. I mean the real deal.
Nurse Managers attend lots of meetings, fill out lots of forms, audit lots of stuff, and spend lots of time at their desk in front of a computer. Somehow, we have to get back to the notion that the NM is also a leader of the clinical practice of the unit. What if a NM spent just 15 min. a day ….every day asking a nurse about a patient story in order to just recognize, or even advance through inspiration a higher level of practice? What if a NM made a point of finding the good stuff the staff does and bragging about it? What can be done to improve the experience for Nurse Managers throughout the current system?
I'm really looking for some feedback from Nurse Managers about Fun and Joy….and what has worked for you to bring those experiences into your challenging role. You deserve it. You are the engine of the system. Take pride in your role and its importance.
Conversations Create Change November 12, 2013
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Recognition of the value of conversations to change ourselves and the world is slowly spreading organically from the experience of Salon conversations ….to using the same format and function in a variety of other settings. I have heard of using the question "What's on your mind about…..?" as a non-judgmental opening for wide-ranging issues. The very openness of the questions removes constraints that might otherwise hinder creativity and deeper dialog.
I continue to be amazed at the directions the conversations take in Salons…..especially the ones where different levels of nurses from different types of settings,with vastly different role experiences come together to talk. And Most Surprising Fact!!!! ….they never, never turn into Bitch Sessions. I'm not exactly sure why…..but I am reporting the truth.
I'm curious… how have you seen that simple question used to stimulate a conversation?


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So who is the Hispanic Fanatic?
Simply put, he has an IQ of 380, the strength of twelve men, and can change the seasons just by waving his hand. Despite these powers, however, he remains a struggling writer.
For the demographically interested, the Hispanic Fanatic is a Latino male who lives in California, where he works as a business writer. He was raised in the Midwest, but he has also lived in New York.
He is the author of the novels Barrio Imbroglio (available here) and Zombie President (serialized here).
He blogs because he must.
He can be reached at firstname.lastname@example.com


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Volume 12, Number 1—January 2006
1918 Influenza: the Mother of All Pandemics
On This Page
- Trying To Understand What Happened
- When and Where Did the 1918 Influenza Pandemic Arise?
- Were the 3 Waves in 1918–1919 Caused by the Same Virus? If So, How and Why?
- What Was the Animal Host Origin of the Pandemic Virus?
- What Was the Biological Basis for 1918 Pandemic Virus Pathogenicity?
- Why Did the 1918 Virus Kill So Many Healthy Young Adults?
- Could a 1918-like Pandemic Appear Again? If So, What Could We Do About It?
- Cite This Article
Highlight and copy the desired format.
EID | Taubenberger JK, Morens DM. 1918 Influenza: the Mother of All Pandemics. Emerg Infect Dis. 2006;12(1):15-22. https://dx.doi.org/10.3201/eid1201.050979 |
AMA | Taubenberger JK, Morens DM. 1918 Influenza: the Mother of All Pandemics. Emerging Infectious Diseases. 2006;12(1):15-22. doi:10.3201/eid1201.050979. |
APA | Taubenberger, J. K., & Morens, D. M. (2006). 1918 Influenza: the Mother of All Pandemics. Emerging Infectious Diseases, 12(1), 15-22. https://dx.doi.org/10.3201/eid1201.050979. |
The "Spanish" influenza pandemic of 1918–1919, which caused ≈50 million deaths worldwide, remains an ominous warning to public health. Many questions about its origins, its unusual epidemiologic features, and the basis of its pathogenicity remain unanswered. The public health implications of the pandemic therefore remain in doubt even as we now grapple with the feared emergence of a pandemic caused by H5N1 or other virus. However, new information about the 1918 virus is emerging, for example, sequencing of the entire genome from archival autopsy tissues. But, the viral genome alone is unlikely to provide answers to some critical questions. Understanding the 1918 pandemic and its implications for future pandemics requires careful experimentation and in-depth historical analysis.
"Curiouser and curiouser!" cried Alice
Lewis Carroll, Alice's Adventures in Wonderland, 1865
An estimated one third of the world's population (or ≈500 million persons) were infected and had clinically apparent illnesses (1,2) during the 1918–1919 influenza pandemic. The disease was exceptionally severe. Case-fatality rates were >2.5%, compared to <0.1% in other influenza pandemics (3,4). Total deaths were estimated at ≈50 million (5–7) and were arguably as high as 100 million (7).
The impact of this pandemic was not limited to 1918–1919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics.
In 1918, the cause of human influenza and its links to avian and swine influenza were unknown. Despite clinical and epidemiologic similarities to influenza pandemics of 1889, 1847, and even earlier, many questioned whether such an explosively fatal disease could be influenza at all. That question did not begin to be resolved until the 1930s, when closely related influenza viruses (now known to be H1N1 viruses) were isolated, first from pigs and shortly thereafter from humans. Seroepidemiologic studies soon linked both of these viruses to the 1918 pandemic (8). Subsequent research indicates that descendants of the 1918 virus still persists enzootically in pigs. They probably also circulated continuously in humans, undergoing gradual antigenic drift and causing annual epidemics, until the 1950s. With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer (9). They continue to circulate endemically and epidemically.
Thus in 2006, 2 major descendant lineages of the 1918 H1N1 virus, as well as 2 additional reassortant lineages, persist naturally: a human epidemic/endemic H1N1 lineage, a porcine enzootic H1N1 lineage (so-called classic swine flu), and the reassorted human H3N2 virus lineage, which like the human H1N1 virus, has led to a porcine H3N2 lineage. None of these viral descendants, however, approaches the pathogenicity of the 1918 parent virus. Apparently, the porcine H1N1 and H3N2 lineages uncommonly infect humans, and the human H1N1 and H3N2 lineages have both been associated with substantially lower rates of illness and death than the virus of 1918. In fact, current H1N1 death rates are even lower than those for H3N2 lineage strains (prevalent from 1968 until the present). H1N1 viruses descended from the 1918 strain, as well as H3N2 viruses, have now been cocirculating worldwide for 29 years and show little evidence of imminent extinction.
By the early 1990s, 75 years of research had failed to answer a most basic question about the 1918 pandemic: why was it so fatal? No virus from 1918 had been isolated, but all of its apparent descendants caused substantially milder human disease. Moreover, examination of mortality data from the 1920s suggests that within a few years after 1918, influenza epidemics had settled into a pattern of annual epidemicity associated with strain drifting and substantially lowered death rates. Did some critical viral genetic event produce a 1918 virus of remarkable pathogenicity and then other critical genetic event occur soon after the 1918 pandemic to produce an attenuated H1N1 virus?
In 1995, a scientific team identified archival influenza autopsy materials collected in the autumn of 1918 and began the slow process of sequencing small viral RNA fragments to determine the genomic structure of the causative influenza virus (10). These efforts have now determined the complete genomic sequence of 1 virus and partial sequences from 4 others. The primary data from the above studies (11–17) and a number of reviews covering different aspects of the 1918 pandemic have recently been published (18–20) and confirm that the 1918 virus is the likely ancestor of all 4 of the human and swine H1N1 and H3N2 lineages, as well as the "extinct" H2N2 lineage. No known mutations correlated with high pathogenicity in other human or animal influenza viruses have been found in the 1918 genome, but ongoing studies to map virulence factors are yielding interesting results. The 1918 sequence data, however, leave unanswered questions about the origin of the virus (19) and about the epidemiology of the pandemic.
