Wednesday 28 November 2018

Urine FEME

The doctor will advise on which urine test or analysis to be done.

1. Urine dispstick

So many urine samples by 12 noon at OPD Lab (85 samples).

Urine dipstick test strip with 3 test patches.
Photos taken at OPD Lab, HUSM. 27 Nov 2018.


Purpose of doing Urine dipstick test

This is done at the first appointment when the doctor wishes to know if there is renal involvement and if the urine content is affected.

If the urine test is just to test for normal or abnormal urine, Urine dipstick is done. The lab report is that based on the test strip findings - positive, negative or trace, for each element tested.

In urine dipstick test, the urine test strips can contain 3 or more test patches. A basic test strip will contain patches for protein, glucose, ketones.

The usual urine test for finding out if a patient has renal involvement is a urine dipstick with 3 patches, in order to save cost.

This 3-patch test strip Urine dipstick test is usually done at the Outpatient Department (OPD) lab.

For more detailed urine test, the test strips may contain more test patches. Some will contain up to 13 test patches. This adds to cost of each test strip.

In hypertensive patients (patient with hypertension), the renal system is monitored. This is because, doctors will need to detect kidney involvement in hypertension. Hypertension is a disease affecting the blood vessels to all vital organs. In hypertension, these small vessels will be damaged (burst or busted), leading to abnormal urine, which is detected by urine dipstick.

Doctors will request hypertensive patients to do "urine test" (dipstick) before coming to see the doctor at the next appointment (ie To Come Again  or TCA). If there is renal involvement (eg protein in urine or microalbuminuria), the doctor will advise the patient accordingly, ie there is renal involvement, ie the disease or condition has worsened, and now the kidneys are affected.


2. Urine FEME

Fixed-angle rotor
Centrifuge
Urine sample after centrifugation

Examination of urinary sediment
Urine FEME test results
Photos above taken at OPD Lab, HUSM 27 Nov 2018.


Purpose of doing Urine FEME

If the doctor wishes to know whether there is infection of the renal system and needs to know the region of origin in the renal system, then the doctor will request for Urine FEME. Urine FEME will involve Urine dipstick test and Microscopic Examination of the urine. Meaning 2 tests will be done on a single urine specimen.

If the doctor wishes to know whether the urine is clear or cloudy (berkeladak) or dark coloured (warna merah kehitaman), the doctor will order Urine FEME.

In the case of bacterial infection (eg severe cough and cold that does not seem to subside in a week), and the patient complains of severe bouts of coughing, sore throat (gatal tekak), nausea (rasa loya nak muntah), loss of appetite (LOA, tak lalu nak makan), and pain (renal colic) in the kidney region (right or left kidney or both) in the back (not back pain), then the doctor will order Urine FEME to be done at OPD lab.

Urine FEME is a walk-in test performed at the OPD lab. The patient takes the green requisition slip from the doctor's office and then walks over to OPD to have it done. The test takes less than 20 minutes. Urine is collected in a small container (10-20 ml) in the toilet. The lab technologist will process and perform Urine FEME. The urine is pipetted and placed in a 10 ml clear glass test-tube. The tube is then centrifuged. Much of the supernatant (cecair bahagian atas) is removed and the sediment mixed and examined under the microscope (high and lower power fields). The lab technologist will look for "formed elements" inside the urine debris. The urine debris or sediment will contain nothing or some "elements". These "elements" can include cells (rbc, wbc) and epilthelial casts (which indicate their origin within the renal system). The lab technologist then fills in the results slip (same green slip) and returns that to the patient to take back to the doctor. The patient then walks back to the doctor's office to have the Urine FEME test results interpreted and explained properly.

In cases where there is renal involvement (of the kidneys, renal tubes and urinary bladder), there will be wbc, rbc, epithelial casts observed in the urine tested for Urine FEME. Otherwise the urine stays normal without any indication (ie negative Urine FEME).

The Urine FEME test is very important because in bacterial infection, the bacteria can go to the kidneys and infect the kidneys, causing excruciating pain. Sometimes breathing is affected. Sometimes sleep at night is impossible because of the excruciating pain. Upon inspection of the urine, rbc, wbc and epithelial casts can appear in the urine. There may also be bacteria present. All these elements will change urine composition and will be detected in Urine FEME.

Monday 12 November 2018

Cancer Therapy: GcMAF, Nagalase and Macrophage

Body's defence system
Our body contains cell stores which help us to generate cells which fight cancer. These stores or nodes are present throughout the body.

Macrophage & phagocyte locations
Macrophages and phagocytes are produced by the skin, gut and intestinal Peyer's patches, lungs, blood, bone marrow, connective tissue, lymphoid tissue, spleen, and thymus.

Types of phagocytes

  1. Skin - macrophages, resident Langerhans cells, dendritic cells, mast cells
  2. Gut and intestinal Peyer's patches - macrophages
  3. Lungs - macrophages, monocyes, mast cells, dendritic cells
  4. Blood - neutrophils, monocytes
  5. Bone marrow - macrophages, monocytes, sinusoidal cells, lining cells
  6. Connective tissue - macrophages, monocytes, dendritic cells, histiocytes
  7. Lymphoid tissue - macrophages, monocytes, dendritic cells
  8. Spleen - macrophages, monocytes, sinusoidal cells
  9. Thymus - macrophages, monocytes


Peyer's patches
The nodes in the intestine are most important. These nodes are called Peyer's patches. They are found beneath the basement membrane of the intestinal mucosa. They are a source of macrophages and immunoglobulin A (Ig A) in response to contents of the food a person consumes.

