عدد المساهمات : 123
تاريخ التسجيل : 23/04/2010
الموقع : http://www.tnb.66ghz.com/vb
|موضوع: البحث نجليزي عن إنفلونزا الطيور (plue الطيور) ، (طاعون الطيور =Search for Avian influenza (bird plue),(The plague of birds) الأربعاء أكتوبر 20, 2010 4:24 am|| |
Avian influenza (bird plue),(The plague of birds)
Influenza viruses belong to the family Orthomyxoviridae under the rank of the rank of Mononegavirales Myxoviruses
Family Orthomyxoviridae contains four genera, including three races of the influenza virus are:
1 - A influenza virus that affects birds and is transmitted to pigs, horses and some other species of animals and some types of rodents also affect some Aatarath rights and move the injured to the proper (H1N1, H3N2, H2N2)
2 - B, and influenza virus in humans only and does not cause medical problems only in school-aged children (5-14 years old) and older and causes respiratory symptoms only.
3 - C influenza virus strains and a weaker humans, pigs, and the symptoms go unnoticed (minor symptoms can not differentiate between them and the symptoms of colds, minor) so little Concern study as well as information available to them.
Description of the virus
Characterized influenza virus multi-forms and change (highlypieomorphic) is either a spherical or oval with a diameter of 80-120 nm, while other forms of it up to (200 nm) or filamentous long length of up to (2000 nm) and a diameter of up to (80-120 nm), and the different strains of the virus in their tendency to form linear forms.
A - outer shell of the virus envelope is composed of fatty highlights from the image protrusions (spines) of the Alglicobrotin of two types:
1 - (HA) haemagglutinin and length of 135 A.
2 - (NA) neuraminidase and length of 60 A.
B - inner surface of the envelope protein of the virus.
Search the thread (piece) of Alraibusom (RNA) carries a single protein code
C - cut the genome and the eight pieces or a string of RNA that carry the genetic code of the virus are in the heart of the virus.* Each thread (piece) of the fees (RNA) carrying code one protein.
* The three major segments (p1, p2, p3) is the internal proteins of the virus and specializes in the process of polymerization (ie converting a string to RNA negative mRNA) in a cell of the family.
* Alraibusom cut three medium-sized, two of them from Itrakban Alglicobrotin carrying the blades HA & NA, second and third bearing code Alnyukliobrotin NP is part of the Alnyukliukabsid.
* Object-seventh, the smallest pieces bear the code M protein, one of the major components of the virus for the cover (envelope)
* Depending on the type Alnyukliobrotin NP and M protein has been divided into three influenza virus types are A, B, C
* Depending on the type of both Alonteginan HA & NA (Alonteginan two major components in the cover of the virus) strain of the virus was determined by their partition numbers (N2 ... H1, H2 .... & NA).
* HA antigen contains about 25% of the protein the virus is a virus-cell adhesion and penetration of host cell membrane and then its entry of the virus within the cell.
* H antigen is divided to 16 under the type (16 subtypes) is (H1, H2, ... H16).
* N is divided into antigenic type to a 9-under (9 subtypes) is (N1, N2, ... N9)
* Antibodies produced by the host against the virus antigen H can be equally efficient with the virus, which contains in its cover if attacked host, therefore, of great importance in the production of influenza vaccines.
* Antibodies produced by the host against the virus N antigen have little effect in slowing or preventing the release of the virus from the host cell (you need very high concentrations of antibodies)
* Spanish influenza H1N1 and H2N2 Asian flu and Hong Kong H3N3.
Mutation of the virus:
Characterized influenza virus ability of big mutation (mutation) in short periods of time and its ability to configure the strains of a new, allowing him to cause infection in the same assembly infected Balaatarp earlier without objection from the immune system and lead to the emergence of strains of a new can finish easily the families were not infected by the mutation and this is what scientists are currently running in fear of the mutated strain of H5N1 to the current striking new strain that could pass easily between humans, triggering a global pandemic such as pandemics that occurred during the last century and killed millions of people.
Mutation of two types:
The first is called - (Antigenic drift)
A mutation of slow onset is through accumulation of point mutations in the gene result in a change of amino acids in a protein the virus, which leads to a change order or complete rupture of Alraibusom and result in a change in the antigen (H1 changed to H2 or N1 to N2 (and thus the virus can escape from the immune system and destroy the host again with the same strain and often mutation occurs in one of the only Alontejinin (H only or N only) and rarely occurs in both.
The second is called (antigenic shift)
A mutation to occur and is fast changing the order of amino acid sequence of the virus also occurs in cells infected with two types of influenza has been observed that the virus occurs in one out of every 10 thousand HIV
Multiplication of the virus:
Facilitate the thorns that contain HA virus to enter the host cell (human - animal - birds Baltsagaha set Almiukubrutin Terminal (NANA = sialic acid ((N-acetyl neuraminic) in the host cell and then link to ingest into the host cell by a currency called endocytosis until it reaches the end Andusumaat to the host cell
To enter the host cell must be divided into two HA protein by enzymes called proteases Onziman Proteolysis is naturally present in secretions of the cells lining the false and the trachea and lungs and there is no secretion from the cells in any other part of the body and this explains that influenza respiratory disease only
But he found too severe strains used another enzyme called (plasmine) to enter the cell, which resides in the secretion of the cells in all tissues of the body as in the case of highly pathogenic strain of H5N1 and other strains of fierce
* Virus strains were classified in terms of intensity, in three groups according to WHO & OIE organizations are:
1. Strain of highly pathogenic HPAI: It is caused by death of a number from 16 to 8 chicks aged 4-8 weeks after intravenous injection solution extract of the virus concentration 1 / 10 over a period of 10 days has been found to contain one of the Alantegnin H5 or H7, and some isolates that contain the H10 antigen, including H10N5 & H10N4.
Note: This strain is included in the list A of the Office International des Epizooties in Paris, which prohibits the importation of birds from countries Alambup them.
2 - strain of medium virulence MPAI: the MOST widespread and caused death of a number 1-5 chicks of the total 8 chicks aged 4-8 weeks after intravenous injection solution extract of the virus concentration 1 / 10 over a period of 10 days, provided it does not contain any of the Alantejinin H5 or H7, and some of these strains used in the work of the influenza vaccine
2 - low pathogenic strains LPAI: They do not cause the appearance of symptoms can be observed.
Influenza A (avian influenza) in humans
* Scientists because the first record of infection of human influenza illness in general to the year 155 AD, the date of the first pandemic in 1580 to spread from one continent where Europe to Asia and Africa (Cunha 2004)
* Join the second infection of human influenza illness in general was in the 18 century, where epidemics have occurred years (1729 to 1730 - 1732-1733.1781 - 1782)
* Join third human bird flu infection in general was in the 19 century, where epidemics have occurred three years (1830 to 1831.1833 - 1834.1889-1890 "Russian Flu)
* So far do not know exactly when she moved strains of influenza A virus from birds to humans for the first time.
* Scientists confirm now that the years 1918-1919 influenza pandemic that struck more than 200 million people and killed more than 50-100 million people (Barry 2004) has moved from birds to humans (scientists expect if a pandemic occurs from the current H5N1 strain the incidence and mortality ranging from 175 to 350 million people) (ASTHO 2004).
* Epidemic appears sharply in the fast-spreading human populations (nurseries, schools, universities, hospitals, exhibitions, etc. ...) where the disease occurs during the short period of time of 1-3 weeks and continue to appear for 3-4 weeks where the disease is usually 20-50 % of the risk of infection.
* Symptoms of infection are more severe and faster prevalent among children (aged 5-14 years) and elderly (over 60-65 years), patients waistcoat or chronic diseases.
* Emerged influenza infection is endemic during the last century in three large epidemics, namely:
1. Spanish influenza H1N1 between 1918 and 1919 that affected more than 200 million people and killed more than 50-100 million people (Barry 2004) in all parts of the world.
2. Asian H2N2 influenza between 1957 and 1958 (that killed nearly a million people).
3. Hong Kong H3N2 avian influenza between 1968 and 1969 (that killed nearly a million people).
• In 1997, he was the cause of infection in humans in Hong Kong is the transmission of influenza strain (H5N1) from birds to humans, causing injury and death of 6 members from among the 18 people injured in this strain.
• In 1999, the infection in humans because of strain (H9N2) in Hong Kong.
• In March 2003 the infection in humans because of strain (H7N7) in the Netherlands and caused the death of a veterinarian after a visit to a poultry farm infected with bird flu.
* Since December 2003 I moved strain of avian influenza (H5N1) to humans in Southeast Asia and killed at least 92 people in Vietnam, Thailand and some other countries, continues to be prevalent in many countries (Thailand - Cambodia - Vietnam - Indonesia - China - Korea - Japan - Malaysia - Iraq - France - Germany - Italy - Iran - Belgium - Cyprus - India - Slovenia - Hungary) n The latest of these countries are (Kazakhstan - Turkey - Greece - Hungary - Croatia - Egypt) so far and are less severe.
