Author Topic: Understanding the Gene: Amytrophic Lateral Sclerosis in case study  (Read 3778 times)

Lorenzo

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I had a lecture in lab today (my last lecture for the semester  :) ). Throughout the course of the semester we instructed the students about concepts of peroxidase sequencing, RNA-ase and DNA-ase abilitities as well as genomic manipulation that can either induce and or inhibit/repress transcriptional factors from binding to the target site of translation-transcription. Gene-specific transcriptional factors will either activate activator-proteins within the open promoter complex to allow the RNA Polymerase to induce the opening of the envelopic fold, thereby manifesting helicase activity as well as kinase activity.

With these complex processes in motion, the open promoter complex of the gene sequence will be translated, then elongated, and then transcribed. Insodoing, one sequence of the  DNA (either it be the complex homo sapiens sapiens, to the simple Arabidopsis thaliana) will be expressed. When all sequences are expressed (there are millions of sequences found in a chromatin within the DNA) then the probability and possibility of proliferation is guaranteed.

Science is an ever-changing field. It is never stable, never secure. As scientists and science-students, we study life in all of its forms and sub-principles. Either it be biology, chemistry,geology,  neuroscience  whatsoever it maybe, it is all part of nature. Nature is always changing, environmental cues will change, plate tectonics will change; always following a rudimentary law of planetary homeostasis.

Just as we, organisms, also too follow in a rudimentary internal homeostasis. A failure to maintain homeostasis either going above limits or below limits, will result in organismal death. Hence, change is manifested. The same is seen in the planet as well.

However

Man, out of all the billions within the continuum of animals, is the only one that can identify a disease, physical and mental degeneracy and trace its causes to the genetic level.

Amytrophic Lateral Sclerosis, per se

     1850 - English scientist Augustus Waller describes the appearance of shriveled nerve fibers

     1869 - French doctor Jean-Marie Charcot first describes ALS in scientific literature

     1881 - "On Amyotrophic Lateral Sclerosis" gets translated into English and published in a three-volume edition of Lectures on the Diseases of the Nervous System

     1939 - ALS becomes a cause célèbre in the United States when baseball legend Lou Gehrig's career—and, two            years later, his life—is ended by the disease.

     1950s - ALS epidemic occurs among the Chamorro people on Guam

     1991 - Researchers link chromosome 21 to FALS

     1993 - SOD1 gene on chromosome 21 found to play a role in some cases of FALS

     1996 - Rilutek® becomes the first FDA-approved drug for ALS

     1998 - El Escorial is developed as the standard for confirming ALS

     2001 - Alsin gene on chromosome 2 found to cause ALS2

As we speak, there are pharmacologists and neurobiologists working in a way to synthesize a gene-specific repressor. This gene-specific repressor will attach itself to the Alsin gene, when it targets the Alsin gene, it will inhibit Alsin transcriptional ability. With this inhibited, there is no translation of ALS2. And since ALS2 is responsible for the manifestation of Amytrophic lateral sclerosis during the developmental stage of the fetus while in the mother's womb, or during adult life, with it totally repressed within the genomic sequence, this therein inhibits the physical degeneracy from manifesting completely.

As we speak, man and science have cooperated in fighting debilitating diseases such as Diabetes, Endocarditis, Alzheimer's, Hypertension, HIV, Basal Carcinoma. The more we research in finding gene-specific sequences, the more we find out what diseases they are responsible, and when we find this out--HOW we can find a way to inhibit and even alter it genetically.

Any questions? 

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #1 on: April 23, 2008, 02:24:59 AM »

Anatomical difference between normal tissue and ALS-affected tissue.
ALS tissue is manifested due to activation of Alsin gene in the chromosome 2 subtaxic sequence,
within the range of phosphodiester bond of the major groove, on the periphery of the nucleotidic sequences in the minor groove.


The Alsin gene--responsible for the translation and transcription of ALS2--which manifests into musculature degeneracy otherwise known as Amytrophic Lateral Sclerosis.

Treating ALS is rather simple; formulate an Alsin gene-specific repressor that will inhibit translational ability of Alsin to proliferate ALS2.



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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #2 on: April 23, 2008, 02:45:10 AM »
Genetic explanation: In TAF level





Why and How does it differ? What happens to manifest it?



A:A common mutation of breakpoint cluster region (Bcr) involves fusion of the Bcr gene on chromosome 22 with the Abl proto-oncogene on chromosome 9. This results in the formation of Bcr–Abl chimaeras that express various portions of N-terminal Bcr sequence fused to the Abl kinase domain: p185 is associated with 20–30% of incidences of acute lymphocytic leukaemia, p210 with 90% of incidences of chronic myelogenous leukaemia (CML), and p230 with a subset of patients that have chronic neutrophilic leukaemia.

 A chimeric protein in which a C-terminal fragment of leukaemia-associated Rho guanine nucleotide-exchange factor (LARG) is fused to the N-terminus of mixed lineage leukaemia (MLL) has been identified in acute myelogenous leukemia. Ala441Gly is a missense mutation in Tiam1 (T-cell lymphoma invasion and metastasis-1) in renal cell cancer cell lines and tumours. Fgd1 mutations result in faciogenital dysplasia (or Aarskog–Scott) syndrome. Mutations include those that introduce premature stop codons and missense mutations that are scattered throughout the protein, with many involving deletion or mutation of the Dbl homology (DH) domain.