Invaders that invade the human body

  1. Viruses (viral infection)
  2. Cancer


Viral infection
(keywords: viral enzymes (nagalases), macrophages, immunity)
When a batch of virus launch an attack on the body, the viruses produce an array of enzymes that weaken the macrophages, rendering them ineffective in fighting off the viruses. This is described as a weakened immune system because the body fails to defend itself and fails to fight off the invading viruses.

Cancer
Cancer cells also produce nagalases which act on macrophages, rendering them weak and inefficient in protecting the body against invading cancer cells. With a weakened immune system, the cancer is able to grow and metastasise.

GcMAF-nagalase loop

  1. GcMAF (contains Gal-GalNAc)
  2. Nagalase


GcMAF
GcMAF is Gc Protein-derived Macrophage Activating Factor. GcMAF is a glycosylated protein bound to vitamin D. There are three forms (subtypes) of GcMAF. They differ in the number of sugar and sialic acid residues in the side chain. The sugar found  in GcMAF are glycosamines.

Structure of Gc protein
The Gc protein contains a threonine (Thr) residue, to which is attached a disaccharide side chain containing galactose (Gal) and Galactosamine (GalNAc) and sialic acid (SA), or simply, Gal-GalNAC-SA. Gal-GalNAC is a cancer biomarker for colon cancer (carcinogenesis). There are three forms of Gc which can be converted to GcMAF. They are Gc1f, Gc1s and Gc2.

(Gc1f):  -aa-aa-aa-aa-Thr-aa-aa-
                                    |
                        Gal-GalNAc
                                    |
                                  SA

Gc1s: -aa-aa-aa-aa-Thr-aa-aa-
                                 |
           (SA)-Gal-GalNAc
                                |
                              SA

Gc2: -aa-aa-aa-aa-Thr-aa-aa-
                               |
                   Gal-GalNAc


Nagalase
Nagalase if one of the viral enzymes. There are two types of nagalases - ie exo- and endo-nagalases. They act at different sies (loci) on GcMAF.

Pathway
When virus or cancer attacks the body, they produce nagalases, which act on macrophages and inactivate them. GcMAF on the other hand, acts opposite of nagalase, ie, they promote macrophage activation. Activated macrophages can transform into natural killer cells (NK cells) which can actively fight a viral infection or cancer.

Production of GcMAF
GcMAF is produced by a laboratory in Japan. There are two productions of GcMAF, ie first and second generations.

  1. First generation GcMAF (1991-2010)
  2. Second generation GcMAF (2011-present)
First generation GcMAF
This GcMAF was less concentrated, unstable at room temperature and had a short half-life.

Second generation GcMAF
This GcMAF was more concentrated, more stable and can last two weeks without refrigeration and up to a year with refrigeration. This is the preferred form for use.


Administration routes of GcMAF
GcMAF can be administered via four routes, ie, skin, muscle, intestine and lungs.

  1. Skin (subcutaneous, SC)
  2. Muscle (intramuscular, IM)
  3. Intestine (oral)
  4. Lungs (inhalation via nebulizer)


Conversion of Gc1f to GcMAF
  1. B cells contain lyso-PC inducible beta-galactosidase. This enzyme removes galactose from the Gal-GalNAc side chain.
  2. T cells contain sialidase. This enzyme removes sialic acid from the GalNAc-SA side chain.

GcMAF: -aa-aa-aa-aa-Thr-aa-aa-
                                      |
                                 GalNAc


Macrophage activation and transformation
GcMAF acts on dormant macrophages to activate them. Activated macrophages transform to NK cells.

Is GcMAF therapy effective?
YES, in the 99 patients who obtained successful treatment.
NO, in one patient in which treatment failed.
Failure rate is 1 in 100 or 1% ineffectiveness, which is negligible.


External links
https://www.immunotherapy-cancer-and-chronic-disease.com/frequently-asked-questions-about-second-generation-gcmaf/

http://gcmaf.timsmithmd.com/book/chapter/53/

https://www.advancedrejuvenationinstitute.com/cancer/3-immunotherapy/cancer-research-gcmaf.html

https://healingoracle.ch/2017/09/06/tutorial-how-to-inject-gcmaf/

https://www.researchgate.net/figure/Plasticity-of-macrophages-in-tumor-microenvironment-and-pathogenesis-of-HCC_fig2_275041931

https://www.immunopaedia.org.za/clinical-cases/infectious-diseases/a-case-of-decreased-joint-function-fever-and-rash/

http://cancerres.aacrjournals.org/content/76/3/513/F1

https://healingoracle.ch/2017/09/06/tutorial-how-to-inject-gcmaf/

https://cancer-cures-plus.com/persecuted-heroes/how-gcmaf-works/new-cancer-fighter-gcmaf-update/

https://thetruthaboutcancer.com/gcmaf/

http://www.brainimmune.com/endogenous-catecholamines-in-immune-cells-discovery-functions-and-clinical-potential-as-pharmacotherapeutic-targets-3/

https://immuno-oncologynews.com/2015/06/09/pd-1-protects-t-cells-burning/

https://www.ncbi.nlm.nih.gov/pubmed/8839767

Sunday 11 November 2018

Mysteries Surrounding Vitamin D

* Emeritus Professor Anthony Norman at the University of California, Riverside campus discovered vitamin D in the 1950s when he was researching hens. Hens which lacked vitamin D had bowed legs. Prof Norman and wife Prof Helen Henry, researched and taught at UCR, Biochemistry and Medicine. Both visited Penang in the 1980s. I met them when I attended UCR in 1980-1982 and when I was working at USM based in Penang.

Photo by Brooke Cagle on Unsplash

* Anorexia nervosa was a fad in the 1960s and 1970s in California. Hippies were often thin and wore Bohemian-styled clothes. They probably suffered from severe acidosis and osteomalacia and vitamin D deficiency.

