Warning-“W32.Koobface.A” على الفيس بوك أحذر هذا الفيروس

أحذر هذا الفيروس للكمبيوتر 

فيروس تتصرف دون إخطارك ، مثل الكتابة على الجدران وأصدقائك إرسال الرسائل الشخصية.

فيروس يسمى "W32.Koobface.A" ، ما يحدث هو إرسال رسالة ، أو كتابة رسالة على الجدار مع أصدقائك التعبير مثل : "كنت تبدو مضحكة في هذا الفيديو الجديد" ، "أنت تنظر فقط رهيبة في هذا الفيديو الجديد" "كليب رائع" و "لقد وجدت فيديو لكنت هنا"

ما يحدث هنا هو :

رسالة تطلب منك النقر على وصلة لعرض الفيديو ، وبعد الضغط سوف يطلب منك لتحميل نسخة جديدة من أدوبي ‘مشغل فلاش لعرض الفيديو وبمجرد أن يتم تحميل الملف وإعدامه ، ويحصل على الكمبيوتر المصابين بهذا الفيروس .

ما يحدث بعد ذلك :

الفيروس عرض مربع رسالة ويبدأ في الانتشار في حد ذاته إلى قائمة أصدقائك. وكذلك ، والسيطرة على جهاز الكمبيوتر ، فإنه ينسخ نفسه وحذف الملفات الهامة.

ما يجب القيام به :

— ابق على برامج مكافحة الفيروسات المحدثة.
— تثبيت أحدث مايكروسوفت ويندوز بقع.

أهمها :
— لا تحاول الوصول إلى أية مواقع غير معروفة أو مشتبه بهم ، وجعل وصلة متأكد من هو معروف وموثوق به.
— فكر قبل النقر!

هذا هو انظروا كيف يعمل على جدار صفحتكم

هذا هو انظروا كيف يعمل على جدار صفحتكم
هذا هو شكله ، وعندما تحصل على رسالة خاصة :

Recently many of Facebook users are being targeted by a virus designed to gather sensitive and personal information about Facebook users.

The virus behave without your notice, such as writing on your friends wall and sending personal messages.

The virus is called "W32.Koobface.A", what happens is sending a message or writing a message on your friends wall with expression like: "you look funny in this new video", "you look just awesome in this new video", "Amazing Video" and "I found video for you here"

Here is what happens:

The message asks you to click on a link to view a video, after clicking you will be asked to download a new version of Adobe’ Flash Player to view the video and once the file is downloaded and executed, the computer gets infected with this virus.

What happens next:

The virus display a message box and starts to spread itself to your friends list. As well as, taking control on the PC, it copies itself and deletes important files.

What to do:

– Keep your antivirus software updated.
– Install the latest Microsoft Windows patches.

Most important:
– Do not try to access any unknown or suspected websites, make sure link is known and trusted.
– Think before clicking!

This is How it Look likes, when you get a wall post:

This is How it Look likes, when you get a private message:

 
 

Simple Ways To prevent Breast Cancer – Dr Usama Fouad Shaalan (MD; PhD )MiniEncyclopedia

 

Simple approch

Dr Usama Fouad Shaalan (MD;PhD) MiniEncyclopedia الموسوعه المصغره للدكتور  أسامه فؤاد شعلان

Breast cancer usually starts with a cancerous, or malignant, tumor located in the breast tissue. Most breast cancers are located in the area around the nipple. For women, breast cancer is the most common cancer and the second leading cause of cancer deaths, following only lung cancer. Although men can get breast cancer, it’s rare (only one half of 1 percent of all breast cancers are in men). Breast cancer is curable if caught early–and is usually treated through some combination of surgery, radiation, chemotherapy, and other medications.

Are you worried about the possibility of breast cancer in your future, or in the future of someone you love? Here are the top ten things you can do to ensure a breast cancer-free future for yourself and your loved ones.

Detection:

 

1. Get regular mammograms. It sounds obvious, but you’d be surprised how many women don’t. Last week an Australian study found that women who get regular mammograms had a 4 percent risk of dying of breast cancer; women who weren’t screened had a 56 percent mortality rate. Ready to make that appointment?

2. Find out whether you or women close to you have dense breasts. What does this mean? It means the breast cells grow and multiply more rapidly, raising your risk. Plus dense breasts make it harder for a mammogram to “see” through the tissue and detect a tumor. While dense breast tissue is more common in younger women who haven’t yet had children, it’s also hereditary and can affect any woman. I have a dear 43-year-old friend whose breast tumor failed to show up on three years’ worth of mammograms before her doctor finally ordered an MRI. How to find out? Schedule a breast exam and ask your doctor. Also talk to the radiologist who’s administering your mammogram.

3. Ask your doctor to recommend other tests. Surprise: Mammograms are only 16 to 40 percent accurate, studies show. Meanwhile, ultrasounds and MRIs can detect breast tumors that may not show up on mammograms. MRIs, the gold standard, are 70 to 100 percent accurate. This fall Dartmouth University published a study showing that MRIs found tumors in 20 percent of patients who’d already “passed” a mammogram or ultrasound. If you have any reason for concern, ask your doctor to refer you for an ultrasound, MRI, or both.

Prevention:

4. Know your BMI–and lower it if necessary. Studies show that women whose body mass index (BMI) is at the lower end of the scale for their height lower their risk of breast cancer. Even more important, though, is getting rid of belly fat, which acts like a “hormone pump” releasing estrogen into the bloodstream as well as raising levels of other hormones.

5. Get 30 minutes a day of exercise. We all know this is one of the best ways to keep our weight down, but research also shows that activity itself helps prevent cancer by keeping hormone levels healthy. This is important for preventing hormone-fueled breast cancer.

6. Limit alcohol to one drink a day–or save it for special occasions. More than one drink a day is associated with a significant increase in breast cancer risk, and teetotalers have the lowest risk of all. It seems that alcohol boosts the effect of other toxins, such as nicotine from smoking, and can directly damage DNA, leading to cancer.

7. Eat those fruits and veggies. For more information, check out these 10 foods known to prevent cancer.

8. Quit smoking. Sorry, I know you don’t want to hear it. But there are great new helpful tools to make it easier to quit–and doing so will reduce your risk of not only breast cancer, but lung, colon, and throat cancer too.

9. Skip the supplemental soy. Soy contains chemicals called isoflavones, which–when concentrated–act like estrogen in your body, so they can stimulate estrogen-sensitive breast cancer. But it’s soy supplements that are the concern; eating tofu or drinking soy milk is fine unless you’re at specific risk of estrogen-sensitive cancer. Overall, women who eat a diet high in soy have a lower breast cancer risk.

10. Don’t take hormones, or limit how long you take them. There’s still plenty of controversy, but most experts agree that long-term use of estrogen and progesterone combination hormone therapy boosts your breast cancer risk. If you or someone you care for is really desperate, ask your doctor to prescribe the lowest possible dose, and plan to use it as a six month respite, and then reevaluate. Five years is considered the maximum time a woman should be on hormones.

More sientific approch

Breast Cancer: What is Breast Cancer?

Affiliation: National Cancer Institute
Last Modified: November 1, 2001

Description

Note: Separate PDQ summaries on Screening for Breast Cancer; Prevention of Breast Cancer; and Male Breast Cancer Treatment are also available.

What is breast cancer?

Breast cancer, a common cancer in women, is a disease in which cancer(malignant) cells are found in the tissues of the breast. Each breast has 15 to 20 sections called lobes, which have many smaller sections called lobules. The lobes and lobules are connected by thin tubes called ducts. The most common type of breast cancer is ductal cancer. It is found in the cells of the ducts. Cancer that begins in the lobes or lobules is called lobular cancer. Lobular cancer is more often found in both breasts than other types of breast cancer. Inflammatory breast cancer is an uncommon type of breast cancer. In this disease, the breast is warm, red, and swollen.

Hereditary breast cancer makes up approximately 5% to 10% of all breast cancer cases. The genes in cells carry the hereditary information that is received from a person’s parents. Several genes have been found to be defective in some breast cancer patients. Relatives of breast cancer patients who carry these defective genes may be more likely to develop breast or ovarian cancer. Some defective genes are more common in certain ethnic groups. Tests are being developed to determine who has the genetic defect long before any cancer appears. (Refer to the PDQ summaries on Screening for Breast Cancer and Prevention of Breast Cancer for more information.)

Hormonal contraceptives may be another factor to consider. Research findings suggest a link between contraceptive use and a slightly increased risk of developing breast cancer.

A doctor should be seen if changes in the breasts are noticed. The doctor may suggest that you have a mammogram. A mammogram is a special x-ray of the breast that may find tumors that are too small to feel. If a lump in the breast is found, the doctor may need to cut out a small piece of the lump and look at it under the microscope to see if there are any cancer cells. This procedure is called a biopsy. Sometimes the biopsy is done by inserting a needle into the breast and drawing out some of the tissue. If the biopsy shows that there is cancer, it is important that certain tests (called estrogen and progesterone receptor tests) be done on the cancer cells.

Estrogen and progesterone receptor tests may tell whether hormones affect the way the cancer grows. They may also give information about the chances of the tumor coming back (recurring). The results help a doctor decide whether to use hormone therapy to stop the cancer from growing. Tissue from the tumor needs to be taken to the laboratory for estrogen and progesterone tests at the time of biopsy because it may be hard to get enough cancer cells later, although newer techniques can be used on tissue that is not fresh.

The chance of recovery (prognosis) and choice of treatment depend on the stage of the cancer (whether it is just in the breast or has spread to other places in the body), the type of breast cancer, certain characteristics of the cancer cells, and whether the cancer is found in the other breast. A woman’s age,weight, menopausal status (whether or not a woman is still having menstrual periods), and general health can also affect the prognosis and choice of treatment.

If a patient is going to have a mastectomy, breast reconstruction (making a new breast mound) may be considered. It may be done at the time of the mastectomy or at some future time. The breast may be made with the patient’s own(non-breast) tissue or by using implants. Different types of implants can be used. The Food and Drug Administration (FDA) has announced that breast implants filled with silicone gel may only be used in clinical trials. Saline-filled breast implants, which contain saltwater rather than silicone gel, may also be used. Before the decision to get an implant is made, patients can call the FDA’s Center for Devices and Radiologic Health at 1-888-INFO-FDA(1-888-463- 6332) to obtain additional information. Additional questions can then be discussed with a doctor.

Stage explanation

Stages of breast cancer
Once breast cancer has been found, more tests will be done to find out if the cancer has spread from the breast to other parts of the body. This is called staging. To plan treatment, a doctor needs to know the stage of the disease. The following stages are used for breast cancer.

Stage 0
Ductal carcinoma in situ (DCIS; also known as intraductal carcinoma) is a very early breast cancer that may develop into an invasive (cancer that has spread from the duct into surrounding tissues) type of breast cancer.

Lobular carcinoma in situ (LCIS) is not cancer, but rather a marker that identifies a woman at increased risk to develop invasive (cancer that has spread into surrounding tissues) breast cancer later in life.

Stage I
The cancer is no larger than 2 centimeters (about 1 inch) and has not spread outside the breast.

Stage II
Stage II is divided into stages IIA and IIB.

Stage IIA is defined by either of the following:

The cancer is no larger than 2 centimeters but has spread to the lymph nodes under the arm (the axillary lymph nodes).

The cancer is between 2 and 5 centimeters (from 1 to 2 inches), but has not spread to the lymph nodes under the arm.

Stage IIB is defined by either of the following:

The cancer is between 2 and 5 centimeters (from 1 to 2 inches), and has spread to the lymph nodes under the arm.

The cancer is larger than 5 centimeters (larger than 2 inches), but has not spread to the lymph nodes under the arm.

Stage III
Stage III is divided into stages IIIA and IIIB.

Stage IIIA is defined by either of the following:

The cancer is smaller than 5 centimeters and has spread to the lymph nodes under the arm, and the lymph nodes are attached to each other or to other structures.

The cancer is larger than 5 centimeters and has spread to the lymph nodes under the arm.

Stage IIIB is defined by either of the following:

The cancer has spread to tissues near the breast (skin or chest wall, including the ribs and the muscles in the chest).