• In 2005 the disease has spread in the countries of North Asia and some European countries, including (Russia - Azerbaijan - Turkey - Romania - Greece - United Kingdom)
* States have become African and European continents susceptible to transmission of avian influenza to it through migratory birds.
Methods of infection in humans:
1. Mixing with sick birds.
2. Eating contaminated food and water Bzark and secretions of infected birds.
3. Inhalation of polluted air Bzark and secretions of infected birds
Symptoms of influenza in humans:
1. Continuous fever.
3. Rhinitis and the descent of the nasal secretions and sneeze
4. Dry cough and inflammation of the Az-Zour
5. Pain in the chest muscles and severe fatigue
6. Shortness of breath
7. Severe pneumonia
8. Gastrointestinal symptoms often appear in children only
Image severe infection occurs in persons in contact with the infected birds and sponsors and circulation of the massacres and contacts or at Zarkha secretions and faeces, and the symptoms continue for several days
Methods of prevention and the prevention of transmission of infection:
1. Good for washing hands with soap and water at intervals, preferably the use of disinfectants in the laundry.
2. Wear protective clothing before exposure to birds or their secretions and Zarkha
3. The use of antiseptic mouth rinses and throat
4. Vitamin C
5. Immunization and the use of antivirals such as amantadine (Amantadine) and rimantadine (Rimantadine) and Rilaniza (Relanza) and Tamiflu (Tamiflue)
1. Comfort in bed.
2. Drink plenty of fluids
3. Eating painkillers such as paracetamol Shirring
4. Address, such as aspirin, antipyrine
5. And the use of antivirals such as amantadine (Amantadine) and rimantadine (Rimantadine) and Rilaniza (Relanza) and Tamiflu (Tamiflue)
6. Inhalation drug (Zanamivir) leads to the short duration of symptoms and reduce the severity.
Influenza A in swine
* Discovered the injury for the first time in pigs in 1918 was not to isolate and diagnose strain (H1N1) that caused the emergence of this infection only in 1930 in the United States of America.
* Serological studies confirmed that was in 1988 and 1989 that this strain (H1N1) is still prevalent in pigs in northern and central United States of America (up to 51%)
* Tested positive for viral isolation and serological presence of the same strain in pigs in many countries of the world, including (France - Japan - England - Bulgaria - Egypt - Thailand - Cambodia).
* Also proved her Baatarp Hong Kong (H3N2) and can be transmitted to the contacts.
• In 1992 was isolated bird flu strain H1N7 from pigs in England, and strain study found that 6 pieces of Alraibusom (RNA) are quite similar to those of human influenza HA antigen, while the Apostle and Alraibusom MRNA was very similar to those of equine influenza.
* Pigs play an important role in the dissemination of influenza viruses because it is the only animal that can be infected with human influenza virus Baatarti and chicken (Kito et al 1994 & Ito et al 1996)
* Focus the seriousness of swine flu in the likeness of the immune system with its counterpart in humans, which gives the virus an opportunity to adapt it, which facilitates the spread of the epidemic from pigs to humans.
* Scientists fear the current transmission of the current strain of H5N1 to wild pigs and mixed with other Balaatarat Pigs play a role because the mixing bowl of different strains and then show the existence of new highly pathogenic strain transmitted from pigs to humans easily.
1. China confirmed 23/08/2004 isolate this strain from a pig in 2002 from samples collected from pigs in 2001 from Fujian Province in southwestern China.
2. In 2003 were collected 1936 from the number of pigs from the same province and 13 other provinces have been isolated strain of a sample of one of the samples taken from pigs from the same province.
3. In 2004 were collected 1.1 million sample 4447 sample of pigs from 10 states, including the province of Fujian has not isolate this strain from pigs.
4. This was confirmed by Chinese scientists that the strain isolated from swine very similar to the H5N1 strain that has been isolated from ducks in China recently and there is no difference between them.
Influenza A in horses
* Been described in horses infected bird flu in the scientific literature since the 17 century, corresponding to its counterparts in humans have not been isolated equine influenza virus only in the 1956.
* Spread of infection in many countries of the world and is of interest to horse breeders, particularly race horses.
* Was isolated influenza virus for the first time the horses in Czechoslovakia in 1956 strain H7N7, known as Equi1 was isolated after in 1956 of horses in many European countries and America, and in 1963 was isolated strain H3N8, known as Equi2 horses in Miami, United States of America followed by isolation of horses in many European countries and North America.
* Appeared mutated strain of the H3N8 strain was isolated from horses in Suffolk, England in 1989 and spread to Asia, where it caused injury to about 80%, and the deaths of nearly 20% of horses in northern China and found that antigens of this strain (A/eq/Jilin/89) as of the strain circulating in ducks on the strain circulating in horses.
Immunization Balaatartin H7N7 & H3N8 together (not every 3 months in all foals 6 months in horses vaccinated mothers publican additional dose before birth to 4-6 weeks) and proper health care, this is vaccination of horses periodically starting in 1981.
Influenza A in the other animals
Rodents play a role in transmission, especially the wedding, and that the discovery of transition strain of H5N1 to domestic cats (the number of 3 cats in the house of Our Lady of THB) and the death of these cats as a result of HIV infection and fauna of the Leopard, one of the largest species of cats are Asian does not exist only in forests in southern East Asia, China and India.
Influenza A in birds
* Birds are infected with all known strains of influenza A have been isolated six species of ten antigen H and nine N types of antigen of influenza
* More sources to isolate strains of virus are migratory waterfowl and wild particularly ducks, followed by ornamental birds, particularly parrots and birds (especially those coming from Southeast Asia, India and Central and South America) and pet birds in the regions of Hong Kong, China (was isolated over 46 strains of different virus Most of the ducks)
* Less sources of virus isolation was one of the domestic birds (chickens, ducks and turkeys).
Ibedemiologip disease and ways to spread
The birds are the natural stores of the virus for many reasons, including:
1. Wild birds and water birds, beaches and migratory birds (especially ducks) is characterized by its susceptibility to infection by more than strain of the virus at the same time there is no evidence of serological for antibodies that could be identified and the diagnosis of influenza viruses, and so can be detected infection tests are performed isolation of viral to isolate the virus from these birds test or rt-PCR (a test not available and difficult procedure and you need to material costs and high-tech).
2. These birds excrete the virus in glaucoma, secretions other for a long time (been isolated the virus from the waters of Lake Inn by wild ducks), which can transfer the virus over large distances (from one continent to another) and that the combination of these birds backyard birds that are raised in backyard plays a major role in the dissemination of infection in other domestic birds.
3. Open markets, where they accumulate live birds from places, farms and multiple different types of display, sale and remain for long periods - these roses related birds are of flu, especially after exposure to enormous stress during transport and handling make it a favorable opportunity for the virus to attack these birds and bird reproduction and growth within the cells and eventually mutate into strains different also gives him the opportunity to return to the farms through the return of these birds from the market, as well as through the means of transport (cars - cages - utensils and tools) as well as rights.
4. Of the distinguishing characteristics of this virus that is excreted in respiratory secretions and Blue (characterized by the virus in its ability to multiply in the digestive tract of birds, one of the characteristics of bird flu is not found the property in human influenza or other animals and excreted in high concentrations in blue) and cold regions of the globe (where he remains capable of causing infection in glaucoma for up to 30 days at a temperature of 4 ˚ m for a period of two days at a temperature of 20 ˚ m) this is the emergence of the disease seasonal in some cases.
5. Virus is transmitted from one farm to another, direct contact and indirect and through the movement of birds and Entries by dust and clothing and all the tools used in the farms and means of transport.
6. The virus has been isolated from sperm and eggs in the turkey, but there is no scientific evidence confirms move vertically through the egg.