* In many poor communities, children do not receive adequate nutritious food. Often, young children had big heads and tummies and bowed legs. Children developed rickets due to malnutrition.

* In the modern world where mothers work, babies and toddlers are left at nurseries. Nurseries can leave the children in walkers for long periods. This adds burden to tiny legs, which will eventually bow as the bones are still soft to bear the body's weight.

* Cancer has become quite common today worldwide. Apart from the effects of the atomic bombing of Hiroshima and Nagasaki, and the Bopal carbide disaster, there is breast cancer, colon cancer, bone cancer, brain tumour, pancreatic cancer, prostate cancer and many other cancers which have afflicted many people, young and old.

* Researchers have tried creating vitamin D analogues for use in alternative cancer therapy. However, lack of evidence-based medicine has plagued its acceptance and adoption for widespread use for otherwise prospective cancer sufferers.

----------------------------------------------
Precursors of vitamin D
  1. cholesterol
  2. 7-dehydrocholesterol (7-DHC)
  3. pre-D3
-----------------------------------------
Forms of vitamin D
  1. Vitamin D3 (cholecalciferol, made by skin via UV light) ... found in fish
  2. Vitamin D2 (ergocalciferol, derived from plant sterol ergosterol) ... used for food fortification ... a vitamin D analogue
  3. 25-hydroxyvitamin D (25OHD)
  4. 1,25-dihydroxyvitamin D (1,25(OH)2D) ... active form, a hormone
----------------------------------------
Enzymes in vitamin D metabolism
  1. CYP2R1 (25-hydroxylase)
  2. CYP27B1 (1-hydroxylase)
  3. CYP24A1 (catabolism)
  4. 3-epimerase
  5. CYP11A1

CYP2R1 is the most important 25-hydroxylase.

CYP27B1 is the key 1-hydroxylase.

Both 25OHD and 1,25(OH)2D are catabolised by CYP24A1.

----------------------------------------
Sources of vitamin D
  1. Vitamin D3 is made in the skin from 7-dehydrocholesterol with exposure to UV light
  2. Vitamin D2 (ergocalciferol) is derived from ergosterol, a plant sterol
----------------------------------------
Production of vitamin D

The production of vitamin D3 (D3) in the skin is not an enzymatic process but requires UV light from sunshine. Both UVB intensity and skin pigmentation level contribute to the rate of D3 formation.

* Exposure of the skin to sunshine in the morning for 15 minutes daily is sufficient for vitamin D production. Babies can also be exposed to the soft sun-rays in the morning for this purpose.

D3 (cholecalciferol) is produced from 7-dehydrocholesterol (7-DHC) through a two-step process in which the B ring is broken by UV light (spectrum 280–320 UVB) radiation from sunshine, forming pre-D3 that isomerizes to D3 in a heat-sensitive but non enzymatic (non catalysed) process.

* Melanin in the skin blocks UVB from reaching 7-DHC, thus limiting D3 production. However, Blacks have large amount of melanin in their skin and yet have good strong bones. Kareem Abdul-Jabbar is a tall, dark and handsome successful famous professional basketball player who played for the National Basketball Association (NBA), USA.

* Sun-screens are worn  for sun bathing or when spending time outdoors as they block sunshine and prevent sunburn, which is painful. Even with sun-screen, basking is limited as sun bathing gives headaches and migraine from excessive UV irradiation.

* Clothing also blocks sunshine from reaching the skin, but not completely. Women who wear thick clothing as a jacket, such as the abaya or jubah, are thought to lack vitamin D or suffer from vitamin D deficiency. This is untrue. These women only wear such long protective jacket when they go out in public, ie for a short time only. They do not wear such clothing at home. This misconception should be corrected among Western researchers and professors.

The intensity of UVB from sunlight varies according to season and latitude. The further one lives from the equator, the less time of the year one can rely on solar exposure to produce D3.

* The Incas of Bolivia live in the highlands of the Andes where the air is thin. They rely on chewed coca leaves or coca drink before climbing to such heights and avoiding dizziness and vomiting. They are exposed to strong levels of UV radiation. La Paz is heavily polluted with brown industrial smog as a result of thinning of the ozone layer and high ozone chemical activity.

Inca women in Copacabana, Lake Titicaca shore, Bolivia 30 Sept 2018.
Courtesy of Noraini Ismail and her travel buddies.
Copacabana is on the shore of Lake Titicaca at 3,841 m (12,602 ft) above sea-level.
Highest navigable lake with surface elevation of 3,812 m (12,507 ft) above sea-level.
Reed boats of the Incas at Lake Titicaca, Bolivia 30 Sept 2018.
Courtesy of Noraini Ismail.
***

Highest capital city at 3,640 m (11,942 ft) above sea-level.
Entering La Paz by coach, Bolivia 30 Sept 2018.
Courtesy of Noraini Ismail.
Highest capital city, La Paz skyline, Bolivia 30 Sept 2018.
Courtesy of Noraini Ismail.

* People who live in the equator have full exposure to sunshine for at least eight hours a day. They have good dentition, dark skin and strong bones. The sea Bajau of Semporna, Sabah (in Borneo) spend a lot of time at sea. They are a great example of sufficient vitamin D intake and exposure to sunshine.

Bajau boy, Semporna, Sabah.
Photo by Logan Lambert on Unsplash

* Apart from the skin, vitamin D can also be obtained from the diet such as milk, liver and eggs.

* Most natural and processed foods, with the exception of freshwater fatty fish (eg ikan patin), contain little vitamin D unless fortified. The Incas consume freshwater trout from Lake Titicaca as a source of EFAs and vitamin D. They have thus good strong bodies.

