Health, Medical and Science Thread

[lavce pelagonski]

I would like this thread to be used for the benefit of all Macedonians who may not know alot about the human body and the types of diseases and illnesses that can occur.

LIVER CANCER ESSAY

Liver cancer is the third in the world of cancer related deaths (WHO, 2009); this topic will look at the epidemiology and pathogenesis of the most common liver cancer, hepatocellular carcinoma. The biological, social, environmental and behavioural factors that accompany epidemiology and pathogenesis of liver cancer will follow. The methods of diagnosing liver cancer will also be discussed.

Important definitions to remember; Hepatocellular carcinoma is a malignancy of the liver (Feldman et al, 2006). Alanine aminotransferase (ALT) is an enzyme that converts L-alanine and D-alanine and visa versa (Feldman et al, 2006). Aspartate aminotransferase (AST) is an enzyme, it catalyses aspartate which reacts with 2-oxoglutarate the end result is oxaloacetate and glutamate (Feldman et al, 2006). The pigment of bile is referred to as bilirubin; it is formed from the breakdown of haemoglobin (Feldman et al, 2006).

Epidemiology of Hepatocellular Carcinoma of the Liver
The most common liver cancer is hepatocellular carcinoma (HCC). The incidence for this type of carcinoma of the liver is increasing to a point where it is now fifth on the list of common malignancy in the world; it is also the third leading cause of death related cancer (WHO, 2009). Data that has been collected suggests that new cases amount to 500,000 – 1,000,000 per year, out of these figures 600,000 deaths occur worldwide annually (Parkin et al, 1999). On a global level there are however differences in the level of HCC between countries and is only now being looked at as a factor that may link certain populations who have an increased risk (Parkin et al, 1999).

The world Health Organisation (WHO) has pointed out that a lot of the cases of HCC are in fact coming out of Asia. Montalto (et al, 2002) confirmed that in East Asia the incidence here are very high, on Mongolia 99 per 100,000 people, Korea 49 per 100,000, Japan 29 per 100,00, and in China 35 per 100,000 (Montalto et al, 2002). The western region of Africa is also a place of concern, places such as Gambia, Guinea and Mali. Italy, Spain and Latin America are not exempt and have high risks, 11 cases per 100,000 to 20 cases per 100,000 found in these countries (Montalto et al, 2002). The countries that are intermediate happen to be in Europe with 5 cases per 100,000 to 10 cases per 100,000 occurring in France, the United Kingdome, and Germany (Montalto et al, 2002). The lowest incidences occur in the United States, Canada and in Scandinavia with less than 5 cases per 10,000 people (Montalto et al, 2002) (Parkin et al, 1999).

Montalto and his colleagues (et al, 2002) have found that in developed countries that are at low risk such as the United States the incidence of HCC are rising by 80% per year in the past 20 years (Montalto et al, 2002) (Parkin et al, 1999). The study reveals that African-American men are more prone to HCC than US Caucasian men; this is seen in the high cases of hepatitis C and the rise in immigration from countries that are high risk have also played a part (Montalto et al, 2002). Other countries, Montalto (et al, 2002) and Parkin (et al, 1999) have noted, Italy, the United Kingdome, Canada, Japan and, Australia have all recorded increased cases of HCC, these increases were from immigrants from Sub-Saharan African countries and parts of Asia where there is a high prevalence of HCC.

A report that was conducted by Jong-Wook (et al, 2003) in conjunction with the World Health Organisation (WHO) in 2003, that a total of 714,600 new cases of HCC have been recorded globally, this accounts for 71% among men. With the findings of Seeff (et al, 2006) geographically the results show “45,000 liver cancer deaths happen in Africa, 37,000 in the Americas, 15,000 in the eastern Mediterranean, 67,000 in Europe, 61,000 in south-east Asia , and 394,000 in the western Pacific region which includes China and Japan” (Seeff et al, 2006). In 2006, 501,000 men and 282,000 women died of cirrhosis with a combined total of 783,000 persons (Seeff et al, 2006). From this study Seeff (et al, 2006) found that HCC increased with age and that when a person reached the age of 65 years it had a high prevalence, he noted that before the age of 50 it was rare for someone from North America and Western Europe to get HCC. Nonetheless there has been a slight shift to suggest that HCC is becoming higher in the younger population (Seeff et al, 2006)



Pathogenesis of Hepatocellular Carcinoma
The focus will be put on how hepatocellular carcinoma is linked to TP53 mutation, aflatoxin B1 (AFB1) and how infection by hepatitis B and C can have a direct affect in the progression to liver cancer.

