Rezultat DNK testa Starchild-a...

Zabranjena_Arheologija

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http://www.abovetopsecret.com/forum/thread601690/pg1


O ovoj lobanji je bilo reci na Nacionalnoj geografiji. Stara je oko 900 godina.

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Lobanja zvezdanog deteta je jedinstvena lobanja otkrivena 1930.godine u Meksiku.Vlasnici lobanje Ray and Melanie Young su 1999.godine pozvali Lloyd Pye -a da prouci neobicnu lobanju.Inace,Lloyd Pye je istraživač sa preko 30 godina iskustva u pisanju i predavanju o poreklu života.Vodeći je zagovornik intervencionističke teorije o poreklu čoveka,koja je suprotna darvinistickoj i kreacionistickoj teoriji. Autor je knjiga Everything You Know is Wrong: Origins of Life and Humans (Sve što znate je pogrešno: poreklo života i ljudi) i The Starchild Skull: Genetic Enigma or Human–Alien Hybrid? (Lobanja Zvezdanog deteta: Genetska enigma ili ljudsko-vanzemaljski hibrid?).


Detaljnim analizama otkriveno je da je lobanja stara 900 godina,iskljucena je mogucnost deformiteta,utvrdjeno je da je lobanja upola tanja i upola laksa od normalne ljudske lobanje,ali je sa druge strane 2-3 puta tvrdja od ljudske lobanje.Ocne jabucice su dosta plitke,a oci su bile postavljene nisko.Vrat je dosta bio kratak i postavljen pod drugacijim uglom u odnosu na normalno ljudsko bice.Otvor na lobanji, koji se zove foramen magnum,bio je daleko od normalnog mesta. Donji stražnji deo bio je bez male kvrge koja se nalazi na svakoj ljudskoj glavi (kao i na glavama simpanza i gorila);nije imala inion.Ceo stražnji deo glave bio je ravan,ali nije bilo znakova manipulisanog spljošćavanja.




Pomislio je da možda drži očuvanu lobanju Sivog vanzemaljca,a na osnovu brojnih cudnij detalja otkrivenih na pronadjenoj lobanji.
Naime,brazdasto udubljenje na gornjem stražnjem delu se ne javlja kod ljudi.Ljudska lobanja je zaobljena na tom delu.
Takozvani «Sivi» («Grays») vanzemaljaci navodno imaju takvo udubljenje na stražnjem gornjem delu glave,što im daje karakterističan «srcolik» oblik. Deo gornje desne vilice (maxilla), pronađena je odvojeno od lobanje (kojoj je nedostajala čitava donja vilica).Bila je veličine vilice dojenčeta,ako ne i manja.To je biće očigledno imalo veoma mali donji deo lica,što su potvrdjivala i mesta na kojima su bili spojeni misici za zvakanje, daleko manja u odnosu na normalne kod ljudi.

2003.godine lobanja je bila podvrgnuta genetskom ispitivanju,sto je i bilo moguce,jer je bila odlicno ocuvana,a sve to zahvaljujuci tome sto nije bila izlozena uticajima spoljasne sredine(nadjena je u tunelu).Analiziranjem DNK lobanje utvrdjeno je da je osoba imala jednog roditelja ljudskog porekla,i to majku,za koju je utvrdjeno da je bila Indijanka,ali se nije moglo utvrditi poreklo oca.
Razvojem nove tehnologije proucavanja DNK-a,ocekuje se da ce do kraja 2009.godine biti moguce otkriti glavnu misteriju:ko je bio otac osobe cija je lobanja pronadjena?






 
Progeria


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Progeria is a condition that resembles premature aging which usually refers specifically to Hutchinson-Gilford Progeria syndrome.
Hutchinson-Gilford Progeria syndrome is an extremely rare condition where symptoms resembling some aspects of aging are manifested at an early age, and few affected children live past age 13. About 1 in 8 million babies are born with this condition. It is a genetic condition, but occurs sporadically and is usually not inherited in families.
Scientists are particularly interested in progeria because it might reveal clues about the normal process of aging.