* The vitamin D in fish is D3, whereas that used for fortification of processed ingredients (eg milled white all-purpose flour) and foodstuff (eg milk, bread, cornflakes, biscuits) is often D2 (ergocalciferol). Many native communities consume fish as a protein and vitamin D source. Fast food outlets offer fish fillet.

Amazon 14 Sept 2018
Brazil 14 Sept 2018
Rio de Janeiro, Brazil 17 Sept 2018
Trout at Copacabana from Lake Titicaca, Bolivia 30 Sept 2018
All photos of fish above are courtesy of Noraini Ismail.

* Phytosterols compete with cholesterol for absorption in the small intestines. When we eat vegetables, phytosterols are preferentially absorbed, and less cholesterol is absorbed. It is therefore advisable to eat vegetables when eating steak and meat dishes.

D2 is produced by UVB irradiation of the ergosterol in plants and fungi (e.g., mushrooms).

* Algae grow to confluence in freshwater. They are a good source of essential fatty acids (EFAs). Seaweeds grow in seawater and are used for making jellies, which can withstand hot temperatures of the equatorial countries.

* Mushrooms, papaya, mangoes and beansprouts are good for encouraging fertility in otherwise barren women.

* Structure-wise, vitamin D resembles cholesterol but with many hydroxyl groups. D2 differs from D3 in having a double bond (C=C) between C22 and C23 and a methyl group (CH3) at C24 in the side chain.

* Since D2 is structurally and chemically different from the active form of vitamin D, D2 can be considered a natural analogue of bioactive vitamin D.

These differences from D3 in the side chain lower its affinity for vitamin D binding protein (DBP), resulting in faster clearance from the circulation, and limit its conversion to 25-hydroxyvitamin D (25OHD) by at least some of the 25-hydroxylases, and alter its catabolism by the 24-hydroxylase (CYP24A1).

Unless given daily, D2 supplementation does not result in as high a blood level of 25OHD as comparable amounts of D3.

On the other hand, 1,25(OH)2D2 and 1,25(OH)2D3 have comparable affinities for the vitamin D receptor (VDR).

----------------------------------------
Metabolism of vitamin D

Once it is made under the skin, vitamin D is metabolised first to 25-hydroxyvitamin D (25OHD) in the liver, then to the hormonal form 1,25-dihydroxyvitamin D (1,25(OH)2D) in the kidneys.

Vitamin D is transported in blood by a vitamin D binding protein (DBP).

----------------------------------------
Vitamin D receptor

The vitamin D receptor (VDR) is found in nearly every tissue except in rbcs (anucleated)

VDR is located in the nucleus and is found in almost all nucleated cells.

1,25(OH)2D is the ligand for the vitamin D receptor (VDR).

1,25(OH)2D is a transcription factor. It binds to sites in the DNA called vitamin D response elements (VDREs).

There are thousands of VDR binding sites throughout the genome, and they regulate hundreds of genes in a cell-specific fashion.

VDR-regulated transcription is dependent on co-modulators, the profile of which is also cell specific.

---------------------------------------
External links

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3968073/

https://www.ncbi.nlm.nih.gov/pubmed/21197695

https://www.nature.com/articles/s12276-018-0038-9.pdf

https://medschool.ucr.edu/faculty_research/faculty_profiles/norman_anthony

https://www.researchgate.net/figure/Vitamin-D-synthesis

https://www.nature.com/articles/nrc2196/figures/1

https://www.nature.com/articles/srep37593/figures/1

https://www.semanticscholar.org/paper/Vitamin-D

https://www.researchgate.net/figure/Vitamin-D-metabolism_fig1

http://www.biochemj.org/content/441/1/61.figures-only

https://www.researchgate.net/figure/Overlay-of-the-systemic-phosphate-homeostasis-with-the-major-players-in-the-phosphate_fig2

https://www.pinterest.com/pin/565905509402816520/?lp=true

https://www.researchgate.net/figure/Photochemical-synthesis-of-vitamin-D-and-main-target-tissues-Classical-pathway-of_fig2

https://www.semanticscholar.org/paper/Vitamin-D Metabolism-Molecular-Mechanism

https://www.researchgate.net/figure/Direct-and-indirect-effects-of-vitamin-D-on-muscle-Data-on-direct-effects-come_fig4

https://www.mdpi.com/1422-0067/18/10/2184

http://acuarios-self-help-health-wellness.blogspot.com/2012/11/vitamin-d.html

http://www.revistanefrologia.com/en-publicacion-nefrologia-articulo-vitamin-d-vitamin-d-receptor-importance-its-activation-in-patients

Saturday 10 November 2018

Civilisation, Traditional Medicine and Biopiracy

Traditional medicine exists in every community that has access to clean freshwater, foliage, flora and fauna. The virgin forest is one of the many assets a community can have.  Sometimes it is not the forest of trees and woods, but a dry desert savanna or a beach vegetation, or wild shrubs and flowers which grow wild by the sandy or dusty roadside. Sometimes they are just plants grown around the house for daily or occasional use. In many communities of Asia, their food is their medicine, which is different from Western medicine.

INDIAN SUBCONTINENT
The Indus Civilisation has provided humans with a myriad of good traditional Ayurvedic herbs that work for many common ailments.

In the hot tropics and the equator, people resort to iced-cold water and ices to quench thirst. Cheap unboiled tap water is used for making ice, and then shaved to obtain ice shavings, which are needed to make attractive, colourful, flavoured ice balls. People who consume such ice-balls (or ABC) can contract hepatitis A after a  month of consuming such food. The patient looks terribly unwell. Hepatitis A is a nasty disease which incapacitates the patient. The patient becomes lethargic and fatigued day by day, and appears at the ER on wheelchair. The patient has no energy to even walk or stand. The skin and sclerae are light yellow (mata kuning). Hepatitis A can be rapidly cured with Jetepar, a fast-healing Indian herbal capsule manufactured in India and useful for modern hospital prescription by specialists in Medicine. Jetepar helps to regenerate liver cells (hepatocytes). Use of Jetepar clears hepatitis within two weeks to a month. Use of Jetepar and Malay traditional medicine clears hepatitis A within two weeks, faster than what modern medicine today possibly can.