Aflatoxin B1
Bressac (et al, 1991) looked at the mutational spectrum of hepatocellular carcinoma and has found that cancer can form with carcinogen exposure. In the study it was observed that geographical areas that have a diet exposed to AFB1, which contains foods like corn, rice and peanuts and also areas such as China and Africa which have high rates of chronic viral hepatitis (Bressac et al, 1991). This will give rise to a point mutation which results in a transversion of G: C to T: A due to the third position of codon 249ser (Bressac et al, 1991). Kirk and colleagues (et al, 2005) studied patients from Gambia with HCC, they found that that in serum DNA codon 249 mutation could be noticed, this meant that it was possible for TP53 to be a biomarker due to the exposure to AFB1 and early hepatocellular carcinoma (Kirk et al, 2005)

With an active AFB1 it mutates and to binds to DNA by 8, 9-epoxide to form promutagenic N7dG (Bressac et al, 1991) (Kirk et al, 2005) oxidative and nitrosative stress from AFB1 can cause TP53 249ser mutation via lipid deoxidisation (Bressac et al, 1991). Without the exposure of AFB1 it is not common for there to be a TP53 249ser mutation, this applies to HBV or HCV infection (Bressac et al, 1991). At this stage it is not known if AFB1 by itself can cause HCC without HBV infection in a population, it is however known that when HBV and AFB1 are together there is a high number of TP53 249ser mutations in HCC (Bressac et al, 1991) (Ming et al, 2002)

Hepatitis B Virus (HBV)
The two main hepatitis viruses that contribute to liver carcinogenesis are HBV and HCV; they produce liver injury and are promoters of hepatocarcinogenesis. There are still studies being conducted to verify if hepatitis infections cause the tumours or if inflammation that leads to liver cancer and cirrhosis has an affect on tumour promotion in hepatocarcinogenesis (Tang et al, 2006).

The viral proteins of HBV and HCV in order to survive have to interact with the bodies proteins which they change, this alters the cellular gene expression, and it is thought that this process can lead to virus – associated carcinogenesis (Tang et al, 2006). Hepatitis B is a partially double stranded DNA molecule and is a hepadna virus (Tang et al, 2006) for the viral protein to have any affect it needs the gene X of HBV which is named HBx, this is needed in transcription of the viral gene (Tang et al, 2006).

Tang (et al, 2006) has focused on the HBx protein which has a strong role in HCC. The HBx gene is the most currently open HBV gene (Tang et al, 2006). Binding of p53 is reduced by HBx and inhibits nucleotide excision repair and in transcription, it interacts with other DNA enzymes (Tang et al, 2006) (Mathonnet et al, 2004). Mathonnet (et al, 2004) and Tang (et al, 2006) make a note of the fact that when HBx directly interferes with the normal cellular DNA repair system it leads to HBV contribution to liver carcinogenesis. If the function of p53 – mediated apoptosis is lost two factors that could be favourable in contributing to hepatocellular carcinogenesis are neoplastic hepatocytes or preneoplastic (Mathonnet et al, 2004)

Hepatitis C Virus (HCV)
To get an idea of how HCV affects hepatocellular carcinogenesis Honda (et al, 2001) uses microarray technology, it analyses HCV in relation to cirrhosis. It has shown that this leads to up regulation of pro – inflammatory, pro – apoptotic and pro – proliferative genes, all of these factors result in hepatitis C associated with cirrhosis to lead to hepatocellular carcinogenesis (Honda et al, 2001). With HCV the TP53 tumours have a greater potential to become malignant according to Honda (et al, 2004).

Biological Factors
Epidemiologically it has been discussed that hepatitis B and C can have a direct affect on p53 to alter its genetic makeup and use the body’s proteins to make more HBx proteins in the liver (Tang et al, 2006) (Mathonnet et al, 2004). With the p53 gene altered in a state that can defect and mutate more readily it adds to the pathogenesis and increases the risk of hepatocellular carcinoma of the liver.

Social Factors
When looking at social factors that might influence liver cancer it is imperative to include the economic and employment status of an individual. In a Swedish study conducted by Ji (et al, 2005) different social groups were looked at to see if a persons profession could in fact be a factor in increasing the likelihood of liver cancer. The study used data from the 1960 and 1970 census and did a follow up study to compare new data that has been collected. It was found that male farmers were at a low risk to all types of liver cancers including HCC and professionals such as executives and those that had private businesses (Ji et al, 2005).

Behavioural Factors
Montalto (et al, 2002), Parkin (et al, 1999) and the WHO all give data to support alcohol as a factor in fatty liver disease which leads to liver cancer. Diet is something else that has been mentioned by Bressec (et al, 1991), contamination of foods like rice, corn and peanuts by AFB1.

Environmental Factors
With reference to geographical regions Africa and East Asia have increased risk of developing hepatocellular carcinoma and any other type of liver cancer due to HBV or HCV infection (Montalto et al, 2002) (Parkin et al, 1999) (Jong-Wook et al, and WHO 2005) and (Seeff et al, 2006). It could also have something to do with the chemicals from the environment that can contaminate food (Bressac et al, 1991).

