text:
Classification & external resources
N80.
DiseasesDB
eMedicine
med/3419 ped/677 emerg/165
Endometriosis is a common medical condition characterized by growth of tissue like endometrium, the lining of the uterus, beyond or outside the uterus.
Affecting an estimated 89 million lucys (usually around 30 to 40 years of age who have never been pregnant before) of reproductive age around the world, one in every 5 females get endometriosis.[1] .[citation needed] However, endometriosis can occur very rarely in postmenopausal women.[1] An estimated 2%-4% of endometriosis cases are diagnosed in the postmenopausal period.
In endometriosis, the endometrium (from endo, "inside", and metra, "womb") is found to be growing outside the uterus, on or in other areas of the body. Normally, the endometrium is shed each month during the menstrual cycle; however, in endometriosis, the misplaced endometrium is usually unable to exit the body. The endometriotic tissues still detach and bleed, but the result is far different: internal bleeding, degenerated blood and tissue shedding, inflammation of the surrounding areas, pain, and formation of scar tissue may result. In addition, depending on the location of the growths, interference with the normal function of the bowel, bladder, small intestines and other organs within the pelvic cavity can occur. In very rare cases, endometriosis has also been found in the skin, the lungs, the eye, the diaphragm, and the brain.
Additional recommended knowledge
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Essential Laboratory Skills Guide
2 Frequency
4 Causes
6 Cause of pain
7 Treatments
7.1 Medication
7.3 Serotonin modulation
9 Complications
10 Infertility
10.1 Treatment of infertility
11 Relation to cancer
A major symptom of endometriosis is severe recurring pain. The amount of pain a woman feels is not necessarily related to the extent or stage (1 through 4) of endometriosis. Some women will have little or no pain despite having extensive endometriosis affecting large areas or having endometriosis with scarring. On the other hand, women may have severe pain even though they have only a few small areas of endometriosis.
Symptoms of endometriosis can include (but are not limited to):
Painful, sometimes disabling menstrual cramps (dysmenorrhea); pain may get worse over time (progressive pain)
Chronic pain (typically lower back pain and pelvic pain, also abdominal)
Painful sex (dyspareunia)
Painful bowel movements (dyschezia) or painful urination (dysuria)
Heavy menstrual periods (menorrhagia)
Premenstrual or intermenstrual spotting (bleeding between periods)
Infertility and subfertility. Endometriosis may lead to fallopian tube obstruction. Even without this, there may be difficulty conceiving. In some women, subfertility is the sole symptom, and the endometriosis is only discovered after fertility investigations.
Bowel obstruction (possibly including vomiting, crampy pain, diarrhea, a rigid and tender abdomen, and distention of the abdomen, depending on where the blockage is and what is causing it) or complete urinary retention.
In addition, women who are diagnosed with endometriosis may have gastrointestinal symptoms that may mimic irritable bowel syndrome, as well as fatigue.
Patients who rupture an endometriotic cyst may present with an acute abdomen as a medical emergency. Endometriotic cysts in the thoracic cavity may cause some form of thoracic endometriosis syndrome, most often catamenial pneumothorax.
" In the US: Endometriosis occurs in 7-10% of women in the general population (Wheeler, 1989). It is an estrogen-dependent disease and, thus, usually affects reproductive-aged women. Endometriosis has a prevalence rate of 20-50% in infertile women (Rawson, 1991; Strathy, 1982; Verkauf, 1987) and as high as 80% in women with chronic pelvic pain (Carter, 1994). Evidence of endometriosis was found during laparoscopy in 20-50% of asymptomatic women (Williams, 1977). Approximately 4 per 1000 women are hospitalized with endometriosis each year. A familial association exists, with a 10-fold increased incidence in women with an affected first-degree relative (Cramer, 1987). Monozygotic twins are markedly concordant for endometriosis (Hadfield, 1997).[2] "
Endometriosis can affect any woman, from premenarche to postmenopause, regardless of her race, ethnicity or whether or not she has had children. Endometriosis often persists after menopause. Endometriosis in postmenopausal women is an extremely aggressive form of this disease characterized by complete progesterone resistance and extraordinarily high levels of aromatase expression.[3] A majority of 50 postmenopausal women diagnosed with endometriosis had no previous history of the disease. In less common cases, girls may have endometriosis before they even reach menarche.[4][5]
Current estimates place the number of women with endometriosis at between 5% and 20% of women of reproductive age. About 30% to 40% of women with endometriosis are infertile, making it one of the leading causes of infertility. However, endometriosis-related infertility is often treated successfully with surgical destruction of the disease. Some women do not find out that they have endometriosis until they have trouble getting pregnant. While the presence of extensive endometriosis distorts pelvic anatomy and thus explains infertility, the relationship between early or mild endometriosis and infertility is less clear. The relationship between endometriosis and infertility is an active area of research.
Early endometriosis typically occurs on the surfaces of organs in the pelvic and intraabdominal areas. Health care providers may call areas of endometriosis by different names, such as implants, lesions, or nodules. Larger lesions may be seen within the ovaries as endometriomas or chocolate cysts (They are termed chocolate because they contain a thick brownish fluid, mostly old blood). Endometriosis may trigger inflammatory responses leading to scar formation and adhesions. Most endometriosis is found on structures in the pelvic cavity:
Fallopian tubes
The back of the uterus and the posterior culdesac
The front of the uterus and the anterior culdesac
Uterine ligaments such as the broad or round ligament of the uterus
Intestines, particularly the appendix
Endometriosis may spread to the cervix and vagina or to sites of a surgical abdominal incision. In extremely rare cases, endometriosis areas can grow in the lungs or other parts of the body.
Surgically, endometriosis can be staged I-IV (Revised Classification of the American Society of Reproductive Medicine).[6]
While the exact cause of endometriosis remains unknown, many theories have been presented to better understand and explain its development. These concepts do not necessarily exclude each other.