Truncation mutations within the amyotrophic lateral sclerosis-2 (ALS2) gene product, Alsin, result in the premature truncation of Alsin and are thought to be causative for juvenile onset amyotrophic lateral sclerosis. Indicated are the locations of breakpoints, missense mutations and sites of protein truncations that result from nucleotide insertions or deletions.


Please, feel free to ask questions.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #3 on: April 23, 2008, 03:10:32 AM »
Insofar,

How is ALS treated?



No cure has yet been found for ALS. However, the Food and Drug Administration (FDA) has approved the first drug treatment for the disease—riluzole (Rilutek). Riluzole is believed to reduce damage to motor neurons by decreasing the release of glutamate. Clinical trials with ALS patients showed that riluzole prolongs survival by several months, mainly in those with difficulty swallowing. The drug also extends the time before a patient needs ventilation support. Riluzole does not reverse the damage already done to motor neurons, and patients taking the drug must be monitored for liver damage and other possible side effects. However, this first disease-specific therapy offers hope that the progression of ALS may one day be slowed by new medications or combinations of drugs.

Other treatments for ALS are designed to relieve symptoms and improve the quality of life for patients. This supportive care is best provided by multidisciplinary teams of health care professionals such as physicians; pharmacists; physical, occupational, and speech therapists; nutritionists; social workers; and home care and hospice nurses. Working with patients and caregivers, these teams can design an individualized plan of medical and physical therapy and provide special equipment aimed at keeping patients as mobile and comfortable as possible.

Physicians can prescribe medications to help reduce fatigue, ease muscle cramps, control spasticity, and reduce excess saliva and phlegm. Drugs also are available to help patients with pain, depression, sleep disturbances, and constipation. Pharmacists can give advice on the proper use of medications and monitor a patient's prescriptions to avoid risks of drug interactions.

Physical therapy and special equipment can enhance patients' independence and safety throughout the course of ALS. Gentle, low-impact aerobic exercise such as walking, swimming, and stationary bicycling can strengthen unaffected muscles, improve cardiovascular health, and help patients fight fatigue and depression. Range of motion and stretching exercises can help prevent painful spasticity and shortening (contracture) of muscles. Physical therapists can recommend exercises that provide these benefits without overworking muscles. Occupational therapists can suggest devices such as ramps, braces, walkers, and wheelchairs that help patients conserve energy and remain mobile.

ALS patients who have difficulty speaking may benefit from working with a speech therapist. These health professionals can teach patients adaptive strategies such as techniques to help them speak louder and more clearly. As ALS progresses, speech therapists can help patients develop ways for responding to yes-or-no questions with their eyes or by other nonverbal means and can recommend aids such as speech synthesizers and computer-based communication systems. These methods and devices help patients communicate when they can no longer speak or produce vocal sounds.

Patients and caregivers can learn from speech therapists and nutritionists how to plan and prepare numerous small meals throughout the day that provide enough calories, fiber, and fluid and how to avoid foods that are difficult to swallow. Patients may begin using suction devices to remove excess fluids or saliva and prevent choking. When patients can no longer get enough nourishment from eating, doctors may advise inserting a feeding tube into the stomach. The use of a feeding tube also reduces the risk of choking and pneumonia that can result from inhaling liquids into the lungs. The tube is not painful and does not prevent patients from eating food orally if they wish.

When the muscles that assist in breathing weaken, use of nocturnal ventilatory assistance (intermittent positive pressure ventilation [IPPV] or bilevel positive airway pressure [BIPAP]) may be used to aid breathing during sleep. Such devices artificially inflate the patient's lungs from various external sources that are applied directly to the face or body. When muscles are no longer able to maintain oxygen and carbon dioxide levels, these devices may be used full-time.

Patients may eventually consider forms of mechanical ventilation (respirators) in which a machine inflates and deflates the lungs. To be effective, this may require a tube that passes from the nose or mouth to the windpipe (trachea) and for long-term use, an operation such as a tracheostomy, in which a plastic breathing tube is inserted directly in the patient's windpipe through an opening in the neck. Patients and their families should consider several factors when deciding whether and when to use one of these options. Ventilation devices differ in their effect on the patient's quality of life and in cost. Although ventilation support can ease problems with breathing and prolong survival, it does not affect the progression of ALS. Patients need to be fully informed about these considerations and the long-term effects of life without movement before they make decisions about ventilation support.

Social workers and home care and hospice nurses help patients, families, and caregivers with the medical, emotional, and financial challenges of coping with ALS, particularly during the final stages of the disease. Social workers provide support such as assistance in obtaining financial aid, arranging durable power of attorney, preparing a living will, and finding support groups for patients and caregivers. Respiratory therapists can help caregivers with tasks such as operating and maintaining respirators, and home care nurses are available not only to provide medical care but also to teach caregivers about giving tube feedings and moving patients to avoid painful skin problems and contractures. Home hospice nurses work in consultation with physicians to ensure proper medication, pain control, and other care affecting the quality of life of patients who wish to remain at home. The home hospice team can also counsel patients and caregivers about end-of-life issues.