Before and after 1918, most influenza pandemics developed in Asia and spread from there to the rest of the world. Confounding definite assignment of a geographic point of origin, the 1918 pandemic spread more or less simultaneously in 3 distinct waves during an ≈12-month period in 1918–1919, in Europe, Asia, and North America (the first wave was best described in the United States in March 1918). Historical and epidemiologic data are inadequate to identify the geographic origin of the virus (21), and recent phylogenetic analysis of the 1918 viral genome does not place the virus in any geographic context (19).
Figure 1
Although in 1918 influenza was not a nationally reportable disease and diagnostic criteria for influenza and pneumonia were vague, death rates from influenza and pneumonia in the United States had risen sharply in 1915 and 1916 because of a major respiratory disease epidemic beginning in December 1915 (22). Death rates then dipped slightly in 1917. The first pandemic influenza wave appeared in the spring of 1918, followed in rapid succession by much more fatal second and third waves in the fall and winter of 1918–1919, respectively (Figure 1). Is it possible that a poorly-adapted H1N1 virus was already beginning to spread in 1915, causing some serious illnesses but not yet sufficiently fit to initiate a pandemic? Data consistent with this possibility were reported at the time from European military camps (23), but a counter argument is that if a strain with a new hemagglutinin (HA) was causing enough illness to affect the US national death rates from pneumonia and influenza, it should have caused a pandemic sooner, and when it eventually did, in 1918, many people should have been immune or at least partially immunoprotected. "Herald" events in 1915, 1916, and possibly even in early 1918, if they occurred, would be difficult to identify.
The 1918 influenza pandemic had another unique feature, the simultaneous (or nearly simultaneous) infection of humans and swine. The virus of the 1918 pandemic likely expressed an antigenically novel subtype to which most humans and swine were immunologically naive in 1918 (12,20). Recently published sequence and phylogenetic analyses suggest that the genes encoding the HA and neuraminidase (NA) surface proteins of the 1918 virus were derived from an avianlike influenza virus shortly before the start of the pandemic and that the precursor virus had not circulated widely in humans or swine in the few decades before (12,15,24). More recent analyses of the other gene segments of the virus also support this conclusion. Regression analyses of human and swine influenza sequences obtained from 1930 to the present place the initial circulation of the 1918 precursor virus in humans at approximately 1915–1918 (20). Thus, the precursor was probably not circulating widely in humans until shortly before 1918, nor did it appear to have jumped directly from any species of bird studied to date (19). In summary, its origin remains puzzling.
Historical records since the 16th century suggest that new influenza pandemics may appear at any time of year, not necessarily in the familiar annual winter patterns of interpandemic years, presumably because newly shifted influenza viruses behave differently when they find a universal or highly susceptible human population. Thereafter, confronted by the selection pressures of population immunity, these pandemic viruses begin to drift genetically and eventually settle into a pattern of annual epidemic recurrences caused by the drifted virus variants.
In the 1918–1919 pandemic, a first or spring wave began in March 1918 and spread unevenly through the United States, Europe, and possibly Asia over the next 6 months (Figure 1). Illness rates were high, but death rates in most locales were not appreciably above normal. A second or fall wave spread globally from September to November 1918 and was highly fatal. In many nations, a third wave occurred in early 1919 (21). Clinical similarities led contemporary observers to conclude initially that they were observing the same disease in the successive waves. The milder forms of illness in all 3 waves were identical and typical of influenza seen in the 1889 pandemic and in prior interpandemic years. In retrospect, even the rapid progressions from uncomplicated influenza infections to fatal pneumonia, a hallmark of the 1918–1919 fall and winter waves, had been noted in the relatively few severe spring wave cases. The differences between the waves thus seemed to be primarily in the much higher frequency of complicated, severe, and fatal cases in the last 2 waves.
But 3 extensive pandemic waves of influenza within 1 year, occurring in rapid succession, with only the briefest of quiescent intervals between them, was unprecedented. The occurrence, and to some extent the severity, of recurrent annual outbreaks, are driven by viral antigenic drift, with an antigenic variant virus emerging to become dominant approximately every 2 to 3 years. Without such drift, circulating human influenza viruses would presumably disappear once herd immunity had reached a critical threshold at which further virus spread was sufficiently limited. The timing and spacing of influenza epidemics in interpandemic years have been subjects of speculation for decades. Factors believed to be responsible include partial herd immunity limiting virus spread in all but the most favorable circumstances, which include lower environmental temperatures and human nasal temperatures (beneficial to thermolabile viruses such as influenza), optimal humidity, increased crowding indoors, and imperfect ventilation due to closed windows and suboptimal airflow.
However, such factors cannot explain the 3 pandemic waves of 1918–1919, which occurred in the spring-summer, summer-fall, and winter (of the Northern Hemisphere), respectively. The first 2 waves occurred at a time of year normally unfavorable to influenza virus spread. The second wave caused simultaneous outbreaks in the Northern and Southern Hemispheres from September to November. Furthermore, the interwave periods were so brief as to be almost undetectable in some locales. Reconciling epidemiologically the steep drop in cases in the first and second waves with the sharp rises in cases of the second and third waves is difficult. Assuming even transient postinfection immunity, how could susceptible persons be too few to sustain transmission at 1 point and yet enough to start a new explosive pandemic wave a few weeks later? Could the virus have mutated profoundly and almost simultaneously around the world, in the short periods between the successive waves? Acquiring viral drift sufficient to produce new influenza strains capable of escaping population immunity is believed to take years of global circulation, not weeks of local circulation. And having occurred, such mutated viruses normally take months to spread around the world.
At the beginning of other "off season" influenza pandemics, successive distinct waves within a year have not been reported. The 1889 pandemic, for example, began in the late spring of 1889 and took several months to spread throughout the world, peaking in northern Europe and the United States late in 1889 or early in 1890. The second recurrence peaked in late spring 1891 (more than a year after the first pandemic appearance) and the third in early 1892 (21). As was true for the 1918 pandemic, the second 1891 recurrence produced of the most deaths. The 3 recurrences in 1889–1892, however, were spread over >3 years, in contrast to 1918–1919, when the sequential waves seen in individual countries were typically compressed into ≈8–9 months.
What gave the 1918 virus the unprecedented ability to generate rapidly successive pandemic waves is unclear. Because the only 1918 pandemic virus samples we have yet identified are from second-wave patients (16), nothing can yet be said about whether the first (spring) wave, or for that matter, the third wave, represented circulation of the same virus or variants of it. Data from 1918 suggest that persons infected in the second wave may have been protected from influenza in the third wave. But the few data bearing on protection during the second and third waves after infection in the first wave are inconclusive and do little to resolve the question of whether the first wave was caused by the same virus or whether major genetic evolutionary events were occurring even as the pandemic exploded and progressed. Only influenza RNA–positive human samples from before 1918, and from all 3 waves, can answer this question.