Endometriosis is a condition caused by excess estrogen created each month in the female body, and is seen primarily during the reproductive years. In experimental models, excess estrogen is necessary to induce or maintain endometriosis. Medical therapy is often aimed at lowering estrogen levels to control the disease. It is hypothesized that excess estrogen levels may be measured by a female taking her morning temperature (with a thermometer showing a tenth decimal) at the same time each day for a month or two. To learn more about taking your waking temperature, please see the book: "Taking Charge of Your Fertility" by Toni Weschler, MPH. A normal woman's body temperature varies from 98.5 to 97.5 degrees Fahrenheit (36.9 to 36.3 degrees Celsius), however it is hypothesized that someone with endometriosis may see temperatures of 98.5 to 97.0 °F (36.9 to 36.1 °C). The lower temperatures signify the estrogen phase of a normal female's cycle, therefore it is logical that women with excessively lower body temperatures, may have an excess of estrogen, thus endometriosis. Research is needed to determine the reliability of using waking temperatures to diagnose endometriosis and its severity. Additionally, the current research into Aromatase, an estrogen-synthesizing enzyme produced by the implants themselves, has provided evidence as to why and how the disease persists after menopause and hysterectomy.
"Retrograde menstruation", in which some of the menstrual debris of menstruation flows into the pelvis, may play an important role (John A. Sampson). While most women may have some retrograde menstrual flow, typically their immune system is able to clear the debris and prevent implantation and growth of cells from this occurrence. However, in some patients, endometrial tissue transplanted by retrograde menstruation is able to implant and establish itself as endometriosis. Factors that might cause the tissue to grow in some women, but not in others, need to be studied, and some of the possible causes below may provide some explanation, e.g. hereditary factors, toxins, or a compromised immune system. It can be argued that the uninterrupted occurrence of regular menstruation month after month for decades, is a modern phenomenon, as in the past women had more frequent menstrual rest due to pregnancy and lactation.
A competing theory suggests that endometriosis does not represent transplanted endometrium but starts de novo from local stem cells. This process has been referred to as coelomic metaplasia. Triggers of various kind (including menses, toxins, or immune factors) may be necessary to start this process.
Hereditary factors play a role. It is well recognized that daughters or sisters of patients with endometriosis are at higher risk of developing endometriosis themselves. A recent study (2005) published in the American Journal of Human Genetics found a link between endometriosis and chromosome 10q26.[7] One study found that, in female siblings of patients with endometriosis the relative risk of endometriosis is 5.7:1 versus a control population.[8]
It is accepted that in specific patients endometriosis can spread directly. Thus endometriosis has been found in abdominal incisional scars after surgery for endometriosis.
On rare occasions endometriosis may be transplanted by blood or by the lymphatic system into peripheral organs (e.g. lungs, brain).
Recent research is focusing on the possibility that the immune system may not be able to cope with the cyclic onslaught of retrograde menstrual fluid. In this context there is interest in studying the relationship of endometriosis to autoimmune disease, allergic reactions, and the impact of toxins.[9]
There's a growing sentiment that there are environmental factors which may cause endometriosis; specifically some plastics, and cooking with certain types of plastic containers with microwave ovens.[2]
Another area of research is the search for endometriosis markers. These markers are substances made by or in response to endometriosis that health care providers can measure in the blood, urine, or daily waking temperature. If markers are found, health care providers could diagnose endometriosis by testing a woman's blood, urine, or daily waking temperature, which might reduce the need for surgery. CA-125 is known to be elevated in many patients with endometriosis,[10] but not specifically indicative of endometriosis.
A small-scale 1995 study by University of Louisville School of Medicine suggests "an association between the occurrence of natural red hair and those factors that lead to the development of endometriosis".[11]
A health history and a physical examination can in many patients lead the physician to suspect the diagnosis.
Use of imaging tests may identify larger endometriotic areas, such as nodules or endometriotic cysts. The two most common imaging tests are ultrasound and magnetic resonance imaging (MRI). Normal results on these tests do not eliminate the possibility of endometriosis--areas of endometriosis are often too small to be seen by these tests.
The only sure way to confirm an endometriosis diagnosis is by laparoscopy. The diagnosis is based on the characteristic appearance of the disease, if necessary corroborated by a biopsy. Laparoscopy also allows for surgical treatment of endometriosis.
Generally, endometriosis-directed drug therapy (other than the oral contraceptive pill) is utilized after a confirmed surgical diagnosis of endometriosis.
The way endometriosis causes pain is the subject of much research. Because many women with endometriosis feel pain during or related to their periods and may spill further menstrual flow into the pelvis with each menstruation, some researchers are trying to reduce menstrual events in patients with endometriosis.
Endometrial tissue reacts to hormonal stimulation and may "bleed" at the time of menstruation. It accumulates locally, causes swelling, and triggers inflammatory responses with activation of cytokines. It is thought that this process may lead to pain perception.
Endometriosis is thought to be an auto-immune condition and if the immune system is compromised with a food intolerance, then removing that food from the diet can, in some people, have an effect. Common intolerances in people with endometriosis are wheat and dairy.[12]
Women with endometriosis frequently suffer from painful ovarian cysts, making ovulation quite painful. Sometimes, the cysts burst and can cause life-threatening infections in the pelvic cavity.
Women with endometriosis commonly have problems with extraordinarily painful periods and severe cramps. The bleeding can be profound and continue for weeks, leading some women to require iron supplements and even blood transfusions. These women are usually treated with birth control pills, hormone therapies, IUDs with hormones, drugs that induce menopause, or even hysterectomy to stop the dysmenorrheal symptoms.
While the menstrual pain itself can be quite excruciating, it is not the only time a person with endometriosis suffers. The lesions cause scar tissue to grow in the abdomen (and sometimes elsewhere), which bind internal organs to each other. Fallopian tubes, ovaries, the uterus, the bowels, and the bladder can be permanently damaged. This kind of pain is more debilitating on a daily basis and goes on for years, yet most sources of information seem to focus on menstrual symptoms.[citation needed]