The cancer has spread to lymph nodes inside the chest wall along the breast bone.

Stage IV
The cancer has spread to other organs of the body, most often the bones, lungs, liver, or brain. Or, tumor has spread locally to the skin and lymph nodes inside the neck, near the collarbone.

Inflammatory breast cancer
Inflammatory breast cancer is a special class of breast cancer that is rare. The breast looks as if it is inflamed because of its red appearance and warmth.

The skin may show signs of ridges and wheals or it may have a pitted appearance. Inflammatory breast cancer tends to spread quickly.

Recurrent
Recurrent disease means that the cancer has come back (recurred) after it has been treated. It may come back in the breast, in the soft tissues of the chest (the chest wall), or in another part of the body.

Treatment option overview

How breast cancer is treated

There are treatments for all patients with breast cancer. Four types of treatment are used: –

  • surgery (taking out the cancer in an operation) –
  • radiation therapy (using high-dose x-rays to kill cancer cells) –
  • chemotherapy (using drugs to kill cancer cells) – hormone therapy (using drugs that change the way hormones work or taking out organs that make hormones, such as the ovaries)

Biological therapy (using the body’s immune system to fight cancer), bone marrow transplantation, and peripheral blood stem cell transplantation are being tested in clinical trials.

Most patients with breast cancer have surgery to remove the cancer from the breast. Usually, some of the lymph nodes under the arm are also taken out and looked at under a microscope to see if there are any cancer cells.

Different types of operations used:

Surgery to conserve the breast:

Lumpectomy (sometimes called excisional biopsy or wide excision) is the removal of the lump in the breast and some of the tissue around it. It is usually followed by radiation therapy to the part of the breast that remains. Most doctors also take out some of the lymph nodes under the arm.

Partial or segmental mastectomy is the removal of the cancer as well as some of the breast tissue around the tumor and the lining over the chest muscles below the tumor. Usually some of the lymph nodes under the arm are taken out. In most cases, radiation therapy follows.

Other types of surgery:

Total or simple mastectomy is the removal of the whole breast. Sometimes lymph nodes under the arm are also taken out.

Modified radical mastectomy is the removal of the breast, many of the lymph nodes under the arm, the lining over the chest muscles, and sometimes part of the chest wall muscles. This is the most common operation for breast cancer.

Radical mastectomy (also called the Halsted radical mastectomy) is the removal of the breast, chest muscles, and all of the lymph nodes under the arm. For many years, this was the operation most used, but it is used now only when the tumor has spread to the chest muscles.

Radiation therapy is the use of high-energy x-rays to kill cancer cells and shrink tumors. Radiation may come from a machine outside the body (external radiation therapy) or from putting materials that produce radiation(radioisotopes) through thin plastic tubes into the area where the cancer cells are found (internal radiation therapy).

Chemotherapy is the use of drugs to kill cancer cells. Chemotherapy may be taken by mouth or it may be put into the body by inserting a needle into a vein or muscle. Chemotherapy is called a systemic treatment because the drugs enter the bloodstream, travel through the body, and can kill cancer cells outside the breast area.

If tests show that the breast cancer cells have estrogen receptors and progesterone receptors, hormone therapy may be given. Hormone therapy is used to change the way hormones in the body help cancers grow. This may be done by using drugs that change the way hormones work or by surgery to take out organs that make hormones, such as the ovaries. Hormone therapy with tamoxifen is often given to patients with early stages of breast cancer. Hormone therapy with tamoxifen or estrogens can act on cells all over the body and may increase the chance of getting cancer of the uterus. A doctor should be seen for a pelvic examination every year. Any vaginal bleeding, other than menstrual bleeding, should be reported to a doctor as soon as possible.

Even if the doctor removes all the cancer that can be seen at the time of the operation, the patient may be given radiation therapy, chemotherapy, or hormone therapy after surgery to try to kill any cancer cells that may be left. Therapy given after an operation when there are no cancer cells that can be seen is called adjuvant therapy.

Biological therapy tries to get the body to fight cancer. It uses materials made by the body or made in a laboratory to boost, direct, or restore the body’s natural defenses against disease. Biological therapy is sometimes called biological response modifier (BRM) therapy or immunotherapy. This treatment is currently only being given in clinical trials.

Bone marrow transplantation is a type of treatment that is being studied in clinical trials. Sometimes breast cancer becomes resistant to treatment with radiation therapy or chemotherapy. Very high doses of chemotherapy may then be used to treat the cancer. Because the high doses of chemotherapy can destroy the bone marrow, marrow is taken from the bones before treatment. The marrow is then frozen and the patient is given high-dose chemotherapy with or without radiation therapy to treat the cancer. The marrow that was taken out is then thawed and given back to the patient through a needle inserted into a vein to replace the marrow that was destroyed. This type of transplant is called an autologous transplant. If the marrow that is given is taken from another person, the transplant is called an allogeneic transplant.

Another type of autologous transplant is called a peripheral blood stem cell transplant. The patient’s blood is passed through a machine that removes the stem cells (immature cells from which all blood cells develop) and then returns the blood back to the patient. This procedure is called leukapheresis and usually takes 3 or 4 hours to complete. The stem cells are treated with drugs to kill any cancer cells and then frozen until they are transplanted back to the patient. This procedure may be done alone or with an autologous bone marrow transplant.

A greater chance for recovery occurs if the doctor chooses a hospital that does more than five bone marrow transplantations per year.

Treatment by stage

Treatment of breast cancer depends on the type and stage of the disease, and the patient’s age, menopausal status, and overall health.

Standard treatment may be considered because of its effectiveness in patients in past studies, or participation in a clinical trial may be considered. Not all patients are cured with standard therapy and some standard treatments may have more side effects than are desired. For these reasons, clinical trials are designed to find better ways to treat cancer patients and are based on the most up-to-date information. Clinical trials are ongoing in most parts of the country for all stages of breast cancer. To learn more about clinical trials,call the Cancer Information Service at 1-800-4-CANCER (1-800-422-6237); TTY at 1-800-332-8615.

Ductal carcinoma in situ

If the patient has ductal carcinoma in situ (DCIS), treatment may be one of the following:

  1. Breast-conserving surgery with radiation therapy, with or without hormone therapy.
  2. Surgery to remove the whole breast (total mastectomy), with or without hormone therapy.
  3. Clinical trials comparing breast-conserving surgery and hormone therapy with or without radiation therapy.

Lobular carcinoma in situ

If the patient has lobular carcinoma in situ (LCIS), treatment may be one of the following:

  1. Biopsy to diagnose the LCIS followed by regular examinations and regular mammograms to find any changes as early as possible.
  2. Hormone therapy to reduce the risk of developing breast cancer.
  3. Clinical trials including a large clinical trial (Study of Tamoxifen and Raloxifene–STAR trial)comparing 2 types of hormone therapy to lower the risk of developing breast cancer and to compare the side effects of treatment. The Cancer Information Service can be called for more information (1-800-4-CANCER).
  4. Surgery to remove all of both breasts (total bilateral mastectomy). This treatment choice is sometimes used in women who have a high risk of getting breast cancer. Most surgeons believe that this is a more aggressive treatment than is needed.

Stage I, ii, and iiia breast cancer

Primary treatment may be one of the following: If the cancer is confined to the breast and lymph nodes under the arm:

  1. Breast-conserving surgery to remove only the cancer and some surrounding breast tissue (lumpectomy) followed by radiation therapy. Some of the lymph nodes under the arm are also removed.
  2. Surgery to remove the whole breast and the lining over the chest muscles (modified radical mastectomy), as well as some of the lymph nodes under the arm with or without breast reconstruction surgery.
  3. A clinical trial evaluating limited lymph node removal (sentinel lymph node biopsy).

Adjuvant therapy (given in addition to the treatments listed above) may include:

  1. Radiation therapy to the lymph nodes under the arm following a modified radical mastectomy.
  2. Systemic chemotherapy with or without hormone therapy.

Stage IIIB, iv, recurrent, and metastatic breast cancer

Treatment for breast cancer that comes back (recurs) to the breast or chest wall may include:

  1. Surgery (radical or modified radical mastectomy) and/or radiation therapy.
  2. Systemic chemotherapy or hormone therapy.

Treatment for Stage IIIB cancer or inflammatory breast cancer may include one or more of the following:

  1. Systemic chemotherapy.
  2. Systemic chemotherapy followed by surgery (breast-conserving surgery or total mastectomy) with lymph node removal followed by radiation therapy. Additional systemic therapy (chemotherapy and/or hormone therapy) may be given).
  3. Clinical trials testing new chemotherapy drugs, new drug combinations, and new ways of giving treatment.

Treatment for Stage IV cancer or metastatic breast cancer may include one or more of the following:

  1. Hormone therapy and/or chemotherapy with or without trastruzumab (Herceptin).
  2. Radiation therapy and/or surgery to relieve the pain caused by the cancer.
  3. Clinical trials testing new chemotherapy and/or hormone therapy. Clinical trials are also studying new combinations of trastruzumab (Herceptin) with chemotherapy drugs.
  4. Clinical trials evaluating other approaches, including high-dose chemotherapy with bone marrow or peripheral stem cell transplantation.
 
 
 

سقوط دولة الموحدين في الأندلس و معركة العُقاب أومعركة لاس ناڤاس دي تولوس – االموسوعه المصغره للدكتور أسامه فؤاد شعلان

 
 
 
Dr Usama Fouad Shaalan MD- PhD MiniEncyclopedia الموسوعه المصغره للدكتور  أسامه فؤاد شعلان

معركة العُقاب أومعركة لاس ناڤاس دي تولوسا هي معركة وقعت في 16 يوليو 1212 م شكلت نقطة تحول في تاريخ شبه جزيرة أيبريا. تجمعت قوات الملك ألفونسو الثامن من قشتالة ومنافسوه السياسيين سانشو السابع من نافاره وأفونسو الثاني من البرتغال وپدرو الثاني من أراگون ضد قوات الموحدين حكام الجزء الجنوبي من شبه الجزيرة الأيبرية ومناطق واسعة من شمال وغرب أفريقيا. قاد قوات الموحدون السلطان محمد الناصر التي جاءت من شتى مناطق الدولة للمشاركة في المعركة.

 التسمية

وقعت المعركة في واد يسميه الإسبان ناڤاس قرب بلدة تولوسا وهذا سبب تسميتها بمعركة لاس نافاس دي تولوزا ووقعت كذلك قرب حصن أموي قديم يسمى العُقاب (بضم العين) ولذلك تسمى في التاريخ العربي باسم معركة العقاب أو معركة حصن العقاب.

 ما قبل المعركة

كان لهزيمة الملك القشتالي ألفونسو الثامن في معركة الأرك التي وقعت عام 1195 م الأثر الكبير في توطيد حكم المسلمين في الأندلس وتوسعة أراضيهم فيها فقد استرجع المسلمون كلا من مدن تروخيو وبلاسينسيا وكوينكا وقلعة رباح وبينافينتي والعديد من المدن والقلاع الأخرى. وقد تركت تلك المعركة أثرا في قلب ألفونسو الثامن الذي كانت تحدث نفسه بالانتقام على الرغم من أنه اضطر إلى عقد هدنة مع الموحدين بعد معركة الأرك.

الشارة الجديدة لناڤاره.

الشارة الجديدة لناڤاره.

استغل الملك ألفونسو الهدنة في تحصين مملكته وكذلك في تأليب بقية مسيحيي أوروبا ضد المسلمين فقد استطاع أن يجلب ود منافسيه السياسيين في أيبريا ملوك البرتغال ونافاره وأراگون. نقض ألفونسو الهدنة عام 1209 م بقيامه باقتحام حصن رباح في وسط الأندلس وأغار على جيان وبياسة وأجزاء من مرسية. إثر ذلك أعلن السلطان محمد الناصر الجهاد وأمر بتجهيز الجيوش لإيقاف المد الصليبي ويذكر بعض المؤرخين المسلمين أن تعداد الجيش الإسلامي وصل لثلاث مئة ألف مقاتل وآخرون يوصلون العدد لنصف مليون مقاتل لكثرة المتطوعين فيه.