What research has been done?



The National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, is the Federal Government's leading supporter of biomedical research on ALS. The goals of this research are to find the cause or causes of ALS, understand the mechanisms involved in the progression of the disease, and develop effective treatment.

Scientists are seeking to understand the mechanisms that trigger selective motor neurons to degenerate in ALS and to find effective approaches to halt the processes leading to cell death. This work includes studies in animals to identify the means by which SOD1 mutations lead to the destruction of neurons. The excessive accumulation of free radicals, which has been implicated in a number of neurodegenerative diseases including ALS, is also being closely studied. In addition, researchers are examining how the loss of neurotrophic factors may be involved in ALS. Neurotrophic factors are chemicals found in the brain and spinal cord that play a vital role in the development, specification, maintenance, and protection of neurons. Studying how these factors may be lost and how such a loss may contribute to motor neuron degeneration may lead to a greater understanding of ALS and the development of neuroprotective strategies. By exploring these and other possible factors, researchers hope to find the cause or causes of motor neuron degeneration in ALS and develop therapies to slow the progression of the disease.

Researchers are also conducting investigations to increase their understanding of the role of programmed cell death or apoptosis in ALS. In normal physiological processes, apoptosis acts as a means to rid the body of cells that are no longer needed by prompting the cells to commit "cell suicide." The critical balance between necessary cell death and the maintenance of essential cells is thought to be controlled by trophic factors. In addition to ALS, apoptosis is pervasive in other chronic neurodegenerative conditions such as Parkinson's disease and Alzheimer's disease and is thought to be a major cause of the secondary brain damage seen after stroke and trauma. Discovering what triggers apoptosis may eventually lead to therapeutic interventions for ALS and other neurological diseases.

Scientists have not yet identified a reliable biological marker for ALS—a biochemical abnormality shared by all patients with the disease. Once such a biomarker is discovered and tests are developed to detect the marker in patients, allowing early detection and diagnosis of ALS, physicians will have a valuable tool to help them follow the effects of new therapies and monitor disease progression.

NINDS-supported researchers are studying families with ALS who lack the SOD1 mutation to locate additional genes that cause the disease. Identification of additional ALS genes will allow genetic testing useful for diagnostic confirmation of ALS and prenatal screening for the disease. This work with familial ALS could lead to a greater understanding of sporadic ALS as well. Because familial ALS is virtually indistinguishable from sporadic ALS clinically, some researchers believe that familial ALS genes may also be involved in the manifestations of the more common sporadic form of ALS. Scientists also hope to identify genetic risk factors that predispose people to sporadic ALS.

Potential therapies for ALS are being investigated in animal models. Some of this work involves experimental treatments with normal SOD1 and other antioxidants. In addition, neurotrophic factors are being studied for their potential to protect motor neurons from pathological degeneration. Investigators are optimistic that these and other basic research studies will eventually lead to treatments for ALS.

Results of an NINDS-sponsored phase III randomized, placebo-controlled trial of the drug minocycline to treat ALS were reported in 2007. This study showed that people with ALS who received minocycline had a 25 percent greater rate of decline than those who received the placebo, according to the ALS functional rating scale (ALSFRS-R).

Source
http://www.ninds.nih.gov/disorders/amyotrophiclateralsclerosis/detail_amyotrophiclateralsclerosis.htm

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Macky Ferniz

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #4 on: April 23, 2008, 02:53:06 PM »
Interesting desease. I am still confused what is the difference between a desease and abnormality. If ALS is a genetic abnormality, then it is not a desease and can not be treated. Abnormality in a gene is something natural with no treatment, but we can only re-divert its fate to make the person better. Or maybe to eliminate the problem genes through breeding techniques so this can not be passed to the next generation. I remembered one of my neighbors said that she will choose the bride of his son because they have some sort of blood abnormalities. Incase her son chooses the wrong pair, her grandson will surely suffer from a rare form of anemia.

Also, I have seen on TV a documentary about a tribe with defective gene which causes thier feet to branch out, thus they are called the "ostrich feet tribe". A defective gene was identified and it was nutralized through selective breeding. So for some period of time, they can not choose their true love.

How is Lou Gehrig's disease compared to Alzheimers desease. Can ALS be treated with the controversial stem cell? By the way, there is now new and easy way to collect stem cell from the placenta instead of the aborted fetus which became controversial during George Bush time.

How about gene therapy, I am also curious, it says it can make you young or change your race from asian to caucasian, is it true?

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #5 on: April 23, 2008, 04:02:40 PM »
Interesting desease. I am still confused what is the difference between a desease and abnormality. If ALS is a genetic abnormality, then it is not a desease and can not be treated. Abnormality in a gene is something natural with no treatment, but we can only re-divert its fate to make the person better. Or maybe to eliminate the problem genes through breeding techniques so this can not be passed to the next generation. I remembered one of my neighbors said that she will choose the bride of his son because they have some sort of blood abnormalities. Incase her son chooses the wrong pair, her grandson will surely suffer from a rare form of anemia.