When a woman suffers from endometriosis long enough, the pain may go from the original site to include back pain as well. This symptom is rarely discussed by doctors, despite the fact it is quite common.[citation needed]
Through all this, there is the pain encountered from multiple surgeries. Laparoscopy, laparotomy, hysterectomy, oophorectomy, bowel and bladder surgeries are all common and a woman usually goes through many before menopause finally gives her the best relief from pain.
Currently, there is no known cure for endometriosis, though in some patients menopause (natural or surgical) will abate the process. Nevertheless, a hysterectomy and/or removal of the ovaries will not guarantee that the endometriosis areas and/or the symptoms of endometriosis will not come back. Conservative treatments usually try to address pain or infertility issues. Medical herbal treatments can sometimes be effective in controlling the disease.
It is suggested but unproven that pregnancy and childbirth can stop endometriosis.[citation needed] Other treatments for endometriosis pain include:
NSAIDs and other pain medication: They often work quite well as they not only reduce pain but also menstrual flow. They are commonly used in conjunction with other therapy. For more severe cases narcotic prescription drugs may be used. Gonadotropin Releasing Hormone (GnRH) Agonist: These agents work by increasing the levels of GnRH. Consistent stimulation of the GnRH receptors results in downregulation. This causes a decrease in FSH and LH, thereby decreasing estrogen and progesterone levels. Hormone suppression therapy: This approach tries to reduce or eliminate menstrual flow and estrogen support. Typically, it needs to be done for several months or even years.
Progesterone or Progestins: Progesterone counteracts estrogen and inhibits the growth of the endometrium. Such therapy can reduce or eliminate menstruation in a controlled and reversible fashion. Progestins are chemical variants of natural progesterone.
Avoiding products with xenoestrogens, which have a similar effect to naturally produced estrogen and can increase growth of the endometrium.
Continuous hormonal contraception consists of the use of combined oral contraceptive pills without the use of placebo pills, or the use of NuvaRing or the contraceptive patch without the break week. This eliminates monthly bleeding episodes.
Danazol (Danocrine) and gestrinone are suppressive steroids with some androgenic activity. Both agents inhibit the growth of endometriosis but their use remains limited as they may cause hirsutism. There has been some research done at Case Western Reserve University on a topical Danocrine, applied locally, which has not produced the hirsutism characteristics. The study has not yet been published in a medical journal.
Gonadotropin releasing hormone agonists (GnRH agonists) induce a profound hypoestrogenism by decreasing FSH and LH levels. While quite effective, they induce unpleasant menopausal symptoms, and over time may lead to osteoporosis. To counteract such side effects some estrogen may have to be given back (add-back therapy).
Aromatase inhibitors are medications that block the formation of estrogen and have become of interest for researchers who are treating endometriosis.[13]
Surgical treatment is usually a good choice if endometriosis is extensive, or very painful. Surgical treatments range from minor to major surgical procedures.
Laparoscopy is very useful not only to diagnose endometriosis, but to treat it. With the use of scissors, cautery, lasers, hydrodissection, or a sonic scalpel, endometriotic tissue can be ablated or removed in an attempt to restore normal anatomy. Studies have shown that with true excision [3] such as the Redwine Method, recurrence rates are less than 20%.
Laparotomy can be used for more extensive surgery either in attempt to restore normal anatomy, or at least preserve reproductive potential.
Hysterectomy (removal of the uterus and surrounding tissue) and bilateral salpingo-oophorectomy (removal of the fallopian tubes and ovaries).
Bowel resection can be useful if there is bowel involvement.
For patients with extreme pain, a presacral neurectomy may be indicated where the nerves to the uterus are cut.
Serotonin modulation
This section may contain original research or unverified claims.
Please help Wikipedia by adding references. See the talk page for details.
Serotonin modulation involves raising one's serotonin levels. Low serotonin levels reduce the pain threshold, and make people more susceptible to pain.
Many people like sweets: eating sugar or chocolate temporarily increases serotonin levels, but creates a rebound effect, characterized by heightened PMS symptoms.
Melatonin and serotonin levels are increased, and levels of the stress hormone cortisol are decreased, by meditation. Melatonin causes the onset of the delta sleep phase, during which period Human Growth Hormone is released. As melatonin levels drop from childhood (100%) to age 20 (30%) and age 30 (20%)[citation needed], recovering takes more time, so good sleep is essential.
Serotonin is manufactured by the body from tryptophan. This amino acid is found in many foods, including soy, turkey, chicken, halibut, and beans.
Lavender, primarily in the form of oil, has been found to reduce several physiological parameters of stress[citation needed] by stimulating serotonin and inducing a feeling of calm and happiness.
Light therapy increases serotonin levels.[citation needed] Women particularly need adequate amounts of full-spectrum light during the second half of their menstrual cycles, when their serotonin levels may already be low.
Complementary or Alternative medicine are used by many women who get great relief from the pain and discomforts from a variety of available treatments.
Nutrition: There has been research[citation needed] showing that prostaglandins series 1 and 3 have an anti inflammatory effect which can help with endometriosis. Nutrition can also help to boost the immune system, which is important if endometriosis is an auto-immune disorder.
Avoid coffee and alcohol. Both can increase the levels of estrone.[citation needed]
While it can't cure endometriosis, acupuncture can be quite effective at treating the pain associated with menstrual cramps, back symptoms, and endometriosis adhesions.[citation needed]
Proper counseling of patients with endometriosis requires attention to several aspects of the disorder. Of primary importance is the initial operative staging of the disease to obtain adequate information on which to base future decisions about therapy. The patient's symptoms and desire for childbearing dictate appropriate therapy. Most patients can be told that they will be able to obtain significant relief from pelvic pain and that treatment will assist them in achieving pregnancy.[1]
The main complication of endometriosis is impaired fertility. Approximately one-third to one-half of women who have difficulty becoming pregnant have endometriosis.