سار محمد الناصر بقواته إلى الأندلس واستقر في إشبيلية وأرسل جزءا من جيشه لتحرير قلعة رباح ذات الموقع الإستراتيجي وبعد حصار دام 8 أشهر استطاع المسلمون أن يفتحوا ذلك الحصن. استغل ألفونسو الثامن ذلك الوضع وبعث إلى البابا إنوسنت الثالث يدعوه لإعلان حرب صليبية في أوروبا وقد استجاب له البابا فأمر بمساعدته وأعلنها حربا صليبية لا يحل الغفران على من لا يساعد أو يشارك فيها. أرسلت الدويلات الإيطالية وفرنسا الجنود والمؤن لدعم التحالف المسيحي.

قلعة رباح الحصينة

قلعة رباح الحصينة

 

تحرك الصليبيون باتجاه قلعة رباح وكانت حامية القلعة الإسلامية لا تزيد عن 100 فارس إلا أنهم قاوموا مقاومة عنيفة ثم استسلموا في نهاية الأمر لعدم تكافؤ الطرفين ولعدم وصول الإمدادات من المسلمين. عندما علم محمد الناصر بذلك حرك جيشه باتجاه الشمال والتقى الطرفان في الثالث عشر من يونيو.

 المعركة

التقى الطرفان على جبال الشارات أو السييرا مورينا وعسكروا في أطراف تلك الجبال. نظمت الصفوف وحمس الجنود وكان الجميع بانتظار شرارة البداية حتى كان السادس عشر من يونيو الموافق الخامس عشر من صفر 609 هـ. في ذلك اليوم التحم الجيشان وفي بادئ الأمر قاومت مقدمة الجيش الإسلامي المؤلفة من المتطوعين المغاربة وصدر الجيش المكون من الجيش النظامي الموحدي قاوموا فرسان التحالف المسيحي مقاومة شرسة حتى بدأت قوات المسيحيين بالتراجع وظهرت عليهم أمارات الخوف.

استشار ألفونسو قادة جيشه وكبار دولته فأشاروا عليه بمحاولة حصار الجيش الإسلامي وكان صوابا أن فعل فانطلق جناحا الجيش المسيحي المكون من قوات نافارة وأراجون وطوقوا جيش محمد الناصر الأمر الذي أدى إلى اضطراب الجيش وانسحاب جناحاه من أرض المعركة المكونان من الأندلسيين والمتطوعين البربر.

بعد ذلك اقتحم المسيحيون الجيش الإسلامي وقتلوا أغلب من فيه وانسحب من استطاع أن ينسحب إلى بلاد المغرب وكان منهم السلطان محمد الناصر ومجموعة من رجاله.

 ما بعد المعركة

فر السلطان محمد الناصر مكرها، فبعد أن رأى هزيمة جيشه ومقتل ابنه على أرض المعركة جلس في خيمته منتظرا الموت أو الأسر إلا أن جموع المسلمين المنسحبة أجبرته على الفرار معها فانطلق حتى وصل إلى إشبيلية ومنها إلى مراكش حيث توفي بعد فترة قصيرة في عام 1213 م. بعد انتهاء المعركة مباشرة تقدم المسيحيون تجاه حصن مدينة أوبيدا واحتلوا الحصن والمدينة وقتلوا 60 ألفا من أهلها.

من أوبيدا انطلق فرديناند الثالث من قشتالة باتجاه قرطبة واستولى عليها عام 1236 وجيان عام 1246 وإشبيلية عام 1248 ثم سقطت كل من آركوس وقادس وصيدا الأندلسية وكان فريديناند الثالث بعد هذه الانتصارات يطمح إلى عبور مضيق جبل طارق وضرب دولة الموحدين في عقر دارها إذ كانت تعاني من الانقسامات والثورات ولا يزال أثر الهزيمة فيها. لم يمنع فريديناند من التقدم سوى موته في إشبيلية عام 1252.

على جبهة أخرى قام ملك أراغون وكونت برشلونة جيمس الأول بالتوسع في مملكته فقام باحتلال جزر الباليار بين عامي 1228 م و 1232 م ومدينة بلنسية عام 1238 م. لم يتبق للإسلام في الأندلس سوى غرناطة التي صمدت خلف حصونها المنيعة وبقي بنو الأحمر يحكموها حتى عام 1492 م.

بعد سقوط دولة الموحدين في الأندلس على يد المسيحين وسقوط معظم أجزائها في أفريقيا على يد القوى المحلية قامت دولة المرينيون على أراضي دولة الموحدين وقاموا بعدة معارك في بلاد الأندلس ولكن النصر لم يكن حليفهم فيها

مرينيون

الدول الحفصية والزيانبة والمرينية

الدول الحفصية والزيانبة والمرينية

المرينوين، بنو مرين: سلالة بربرية أمازيغية تولت الحكم في المغرب 1244-1465 م.

المقر: فاس.

ينحدر المرينيون من فبيلة زناتة البربرية والتي استوطنت المناطق الشرقية على الحدود مع الصحراء. نزح هؤلاء إلى المغرب مطلع القرن الـ12 م واستقروا في المناطق الشرقية و الجنوب شرقية. بعد صولات وجولات مع الموحدين استطاع المرينيون في عهد الأخوين أبو يحي عبد الحق (1244-1258 م) ثم أبو يوسف (1258-1286 م) أن يستولو على العديد من المدن، مكناس: 1244 م، فاس: 1248م. مع حلول سنة 1269 م استطاعوا التخلص من آخر الموحدين في مراكش، وبدأوا بعدها في تنظيم جيش قوي حتى يمكنهم الاحتفاظ بالمناطق التي انتزعوها. خاضوا عدة حروب على أرض الأندلس في عهد أبو يعقوب يوسف (1286-1307 م)، توسعوا إلى الجزائر (الاستيلاء على وهران و مدينة الجزائر). عرفت الدولة أوجها أثناء عهدي أبو الحسن علي (1331-1351 م) ثم ابو عنان فارس (1351-1358 م) وازدهرت حركة العمران. استطاع الأخير صد سلاطين عبد الواد والاستيلاء على عاصمتهم تلمسان، ثم واصل في غزواته حتى بلغ تونس واحتلها على حساب الحفصيين.

منذ 1358 م بدأت الدولة المرينية تتهاوى سريعا. تولى الحكم سلاطين دون سن الرشد (1358-1374 م ثم 1393-1458 م) كانو بلا رأي، وضع هؤلاء تحت وصاية أقرابائهم من الوطاسيين، كما قام أصحاب غرناطة بتولى دور الوصتية (1373-1393 م). آخر السلاطين عبد الحق (1421-1465 م) استطاع أن يتخلص من أقربائه الوطاسيين بعد أن أقام لهم مذبحة كبيرة سنة 1458 م. لم يدم الأمر على حاله وقام سكان فاس بثورة على المرينيين ثم صار أمر المغرب بعده في أيدي الوطاسيين.

قائمة السلاطين

   الحاكم  الحياة  الحكم
1 أبو يوسف يعقوب بن عبد الحق  1210-1286   1269-1286 
2 أبو يعقوب يوسف الناصر  ….-….   1286-1307 
3 أبو ثابت عامر  ….-….   1307-1308 
4 أبو الربيع سليمان  ….-….   1308-1310 
5 أبو سعيد عثمان بن يعقوب  ….-….   1310-1331 
6 أبو الحسن علي بن عثمان  ….-….   1331-1348 
7 أبو عنان فارس بن علي  ….-….   1348-1358 
8 أبو سالم محمد بن فارس  ….-….   1358-1361 
9 محمد بن يعقوب  ….-….   1361-1366 
10 أبو العزيز الأول  ….-….   1366-1372 
  الحرب الأهلية  ….-….   1372-1384 
11 موسى بن فارس  ….-….   1384-1387 
12 أبو العباس  ….-….   1387-1393 
13 عبد العزيز  ….-….   1396-1393 
14 عبد الله  ….-….   1396-1398 
15 عثمان  ….-….   1398-1421 
16 عبد الحق  ….-….   1421-1465 
17 الحرب الأهلية  ….-….   1465-1472 

.

حنبعل برقا القائد العظيم الشهير هانيبال أو هانيبعل أو حنا بعل الفنيقى الاصل القرطاجى المولد والاناضولى المقتل – الموسوعه المصغره للدكتور أسامه فؤاد شعلان

 
Dr Usama Fouad Shaalan MD- PhD MiniEncyclopedia الموسوعه المصغره للدكتور  أسامه فؤاد شعلان
 

             

 

حرب بونيقية أولى

حرب بونيقية أولي

جزء من حرب رومانية قرطاجية
التاريخ 264-241 ق.م
المكان البحر المتوسط,صقلية,سردينيا
النتيجة انتصار الجمهورية الرومانية
المتحاربون
الجمهورية الرومانية قرطاج
القادة
ماركوس اتيليوس ريجولوس، جايوس لاتاتيوس, جايوس دويليوس حانيبعل، هانو الكبير، حاسدروبعل

قالب:حروب رومانية قرطاجية

تاريخ

لما مات اليوناني اغاثوقليس عام 288 ق م، كان الأجراء الإيطاليون في جيشه قد فقدوا خدمتهم، فغضبوا وحكموا مدينة مسينا اليونانية في صقلية وسموا أنفسهم "ماميرتين" يعني "تابعي اله الحرب" وأخذوا يحاربون على كل مدن صقلية. فبعدما أصبح هييرون الثاني طاغية سيراقوسة في عام 265 ق م هجم عليهم، فأرسل الماميرتين سفير إلى روما ليطلب عونهم، وسفير ثان إلى قرطاجة. وأجابت قرطاجة وبعثت جيش إلى مدينة مسينا اليونانية ومجلس أعيان روما لم تزل تتناق. لكن بعد قليل اتفق القرطاجيون مع سيراقوسة، فطلب الماميرتين عون روما ليخرجوا جيش قرطاجة. قبل الرومان الطلب المامرتيني لأن روما لم تقبل أن تكون دولة قوية مثل قرطاجة في مسينا لأنها قريبة جدا إلى جنوب إيطاليا (اليونان الكبرى التي أصبحت تحت السيطرة الرومانية)، فقرروا أن يبعثوا بجيش لتأييد الماميرتين، وبدأت الحرب البونيقية الأولى.

الجيش الروماني الأول لم يربح، لكن في عام 263 ق م، بعثت روما جيشا ثان يقدر ب 40،000 ألف مقاتل ، لترهيب و تخويف هييرون الثاني طاغية سيراقوسة ، الذي سرعان ما نقض تحالفه مع قرطاجة و تحالف مع الرومان وعقد معهم معاهدة عدم إعتداء لمدة 15 سنة.

أخذ الرومان يعدون لمهاجمة قرطاجة نفسها إنطلاقا من جزيرة صقلية حيث ثبتوا أقدامهم. فتمكنوا من إعداد أسطول كبير تألف من 250 سفينة حربية، فضلا عن 80 سفينة نقل . ولما علمت قرطاجة أخذت هي الأخرى بالإستعداد و إن كان أسطولها الباقي أقل من الروماني بقليل.

في سنة 256 ق.م بعد أبحر الرومان نحو قرطاجة فالتقوا بالأسطول القرطاجي عند رأس أقنوموس جنوب صقلية حيث أشتبكا و انتهت المعركة بهزيمة القرطاجيين ، تابع بعدها الاسطول الروماني ابحاره بقيادة القنصل مرقس اتيليوس رجولوس و نزل على الشاطىء الأفريقي حيث أنزل عدة هزائم متتابعة بالقرطاجيين مكنته من التوغل بعيدا عن الشاطىء لقضاء فصل الشتاء في مكان قريب من قرطاجة مما جعل الأخيرة تطلب الصلح منه . عرض القنصل الروماني مرقس شروطا قاسية على قرطاجة فرفضتها ثم أخذت تستعد للقتال في نهاية الشتاء باستقدام فرقة من المرتزقة المشهود لهم في القتال و التدريب و على رأسهم قائد إسبارطي محترف هو زانتيبوس الذي عمل على فوره على تدريب الجيش القرطاجي وفقا لأفضل الأساليب القتالية الإغريقية.