Routes of infection in birds:
1. Contact with infected birds
2. Eating contaminated food and water Bzark and secretions of infected birds
3. Inhalation of polluted air Bzark and secretions of infected birds
Stop the emergence and severity of symptoms of influenza virus on many factors, including:
1. Type strain of the virus (fierce - medium intensity - low intensity)
2. The type of birds infected
3. Health status and immunity of the herd
4. Breeding systems
5. Environmental conditions surrounding the herd
6. The presence of secondary infection
7. Age of the infected herd
(Is the period between the entry of the virus and onset of the first presentation of the injury), ranging from 3-7 days and less in the event of injury Balaatarp fierce
The symptoms of bird flu virus in several photographs, including:
Evidenced by the presence of the disease through:
1. The presence of antibodies periodic serological tests
2. A slight decrease in feed intake and loss of appetite, slight
3. Minor respiratory symptoms (discharge water from the nose - cough - the speed of breathing)
4. Gastrointestinal symptoms (diarrhea)
1. Sudden death without any symptoms of pre-
2. High body temperature
3. Loss of mobility and inability to stand
4. Loss of appetite and severe shortage of feed consumption
5. A sharp drop in egg production and egg production flabby crust or without crust or distorted
6. Edema (water swelling) in the head and eyelids, custom Aldalitin and around the claws.
7. Congestion and the blue color custom Aldalitin and legs, and body parts free of feathers
8. Nasal secretions of water and mucus, cough and difficulty in breathing, sinusitis and rattle sound
9. Gastrointestinal symptoms (diarrhea)
10. Neurological symptoms (idle - the inability to walk or stand - ruffled feathers and roughness)
11. Symptoms in ducks and turkeys are similar to those of the poultry, but less evident than unity in the chicken
* Percentages of injury to 100% within 2-10 days of onset of symptoms.
* Percentages of deaths to 100% in case of injury Balaatarp too severe HPAI during 2-10 days.
1. Congestion conjunctivitis eye is accompanied in some cases the presence of patches Tnkerzip them.
2. Edema under the skin zones for head and neck
3. Accumulation of large amounts of tracheal mucus may be present Onzvp similar to those in disease inflammation of the larynx, trachea, gastric
4. Onzvp muscle
5. Splanchnic congestion in
6. Hemorrhagic spots the size of a pinhead on the outer surface of the sternum
7. Hemorrhagic spots on the abdominal fat (appears as if it had been sprayed with red dye)
8. Onzvp on the mucous membrane lining of the stomach, especially when they relate to Proventriculus Balqansp (similar to the patches of haemorrhagic disease, Newcastle disease and other diseases).
9. Renal congestion and the filling of the ureter and kidney channels urinary uric acid salts sometimes
10. Peritoneal cavity filled Besvar white eggs result of the explosion, resulting in an acute inflammation of air bags and acute peritonitis (in birds, which remain alive for 7-10 days of the start of infection)
11. Ovarian atrophy and there may be some haemorrhagic spots and stains on the surface Altnkerzip
12. Anatomical lesions in ducks and turkeys, and less evident than in poultry
13. Anatomical lesions of the flu can not be easily distinguishable from its counterpart in the Newcastle disease, which gives the opportunity for influenza virus to spread before reaching the exact diagnosis of the disease.
Field diagnosis (suspected):
Is based on:
1. Medical history in terms of a disease in an area close or the presence of migratory birds or wild ducks near the farm or the presence of a lake ... Etc..
2. Symptoms of the phenomenon on the herd and in particular sudden death and the sharp drop in egg production ... Etc
3. Anatomical lesions
Is to isolate the virus strain causing the disease and determine the severity of ferocity.
Samples must be sent to the lab are:
1. Swabs of the trachea and anal swabs
2. Internal organs (trachea - lungs - the spleen - the compound - the brain)
3. Blood samples for testing Sero to indicate the presence of antibodies in the serum of the disease.
And taking into account that the samples are collected from a large number of birds that show symptoms and birds mixing with them and sent to the lab saved on ice.
Intended to distinguish between avian flu and similar diseases, such as:
1. Intestinal fierce strain of Newcastle disease VVND
2. The acute phase of disease, fowl cholera
3. Some respiratory diseases such as acute in the image LT & E Coli
Influenza viruses were isolated from the Ratites for the first time in 1991
* Strains were isolated from the ostrich, Alaembo and other bird species which do not fly (H3N2, H4N2, H4N6, H5N2, H5N9, H7N1, H7N2, H9N2, H10N7)
Search the strains of influenza virus that was isolated from birds (which do not fly, such as ostriches) strains of medium intensity MPAI
* Infection in the birds do not fly the symptoms do not occur Nfoqa simple but her role in the transfer of infection to poultry and other birds
* South Africa announced that the bird flu hit the wild ostriches for the first time in the month of August 2004 and it caused the death or culling of more than 13,000 ostrich in 5 of the largest ostrich farms in the world during that month were identified as H5 strain
* The virus has been isolated from many types of wild birds in addition to the foregoing, including some types of hawks and other birds of prey
Methods of prevention and elimination of the disease:
For the prevention of infection with avian influenza should know that:
1. The virus is sensitive to most detergents and disinfectants traded markets
2. The virus is sensitive to temperature and drought
3. Virus requires the presence of organic materials damp (was removed alive from the wet blue, 105 days)
1. Hygienic disposal of infected poultry and Entries by burning or deep burial in a pit of quicklime and covers a layer of quicklime in the hole before backfilling
2. Raise the temperature of amber over in 1930 for several days, then wash and cleanse well is not used for breeding again until after 3 months of the end of the disease
For the prevention of the disease are the following procedures:
First, prevention Bio:
1. On the farm:
To prevent the entry of the virus to the farm taking into account the following:
* Continue to farm closed on what is in it from home and abroad (Farm closed less vulnerable to the disease has recently been in some European countries to prevent breeding birds outside the barns closed - in courtyards or open spaces - not to be subject to mixing with wild birds or migratory directly or pollution caused by these birds to water or food)
* Farm workers to wear special clothing, blankets and Bao inside
Prevent visitors from approaching or entering the farm scale
• Prevent the entry of personnel management and supervisors of any other farms
* Change of clothes and clean the various parts of the body after the care of herds and before leaving the farm
* Visitors who can not be denied entry, such as the owner and the truck drivers transport of fodder and fuel ... Etc. must before entering the farm to wear protective clothing and headgear Pot and a good cleansing
* Cars and other means of transportation must be disinfected before entering the farm and when you exit
* Pots and tools used in the farm tools and transport must be kept clean and are disinfected before use and after
* Hygienic disposal of sick and dead birds
* Individuals who are dealing with wild birds and pet birds should be prevented from entering within the scope of the farm prior to change clothes and wash and clean thoroughly before entering into the scope of the farm
Must set warning signs to prevent entry of vehicles in the scope of the farm
2. Procedures for the sale and circulation of influenza:
* The use of plastic cages for easy laundered and disinfected
Maintaining the cleanliness of the scales and floor sales area of pollution glaucoma and feathers and other residues and cleaned and disinfected after the end of the sale
* Cleaning and disinfection of all pots and cages and transport of poultry prior to entering into the scope of the farm again
Prevent re-birds came out of the sale have not been sold to the farm again
Surveillance and control of the disease:
1. Serological examination routine periodic monitoring the presence of antibodies in the blood and eggs on farms which may be suspected by the presence of infection (early detection of disease - a preventive measure)
2. The total isolation of herds infected until they are disposed of health, including necessary action to prevent the spread of infection (the responsibility of a breeder in the first place the need for rapid reporting of infection satisfactory ranch so that the Veterinary speed to take the necessary measures to control the disease and prevent spread of the farms nearby, close to the farm affected)
3. Re-examine the education status quo and not a new education in the same ward only after completely sure of the absence of any viral activity of the farm and surrounding areas.
4. Follow-up to wild birds and migratory birds and testing Serological routine to monitor the presence of antibodies.
Although he faces many objections, including:
1. Immunization does not prevent infection Balaatarat other strains of the virus or high pathogenic HPAI
2. Medium-intensity field strains MPAI hit if the herd could grow unnoticed Serological tests may even mutate into new strains of highly pathogenic HPAI
3. Immunization does not prevent the secretion of the virus in respiratory secretions or blue of the bird
4. Immunization can not be of the early detection Balaatarat field where you can not distinguish between antibodies resulting from immunization and antibodies resulting from infection Balaatarp field Serological tests
5. Vaccinated herds may contribute to the dissemination of infection among non-vaccinated herds (vulnerability to HIV infection less in vaccinated herds and symptoms is less clear, especially in the event of injury Balaatarp field medium intensity MPAI
However, the immunization Balaatarat isolated from herds infected or carriers of many advantages, including:
1. Prevents or greatly reduces the secretion of the virus (immunized chickens stopped Alljhorn College secretion of the virus in turkeys in the secretion rate was less fortified by 99-99.99% of the excretion in the turkey was not married and in laboratory experiments)
2. Field results of immunization indicated that will help many control programs and control the disease and prevent its spread
3. Reduces or prevents the emergence of symptoms of infection
4. Reduces or prevents decline in egg production
5. Leads to a reduction of material loss to the poultry industry
Immunization is currently used in some States in herds exposed to infection (farms surrounding the infected farm, which lies outside the circle to which the infected farm status and 3 km radius and within the circle radius of 10 km around the infected farm).
Been vaccinated turkey flocks in the United States of America Balaatarp H1N1, especially in states that spread by pig-raising.