Symptoms

The earliest symptoms include failure to thrive (FTT) and a localized scleroderma-like skin condition. As the child ages past infancy, additional conditions become apparent. Limited growth, alopecia, and a distinctive appearance with small face and jaw and pinched nose all are characteristic of progeria. The people diagnosed with this disease usually have small, fragile bodies like those of elderly people.
Later the condition causes wrinkled skin, atherosclerosis and cardiovascular problems.

Cause

Hutchinson-Gilford Progeria Syndrome (HGPS) is a childhood disorder caused by mutations in one of the major architectural proteins of the cell nucleus.
Unlike most other “accelerated aging diseases” (such as Werner’s syndrome, Cockayne’s syndrome or xeroderma pigmentosum), progeria is not caused by defective DNA repair. Because these “accelerated aging” diseases display different aspects of aging, but never every aspect, they are often called “segmental progerias”.

Diagnosis

In HGPS patients, the cell nucleus has dramatically aberrant morphology (bottom, right) rather than the uniform shape typically found in healthy individuals (top, right) Diagnosis is suspected according to signs and symptoms, such as skin changes, abnormal growth, and loss of hair. It can be confirmed through a genetic test.

Treatment

No treatments have been proven effective. Most treatment focuses on reducing complications such as cardiovascular disease, such as heart bypass surgery or low-dose aspirin. Children may also benefit from a high-calorie diet.
Growth hormone treatment has been attempted.
A type of anti-cancer drug, the farnesyltransferase inhibitors (FTIs), have been proposed, but their use has been mostly limited to animal models. A phase II clinical trial using the FTI Lonafarnib began in May 2007.

Prognosis

There is no known cure. Few people with progeria exceed 13 years of age. At least 90% of patients die from complications of atherosclerosis, such as heart attacks or strokes.
Mental development is not affected. The development of symptoms is comparable to aging at a rate six to eight times faster than normal, although certain age-related conditions do not occur. Specifically, patients show no neurodegeneration or cancer predisposition. They do not develop “wear and tear” conditions commonly associated with aging, like cataracts and osteoarthritis.

Epidemiology

One study from the Netherlands has shown an incidence of 1 in 4 million births. Currently, there are 48 known cases in the world. Approximately 100 cases have been formally identified in medical history.http://en.wikipedia.org/wiki/Progeria#cite_note-13http://en.wikipedia.org/wiki/Progeria#cite_note-USA_T-9
Classical Hutchinson–Gilford Progeria Syndrome is almost never passed on from parent to child. It is usually caused by a new (sporadic) mutation during the early division of the cells in the child. There has been one case in which became evident that a healthy parent can carry the LMNA-mutation that causes progeria in her or his egg- or spermcells. In this case two siblings were born with HGPS. But Hutchinson–Gilford Progeria Syndrome is usually genetically dominant, therefore parents who are healthy will normally not pass it on to their children. Affected children do not live long enough to have children themselves.
However, there are milder cases in which either the gene is not expressed in parents, or a different gene is responsible for a different form of progeria, and healthy parents can pass on their children.
Four families have been identified as having more than one child with the disease.

Research areas

Several discoveries have been made that have led to greater understanding and perhaps eventual treatment.
A 2003 report in Nature said progeria may be a de novo dominant trait. It develops during cell division in a newly conceived child or in the gametes of one of the parents. It is caused by mutations in LMNA (Lamin A protein) gene on chromosome 1; The mutated form of Lamin A is commonly known as progerin. One of the authors, Leslie Gordon, was a physician who didn’t know anything about progeria, until her own son, Sam, was diagnosed at 21 months. Gordon and her husband, pediatrician Scott Berns, founded the Progeria Research Foundation.