وفي ربيع عام 255 ق.م بعد ان أنهى الجيش القرطاجي تدريباته ، أشتبك مع الجيش الروماني الذي هزم و أسر قائده القنصل مرقس . ولكن الأسطول القرطاجي تصدى للأسطول الروماني الذي كان قادما بتعزيزات لمرقس قد مني بخسارة فادحة شلت قدرة قرطاجة البحرية لمدة ال5 أعوام التالية. وكان الأسطول الروماني وصل بعد أنتهاء المعركة البرية فأنقذ فلول جيشه تجاه شاطىء صقلية الجنوبي و لكن تحطمت أكثر من 250 سفينة– من بينها 100 سفينة قرطاجية كان الرومان قد اغتنموها فلم يتبق من الأسطول الروماني الناجي سوى أكثر من 100 سفينة فقط.

أعاد الرومان بسرعة كبيرة بناء أسطولهم الذي دمرت معظمه الأنواء و ركزوا هجومهم على القواعد القرطاجية في غرب صقلية . فسقطت مدينة بانورموس (باليرمو) في أيدي الرومان عام 254 ق.م لتتوقف الحرب بين الطرفين لمدة سنتين فقد أشتعلت الحرب بين قرطاجة و نوميديا في شمال أفريقيا عام 253 ق.م.

عام 250 ق.م حاولت قرطاجة استعادة بانورموس و لكنها منيت بالفشل مما شجع الرومان في العام التالي على مهاجمة مدينة ليلوبايوم و محاصرتها برا وبحرا. إلا أن القرطاجيين تمكنوا من هزيمة الرومان برا و بحرا هذه المرة و أستعادوا سيادتهم البحرية مؤقتا.

ووصل إلى صقلية في عام 247 ق.م القائد القرطاجي حملقارت برقا الذي اسندت إليه القيادة القوات القرطاجية في صقلية يعاونه القائدان أذربعل و قرتالو الذان كانا يقومان بتخريب سواحل إيطاليا . كما كان حملقارت يشن حرب عصابات أقضت مضاجع الرومان و أوقعتهم في مأزق مالي بسبب الخسائر و إزدياد النفقات و أستولى حملقارت على موقعين منيغين هما جبل هرقيتي قرب بانورموس و جبل إيريكس قرب دربانا و أإتخذ منهما قاعدتين لشن الغارات على القوات الرومانية.

كاد القرطاجيون أن يححقوا نصرا حاسما في صقلية لولا قرارها المبهم في إستدعاء أسطولها من صقلية لتجمع قواتها للتحكم في مناطق شمال أفريقيا الداخلية جنوب غرب قرطاجة بسبب الحرب مع نوميديا.

أستغل الرومان الفرصة فأعادوا بناء أسطولهم حيث أنزلوا 200 سفينة إلى البحر بقيادة القنصل النوميدي ماسينيسا وأرسلو جيش ليهجم على أفريقيا نفسها، فبعد قليل نجت روما وأخذت اسبانلوتاتيوس كاتولوس ليضيق الحصار حول مدينتي دربانا و ليلوبايوم القلعتين القرطاجيتين. عجزت فرطاجة عن غعداد اسطول لإنقاذ هاتين القلعتين . ولم تسطع سوى إرسال حملة بحرية هزمها الرومان قرب دربانا في ربيع 241 ق.م أضطر القرطاجيون إلى قبول الصلح مع الرومان في معاهدة(قاتولوس) و الذي تتضمن تخلي قرطاجة النهائي عن جزيرة صقلية، تتعهد قرطاجة بدفع غرامة مالية قدرها 320 وزنة تسددها سنوبا على شكل أقساط لمدة 20 عاما وأن تسلم قرطاجة كل الرهائن الرومان بدون أية فدية.

 الحرب البونيقية الثانية

بعد ما عبر الايبرو سار حنبعل وجيشه بسرعة، وعبروا جبال الالب في 218 ق م. لما وصلوا إلى إيطاليا دخل في جيشهم كثير الأجراء والحلفاء من عند قبيلة الگول وهزم الجيوش الرومانية في المنطقة بسهولة، ولما رأوا هذا حالفه الكثير من مدن إيطاليا ومنهم سيراكوزا. في نفس الوقت كان جيش روماني يحارب في اسبانيا. وقرب إلى روما حتى وصل إلى كابوا في 211 ق م، لكن بعد موت أخوه عزربعل في عام202 رجع إلى مدينة بروتيوم في جنوب إيطاليا. وأخيرا حالف الرومان الملكيا كلها في اتفاق السلام، ومنعت قرطاج من أي حرب – حتى ولو كانت في دفاع نفسها – إلا بإذن روما

حنبعل برقا الشهير هانيبال أو هانيبعل أو حنا بعل هو من أعظم القادة العسكريين في التاريخ. اكتسح شمال أفريقيا و إسبانيا و فرنسا وسويسرا و إيطاليا و حاصر روما 15 عاما و كادت تسقط لولا أن قامت عليه ثورة في قرطاج في القرن الأول قبل الميلاد غيرت روما ساحة القتال إلى شمال أفريقيا.و يعتقد الباحثون ان هانيبعل ينحدر من اسرة الملكة الفينيقية السورية اليسار التي جاءت هاربة مع انصارها من صور إلى شمال أفريقيا حيث اسست اليسار قرطاج عام 814 قبل الميلاد

ولد بقرطاج سنة 247 قبل الميلاد، ورافق وهو في التاسعة من عمره والده أميلكار برقا في إلى اسبانيا. وفي سنة 221 اختاره الجنود قائدا بعد اغتيال صدربعل زوج أخته صلامبو، فتمكن من بسط نفوذ قرطاج على كامل شبه الجزيرة الإيبيرية بما في ذلك صاغنتوم، إحدى المحميات الرومانية. وقد رأت روما في ذلك خرقا للمعاهدة التي عقدت إثر الحرب البونيقية الأولى، وطالبت بتسليمها حنبعل، وقد كان رفض هذا الطلب سببا في اندلاع الحرب البونيقية الثانية بين سنتي 218 و201 قبل الميلاد.

حنبعل ّّدارت بين روما و قرطاج 3 حروب دامت قرنا كاملا بصفة متقطعة من 246 ق.م إلى 146 ق.م. حنبعل ولد في المستعمرة الفينيقية قرطاج قاد جيوش قرطاج في الحرب الثانية التي دارت بين روما و قرطاج في واقعة كانة وقد اجتاز جبال الالب حتى وصل إلى حوض نهر البو بايطاليا.

 من أفكار حنبعل

عندما حاول حنبعل قطع جبال الآلب عمد إلى دهن أجسام جيوشه الزيت كي تبقى أجسادهم دافئة .

 هيئة أركان جيشه

كانت هيئة أركان جيشه تتكون من: هانو بن هاملقار ، و مهر بعل (مار بال) قائد سلاح الفرسان الأمازيغي (البربري)، الذي تقلد هذه القيادة منذ عهد والد حنابعل أميلكار برقه، ويكن له حنا بعل حبا فائقا، و هيرت ، و سينهالوس المصري كبير الأطباء، والاغريقيين سوسيلوس ، و وسلينوس ، و بوح الهندي منجم الحملة، والاسبرطي سوسيليوس الذي علم حنا بعل اليونانية .

غزو روما و عبور جبال الألب

في سنة 218 ق.م قرر حنا بعل التقدم بجيشه بعد أن ترك شقيقه صدر بعل (هزدروبال) علي رأس ولاية قرطاجنة بإسبانيا التي كانت تابعة لامبراطورية قرطاج.

وقد قرر حنا بعل الاسراع في بدء حملته البرية، بعد أن وصلته أنباء من جواسيسه بأن الرومان يستعدون لتطبيق خطة بنقل الحرب الي أفريقيا في عقر دار قرطاج.

كان حنا بعل يقول لقادة أركان جيشه: في حالة وصولنا لنهر البو قبل فوات الأوان، نستطيع أن نمسك بتلابيب جيوش الغزو الرومانية داخل إيطاليا نفسها، فلا تصبح مدينة قرطاج ميدانا للحرب، وحينئذ تقع تكاليف الحرب ولأول مرة، علي الرومان وعلي بلادهم فيكتوون بآلامها، ويحرقون بنارها.. فالسرعة ثم السرعة.

وتقدم حنا بعل الذي يحب دائما ترديد قول القنصل الروماني جيولاس: اما أن تقهر عدوك، واما أن تقبل مصير المقهورين . وتمكن من عبور جبال الألب بجيش قوامه ثلاثون ألفالألب في خمسة عشر يوما، مات جزء من جيشه في الطريق، وبقي قسمه الأكبر.

 معركة تسينو

وخاض حنا بعل أول معركة وهي معركة تسينو التي دارت علي شواطئ نهر تسينو. حسمها حنا بعل لصالحه بخطة سريعة لعب فيها الفرسان الأمازيغ ـ البربر دورا حاسما عندما طوقوا من الخلف كتائب الرومان الثقيلة بحيث لم تصمد برماحهم الطويلة أمام حراب الأمازيغ القصيرة والخفيفة والنافذة، وما هي الا لحظات حتي سقط القنصل ببليوس قائد الجيش تحت سنابك خيل هؤلاء الفرسان المردة. عاد هذا القنصل لروما جريحا وهو يردد لخاصته كيف وقع من صهوة جواده وسط فرسان غرباء لم ير مثلهم في حياته من قبل في سرعة الكر والفر ، ويقصد الفرسان النوميديين الأمازيغ ـ البربر.

 معركة تريبيا

ووجهت روما جيشا ثانيا ضخما بقيادة قنصل جديد هو طيباريوس سمبرونيوس لمسح هزيمة معركة تسينو، وأعد حنا بعل له فخا علي ضفاف نهر تريبيا حيث دارت معركة تريبيا حسمها حنا بعل باختيار مكان المعركة وهو سهل غمره الفيضان فأوحلت تربته ولم يره خصمه، اختاره وهو يردد قول أبيه هملقار برقة: دع الأرض تقاتل عنك .

أمر حنا بعل خمسمائة من خيرة الفرسان النوميديين الأمازيغ ـ البربر وأصدر توجيهاته لقائدهم فقال له: توجهوا في بداية الليل الي معسكر العدو، اقتربوا من خنادقهم راكضين، وعندما يتصدي لكم فرسانه، التحموا معهم في معركة، ثم ولوا هاربين ممثلين اندحارا، فسيتبعكم العدو، وجهوه عند ذلك السهل الضحل حيث الكمين . ووقع القائد الروماني في الفخ.. وانطلقت المعركة فأعطي القنصل الأمر ببدء المعركة بتعقب النوميديين الأمازيغ المراوغين… وهُزم الرومان شر هزيمة.

وأهم ما أسفرت عنه هذه المعركة تحالف حنا بعل مع شعب غال سيسالبين وانضم له في الشهرين التاليين 14000 من مقاتليهم الأشداء، فاستقبلهم وهو يردد قولته المشهورة: اذا أحرزت نصرا انضم اليك الجميع حتي خصومك، أما اذا حاقت بك الهزيمة تخلي عنك حتي محبوك .

وبعد انقضاء شهري الشتاء قرر التوجه جنوبا نحو روما، ووقع في مستنقعات، وانتشرت الحمي بين جيشه وفقد نتيجة لاصابته بها احدي عينيه.

 موقعة ترازايمين

في اليوم الحادي والعشرين من شهر حزيران ـ يونيو 217 ق. م. تقدم جيش روماني ضخم تعداده أربعون ألفا بقيادة جايوس فلامنيوس نحو بحيرة ترازايمين تحت رقابة الفرسان البربر الأمازيغ، كان يلفه ضباب كثيف، وكان حنا بعل قد رصده بواسطة جواسيسه من بعيد، وترصد للمكان الذي سيخرج منه وهو يسيطر علي المرتفعات التي تشرف علي مكان مروره. وفجأة ومن خلال الضباب هاجم القرطاجيون من مواقع مثالية، فكانت الصاعقة المفاجئة تحل علي رؤوس الرومان.