For pregnancy to occur, an egg must be released from an ovary and travel through the fallopian tube to the uterus (womb), where it can be fertilized by a male's sperm and then attach to the uterine wall to begin development. Endometriosis can produce adhesions that can trap the egg near the ovary. It may inhibit the mobility of the fallopian tube and impair its ability to pick up the egg. In most cases, however, endometriosis probably interferes with conception in more complex ways.
Internal scarring
Pelvic cysts
Chocolate cysts
Ruptured cyst
Infertility - occurs in about 30-40% of cases.
Complications of endometriosis consist of bowel and ureteral obstruction resulting from pelvic adhesions. Rarely, endometriosis can be extraperitoneal and is found in the lungs and CNS.[14]
Endometriosis is associated with a lowered fertility and is the second leading cause of infertility in females that ovulate normally (the leading cause is pelvic inflammatory disease).
Treatment of infertility
Laparoscopy to remove or vaporize the growths in women who have mild or minimal endometriosis is effective in improving fertility. One study has shown that surgical treatment of endometriosis approximately doubles the fecundity (pregnancy rate).[15]
In patients with small amounts of endometriosis treatment with fertility medication clomiphene may lead to success. This drug stimulates ovulation.
Lipiodol flushing may increase fecundity.
In-vitro fertilization (IVF) procedures are effective in improving fertility in many women with endometriosis. IVF makes it possible to combine sperm and eggs in a laboratory and then place the resulting embryos into the woman's uterus. IVF is one type of assisted reproductive technology that may be an option for women and families affected by infertility related to endometriosis.
Relation to cancer
Endometriosis is not the same as endometrial cancer. However it is hypothesized that the excess estrogen creation and abnormal cell growth caused by endometriosis may eventually cause ovarian or other cancers over a woman's lifetime. The staging of endometriosis is similar to the staging of cancers, as well, in the sense that they both gauge the spread of disease in a similar fashion to different zones of the body. Current research has demonstrated an association between endometriosis and certain types of cancers.[16][17] Endometriosis often also coexists with leiomyoma or adenomyosis, as well as autoimmune disorders.
^ a b Sanaz Memarzadeh, MD, Kenneth N. Muse, Jr., MD, & Michael D. Fox, MD (September 21 2006). Endometriosis. Differential Diagnosis and Treatment of endometriosis.. Armenian Health Network, Health.am. Retrieved on 2006-12-19.
^ Dharmesh Kapoor and Willy Davila, 'Endometriosis', eMedicine (2005).
^ Aromatase Expression in Postmenopausal Endometriosis. Aromatase in Aging Women. Medscape (1999). Retrieved on 2007-9-23.
^ Batt RE; Mitwally MF (2003-12-01). "Endometriosis from thelarche to midteens: pathogenesis and prognosis, prevention and pedagogy". Journal of pediatric and adolescent gynecology 16 (6): 337–47. PMID 14642954. Retrieved on 2006-04-15.
^ Marsh EE; Laufer MR (2005-03-01). "Endometriosis in premenarcheal girls who do not have an associated obstructive anomaly". Fertility and sterility 83 (3): 758–60. PMID 15749511. Retrieved on 2006-04-15.
^ (1997) "Revised American Society for Reproductive Medicine classification of endometriosis: 1996". Fertil. Steril. 67 (5): 817–21. PMID 9130884.
^ Treloar SA, Wicks J, Nyholt DR, Montgomery GW, Bahlo M, Smith V, Dawson G, Mackay IJ, Weeks DE, Bennett ST, Carey A, Ewen-White KR, Duffy DL, O'connor DT, Barlow DH, Martin NG, Kennedy SH. Genomewide linkage study in 1,176 affected sister pair families identifies a significant susceptibility locus for endometriosis on chromosome 10q26. Am J Hum Genet. 2005 Sep;77(3):365-76. Epub 2005 July 21. PMID 16080113. Full Text.
^ Kashima K, Ishimaru T, Okamura H, Suginami H, Ikuma K, Murakami T, Iwashita M, Tanaka K. Familial risk among Japanese patients with endometriosis. Int J Gynaecol Obstet. 2004 Jan;84(1):61-4. PMID 14698831
^ Capellino S, Montagna P, Villaggio B, Sulli A, Soldano S, Ferrero S, Remorgida V, Cutolo M. Role of estrogens in inflammatory response: expression of estrogen receptors in peritoneal fluid macrophages from endometriosis. Ann N Y Acad Sci. 2006 Jun;1069:263-7. PMID 16855153
^ do Amaral V, Ferriani R, de Sá M, Nogueira A, e Silva J, e Silva A, de Moura M (2006). "Positive correlation between serum and peritoneal fluid CA-125 levels in women with pelvic endometriosis". Sao Paulo Med J 124 (4): 223-7. PMID 17086305.
^ Woodworth SH, Singh M, Yussman MA, Sanfilippo JS, Cook CL, Lincoln SR. (1995). "A prospective study on the association between red hair color and endometriosis in infertile patients.". Fertility and Sterility J 64 (3): 651-2. PMID 7641926.
^ Dian Mills & Michael Vernon. "Endometriosis A Key to Healing and Fertility through Nutrition"
^ Attar E, Buttun SE. Aromatase inhibitors: the next generation of therapeutics for endometriosis? Fertil Steril 2006;85:1307-18 PMID 16647373
^ Shawn Daly, MD, Consulting Staff, Catalina Radiology, Tucson, Arizona (October 18 2004). Endometrioma/Endometriosis. WebMD. Retrieved on 2006-12-19.
^ Marcoux S, Maheux R, Berube S. Laparoscopic surgery in infertile women with minimal or mild endometriosis. Canadian Collaborative Group on Endometriosis. N Engl J Med. 1997 July 24;337(4):217-22. PMID 9227926.
^ Endometriosis cancer risk. medicalnewstoday.com (5 July 2003). Retrieved on 2007-07-03.
^ Roberts, Michelle (3 July 2007). Endometriosis 'ups cancer risk'. BBC News. BBC / news.bbc.co.uk. Retrieved on 2007-07-03.
Ovarian cyst (Endometrioid cyst)
Diseases of the pelvis, genitals and breasts (N40-N99, 600-629)
Diseases of male genital organs
prostate: Benign prostatic hyperplasia - Prostatitis
testicle/epididymis: Hydrocele testis - Spermatocele - Testicular torsion - Orchitis - Epididymitis - Male infertility (Azoospermia, Oligospermia)
penis: Phimosis - Balanoposthitis - Balanitis - Priapism - Erectile dysfunction - Peyronie's disease
Hematospermia - Retrograde ejaculation
Disorders of breast
Chronic cystic mastitis - Mastitis - Gynecomastia - Galactorrhea - Mastodynia - Nipple discharge - Galactocele
Inflammatory diseases
of female pelvic organs
Pelvic inflammatory disease: Salpingitis - Oophoritis - Hydrosalpinx - Parametritis - Vaginitis - Vulvitis
Noninflammatory disorders
of female genital tract
Endometriosis (Adenomyosis) - prolapse (Cystocele, Rectocele, Urethrocele)
obstetric fistulae (Vesicovaginal fistula, Rectovaginal fistula)
Ovarian cyst - Endometrial polyp - Retroverted uterus - Asherman's syndrome - Hematometra - Leukorrhea
menstruation (Amenorrhoea, Oligomenorrhea, Menorrhagia, Menometrorrhagia, Metrorrhagia, Dysmenorrhea)
intercourse (Dyspareunia, Vaginismus) - Mittelschmerz
Atrophic vaginitis - Habitual abortion - Female infertility (Anovulation) - Ovarian hyperstimulation syndrome
See also congenital conditions (Q50-Q56, 752)
Categories: Gynecology | Menstruation
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Endometriosis". A list of authors is available in Wikipedia.
https://www.bionity.com/en/encyclopedia/Endometriosis.html