Also, I have seen on TV a documentary about a tribe with defective gene which causes thier feet to branch out, thus they are called the "ostrich feet tribe". A defective gene was identified and it was nutralized through selective breeding. So for some period of time, they can not choose their true love.

How is Lou Gehrig's disease compared to Alzheimers desease. Can ALS be treated with the controversial stem cell? By the way, there is now new and easy way to collect stem cell from the placenta instead of the aborted fetus which became controversial during George Bush time.

How about gene therapy, I am also curious, it says it can make you young or change your race from asian to caucasian, is it true?

Mr. Ferniz, you raise scintillating questions.

A)
Disease in its basic sense is an abnormal condition of an organism that impairs bodily functions, which comes with physical symptoms that leads to its identification and thus possible modes of treatment are prescribed by the physician and/or a surgical procedure is implemented to alleviate the certain condition.

Genetic abnormality is a result of gene-sequential mutanogensis, meaning that there was an error in the protein synthesis, either it be alteration in the production of proteins in the ribosome, some kind of malfunction of the RNA Polymerase I, II, III to bind to the open promoter complex thus leads to a ceasure of helicasization, kinasization. When this occurs, there is no translation of the gene, there is no elongation of the gene, and if there is no translation or elongation, then there is no transcription. We have abortive transcription. If we have abortive transcription, then certain genetic sequences that are responsible for proper formation of tissue types (endothelium, cardiac, smooth muscle, rough muscle, neural, genital, osteolithic (bone tissue), occipital (eye) etc) will not manifest. With these tissue-specific gene sequences inhibited, then as a result diseases and physical degeneracy will manifest outright.

Every disease, physical and mental degeneracy is a result of genetic failure. In example, for those who suffer Alzheimer's. Alzheimer's disease is a result of neural degeneracy in which our neural synapse is unable to transmit information into the cortical apex of the brain and allow retrieval. As a result of this, we have inability to remember, inability to integrate the present to the past. Two abnormal structures called plaques and tangles are prime suspects in damaging and killing nerve cells. Plaques build up between nerve cells. They contain deposits of a protein fragment called beta-amyloid. Tangles form inside dying cells. Though most people develop some plaques and tangles as they age, those with Alzheimer’s tend to develop far more. The plaques and tangles tend to form in a predictable pattern, beginning in areas important in learning and memory and then spreading to other regions.

Why does Alzheimer's manifest in the elderly? It is because of genetic degeneracy. As we age, the wear and tear of genetic transcription damages the RNA Polymerase I, II, III, and as we age site-specific mutanogenisis is common due to the protein inhibition, weakness of protein folding. This simple error translates into a gigantic error in the visceral-organismal level. Proper gene sequences that are responsible for creating the axon and the myelin sheath (which is the protein coating that covers the axon--allowing neural messages to be sent down and up the neural interface) will be damaged, and or unable to repair itself. Another genetic mutanogenisis is that the wrong TAFII (Tata promoter-associated factor) will bind to the wrong protein activator, or a lead to the truncation of a particular DNA plasmid nucleosome. When this happens, we have the wrong sequences binding, and mutation is manifest over 10 million fold. Thus we have the formation of plagues and tangles. Thus Alzheimer's is present. It is mostly an age-specific neural degeneracy (abnormality/disease) in that it is a result of genetic impudence--a result of age.

Diseases, therefore, manifests as a result of genetic mutanogensis. Every disease known to man is a result of genetic mutanogensis. Diabetes is a disease in the American Medical Association, but we all known that it is a result of the body's inability to produce Insulin, which is regulated by the Insulin gene. What happens is that there is a repressor that inhibits the insulin gene from expressing itself in the open promoter complex. When this happens, there is no elongation, no translation, no transcription. Thus, no insulin gene being expressed in the DNA chromatin, and DNA structure. Therefore we have the body's inability to produce Insulin, therefore we have diabetes.
Chemical therapy is present in that we have diabetic medical that provides insulin to the body.

Every disease is genetically-linked. The quicker we locate the peroxidase sequence-specific areas of a disease, the faster we can find a way to develop drugs and models that can over-express that gene or create an anti-repressor that can nullify the repression in mutanogenesis.

B)Amytrophic Lateral Sclerosis can be properly treated by chemical therapy. As we speak, there are scientists researching in the creation of repressors that can nullify the  ability of the mutanogensis that resulted in the production of Alsin. And since the Alsin gene is responsible for the production of ALS2, its inhibition and inability to express itself in the DNA chromatid structure of the DNA strand, will allow the body's ability to developing properly. However, if there is no inhibition of the Alsin gene, then ALS2 will be transcribed and thus we have manifestation of Amytrophic Lateral Sclerosis.

The Alsin gene, if mutated, will allow this. There are studies, as we speak, that is indentifying the cause of this mutation of the Alsin gene.