وأرسل حنا بعل بسائر فرقه لتهاجم في وقت واحد، وكان يراقب من موقع عال فوق الطرف الأقصي من طريق البحيرة، وسد فرسان مهر بعل النوميديون الأمازيغ ـ البربر، مصحوبين بمشاة الأفارقة، مدخلَ شاطئ البحيرة الهلالي الشكل. وهكذا وقع القنصل في نفس المصيدة الذي كان ينوي ايقاع حنا بعل فيها. وأطبقت كماشة الجيش القرطاجي من كل ناحية، بحيث لم تجد كتائب الرومان مجالا للمناورة ولا حتي للهروب. وما كادت تحل الساعة العاشرة صباحا حتي كانت موقعة بحيرة ترازايمين قد انتهت. وصار بذلك ستة آلاف من الجنود الأشداء أسري حنا بعل. وهكذا تمكن الجيش القرطاجي الذي أنهكته الحمي قبل أيام، بجياد هزيلة من ابادة جيش قوي خارج للتو من معسكراته ينعم بالصحة والعافية، تمكن من هزمه وأسر خمسة عشر ألفا من خيرة جنوده. وأطلق سراح الأسري من الشعوب الأخرى وهو يقول لهم: ما جئت لأشن الحرب علي الشعوب المستعمََـرة، بل ولا حتي علي الايطاليين، وانما جئت لأساعد الجميع ضد حكام روما الظالمين .

تجمعت جماهير روما بساحة الفوروم، بعد أن وصلت أنباء كوارث الهزائم. وبقيت أبواب مجلس الشيوخ مغلقة أمام الجماهير، وبعد طول الحاح خرج اليهم القنصل بومبونيوس ماثو بمفرده واعتلي درج مدخل المجلس، وألقي عليهم خطابا يتكون من اثنتي عشرة كلمة: لقد قهر العدو جيوش روما في موقعة عظيمة مات فيها أحد القنصلين .

 موقعة كناي العظمى

واستمرت القوات الرومانية في تكتيك العرقلة، لكن حنا بعل بمجرد أن تأكد أن جنوده أخذوا ما ينبغي أخذه من الراحة، واستوعبوا تدريبات عالية، قرر المرور الي الاستدراج، وخلق سائر الظروف علي مدي أشهر لموقعة كناي العظمي التي بدأت في فجر اليوم الثالث من شهر آب ـ أغسطس سنة 216 ق.م. قام حنا بعل بمناورات علي مدي أشهر جعلت العدو يحرك قوات جبارة الي كناي.

كان منيوسياس روفوس صغير السن، وقام حنا بعل بمناورة فهم منها الضابط الروماني أنه صار يخاف المواجهة ويهرب . وهكذا انطلت عليه مناورة حنا بعل الذي أظهر تقهقرا منهزما زيادة في اتقان حبكة الاستدراج الكبير الذي يعده لخصمه المغرور. كان حنا بعل يقود جيشا من أربعين الفا، بينما كان جيش عدوه يتجاوز المائة ألف، نصفهم من المجندين حديثا، واعتبر أنه أقوي جيش علي الإطلاق جمعته روما في تاريخها. وزيادة في الخديعة قام الفرسان النوميديون (البربر) في خفة الأشباح بغارة صدتها القوات الرومانية بنجاح، وتقهقر الفرسان البربر مظهرين انهزامهم، فقرر عند ذاك القنصلان فارو وأميليوس مطاردة العدو المنهزم، وتقهقر القائد الأمازيغي مهر بعل عبر نهر أوفيدوس هاربا وجيشا القنصلين بتعقبانه، وضيق عليهما الخناق شيئا فشيئا فوق سهل كناي المكشوف، وذلك في اليوم الثالث من شهر آب ـ أغسطس.

عندما التقي الجيشان أعطي حنا بعل إشارة البدء… ووجد الرومانيون أنفسهم يقاتلون في ظروف مزدوجة السوء، كانوا منكفئين بعضهم علي بعض، محصورين الكتف الي الكتف، بينما كان أعداؤهم يحومون حولهم بكامل حريتهم، كانوا منهوكي القوي، يواجهون عدوا متجدد القوة شديد البأس. كان حنا بعل يستعمل من بعيد إشارات معينة بدخان منطلق من حزم أعشاب خاصة تطلق دخانا عاليا، وكل عدد من هذه المشاعل الدخانية يعني أمرا معينا. ولم تكد تحل الظهيرة حتي اختفي الفرسان، فلم يبق فارس واحد بين مرتفعات كناي والمقر الصخري المرتفع لقيادة حنا بعل، وبقيت في هذا الامتداد كتائب مشاة الرومانيين مكدس بعضها علي بعض، في كتلة بشرية هائلة صماء. وانطلق الفرسان النوميديون الخفاف كالبرق وعلي رأسهم قائدهم مهر بعل فسدوا ثغرة فرار العدو المنهزم الهارب الي النهر. وكانت الأرض في سائر الاتجاهات ضد الرومان، وتمعن حنا بعل في هذا الموج البشري، وردد، في نشوة، وصية والده هملقار برقة: دع الأرض تقاتل عنك.. . وترك قادة وحداته ينفذون حرفيا خطته. وأبيد هذا الجيش الضخم. وعندما طلب منه رجاله أن يستريح أجابهم: ينبغي علي الطهاة أن يعدوا وجبة شهية، ويسخروا لها كل فنونهم، وتقدم مصحوبة بالخمر الي الجنود من سائر الرتب، فقد آن للجيش أن يستريح .

وهنا صاح العجوز مهر بعل الأمازيغي ـ البربري في غضب: حنا بعل.. اسمع لي جيدا، في خمسة أيام يستطيع الجيش أن يتناول هذه الوجبة في روما نفسها، سيسبقك فرساني كالبرق اليها، فيكتشف الرومانيون بحلولك بينهم من خلال هؤلاء الفرسان المردة قبل أن يعلموا بخروجك اليهم.. . وتطلع حنا بعل مليا في وجه مساعده العجوز، ثم أجابه: هذا مما يسهل قوله، ويبهج القلب سماعه، يا عمنا البطل، لكن امعان التفكير في الأمر وتقليبه علي عدة وجوه، يحتاج الي وقت طويل . وهنا لم يتمالك مهر بعل نفسه فصاح فيه في غضب، وقال له قولته الخالدة: حنا بعل.. لقد حبتك الآلهة بنعم كثيرة، فأنت تعرف كيف تحرز النصر، ولكنك لا تعرف كيف تستخدمه وتستغله.. . واستمع حنا بعل لمساعده الأمازيغي العجوز رفيق وصديق والده، ومعلمه سائر أنواع القتال والفروسية والرياضة، تمعن مليا فيه ثم أمر باطعام الرجال. وعند انتهاء جولته التفتيشية عاد الي مقر قيادته لينام نوما عميقا بين حراسه.

ويعقب مؤرخو سيرة حنا بعل فيجمعون علي أنه لو عمل برأي القائد الفارس الأمازيغي مهر بعل لتمكن من احتلال روما وتغيير مجري التاريخ.. بدون حسم سريع ـ مثلما يراه مهر بعل ـ لا أمل في أن يكسب القرطاجيون الحرب في النهاية، لأنهم يقاتلون عدوا في بلاده، يملك تحت يده الشعب والغذاء والمال، بينما هو بعيد عن قرطاج، قطعت عنه الامدادات من إسبانيا التي تمكن سيبيو من السيطرة عليها، وعبر البحر المتوسط الذي تسيطر عليه الأساطيل الرومانية سيطرة مطلقة، ولا أمل في أن ترسل قرطاج نجدات عبره لحنا بعل.

 تدمير قرطاجة

انتهت هذه الملحمة البطولية ملحمة الدفاع عن قرطاج. واذا كانت هذه الحرب أسفرت عن وفاة مدينة، فقد أكدت أن الإنسان أقوي من القهر، وأن ارادته لا تردع بسهولة. ولقد تأثر لهذه المأساة حتي بعض المؤرخين الأوروبيين، يقول وارمنغتون: ألقي سيبيو أميليانوس نظرة علي المدينة التي ازدهرت أكثر من سبعمائة سنة منذ انشائها، والتي حكمت مناطق كثيرة، جزرا وبحارا، وكانت ثرية في السلاح والأساطيل والفيلة والمال، مثل الامبراطوريات العظمي، بل والتي فاقتها في الإقدام والشجاعة الفائقة. فبالرغم من أنها جردت من كافة أسلحتها وسفنها، فقد صمدت أمام حصار شديد، ومجاعة دامت ثلاث سنوات، ووصلت الي نهايتها بالتدمير الكلي .

ويروي المؤرخ اليوناني بوليبيوس الذي رافق القائد الروماني في عملية التدمير، فيقول: أن سيبيو أمليانوس بكي تأثرا بما آل له عدوه، فاستعرض أمامه الحقيقة المتمثلة في أن الأفراد والأمم والامبراطوريات نهايتها محتومة، وكذلك نصيب مدينة طروادة العظيمة، ونهاية الامبراطوريات الأشورية، والميدية، والفارسية، والتدمير الأخير لامبراطورية مقدونية الكبيرة. تمعن في هذا كله ثم ردد بقصد أو بدون قصد، كلمات هكتور في الياذة هوميروس: (سيأتي اليوم الذي تسقط فيه طروادة المقدسة، وكذلك الملك بريام وجميع رجاله المسلحين معه) ، وعندما سأل المؤرخ بوليبيوس، سيبيو، ماذا تقصد بهذا؟ ، التفت اليه القائد الروماني وقال بتأثر: هذه لحظة عظيمة يا بوليبيوس..ان الخوف يتملكني من أن نفس المصير سيكون لوطني في يوم من الأيام .

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Skin you live in – Dr Usama Fouad Shaalan MD- PhD MiniEncyclopedia

 

Dr Usama Fouad Shaalan MD- PhD MiniEncyclopedia الموسوعه المصغره للدكتور  أسامه فؤاد شعلان

Most people know that beauty is more than skin-deep but our social emphasis on physical appearance can make even the most flawless-skinned beauty self-conscious. Supermodels sporting perfect, made-up, and airbrushed skin and not much else adorn the pages of magazines and television ads reminding onlookers to strive for the impossible.

Not surprisingly, anyone suffering from skin problems may find it difficult to look beyond their skin’s surface to the beauty within. With some help from foods, water, herbs, and of course, a healthy dose of self-appreciation, it is possible to not only love the skin you are in, but improve its health and appearance as well.

Skin
Skin is the body’s largest organ. It shields our bodies from the elements around us (sometimes taking a beating in the process), assists with detoxification, and protects our tissues and organs from damage. It is also a mirror into the condition of our bodies at a deeper level. Skin reflects our inner health. It may show toxic overload, stress, hormonal imbalances, and nutritional deficiencies.

Living in a Toxic World
There are literally thousands of toxins and harmful synthetic chemicals found in our food, air, water, homes, and workplaces. They take the shape of pesticides; herbicides; cigarette smoke; synthetic chemicals found in beauty and hygiene products; food additives, colours, and fillers; medications; or stress hormones. Our bodies must attempt to filter this toxic onslaught to prevent toxic overload, which can occur when our bodies take in more toxins than they can eliminate. Numerous organs play a role in cleansing the body, namely the kidneys, liver, intestines, and of course, the skin. Problems with the skin can suggest that the other elimination organs are overloaded.

Water, Water Everywhere
One of the most critical components of healthy skin is water. The body is made up of approximately seventy percent water and needs its stores replenished. Every cell in the body is dependent on water for good health, including skin cells. Water helps to keep the skin properly hydrated. While the standard recommendation for water is eight cups per day, the number may vary from person to person. And if you drink caffeinated or alcoholic beverages, add two additional cups of water for every cup of coffee, tea, or alcohol you drink.