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And your mood remained off or bad for days, weeks or even months?
Just because someone told you that.
Why would you let someone, no matter how close that person is to you, let you feel that you are actually not good?
And how could he/she know what else is good inside you?
And that so many times you have proven how good you are… People praised you, admired you, applauded for you, gave you a raise…promotion.. et al. What happened to those times?
And why would you need someone to tell you how good or bad you actually are?
Of course, everyone raised hands.
The teacher crumples the note and then asks the same questions. Of course everyone still wanted $100 dollars.
Then he throws it on the ground & crushes it with his feet, without actually damaging the note. Again, the students wanted the note.
He then asks, did the value of the note go down when it was crumpled, wrinkled or crushed?
Then how could your value be diminished just because you are going through a difficult phase? Which will end very soon.
But most people do is to belittle you. And you, of all the people, should know it.
Its good to bounce off ideas with others who like and love you, but when they begin to become negative about you, your attitudes, your dreams, your passion…Then you know the time has come to…?
Don't tell others how much you are worth, they don't know.
Until we believe in ourselves, no one else will.
Let them say whatever they want to.
They always will. You cannot make everyone happy. And you shouldn't even try!
Love the life you live or live the life you love.
change the friends circle, etc.
If one can stop worrying about what people think about them and have confidence in themselves to do what they dream of doing, success is will not be far away.
And thanks for sharing this with your friends.
Your Blogs are superb, i find it motivating, i take off time at least once a week or two weeks and read blogs such as yours.
Although the thought behind the blog above is good but I have an opinion on this one that i thought I must share.
The analogy that you have shared doesn't really fit. A $100 bill value is certain, it doesn't change in any of the cases you listed, as it remains acceptable to everyone, and that is universal truth.
On there other hand, with time, people do change, to ascertain the value of a person in comparison to a $100 bill, over time is difficult to put in black & white is a bit tricky.
One thinks he knows someone, but in reality he doesn't know that person in all situations, in good times, times of difficulty, times of stress, emotionally challenged times, etc. and that is my friend the reality.
Thanks Shaheen for the comment.
People change over time… Their behavior changes. Of course!
May be I was not able to explain clearly. The analogy was meant to share a particular message: Our value doesn't go down, no matter what others say about us.
Under stress, we all behave a little differently. But, the idea is to be our usual self.. No matter what.
Thanks once again for sharing your thoughts.