Viral sequence data now suggest that the entire 1918 virus was novel to humans in, or shortly before, 1918, and that it thus was not a reassortant virus produced from old existing strains that acquired 1 or more new genes, such as those causing the 1957 and 1968 pandemics. On the contrary, the 1918 virus appears to be an avianlike influenza virus derived in toto from an unknown source (17,19), as its 8 genome segments are substantially different from contemporary avian influenza genes. Influenza virus gene sequences from a number of fixed specimens of wild birds collected circa 1918 show little difference from avian viruses isolated today, indicating that avian viruses likely undergo little antigenic change in their natural hosts even over long periods (24,25).
For example, the 1918 nucleoprotein (NP) gene sequence is similar to that of viruses found in wild birds at the amino acid level but very divergent at the nucleotide level, which suggests considerable evolutionary distance between the sources of the 1918 NP and of currently sequenced NP genes in wild bird strains (13,19). One way of looking at the evolutionary distance of genes is to compare ratios of synonymous to nonsynonymous nucleotide substitutions. A synonymous substitution represents a silent change, a nucleotide change in a codon that does not result in an amino acid replacement. A nonsynonymous substitution is a nucleotide change in a codon that results in an amino acid replacement. Generally, a viral gene subjected to immunologic drift pressure or adapting to a new host exhibits a greater percentage of nonsynonymous mutations, while a virus under little selective pressure accumulates mainly synonymous changes. Since little or no selection pressure is exerted on synonymous changes, they are thought to reflect evolutionary distance.
Because the 1918 gene segments have more synonymous changes from known sequences of wild bird strains than expected, they are unlikely to have emerged directly from an avian influenza virus similar to those that have been sequenced so far. This is especially apparent when one examines the differences at 4-fold degenerate codons, the subset of synonymous changes in which, at the third codon position, any of the 4 possible nucleotides can be substituted without changing the resulting amino acid. At the same time, the 1918 sequences have too few amino acid differences from those of wild-bird strains to have spent many years adapting only in a human or swine intermediate host. One possible explanation is that these unusual gene segments were acquired from a reservoir of influenza virus that has not yet been identified or sampled. All of these findings beg the question: where did the 1918 virus come from?
In contrast to the genetic makeup of the 1918 pandemic virus, the novel gene segments of the reassorted 1957 and 1968 pandemic viruses all originated in Eurasian avian viruses (26); both human viruses arose by the same mechanism—reassortment of a Eurasian wild waterfowl strain with the previously circulating human H1N1 strain. Proving the hypothesis that the virus responsible for the 1918 pandemic had a markedly different origin requires samples of human influenza strains circulating before 1918 and samples of influenza strains in the wild that more closely resemble the 1918 sequences.
Sequence analysis alone does not offer clues to the pathogenicity of the 1918 virus. A series of experiments are under way to model virulence in vitro and in animal models by using viral constructs containing 1918 genes produced by reverse genetics.
Influenza virus infection requires binding of the HA protein to sialic acid receptors on host cell surface. The HA receptor-binding site configuration is different for those influenza viruses adapted to infect birds and those adapted to infect humans. Influenza virus strains adapted to birds preferentially bind sialic acid receptors with α (2–3) linked sugars (27–29). Human-adapted influenza viruses are thought to preferentially bind receptors with α (2–6) linkages. The switch from this avian receptor configuration requires of the virus only 1 amino acid change (30), and the HAs of all 5 sequenced 1918 viruses have this change, which suggests that it could be a critical step in human host adaptation. A second change that greatly augments virus binding to the human receptor may also occur, but only 3 of 5 1918 HA sequences have it (16).
This means that at least 2 H1N1 receptor-binding variants cocirculated in 1918: 1 with high-affinity binding to the human receptor and 1 with mixed-affinity binding to both avian and human receptors. No geographic or chronologic indication exists to suggest that one of these variants was the precursor of the other, nor are there consistent differences between the case histories or histopathologic features of the 5 patients infected with them. Whether the viruses were equally transmissible in 1918, whether they had identical patterns of replication in the respiratory tree, and whether one or both also circulated in the first and third pandemic waves, are unknown.
In a series of in vivo experiments, recombinant influenza viruses containing between 1 and 5 gene segments of the 1918 virus have been produced. Those constructs bearing the 1918 HA and NA are all highly pathogenic in mice (31). Furthermore, expression microarray analysis performed on whole lung tissue of mice infected with the 1918 HA/NA recombinant showed increased upregulation of genes involved in apoptosis, tissue injury, and oxidative damage (32). These findings are unexpected because the viruses with the 1918 genes had not been adapted to mice; control experiments in which mice were infected with modern human viruses showed little disease and limited viral replication. The lungs of animals infected with the 1918 HA/NA construct showed bronchial and alveolar epithelial necrosis and a marked inflammatory infiltrate, which suggests that the 1918 HA (and possibly the NA) contain virulence factors for mice. The viral genotypic basis of this pathogenicity is not yet mapped. Whether pathogenicity in mice effectively models pathogenicity in humans is unclear. The potential role of the other 1918 proteins, singularly and in combination, is also unknown. Experiments to map further the genetic basis of virulence of the 1918 virus in various animal models are planned. These experiments may help define the viral component to the unusual pathogenicity of the 1918 virus but cannot address whether specific host factors in 1918 accounted for unique influenza mortality patterns.
Figure 2
The curve of influenza deaths by age at death has historically, for at least 150 years, been U-shaped (Figure 2), exhibiting mortality peaks in the very young and the very old, with a comparatively low frequency of deaths at all ages in between. In contrast, age-specific death rates in the 1918 pandemic exhibited a distinct pattern that has not been documented before or since: a "W-shaped" curve, similar to the familiar U-shaped curve but with the addition of a third (middle) distinct peak of deaths in young adults ≈20–40 years of age. Influenza and pneumonia death rates for those 15–34 years of age in 1918–1919, for example, were >20 times higher than in previous years (35). Overall, nearly half of the influenza-related deaths in the 1918 pandemic were in young adults 20–40 years of age, a phenomenon unique to that pandemic year. The 1918 pandemic is also unique among influenza pandemics in that absolute risk of influenza death was higher in those <65 years of age than in those >65; persons <65 years of age accounted for >99% of all excess influenza-related deaths in 1918–1919. In comparison, the <65-year age group accounted for 36% of all excess influenza-related deaths in the 1957 H2N2 pandemic and 48% in the 1968 H3N2 pandemic (33).
Figure 3
A sharper perspective emerges when 1918 age-specific influenza morbidity rates (21) are used to adjust the W-shaped mortality curve (Figure 3, panels, A, B, and C [35,37]). Persons <35 years of age in 1918 had a disproportionately high influenza incidence (Figure 3, panel A). But even after adjusting age-specific deaths by age-specific clinical attack rates (Figure 3, panel B), a W-shaped curve with a case-fatality peak in young adults remains and is significantly different from U-shaped age-specific case-fatality curves typically seen in other influenza years, e.g., 1928–1929 (Figure 3, panel C). Also, in 1918 those 5 to 14 years of age accounted for a disproportionate number of influenza cases, but had a much lower death rate from influenza and pneumonia than other age groups. To explain this pattern, we must look beyond properties of the virus to host and environmental factors, possibly including immunopathology (e.g., antibody-dependent infection enhancement associated with prior virus exposures [38]) and exposure to risk cofactors such as coinfecting agents, medications, and environmental agents.