As we go about our daily lives, we tend to be careless at times, and often fall. Sometimes a slight sudden movement (jerk) can give us a fracture. Children tend to get fractures when they fall down from trees. Adults tend to get fractures as they carry or shift heavy objects about in the house. Some adults get injury while at work, carrying or moving heavy packages. The Indians use ingu for fractures and bone pain. Ingu is a dark (black) herbal paste which can be purchased from well-stocked Indian stores in most Malaysian cities. It is sold in small plastic wrapped balls and smells. Ingu is applied on the skin at the fracture site and then wrapped overnight. It can be replaced if the pain continues. With use of ingu, pain usually subsides after 3 days. Fracture will take about a month to heal and longer to have functional strength.

Indian black tea is served with dusted cinnamon and a dash of honey. This tea is consumed to overcome diabetes. It  may work in some people. It may not work in people who are sensitive to cinnamon and suffer allergy and migraine as a consequence of consuming this type of tea.

INDIA & SOUTH-EAST ASIA
Indian cuisine has curries. Indians do not consume beef, but consume mutton, chicken and fish curries instead. Indian curries have many spices, including seeds, nuts and beans. Indian curries contain coriander seeds (biji ketumbar), star anise (bunga lawang), cinnamon (kayu manis), cloves (cengkih), mustard seed (biji sawi), fenugreek (halba), ginger (halia), galangal (lengkuas), tamarind (asam jawa) and asam keping. Indian curries also have ladies finger (bendi or bendeh), long beans (kacang panjang), moringa (keloh), brinjals/eggplants (terung) and curry leaves (daun kari). When the Malays make curries, they add more spices (jintan), turmeric (kunyit), lemon grass (serai), daun limau purut and extra spicy ground chili (cili boh or cili giling).

The Indian, Indonesians and Malays then add coconut milk and macademia nuts to thicken curries. Salt and MSG are added to taste. Curries are a good source of minerals. Moringa is a rich and cheap source of iron in many countries where the tree grows wild. Drumsticks (beans) of the moringa tree are consumed by mothers who are about to deliver and expedites labour. Moringa seeds are sold commercially at speciality food stores. Brinjals give good clear vision. Lemon grass helps in arthritic conditions. Coconut water is used to cool down the body and expand blood volume in fever and dehydration. Plain water is drank immediately after a fall to overcome shock.

MALAY CIVILISATION
The Malay Archipelago is vast and mainly covers hundreds of scattered islands and a peninsula in SEA in addition to a belt around the equator. It includes Indonesia, Malaysia, Brunei. Borneo, Philippines, Sulu, parts of China, Taiwan, Japan, Polynesia, Melanesia, Guam, Hawaii, Ceylon, South India, Madagascar, South Africa and parts of the Amazon forest also contain Malays.

The Malays use coconut water for healing heat conditions and fever. Coconut water is like blood plasma and is a plasma expander. Guava shoots are used for dengue to increase platelet count. Quinine is consumed fresh to overcome malaria and its fatal outcome. Quinine is close to machang/macang, a fragrant fruit from a perennial very tall tree. Macang is grown and sold in the fresh market, but quinine is rarely sold. Inai leaves are pounded to a paste and applied on severe skin afflictions without bandage. Betel leaves (daun sireh) are chewed and spat onto children to remove evil spirits and to break away a mother from her clinging child. Turmeric is either eaten raw or cooked. Raw turmeric is pounded to make sambal belacan and eaten with hot rice to increase milk in breastfeeding and improve appetite. Fresh fish is covered with a mixture of pounded or ground turmeric, chilli and salt, then deeply fried and eaten with hot rice. Turmeric contains curcumin, and curcumin kills cancer. Betel leaves, pandan (Pandanus leaves), daun cermai and fragrant flowers, are used for mothers to bathe in the post-partum period; they reduce body itch. Soaked crushed watercress (air kangkung) makes a good light latex emulsion for treating itch and warding off chickenpox. It stops chickenpox infection from spreading.

The Malays are noted for their salads (ulam). They eat a variety of salads not found in many other communities. The Malay ulam includes boiled or fresh four-angled beans (kacang botol), watercress (kangkong), ladies finger, big & small brinjals (terung & terung pipit), big & small cucumber (timun & timun susu), cashew shoots (daun ketereh/gajus), long beans, drumstick (kacang keloh), marrows (labu air), young corn (ketiak jagung), jering, petai, etc. These fresh vegetables are dipped in anchovy sauce (budu) or peanut sauce (kuah rojak). Blanching or boiling kills E. coli and flatulence is minimal. Ulam helps to overcome problems of constipation. However, vegetables are regarded as cold food and are avoided by mothers in the post-partum period. As such these mothers suffer from constipation.

Tropical fruits which are grown around the house are eaten fresh by the Malays. They include big & small bananas, big & small papayas, hard & soft guava, durian, mango (mangga), rambutan, pulasan, mangosteen (manggis), langsat, dokong, laichi, grapes, pomegranate (delima), soursop (durian belanda, Graviola), ciku, custard apple (nona), etc. Some fruits are used for making fruit preserves such as acar buah (chutney) and jeruk buah. Pak Ali is a famous fruit preserve brand in Malaysia. It includes nutmeg, prunes, cherries, buah bidara, buah cermai, etc. Preserved fruit is eaten as snacks or made into acar buah.