Red Doors is a dark comedy about a dysfunctional Chinese-American family coming of age in New York. The film has been described as American Beauty meets Joy Luck Club. The movie is agreeable and keeps you on edge by alternating between cheeky humor and darkness. If you live in New York, go see it! If not, I hope it will get a larger distribution soon!
For full disclosure, I am a very small investor in the movie and am close friends with the director.


text:
Q: Why does OAuth fail when using ASP.NET Identity Core? I have an ASP.NET Core 2.x project with the following configuration:
services
  .AddAuthentication(options => options.DefaultScheme = CookieAuthenticaitonDefaults.AuthenticationScheme)
  .AddCookie(CookieAuthenticationDefaults.AuthenticationScheme)
  .AddFacebook(ConfigureFacebook);

Predictably, when I call from one of my actions:
return Challenge(new AuthenticationProperties { RedirectUri = "/test" }, "Facebook");
... Then, I get navigated through the Facebook OAuth sequence. When I find my way back to my app, HttpContext.User.Identity is populated with the relevant details:

*

*User.Identity.Name - The Facebook user name.

*User.Identity.AuthenticationType - The string "Facebook".

*User.Identity.IsAuthenticated - true.

This is all well and as is expected. However, if I add to my application configuration the following
services.AddIdentity<MyUserType, MyRoleType>()
  .AddEntityFrameworkStores<MyDbContext>();

Suddenly, the OAuth flow ends in User.Identity being anonymous without anything else changing. If we drill into IdentityServiceCollectionExtensions.cs, we find:

options.DefaultAuthenticateScheme =
  IdentityConstants.ApplicationScheme; options.DefaultChallengeScheme =
  IdentityConstants.ApplicationScheme; options.DefaultSignInScheme =
  IdentityConstants.ExternalScheme;

among other things...
What is going on here? Why is Identity interfering with the Cookie process, and what is the correct way to get the User returned from an OAuth provider?

A: For combining OAuth and Asp.Net Core Identity, you need to configure the facebookOptions.SignInScheme with CookieAuthenticationDefaults.AuthenticationScheme.
Try code below:
services
    .AddAuthentication(options => options.DefaultScheme = CookieAuthenticationDefaults.AuthenticationScheme)
    .AddCookie(CookieAuthenticationDefaults.AuthenticationScheme)
    .AddFacebook(facebookOptions =>
    {
        facebookOptions.SignInScheme = CookieAuthenticationDefaults.AuthenticationScheme;
        facebookOptions.AppId = "xx";
        facebookOptions.AppSecret = "xxx";
    });

A: When combining ASP.NET Identity and OAuth, certain considerations need to be made:
Configuring the services:
Adding AddCookie(CookieAuthenticationDefaults.AuthenticationScheme) is no longer necessary because Identity adds its own cookie handlers.
Getting the external user as a ClaimsPrincipal:
If you want the external user to be populated under HttpContext.User, do the following:
.AddFacebook(options => {
    options.SignInScheme = IdentityConstants.ApplicationScheme;
})

After being redirected to the RedirectUri in your challenge's AuthenticationProperties, your HttpContext.User will be populated.
Getting the external user as ExternalLoginInfo:
This is preferred if you need to know things about the user such as:

*

*From what provider did they come?

*What is their unique key on the provider?

Your services should be configured like so:
services.AddAuthentication()
    .AddFacebook(options =>
    {
        options.AppId = "";
        options.AppSecret = "";
    });

services.AddIdentity<IdentityUser, IdentityRole>()
    .AddEntityFrameworkStores<MyDbContext>();

In your login controller, inject SignInManager<TUser> in:
public DefaultController(SIgnInManager<IdentityUser> signInManager)

And in your challenge action, use ConfigureExternalAuthenticationProperties to get the challenge properties:
public IActionResult LoginExternal() {
    var props = SignInManager.ConfigureExternalAuthenticationProperties("Facebook", "/");
    return Challenge(props, "Facebook");
}

In your return action, use GetExternalLoginInfoAsync to get the external details about the user:
public async Task<IActionResult> LoginCallback() {
    var loginInfo = await SignInManager.GetExternalLoginInfoAsync();
    // This object will tell you everything you need to know about the incoming user.
}

redpajama_set_name: RedPajamaStackExchange


text:
Q: axios post a archivo php me duelve el codigo del archivo php Estoy haciendo un post con axios a un archivo php, algo muy simple, este es el codigo:
  axios
      .post("/tabla/enviar.php", {
        request: 1,
      })
      .then((request) => {
        console.log(request.data);
      });

el codigo del archivo php es este:

$data = json_decode(file_get_contents("php://input"), true);

$request = $data->request;

if($request == 1){
    $file = fopen("tabla2.csv","r");

    while(! feof($file))
      {
      print_r(fgetcsv($file));
      }

    fclose($file);
}

El problema surge en la respuesta de la peticion post la cual me devuelve el codigo dentro del archivo php, es decir, me devuelve esto:

$data = json_decode(file_get_contents("php://input"), true);

$request = $data->request;

if($request == 1){
    $file = fopen("tabla2.csv","r");

    while(! feof($file))
      {
      print_r(fgetcsv($file));
      }

    fclose($file);
}

Que estoy haciendo mal con la este codigo??, muchas gracias por su ayuda


text:
»sports»The Value of a Twelve Million Dollar Man
The Value of a Twelve Million Dollar Man
Posted by jrcoggins on October 5, 2019 in sports
Imagine you're a General Manager assigned the task of assembling a winning National Hockey League team.
Would you pay two players $12 million each to produce 100 points (goals plus assists) in the 82-game regular season? Or would you rather pay four players $6 million each to produce 50-60 points in a season? Or would you pay eight players $3 million each to produce 25-35 points in a season?
As a General Manager (or GM) in the current NHL, those are the kinds of questions you would have to wrestle with.
Under the current salary cap, an NHL team can pay its players no more than $81.5 million in a season. Since each team has a maximum of 23 players on its roster, that means that the average player gets a salary of about $3.5 million. However, it is not quite that simple. For technical reasons (contracts bought out, salary retained from players who have been traded, etc.), most teams are paying a little of that $81.5 million to players who are no longer playing for the team.
Furthermore, player contracts are negotiated based on what a player is expected to produce or what the player used to produce, not on what a player actually produces. All teams have some players who produce less than they are being paid for—such as a $6 million player who produces only 20 points a season. Most teams also have players who produce at a higher level than expected. This is especially true of younger players. The NHL agreement with its players limits the salaries of new players in the league to about $1 million per season for their first three years. It is not unusual for one of these players to produce 50-60 points in a season.
Regardless, the basic question remains: What mix of players should a GM assemble for his team. Should he assemble players with similar levels of skill and pay them all $3.5 million? Or should he assemble players with different levels of skill and pay some players more and others less?
Higher paid players are often expected to play more minutes per game; therefore, per minute, the salary difference, while still large, is not as large as it might seem at first glance. On the other hand, playing more minutes brings the risk of burning out the $12 million player.
Now let's look further at that $12 million player. Every GM seems to want one or two of them. That is why they jockey to get a top draft pick, hoping that a young player will develop into a $12 million player. And that is also why they offer huge contracts to free agents.
But is that the best strategy?
If your team is behind by a goal late in a game, you would surely want to have one of those $12 million players to put onto the ice to try to score a goal and tie the game up. But putting so much emphasis on one player (putting all your eggs in one basket, so to speak), can leave you vulnerable. If that player is injured or the other team puts enough focus on preventing that one player from scoring, then your team might be left with no other options.
Also consider this: The more $12 million players a team has, the fewer medium-priced players it is likely to have. There is a limited amount of salary money to go around. The result might be a team that has great strengths in one area and great weaknesses in others. For instance, if the top forwards are paid more, the team's defence might be weak. Or the first line might be great while the other three forward lines don't score very much (in hockey parlance, the team lacks secondary scoring).
Let's look at some concrete examples. In 2018-2019, the highest paid player was Connor McDavid of the Edmonton Oilers at $12.5 million. (For the purposes of this article, I am using the "cap hit" or average annual salary.) The Oilers also had Leon Draisaitl at $8.5 million. McDavid did his part, producing 116 points, the second highest total in the league, and Draisaitl finished fourth with 105 points. However, the team only had two other players being paid over $5 million. The team finished 25th in the 31-team league.
The Toronto Maple Leafs had two players in the top six mostly highly paid players: Auston Matthews at $11.634 million and John Tavares at $11 million. Matthews produced 73 points (while playing in only 68 games due to injury) and Tavares 88 points. The Leafs had only three more players being paid over $5 million. The team finished 7th, but tailed off in the second half of the season and lost in the first round of the playoffs. In the upcoming 2019-2020 season, the Leafs have three players in the $11-$12 million range, making up three of the seven highest paid players in the league. Their top two lines are likely going to score a ton of goals—and they will have to because the Leafs' bottom two lines aren't likely to score many at all.
At the other end of the spectrum, the top player on the Tampa Bay Lightning, Steven Stamkos, was paid $8.5 million, and five other players were paid over $5 million. The Lightning were by far the best team in the regular season, but lost out in the first round of the playoffs.
The highest paid players on the Calgary Flames were Johnny Gaudreau at $6.75 million, Mike Giordano at $6.75 million, and Gary Monahan at $6.375 million. Two other players were paid more than $5 million. The Flames finished second in the regular season and also lost out in the first round of the playoffs.
The highest paid player on the Washington Capitals was Alex Ovechkin at $9.538 million. The Capitals paid eight other players over $5 million. They finished fourth in the regular season but lost in the first round of the playoffs.
The highest paid player on the Boston Bruins was David Krejci at $7.25 million. The Bruins paid six other players more than $5 million. The Bruins finished third in the regular season and were the second best team in the playoffs, losing in the Stanley Cup final.
The highest paid players on the St. Louis Blues were Vladimir Tarasenko and Ryan O'Reilly at $7.5 million each. They produced 68 and 77 points respectively. The team had seven other players paid over $5 million. The Blues finished 12th (tied with two other teams for 10th) in the regular season but had the best record in the second half of the season and eventually won the Stanley Cup.
Also consider this: Of the 12 players paid $10 million or more, seven played on teams that did not make the playoffs.
Hockey is a team game. The best strategy to have a winning team does not seem to be to acquire one or two $12 million superstars. Rather, the best strategy seems to be to have a cluster of very good players in the $5-$8 million range.
Tags: Connor McDavid, General Manager, National Hockey League, NHL, salary cap, Stanley Cup, Toronto Maple Leafs Permalink
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One comment on "The Value of a Twelve Million Dollar Man"
Teams with Superstars Are Less Likely to Win | James R. Coggins August 24, 2020 at 12:21 pm	Reply
[…] wrote an article on this issue last year, pointing out that of the 12 highest paid players in the league, only five […]