Lessen Toxic Exposure
Switch to natural body- and skincare products that are free of fragrances, colours, or other synthetic chemicals that have a tendency to irritate skin. Lessen your intake of the following foods:

  • Processed, packaged, or fast foods
  • Hydrogenated fats (margarine, shortening, lard or products made with them such as cookies, pies, packaged foods, buns, pizza, etc.)
  • Fried foods (French fries, onion rings, potato chips, nachos, hamburgers, etc.) or foods containing oils that have been excessively heated. Most grocery store oils have been heated excessively even before they reach the shelves. Extra-virgin olive oil is an excellent choice for cooking; cold-pressed oils found in most health food stores are also a healthy choice
  • Sugar and foods that contain sugar
  • Synthetic sweeteners (Nutrasweet, saccharin, aspartame, etc.)
  • Salt (use Celtic sea salt instead)
  • Food additives: colours, flavour enhancers, stabilizers, preservatives, etc.
  • Non-organic meat and poultry contains hormones, sugar, and antibiotics, all of which increase your body’s toxic load. In addition, many people are sensitive to the hormones and other chemicals in meat. Skin problems can be an indication of a sensitivity or allergy. If possible, switch to organic meat and poultry

Hormonal Imbalances
If your skin problems coincide with your menstrual periods, hormonal imbalances may be at fault. Alternatively, if you started experiencing skin problems such as dry skin along with other menopausal problems, hormonal imbalances may also play a role.

Lessening your intake of the above foods can have dramatic results on hormonal imbalances over time. Additionally, there are numerous herbs that are effective for hormone balancing. Dong quai or Vitex are excellent choices for women women suffering from hormone imbalances. For menopausal women, black cohosh, vitex (chasteberry), wild yam, sage, St. John’s wort, primrose oil, sage, and dong quai can be helpful for skin conditions. Be sure to consult with a natural medicine specialist or herbalist before supplementing with herbs.

Regular exercise and avoidance of caffeine and alcohol can also be helpful in balancing hormones that may be linked to dry skin during the menopausal years.

Give Your Skin an Oil Change
Healthy skin requires plenty of health-boosting essential fats like Omega 3s, yet most people don’t get enough of them. Flax, hemp, walnuts, and fatty fish like salmon, mackerel, and sardines tend to have high levels of Omega 3s. Be sure to choose cold-pressed flaxseed or hempseed oil and raw, unsalted walnuts that have been stored in the refrigerator section of your natural food store since the Omega 3 fats are sensitive to heat.

Caring for your body by avoiding harmful foods, eating healthily, and using herbs will yield greater results than slathering on creams and ointments on your skin. By creating a healthier body from the inside out, you’ll experience healthier skin too.

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The skin is the outer covering of the body. In humans, it is the largest organ of the integumentary system made up of multiple layers of mesodermal tissue, and guards the underlying muscles, bones, ligaments and internal organs.[1] Skin of a different nature exists in amphibians, reptiles, birds.[2] Human skin is not unlike that of most other mammals except that it is not protected by a pelt and appears hairless though in fact nearly all human skin is covered with hair follicles. The adjective cutaneous literally means "of the skin" (from Latin cutis, skin).

Because it interfaces with the environment, skin plays a key role in protecting (the body) against pathogens[3] and excessive water loss.[4] Its other functions are insulation, temperature regulation, sensation, synthesis of vitamin D, and the protection of vitamin B folates. Severely damaged skin will try to heal by forming scar tissue. This is often discolored and depigmented.

In humans, skin pigmentation varies among populations, and skin type can range from dry to oily. Such skin variety provides a rich and diverse habit for bacteria which number roughly a 1000 species from 19 phyla.[5][6]

 Skin components

See also: Skin layers

Skin has mesodermal cells, pigmentation, or melanin, provided by melanocytes, which absorb some of the potentially dangerous ultraviolet radiation (UV) in sunlight. It also contains DNA-repair enzymes that help reverse UV damage, and people who lack the genes for these enzymes suffer high rates of skin cancer. One form predominantly produced by UV light, malignant melanoma, is particularly invasive, causing it to spread quickly, and can often be deadly. Human skin pigmentation varies among populations in a striking manner. This has led to the classification of people(s) on the basis of skin color.[7]

Mammalian skin often contains hairs, which in sufficient density is called fur. The hair mainly serves to augment the insulation the skin provides, but can also serve as a secondary sexual characteristic or as camouflage. On some animals, the skin is very hard and thick, and can be processed to create leather. Reptiles and fish have hard protective scales on their skin for protection, and birds have hard feathers, all made of tough β-keratins. Amphibian skin is not a strong barrier to passage of chemicals and is often subject to osmosis. A frog sitting in an anesthetic solution could quickly go to sleep.

The skin is the largest organ in the human body. For the average adult human, the skin has a surface area of between 1.5-2.0 square meters (16.1-21.5 sq ft.), most of it is between 2–3 mm (0.10 inch) thick. The average square inch (6.5 cm²) of skin holds 650 sweat glands, 20 blood vessels, 60,000 melanocytes, and more than a thousand nerve endings.

 Functions

Skin performs the following functions:

  1. Protection: an anatomical barrier from pathogens and damage between the internal and external environment in bodily defense; Langerhans cells in the skin are part of the adaptive immune system.[3][4]
  2. Sensation: contains a variety of nerve endings that react to heat and cold, touch, pressure, vibration, and tissue injury; see somatosensory system and haptics.
  3. Heat regulation: the skin contains a blood supply far greater than its requirements which allows precise control of energy loss by radiation, convection and conduction. Dilated blood vessels increase perfusion and heatloss, while constricted vessels greatly reduce cutaneous blood flow and conserve heat. Erector pili muscles are significant in animals.
  4. Control of evaporation: the skin provides a relatively dry and semi-impermeable barrier to fluid loss.[4] Loss of this function contributes to the massive fluid loss in burns.
  5. Aesthetics and communication: others see our skin and can assess our mood, physical state and attractiveness.
  6. Storage and synthesis: acts as a storage center for lipids and water, as well as a means of synthesis of vitamin D by action of UV on certain parts of the skin.
  7. Excretion: sweat contains urea, however its concentration is 1/130th that of urine, hence excretion by sweating is at most a secondary function to temperature regulation.
  8. Absorption: Oxygen, nitrogen and carbon dioxide can diffuse into the epidermis in small amounts, some animals using their skin for their sole respiration organ (contrary to popular belief, however, humans do not absorb oxygen through the skin).[8] In addition, medicine can be administered through the skin, by ointments or by means of adhesive patch, such as the nicotine patch or iontophoresis. The skin is an important site of transport in many other organisms.
  9. Water resistance: The skin acts as a water resistant barrier so essential nutrients aren’t washed out of the body.

 Hygiene and skin care

See also: Exfoliation (cosmetology)

The skin supports its own ecosystems of microorganisms, including yeasts and bacteria, which cannot be removed by any amount of cleaning. Estimates place the number of individual bacteria on the surface of one square inch (6.5 square cm) of human skin at 50 million, though this figure varies greatly over the average 20 square feet (1.9 m2) of human skin. Oily surfaces, such as the face, may contain over 500 million bacteria per square inch (6.5 cm²). Despite these vast quantities, all of the bacteria found on the skin’s surface would fit into a volume the size of a pea.[9] In general, the microorganisms keep one another in check and are part of a healthy skin. When the balance is disturbed, there may be an overgrowth and infection, such as when antibiotics kill microbes, resulting in an overgrowth of yeast. The skin is continuous with the inner epithelial lining of the body at the orifices, each of which supports its own complement of microbes.

Proper skin hygiene is important because unclean skin favors the development of pathogenic organisms. The dead cells that continually slough off the epidermis mix with the secretions of the sweat and sebaceous glands and the dust found on the skin form a filthy layer on its surface. If not washed away, the slurry of sweat and sebaceous secretions mixed with dirt and dead skin is decomposed by bacterial flora, producing a foul smell. Functions of the skin are disturbed when it is excessively dirty; it becomes more easily damaged, the release of antibacterial compounds decreases, and dirty skin is more prone to develop infections.

Cosmetics should be used carefully on the skin because these may cause allergic reactions. Each season requires suitable clothing in order to facilitate the evaporation of the sweat. Sunlight, water and air play an important role in keeping the skin healthy.

 Oily Skin

Oily skin is caused by over-active sebaceous glands, that produce a substance called sebum, a naturally healthy skin lubricant.[1] When the skin produces excessive sebum, it becomes heavy and thick in texture. Oily skin is typified by shininess, blemishes and pimples.[1] The oily-skin type is not necessarily bad, since such skin is less prone to wrinkling, or other signs of aging,[1] because the oil helps to keep needed moisture locked into the epidermis (outermost layer of skin).

The negative aspect of the oily-skin type is that oily complexions are especially susceptible to clogged pores, blackheads, and buildup of dead skin cells on the surface of the skin.[1] Oily skin can be sallow and rough in texture and tends to have large, clearly visible pores everywhere, except around the eyes and neck.[1]

The goal of treating oily skin is to remove excess surface sebum without complete removal of skin lipids.[1] Severe degreasing treatment can foster an actual worsening of sebum secretion, which defeats the aim of the cleansing.[1] A method of cleansing oily skin is to cleanse with a natural face cleanser formulated especially for oily skin. The cleansers pH should be 4.5 – 5.5, since the skin’s pH value is approximately 5.4. Gel cleansers work best on oily skin.[1] (see: surfactant) Oily skin products should contain very little natural oils. They should not contain waxes or other synthetic lipid agents that could aggravate the oily condition of the skin. A toning lotion should also be natural and have a pH of 4.5-5.5 and formulated especially to help balance and hydrate oily skin. Some cleansing products have lower concentrations of hydroxy acids, which remove dead cells from the upper levels of the stratum corneum.[1] Those products should be used on a regular basis to work adequately.

In cases of excessive output of sebum, there have been anecdotal reports of successful control using dietary supplementation of Niacin (Vitamin B3) at a dosage of 500 mg to 1000 mg a day

 Aging

For more details on this topic, see senescence.

For more details on this topic, see Intrinsic and extrinsic aging.

A typical rash

Skin infected with Scabies

As skin ages, it becomes thinner and more easily damaged. Intensifying this effect is the decreasing ability of skin to heal itself as a person ages.

Among other things, skin aging is noted by a decrease in volume and elasticity. There are many internal and external causes to skin aging. For example: Aging skin receives less blood flow and lower glandular activity.

Cortisol causes degradation of collagen[10], accelerating skin aging.[11]

 Disease

For more details on this topic, see skin disease.

Dermatology is the branch of medicine that deals with conditions of the skin.[12]

 Variability in skin tone

Individuals with ancestors from different parts of the world can have highly visible differences in skin pigmentation. Individuals with sub-Saharan African ancestry (black people) tend towards darker skin, while those of Northern European descent (white people) have paler skin. Between these extremes are individuals of Asian, South-East Asian, Native American, Middle Eastern, Polynesian and Melanesian descent.

The skin of black people has more variation in color from one part of the body to another than does the skin of other racial groups, particularly the palms of the hands and soles of the feet. Part of this is the result of the variations in the thickness of the skin or different parts of the body. The thicker the skin, the more layers of cells with melanin in them, and the darker the color.[13] In conclusion, these parts of the body have melanin-producing cells.

Darker skin hinders UVA rays from penetrating. Because UVA degrades folate (a B vitamin) and is required for vitamin D synthesis, people with darker skin tones are more susceptible to deficiencies of these vitamins.

 Skin types

Skin can be classified based on its reaction to ultraviolet radiation:[14]

Type
Definition
Description

I
Always burns, never tans
Pale, Fair, Freckles

II
Usually burns, sometimes tans
Fair

III
May burn, usually tans
Light Brown

IV
Rarely burns, always tans
Olive brown

V
Moderate constitutional pigmentation
Brown

VI
Marked constitutional pigmentation
Black

 Skin flora

Main article: Skin flora

The human skin is a rich environment for microbes.[5][6] Around 1000 species of bacteria from 19 bacterial phyla have been found. Most come from only four phyla: Actinobacteria (51.8%), Firmicutes (24.4%), Proteobacteria (16.5%), and Bacteroidetes (6.3%). Propionibacteria and Staphylococci species were the main species in sebaceous areas. There are three main ecological areas: moist, dry and sebaceous. In moist places on the body Corynebacteria together with Staphylococci dominate. In dry areas, there is a mixture of species but dominated by b-Proteobacteria and Flavobacteriales. Ecologically, sebaceous areas had greater species richness than moist and dry one. The areas with least similarity between people in species were the spaces between fingers, the spaces between toes, axillae, and umbilical cord stump. Most similarly were beside the nostril, nares (inside the nostril), and on the back.