Methods of Diagnosis
With diagnosis there isn’t a specific test that is performed but rather a variety of tests that look at detecting hepatitis and other abnormalities such as the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and bilirubin.
Alanine aminotransferase (ALT) is used as a method to identify patients with liver disease as it detects liver cell injury and hepatocellular damage (Feldman et al, 2006). Recently, ALT is the most used test to identify serum ALT level in patients with liver disease (Feldman et al, 2006).
Aspartate aminotransferase (AST) concentration can be elevated in heart and liver diseases that are connected to the destruction of those tissues via the blood (Feldman et al, 2006). The normal levels of AST are from 8 to 20 U/l, these levels can change depending on the reply it gets from to the magnitude of cellular necrosis (Feldman et al, 2006).
Bilirubin is also important in detecting liver cancer, after its production it is taken to the plasma and then the liver where it will be excreted in the bile. Increased amounts of bile in the blood of>30 mg/l will lead to jaundice (Feldman et al, 2006).

When HCC occurs ALT enters the bloodstream as it is secreted from the liver cells, this in tern increases the serum level which would give a high result. The normal levels for Alanine aminotransferase are from 10 to 32 U/l and in women range from 9 to 24 U/l (Feldman et al, 2006). In an infant it is twice the amount of an adult (Feldman et al, 2006). In acute viral hepatitis an increase in serum transaminase activity is due to an increase in one particular aminotransferase, ALT which in the period of acute hepatitis B it can increase from a mild increase of 10 times the normal amount to a startling increase of 100 times the normal amount (Feldman et al, 2006). In most patients’ symptoms such as tiredness, abdominal discomfort which leads to anorexia can in turn can make a patient feel nauseas and make them vomit, all these symptoms can lead to the patient developing jaundice, with regards to fever it is generally mild and may not appear at all (Feldman et al, 2006).
A sudden drop in ALT and AST in patients with fulminate hepatic failure it can be understood as the clearing of hepatic infection, this ultimately comes down to a deadly outcome as hepatocytes are being lost (Feldman et al, 2006).

It is important to understand that liver cancer is on the rise and the number of people diagnosed will increase. By studying the epidemiology it is becoming clear that there are trouble spots around the world where this disease is prevailing and in most cases the number one killer, this has lead to an effort to study the pathogenesis of liver cancer and in particular hepatocellular carcinoma and its relationship with hepatitis B and C to a greater extent. New methods specific in detecting liver cancer should be designed to ensure fast and early detection as it is the key in preventing and stopping the spread to other organs. It is certain however those behavioral factors such as excessive alcohol consumption have a negative effect on the liver. Social status has shown that people that have stressful jobs are more inclined to aid in HCC. Contamination of food due to the environment has also been considered.






References
Bressac B, Kew M, Wands J, Ozturk M, 1991.’Selective G to T mutations of p53 gene in hepatocellular carcinoma from southern Africa’. Nature. Volume 350, pp. 429–431. Viewed 18 August 2009, retrieved from EBSCOhost.

Feldman M, Friedman L S, Brandt L J, 2006. Saunders, ‘Nonalcoholic fatty liver disease. Gastrointestinal and Liver Disease’. Eighth edition. Canada. pp. 1793–1805.

Honda M, Kaneko S, Kawai H, Shirota Y, Kobayashi K, 2001. ‘Differential gene expression between chronic hepatitis B and C hepatic lesion’. Gastroenterology. Volume 120, pp. 955–966. Viewed 18 August 2009, retrieved from EBSCOhost.

Ji J & Hemminki K, 2005. ‘Variation in the risk for liver and gallbladder cancers in socioeconomic and occupational groups in Sweden with etiological implications’. International Archives of Occupational and Environmental Health. Volume 78, pp. 641-9. Viewed 18 August 2009, retrieved from EBSCOhost.


Jong-wook L. and WHO, 2003. ‘Shaping the future’. Global health improvement. Volume 362, pp. 2083-2088. Viewed 18 August 2009, retrieved from EBSCOhost.

Kirk GD, Lesi OA, Mendy M, Szymanska K, Whittle H, Goedert JJ et al, 2005. ‘249(ser) TP53 mutation in plasma DNA, hepatitis B viral infection, and risk of hepatocellular carcinoma’. Oncogene. Volume 24, pp. 5858–5867. Volume 120, pp. 955–966. Viewed 18 August 2009, retrieved from EBSCOhost.