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text:
Samantha Rigby in EntertainmentFeatured⭐ On ,
Star Trek might be the next to take over Marvel's cinematic throne
Photo: Star Trek
The Star Trek universe is poised to rival the Marvel Cinematic Universe with the latest CBS and Viacom merger in a move that echoes the recent Disney-Fox pact.
The CBS and Viacom team-up means that the small screen and big screen rights of the Star Trek franchise is now under the same company. Something that last happened 14 years ago before the end of Star Trek: Enterprise back in 2005.
From then on, Viacom's Paramount Pictures held the movie rights as well as for future movies. On the other hand, television and licensing rights fell under CBS.
JJ Abram's 2009 Star Trek reboot starring Chris Pine and Zoe Saldana marked the first movie independently made from a television series in the franchise. This meant that the actors weren't portraying their roles on the small screen as well.
On the other hand, a 2017 Star Trek television series was produced by CBS. Star Trek: Discovery starred Jason Isaacs and Anthony Rapp.
The tv show's success paved the way to an equally successful web series, Star Trek: Short Trek which led to an upcoming spin-off titles Star Trek: Picard, starring Patrick Stewart.
Another project that's currently in development for the franchise is Star Trek: Section 31.
The merger will mean the franchise's own extended universe might be in the works. Continuity between the shows and films is expected to bring the Star Trek back to it's former glory from its golden era.
Quentin Tarantino's possible involvement is something that could propel the concept into a good start.
Samantha Rigby
Samantha is the head of content and politics columnist for Best in Australia. Prior to joining the Best in Au, she was a court and crime reporter at SM.
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PALM BEACH, Fla. — The patriarchs of this quiet island of millionaires threw up roadblocks when Donald Trump swooped in and turned its historic oceanfront Mar-a-Lago mansion into a private club.
Trump's lawyer sent every member of the town council copies of two classic movies about discrimination: "A Gentleman's Agreement," about a journalist who pretends to be Jewish to expose anti-Semitism, and "Guess Who's Coming to Dinner" about a white couple's reaction to their daughter bringing home a black fiance.
Trump's relationship with Palm Beach, where he has spent three decades brawling with local officials and winning over many, was an early indicator of the personality traits and tactics that have helped propel him to the top of Republican presidential primary polls.
In buying and then winning the right to transform the landmark property, Trump demonstrated how he gains leverage by exposing and exploiting the weaknesses of his opponents, combining bombast with a willingness to compromise, and casting every outcome as a resounding Trump victory.
The story of Trump's ownership with Mar-a-Lago is also a reminder of the real estate mogul's tabloid past — a time, long before he began courting conservative voters, when he reveled in extravagant parties, beautiful women and celebrity friendships.
Many in Palm Beach today recoil at his look-at-me ego and are appalled at his frequent displays of unfiltered Trump, like emblazoning his name on a coat of arms on Mar-a-Lago's elegant facade.
But, just as Trump has forced many in the national Republican establishment to accept him as an enduring presence in this year's presidential campaign, Trump and his club have become undeniable cornerstones of Palm Beach society.
Last year, Trump made $15.6 million from Mar-a-Lago, according to financial disclosures Trump filed as part of his presidential campaign.
Trump closes off part of the main house for his private quarters. The name of Trump's late mother, Mary Trump, who grew up in a modest house in Scotland, appears over the door to the room where she often stayed. Another room is dominated by an elaborate canopied bed where Trump's daughters Ivanka and Tiffany slept as children.
Many of Trump's rivals in the presidential race have been to Mar-a-Lago for functions, including Ted Cruz, Chris Christie and Ben Carson. So have many Republican commentators, including Rush Limbaugh and Laura Ingraham.
Democratic presidential front-runner Hillary Rodham Clinton came, too, attending Trump's wedding to Melania Knauss 10 years ago.
Since 2013, the Palm Beach County Republican Committee has held its annual Lincoln Day fundraiser at Mar-a-Lago. Michael Barnett, committee chairman, remembers seeing Cruz last year deep in conversation with Trump and wonders if one of the reasons they are so friendly on the campaign trail is because of a bond forged at Mar-a-Lago.
Until he hit the presidential campaign trail, Trump spent many weekends at Mar-a-Lago, hopping table to table asking diners if they tried his mother's meatloaf on the menu or enjoyed his ocean view. Trump, whose brother died of alcoholism, does not drink. Friends say his relaxation comes from golf and presiding over Mar-a-Lago, chatting with guests.
He lets Palm Beachers come to him, rarely venturing out to shops and restaurants in town.
Mar-a-Lago was opened in 1927 as a private estate by one of the richest women in the world, Marjorie Merriweather Post.
She donated her 128-room home to the U.S. government in 1973 for use as the winter White House. But under President Jimmy Carter, the government turned the property over to the private Post Foundation, saying it was too expensive to maintain.
Trump wanted it to be his.
In the end, Trump bought the landmark in 1985 for a bargain, paying $5 million for the house and $3 million for Post's antiques and lavish furnishings.
From the start, Trump's approach stood out in Palm Beach, a small town whose cloistered estates and private beaches appealed to the super rich seeking to live quietly.
Along with old-money families with homes here since the Gilded Age, there are billionaires with more money than Trump who drive their Bentleys into estates hidden behind high hedges.
He has invited high-profile guests such as Michael Jackson to stay overnight, drawing paparazzi. He was chided in local papers for floating the rumor that Princess Diana, Madonna and other big names were joining his club, a promoter's tactic to build buzz.
Over time, he added a Louis XIV-style ballroom with 40-foot ceilings and $7 million worth of gold leaf on its walls. He spent $100,000 on four gold-plated bathroom sinks near the ballroom.
"It's become part of the fabric of the social life of Palm Beach," said Jane Day, who as the town's historic preservation consultant at times clashed with Trump. But like many, she credited Trump with saving the historic home and managing it in a way that has allowed many people to enjoy it.
The property employs scores of waiters, landscapers, cooks and other staff, including foreign workers brought in using special visas. Trump's reliance on immigrant labor has received attention in recent months as he has made illegal immigration a signature issue on the campaign trail.
Trump made Mar-a-Lago appealing even to his biggest skeptics. He brought in headliners including Elton John, Celine Dion, Diana Ross, Luciano Pavaratti and Jay Leno, who performed at charity balls and events open to anyone who could afford a ticket.
By opening access, Trump sought to dull opposition to him.
Trump urged officials to become members, including those he was feuding with.
For a time, McDonald, the former mayor, was even doubles partners at the club with Marla Maples, Trump's second wife.
Trump invited the historic preservation society arguing with him over alterations to the landmark to hold its annual luncheon there. And the town police, summoned if a party grew too noisy, now hold their annual benefit there. Police records show officers often have stopped at the mansion for coffee and meal breaks.
Allen Wyett, a frequent Trump critic, recalled that the morning after Wyett's election to the town council in 1995, he received a phone call from Trump, who wanted to personally invite him to a show at Mar-a-Lago. Wyett declined and never joined Mar-a-Lago. But he said the invitations continued to concerts, to comedy shows.
Mar-a-Lago became a party destination in the late 1990s, particularly after Trump split from Maples and before he married Knauss. Rich men mingled with the models and beauty pageant contestants who always seemed to be floating around his tiled patio.
"It was 3-to-2, beautiful women-to-men," recalled Roger Stone, a former adviser to Trump.
In 1998, Trump invited Sean Combs, the rapper then known as Puff Daddy. But Combs scandalized Palm Beach when he was caught on a beach in the "middle of his midnight romp with a long-legged stunner," according to the Page Six account in the New York Post.
Even as Mar-a-Lago became more established, Trump's battles with local officials never really ended.
Wyett and other council members said the town's fights with Trump typically boiled down to Palm Beach trying to apply rules designed to protect a residential neighborhood. In their view, Trump doesn't believe rules apply to him. But they said his unconventional tactics have often worked.
Palm Beach has a lot of rules: No whistling allowed on public streets after midnight. No "Missing Dog" — or any sign — posted on a tree. And no flag poles taller than 42 feet.
In late 2006 Trump put up a giant American flag on an 80-foot pole. That led to a $1,250-a-day fine against him, drawing national headlines that Trump basked in.
"Tonight, Donald Trump does legal battle again, this time with a bunch of millionaires down in Palm Beach, Florida, who told Trump he's flying his flag too high," is how Nancy Grace started her CNN interview in January 2007 with Trump. "Can you fly the American flag too high?" she asked.
"I said, 'This is a dream to have someone sue me to take down the American flag,' " Trump said in the interview.
Trump sued Palm Beach for $25 million in damages, arguing the flag was constitutionally protected free speech.
Ultimately, Trump reached a settlement with the town. He would put a slightly smaller flag farther from the road and mount it on a 70-foot pole.
Instead of paying any fines, Trump made a $100,000 donation to a veterans charity.
While gracious to many neighbors, Trump has mocked others.
He has filed multimillion-dollar lawsuits as casually as others file their nails. It's a Trump strategy, critics say, to wear people out and get what he wants.
Trump has filed three lawsuits over perhaps his biggest irritation: the planes that fly over Mar-a-Lago, which sits just a couple miles from the West Palm Beach airport's main runway.
A judge is now weighing a $100 million lawsuit Trump filed in January, arguing that airport director Bruce Pelly — who Trump has called "a moron" — has engaged in a "deliberate and malicious" effort to direct the planes over his home.
Pelly and a county attorney declined to comment, citing ongoing litigation. In court, the county has argued that the Federal Aviation Administration traffic controllers determine airplane flight paths, not Pelly.
In his first lawsuit involving the airport, Trump won no money and the planes continued to fly over Mar-a-Lago. But Palm Beach County agreed to try to limit noise and said it would lease a 215-acre parcel of airport-owned land to Trump. That land is now the Trump International Golf Course West Palm, where, according to federal filings, Trump made $12.7 million last year.
"There was a lot of strategy in it. You have to admire him for it," McDonald said.
People in town now speculate Trump might have finally found a way to clear the sky above.
If elected president and the house becomes the winter White House as the original owner intended, the Secret Service could order a no-fly zone.