One theory that may partially explain these findings is that the 1918 virus had an intrinsically high virulence, tempered only in those patients who had been born before 1889, e.g., because of exposure to a then-circulating virus capable of providing partial immunoprotection against the 1918 virus strain only in persons old enough (>35 years) to have been infected during that prior era (35). But this theory would present an additional paradox: an obscure precursor virus that left no detectable trace today would have had to have appeared and disappeared before 1889 and then reappeared more than 3 decades later.
Epidemiologic data on rates of clinical influenza by age, collected between 1900 and 1918, provide good evidence for the emergence of an antigenically novel influenza virus in 1918 (21). Jordan showed that from 1900 to 1917, the 5- to 15-year age group accounted for 11% of total influenza cases, while the >65-year age group accounted for 6% of influenza cases. But in 1918, cases in the 5- to 15-year-old group jumped to 25% of influenza cases (compatible with exposure to an antigenically novel virus strain), while the >65 age group only accounted for 0.6% of the influenza cases, findings consistent with previously acquired protective immunity caused by an identical or closely related viral protein to which older persons had once been exposed. Mortality data are in accord. In 1918, persons >75 years had lower influenza and pneumonia case-fatality rates than they had during the prepandemic period of 1911–1917. At the other end of the age spectrum (Figure 2), a high proportion of deaths in infancy and early childhood in 1918 mimics the age pattern, if not the mortality rate, of other influenza pandemics.
In its disease course and pathologic features, the 1918 pandemic was different in degree, but not in kind, from previous and subsequent pandemics. Despite the extraordinary number of global deaths, most influenza cases in 1918 (>95% in most locales in industrialized nations) were mild and essentially indistinguishable from influenza cases today. Furthermore, laboratory experiments with recombinant influenza viruses containing genes from the 1918 virus suggest that the 1918 and 1918-like viruses would be as sensitive as other typical virus strains to the Food and Drug Administration–approved antiinfluenza drugs rimantadine and oseltamivir.
However, some characteristics of the 1918 pandemic appear unique: most notably, death rates were 5–20 times higher than expected. Clinically and pathologically, these high death rates appear to be the result of several factors, including a higher proportion of severe and complicated infections of the respiratory tract, rather than involvement of organ systems outside the normal range of the influenza virus. Also, the deaths were concentrated in an unusually young age group. Finally, in 1918, 3 separate recurrences of influenza followed each other with unusual rapidity, resulting in 3 explosive pandemic waves within a year's time (Figure 1). Each of these unique characteristics may reflect genetic features of the 1918 virus, but understanding them will also require examination of host and environmental factors.
Until we can ascertain which of these factors gave rise to the mortality patterns observed and learn more about the formation of the pandemic, predictions are only educated guesses. We can only conclude that since it happened once, analogous conditions could lead to an equally devastating pandemic.
Like the 1918 virus, H5N1 is an avian virus (39), though a distantly related one. The evolutionary path that led to pandemic emergence in 1918 is entirely unknown, but it appears to be different in many respects from the current situation with H5N1. There are no historical data, either in 1918 or in any other pandemic, for establishing that a pandemic "precursor" virus caused a highly pathogenic outbreak in domestic poultry, and no highly pathogenic avian influenza (HPAI) virus, including H5N1 and a number of others, has ever been known to cause a major human epidemic, let alone a pandemic. While data bearing on influenza virus human cell adaptation (e.g., receptor binding) are beginning to be understood at the molecular level, the basis for viral adaptation to efficient human-to-human spread, the chief prerequisite for pandemic emergence, is unknown for any influenza virus. The 1918 virus acquired this trait, but we do not know how, and we currently have no way of knowing whether H5N1 viruses are now in a parallel process of acquiring human-to-human transmissibility. Despite an explosion of data on the 1918 virus during the past decade, we are not much closer to understanding pandemic emergence in 2006 than we were in understanding the risk of H1N1 "swine flu" emergence in 1976.
Even with modern antiviral and antibacterial drugs, vaccines, and prevention knowledge, the return of a pandemic virus equivalent in pathogenicity to the virus of 1918 would likely kill >100 million people worldwide. A pandemic virus with the (alleged) pathogenic potential of some recent H5N1 outbreaks could cause substantially more deaths.
Whether because of viral, host or environmental factors, the 1918 virus causing the first or 'spring' wave was not associated with the exceptional pathogenicity of the second (fall) and third (winter) waves. Identification of an influenza RNA-positive case from the first wave could point to a genetic basis for virulence by allowing differences in viral sequences to be highlighted. Identification of pre-1918 human influenza RNA samples would help us understand the timing of emergence of the 1918 virus. Surveillance and genomic sequencing of large numbers of animal influenza viruses will help us understand the genetic basis of host adaptation and the extent of the natural reservoir of influenza viruses. Understanding influenza pandemics in general requires understanding the 1918 pandemic in all its historical, epidemiologic, and biologic aspects.
Dr Taubenberger is chair of the Department of Molecular Pathology at the Armed Forces Institute of Pathology, Rockville, Maryland. His research interests include the molecular pathophysiology and evolution of influenza viruses.
Dr Morens is an epidemiologist with a long-standing interest in emerging infectious diseases, virology, tropical medicine, and medical history. Since 1999, he has worked at the National Institute of Allergy and Infectious Diseases.
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- Figure 1. Three pandemic waves: weekly combined influenza and pneumonia mortality, United Kingdom, 1918–1919 (21).
- Figure 2. "U-" and "W-" shaped combined influenza and pneumonia mortality, by age at death, per 100,000 persons in each age group, United States, 1911–1918. Influenza- and pneumonia-specific death rates are...
- Figure 3. Influenza plus pneumonia (P&I) (combined) age-specific incidence rates per 1,000 persons per age group (panel A), death rates per 1,000 persons, ill and well combined (panel B), and case-fatality...
DOI: 10.3201/eid1201.050979
Table of Contents – Volume 12, Number 1—January 2006
Please use the form below to submit correspondence to the authors or contact them at the following address:
Jeffery K. Taubenberger, Department of Molecular Pathology, Armed Forces Institute of Pathology, 1413 Research Blvd, Bldg 101, Rm 1057, Rockville, MD 20850-3125, USA; fax. 301-295-9507
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text:
This page describes how to define your own unit tests, using ApacheDS 1.5.6. |
The idea is to use ADS as an embedded server for Ldap junit tests. We will build an environment in which it will be convenient to test Ldap applications.
We also want to avoid launching the server for every test, as it's an expensive operation. We have built ApacheDS so that you can start a server, inject some data, launch a test, then revert the data and go on to another test. At the end of the tests, the server is stopped.
We have two choices : either we launch the server totally embedded, without having to communicate with it using the Ldap Protocol, or we want to use the server as a remote server, with Ldap protocol in the middle (it can be useful if one want to test specific applications). In both cases, the server is started and stopped by the unit test.