The preparation of vaccines suppressive immunization Alaatartin H7, H5 of strains highly pathogenic HPAI experiments are currently under study could be used in vaccination in endemic areas such as East Asia (China announced recently that it has succeeded in producing a vaccine strain of H5N1 and the use of already in the vaccination of poultry by) where it has become necessary to control the current epidemic of influenza.
1. Closed farms are less prone to infection than open fields and easier to take action to prevent common diseases.
2. Vital prevention measures should be carried out strictly in all types of poultry activity.
3. Serological examination of routine action is necessary to monitor any possible epidemics and officials from the speed to take appropriate measures to control the epidemic and control it and prevent its spread if it occurs.
4. In the case of epidemics in any country can be borne wild birds and migratory birds should follow up on these birds and testing Serological her routine to monitor the presence of antibodies to those diseases.
5. Immunization Balaatarat isolated from field cases necessary action on the farms surrounding the affected farm, which lies outside the region that are taking action to get rid of herds infected with highly pathogenic HPAI Balaatarat In all farms around the infected farm field Balaatarat medium intensity MPAI
Organizations recommended that the three global WHO, OIE & FAO these precautions in affected countries:
1. Testing on humans should be exposed to include the duck, as it is with the risk of infected poultry and dead.
2. Rights should take precautions as in the case of exposure to poultry infected with the apparently healthy ducks.
3. Education should not be allowed home for the ducks.
4. Sources of drinking man should be the water is not frequented by ducks and stored in a manner to prevent access to the ducks.
5. Equipped with well-cooked duck meat and duck eggs do not represent a risk to human
6. Exposure to the most dangerous to humans is during the home slaughtering and processing before cooking.
The organizations also pointed to the role played by ducks in the transmission cycle of H5N1 strain and that there is a great need to do research on the phenomenon of non-infection in ducks.
* Should be the FAO, OIE to develop long-term strategy to control the current strain
* Must be fundamental changes in poultry farming systems, particularly in rural areas
* The continuing investigation in animals is the key to control the infection and prevention of this investigation should be strengthened and intensified.
Should know that:
1. Trading a healthy poultry prevents or reduces the chance of transmission of influenza between the farmer and also for the human being and that of handling and eating poultry meat and eggs cooked does not transmit the disease.
2. The virus of avian influenza viruses and most can be eliminated easily by
* Washing hands with soap and water
* The use of disinfectants available homes and farms
* Use of materials such as acid anhydride used in homes for the work of the authorities and other destroys the virus
* The spraying a dilute solution of iodine 1 cm / L in the wards and around enough to eradicate the virus by imposing presence in the air.
Why is the bird flu risk to public health?
Disease is at present a specific threat geographically linked to direct contact with birds, but the property of these viruses in the formation of false patterns. Through mutation and the possibility of pigs and humans play the role of the mixing bowl and make a dent emergence of new patterns more dangerous than SARS.
With respect to the position of Arab Republic of Egypt from the disease, it has been taken the following actions:
Issuance of ministerial decisions in this regard:
1. Ministerial Decree No. 1536 of the year 2004 the position of import of poultry and poultry products from Asia and countries affected by bird flu
2. Ministerial Decree No. 1327 for the year in 2005 to stop the importation of fodder origin poultry
3. Ministerial Decree No. 1326 of the year in 2005 stopping the importation of chicks and poultry from all countries of the world for 3 months and re-innovation in accordance with the position of the global epidemic
4. Ministerial Decree No. 1389 for the year in 2005 to prevent the import of birds and feathers Poultry waste used in the manufacture of fodder concentrates
5. Ministerial Decree No. 168 of 2005 permits the prohibition of hunting and a ban on hunting of birds and migratory Albraio of the Year 2005/2006
6. Decision of the Prime Minister to prevent hunting of migratory birds.
Hold training courses for veterinarians directorates for training on monitoring and surveillance and the role of migratory birds in the transmission of the disease and immediate actions to be taken in case of suspicion of the disease.
Preparation of a scientific bulletin on avian influenza for doctors and other simple bulletin on the disease to poultry farmers
Joint meetings with the responsible authorities such as the Ministry of Health and the Ministry of Environment to determine the responsibilities and coordination between these actors.
Agreement with both:
* Food and Agriculture Organization for the accession of Egypt to the early warning countries of the Near East
* American project for the infrastructure to support Egypt's efforts in monitoring procedures, surveillance, prevention and control.
Convene a meeting of directors of directorates in the governorates of Veterinary Medicine to inform them of the current situation of the disease and the measures taken by the authority and role of the Directorate of Veterinary Medicine in the implementation of these procedures.
Limited to poultry farms and Arab Republic of Egypt is divided into:
* High-risk areas (15 counties)
* Medium-risk areas (8 provinces)
* Low-risk areas (4 provinces)
According to the population density of migratory birds to those provinces and to establish priorities for surveillance and control
Develop and implement a plan of survey Field and laboratory, with the formation of committees to collect samples from migratory birds in the governorates of coastal as well as poultry farms and note any symptoms may appear by The Commissions started their work as of 23/10/2005 and the results of examination of samples that have been withdrawn according to the non-existence of the disease in Egypt until the date of 02/17/2006.
A meeting between the Commission and representatives of the General Federation of Producers of poultry and poultry disease specialist teachers colleges of veterinary medicine and research institutes and the Institute for vaccine production where it was agreed the following recommendations:
1. Prevention of breeding birds on the roofs of houses, homes, barns and open around the homes of peasants, chickens and ducks roaming on the canals.
2. Hygienic disposal of the dead in a scientific manner by the concerned authorities through deep burial
3. Legislation (Ministerial Decree) to collect the amount of twenty pounds for each ton of maize or soybeans to be imported and placed in a special fund costs of the security program and biosecurity of poultry farms.
4. Legislation (Ministerial Decree) to compensate the affected farms and veterinary authorities have taken the decision to execute the poultry in the event of an outbreak of bird flu.
5. Legislation (Ministerial Decree) to prevent the transfer of live poultry between provinces and limited trading in poultry slaughtered only
6. The speed of the potential for a Research Institute of vaccine production to produce a vaccine against avian flu.
A. Was formed several specialized committees of the General Authority for Veterinary Services Authority poultry specialists, institutes and universities to determine the actions to be taken to prevent the disease from entering the country as well as actions required in the case of entry and recommended the following:
Determine how the reporting of the disease? And actions taken in case of suspicion of injury and reported to the departments of veterinary medicine in the governorates, as the alarm on the veterinary departments of all provinces need to quickly inform the General Authority for Veterinary Services in the case of suspicion of the presence of bird flu (sudden death more than 30% of the herd during the period of time 3 days + virtual symptoms of the disease + anatomical lesions which refers to the suspected presence of disease) in order to be able to take all measures necessary for the diagnosis and control and prevention in the case of God forbid occur (reported to district)
B. Formed a scientific committee of specialists poultry Authority, colleges and universities to determine the required samples and methods of screening and diagnosis in the case of suspicion of the presence of bird flu.
T.. Contact was the world reference laboratory for providing the Arab Republic of Egypt Balaatarat work necessary for a vaccine has been coordinated with the Research Institute of serums and vaccines Abbasia to speed processing in the case of vaccine needed to vaccinate poultry.
7. The General Authority for Veterinary Services (Directorate General of epidemics and diseases of poultry) to monitor the disease locally and internationally with some of the scientific centers (Research Unit of the U.S. Navy "example 3" in cooperation with the Ministry of Environment in migratory birds - National Laboratory for control of poultry in collaboration with the Academy of Scientific Research in domestic birds - Some veterinary colleges to universities and research centers on migratory birds and local) that collects samples from migratory birds and domestic birds and the work of the laboratory tests where the results of these tests proved the absence of highly pathogenic strain in the Arab Republic of Egypt.
8. Body (General Directorate for Epidemiology and Poultry Diseases) following the development of the spread of bird flu virus in all around the world to take the necessary measures to prevent entry into the country immediately, through international organizations, the three OIE, FAO, WHO and international information network and other means of publishing a daily basis.
9. The General Authority for Veterinary Services to the work program of finding a permanent avian flu in the Arab Republic of Egypt in conjunction with the National Laboratory for control of poultry to prevent the disease from entering the country by migratory birds or any other means tightly control the lessee on the ports so as to ensure the protection of livestock from pests and diseases Expat and non-diversion of the country with the speed to take the necessary measures to prevent the spread of the disease and control in case it occurs
Kingdom of Saudi Arabia
Ministry of Higher Education
University of Northern Border
Faculty of Engineering


Briefly introduce the concept of wildlife safaris and their popularity among adventure seekers and nature enthusiasts.
Highlight the diversity and richness of Asia’s wildlife and the continent’s appeal as a safari destination.
Kaziranga National Park, India
Describe the unique ecosystem and wildlife found in Kaziranga National Park.
Highlight the park’s population of the iconic one-horned rhinoceros.