Unfortunately, Mr. Ferniz, drug formation and creation takes years. Research is a conservative process that undergoes countless trials (animals) before making it into human trials. And even if there is a positive confidence in treatment, the drug companies decide in its marketing ability. Cost, is always a factor.

Right now, the only mode of treatment are pain killers, bed side care and tertiary prescriptions that targets bacterial activity in ALS patients (who tend to be more immunosuppressed than non-ALS patients).

Every mode of disease is understood in pure sample. Every treatment created by man for diseases has been a product of stem cell harvesting. The reason for this, Mr. Ferniz, is that stem cells are non-specific cells. Thereby it can develop into any tissue, if placed in that area. If we take a stem cell and place it on top of a damaged cardiac tissue, the stem cell (because of God's brilliance) will actually mold itself and transform itself into a cardiac muscle cell and begin to replicate. They will then repair the damaged heart tissue. If stem cell is placed near a damaged neural tissue, the stem cell will mold itself and transform itself into a precious neural tissue (neural tissue does not replicate btw, that is why any damage on neural tissue is irreversible without stem cell intervention/utilization) and repair itself. Stem cells are uni-specific. They will become whatever their surroundings are.

This is the reason why they are so imperative to medical and scientific research. Stem cells are pure and unadulterated. Yes, we can take stem cell samples from fetuses, however one needs to understand that if we do that there is a high risk of killing the fetus since the stem cells in the fetus are molding itself into either neural tissue, cardiac tissue, osteolithic tissue (bone), occipital tissue (eye), occular tissue (ear), etc. That is why no parent of mother is willing to allow that.

C)Caucasians, Mongoloids and Negroids are all of the same genus: Homo sapiens sapiens. Any differences we have are primarily phenotypic and a result of evolution and of the climactic extremes the said races lived in. Skin tone differences are merely mutations in the endothelium in that there are overactive melnocytes, which are responsible for skin tone and color. Negroids lived in the central plain near the equalitorial range, hence they were bombarded with solar rays, to survive in such harsh and hot climates, they developed overactive melanocytes and thus are dark. Their hair is also kinky as an evolutionary change to repel heat. Caucasoids, who lived above the equalitorial range and were subjected to significantly less solar ray developed less melanocytes thus their skin tone are light. Their eye color differentiation is nothing more than genetic mutation and recessivity. The dominant human trait is brown eyes. This is seen in negroid and mongoloids. Mongoloids developed differently due to the harsh weather of the Pleistocene. Mongoloids came from the Siberian region, where snow was constant and sun irregular. That is why the eye fold of Mongoloids are prominent, the short stature is a result of lack of sun, lack of food in the Siberian region. Lack of calcium intake.

All races are inter-breedable; and thus all similar. Any differences we have are only phenotypic and slight genetic differences. Hypothetically, Mr. Ferniz, one can use gene therapy to change the phenotype of a fetus while developing.

In my opinion that is unnecessary and unnatural for the parents to do. I believe in gene richness. Any mixing of children due to the inter-racial marriage of both parents combines the genotypes. Thereby making the offspring genetically superior to both parents. As they have the best of both worlds.

I hope I answered your questions appropriately, sir.


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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #6 on: April 23, 2008, 06:06:07 PM »
On that note,

Development of repressors, anti-repressors, inhibitors, inducer drugs is a difficult endeavor. The reason for this is that all gene sequences are composed of specific nucleotide base pairs:
C (Cytosine), A (Adenine), T (Thymine) and G (Guanine) and therefore gene sequences are sensitive to changes in these base pairs. Some drugs that have repressive,anti-repressive ability, inhibitory, inducer ability have been known to alter nucleotides and the amino-acids in base.

This is why it is so difficult. I myself have aided some of my Professors in developing a specific transcription abolisher in the plant tissue of Brassica Rapa as well as in the Arabidopsis thaliana. In studies, we have been able to locate a particular peroxidase primer sequence that induces or inhibits transcription. This resulted in over-expression of root growth, or nullificiation of growth.

One of our concerns, as we have noted in studies, is that these sequences are protein-based. And proteins are extremely sensitive to heat. Any diminishment of heat or heightening of heat can manifest problems. In either over expression or sub-expression.

This is why there have been failed trials, in research. Life, is unstable. And every time we set standards to learn, we always end up learning something new, a new dimension in the reality of science and molecular genetics.

I sometimes am agape and wonder in the brilliance of God. In how he designed these templates, the intricacies of the subsystems within a gene is gloriously vast. The gene is as vast as the oceans of the earth compressed into one. And man is paddling in this so called 'gene ocean' with a needle, while attempting to understand it.



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Macky Ferniz

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #7 on: April 23, 2008, 06:43:03 PM »
Trying to deciper the mechanics of a simple gene will only cause wonder on how great the wisdom and power of the Creator.

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #8 on: April 23, 2008, 06:57:57 PM »
You remembered the thread Wajde tribe in Bohol?

I wondered if there is any company in the US who is providing free genotyping services.

I have a strong doubt that the Wajde tribe did not originate in India but in Wajdi New Guinea. Based on physical characteristics of those tribes, there is no evidence/manifistation of Indian features. However, there is a huge resemblance to the Aborigine race.