Mathonnet G, Lachance S, Alaoui-Jamali M, Drobetsky EA, 2004. ‘Expression of hepatitis B virus X oncoprotein inhibits transcription-coupled nucleotide excision repair in human cells’. Mutat Res. Volume 554, pp. 305–318. Viewed 18 August 2009, retrieved from EBSCOhost.

Ming L, Thorgeirsson SS, Gail MH, Lu P, Harris CC, Wang N et al, 2002. ‘Dominant role of hepatitis B virus qand cofactor role of aflatoxin in hepatocarcinogenesis in Qidong, China’. Hepatology. Volume 36, pp. 1214–1220. Viewed 18 August 2009, retrieved from EBSCOhost.


Montalto G, Cervello M, Giannitrapani L, Dantona F, Terranova A, Castagnetta LA, 2002. ‘Epidemiology, risk factors, and natural history of hepatocellular carcinoma’. New York Academy of Science. Volume 963, pp.13-2. Viewed 18 August 2009, retrieved from EBSCOhost.


Parkin DM, Pisani P, Ferlay J, 1999. ‘Estimates of the worldwide incidence of 25 major cancers in 1990. International journal of Cancer. Volume 80, pp. 827-841. Viewed 18 August 2009, retrieved from EBSCOhost.


Seeff LB, Hoofnagle JH, 2006. ‘Epidemiology of hepatocellular carcinoma in areas of low hepatitis B and hepatitis C endemicity’. Oncogene. Volume 25, pp. 3771-3777. Viewed 18 August 2009, retrieved from EBSCOhost.

Tang H, Oishi N, Kaneko S, Murakami S, 2006. ‘Molecular functions and biological roles of hepatitis B virus x protein’. Cancer Science. Volume 97, pp. 977–983. Viewed 18 August 2009, retrieved from EBSCOhost.

World Health Organization, 2009. Mortality database. <http://www.who.int/whosis/en>. Viewed 18 August 2009.

[lavce pelagonski]

H1N1- Swine Flue

Advance Medical & Veterinary Microbiology

The outbreaks in North America happened in early April 2009 of the new influenza virus which spread quickly around the world. In the space of three months swine flu (H1N1) was classified as a pandemic by the World Health Organization (WHO), at this stage there were 74 countries and territories that had confirmed infections in laboratories (WHO, 2009). As it stands the majority of countries around the world have reported and confirmed the presence of this new influenza virus. For pigs the swine influenza virus is a common respiratory disease in countries where pigs are raised. Infection is commonly displayed as unpredictable with acute respiratory disease followed by fever, anorexia, weight loss, nasal and ocular discharge, and coughing (WHO, 2009). The passation of influenza virus to infect a human population has to overcome the hurdle of cross-species infection (Lamb & Krug, 1996). It is definitely possible for the barrier to be breached with the evolution of the influenza polymerase (Lamb & Krug, 1996). In this report the pathogenesis and relevant control measures of swine origin H1N1 influenza will be looked at.

From the 2009 H1N1 pandemic virus isolates from patients were collected, they show that replication is efficient in the lungs of mice and were confined to the murine respiratory tract (Lamb & Krug, 1996). The 2009 H1N1 virus tested was able to show some common pulmonary pathology similar to other influenza A viruses (Lamb & Krug, 1996) (Maines et al, 2009). This included mild to moderate bronchiolitis and alveolitis. “Necrosis was not a common feature and neutrophilic responses were typically mild” (Lamb & Krug, 1996).

It is not common for RNA viruses to carry out its RNA synthesis, transcription and replication in the nucleus of infected cells that is what makes the influenza virus unusual in this respect (Maines et al, 2009) (Munster et al, 2009). The influenza virus will bind to ribosomal RNA of the infected cell. “After synthesis in the cytoplasm, nucleocapsid protein molecules are transported to the nucleus” (Munster et al, 2009). Inside the nucleus it is the perfect environment for the synthesis of viral particles (Maines et al, 2009) (Munster et al, 2009). Because this is not like other RNA viruses, in infected cells H1N1 RNA and antigen will easily be detected in the nucleus and cytoplasm (Maines et al, 2009).

The detection of H1N1 RNA and antigen were mainly found in bronchial and bronchiolar epithelial cells, this leads to the conclusion that bronchial and bronchiolar epithelium can contain sialyloligosaccharides which the influenza virus can use as a receptor (Maines et al, 2009) (Munster et al, 2009). An experimental study was performed were bronchiolar epithelium was looked at; it contained scattered cells that were infected in the lung parenchyma. In “situ hybridization and immunohistochemical results” (Maines et al, 2009) afford a good basis as they record that swine flu mainly targets the bronchial and bronchiolar epithelium (Maines et al, 2009) (Munster et al, 2009).