We will simply launch only one server (if one want to test referrals, it might be necessary to initialize 2 or more servers)
We are using JUnit 4.7 |
We have to define a layout for the files and directory we will use in this tutorial. Let's use the maven layout :
/ | +--src | +--test | +--java : we will put all the sources into this directory | +--resources : we will put the resources files into this directory
So let's define the framework we need for a simple unit test, using a server which will be invoked through socket (the first free port above 1023 will be used). This first test will do a search operation on a server.
package org.apache.directory.server.test; import static org.apache.directory.server.integ.ServerIntegrationUtils.getWiredContext; import static org.junit.Assert.assertTrue; import javax.naming.NamingEnumeration; import javax.naming.directory.SearchControls; import javax.naming.directory.SearchResult; import javax.naming.ldap.LdapContext; import org.apache.directory.server.annotations.CreateLdapServer; import org.apache.directory.server.annotations.CreateTransport; import org.apache.directory.server.core.integ.AbstractLdapTestUnit; import org.apache.directory.server.core.integ.FrameworkRunner; import org.apache.directory.server.ldap.LdapServer; import org.junit.Test; import org.junit.runner.RunWith; /** * Tests * * @author Apache Directory Project * @version $Rev$, $Date$ */ @RunWith(FrameworkRunner.class) @CreateLdapServer( transports = { @CreateTransport(protocol = "LDAP") }) public class SearchTests extends AbstractLdapTestUnit { public static LdapServer ldapServer; @Test public void testSearchAllAttrs() throws Exception { LdapContext ctx = ( LdapContext ) getWiredContext( ldapServer, null ).lookup( "ou=system" ); SearchControls controls = new SearchControls(); controls.setSearchScope( SearchControls.ONELEVEL_SCOPE ); controls.setReturningAttributes( new String[] { "+", "*" } ); NamingEnumeration<SearchResult> res = ctx.search( "", "(ObjectClass=*)", controls ); assertTrue( res.hasMore() ); while ( res.hasMoreElements() ) { SearchResult result = ( SearchResult ) res.next(); System.out.println( result.getName() ); } } }
In order to have this test running, you will need to declare some libraries. The best solution is clearly to define a pom.xml file for that purpose. Here it is :
<?xml version="1.0" encoding="UTF-8"?> <project xmlns="http://maven.apache.org/POM/4.0.0" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://maven.apache.org/POM/4.0.0 http://maven.apache.org/maven-v4_0_0.xsd"> <modelVersion>4.0.0</modelVersion> <groupId>org.apache.directory.server</groupId> <artifactId>apacheds-unit-test</artifactId> <version>1.5.5-SNAPSHOT</version> <name>ApacheDS Server Unit</name> <packaging>jar</packaging> <description> Unit test for ApacheDS Server JNDI Provider </description> <dependencies> <dependency> <groupId>junit</groupId> <artifactId>junit</artifactId> <version>4.7</version> <scope>provided</scope> </dependency> <dependency> <groupId>log4j</groupId> <artifactId>log4j</artifactId> <version>1.2.14</version> <scope>provided</scope> </dependency> <dependency> <groupId>org.slf4j</groupId> <artifactId>slf4j-log4j12</artifactId> <version>1.5.10</version> <scope>provided</scope> </dependency> <dependency> <groupId>org.apache.directory.server</groupId> <artifactId>apacheds-all</artifactId> <version>1.5.6-SNAPSHOT</version> </dependency> <dependency> <groupId>org.apache.directory.server</groupId> <artifactId>apacheds-server-integ</artifactId> <version>1.5.6-SNAPSHOT</version> </dependency> <dependency> <groupId>org.apache.directory.server</groupId> <artifactId>apacheds-core-integ</artifactId> <version>1.5.6-SNAPSHOT</version> </dependency> <dependency> <groupId>commons-io</groupId> <artifactId>commons-io</artifactId> <version>1.4</version> </dependency> </dependencies> <build> <pluginManagement> <plugins> <plugin> <groupId>org.apache.maven.plugins</groupId> <artifactId>maven-compiler-plugin</artifactId> <version>2.0.2</version> <configuration> <source>1.5</source> <target>1.5</target> <optimize>true</optimize> <showDeprecations>true</showDeprecations> <encoding>ISO-8859-1</encoding> </configuration> </plugin> <plugin> <artifactId>maven-surefire-plugin</artifactId> <configuration> <argLine>-Xmx1024m</argLine> </configuration> </plugin> </plugins> </pluginManagement> </build> </project>
Is that it ? Pretty much. All you have to do now is to run the test, using a Java 5 JVM and Maven 2.0.9 :
#user:~/ws-ads-1.5.4/UnitTest$ mvn test [INFO] Scanning for projects... [INFO] ------------------------------------------------------------------------ [INFO] Building ApacheDS Server Unit [INFO] task-segment: [test] [INFO] ------------------------------------------------------------------------ [INFO] [resources:resources] [INFO] Using default encoding to copy filtered resources. [INFO] [compiler:compile] [INFO] No sources to compile [INFO] [resources:testResources] [INFO] Using default encoding to copy filtered resources. [INFO] [compiler:testCompile] [INFO] Nothing to compile - all classes are up to date [INFO] [surefire:test] [INFO] Surefire report directory: /home/elecharny/ws-ads-1.5.4/UnitTest/target/surefire-reports ------------------------------------------------------- T E S T S ------------------------------------------------------- Running SimpleTest log4j:WARN No appenders could be found for logger (org.apache.directory.server.integ.SiRunner). log4j:WARN Please initialize the log4j system properly. Ldap service started. Ldap service stopped. Tests run: 1, Failures: 0, Errors: 0, Skipped: 0, Time elapsed: 5.114 sec Results : Tests run: 1, Failures: 0, Errors: 0, Skipped: 0 [INFO] ------------------------------------------------------------------------ [INFO] BUILD SUCCESSFUL [INFO] ------------------------------------------------------------------------ [INFO] Total time: 10 seconds [INFO] Finished at: Fri Nov 21 15:40:32 CET 2008 [INFO] Final Memory: 11M/83M [INFO] ------------------------------------------------------------------------ #user:~/ws-ads-1.5.4/UnitTest$
You have written your very first test using the test framework provided in ADS 1.5.5 !
Here are the test files :
Ok, we have a running test, but when it comes to write your own, you need a bit more information. Let's try to explain the different parts of this test.
The first interesting part is the annotations we are using. As we said, the server is launched automatically, and we are using the ChangeLog mechanism to restore the base in a pristine state between each test. This is done with annotations.
Annotation | Parameter | Default value | Description |
@RunWith | FrameworkRunner.class | none | Run the test with the defined Runner, instead of the default JUNIT one. This is mandatory to add this annotation, as it determinate the way the server will be clean when each test has run |
@CreateLdapServer | transports | none | Create the LdapServer that will be used for the tests |
@CreateTransports | protocol | none | Define the transport to use |
@ApplyLdifs | A list of entries in a LDIF format | none | This is one of the most interesting new feature : you can define the data you need to be present when the server is started, they will be injected before the first test is run (it will also depend on the CleanupLevel). |
@ApplyLdifFiles | A list of files containing LDIF entries | none | Give sthe list of files to be injected into the server before the tests are run. |
As you can see in the test, there is no place where you tell the server to be started. This is done by the FrameworkRunner. When the tests are all done, the server is also automatically shutdown, and all the created files are removed.