Discuss the opportunities for elephant safaris and birdwatching in the park.
Mention the best time to visit for optimal wildlife sightings.
Ranthambore National Park, India
Discuss the historical significance of Ranthambore and its transformation into a wildlife sanctuary.
Focus on the park’s population of Royal Bengal tigers and their conservation efforts.
Explain the various safari options, including jeep safaris and canter safaris.
Talk about the picturesque landscape and the fort within the park.
Yala National Park, Sri Lanka
Highlight the diverse range of wildlife species found in Yala National Park.
Discuss the park’s population of leopards and the chance to spot these elusive creatures.
Describe the safari experiences offered, such as jeep safaris and camping.
Discuss the park’s proximity to beautiful coastal areas for a complete wildlife and beach vacation.
Taman Negara National Park, Malaysia
Introduce Taman Negara National Park as one of the oldest rainforests in the world.
Describe the incredible biodiversity and unique flora and fauna found in the park.
Discuss the various activities available, such as jungle trekking, night safaris, and river cruises.
Mention the indigenous culture and the opportunity to learn about local communities.
Chitwan National Park, Nepal
Discuss Chitwan National Park’s UNESCO World Heritage status and its importance for conservation.
Describe the park’s diverse wildlife, including the endangered Bengal tiger and one-horned rhinoceros.
Talk about the elephant safaris and canoe rides along the Rapti River.
Highlight the Tharu culture and the chance to experience their traditional lifestyle.
Kinabatangan Wildlife Sanctuary, Borneo
Describe the unique ecosystem of Kinabatangan Wildlife Sanctuary, including the mangrove forests and oxbow lakes.
Discuss the sanctuary’s population of proboscis monkeys, orangutans, and pygmy elephants.
Explain the opportunities for river cruises and night safaris to spot wildlife.
Mention the conservation efforts and eco-lodges available for visitors.
Embarking on a wildlife safari is an exhilarating experience that allows adventure seekers and nature enthusiasts to immerse themselves in the untamed beauty of the natural world. From the majestic creatures that roam the plains to the vibrant ecosystems that support a wide array of flora and fauna, Asia offers an enticing selection of destinations for safari lovers. This blog will delve into some of the top wildlife destinations in Asia, each offering a unique glimpse into the continent’s rich biodiversity and captivating landscapes.
Kaziranga National Park, India: The Realm of the One-Horned Rhinoceros
Nestled in the northeastern state of Assam, Kaziranga National Park stands as a testament to India’s commitment to wildlife conservation. Boasting a unique ecosystem of tall elephant grass, dense forests, and marshy swamps, the park provides a sanctuary for a remarkable diversity of wildlife. The crown jewel of Kaziranga is undoubtedly the one-horned rhinoceros, with the park hosting the largest population of this iconic species in the world. Visitors can embark on thrilling elephant safaris to get up close to these magnificent creatures while also enjoying the opportunity for birdwatching as Kaziranga is a haven for avian species. To make the most of the wildlife sightings, the best time to visit is from November to April, when the park is accessible and the animals are more active.
Ranthambore National Park, India: In the Footsteps of Royal Bengal Tigers
Ranthambore National Park, situated in the state of Rajasthan, holds a significant place in India’s wildlife conservation efforts. Once a hunting ground for maharajas, it has now transformed into a thriving wildlife sanctuary. The park’s main attraction is its population of Royal Bengal tigers, offering visitors a rare chance to witness these majestic predators in their natural habitat. Safaris in Ranthambore come in the form of exciting jeep safaris or canter safaris, where knowledgeable guides navigate through the park’s rugged terrain, increasing the chances of tiger sightings. Besides the captivating wildlife, Ranthambore is adorned with picturesque landscapes, dotted with ancient ruins, including the iconic Ranthambore Fort that adds a touch of history to the safari experience.
Yala National Park, Sri Lanka: Leopards and Coastal Charms
Located on the southeastern coast of Sri Lanka, Yala National Park is a wildlife enthusiast’s paradise. Renowned for its diverse range of wildlife species, Yala offers an unforgettable safari experience. The park is home to the elusive leopard, with Yala having one of the highest densities of leopards in the world. As visitors traverse the park’s untamed wilderness on thrilling jeep safaris, they have the opportunity to spot these graceful cats in their natural habitat. Yala National Park’s allure extends beyond its wildlife wonders, as it is situated near beautiful coastal areas. This makes it a perfect destination for those seeking a blend of wildlife adventure and serene beachside relaxation.
Taman Negara National Park, Malaysia: Unveiling the Ancient Rainforest
Venturing into Taman Negara National Park in Malaysia is like stepping back in time. As one of the oldest rainforests in the world, this sprawling wilderness showcases unparalleled biodiversity and a rich tapestry of unique flora and fauna. The park offers a range of activities for visitors, including thrilling jungle trekking trails, enchanting night safaris to observe nocturnal creatures, and mesmerizing river cruises along the meandering waterways. Taman Negara is not only a haven for wildlife enthusiasts but also an opportunity to learn about the indigenous culture of the Orang Asli people who call this ancient rainforest home.
Chitwan National Park, Nepal: Where Conservation Meets Cultural Heritage
Designated as a UNESCO World Heritage site, Chitwan National Park in Nepal is a testament to the importance of preserving fragile ecosystems and protecting endangered species. The park’s diverse wildlife includes the Bengal tiger and the one-horned rhinoceros, both of which have faced severe threats to their survival. Visitors to Chitwan can participate in elephant safaris, traversing through dense grasslands and lush forests in search of these remarkable creatures. Additionally, tranquil canoe rides along the Rapti River offer glimpses of aquatic species and the park’s stunning natural beauty. Chitwan National Park also provides an opportunity to immerse oneself in the Tharu culture, an indigenous community known for their harmonious relationship with nature. Experiencing their traditional lifestyle adds a unique cultural dimension to the wildlife adventure.
Kinabatangan Wildlife Sanctuary, Borneo: Exploring the Biodiversity of the Mangrove Ecosystem
Nestled in the heart of Borneo, the Kinabatangan Wildlife Sanctuary captivates visitors with its remarkable and fragile ecosystem. The sanctuary is characterized by dense mangrove forests, winding rivers, and oxbow lakes that serve as vital habitats for an array of wildlife. Visitors have the chance to encounter proboscis monkeys swinging through the treetops, orangutans hanging from branches, and pygmy elephants gracefully moving along the riverbanks. River cruises and night safaris offer immersive experiences to witness these incredible creatures in action. Kinabatangan Wildlife Sanctuary’s commitment to conservation is evident through its various conservation efforts and eco-lodges that provide sustainable accommodation options for visitors.
Asia’s top wildlife destinations offer an escape into untamed beauty and the chance to witness extraordinary creatures in their natural habitats. From the vast grasslands of Kaziranga to the ancient rainforests of Taman Negara, these destinations provide captivating safari experiences that awaken a sense of wonder and appreciation for the natural world. Whether it’s spotting the elusive one-horned rhinoceros, tracking Royal Bengal tigers, or immersing in the diverse ecosystems of mangroves and rainforests, Asia’s wildlife safaris promise unforgettable adventures. Embark on a journey through these wildlife havens, support their conservation efforts, and create memories that will last a lifetime.


Did you know women are more likely to be diagnosed with anxiety and depression than men? They are also more likely to develop Alzheimer’s disease – ⅔ of people suffering from this disease are women. Could it be that women live longer and are therefore more likely to go on to develop Alzheimers? Or is it something else?
The key thing, according to Lisa Marconi and the women’s brain institute research, is that women’s brains age differently and menopause is the key to understanding why that is.
Remember that the brain is in constant communication with the rest of the body – part of which is the reproductive system which is crucial to brain ageing due to the hormones – men have more testosterone and women more estrogen, but the main issue is that although testosterone gradually declines as men get older, estrogen takes a precipitous drop in women as they go through menopause.
Hot flushes, night sweats, anxiety, memory lapses, insomnia, depression – all common symptoms associated with menopause – all start in the brain. How is that? The brain and ovaries are part of the neuro-endocrine system – which means there is constant communication between the brain and the ovaries. When the ovaries function starts to decline in menopause, estrogen levels drop – estrodial is a key hormone that facilitates energy production in the brain by pushing the neurons to burn glucose. So while estrogen is high, brain energy is high, when estrogen is low, the neurons slow down and age faster. Studies have shown that this leads to the plaques that are associated with Azheimers disease. Some brain regions are more affected than others.
The hypothalamus is in charge of temperature regulation – cue hot flushes and night wears. The brain stem is in charge of your sleep pattern – cue insomnia. The amygdala – responsible for emotion – cue anxiety and depression/ mood swings. The hippocampus which is the memory center of the brain – cue forgetting your children’s names, or even how to do basic tasks.