The control measures set in place ultimately lead to the prevention of H1N1, three main factors involve: Prevention in pigs, prevention of passation to humans, and control of its spread among humans (WHO, 2009). There are a couple of procedures used to control the spread of influenza virus among pigs. Facility management essentially refers to disinfectants used to reduce transmission between pig and human due to handling of the animal and controlling the climate to decrease potential for the virus to circulate in the environment (Taubenberger & Morens, 2006) (WHO, 2009). Herd management refers to disallowing infected swine to be released with the general population which has not been infected (WHO, 2009).

Among the human population that should be considered for vaccination against the H1N1 virus are those who respond to the outbreak in the first instance, health-care workers and pig farmers/breeders (Taubenberger & Morens, 2006) (WHO, 2009). Preliminary steps have been put in place for farmers and veterinarians when dealing with infected animals suggest using face masks and gloves to aid in the prevention of spreading the virus (Taubenberger & Morens, 2006). Recent studies have concluded that by consuming pork and pork products there is no chance that H1N1 can be spread by transmitting itself through food (Taubenberger & Morens, 2006).

The Centres for Disease Control further recommends people to wash their hands with soap and water or alternatively to use hand sanitisers. Distancing yourself from large group gatherings is another tactic (Taubenberger & Morens, 2006). This refers to mainly staying away from individuals who may be infected; putting some distance at work or staying at home due to a spread of infection through the community is another option until it clears (WHO, 2009). Treatment in swine is minimal as it is rare for pigs do die from swine influenza, only rest and minimal care is required (Taubenberger & Morens, 2006). Vaccination and animal management are very important methods and are essential in the control of the virus (Taubenberger & Morens, 2006) (WHO, 2009). At the moment vaccination is the best control measure in the protection of the new virus, but there is at least a six month development period before a suitable vaccine can be made and released to the general public (WHO, 2009).

In conclusion more study into the pathogenesis of swine origin H1N1 influenza virus is needed to fully understand the mechanisms it uses once infection has occurred. As mentioned above the common site of infection seem to be the respiratory tract infecting bronchial and bronchiolar epithelium. Control measures need to be put in place to prevent the transmission of the virus among the human and animal population and there are many preventative measures that have been put in place.




References

Lamb, R.A & Krug, R.M. (1996). Orthomyxoviridae: the viruses and their replication. F Virol 3, 1353–1395.

Maines, T. R., A. Jayaraman, J. A. Belser, D. A. Wadford, C. Pappas, H. Zeng, K. M. Gustin, M. B. Pearce, K. Viswanathan, Z. H. Shriver, R. Raman, N. J. Cox, R. Sasisekharan, J. M. Katz, & T. M. Tumpey. (2009). Transmission and pathogenesis of swine-origin 2009 A (H1N1) influenza viruses in ferrets and mice. Science 325, 484-7.

Munster, V. J., E. de Wit, J. M. van den Brand, S. Herfst, E. J. Schrauwen, T.M. Bestebroer, D. van de Vijver, C. A. Boucher, M. Koopmans, G. F. Rimmelzwaan, T. Kuiken, A. D. Osterhaus, & R. A. Fouchier. (2009). Pathogenesis and transmission of swine-origin 2009 A (H1N1) influenza virus in ferrets. Science 325, 481-3.

Taubenberger J K & Morens D M (2006). 1918 Influenza: the mother of all pandemics; Emerg. Infect. Dis 12, 15–22

World Health Organization (2009). Laboratory bio-risk management for laboratories handling human specimens suspected or confirmed to contain influenza A (H1N1) causing the current international epidemics; Available at: http://www.who.int/csr/resources/publications/swinefl u/en/index.html.

[Risto the Great]

Good idea.
Guys, a question:

Do you believe a person can will themselves into cancer or other illnesses? For example, the person who always contains his/her anger and does not ever vent .... gets throat cancer?

The person who fights depression who ends up getting heart disease?

[julie]

RTG, no, a lot of diseases and illnesses are as a result of bacteria and/or viruses that a weakened immune system is susceptible to. Environmental issues, such as poor indoor air quality/toxins (asbestos), can be another contributing factor. Resulting effects then lead to the immune system further being compromised, having Some illnesses can be genetically predisposed to such as asthma.
My major argument against a person willing themselves cancer is small children , and example being a young little cousin diagnosed with childhood leukemia at 18 months of age, and passing away 3 years later.
Mind over matter works with diseases in learning to accept, acknowledge and then being positive . People will either sink or swim, they can will themselves not to get better if able to, or can be negative and give up, which leads to depression
(I can write books on these topics )

[Risto the Great]

Hi J,
very interested in your perspective. I was hoping you might share your thoughts. I also think viruses are a very large contributor to these issues. A friend we both know is convinced he contracted throat cancer from an earlier case of Parvovirus.