Lamin A

Nuclear lamina is a protein scaffold on the inner edge of the nucleus that helps organize nuclear processes such as RNA and DNA synthesis.
preLamin A contains a CAAX box at the C-terminus of the protein (where C is a cysteine and A is any aliphatic amino acids). This ensures that the cysteine is farnesylated, and this allows preLamin A to bind membranes, specifically the nuclear membrane. After Prelamin A has been localized to the cell nuclear membrane the C-terminal amino acids, including the farnesylated cysteine, are cleaved off by a specific protease. The resulting protein is now Lamin A, is no longer membrane-bound and carries out functions inside the nucleus.
In HGPS the recognition site that the enzyme requires for cleavage of Prelamin A to Lamin A is mutated. Lamin A cannot be produced and preLamin A builds up on the nuclear membrane, causing a characteristic nuclear blebbing. This results in the premature aging symptoms of progeria, although the mechanism connecting the misshapen nucleus to the symptoms is not known.
A study which compared HGPS patient cells with the skin cells from LMNA young and elderly human subjects found similar defects in the HGPS and elderly cells, including down-regulation of certain nuclear proteins, increased DNA damage and demethylation of histone leading to reduced heterochromatin. Nematodes over their lifespan show progressive lamin changes comparable to HGPS in all cells but neurons and gametes. These studies suggest that lamin A defects contribute to normal aging.

Mouse model of progeria

A mouse model of progeria exists, though in the mouse the LMNA preLamin A is not mutated, but instead ZMPSTE24, the specific protease that is required to remove the C-terminus of preLamin A is missing. Both cases result in the build up of farnesylated preLamin A on the nuclear membrane and in the characteristic nuclear LMNA blebbing. Fong et al use a farnesyl transferase inhibitor (FTI) in this mouse model to inhibit protein farnesylation of preLamin A. Treated mice had greater grip strength, lower likelihood of rib fracture and may live longer than untreated mice.
This method does not directly ‘cure’ the underlying cause of progeria. This method prevents Prelamin A going to the nucleus in the first place so no preLamin A can build up on the nuclear membrane, but equally there is no production of normal Lamin A in the nucleus. Luckily Lamin A does not appear to be essential, indeed mouse models in which the genes for preLamin A and C are knocked out show no symptoms. This also shows that it is the build up of Prelamin A in the wrong place, rather than the loss of the normal function of Lamin A that causes the disease.
It was hypothesized that part of the reason that treatment with an FFI such as alendronate is inefficient due to prenylation by geranylgeranyltransferase. Since statins inhibit geranylgeranyltransferase, the combination of an FFI and statins was tried, and markedly improved “the aging-like phenotypes of mice deficient in the metalloproteinase Zmpste24, including growth retardation, loss of weight, lipodystrophy, hair loss and bone defects”.

History

Progeria was first described in 1886 by Jonathan Hutchinson and also described independently in 1897 by Hastings Gilford. The condition was later named Hutchinson-Gilford Progeria syndrome (HGPS).
 
Poslednja izmena:
Crozuon Syndrome


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Crouzon Syndrome is a craniofacial condition. The word "craniofacial" refers to conditions or syndromes that affect the skull and/or face. Myself, my daughter and my son have this syndrome.
What is Crouzon Syndrome?
Crouzon Syndrome (also known as Craniofacial Dysostosis) was originally described in 1912 by O. Crouzon in Paris in a mother and her daughter. It is caused by a mutation in the FGFR2 (fibroblast growth factor receptor-2) gene or in the FGFR3 gene (known as acanthosis nigricans when a dark discolouration occurs with rough skin in the armpits and groin). These genes were first reported in 1994 by Reardon. Basically this means that when the baby's face and skull are forming in the womb, things go 'haywire' and these parts of the body do not develop properly. The reason why is still being discovered - the current thought is that the mutation makes the receptor overly active and it sends false signals or it binds to the wrong signals (Little, 1996). Characteristics of a person with Crouzon's are described below. Though like in any condition, symptoms can range from mild to severe, and not all people display all characteristics. Also symptoms can be different in each generation. And from talking to other people who have Crouzon's or their children do, there are also other characteristics that have not been documented.
The main symptoms are:

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Craniosynostosis (also known as craniostenosis)

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Facial features - large bulging eyes and a flat face (due to a recessed mid-face)

Craniosynostosis
Before birth and early in infancy, a child's brain grows very rapidly, reaching 70% of its eventual adult size in the first year. To keep up with this growth, the head must expand rapidly while keeping the brain protected. This is able to happen because a baby's skull bone is made up of a collection of many smaller bones. Where these bones meet are called sutures. Each of these sutures has a name (see the diagram). As the brain grows the sutures expand allowing for rapid symmetrical expansion. In babies with Crouzon Syndrome these sutures 'close' or fuse together which means these bones cannot expand for brain growth. If there are sutures which are not fused then that is where the brain will grow towards leading to abnormal head shapes. Because the brain is growing but the skull does not in most cases expand adequately enough for the brain's size, pressure is also put on the brain which if not eased, will lead to mental retardation and eventually death. The brain can also put pressure on the optic nerves at the back of the eye which can lead to blindness.