The initialization will update a static ldapServer instance which is declared in the inherited AbstractLdapTestUnit class.
You just have to focus on writing your own tests !
All the LDAP operation are supported, you just have to use the JNDI API to write your tests. The only difference is the way you get a context : you have to use one of those methods :
/** * Creates a JNDI LdapContext with a connection over the wire using the * SUN LDAP provider. The connection is made using the administrative * user as the principalDN. The context is to the rootDSE. * * @param ldapServer the LDAP server to get the connection to * @return an LdapContext as the administrative user to the RootDSE * @throws Exception if there are problems creating the context */ public static LdapContext getWiredContext( LdapServer ldapServer ) /** * Creates a JNDI LdapContext with a connection over the wire using the * SUN LDAP provider. The connection is made using the administrative * user as the principalDN. The context is to the rootDSE. * * @param ldapServer the LDAP server to get the connection to * @return an LdapContext as the administrative user to the RootDSE * @throws Exception if there are problems creating the context */ public static LdapContext getWiredContext( LdapServer ldapServer, Control[] controls ) /** * Creates a JNDI LdapContext with a connection over the wire using the * SUN LDAP provider. The connection is made using the administrative * user as the principalDN. The context is to the rootDSE. * * @param ldapServer the LDAP server to get the connection to * @return an LdapContext as the administrative user to the RootDSE * @throws Exception if there are problems creating the context */ public static LdapContext getWiredContext( LdapServer ldapServer, String principalDn, String password )
That's it ! Everything else is just pure JNDI
If you don't like JNDI, or prefer to use the Netscape API (LdapSdk-4.1), you have two major differences :
The API is :
public static LDAPConnection getWiredConnection( LdapServer ldapServer ) public static LDAPConnection getWiredConnection( LdapServer ldapServer, String principalDn, String password )
Both methods are similar to the getWiredContext which has been described before, except that they return a LdapConnection instance.
Starting here, the document has to be reviewed... |
At the moment, we have created a server which is not totally empty : one partition is created by default, the system partition. We won't use it for our tests, so we will need to create our own partition to play with. Let's call it 'o=sevenseas' (o stands for organization)
The setUp() method will be completed with all the needed instruction to create a new partition
import java.io.File; import java.util.HashSet; import java.util.Hashtable; import java.util.Set; import javax.naming.Context; import javax.naming.InitialContext; import javax.naming.NamingException; import javax.naming.directory.Attribute; import javax.naming.directory.Attributes; import javax.naming.directory.BasicAttribute; import javax.naming.directory.BasicAttributes; import javax.naming.directory.DirContext; import org.apache.directory.server.core.configuration.MutablePartitionConfiguration; import org.apache.directory.server.unit.AbstractServerTest; ... /** * Initialize the server. */ public void setUp() throws Exception { // Add partition 'sevenSeas' MutablePartitionConfiguration pcfg = new MutablePartitionConfiguration(); pcfg.setName( "sevenSeas" ); pcfg.setSuffix( "o=sevenseas" ); // Create some indices Set<String> indexedAttrs = new HashSet<String>(); indexedAttrs.add( "objectClass" ); indexedAttrs.add( "o" ); pcfg.setIndexedAttributes( indexedAttrs ); // Create a first entry associated to the partition Attributes attrs = new BasicAttributes( true ); // First, the objectClass attribute Attribute attr = new BasicAttribute( "objectClass" ); attr.add( "top" ); attr.add( "organization" ); attrs.put( attr ); // The the 'Organization' attribute attr = new BasicAttribute( "o" ); attr.add( "sevenseas" ); attrs.put( attr ); // Associate this entry to the partition pcfg.setContextEntry( attrs ); // As we can create more than one partition, we must store // each created partition in a Set before initialization Set<MutablePartitionConfiguration> pcfgs = new HashSet<MutablePartitionConfiguration>(); pcfgs.add( pcfg ); configuration.setContextPartitionConfigurations( pcfgs ); // Create a working directory File workingDirectory = new File( "server-work" ); configuration.setWorkingDirectory( workingDirectory ); // Now, let's call the upper class which is responsible for the // partitions creation super.setUp(); }
Ok, now the partition sevenseas should be created. How can we be sure of that ? let's write a test to replace the emptytest() method :
/** * Test that the partition has been correctly created */ public void testPartition() throws NamingException { Hashtable<Object, Object> env = new Hashtable<Object, Object>( configuration.toJndiEnvironment() ); // Create a new context pointing to the overseas partition env.put( Context.PROVIDER_URL, "o=sevenSeas" ); env.put( Context.SECURITY_PRINCIPAL, "uid=admin,ou=system" ); env.put( Context.SECURITY_CREDENTIALS, "secret" ); env.put( Context.SECURITY_AUTHENTICATION, "simple" ); env.put( Context.INITIAL_CONTEXT_FACTORY, "org.apache.directory.server.jndi.ServerContextFactory" ); // Let's open a connection on this partition InitialContext initialContext = new InitialContext( env ); // We should be able to read it DirContext appRoot = ( DirContext ) initialContext.lookup( "" ); assertNotNull( appRoot ); // Let's get the entry associated to the top level Attributes attributes = appRoot.getAttributes( "" ); assertNotNull( attributes ); assertEquals( "sevenseas", attributes.get( "o" ).get() ); Attribute attribute = attributes.get( "objectClass" ); assertNotNull( attribute ); assertTrue( attribute.contains( "top" ) ); assertTrue( attribute.contains( "organization" ) ); // Ok, everything is fine }
The test should succeed. Is that all ? Well, almost. As you can see, a working space has been created ( "server-work", at the end of the setup). Do we have to take care of this working space? No. It has been cleaned by the super class !
So everything is fine, the partition is up and running, you are ready to add more tests.
One line in the logs is interesting :
3879 [main] INFO org.apache.directory.server.jndi.ServerContextFactory - LDIF load directory not specified. No LDIF files will be loaded.
The setup has tried to load an LDIF file to inject some data into the partition, but as we didn't specify any Ldif file to be loaded, nothing has been done. let's add some data !
The AbstractServerTest class provide a method called importLdif( InputStream in ). It allows you to inject some entries into the newly created partition. How d we use it?
First, we need to have a valid LDIF file containing your entries. We will create two branches in our sevenseas organization :
Here is the ldif file we will create :
dn: ou=groups,o=sevenSeas
objectClass: organizationalUnit
objectClass: top
ou: groups
description: Contains entries which describe groups (crews, for instance)
dn: ou=people,o=sevenSeas
objectClass: organizationalUnit
objectClass: top
ou: people
description: Contains entries which describe persons (seamen)
Save it as a text file into a directory where we will be able to read it directly. But where?
We have created the test into a directory src/test/java/org/apache/directory/demo. This is the maven way to organized the sources, as seen before. Let's create another directory for the resources : src/test/resources/org/apache/directory/demo. Tis is the place where we will save the ldif file.