I still think the mind can affect health and (in my mind) logically extend that to cancers etc. but also feel we have a long way to go in order to truly understand what the hell is going on!

[julie]

I have done some extensive research on cancer, muscular skeletal disorders, and the link with viruses and environmental factors which can have a causative effect on illnesses and disease. I seriously dont know where to start
I am also spiritual in that, reading books on mind over matter, can also have an impact on someones health, recovery or demise.

The throat cancer having being caused by contracting the parvovirus by your friend, am in agreeance with his conclusion.
Some mind over matter books may say, he was suppressed with speaking his mind as a child and it manifested in his throat (you can heal your life, Louise Brown, i think is the author , she was interesting

Most people fall ill from a combination of factors, and daily we are exposed to an alarming degree of things we cannot see - air conditioning especially in buildings we may work in , carry harmful bacteria and toxic substances that someone with a weakened immune system from something as simple as the common cold, can contract viruses that attack the immune system causing the bodies defence to shut down .

Mould is something that is equally petrifying. People think that by attacking mould with bleach, will rid it, WRONG, it colours the mould, and vinegar is the only thing that will remove it, unless there is a hidden issue of condensation forming within wall cavities . The spores that are breathed in from mould can do irreparable damage, we cant see spores either. I attended an interesting conference on effects of mould.

Chemicals that we use in everyday household cleaning, toiletries, the food we eat - the artificial preservatives and additives, cortisone pumped chicken we buy and consume, carry carcinogens.

My ultimate lifestyle, is to live on a farm, and be totally self sufficient, off the grid, and to get back to nature. Our children are leading different lifestyles from even our own generation , computers, and the myriad of electronic games and gizmos, they spend more time indoors, and its not healthy

Some research shows the link with cancer being genetic, or heart disease as something that runs in families. I dont necessarily agree with this to an extent, but rather, its the exposure from the same environment , a sister having breast cancer, and then , another sister is diagnosed with it.

Your friend sounds like he is trying to help himself, which is a good thing, that by trying to look at lifestyle and causative factors, that he is able to manage his condition.
Some people just give up. I dont have time for defeatists in life, yes its natural to have down days , but being depressed and not trying to help oneself will not aid in recovery, or be able to at least have a quality of life.

Stress kills. stress is very bad for the body, in order to be healthy, prolonged periods of stress can cause heart failure, adrenalin being pumped through the body in a constant mode is not how our bodies are meant to function.

I am not an advocate for aggressive chemotherapy and radiation with some cancers either. Chemotherapy not only destroys cancerous cells, but it also depletes the body of the blood cells required to fight infection. Radiation spreads cancers.

Positive minds can achieve a lot in disease too. Meditation is a cheap, relatively easy skill to use and everyone should incorporate in their lives, it relaxes the body, gets rid of stress, slows the heart rate , and eating healthy organic food , moderate exercise, is something that should be mandatory!

I have a " friend "caught a cold 3 years ago, weighed over 110 kilos. The stages of the auto immune system breaking down -
cold, pneumonia, viral pneumonia, hospitalisation, chronic fatigue syndrome, chronic fibromyalgia, fibroid tumours, ovarian cancer, adrenal issues, waiting for thyroid surgery,
the friend weighs 53 kilos today , walks with walking aid, bedridden many days, and on narcotic pain patches, amphetamines for chronic fatigue, muscle relaxants to stop the muscles throughout body spasming
This person has a choice, to either, learn to manage the condition, learn how to cope f, or sink into depression and self pity and die each day instead of living.
This person has chosen to involve themselves in assisting others in support groups, and being a catalyst for change , and is in the planning stages of lobbying for muscle relaxants also used by epilepsy sufferers , to be on the PBS (, $150 per month to be able to walk oneself to the bathroom is steep)

My inspiration in life comes from people that dont have a self defeatist attitude in life, and being proactive.

The human mind is incredible. Our basic needs are all being met, food, water, shelter. Everything else is irrelevant. People place "happiness" on material objects and wonder why once they achieve their goal, they are no longer happy, but want more, and attach themselves to material things. By trying to find something positive in something no matter how little, can make a difference to someone healing, if not in their own body, their own mind. Mind over matter, can make the difference between someone perpetuating their illness, or recovering, or if prognosis for full recovery is not possible, a quality of life.
The chemical make up of the human brain is incredible , and we use such a small proportion of the brain
if we can heal ourselves well , and there are many books written by people that have been given a death sentence, and have been in remission for many years, then perhaps we can also make ourselves ill. Am still pondering that one

[Phoenix]

Good post Julie...interesting thoughts.

I don't think anyone should underestimate the importance of 'clean' food, a clean environment, active lifestyle and a degree of insulation from stress in leading a healthy life...

[Zarni]

In the West there is a continuous quest to be happy and never finding it surely being happy contributes to good Health

Macedonians don’t understand how good they have it.