CHINESE CIVILISATION
Herbs used in Chinese traditional medicine include garlic, ginger, ginseng, lotus seeds, barley, red dates, white fungus, and spices. Mothers are fed garlic and ginger-rich chicken soup in the post-partum period to expedite recovery. Babies get a lime oil rub for colic. There is a plain cabbage soup to avoid constipation. The hot or cold beans drink, leng chi kang, helps to overcome thirst and is nutritious. Barley water is alkaline and is used to cool down the body, for hypertension, diabetes and renal problems. Chinese children eat a lot of oranges for vitamin C.

Barley, basil and pandan drink

Chinese fruit preserves and seeds are widely marketed in Malaysia. It includes dried orange skin, dried plums, dried prunes, pumpkin & melon seeds (kuaci), and crystallised fruits.

In the old days in China, excess oranges were cooked in sugar and made into crystallised oranges. These were consumed in winter when there were no fresh oranges to consume. Crystallised oranges were also used as gifts when the Chinese travelled the world. In California where the Chinese arrived and set up trading posts, crystallised oranges were gifts for exchange with Californian sweet jelly-apple-walnuts clusters dusted with powdered glucose.

Chinese coffee shops offer sweet black coffee to go with char koay. This is good for overcoming hypoglycaemia when rising from overnight sleep. Light unsweetened Chinese green tea is consumed at coffee-break and in the afternoon. This is good for avoiding a multitude of afflictions such as hypertension, hyperlipidaemia and diabetes.

THAI CIVILISATION
Thai snacks include sugar-coated tamarind, skewed honey squids, puffed rice crackers, cashew nuts, coated groundnuts, honey fried anchovies, popcorn, etc. These are cheap nutritious food. Some help to overcome protein needs of poor communities, which is prevalent in South-east Asia (SEA).

The Thais have a special spice mix that is used in terminal cases to overcome near death. This is a fragrant spice mix and is not sold in the open market. This is a protected spice mix and is only available upon request through special people. Not everyone can get hold of this spice. Even if it is made available, it is only available less a teaspoonful and once only.

The Thais have a rich thick sweet green tea recipe. This tea has recently crossed borders and come into the Malaysian market, especially at universities, fresh markets and Ramadan food fair. This tea can be dark green or light green. Its green colour does not resemble that of green algae or natural chlorophyll. It could be artificial edible food colouring or other. It has a metallic odour. Whether this type of green tea is good for health or otherwise is a wonder.

The Thais have invented a soy-based health drink that combines black seed. Black seed is mostly used in Arabic medicine. Black seed is the Mother of Medicine in Arabic medicine. Black seed is especially useful for dissolving tumors (any organic solid mass). Its proper usage is unknown. There is scarce knowledge of its proper use in medicine in order to obtain maximum benefits.

PHILIPPINES CIVILISATION
The Filipinos eat manuk - eggs containing unborn chicks (with feathers, beak, eyes, wings and legs. It is eaten with chilli sauce. It is a good source of protein.

OTHER
There are isolated communities who rely on human flesh and brain for protein. These communities are dying out. Cannibalism and head hunters are a dying tradition. The wild boar and pythons are main sources of protein for isolated communities, especially in hilly regions far from the sea or rivers. Protein malnutrition is rare in these communities. However, transmission of viruses from consuming infected human or animal brains is a possibility.

BIOPIRACY
Patients are always hoping for a miracle drug, only to find out that they are consuming an illegally patented drug in a first world nation but the original source was actually smuggled out from a civilised community of a third world country. It may be too late when this happens.

When entrepreneurs and researchers in biotechnology and pharmaceutical products take a plant, flower, fruit, seed, bark, root, sap or gum out of a country, and do R&D to obtain a patent for a new drug or cure, this is a bad thing for the original country where the plant was first sourced. When this happens, the original country loses its ownership of the original plant source and the newly developed drug. Money may mean everything for big pharma.

Biopiracy did not just  suddenly come into the world. It has been around since rubber seeds were smuggled out from Brazil to Kew Gardens in England and then brought to Malaya for R&D and commercial cultivation. Bitangor is a useful tree for cure of hepatitis. It was smuggled out from Malaysia and now patented for a new drug in the USA. The Chinese eat red yeast rice as part of their normal routine to keep optimal health. Red yeast rice has been exploited to produce statin drugs by pharma in USA. Statins are expensive drugs used in the treatment of hypercholesterolaemia.

External links
Mongabay
https://news.mongabay.com/2015/06/amazon-tribe-creates-500-page-traditional-medicine-encyclopedia/


Sunday 2 September 2018

Eduaid.net

I have C&P this text from a comment posted in the wrong place.

http://eduaid.net is a leading Australian Registered Immigration Law Firm, which is recognized by the immigration authorities of both Australia and New Zealand.

Monday 25 June 2018

Endogenous Pathway of Lipoprotein Metabolism (June 2018)

In an integrated curriculum, which our Medical School deploys, temporal distribution of related topics can be an issue which may seriously affect students' learning. This problem can go unnoticed by both lecturers and students. It is a worry when scheduling related topics far apart. They would be close together in a conventional curriculum.