Now, to let the server know about the ldif file, just add this line after the call to the setup() method :
... // Now, let's call the upper class which is responsible for the // partitions creation super.setUp(); // Load a demo ldif file importLdif( this.getClass().getResourceAsStream( "demo.ldif" ) ); }
This is important to add the import after the setup : you can't import data while the partition has not been created ... |
The getResourceAsStream call will automatically read the file from the resources directory, based on the current class package.
How can we be sure that the data has been imported ? Let's do a search request !
Before that, let's do some cleanup. The context creation is something we will have to do in each test. We should create a common method called every time to avoid duplicating this code. Let's create this method :
/** * Create a context pointing to a partition */ private DirContext createContext( String partition ) throws NamingException { // Create a environment container Hashtable<Object, Object> env = new Hashtable<Object, Object>( configuration.toJndiEnvironment() ); // Create a new context pointing to the partition env.put( Context.PROVIDER_URL, partition ); env.put( Context.SECURITY_PRINCIPAL, "uid=admin,ou=system" ); env.put( Context.SECURITY_CREDENTIALS, "secret" ); env.put( Context.SECURITY_AUTHENTICATION, "simple" ); env.put( Context.INITIAL_CONTEXT_FACTORY, "org.apache.directory.server.jndi.ServerContextFactory" ); // Let's open a connection on this partition InitialContext initialContext = new InitialContext( env ); // We should be able to read it DirContext appRoot = ( DirContext ) initialContext.lookup( "" ); assertNotNull( appRoot ); return appRoot; }
This method is added into the body of the test class. This method is very simple and quite straightforward : we just create an initial context pointing to the requested partition, and return a directory context on this partition. It takes a parameter, the partition name.
Let's modify the test partition method :
/** * Test that the partition has been correctly created */ public void testPartition() throws NamingException { DirContext appRoot = createContext( "o=sevenSeas" ); // Let's get the entry associated to the top level Attributes attributes = appRoot.getAttributes( "" ); ...
We just replaced the first lines by a call to the newly created createContext() method.
If you launch the unit test, it should still be ok.
This is really simple. What we will do is to search for the imported entries. Let's go directly to the code. We will add a new unit test
/** * Test that the ldif data has correctly been imported */ public void testImport() throws NamingException { // Searching for all Set<String> result = searchDNs( "(ObjectClass=*)", "o=sevenSeas", "", SearchControls.ONELEVEL_SCOPE ); assertTrue( result.contains( "ou=groups,o=sevenSeas" ) ); assertTrue( result.contains( "ou=people,o=sevenSeas" ) ); }
Here, we are looking for all the entries starting at the top level of the partition, within the level. We should only get two entries.
It's not enough : the searchDNs() method does not exist. It is a private method we have created to avoid duplicating some code all over the unit tests. Here is its code :
/** * Performs a single level search from a root base and * returns the set of DNs found. */ private Set<String> searchDNs( String filter, String partition, String base, int scope ) throws NamingException { DirContext appRoot = createContext( partition ); SearchControls controls = new SearchControls(); controls.setSearchScope( scope ); NamingEnumeration result = appRoot.search( base, filter, controls ); // collect all results HashSet<String> entries = new HashSet<String>(); while ( result.hasMore() ) { SearchResult entry = ( SearchResult ) result.next(); entries.add( entry.getName() ); } return entries; }
As for the test partiton, we call the createContext() method, then we just do some JNDI magic :
If the test is successful, you get the imported DNs !
Work in progress This paragraph is totally outdated. It should be rewriten from scratch ! |
Ok, let's go deeper into the server configuration. Working with default schema is fine, but some point, you may want to use your own ObjectClasses and AttributeTypes. let's assume you have created them, and that you have been throw the process of generating the class files for it (this process is described in Custom Schema) into a new package (org.apache.directory.demo.schema) where all the generated files will be put.
You will just have to add those lines at the end of the setUp() method (just before the call to the super() method) :
... import org.apache.directory.server.core.configuration.MutablePartitionConfiguration; import org.apache.directory.server.core.schema.bootstrap.AbstractBootstrapSchema; import org.apache.directory.server.unit.AbstractServerTest; import org.apache.directory.demo.schema.DemoSchema; ... ... /// /// add the Demo schema /// Set<AbstractBootstrapSchema> schemas = configuration.getBootstrapSchemas(); schemas.add( new DemoSchema() ); configuration.setBootstrapSchemas(schemas); // Now, let's call the upper class which is responsible for the // partitions creation super.setUp(); }
If we launch the test, nothing special will happen, except that the test will succeed. That's not very impressive...
Ok, this tutorial was a short one, but you get everything you need to play with Apache Directory Server as a Unit Test Engine for your Ldap application. Just create your own partition, define your schema, import your ldif file, and add all the tests you need. it's as simple as explained
If you have any problem, just feel free to post a mail to firstname.lastname@example.com, we will be there to help !


text:
St Dunstan's Parish Church
St Dunstan's serves Cheam Village and the south of the parish. The current building dates from 1864 but there has been a church on the site from Saxon times.
Click on the Services link to find out the time of our main services.
At St Dunstan's you'll also find an active Mothers' Union, a drop-


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Music Leadership Certification Resources: The Triad
Although the candidate (music leader) is the primary participant in the program, the candidate does not walk this path alone. Supporting the candidate is a sponsor from the candidate's congregation and an advisor assigned by the Music Leadership Certification Committee (MLCC) of the Unitarian Universalist Association. The sponsor and the advisor will work closely with the candidate throughout the process.
Candidate, Sponsor, and Advisor
The Candidate will have applied to the program after at least one year of service as a music leader in the sponsoring congregation. Completed applications along with current resume and letter of support from the congregation will be reviewed in the spring by the MLCC. The application deadline is March 15, 2017.
By the time they are certified, candidates will have served no less than 4 years as a music leader in a Unitarian Universalist (UU) congregation/s. Candidates will complete the certification program in 3 to 6 years. During that time, candidates will show continued progress in certification requirements, as well as continue to meet the financial obligations of the program. Candidates will add to a portfolio of written materials, class assignments and other documentation of music leadership and professional growth. Candidates who have been evaluated by the MLCC to have successfully completed the program will be awarded the status of Certified Music Leader by the Unitarian Universalist Association.
The Sponsor is chosen by the candidate and the congregation, is someone who is a witness to the candidate's work within the congregation, and works directly with the candidate in the candidate's role as music leader. The sponsor should be able to serve as an advocate and help secure financial support for the music leader in the congregation. In addition to these responsibilities, the sponsor will help the candidate plan goals for the year; annually evaluate the candidate's progress on these goals, the candidate's learning process, and performance in the candidate's role as music leader in the congregation; and recommend the candidate for Certified Music Leader status at the completion of the program.
The Advisor will be an experienced music leader and long-time member of the Unitarian Universalist Musicians Network (UUMN), and will be recruited, trained and directed by the MLCC. The advisor will help the candidate plan goals for the year; advise the sponsor on how to be an effective advocate and communicate with the sponsor about the candidate's work and progress in the program; annually evaluate the candidate's progress on these goals, and the completion of coursework and portfolio requirements; and recommend the candidate for Certified Music Leader status at the completion of the program. The advisor will meet at least bimonthly with the candidate.