PET scans show that the brain energy levels drop around 30% in women once they have gone through menopause – this is independent of age – which will account for so many of the symptoms women go through during menopause. This is really crazy making as your brain is going through a transition and adjustments need to be made – even if we show no cognitive difference to men, how hard it is for us to do those tasks certainly is different! Cue ‘tired all the time’!
Certain scans also show that the amyloid plaques (associated with Alzheimers) increase with 20% during menopause. This is a risk factor rather than a definitive cause. We need to bear this is mind when women are going through menopause – whether natural or surgical which can often be years earlier. Studies show that removal of the uterus, but more so the ovaries, correlate with a higher risk of dementia in women. Although this is surely upsetting news for women – knowledge is power and there is much that can be done to offset this effect and protect our brains.
Should we take HRT? Although helpful for many of the symptoms of menopause, it is not currently recommended for dementia prevention, but many studies are under way in this field so hopefully we will see a change in this in years to come.
Lifestyle seems to be the best known way to help protect the brain – what foods we eat, how much sleep we get, how much exercise we get, how much stress we have in our lives all impact our hormone levels and therefore our brain health.
The best diet for hormone health seems to be the Mediterranean diet – women on this diet have a much lower risk of cognitive decline, cardiovascular disease, mood disorders, cancer and less hot flashes to boot. It is rich in foods that are rich in phytoestrogens – foods like flax seeds, sesame seeds, dried apricots, legumes, berries and melons – and don’t forget dark chocolate!
Then avoiding things like stress that can bring cortisol levels up which takes estrogen levels down as they work in balance with each other. So having a mindfulness practice or going for that walk or workout after a stressful day can be really helpful in protecting your brain and boosting your feel good hormones at the same time!
Remember, we are here to help – if you need some help in managing your menopausal symptoms, we offer individual education, acupuncture and lifestyle advice and support to get you back on track. The women’s health discovery session is aimed at looking at all of you and helping you make a plan that gets you back to thriving at life rather than just surviving!


There are several kinds of treatment available for doing away with spider veins or the thin red lines or the network of blood vessels.
Actually speaking, spider veins are not harmful, per se. However, they can result in aching or burning sensation. There are different kinds of treatment available to treat this condition.
What is sclerotherapy?
This is a process by which the physician or surgeon injects a chemical into the veins which scar and closes the veins. With this, the blood then gets re-routed towards other and more healthy veins. Within a duration of a few weeks, the spider veins fade out. However, this treatment may need to be performed more than once. Nonetheless, if done properly, this line procedure is usually successful. No local or general anesthesia is required to be administered for this treatment. There may be a few side effects of the procedure. These are: swelling, itching, and skin color change.
How is laser surgery performed?
Laser surgery is done by thrusting in powerful doses of light into the vein. With time, the vein disappears away. For this, no cuts are required to be made. However, this treatment may not be as effective as sclerotherapy and more so if larger veins are being treated. This also results in some side effects like redness, bruising, itching, swelling and changes in skin color. Blood vessels treated with this procedure may fade out but will not totally disappear. In addition, new spider veins can also come up.
How can spider veins form?
Spider veins, actually speaking, are a minor variant of varicose veins and can be a precursor to them. Exposure to the sun can cause a worsening of this condition. A number of reasons can lead to this condition. These could be heredity; if you working as a nurse, hair stylist or a teacher who needs to stand for a long time while working; during pregnancy, puberty and menopause when there is a fluctuation of hormones; if one is on birth control pills; during postmenopausal hormonal replacement; if one has a history of blood clots, if there is undue pressure in the abdominal area due to tumors, constipation et al. Spider veins can also form if a person has undergone severe trauma of some kind or has had a skin injury or a vein surgery.
It is a fact that varicose and spider veins are more commonly found in women than in men. Also, the chances of their occurrence are more with increasing age. In accordance with available data, it is estimated that about 30 to 60 percent of all adults suffer from a condition of either varicose or spider veins. As per data from the US Department of Health and Human Services’ Office on Women’s Health, it is reported that about 55 percent of all women have some type of vein issue or another.
For details, contact: Center for Cosmetic Dermatology. Phone: 717-741-5512.


All available TRiP-CRISPR guide RNA lines are listed here. The insertions must be combined with a source of Cas9 to induce gene knockout or overexpression. See the TRiP-CRISPR toolbox for a list of available stocks with both Cas9 and a GAL4 driver.
There are two TRiP-CRISPR gRNA stock collections (for specifics, please see the TRiP in vivo CRISPR site):
TRiP-CRISPR Overexpression (TRiP-OE) - activate expression of the target gene in somatic and/or germline cells by crossing to a line expressing GAL4 and dCas9-VPR
TRiP-CRISPR KnockOut (TRiP-KO) - generate indels (small insertion or deletion mutations) in somatic and/or germline cells by crossing to a line expressing GAL4 and Cas9
TRiP-CRISPR lines are generated in either pCFD3 or pCFD4 vectors (Port et al., 2014) which are designed to ubiquitiously express either one or two sgRNAs, respectively. Both vectors contain attB sites for phiC31-recombination, as well as the vermillion selection marker. In pCFD3, a single sgRNA is driven by the snRNA:U6:96Ac (U6:3) promoter and in pCFD4 the sgRNAs are driven by snRNA:U6:96Aa (U6:1) and snRNA:U6:96Ac. Detailed descriptions of these vectors are available at the CRISPR Fly Design site.
The TRiP encourages the community to nominate genes for TRiP-OE and TRiP-KO production via the TRiP sgRNA Database. If use of any of the TRiP-CRISPR stocks results in data used in a publication, please cite the TRiP in your publication.
** If indicated, this insertion targets more than one gene. To see the other targets, either search this page with the stock number or click on the stock number to read the stock report.


Talk delivered at the American Museum of Natural History, 23 April 2002 at a discussion titled “Evolution or Intelligent Design?” The participants included ID proponents William A. Dembski and Michael J. Behe as well as evolutionists Kenneth R. Miller and Robert T. Pennock. Eugenie C. Scott moderated the discussion. An introduction was given by National History Editor, Richard Milner. For coverage of this debate, see Scott Stevens’ article in The Cleveland Plains Dealer.
Evolutionary biology teaches that all biological complexity is the result of material mechanisms. These include principally the Darwinian mechanism of natural selection and random variation, but also include other mechanisms (symbiosis, gene transfer, genetic drift, the action of regulatory genes in development, self-organizational processes, etc.). These mechanisms are just that: mindless material mechanisms that do what they do irrespective of intelligence. To be sure, mechanisms can be programmed by an intelligence. But any such intelligent programming of evolutionary mechanisms is not properly part of evolutionary biology.
Intelligent design, by contrast, teaches that biological complexity is not exclusively the result of material mechanisms but also requires intelligence, where the intelligence in question is not reducible to such mechanisms. The central issue, therefore, is not the relatedness of all organisms, or what typically is called common descent. Indeed, intelligent design is perfectly compatible with common descent. Rather, the central issue is how biological complexity emerged and whether intelligence played a pivotal role in its emergence.
Suppose, therefore, for the sake of argument that intelligence — one irreducible to material mechanisms — actually did play a decisive role in the emergence of life’s complexity and diversity. How could we know it? To answer this question, let’s run a thought experiment. Imagine that Alice is sending Bob encrypted messages over a communication channel and that Eve is eavesdropping. For simplicity let’s assume all the signals are bit strings. How could Eve know that Alice is not merely sending Bob random coin flips but meaningful messages?
To answer this question, Eve will require two things: First, the bit strings sent across the communication channel need to be reasonably long — in other words, they need to be complex. If not, chance can readily account for them. Just as there’s no way to reconstruct a piece of music given just one note, so there is no way to preclude chance for a bit string that consists of only a few bits. For instance, there are only eight strings consisting of three bits, and chance readily accounts for any of them.
There’s a second requirement for Eve to know that Alice is not sending Bob random gibberish: Eve needs to observe a suitable pattern in the signal Alice sends Bob. Even if the signal is complex, it may exhibit no pattern characteristic of intelligence. Flip a coin enough times, and you’ll observe a complex sequence of coin tosses. But that sequence will exhibit no pattern characteristic of intelligence. For cryptanalysts like Eve, observing a pattern suitable for identifying intelligence amounts to finding a cryptographic key that deciphers the message. Patterns suitable for identifying intelligence I call specifications.
In sum, Eve requires both complexity and specification to infer intelligence in the signals Alice is sending to Bob. This combination of complexity and specification, or specified complexity as I call it, is the basis for design inferences across numerous special sciences, including archaeology, cryptography, forensics, and the Search for Extraterrestrial Intelligence (SETI). I detail this in my book The Design Inference, a peer-reviewed statistical monograph that appeared with Cambridge University Press in 1998.