Reflecting upon the diversity of the human skin researchers on the human skin microbiome have observed: "hairy, moist underarms lie a short distance from smooth dry forearms, but these two niches are likely as ecologically dissimilar as rainforests are to deserts."[5]

The NIH has been launched the Human Microbiome Project to characterize the human microbiota which includes that on the skin and the role of this microbiome in health and disease.[15]

 Animal skin products

The term skin refers to the covering of a small animal, such as a sheep, goat (goatskin), pig, snake (snakeskin) etc or the young of a large animal.

The term hides or rawhide refers to the covering of a large adult animal such as a cow, buffalo, horse etc.

Skins and hides from different animals are used for clothing, bags and other consumer products, usually in the form of leather, but also furs.

Skin can also be cooked to make pork rind or cracklin. The skin on roasted chicken and turkey is another coveted delicacy.

 Skin layers

Skin is composed of three primary layers:

  • the epidermis, which provides waterproofing and serves as a barrier to infection;
  • the dermis, which serves as a location for the appendages of skin; and
  • the hypodermis (subcutaneous adipose layer).
[edit] Epidermis

Epidermis, "epi" coming from the Greek meaning "over" or "upon", is the outermost layer of the skin. It forms the waterproof, protective wrap over the body’s surface and is made up of stratified squamous epithelium with an underlying basal lamina.

The epidermis contains no blood vessels, and cells in the deepest layers are nourished by diffusion from blood capillaries extending to the upper layers of the dermis. The main type of cells which make up the epidermis are Merkel cells, keratinocytes, with melanocytes and Langerhans cells also present. The epidermis can be further subdivided into the following strata (beginning with the outermost layer): corneum, lucidum (only in palms of hands and bottoms of feet), granulosum, spinosum, basale. Cells are formed through mitosis at the basale layer. The daughter cells (see cell division) move up the strata changing shape and composition as they die due to isolation from their blood source. The cytoplasm is released and the protein keratin is inserted. They eventually reach the corneum and slough off (desquamation). This process is called keratinization and takes place within about 27 days. This keratinized layer of skin is responsible for keeping water in the body and keeping other harmful chemicals and pathogens out, making skin a natural barrier to infection.

 

[also see:  image rotating (1.1 mb) ]
Optical Coherence Tomography tomogram of fingertip, depicting stratum corneum (~500 µm thick) with stratum disjunctum on top and stratum lucidum (connection to stratum spinosum) in the middle. At the bottom superficial parts of the dermis. Sweatducts are clearly visible.

 Components

The epidermis contains no blood vessels, and is nourished by diffusion from the dermis. The main type of cells which make up the epidermis are keratinocytes, melanocytes, Langerhans cells and Merkels cells. The epidermis helps the skin to regulate body temperature.[citation needed]

Layers

Epidermis is divided into several layers where cells are formed through mitosis at the innermost layers. They move up the strata changing shape and composition as they differentiate and become filled with keratin. They eventually reach the top layer called stratum corneum and are sloughed off, or desquamated. This process is called keratinization and takes place within weeks. The outermost layer of the epidermis consists of 25 to 30 layers of dead cells.

 Sublayers

Epidermis is divided into the following 5 sublayers or strata:

Mnemonics that are good for remembering the layers of the skin (using "stratum basale" instead of "stratum germinativum"):

  • "Cher Likes Getting Skin Botoxed" (from superficial to deep)
  • "Before Signing, Get Legal Counsel" (from deep to superficial)

Blood capillaries are found beneath the epidermis, and are linked to an arteriole and a venule. Arterial shunt vessels may bypass the network in ears, the nose and fingertips.

Dermis

Gray942.png

The distribution of the bloodvessels in the skin of the sole of the foot. (Corium – TA alternate term for dermis – is labeled at upper right.)

Gray940.png

A diagrammatic sectional view of the skin (click on image to magnify). (Dermis labeled at center right.)

Gray’s
subject #234 1065

MeSH
Dermis

Dorlands/Elsevier
Skin

 Dermis

The dermis is the layer of skin beneath the epidermis that consists of connective tissue and cushions the body from stress and strain. The dermis is tightly connected to the epidermis by a basement membrane. It also harbors many Mechanoreceptor/nerve endings that provide the sense of touch and heat. It contains the hair follicles, sweat glands, sebaceous glands, apocrine glands, lymphatic vessels and blood vessels. The blood vessels in the dermis provide nourishment and waste removal from its own cells as well as from the Stratum basale of the epidermis.

The dermis is structurally divided into two areas: a superficial area adjacent to the epidermis, called the papillary region, and a deep thicker area known as the reticular region.

 Papillary region

The papillary region is composed of loose areolar connective tissue. It is named for its fingerlike projections called papillae, that extend toward the epidermis. The papillae provide the dermis with a "bumpy" surface that interdigitates with the epidermis, strengthening the connection between the two layers of skin.

In the palms, fingers, soles, and toes, the influence of the papillae projecting into the epidermis forms contours in the skin’s surface. These are called friction ridges, because they help the hand or foot to grasp by increasing friction. Friction ridges occur in patterns (see: fingerprint) that are genetically and epigenetically determined and are therefore unique to the individual, making it possible to use fingerprints or footprints as a means of identification.

 Reticular region

The reticular region lies deep in the papillary region and is usually much thicker. It is composed of dense irregular connective tissue, and receives its name from the dense concentration of collagenous, elastic, and reticular fibers that weave throughout it. These protein fibers give the dermis its properties of strength, extensibility, and elasticity.

Also located within the reticular region are the roots of the hair, sebaceous glands, sweat glands, receptors, nails, and blood vessels.

Tattoo ink is held in the dermis. Stretch marks from pregnancy are also located in the dermis.

 Hypodermis

The hypodermis is not part of the skin, and lies below the dermis. Its purpose is to attach the skin to underlying bone and muscle as well as supplying it with blood vessels and nerves. It consists of loose connective tissue and elastin. The main cell types are fibroblasts, macrophages and adipocytes (the hypodermis contains 50% of body fat). Fat serves as padding and insulation for the body.

Microorganisms like Staphylococcus epidermidis colonize the skin surface. The density of skin flora depends on region of the skin. The disinfected skin surface gets recolonized from bacteria residing in the deeper areas of the hair follicle, gut and urogenital openings.

 See also


Look up skin in Wiktionary, the free dictionary.

 External links

] References

  1. ^ a b c d e f g h i j "Skin care" (analysis), Health-Cares.net, 2007, webpage: HCcare.
  2. ^ Alibardi L. (2003). Adaptation to the land: The skin of reptiles in comparison to that of amphibians and endotherm amniotes. J Exp Zoolog B Mol Dev Evol. 298(1):12-41. PMID 12949767
  3. ^ a b Proksch E, Brandner JM, Jensen JM. (2008).The skin: an indispensable barrier. Exp Dermatol. 17(12):1063-72. PMID 19043850
  4. ^ a b c Madison KC. (2003). Barrier function of the skin: "la raison d’être" of the epidermis. J Invest Dermatol. 121(2):231-41. PMID 12880413
  5. ^ a b c Grice EA, Kong HH, Conlan S. (2009). Topographical and Temporal Diversity of the Human Skin Microbiome, Science, 324: 1190 – 1192. doi:10.1126/science.1171700
  6. ^ a b Pappas S. (2009). Your Body Is a Wonderland … of Bacteria. ScienceNOW Daily News
  7. ^ Maton, Anthea; Jean Hopkins, Charles William McLaughlin, Susan Johnson, Maryanna Quon Warner, David LaHart, Jill D. Wright (1993). Human Biology and Health. Englewood Cliffs, New Jersey, USA: Prentice Hall. ISBN 0-13-981176-1.
  8. ^ Connor, Steven: The book of skin, Cornell University Press, 2003, pg. 176
  9. ^ Theodor Rosebury. Life on Man: Secker & Warburg, 1969 ISBN 0-670-42793-4
  10. ^ http://www3.interscience.wiley.com/journal/107640112/abstract
  11. ^ http://www.ingentaconnect.com/content/bsc/ics/2004/00000026/00000002/art00010
  12. ^ Marks, James G; Miller, Jeffery (2006). Lookingbill and Marks’ Principles of Dermatology (4th ed.). Elsevier Inc. ISBN 1-4160-3185-5.
  13. ^ Smith, Wilma and Burns, Catherine. (1999) "Managing the hair and skin of African American pediatric patients." Journal of Pediatric Health Care 13(2):72-8.
  14. ^ Weller, Richard; John Hunter, John Savin, Mark Dahl (2008). Clinical Dermatology (4th ed.). Malden, Massachusetts, USA: Blackwell Publishing. pp. 268. ISBN 978-1-4051-4663-0.
  15. ^ NIH Human Microbiome Project.

Mitral Valve Prolapse -ارتخاء الصمام المترالى

Usama Fouad Shaalan MD- PhD MiniEncyclopedia الموسوعه المصغره للدكتور  أسامه فؤاد شعلان

Mitral Valve Prolapse
Mitral valve anatomy
The mitral valve consists of the mitral annulus, anterior and posterior leaflets, chordae tendineae, and the papillary muscles. Mitral regurgitation may be due to a disease that primarily affects the valve leaflets, such as mitral-valve prolapse or rheumatic mitral-valve disease, or may result from alterations in the function or structure of the left ventricle, such as those induced by ischemic disease or dilated cardiomyopathy. Reproduced with permission from: Otto, CM. Clinical practice. Evaluation and management of chronic mitral regurgitation. N Engl J Med 2001; 345:740. Copyright © 2001 Massachusetts Medical Society.

Mitral valve prolapse, is a common condition in which the mitral valve leaflets are floppy or loose. Mitral valve prolapse is diagnosed by echocardiography (EKG) which records the heart’s electrical activity. Most patients with mitral valve prolapse do not have a leaky mitral valve and do not require surgery. When a valve with prolapse has a severe leak, surgery should be considered.

 Illustration of the mitral valveIn a normal valve, the flow of blood goes from the left atrium to the left ventricle. Upon closing, it prevents blood from going back into the left atrium. With MVP the flaps fail to close evenly. One or both flaps collapse backwards, sometimes allowing a small amount of blood to leak through the valve.

Mitral valve prolapse, sometimes known as mitral insufficiency or mitral valve regurgitation, is a genetic disorder and seems to affect women three times more than men. It is one of the most common cardiac conditions.

Infection of the mitral valve or endocarditis, is extremely rare. But, people with MVP have a slightly greater risk of contracting it. 1

About the Mitral Valve

The heart has four valves that open and close to keep blood flowing in the proper direction through the heart. The mitral valve connects the heart’s upper-left chamber (atrium) to the heart’s lower-left chamber (ventricle).

Mitral valve stenosis?or mitral stenosis?is a narrowing of the mitral valve. This narrowing causes the valve to not open properly and to obstruct blood flow between the left chambers of the heart.

Mitral valve regurgitation, or mitral regurgitation, occurs when the mitral valve doesn’t close tightly and allows blood to flow backward in the heart.

Other names for mitral valve prolapse:

  • Barlow’s Syndrome
  • Floppy mitral valve
  • Myxomatous mitral valve
  • Billowing mitral valve
  • Systolic click-murmur syndrome
  • Prolapsing mitral leaflet syndrome. 2

Symptoms of Leaky Heart Valve

Many patients with mitral valve disease have no symptoms, even with a leak that is severe. When symptoms develop, they include shortness of breath, fatigue, loss of energy, swelling of the ankles and palpitations (extra or skipped heart beats).