If we could identify the dominant genetic marker of that population, then only we can conclude.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #9 on: April 24, 2008, 02:15:37 AM »
I've read reports on ethnic genetics, there was one study that tried to locate any differences of loci from different samples around the world. In the experiment, the data were grouped into 9 regional populations studied for 49 alleles and haplotypes belonging to 20 polymorphic loci. Average genetic distances from the all-world human gene pool to each of regional one, and from these to gene pools of ethnic groups within regions were estimated and compared.

It is possible to do a specified research; a case study on Aboriginal gene presence in certain south east asian regions. The problem we come into is funding. Gene sequencing and analysis for a large population sample (it would be necessary to evade Type II analysis error) would cost millions of dollars.

Isn't it funny how in the long run, money always is the last indicator? The prime factor?

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #10 on: April 24, 2008, 02:52:15 PM »
There was one case study conducted by an Indian geneticist regarding one tribe located East of Sumatra "the Andamans", where their genetic marker did not fit to the puzzle of human migration patern. They even suggests that these tribes exists before the ice age, before man migrated from Africa to Central Asia.

Such case sparked controversy that scientists, researchers and the media flocked the place.

Our case, is only of local interest and very isolated. However, if exposed, some may be interested like independent researchers and masteral students of these field conducting thesis. Going through a private company would cost millions.

On the other hand, genetics plays an important role in world health, but it is also a very dangerous tool to wipe out an entire species, like carrying a bomb in your pocket.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #11 on: April 28, 2008, 11:54:37 AM »
That is why it is key that all scientists who partake in the elucidation of humanity to genetics , be respectful towards human rights, animal rights, and assure the goal of research is for the betterment of man. Not the antithesis.

The grasp of genetics can either unravel the causes of certain disease pathways, certain genetic abnormalities and plausible treatments. However, there are those who would take advantage of such discoveries to create and genetically enhance known diseases/viruses for purposes of destruction. For death. For War.

As we speak, there are those who engage in both sides of the spectrum.



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Macky Ferniz

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #12 on: April 28, 2008, 07:38:01 PM »
Let me share you one real story of applied genetics.

Last Nov, we bought a land in Mindanao at a very cheap price of Php20,000 with an area of 2 hectares. We decided to plant corn, so we asked my wife's sister to watch the land and plant corn.

During harvest time, we sent her a note to keep some sacks for their consumption.

To my surprise, they told me that the corn they planted is not edible nor safe for human consumption. They have planted a genetically engineered corn for fuel production. They said if you eat the corn it will make you sick due to it's high starch level. This corn will be processed by one company to be converted fuel additive to gasoline or diesel and the stems will be processed as animal feed.

They harvested last Feb and the company who bought the corn harvested the crops for free.

If this is the trend of genetics, then it is a good progress to humanity.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #13 on: April 29, 2008, 12:34:29 AM »
I am truly amazed that such programs are occurring in the Philippines. Genetically-designed plants for environmental and energy purposes is what defines the progress of a certain nation towards the future.

I currently work with Dr. Klein, who herself is doing research with other colleagues in other research universities in designing a peroxidase sequence that identifies what part of synergy and during embryogenesis of a plant that certain stages of Phytophthora Root Rot occurs. They are right now, successfully cloning and identifying a particular peroxidase sequence and within that sequence, the basal nucleotides that composes the protein sequence that makes up the greater peroxidase. When they completely identify a particular peroxidase sequence responsible for the manifestation of Phytophthora Root Rot, they can, thereby, go in and suppress that particular protein sequence through genetic therapy. Through seed-by-seed oversuppression techniques.

I have worked with Dr. Klein in the genetic cloning of Brassica Rapa and Arabidopsis Thaliana tissues, in order to harvest specific peroxidase sites (cotyledons, stem, root, tissue). For purposes of finding a genetic comparison.

The effects of this, if Dr. Klein and her research colleagues are able to identify it, translates in the hundreds of millions of dollars saved for farmers in the United States and abroad. The positives of plant-based cloning is that we clone ever part of a plant, and sequentially identify and mark every aspect of a particular species' genome.

We cannot do that to humans. As it would be a violation of most (if not all) moral and ethos practices.

OT: What part of Mindanao did you buy your land, Mr. Ferniz? I am impressed with the energy-oriented activities in the agrarian industry in the Philippines. The country really is going progressive. Even if it is only in a case-by-case basis.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #14 on: April 29, 2008, 12:57:15 AM »
You know what I also find rather amazing, Mr. Ferniz?
Life. And its uncontrollable nature.


I recently read a manuscript entitled  Environmental Science Today, there was one article in there that caught my attention. The basis of the study was the mutative capabilities of genetically designed potatoes and tomatoes. The study focused on these said vegetables, which were designed so that during  embryogenesis, these plants would over-express fruit formation therefore it translates in a larger potatoe plant, or tomatoe plant despite soil concentration, richness of soil etc.