So, what’s all the fuss about specified complexity? The actual term specified complexity is not original with me. It first occurs in the origin-of-life literature, where Leslie Orgel used it to describe what he regards as the essence of life. That was thirty years ago. More recently, in 1999, surveying the state of origin-of-life research, Paul Davies remarked: “Living organisms are mysterious not for their complexity per se, but for their tightly specified complexity” (The Fifth Miracle, p. 112).
Orgel and Davies used specified complexity loosely. In my own research I’ve formalized it as a statistical criterion for identifying the effects of intelligence. For identifying the effects of animal, human, and extraterrestrial intelligence the criterion works just fine. Yet when anyone attempts to apply the criterion to biological systems, all hell breaks loose. Let’s consider why.
Evolutionary biologists claim to have demonstrated that design is superfluous for understanding biological complexity. The only way to actually demonstrate this, however, is to exhibit material mechanisms that account for the various forms of biological complexity out there. Now, if for every instance of biological complexity some mechanism could readily be produced that accounts for it, intelligent design would drop out of scientific discussion. Occam’s razor, by proscribing superfluous causes, would in this instance finish off intelligent design quite nicely.
But that hasn’t happened. Why not? The reason is that there are plenty of complex biological systems for which no biologist has a clue how they emerged. I’m not talking about handwaving just-so stories. Biologists have plenty of those. I’m talking about detailed testable accounts of how such systems could have emerged. To see what’s at stake, consider how biologists propose to explain the emergence of the bacterial flagellum, a molecular machine that has become the mascot of the intelligent design movement.
Howard Berg at Harvard calls the bacterial flagellum the most efficient machine in the universe. The flagellum is a nano-engineered outboard rotary motor on the backs of certain bacteria. It spins at tens of thousands of rpm, can change direction in a quarter turn, and propels a bacterium through its watery environment. According to evolutionary biology it had to emerge via some material mechanism. Fine, but how?
The usual story is that the flagellum is composed of parts that previously were targeted for different uses and that natural selection then co-opted to form a flagellum. This seems reasonable until we try to fill in the details. The only well-documented examples that we have of successful co-optation come from human engineering. For instance, an electrical engineer might co-opt components from a microwave oven, a radio, and a computer screen to form a working television. But in that case, we have an intelligent agent who knows all about electrical gadgets and about televisions in particular.
But natural selection doesn’t know a thing about bacterial flagella. So how is natural selection going to take extant protein parts and co-opt them to form a flagellum? The problem is that natural selection can only select for pre-existing function. It can, for instance, select for larger finch beaks when the available nuts are harder to open. Here the finch beak is already in place and natural selection merely enhances its present functionality. Natural selection might even adapt a pre-existing structure to a new function; for example, it might start with finch beaks adapted to opening nuts and end with beaks adapted to eating insects.
But for co-optation to result in a structure like the bacterial flagellum, we are not talking about enhancing the function of an existing structure or reassigning an existing structure to a different function, but reassigning multiple structures previously targeted for different functions to a novel structure exhibiting a novel function. The bacterial flagellum requires around fifty proteins for its assembly and structure. All these proteins are necessary in the sense that lacking any of them, a working flagellum does not result.
The only way for natural selection to form such a structure by co-optation, then, is for natural selection gradually to enfold existing protein parts into evolving structures whose functions co-evolve with the structures. We might, for instance, imagine a five-part mousetrap consisting of a platform, spring, hammer, holding bar, and catch evolving as follows: It starts as a doorstop (thus consisting merely of the platform), then evolves into a tie-clip (by attaching the spring and hammer to the platform), and finally becomes a full mousetrap (by also including the holding bar and catch).
Ken Miller finds such scenarios not only completely plausible but also deeply relevant to biology (in fact, he regularly sports a modified mousetrap cum tie-clip). Intelligent design proponents, by contrast, regard such scenarios as rubbish. Here’s why. First, in such scenarios the hand of human design and intention meddles everywhere. Evolutionary biologists assure us that eventually they will discover just how the evolutionary process can take the right and needed steps without the meddling hand of design.
But all such assurances presuppose that intelligence is dispensable in explaining biological complexity. The only evidence we have of successful co-optation, however, comes from engineering and confirms that intelligence is indispensable in explaining complex structures like the mousetrap and by implication the flagellum. Intelligence is known to have the causal power to produce such structures. We’re still waiting for the promised material mechanisms.
The other reason design theorists are less than impressed with co-optation concerns an inherent limitation of the Darwinian mechanism. The whole point of the Darwinian selection mechanism is that you can get from anywhere in configuration space to anywhere else provided you can take small steps. How small? Small enough that they are reasonably probable. But what guarantee do you have that a sequence of baby-steps connects any two points in configuration space?
Richard Dawkins compares the emergence of biological complexity to climbing a mountain — Mount Improbable, as he calls it. According to him, Mount Improbable always has a gradual serpentine path leading to the top that can be traversed in baby-steps. But that’s hardly an empirical claim. Indeed, the claim is entirely gratuitous. It might be a fact about nature that Mount Improbable is sheer on all sides and getting to the top from the bottom via baby-steps is effectively impossible. A gap like that would reside in nature herself and not in our knowledge of nature (it would not, in other words, constitute a god-of-the-gaps).
The problem is worse yet. For the Darwinian selection mechanism to connect point A to point B in configuration space, it is not enough that there merely exist a sequence of baby-steps connecting the two. In addition, each baby-step needs in some sense to be “successful.” In biological terms, each step requires an increase in fitness as measured in terms of survival and reproduction. Natural selection, after all, is the motive force behind each baby-step, and selection only selects what is advantageous to the organism. Thus, for the Darwinian mechanism to connect two organisms, there must be a sequence of successful baby-steps connecting the two.
Again, it is not enough merely to presuppose this — it must be demonstrated. For instance, it is not enough to point out that some genes for the bacterial flagellum are the same as those for a type III secretory system (a type of pump) and then handwave that one was co-opted from the other. Anybody can arrange complex systems in a series. But such series do nothing to establish whether the end evolved in a Darwinian fashion from the beginning unless the probability of each step in the series can be quantified, the probability at each step turns out to be reasonably large, and each step constitutes an advantage to the organism (in particular, viability of the whole organism must at all times be preserved).
Convinced that the Darwinian mechanism must be capable of doing such evolutionary design work, evolutionary biologists rarely ask whether such a sequence of successful baby-steps even exists; much less do they attempt to quantify the probabilities involved. I attempt that in chapter 5 of my most recent book No Free Lunch. There I lay out techniques for assessing the probabilistic hurdles that the Darwinian mechanism faces in trying to account for complex biological structures like the bacterial flagellum. The probabilities I calculate — and I try to be conservative — are horrendous and render natural selection entirely implausible as a mechanism for generating the flagellum and structures like it.
If I’m right and the probabilities really are horrendous, then the bacterial flagellum exhibits specified complexity. Furthermore, if specified complexity is a reliable marker of intelligent agency, then systems like the bacterial flagellum bespeak intelligent design and are not solely the effect of material mechanisms.
It’s here that critics of intelligent design raise the argument-from-ignorance objection. For something to exhibit specified complexity entails that no known material mechanism operating in known ways is able to account for it. But that leaves unknown material mechanisms. It also leaves known material mechanisms operating in unknown ways. Isn’t arguing for design on the basis of specified complexity therefore merely an argument from ignorance?
Two comments to this objection: First, the great promise of Darwinian and other naturalistic accounts of evolution was precisely to show how known material mechanisms operating in known ways could produce all of biological complexity. So at the very least, specified complexity is showing that problems claimed to be solved by naturalistic means have not been solved. Second, the argument from ignorance objection could in principle be raised for any design inference that employs specified complexity, including those where humans are implicated in constructing artifacts. An unknown material mechanism might explain the origin of the Mona Lisa in the Louvre, or the Louvre itself, or Stonehenge, or how two students wrote exactly the same essay. But no one is looking for such mechanisms. It would be madness even to try. Intelligent design caused these objects to exist, and we know that because of their specified complexity.
Specified complexity, by being defined relative to known material mechanisms operating in known ways, might always be defeated by showing that some relevant mechanism was omitted. That’s always a possibility (though as with the plagiarism example and with many other cases, we don’t take it seriously). As William James put it, there are live possibilities and then again there are bare possibilities. There are many design inferences which, to question or doubt, require invoking a bare possibility. Such bare possibilities, if realized, would defeat specified complexity. But defeat specified complexity in what way? Not by rendering the concept incoherent but by dissolving it.