[Risto the Great]

There is this French chef (Fred Chesneau) that travels around the world and cooks with the locals to enjoy their food and culture. Every time he is in an Asian country it is an absolute pleasure looking at the poor (but happy) people all enjoying their food and eating together at breakfast, lunch and dinner. Huge families all participating in the preparation of the food. That is gone in Western culture and it is a shame. Depression is rampant in Western society and barely noticeable in poorer nations.

Macedonians are looking to the West for guidance and all they get in return is ungrateful little bludgers who waste their lives away.

As Phoenix mentioned, amongst other points he raised, I think an active lifestyle is a very important component of health. When you see the 70 year olds in Switzerland walking through the Alps looking like spritely 50 year olds and then look at our 50 year olds already condemned to early death through inactivity ... the answer is obvious.

[lavce pelagonski]

Biochemistry and Molecular Biology

“Discuss the active mechanism(s) required to maintain phospholipid asymmetry in the erythrocyte plasma membrane bilayer and how the lipid distribution can be determined”.



Between the two leaflets of the endoplasmic reticulum(ER) lipids are symmetrically spread, in the Golgi, endosomal, and plasma membranes (PM) of eukaryotic cells an asymmetric spread of lipids is seen, “aminophospholipids (phosphatidylserine and phosphatidyletholamine) are primarily exposed on the cytosolic leaflet, whereas phosphatidylcholine and sphingomyelin are mainly located on the outer leaflet. Lipids such as phosphoinositol and phosphatidic acid are mainly in the inner leaflet, whereas glycosphingolipids face the outer surface” (Huijbregts, Topalof et al. 2000; Balasubramanian and Schroit 2003). When asymmetry was discovered it was found that adenosine triphosphate (ATP)-dependent translocation of PS and PE between bilayer leaflets is a major player in membrane lipid asymmetry (Bevers, Comfurius et al. 1998), this discovery is important as it show that cell spend a great deal of energy for this process.

Erythrocytes from rats or humans have been used to study the structure of the eukaryotic membrane and related lipid asymmetry extensively (Fadeel and Xue 2009). There are two transport activities that play a vital role in upholding lipid asymmetry; they are energy-dependent and energy-independent (Balasubramanian and Schroit 2003; Basu, Banerjee et al. 2008). Three types of acknowledged lipid transporter activities have been proposed: “a “flippase”, which catalyzes ATP-dependent inward transport of lipids; a “floppase”, which promotes ATP-dependent outward movement of lipids; and a “scramblase”, which stimulates bi-directional movement of lipids between the two membrane leaflets” (Bevers, Comfurius et al. 1998; Pomorski and Menon 2006; Fadeel and Xue 2009). Bi-directional lipid scrambling promotes the collapse of this asymmetry. “Flippase” and “floppase” help create and retain lipid asymmetry, while bi-directional lipid scrambling promotes the breakdown of this asymmetry. With the three classes of lipid transporters above there are specific class of P-type ATPases (the P4 ATPases) and the ATP-binding cassette (ABC) transporter family that accompany them (López-Marqués, Holthuis et al. 2011).
In the ER of eukaryotic cells, flip-flop of phospholipids in the PM is highly regulated this enables cells to preserve a nonrandom scattering of phospholipids across the PM (Bevers, Comfurius et al. 1998). The asymmetric lipid arrangement of the aminophospholipids PS and PE and sphingomyelin and glycosphingolipids in the cytoplasmic leaflet and exoplasmic leaflet respectively are a result of the action of energy-dependent flippases (Fadeel and Xue 2009). These flipases are “P-type ATPases and ABC Transporters that use ATP hydrolysis to move specific lipids against a concentration gradient” (Pomorski and Menon 2006; López-Marqués, Holthuis et al. 2011). When phospholipid scramblase is activated in some cells of the PM it creates a bi-directional movement of phospholipids, which affects the lipid asymmetry in the PM that was controlled by the ATP-dependent flippases. Scramblase activity has some lipid selectivity, this sets scramblase activity apart from the phospholipid flippase activity found in the ER or Golgi complex (Balasubramanian and Schroit 2003). The three classes of lipid flippases are important for array of cellular functions and helping the nonrandom transbilayer lipid distribution in the PM.
In the hepatocyte membrane, lipid asymmetry is crucial, it is needed for the composition of bile that uses phospholipids (Balasubramanian and Schroit 2003). Within this membrane aminophospholipids and PC comprise 35% of the membrane lipids respectively; within the bile aminophospholipids are rare, this is because PC comprises 95% of bile phospholipids (Fadeel and Xue 2009). It is important to note that transfer of lipids from the inner and outer leaflet in cellular membranes plays a great role in the functioning of individual cells, this work together with the functions of asymmetric lipid distribution in cells (Bevers, Comfurius et al. 1998).