The years of the geneticists in developing the perfect promoter sequence that would induce transcription of a certain gene that would allow the bearing of fruit. They were meticulous in making sure that repressors that would inhibit growth would be genetically and completely removed. All of this was designed in a sterile environment in a laboratory.

However, when the seeds were planted in a particular farm, the vegetables did not grow according to expectations under stressful environment. Even though it was genetically designed to grow effectively under trying environment.

The reason for this, they concluded after post-mortem examination of said plant tissue, was the fact that plants, like any life, have a counter-repression ability.

These genetically engineered plants, despite man-made, have the ability to repress man-made promoters. This tells us that within the genome of a plant, deep regions of the genome, there is some kind of marker--some kind of activator that tells a plant to do something totally unexpected. Beyond our knowledge, we don't know what causes this. This is so called 'mutanogenisis'; the same pathway that causes diseases and causes breakdown.

Life, truly is unpredictable and can never be truly contained or retained. As even man-made, genetically modified man-made mutants can revert back to pre-mutation. I am awed by that ability. For a plant to do that! Now if a simple prokaryotic plant can do that, can you imagine the abilities of higher tiered organisms, such as Humans (the apex of animalia).

It is as if nature beckons to us that man-made procedures are sometimes unnatural. Untrue.
Life, as it is unstable, unpredictable, is also designed to last for a finite amount of time. As a seed plant is born, so will it grow, reproduce, and eventually abate. There is a simple and beautiful cycle in it, and in my belief--as though I would like to think there is a way to maintain longevity in humans--maybe a way to genetically turn 'off' death. I know it cannot be so. Though there are many scientists who believe that it can be so.

I personally think it cannot be. If we cannot even completely understand a simple tomatoe or potatoe, how can we even begin to fathom the ability of man-induced immortality. Nature, as it always has, would just find a way to over-express death, or inhibit man-made promoters.



The brilliance of God in how he made his creations, all organisms from the little fruit to the great Elephant, never ceases to amaze me. What a beautiful and powerful creator and designer of life. Of nature.


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Macky Ferniz

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #15 on: April 29, 2008, 05:24:02 PM »

OT: What part of Mindanao did you buy your land, Mr. Ferniz? I am impressed with the energy-oriented activities in the agrarian industry in the Philippines. The country really is going progressive. Even if it is only in a case-by-case basis.

The land is in Esperanza, Agusan Del Sur, a boundary between Agusan and Bukidnon Provinces.

During the 1960's this place was destroyed by a logging. They sold thier trees to Entrepreneurs which leave them with unproductive soil, landslides and floods. Nowadays people realized thier mistakes and started planting back native trees, as well as commercial trees. This initiative started a decade back during the time of President Ramos and now, the people are harvesting thier trees and you can see the hills are green again. Amazingly, since 5 years back, the annual flood stopped even it rained hard last year.

We also planted commercial trees in one of our land. The commercial name of the tree is "Palcata". I don't know the scientific name of that tree, but they told it is a mutation of the Acacia. It is fast growing tree and in 5 years you can start harvesting. The good thing about this tree is you cut it halfway during harvest and it grows back branches and again you will harvest a year after and so on.

This is used for paper production and the company buying will harvest free of charge. The profitability of the harvest is around P200,000 per hectare per year. Hopefully, I will start harvesting after 3 years from now.

My inlaws who is taking care of the land told that a Malaysian aproached them and asked if we would sell the land for Palm Tree plantation. I instructed them not to sell. Also the Mayor of the place refused to sell any land to the Malaysians or any foreigner. The mayor being a native "Manobo" elder, told that this land is sacred for thier tribe.

Sadly, in Bukidnon, the people are selling thier lands and many Malaysian companies are already cultivating Palm for oil production. They pay minimum taxes to Phil. Govt. and all profits will go to their banks in Malaysia.

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #16 on: April 30, 2008, 02:14:56 AM »
OT: The Malaysians are so greedy and taking advantage of the poverty of Filipinos. Are they not satisfied with the vast land of Sabah that they stole from the Philippines? The states of Sabah and Sarawak in Eastern Malaysia are practically un-used and still ripe with rubber trees; the soil in those states are so rich in nutrients.

And they have the audacity to come to the Philippines?

Wake up Philippine government! Why are we prostituting ourselves to businessmen of Malaysia and other south east asian nations? Keep Philippines for the Filipino!

The Philippines needs to implement a law that prohibits foreigners to ever purchase land, only if they are willing to become Philippine citizens and pay Philippine taxes can they purchase land.

I like China's and India's stance on their territory. No foreign national can purchase Chinese or Indian soil. And even if one marries into a Chinese or Indian family, the foreigner cannot own the land; technically his or her child can. So long as the child is born and recognizes China or India as their motherland.

Mr. Ferniz, Malaysians are known to take advantage of their poorer neighbors. They take advantage of poor Indonesians as well, using them as domestic workers, and encroach on Indonesia's land. It is a shame that they are doing this as well in the Philippines.

Mr. Ferniz, I salute you for your refusal to sell land to these Malaysian businessmen. It is a total shame that they would take advantage of their own Malay brothers. Beyond the name and our religions, the Filipino, Malaysian and Indonesian are brothers. Of the great Malay race.