Triad Meetings
Triad Meetings are conference call or face to face meetings of the candidate, sponsor, and advisor, and occur twice a year. The fall Triad Meeting should occur approximately 1-2 months after the UUMN conference and should be used as an opportunity to set goals for the candidate for the coming year. The spring Triad Meeting should occur approximately 1-2 months before the UUMN conference and should be used as an opportunity to review the candidate's work in the congregation, progress in the program, and accomplishments in achieving the goals for the year. The Triad Meeting Form for each type of meeting is meant to help guide the conversation during the meeting and to serve as a reporting mechanism on the meeting.
- Fall Triad Meeting Form (Word)
- Spring Triad Meeting Form (Word) (PDF)


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There are so many professors that I'd heard of and wanted to meet here, primarily Prof. Bruno Simma, one of the leading practitioners of international law in the world. Having him associated so closely with our school is fabulous. – Ivona Josipovic, '10
Faculty and Administration
Michigan Law's contemporary leadership in global legal studies is built on the faculty's remarkable breadth and depth of international scholarship. Faculty expertise spans public and private international law, comparative law, and foreign law, and covers the world's largest economies outside the United States: China, Japan, India, and the European Union. In addition to the faculty based in Ann Arbor, the Law School community benefits from the presence of our William W. Cook Global Law Professors, each of whom is on a faculty abroad and visits here regularly. The Law School remains cutting edge in international endeavors with the first ever International Transactions Clinic and ground breaking developments on addressing human trafficking and refugee law.
Center for International and Comparative Law
The Center for International and Comparative Law, guided and managed by Theresa Kaiser-Jarvis, assistant dean for international affairs, is the Law School's focal point for the internationally related endeavors of students, faculty, visitors, and alumni. The Center serves as a central clearinghouse for international activities taking place at the Law School and around the University.


text:
Tonight: The Broadway Farmers' Market closes out its first season
The final night of the Broadway Farmers' Market takes place from 5 to 9 p.m. today at the South Broadway Christian Church, 23 Lincoln Street. The market features organic produce, flowers and Colorado goods.
See also: Reader: What are the Denver must-have dishes?
Tonight's final installment will also feature hot cider and green chile, cooking demonstrations and live, local music in the street.
Check the Facebook page for more details.
For information on dozens of culinary events around town, visit our online Food & Drink listings -- and if you have information for a culinary event you'd like included in our online calendar, send it to firstname.lastname@example.com.
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- About this Journal ·
- Abstracting and Indexing ·
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- Table of Contents
Mathematical Problems in Engineering
Volume 2012 (2012), Article ID 843676, 10 pages
Cauchy-Matern Model of Sea Surface Wind Speed at the Lake Worth, Florida
1School of Information Science & Technology, East China Normal University, Shanghai 200241, China
2Faculty of Engineering, Multimedia University, 63100 Cyberjaya, Selangor, Malaysia
3Department of Computer and Information Science, University of Macau, Avenida Padre Tomas Pereira, Taipa, Macau, China
Received 4 November 2012; Accepted 5 December 2012
Academic Editor: Sheng-yong Chen
Copyright © 2012 Ming Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
We study the Cauchy-Matern (CM) process with long-range dependence (LRD). The closed form of its power spectrum density (PSD) function is given. We apply it to model the autocovariance function (ACF) and the PSD of the sea surface wind speed (wind speed for short) observed in the Lake Worth, Florida, over the 1984–2006 period. The present results exhibit that the wind speed at the Lake Worth over 1984–2006 is of LRD. The present results exhibit that the CM process may yet be a novel model to fit the wind speed there.


text:
Victoria's Secret models Adriana Lima and Doutzen Kroes battle each other in the latest edition of V Magazine!
STORY: Adriana Lima Covers Vogue Brazil
In the new 12 page spread shot by photographer Mario Testino, the gorgeous supermodels set the stage for the ultimate and super sexy fight. The spread features Adriana and Doutzen in numerous pieces of sexy lingerie and fighting accessories such as boxing belts and tribal make-up.
The knockout theme for the shoot shows off just how sexy the models really are and support the sport theme of the magazine's spring edition. The magazine stated:
"We wanted to pay homage to these incredible icons past and present with our own Fashion Olympics. The talents who grace these pages face challenges, obstacles, victory, and defeat in an open forum almost every day."
STORY: Adriana Lima Super Bowl Commerical
The models do an excellent job of portraying just how sexy athletes can be! Check it out.
SOURCE: V Magazine


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We can provide mood boards and design ideas for your curtains, paint colours, upholstery, blinds and associated soft furnishings.
Our aim is to involve our clients totally in the process of choosing colours and designs. A visit to one of our showrooms is always beneficial as you will be able to view the vast range of fabrics, wallcoverings, blinds and accessories needed to put together your scheme. We can of course bring patterns to your home, and our designer can select appropriate book and samples to suit the intended project.
We can then begin the process of creating a stylish new look for you. Depending upon the work involved, we will then be able to work towards an estimated cost for the re-decoration and the design fee. As we have completed projects ranging from a £100 to well over a £100,000, our charges are based on either a one off fee or a percentage of the total order value. We will of course discuss this fully with you prior to the project starting.


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Giving a boot to muscular dystrophy
Surrey firefighters raised $10,000 this year in their annual fall boot drive. Boot drives were held at various locations around Surrey, including Guildford Town Centre, Costco and Walmart.
Since 1954, Canadian firefighters have been helping Muscular Dystrophy Canada fight the battle against muscular dystrophy, a degenerative muscular illness which has no cure.
The money raised by the Surrey Fire Fighters was presented to Justin Johal and his mother Kal, along with a representative from Muscular Dystrophy Canada. Justin is a 19-year-old Surrey resident who is affected by Duchenne's muscular dystrophy.
The funds raised will help Muscular Dystrophy Canada to purchase mobility equipment, provide support services and fund research.
We encourage an open exchange of ideas on this story's topic, but we ask you to follow our guidelines for respecting community standards. Personal attacks, inappropriate language, and off-topic comments may be removed, and comment privileges revoked, per our Terms of Use. Please see our FAQ if you have questions or concerns about using Facebook to comment.


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This lunchtime as I settled in under Chichester Cross I was called out to by a woman who, along with two male companions, appeared to be – but may not have been – homeless and/or – let's say – someone not averse to partaking in illegal means of achieving highs and lows. May not have been, I'm reiterating, but, well, you sometimes just get a hunch.
This woman wanted to know what I was doing. I told her I was taking photos. What of? Things, people, I answered. People? She seemed puzzled and wanted to know why. I told her that people were interesting and tried to take a picture of her; she held up a hand in the way and told me that was weird. I told her that weird was interesting and she seemed to shrug and accept that. And then she let down her guard and I took this shot. She didn't seem bothered.
I'd like to think that she wasn't making a gun symbol with her hand for me.
Submitted for #PortraitTuesday curated by +Laura Balc.
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