Let me give you an example of what I mean.
  1. The topic Exogenous Pathway of Lipoprotein Metabolism was covered in two ways - guided self-learning (GSL5) and a class lecture. However, these two inputs were spaced far apart on the time-table.
  2. The GSL5 module was made available to students at the e-learning portal on 21 Sept 2017
  3. The lecture Lipoprotein Metabolism was delivered in the lecture hall on 28 February 2018
  4. Time difference between GSL5 and the lipoprotein lecture was 5 months plus 1 week
  5. A semester exam was conducted on 25 June 2018 (9 months after GSL5 and 4 months after the lipoprotein lecture)
Module:
CELL AND TISSUE
COURSE (GMT 101)
PHASE I MD 2017/2018
GUIDED SELF-LEARNING (GSL) ON
STRUCTURE AND FUNCTION OF LIPIDS
Prepared by
PROF. FARIDAH ABDUL RASHID
DEPARTMENT OF CHEMICAL PATHOLOGY
SCHOOL OF MEDICAL SCIENCES
KUBANG KERIAN, KELANTAN
Updated on
11 September 2017
------
Medical Doctor (MD) Programme Phase I
Academic Session 2017/2018
Cell & Tissue Course (GMT 101)
Week 2
GSL 5: Structure and Function of Carbohydrates, Lipids, Amino Acids
and Nucleic Acids (Biomolecules) ... uploaded at e-learning portal
KNSS, IZA, FAR
21 Sept 2017
Contents:
PLASMA LIPOPROTEINS (page 6)
1, Describe the structure and function of plasma lipoproteins.
2. Describe the exogenous pathway of plasma lipoprotein metabolism.
3. Describe the endogenous pathway of plasma lipoprotein metabolism.
4. Describe reverse cholesterol transport.
5. Describe how lipids can cause heart disease.
-----------
Phase I
Year 1 Sem 2
MEDICAL DOCTOR (MD) PROGRAMME PHASE I (YEAR 1)
Academic Session 2017/2018
CVS Course (GMT 107)
Week 3
Lecture
Lipoprotein Metabolism
28 February 2018

Even though the lecture on Lipoprotein Metabolism was given late in first year (Sem 2), in the CVS Course (GMT 107), it should not be an excuse for students who are unable to connect with or recall earlier topics (Learning Issues, LI, or Learning Objects, LO).

Students may not be able to recall or connect that the same topic and essay questions have appeared earlier - in the self-learning module or guided self-learning (GSL), in their first week of Medical School (Sem 1, Cell & Tissue Course (GMT 101).

This shows that students often do not revise, re-study or check back on what they have learned very early in their medical course. There is a gap and topics early in their medical studies may have been forgotten altogether. However, they only need to revise, re-study or check back. They may not be able to connect past topics if they did not re-check, revise or re-study the topics that they have learned many months before to exam.

There are 3 possible essay questions concerning the topic Lipoprotein Metabolism. Any of these 3 essay questions can pop up on any exam - Term and Professional. Therefore, students should be aware that there are these 3 options. They should be prepared, rather than not be aware and be unprepared or go blank during exam.

For June 2018 exam, though half the students passed (73/134 or 54%), I am quite disappointed that quite a large number of students (61/134 or 46%) still failed a repeat essay question on lipoprotein metabolism, which had been made available to students in their first week of Medical School since 2014 (and even earlier). What a shame!

The essay question below was taken directly from GSL5, that was made available online on the e-learning portal on 21 Sept 2017, to all incoming first-year medical students. Students either saw it but overlooked it, or took it seriously, studied and attempted to answer it! There is no excuse for failing this essay question.


Essay
Describe the endogenous pathway of lipoprotein metabolism. (10 marks)

How often has this question been used?
This question has been used repeatedly since 2014.

Proposed Model Answer

(i) Diagram
Is a diagram required?
No and it is not necessary.
A diagram is not required since it is not specifically asked.
However, you can draw a labelled diagram or flowchart if it helps and guides you to answer the question.
Refer to any diagram on "endogenous pathway of lipoprotein metabolism" in any textbook or Google it. 
Be careful when drawing for an essay question. You can use simple ball and arrow diagram and label everything using abbreviations. But students often go wrong here because they cannot recall the lipoprotein abbreviations correctly, and which way the LDL cascade should go. Many remember it wrongly. There are 3 distinct pathways of lipoprotein metabolism, and they do not merge. Be extra careful. 

(ii) Text


Any 10 Statements pertaining to the following, or other statements relevant to the topic.
Max. 10 Marks
1.       
Endogenous pathway happens all the time.
1
2.       
It involves VLDL-LDL metabolism or “LDL cascade” and LDL receptor-mediated uptake in liver.
1
     
Synthesis of VLDL:

3.       
The liver synthesizes VLDL. Hepatocytes release nascent VLDL into the Space of Disse Ã VLDL enter sinusoids Ã  VLDL enter systemic circulation.
1
    
VLDL have several fates:

4.       
a)      VLDL transport triglycerides from liver to peripheral tissues for utilization.
1
5.       
b)      When VLDL reach vascular/capillary beds, they undergo hydrolysis (lipolysis) by LPL where their triglycerides contents are hydrolysed to free fatty acids (FFAs) and glycerol.
1
6.       
c)      VLDL remnants are taken up by liver via LDL (B,E) receptors.
1
7.       
d)     The VLDL are reduced in size (but increased density) and are converted into VLDL remnants and IDL, as a result of lipoprotein lipase (LPL) activity, hydrolysis or delipidation, which requires apolipoprotein C-II as cofactor.
1

Unesterified FFAs have several fates:

8.   
a)      During lipolysis, some FFA can be carried by plasma albumin and dispersed in plasma for delivery to other cells. Not much of this happens.
1
9.   
b)      Normally, FFA can enter underlying adipocytes by simple diffusion. Inside the adipocytes, the FFA are re-esterified to form triglycerides (TG) once more. Adipocytes store TG until required (as an energy source during fasting or starvation). A majority of FFA are stored in adipocytes following lipolysis.
1
10.   
c)      In times of starvation, when blood glucose is low and glycogen reserves are low, triglycerides stored in adipose tissues are hydrolysed by hormone sensitive lipase (HSL) and the FFAs are released from adipose tissue. FFAs then attach to circulating albumin and are brought to liver for beta-oxidation, for continued energy supply.
1

