The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
The PDC deficiency cause lactic acid accumulation in the body part. In the absence of deficiency of PDC, the pyruvate will be unable to convert into acetyl Co- A and hence the pyruvate undergoes anaerobic respiration to form lactic acid leading to the damage of the tissue in absence of energy in form of ATP. In this case the body unable to break down nutrients efficiently and no ATP is formed to be used for energy.
Some cells are more vulnerable to the PDC deficiency because they are totally relied on the presence of glucose that undergo glycolsis and then enter the TCA cycle and ATP formed which is used for proper function. Tissue like brain is such example that utilizes only glucose as a source of energy aerobically. So it is highly vulnerable to the PDC dysfunction or deficiency.
Clinical manifestations: metabolic dysfunction(lethargy and increased breathing rate), neurological dysfunction (ataxia, hypotonia, developmental delay, abnormal seizures), brain abnormalities, low birth weight in infants, frontal bossing in babies etc,.
3. Why are some tissues more vulnerable to inhibition of PDC activity and how does this...
Describe why the world is more vulnerable to spread of viral infections today compared to 100 years ago? Using HIV as an example, explain how new human pathogens emerge due to viruses jumping from animals to humans.
In plants, germ cells are derived from tissues late in plant growth. How does this fact relate to inheritance patterns observed in plants versus animals? a. This explains the presence of Barr bodies found in the cells of animals but not in plants. b. This explains why some genes in both the egg and sperm of animals contain special methylation patterns, whereas in plants all gametes have the same methylation patterning. c. This explains why epigenetic modifications are heritable in...
3. explain why more companies are changing their costing system to Activity Based Costing. (8 marks)
3. Why is an allosteric enzyme more sensitive to substrate concentration around Km values than a Michaelis-Menten enzyme with the same Vmax? 4. Explain how pH and temperature influence enzyme activity. ( A Lineweaver-Burk (double reciprocal) plot was used to compare the effects of three different reversible inhibitors (A, B and C) on an enzyme. The plot of 1/V vs 1/[S] for the enzyme with no inhibitor is shown in a solid black line. The plot of 1/V vs 1/[S]...
Correct answer and why the other ones are wrong
3. How does phosphorylation regulate protein activity? a. It adds energy to the protein b. The negative charge associated with the phosphate group blocks the binding of negatively charged molecules c. It causes a conformational change in the protein d. It denatures the protein.
Using suitable examples explain why does Hoffman product (more substituted alken) predominates in some Elimination reactions whilst the Hoffrman product (less substituted alkene) form in others Using suitable examples, explain the differences in mechanism, mechanism, substrates, nucleophile and solvents in a SN1and SN2, Using suitable examples, explain the differences in mechanisms, substrates, bases in an El and an E2 reaction.
How is activity based costing used to measure customer profitability and why does it need to be tracked by customer?
VI. Some more assignments for practice. See how understanding of Sn1, SN2, E1, E2 is essential here. • the substrate produces a cyclized product in presence of acid/base (circle one) • draw the structure of the cyclized product Сн,он olyo CHOW .no optical activity in the product explain why einen H3PO4 heat NaOEt product and configuration? (E2) EtOH, heat NaOH why no reaction?
why do some people put more faith in testimonials than in proven research. (this question does not have to do with celebrity testimonial).
Use the sources below to learn more about African trypanosomiasis. "Parasites-African Trypanosomiasis, " Centers for Disease Control and Prevention http://www.cdc.gov/parasites/sleepingsickness/"Trypanosomiasis, African, " World Health Organization (WHO) http://www.who.int/topics/trypanosomiasis_african/en/After thoroughly investigating these and other relevant sources, answer the questions below. What is a protozoan? How is a protozoan parasite different from bacteria and multi-celled parasites such as intestinal worms? How does T. brucei differ from the closely related American trypanosome T. cruzi, the causative agent of Chagas disease, and from the P....