In fact, that is how Darwinists, complexity theorists, and anyone intent on defeating specified complexity as a marker of intelligence usually attempts it, namely, by showing that it dissolves once we have a better understanding of the underlying material mechanisms that render the object in question reasonably probable. By contrast, design theorists argue that specified complexity in biology is real: that any attempt to palliate the complexities or improbabilities by invoking as yet unknown mechanisms or known mechanisms operating in unknown ways is destined to fail. This can in some cases be argued convincingly, as with Michael Behe’s irreducibly complex biochemical machines and with biological structures whose geometry allows complete freedom in possible arrangements of parts.
Consider, for instance, a configuration space comprising all possible character sequences from a fixed alphabet (such spaces model not only written texts but also polymers like DNA, RNA, and proteins). Configuration spaces like this are perfectly homogeneous, with one character string geometrically interchangeable with the next. The geometry therefore precludes any underlying mechanisms from distinguishing or preferring some character strings over others. Not material mechanisms but external semantic information (in the case of written texts) or functional information (in the case of polymers) is needed to generate specified complexity in these instances. To argue that this semantic or functional information reduces to material mechanisms is like arguing that Scrabble pieces have inherent in them preferential ways they like to be sequenced. They don’t. Michael Polanyi offered such arguments for biological design in the 1960s.
In summary, evolutionary biology contends that material mechanisms are capable of accounting for all of biological complexity. Yet for biological systems that exhibit specified complexity, these mechanisms provide no explanation of how they were produced. Moreover, in contexts where the causal history is independently verifiable, specified complexity is reliably correlated with intelligence. At a minimum, biology should therefore allow the possibility of design in cases of biological specified complexity. But that’s not the case.
Evolutionary biology allows only one line of criticism, namely, to show that a complex specified biological structure could not have evolved via any material mechanism. In other words, so long as some unknown material mechanism might have evolved the structure in question, intelligent design is proscribed. This renders evolutionary theory immune to disconfirmation in principle, because the universe of unknown material mechanisms can never be exhausted. Furthermore, the evolutionist has no burden of evidence. Instead, the burden of evidence is shifted entirely to the evolution skeptic. And what is required of the skeptic? The skeptic must prove nothing less than a universal negative. That is not how science is supposed to work.
Science is supposed to pursue the full range of possible explanations. Evolutionary biology, by limiting itself to material mechanisms, has settled in advance which biological explanations are true apart from any consideration of empirical evidence. This is arm-chair philosophy. Intelligent design may not be correct. But the only way we could discover that is by admitting design as a real possibility, not ruling it out a priori. Darwin himself agreed. In the Origin of Species he wrote: “A fair result can be obtained only by fully stating and balancing the facts and arguments on both sides of each question.”


There are over 22 types of headaches and everyone gets one from time to time. Nowadays it being a symptom of Covid19 it’s important to be extra aware of them along with other symptoms. If it’s reoccurring and progressively worsens its best to consult your medical professional since outside of the current wave of covid, headaches can be an alarm for brain and neurological issues that could be serious.
On the flip side a headache could very well just be a headache caused by stress, tension, anxiety, fatigue, low or high blood sugar, sinusitis, allergies, vitamin deficiencies, constipation, hunger, hormonal imbalances, caffeine consumption, perfumes, alcohol and other irritants.
Headache experts do estimate that about 90% of all headaches are tension headaches (caused by muscular tension) and we often grab our go to over the counter headache medicines to temporarily solve the discomfort.
It’s important to know that its better to treat the cause of the headache vs the symptom and that long over reliance on asprin and acetaminophen and other painkillers can interfere with your brains’ natural ability to fight headaches.
However adding a regiment of certain nutrients and herbs can potentially help quiet and or eliminate headaches and the deficiencies that are causing them .
Some of the nutrients include:
Calcium and Magnesium to relax the muscles.
Coenzyme Q10 to oxygenate the tissues and detox many dangerous substances that may be causing the headache.
Bromelain helps regulate the inflammatory response.
Vitamin B3 and B Complex together improve circulation aids nervous system and removes excess water from tissues.
Vitamin C aids in defense against harmful pollutants in the body and production of antistress hormones
Vitamin E improves circulation
Herbs that are helpful include:
Cayenne that thins blood which reduces pain and allows beneficial blood flow.
Chamomile relaxes muscles.
Ginkgo Biloba improves circulation to the brain.
Kava Kava for tension relief.
Scullcap has antispasmodic agents.
Valerian Root a good sedative.
Of course a good diet, ample water, m,oderate exercise and plenty of sleep is key for best health.
Experts say foods that contain tyramine can likely cause headache discomforts if you are over consuming them. Some of those foods include alcohol, bananas, cheese, chocolate, cold cuts, onions, pork, smoked foods, peanut butter, chicken, citrus fruits, dairy/sour cream vinegar, wine. Through process of elimination of these foods you may find your headache culprit.
( supplement regiment found in prescription for Nutritional Healing 4th edition)


“They tried to bury us, but they didn’t know we were seeds” is a powerful saying because it alludes to the promise of growth, to the potential of life despite the heavy weight piled on. After a period of dormancy, a seed’s growth is triggered by internal and external conditions. Only when the circumstances align are the seeds automated to begin their true act of defiance; to grow. That initial step is taken by the brave first organ to appear during germination; the radicle. Pronounced radical, it pushes through and grows downward into the soil, anchoring the seedling for its next phase of life.
The radicle, also known as the primary root, can then grow a network of roots or store food (like potatoes or carrots). Roots (for the most part) are what hold a plant to the dirt, what brace it to the earth. They feed and nurture the blooming and fruiting of plants. Roots themselves are sustenance and can heal through medicinal properties, but they can also be a force of disruption. As Daniel Murphy states, “A tiny seed finds its way into a small crack in the sidewalk. The radical emerges. Before you know it, a plant strong enough to push apart two concrete slabs has grown.”
Metaphorically, roots can refer to our ancestral history, culture, and traditions. A successful seed can traverse miles- carried by the wind, stuck on roaming creatures, floating in the sea. When seeds find themselves in new environments, “radicals rise up as radicles force themselves downward, rooting in new lives.” Like with flora, many of our ancestors and the individuals migrating now- rooting oneself is a radicle and natural act.
Rooted in the Lower Rio Grande Delta
The Valley is the land on which we stand, but it is also the ideological apparatus that has crafted us. Traditions and culture have shaped our ideas of community and informed our interaction with our environment. Dominant forces have divided us, these forces have separated us from our land, but our roots in this area are deep. They have been tended by indigenous/Tejanos, both our ancestors and contemporaries. They look like your tio, your grandma, your siblings, and you.
We’ve tilled these soils, harvested its bounty, and cared for our seedlings. Our work has amassed a rich history and knowledge. We’ve connected; through food, language, and love. We’ve shared recipes and remedios, work and its rewards.
We move like plants. Our seeds dispersed through the waves, carried by the wind over boundaries and barriers. They spread for miles in all directions. We’ve traveled far and wide for freedom, liberty, and the right to live comfortably. We aspire to labor and continue to tend to our roots. When we connect with these roots, we are able to cultivate cultural and institutional change.
Our roots aren’t stopped by the river, they’re reinforced and grow strong and dense. Only with water can we bloom, only in water do lotuses flower.


A life of constant burning pain
An individual with EB lacks a critical protein that binds the layers of skin together. Without this protein, the skin tears apart, blisters and sheers off, leading to severe pain, disfigurement, and constant gaping open wounds. EB affects the body inside and out. Blisters occur all over the body, as well as in the eyes, mouth, esophagus, and other internal organs. Living with EB is like living with third degree burns.
Sufferers can spend hours everyday being bandaged with dressings to protect and medicate their wounds. EB causes severe pain, disfigurement, and in too many cases, an early death from systemic failure, infection or from aggressive forms of skin cancer. And because most people have never heard of EB, a lack of research holds back an end to this devastating condition.


Benefits of Turmeric
Within turmeric, there’s a chemical called curcumin, its primary active component, which is the compound that most of its health benefits are attributed to. Curcumin is a natural antioxidant that has anti-inflammatory properties. Studies previously carried out even go so far as to say that, if the right amount is taken, curcumin can have greater anti-inflammatory effects than common medications taken for that purpose, such as aspirin.
Not only that, but it has been shown to potentially have anti-aging qualities as well as being a candidate for preventing Alzheimer’s disease and even depression. Cancer, heart disease, arthritis and diabetes are just a number of other potential areas where it’s use can be of great consequence.
To experience these benefits, however, it wouldn’t be sufficient to simply add turmeric to the occasional meal, but to employ the use of supplements.
It’s important to note that though it may be of use to the listed health issues, combining it with medication being taken for those specific issues should be avoided before consulting a doctor.
For example, there’s evidence that taking turmeric along with diabetes medication can lead to very low blood sugar levels. Turmeric also restricts your body absorbing iron, so combining it with iron supplements is not advised.
So, despite its benefits, turmeric is no different to many other helpful substances. Caution should always be applied before admitting it to your body.