Usually symptoms do not show up before the age of 14 or 15, but more and more children display central nervous system symptoms before the MVP shows up. Ninety-eight percent of people with Mitral Valve Prolapse Syndrome have nothing wrong with their heart. The majority of symptoms are caused by an out-of-balance nervous system. 3

Diagnosis

The first step in diagnosing mitral valve prolapse involves listening with a stethoscope. This allows the doctor to hear a murmur, which represents turbulent blood flow across an abnormal valve. The diagnosis is confirmed by an echocardiogram. Ultrasound is used in an echocardiogram which allows the doctor to visualize the heart valves and determine the severity and cause of the leak. In most patients, a standard transthoracic echocardiogram (a probe placed on the skin of the chest) is adequate to visualize the valve. Sometimes a transesophageal echocardiogram (a probe passed through the mouth into the esophagus) is necessary to more closely visualize the valve. This is an outpatient procedure.

» Continue to Treatment of Mitral Valve Conditions

1. “Mitral valve prolapse,” Medline Plus Medical Encyclopedia, http://www.mlm.nih.gov. URL: http://www.nlm.nih.gov/medlineplus/ency/article/000180.htm . See also: “Mitral valve prolapse,” MayoClinic.com. URL: http://www.mayoclinic.com/health/mitral-valve-prolapse/DS00504
2. “Mitral valve prolapse,” Medline Plus Medical Encyclopedia, http://www.mlm.nih.gov. URL: http://www.nlm.nih.gov/medlineplus/ency/article/000180.htm
3, Kristine A. Scordo, M.D., “Understanding the Mitral Valve Prolapse Syndrome,” http://www.wright.edu. URL: http://www.wright.edu/nursing/practice/mvp/default.htm  

While clinical studies support the effectiveness of the da Vinci® System when used in minimally invasive surgery, individual results may vary. Surgery with the da Vinci Surgical System may not be appropriate for every individual. Always ask your doctor about all treatment options, as well as their risks and benefits.

Treatment of Mitral Valve Conditions

Most of the time, there are few or no symptoms for mitral valve conditions and treatment is not needed. But, if you have severe mitral valve prolapse, you may need to stay in the hospital. Surgery to repair or replace the valve may be needed if you have severe mitral regurgitation or your symptoms get worse. Mitral regurgitation is a condition in which your heart’s mitral valve does not close tightly, allowing blood to flow backward in your heart.

Commonly Prescribed Medications

  • Anti-arrhythmics drugs to help control irregular heart beats.
  • Vasodilators dilate (widen) blood vessels, which makes it easier for the heart to work.
  • Digitalis is used to strengthen the heartbeat.
  • Diuretics (water pills) help remove excess fluid in the lungs.
  • Propranolol is given for palpitations or chest pain.
  • Anticoagulants (blood thinners) help prevent blood clots in people who also have an irregular heartbeat.1

Surgery

Surgery should be considered in virtually all patients with a leak that is graded as a 4 (severe) and in some patients with a leak that is graded as a 3 (moderately severe). When a patient with mitral valve regurgitation develops symptoms, a decrease in heart function, or an increase in heart size, surgery is recommended. Surgery should also be considered when a patient develops atrial fibrillation – an irregular heartbeat. Surgery is also recommended in many patients who don’t have any symptoms but have a severe leak; in these patients, surgery improves long-term survival.2 During surgery, a sternotomy is typically required. This is when surgeons access the heart by making an 8- to 10-inch incision down the chest, cut through the breastbone (the sternum) and open the ribs.

Minimally Invasive Surgery

Comparison of Traditional Open Incision to Robotic Incision

Recently, minimally invasive approaches to Mitral Valve Repair are replacing sternotomy as the surgical method of choice. Of the minimally invasive approaches, robotic surgery ( da Vinci Surgery) has many practical advantages for both the patient and the surgeon: precision, fewer complications, reduced blood loss and shorter hospital stays. According to the world-renowned Cleveland Clinic, there is a 95% chance that a leaky mitral valve can be repaired using minimally invasive techniques. 3

1. “Treatment Options for Mitral Valve Disease,” Mayo Clinic, http://www.mayoclinic.org. URL: http://www.mayoclinic.org/mitral-valve-disease/treatment.html
2. “Mitral Valve Repair: Answers to our most common questions,” Cleveland Clinic Heart & Vascular Institute, http://www.clevelandclinic.org. URL: http://www.clevelandclinic.org/heartcenter/pub/guide/disease/valve/mvrepairfaq.htm
3. Ibid.

While clinical studies support the effectiveness of the da Vinci® System when used in minimally invasive surgery, individual results may vary. Surgery with the da Vinci Surgical System may not be appropriate for every individual. Always ask your doctor about all treatment options, as well as their risks and benefits.

 

 

 

 

 

H1N1 Critical Illness Mostly Affects Young Patients and Is Often Fatal- Dr Usama Fouad Shaalan MD- PhD MiniEncyclopedia الموسوعه المصغره للدكتور أسامه فؤاد شعلان

rH1N1 Critical Illness Mostly Affects Young Patients and Is Often Fatal
 
 
 

October 12, 2009 — H1N1 critical illness mostly affects young patients and is often fatal, according to the results of a Canadian and Mexican study and an editorial published online October 12 in the Journal of the American Medical Association (JAMA).

"Between March and July 2009, the largest number of confirmed cases of 2009 influenza A(H1N1) infection occurred in North America," write Anand Kumar, MD, from the Health Sciences Centre and St. Boniface Hospital in Winnipeg, Manitoba, Canada, and colleagues with the Canadian Critical Care Trials Group H1N1 Collaborative.

The goal of this prospective observational study was to evaluate clinical characteristics, treatment, and outcomes of critically ill patients who had 2009 influenza A (H1N1) infection in Canada. Between April 16 and August 12, 2009, 168 critically ill patients with 2009 influenza A (H1N1) infection in 38 adult and pediatric intensive care units (ICUs) in Canada were followed up for 28-day and 90-day mortality. Secondary study endpoints included frequency and duration of mechanical ventilation and duration of ICU stay.

Of 215 patients with critical illness, 162 had confirmed, 6 had probable, and 47 had suspected community-acquired 2009 influenza A (H1N1) infection. Mean age was 32.3 ± 21.4 years in the 168 patients with confirmed or probable 2009 influenza A (H1N1); 113 patients (67.3%) were women and girls, 50 patients (29.8%) were children, and 43 patients (25.6%) were aboriginal Canadians.

Among critically ill patients, overall 28-day mortality was 14.3% (95% confidence interval [CI], 9.5% – 20.7%), and shock and nonpulmonary acute organ dysfunction were common (sequential organ failure assessment mean score 6.8 ± 3.6 on day 1). At 90 days, overall mortality was 17.3% (95% CI, 12.0% – 24.0%; n = 29).

At ICU admission, all patients were severely hypoxemic (mean ratio of partial pressure of oxygen in arterial blood [PaO2] to fraction of inspired oxygen [FIO2] of 147 ± 128 mm Hg). Median time from symptom onset to hospital admission was 4 days (interquartile range [IQR], 2 – 7 days) and from hospitalization to ICU admission was 1 day (IQR, 0 – 2 days).

Most critically ill patients received neuraminidase inhibitors (n = 152 [90.5%]) and mechanical ventilation (n = 136 [81.0%]). Median duration of ventilation was 12 days (IQR, 6 – 20 days) and of ICU stay was 12 days (IQR, 5 – 20 days). Some patients also required lung rescue therapies, including neuromuscular blockade in 28% of patients, inhaled nitric oxide in 13.7%, high-frequency oscillatory ventilation in 11.9%, extracorporeal membrane oxygenation in 4.2%, and prone positioning ventilation in 3.0%.

"Critical illness due to 2009 influenza A(H1N1) in Canada occurred rapidly after hospital admission, often in young adults, and was associated with severe hypoxemia, multisystem organ failure, a requirement for prolonged mechanical ventilation, and the frequent use of rescue therapies," the study authors write. "Our data suggest that severe disease and mortality in the current outbreak is concentrated in relatively healthy adolescents and adults between the ages of 10 and 60 years, a pattern reminiscent of the W-shaped curve previously seen only during the 1918 H1N1 Spanish pandemic."

Limitations of this study include focus on severe disease requiring ICU admission, possible late deaths occurring after the observation period, and possible overrepresentation or underrepresentation of certain comorbidities and clinical features.

"We have demonstrated that 2009 influenza A(H1N1) infection–related critical illness predominantly affects young patients with few major comorbidities and is associated with severe hypoxemic respiratory failure, often requiring prolonged mechanical ventilation and rescue therapies," the study authors conclude. "With such therapy, we found that most patients can be supported through their critical illness."

Mexican Study

The goal of the second observational study was to describe baseline characteristics, treatment, and outcomes of critically ill patients with confirmed, probable, or suspected 2009 influenza A (H1N1) in 6 Mexico hospitals. Between March 24 and June 1, 2009, the investigators collected demographic data, symptoms, comorbid conditions, illness progression, treatments, and clinical outcomes from 58 critically ill patients with 2009 influenza A (H1N1). The main study endpoint was mortality, and secondary endpoints were rate of 2009 influenza A (H1N1)–related critical illness and mechanical ventilation and length of stay in the hospital and ICU.

Of 899 patients hospitalized with confirmed, probable, or suspected 2009 influenza (A) H1N1, 58 (6.5%) were critically ill. All presented with fever, and 57 of 58 presented with respiratory symptoms; median age was 44.0 years (range, 10 – 83 years). Although comorbid respiratory disorders occurred in few patients, 21 patients (36%) were obese. Median time from hospital to ICU admission was 1 day (IQR, 0 – 3 days). Mechanical ventilation for severe acute respiratory distress syndrome and refractory hypoxemia was needed in 56 of 58 patients. Median day 1 ratio of PaO2 to FIO2 was 83 mm Hg (IQR, 59 – 145).

Mortality by 60 days was 41.4% (24 deaths; 95% CI, 28.9% – 55.0%), with 19 deaths occurring within the first 2 weeks. Factors associated with mortality were greater initial severity of illness, worse hypoxemia, higher creatine kinase levels, higher creatinine levels, and ongoing organ dysfunction. Neuraminidase inhibitor treatment (vs no treatment) was associated with better survival, after adjustment for a reduced opportunity to receive neuraminidase inhibitors among patients dying early (odds ratio, 7.4; 95% CI, 1.8 – 31.0).

"Critical illness from 2009 influenza A(H1N1) in Mexico occurred in young individuals, was associated with severe acute respiratory distress syndrome and shock, and had a high case-fatality rate," write Guillermo Domínguez-Cherit, MD, from Instituto Nacional de Ciencias Médicas y Nutrición "Salvador Zubirán," Mexico City, and colleagues. "Fever and respiratory symptoms were harbingers of disease in almost all cases. There was a relatively long period of illness prior to presentation to the hospital, followed by a short period of acute and severe respiratory deterioration."

Study limitations include relatively early examination of the epidemiology of a severe infectious disease with possible overestimation of case-fatality rate.

"Early recognition of disease by the consistent symptoms of fever and a respiratory illness during times of outbreak, with prompt medical attention including neuraminidase inhibitors and aggressive support of oxygenation failure and subsequent organ dysfunction, may provide opportunities to mitigate the progression of illness and mortality observed in Mexico," the study authors conclude.

In an accompanying editorial, Douglas B. White, MD, MAS, and JAMA Contributing Editor Derek C. Angus, MD, MPH, from the University of Pittsburgh School of Medicine in Pennsylvania, note that many US hospitals may be inadequately staffed to provide treatment of the most seriously ill patients with 2009 influenza A (H1N1) in a timely fashion.

"Hospitals must develop explicit policies to equitably determine who will and will not receive life support should absolute scarcity occur," Dr. White and Dr. Angus write. "Any deaths from 2009 influenza A(H1N1) will be regrettable, but those that result from insufficient planning and inadequate preparation will be especially tragic."

The Canadian Public Health Agency of Canada, the Ontario Ministry of Health and Longterm Care, the Heart and Stroke Foundation Canada, and the Canadian Institutes of Health Research supported the Canadian study. The authors of both studies have disclosed no relevant financial relationships.

JAMA. Published online October 12, 2009.

 

 
 
 
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