But even in some sibling relationship, I guess there is always one brother who takes advantage of his poorer relatives. And Cheats them from what they truly own and deserve. :(



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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #17 on: April 30, 2008, 11:30:56 AM »
Back to the topic tho, lets address the concept of mutation. And how does mutation occur within the molecular model. As mutation can conflict with treatment, even alter the mode of treatment.

Shall we?

:)

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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #18 on: May 08, 2008, 03:46:56 PM »
As said earlier, mutation within a gene, also known as mutanogenesis, is the prime cause of most physical and neural degeneracy.

I can think of thousands of mutanogenetics, the two forms that I'm well acquainted with is the inhibitory/repressive abilities of certain transcriptional proteins.

Within molecular genetics, our understanding is rather elucidated, however, there are anomolies that defy traditional concepts such as basal understanding of the translational pathway, the elongation pathway, and the transcriptional pathway.

For a specific example, what happens in genetics is that we have a protein base, composed of multiple amino acids that form a nucleotidic chain. When this happens we have interaction of certain protein charges, which will attract positive or negative charged diatoms. Basically what happens is that such charges will attract the arrival of RNA Polymerase I, II or III. The RNA polymerase is imperative in that it carries with it a CTD (Cytosine Terminal Domain) which will allow it to be kinased (phosphorylated) by an important subunit known as the HAT (Histone acetyl transferase), this will acetylize all histon chains and surrounding nucleosomes, including the CTD of the RPB1 of the RNA Polymerase I, II, III. When we have this, this will allow the attraction of specific kinds of promoter complexes.

When the promoter complexes are formed, we will have the ability of elongation, then translation. When this happens, the chromatin will form. When the chromatin is formed, so long as it is induced, we will have ability for transcriptional pathway--which leads to transcription of a gene. Which, if transcribed, will mean that that particular gene (ex; a gene that is in charge of nose formation, eye formation, hair formation, activity of the left brain, right brain, formation of the lung, formation of heart, etc etc). So, as you see, the proper transcription of one simple gene resonates as an important truth for the organism.

Any inhibition of gene formation and proper transcription will lead to organismal degeneracy and instability. An example of genetic failure, natural imbalance, a genetic mistake.

This is the real life example of mutanogenesis.

What puzzles us, scientists, is that we are able to utilize ChIP analysis (chromatin immunoprecipitation analysis), Electrophoresis, genetic cloning, as well as genetic modeling through DNA linker analysis; however there are anomalies that lie beyond our understanding. These anomolies are what drives our interest to study deeper; to have a better understanding of what causes such anomaly.

Specifically, one example of a genetic anomoly that puzzles us is TAF (Transcriptional-Associated factors) mutanogenesis. Normally, TAFs will link to each other with the TFIID to allow the transcription within a TATA box of the genetic line. Even in preferred circumstances, some TAFs will not bind to TAF-linked co-activator protein syndicates. Usually the TAF will bind to the TAF-linked co-activator protein syndicates. By natural law, positive will bind to negative; and in this case an Adenosine-based factor will bind to a thymine based factor; or a cytonsine-based will bind to a guanine-based. However, in TAF mutanogenesis, these TAFs will just not bind. Or bind to one and not to others. But why do they do this?
All components necessary for proper linkage and binding and processing is there--but still problems arise.




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Lorenzo

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Re: Understanding the Gene: Amytrophic Lateral Sclerosis in case study
« Reply #19 on: May 08, 2008, 03:47:44 PM »
It is in my firm belief, as a student-scientist, that prooves the concept of Divine Plan. Divine Intelligence. Divine Design. Mutations of genetic level is, in my opinion, is proof of Divine presence. The fact that it occurs without a reason--it happens because it just does. Many molecular biologists say that it is not the presence of the divine, but by a subjects innate inferiority that leads to such genetic impudence.

However, it is impossible to repudiate the existence of a Divine Planner. The odds that our genetic pathways, which are perfect in my opinion, developed from nothing is already in astronomical numbers. It is too perfect to have come from chance.

Mutanogenesis is not only a scientific anomoly. Mutanogenesis is proof of our Maker's Imprint. His Presence.

The evolution of life from a simple prokaryote to the multiple tiered eukaryotic species in the world is proof of that intelligence. All living beings, are genetically related.

Why is it that a simple fly, Drasophola, has 75% of the same genetic homolog as that of the Homo Sapiens sapiens? This means that humans and flies share 75% of the same genes. Why is it that a simple pea has the same hnRNAs, rnRNAs, SM Proteins, RNA Polymerase I, II, III; same formation and same replication of cells as that of a mammal? A cow? A dog? etc?

Evolution, is proven to us through molecular genetics. And is the basis of Truth.

One thing that I take from this, is that our GOD's intelligence is BEYOND this world. Our genetic complexities resounds to the Maker's unassailable brilliance.

Those who disagree with me, please do so. And provide scientific fact to support it.
Because as a believer, science, is testament to the Infinity and Divinity of the Lord.
It is PROOF.


 8)

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