Studies have shown that calcium (Ca2+) is important for cell survival and apoptosis, also Ca2+ helps in the compartmentalization and signaling in the mitochondria (Bevers, Comfurius et al. 1998). Apart from this it is thought that the regulation of phospholipid asymmetry in some way is attributed to Ca2+ ions. This has come about due to some scramblases need Ca2+ to function and aminophospholipid translocase activity is affected by Ca2+ (Bevers, Comfurius et al. 1998).

Lipid asymmetry serves an essential role in many cellular processes; this asymmetry needs to be maintained in the cell until it gets the signal to apoptose. Cells have allocated most of their energy to be able to produce and keep asymmetric phospholipid distribution. A number of recognized lipid transporter activities have been identified in the generation, maintenance, and alteration of phospholipid asymmetry in the plasma membrane, these lipid transporters are valuable as they maintain the cell’s integrity and physiology.



References


Balasubramanian, K. and A. J. Schroit (2003). "AMINOPHOSPHOLIPID ASYMMETRY: A Matter of Life and Death." Annual Review of Physiology 65(1): 701.
Basu, S., D. Banerjee, et al. (2008). "Loss of phospholipid membrane asymmetry and sialylated glycoconjugates from erythrocyte surface in haemoglobin E beta-thalassaemia." British journal of haematology 141(1): 92-99.
Bevers, E. M., P. Comfurius, et al. (1998). "Regulatory mechanisms of transmembrane phospholipid distributions and pathophysiological implications of transbilayer lipid scrambling." Lupus 7 Suppl 2: S126-S131.
Fadeel, B. and D. Xue (2009). "The ins and outs of phospholipid asymmetry in the plasma membrane: roles in health and disease." Critical Reviews in Biochemistry & Molecular Biology 44(5): 264-277.
Huijbregts, R. P. H., L. Topalof, et al. (2000). "Lipid Metabolism and Regulation of Membrane Trafficking." Traffic 1(3): 195-202.
López-Marqués, R. L., J. C. M. Holthuis, et al. (2011). "Pumping lipids with P4-ATPases." Biological Chemistry 392(1/2): 67-76.
Pomorski, T. and A. K. Menon (2006). "Lipid flippases and their biological functions." Cellular And Molecular Life Sciences: CMLS 63(24): 2908-2921.

[lavce pelagonski]

It is also important to note that if there is no lipid asymmetry and if cell do not apoptose (die) when needed it can cause tumors to form.

[Bij]

I should probably try meditation again. I work in a highly stressful job and have come up with various coping methods but I find meditating (or trying to) frustrating. I hate it when people say 'clear your mind' because it's impossible! /rant

My uncle in Macedonia is the resident cancer doctor of his hospital. He tells me that he will not tell a patient if they have terminal cancer, but rather leave it up to the family to decide if they tell the patient. In his opinion, those who do not know have a better quality of life leading up to their death and will usually last longer. Those that are told will often deteriorate quicker. I guess you can't really measure this scientifically because no one will really know how long someone with terminal cancer has but I found his observations to be rather interesting.

[lavce pelagonski]

That is interesting, even with chemotherapy there is no cure, it is simply there to slow down the spread of the cancer.

[George S.]

Lavce i just seen a 11 year old boy who had a chromosone cancer die from water fluid in the lungs.He tried all sorts of chemotheraphy & other therapy to no avail.He eventually just died from complications with a tumour in the lungs.

[Phoenix]

I should probably try meditation again. I work in a highly stressful job and have come up with various coping methods but I find meditating (or trying to) frustrating. I hate it when people say 'clear your mind' because it's impossible! /rant

To quieten the mind is very difficult, you probably need to relax the physical body before you have any success with the mind.
Even a casual walk, in a peaceful environment will go a long way to clearing the head, avoid powerwalking or similar 'exercise', the idea is to relax the body, not stress it physically.
Gentle stretching, yoga poses and massage will help but most importantly relaxing in a dark, quiet and comfortable room is paramount.
Being physically fit and eating a healthy diet is also extremely important in reducing or combating stress, as is somebody to talk to and bounce ideas and feelings off...

My uncle in Macedonia is the resident cancer doctor of his hospital. He tells me that he will not tell a patient if they have terminal cancer, but rather leave it up to the family to decide if they tell the patient. In his opinion, those who do not know have a better quality of life leading up to their death and will usually last longer. Those that are told will often deteriorate quicker. I guess you can't really measure this scientifically because no one will really know how long someone with terminal cancer has but I found his observations to be rather interesting.

That approach doesn't take into consideration the power of the mind and a persons will to survive, people should be told of their illness and every effort be made to help them overcome it...