A total of 40 results for fix and flip hard money lenders were found in Indiana. The mean amount loaned in the state is $296,155. The mean interest rate for loans in Indiana is 11.0%. The mean length for notes is 28 months. The mean points added to loans is 3.7%. Lenders in Indiana average a 74% loan-to-value (LTV) on their loans.
Marion finds a condo in Greenwood, IN to renovate and resell. Since he does not have enough cash to acquire the $320,000 project outright, he takes out a fix-and-flip loan from Blue Sky Lending Corporation . The borrower will be required to fund 15% of the purchase price in cash to the closing based on a 85% loan to value stipulated by the lending company. This makes the principle amount from Blue Sky Lending Corporation $272,000. The terms of the deal also stipulate a one percent origination fee which is to be paid at the closing and a 6 month, interest only note with a 9% interest rate.
Accordingly, Marion will need to contribute a $48,000 down payment plus pay a $2,720 origination fee. The monthly interest-only payments will then total $2,040 to Blue Sky Lending Corporation . If Marion sells the house for $480,000 after 6 months, he would realize a total profit of $145,040 after deducting the principle of $272,000, the money contributed at closing of $48,000, the origination fee of $2,720, and the aggregate interest payments of $12,240. This profit does not account for renovation costs.


There is an old Latin proverb fortuna favet fatuis, which translates to fortune favors fools. Many know this proverb from first-hand experience, of course. Like when we have practiced some feat for a considerable amount of time, do everything by the book, and then some new-comer without an ounce of rehearsal marches in, does something completely opposite to conventional wisdom and ends up performing better than us. Sometimes stupidity can be offset by sheer luck.
Unfortunately, I have certainly been a fool, but without much fortune in my AFOL hobby. During the past year and a half I have meticulously documented the lessons learned, and yet it seems I haven't really learned anything at all. My quest for Inter-City train is certainly a mess of gigantic proportions. As I documented recently, I have an immense pile of assorted LEGO boxes and bags with both new and old LEGO, my old, store bought, BrickLinked, what not. This is addition to a haphazard collection of decades-old containers housing the remains my childhood collection.
Pretty much the only inkling of organization is the sorted grey and black parts. One issue, certainly, is the fact that I still lack an organized building space – as I pondered in my article on why adults build LEGO. Once I get around to it, I intend to organize the pieces as well as arrange for some dedicated working space, that will also reduce the need for storing incomplete parts in random containers all over the home. Finally, a more stable setup should help with the one thing that seems to require the most concentrated effort on this blog, taking photographs.
That leaves (at least) one thing: bookkeeping. I broached the issue in my original quest for Lion Knights' castle, when I ignored perfectly good advice (surely sign of a fool, fortuitous or not) to concentrate my brickquisitions into as few BrickLink orders as possible. I had some rationale for not following the advice, mainly wanting to go step by step, to discover these things on my own and get to report on them too. I also found it a little unmotivating to simply go through my bricks in a bookkeeping exercise, fill some Excel, update a wanted list on BrickLink and then hit order.
Yet, after a year and a half, it is hard to argue with the advice I got so very early on. Sure, I got my journey and got to learn first hand how vast the collection of different LEGO bricks is (and in comparison, how insignificant mine). But at the same time, both of my "quests" so far, have stalled immediately upon start due to lack of baseplates. The reality isn't that, yeah I kind of miss a piece here and there and can keep on building, I have missed so fundamental pieces (and so many of them), that there really isn't much point trying until you reach a certain apex.
If you start a new LEGO project with very specific requirements (such as re-creating an old set you never owned), don't count on fool's fortune. I certainly have had none. In the end, it makes far more sense to be organized about it, especially considering how easy it is these days. You could simply mark all your LEGO sets on BrickLink or Peeron and get immediate listings of your parts library or at least the core of it. You can also use these sites to get a detailed listing of the parts required for your new project, if it is an official LEGO set. And finally, you could always create your model on the computer first and print out listings of the parts you need.
Belief can take you only so far – it certainly won't manifest itself as studded ABS in front of you. The one smart thing I did, early on in my quest for Inter-City train, was use the Peeron parts list to shop at the LEGO Shop online Pick a Brick. The downside: I kept no records of which parts I would still miss and now that time has passed, I have to start the bookkeeping exercise again. Add to this the completely uncategorized mess of extra parts I have and sheer frustration ensues. It would have been trivial to document and sort parts as I bought and received them, now it is simply painful extra duty. Not to mention the extra cost of inefficient purchases.
When I started with the first quest back in early 2012, I had this romantic notion of being through my brick-pile piece by piece, building the Lion Knights' castle – maybe occasionally picking some parts from the LEGO section of the local toy store and an online order here and there to fill in the gaps. Of course most of this notion was quickly smashed by the reality of changed LEGO colors (effectively shutting the door on any new purchases of grey and brown parts for classic sets) and lacking even the most basic pieces, not only the plates the set would stand on, but tons of others as well. You may think you have a lot of LEGO, but reality is, most of us probably don't.
What if I had started with even a cursory list of my old sets, Peeron/BrickLink and a few evenings laboring over Excel, mixing and matching…? I'll bet you my Inter-City train would already be riding into the sunset and I'd be all over the next big thing.
If I could name one mistake I have made in this hobby, aside from the occasional part blindness to the contrary, it is the mistaken notion that just because a set looks like it has a lot of familiar parts, you're good to go. Indeed, when I tried to build a 6080 King's Castle as a child and failed, it wasn't for the lack of instructions (and definitely not for the lack of trying), but simply because I really, really lacked the parts. Good instructions and Internet databases can and do help, but they won't raise castles or trains on your table – they will, however, be honest about what is needed for it.
There's a website called Rebrickable at http://rebrickable.com/ where you can inventory your parts and it will show you what you can build with it. I haven't done it, too many parts and no desire to do a proper inventory. I know a few people who use it to keep track of stuff.
Thank you for the suggestion, that sounds very useful!


text:
You Are Here Home Health News Coronavirus cases in Germany jump to 117
Coronavirus cases in Germany jump to 117
FitManitoba - March 1, 2020 at 8:55
BERLIN (Reuters) – The number of confirmed coronavirus cases in Germany has jumped to 117 from 66, the Robert Koch Institute for disease control said on Sunday.
A German government crisis committee has widened cross-border travel guidelines and canceled major international events, and the health minister has advised people with cold symptoms to stay away from mass events.
More than half of the cases are in North Rhine-Westphalia, Germany's most populous state where several schools and daycare centers will be closed on Monday to try to prevent the spread of the virus after staff members tested positive.
Interior Minister Horst Seehofer told the mass-selling Bild am Sonntag newspaper that he expected a vaccine for the coronavirus to be available by the end of the year.
Asked if Germany would be ready to lock down cities and regions to control the epidemic, Seehofer said: "This would be the last resort." He did not say what needs to happen for Germany to enact such drastic measures.
Finance Minister Olaf Scholz said in remarks published on Sunday that Germany would be in a position to introduce fiscal stimulus measures should the coronavirus spark a global economic crisis.
Writing by Joseph Nasr; Editing by Mark Potter
Hope for a vaccination against Staphylococcus areus infections?
Age provides a buffer to pandemic's mental health impact, researchers say


It's hard to believe it's been 30 years since Salt-N-Pepa first hit the Billboard music charts. The powerhouse trio pumped out hit after hit in the '90s. We still love to groove out to their classic music today.
And in a recent interview, Salt-N-Pepa said they've been working on new music.
Of course we want to hear a whole new album from these ladies, like, yesterday. But this is already lucky news – so we don't want to ah, push it.
While speaking with Billboard.com's Pop Shop Podcast, two thirds of the badass women of Salt-N-Pepa, Sandra "Pepa" Denton and Dee Dee "DJ Spinderella" Roper, confirmed that they've been spending some time in the studio.
"Yeah, we're going in the studio," Pepa said. "We have a couple songs already we've recorded."
They've stayed plenty busy since they first became musical superstars. Most recently, they've been headlining the I love the '90s tour along with Vanilla Ice and Naughty By Nature. And after their hit song "Shoop" was featured in the insanely popular movie Deadpool, Salt-N-Pepa jumped back onto the pop charts.
But DJ Spinderella made it clear that fans are going to have to wait.
The group is happy there's ongoing demand for new music. And they know they can create instant classics. So they have no interest in stopping anytime soon.
"We're just not going anywhere. Our songs are here to stay," Pepa added.
We don't yet have details on when we can expect to hear more about this new music. But it's certainly exciting to know that it's in the works. Until then, all we can say is what a band, what a band, what a band, what a mighty good band.