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Which sutures are affected varies widely. In typical cases of Crouzons, the coronal sutures which run along the top of the head from ear to ear, are affected making the head high and thin, like in the photo below.
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Who Looks after these Children?
All over the world there are clinics set up in the major hospitals. The clinics consist of a multi-disciplinary team of doctors. Usually a team consists of a plastic surgeon, neurosurgeon, geneticist, speech pathologist, orthodontist, audiologist and opthamologist. Other specialists may also be involved depending on the symptoms.

Genetics
Crouzon Syndrome can 'just happen' or it can be congenital. In my case there is no family history of the syndrome so it is said to have 'just happened' (medically called a 'sporadic mutation' and is said to occur in 25% - 50% of cases). I have been told that the medical fraternity do not know why the gene mutates, the only factor they have currently identified is the father's age. The gene change though is present in only one of the approximately 30,000 genes which we have.
Now that I have the syndrome, I have the gene (it is now called 'familial'). The three of us have had genetic testing done which has confirmed the syndrome. The gene identified in each of us is the FGFR2 (fibroblast growth factor receptor-2) exon 7 cDNA 833G->T (cys278phe). This basically means that in the FGFR2 gene, the amino acid in the protein at position 278 changed from a cystine which it should have been, to a phenylalanine. This simple change, or mistake, in the type of amino acid caused the face to not grow normally.
Now I need to say that because my family is not 'typical' Crouzon - we do not fit into the normal definition that you find on-line of Crouzon Syndrome (see http://www.thecraniofacialcenter.org/crouzon.html, http://www.worldcf.org/crouzon.cfm). We fit more into the Pfeiffer Syndrome definition because we have feet and hands involved (see http://ghr.nlm.nih.gov/condition=pfeiffersyndrome, http://www.worldcf.org/pfeiffer.cfm). Pfeiffer Syndrome I seems to be the same as Crouzon Syndrome but has additional characteristics. But our genetic testing showed that we have the gene that other families with Crouzon Syndrome have. So we have been given the official title of 'Craniosynostosis syndrome secondary to FGFR2 cys278phe" by our geneticist... aka Crouzon Syndrome for my sanity! Basically our genetic testing has proven that the medical book categories are incorrect.
The chance of me passing on the gene to each of my children is 50/50 per pregnancy. Melissa received the gene so she has the syndrome and she too has a 50/50 chance of passing the gene on to each of her children and Nicholas received the gene so he has the syndrome and he too has a 50/50 chance of passing the gene on to each of his children. Boys and girls are affected equally. If a child is born without the syndrome then they have the same chance of passing on the gene as the general population. The syndrome does not skip generations but can be so mild that no one realises that someone has it. The incidence is inconsistently reported but seems to range from 1 in 25,000 to 1 in 100,000.
 
Poslednja izmena:
hah, paganko je objasnio

nisam. ni sebi, još uvek. trenutno mi je malo muka od ovih genetskih bolesti koje sam ispronalazio. Evo još jedne koja je blago rečeno, odvratna:


Hydrocephalus


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The term hydrocephalus is Greek in origin — hydro (water), cephalus (head). It means an abnormal increase in the amount of fluid within the cranial (skull) cavity. Until approximately 30 years ago, no effective treatment for this condition was known. Those diagnosed with hydrocephalus, usually babies and young children, died or were institutionalized for mental retardation and an extremely large head size. Today the outlook is much brighter, and, with early diagnosis and medical management, many hydrocephalic children will develop with only minimal physical and intellectual delays.
Causes of Hydrocephalus. Hydrocephalus is noted in about four out of every 1,000 children from birth to three months of age. It is commonly seen in premature babies, of which there are now 250,000 born annually. One can be born with hydrocephalus (usually due to a brain or spinal malformation which commonly occurs during the first eight weeks a woman is pregnant) or it can be acquired after birth due to a variety of causes (injury to the head, brain tumors, spontaneous bleeding within the brain, and meningitis as well as other serious infections).
How Does Fluid Accumulate in the Brain? The human head is made up of three main components: a bony covering (skull), brain matter, and cerebrospinal fluid (CSF). The CSF cushions and protects the brain and also carries nutrients throughout the brain and spinal canal. This fluid is produced in and travels throughout four lakes or cavities deep within the head called "ventricles." It then bathes the outer surface of the brain and spinal cord and is eventually absorbed into the bloodstream. We produce continuously about one cup of this CSF per day (.35 cc per minute).
Hydrocephalus occurs when there is obstruction anywhere along the normal pathway of the brain fluid. The result is a dam-like effect: the ventricles can t empty properly, so they become fluid-filled and enlarge. Brain damage takes place if the ventricles then "squash" the brain against the skull, thereby harming brain cells. Babies luckily have both a very pliable skull and soft spots (fontelle) that allow the brain to expand without much injury if the problem is diagnosed and taken care of early.
Does My Child Have Hydrocephalus? The head size of babies is measured daily while they are still in the hospital and at each pediatric visit thereafter. If the doctor detects that the head is growing too fast, a special x-ray of the brain called a computerized topographic (CT) scan may be ordered. This will reveal the size of the ventricles and status of the surrounding brain tissue. If your baby is in the premature nursery, serial ultrasound (sound wave) studies may be done routinely to check for this. Premature babies have more hydrocephalus because their brains bleed rather easily, and the blood can sometimes cause a permanent blockage within the fluid channels.)
Other signs of hydrocephalus in a child may be: 1) a bulging fontanelle, 2) forceful vomiting, 3) prominent veins on the forehead, 4) a high-pitched, shrill cry, 5) irritability, 6) increasing drowsiness, 7) difficulty sucking or swallowing, 8) periods where he or she stops breathing, 9) seizures, 10) or stiffness of the legs. Call your doctor if you notice a combination of these symptoms.
Types of Treatment Available Unfortunately it is almost impossible to slow down the production of CSF with medication. Therefore, a surgical diversion of this fluid from the brain to another part of the body where it can readily be absorbed is the treatment of choice. A elastic rubber tube called a shunt is usually threaded from the brain down to the abdomen or heart in a relatively easy and quick procedure performed by a neurosurgeon. The shunt contains a one-way valve which opens when a certain pressure is reached inside the ventricles, and which allows fluid only to go out of the brain. Although a shunt is usually left in throughout a person s life, it is virtually unnoticeable. The tubing may need to be lengthened at some point as the child grows and might need to be totally replaced if it should become blocked or infected.
Will Children with Hydrocephalus Be Handicapped? This is the most difficult question which is posed to health care personnel. The extent of disability from hydrocephalus will be determined by many factors: the cause of the hydrocephalus , age at which detected, promptness of treatment, presence of other medical problems, and shunt function. Parents of a hydrocephalic child, however, can do two important things to assure their child of the best possible outcome. See the child's doctor and neurosurgeon regularly (and call with suspected problems), and seek out all types of physical and mental stimulation available for children with neurological problems. A child's brain is an amazing machine, and the earlier he or she begins to use it, the greater the potential for physical and intellectual development!
 
Citat sa sajta sa pocetka teme: "Preliminary new DNA results from the 900 year old Starchild Skull, providing proof that a percentage of the DNA in the bone is not from Earth (Alien).

"

Citat sa wikipedie:

DNA testing in 1999 at BOLD, a forensic DNA lab in Vancouver, British Columbia found standard X and Y chromosomes in two samples taken from the skull, "conclusive evidence that the child was not only human (and male), but both of his parents must have been human as well, for each must have contributed one of the human sex chromosomes"

Obratite pažnju na rapidnu razliku citatima, pogotovo po pitanjima ko, gde, kada.
 
Znaci nije ljudsko bice?

u bukvalnom prevodu sa engleskog:

Tokom DNA testiranja 1999. godine u forenzičkoj laboratoriji BOLD, Vankuver, Britanska Kolumbija, pronadjeni su standardni Semplovi X i Y hromozoma u dva uzorka koji su pokazali nedvosmislen argument da je dete ne samo čovek i muško, već i da su mu roditelji morali biti ljudi prilažući po jedan ljudski polni hromozom.

Žao mi je, ali dok neki drugi test ne potvrdi suprotno, ovo ostaje siroti bednik koji se rodio sa nekom od gorenavedenih genetskih bolesti. Pri tome ne vidim nšta sporno da se takvo dete moglo roditi i tada kao što se i sada radjaju sa raznim izvitoperenim lobanjama i slično. Ovih par gore koje sam prikazao, daju otprilike najsličnije deformitete lobanje sa ovom, pronadjenom.

Ipak, diskusija ostaje otvorena, jer ću sa zadovoljstvom sačekati da ljudi koji su vršili nova testiranja, konačno potvrde ili opovrgnu svoje nalaze.
 
Moje misljenje je da su ova deca nastala parenjem ljudi i vanzemaljaca,a "bolest" koje nema,odnosno njihov izgled je objasnjen tim nazivom "hidrokefalijom",kako bi se otklonila sumnja da su oni nastali ukrstanjem aliena i ljudi.

Mozda gresim,ali....

Hmmm, a kako objasniti ukrstanje genetskog materijala ljudi i vanzemaljaca kada je nemoguce ukrstiti parenjem konja i coveka npr. a kamoli 2 bica zasnovana na totalno drugim platformama?! Nesto mi to ne drzi vodu, ali dobro...
 
Pa sigurno se vanzemaljci i ljudi ne pare prirodnim putem vec putem genetske manipulacije i inzinjeringa.
S' obzirom da su njihova tehnologija, nauka i medicina mozda hiljadama godina ispred nase sigurno im nije problem da naprave jednog ljudsko-vanzemaljskog hibrida, pa ko zna cak mozda i hibrida coveka i konja ( Kentaur)

Mislim ko zna mozda je Kentuar iz grcke mitologije zaista i postojao , kao i neka druga bica iz mitova i legendi i mozda ta mitoloska bica su ustvari bila samo proizvod nekog eksperimenta genetskog inzenjeringa i manipulacije.
 
Pa sigurno se vanzemaljci i ljudi ne pare prirodnim putem vec putem genetske manipulacije i inzinjeringa.
S' obzirom da su njihova tehnologija, nauka i medicina mozda hiljadama godina ispred nase sigurno im nije problem da naprave jednog ljudsko-vanzemaljskog hibrida, pa ko zna cak mozda i hibrida coveka i konja ( Kentaur)

Mislim ko zna mozda je Kentuar iz grcke mitologije zaista i postojao , kao i neka druga bica iz mitova i legendi i mozda ta mitoloska bica su ustvari bila samo proizvod nekog eksperimenta genetskog inzenjeringa i manipulacije.


Otkud ti znas da je medicina i nauka razvijenija nego kod nas... Sa filmova i sa crtanih ... Daj ne seri...
 
Moje misljenje je da su ova deca nastala parenjem ljudi i vanzemaljaca,a "bolest" koje nema,odnosno njihov izgled je objasnjen tim nazivom "hidrokefalijom",kako bi se otklonila sumnja da su oni nastali ukrstanjem aliena i ljudi.

Mozda gresim,ali....

Znaci svi oni koju su studirali medicinu i upoznali se sa ovim lazu kada kazu da je to oboljenje a jedino ti znas pravu istinu. Daj covece imaj malo obzira prema roditeljima... JEsi li video glave ljudi iz onih plemena u ( sada mi stao mozak kako se zove mesto ) gde im glava izgleda kao kupa...

Ne da gresis nego.... Sada bas lupas...
 
Znaci svi oni koju su studirali medicinu i upoznali se sa ovim lazu kada kazu da je to oboljenje a jedino ti znas pravu istinu. Daj covece imaj malo obzira prema roditeljima... JEsi li video glave ljudi iz onih plemena u ( sada mi stao mozak kako se zove mesto ) gde im glava izgleda kao kupa...

Ne da gresis nego.... Sada bas lupas...


To su majanska plemena,i oni su oblikovali te lobanje,nisu rodjeni sa takvim lobanjama.

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Nacin na koji se to radilo:

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Izvrces reci. Ja sam rekao da je to moje misljenje,a ne prava istina.
 

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