IDL have several fates:

11.   
a)      IDL can be converted into LDL by LPL in blood (intravascular).
1
12.   
b)      IDL can be taken up by hepatic receptors.
1
13.   
c)      IDL can be converted into LDL by hepatic lipase (HTGL) in liver.
1

LDL have several fates:

14.   
a)      Normally, LDL are taken up by hepatic LDL (B,E) receptors. The contents of LDL are broken down into FC, CE, PL, TG/ DG/ MG/ FFA and amino acids. These are kept within the hepatocytes or recycled for use by other cells. Hepatic contents of FC and CE are regulated by acyl cholesterol acyltransferase (ACAT). Few things can happen if cholesterol is low, specifically in the cell or in the blood. If there is low cellular FC, stored cholesterol (as cholesteryl ester, CE) is broken down to free cholesterol (FC) by ACAT. If there is low plasma FC, the liver cell makes more FC via increased HMG-CoA reductase activity. The 2 enzymes, ACAT and HMG-CoA reductase, are sensitive to cellular and blood cholesterol levels, and combined, they regulate cholesterol levels in cells and blood.
1
15.   
b)      LDL can also deliver its contents directly to cells, eg adrenal glands, for synthesis of steroid hormones.
1
16.   
c)      Under abnormal levels of LDL in the blood (eg hyperlipidaemia), LDL can be taken up by the scavenger receptors present on extrahepatic tissues (EHT).
1
17.   
d)     LDL apoB-100 will be oxidized due to the prolonged presence of LDL in blood. Also, the LDL particle is now smaller and apoB-100 is unstable at this stage. ApoB-100 becomes easily oxidised. Oxidised apoB-100 has higher affinity for macrophages. Thus, oxidised LDL will be taken up by macrophages in EHT.
1
18.   
e)      Macrophages contain scavenger receptors on their surface. Macrophages are present on blood vessel walls. Oxidised LDL will attach to the receptors and be internalised by macrophages.
1
19.   
f)       The oxidised LDL are hydrolysed into component cholesterol, fatty acids, glycerol and amino acids, which are stored within the macrophages.
1
20.   
g)      This uptake of oxidised LDL is unregulated (ie, uncontrolled). The macrophages take up as much LDL as they can until they stop functioning and die - becoming foam cells.
1


OUTCOMES

Students' English proficiency
  1. Some can write well
  2. A few cannot write correct English sentences and seemed to struggle
  3. Not knowing how to properly use some words in sentences makes it difficult to comprehend what students are writing or trying to convey. Use of certain words seem difficult for students: constituent, composition, comprise, compose; retained, remained, degrade, bind, combine, uptake, consumed, utilised, undergo, etc
  4. Understanding of reciprocal relationships - lipoprotein density increases as size decreases
  5. Practice will make essay writing perfect, but there is lack of written assignments in first-year Medical School.
  6. There may be greater underlying problems such as learning the relevant science subjects in Bahasa Malaysia in primary and secondary schools. Subjects such as Biology, Chemistry, Physics, may have been taught in Bahasa. They should be taught in English if students have to master English at university level, and especially in a medical course.
  7. Students have tried their best to answer in English.
Students' answering difficulties
  1. No schema or outline to use to answer the question
  2. Careless writing 
  3. Haphazard writing 
  4. Don't know how & where to begin
  5. No proper writing style
  6. Page improperly utilised
  7. Considerable amount of scribbling at edges
  8. Diagrams in pencil and not ink 
  9. Thinking and writing at full speed 
  10. No knowledge to even write anything
  11. Blank or stuck
  12. Unexpected essay question
  13. No time to check answers
Students' handwriting
  • Handwriting was terrible for a majority of the scripts.
  • Most handwriting were tiny and had to be read close-up.
  • 1 script was intelligible (hard to read and comprehend)
Students' creativity
  • Abbreviations for VLDL, IDL and LDL were various and incorrect
  • Swapped functions of LDL and HDL
  • New abbreviations for lipoproteins were created!  
  • New terminologies were created! 
  • One student wrote on ADP and ATP
Diagrams drawn by students
  • Interesting diagrams, but some were incomplete or wrong
  • There were a few little diagrams of sorts. 

PROBLEMS FACED BY STUDENTS
26 students (19.4%) scored 0 marks in June 2018

Breakdown of problems faced by students who scored 0 marks:
  • 18 students handed in empty answer scripts (completely no answer; nothing written).
  • 1 student answered: formation of Chylomicron (with a smiley) [False]
  • 1 student answered wrongly on Chylomicron Metabolism [Chylomicron Metabolism is Exogenous pathway of lipoprotein metabolism.]
  • 1 student wrote: In endogenous pathway, lipoprotein is metabolised into chylomicrons. [False. This never happens!]
  • 2 students wrote on Bile Metabolism / Cholesterol Synthesis and HMG-CoA [wrong answers]
  • 2 students wrote on Lipid Digestion / Micelles and Chylomicron / Stomach Functions and Chylomicron [wrong answers]
  • 1 student wrote: Lipoprotein mechanism is breakdown of lipoprotein into amino acids. [False]

FOCUS of this essay question

Since this essay question is specifically about VLDL-IDL-LDL metabolism or endogenous pathway, any answer on chylomicron metabolism or exogenous pathway will be incorrect. Since HDL metabolism is not asked, there is no need to touch on HDL metabolism, except its associated role in the endogenous pathway.

Other answers such as stomach contents and functions, lipid digestion (formation of micelles, enzymic digesiton of lipids), lipid absorption, formation of chylomicron in enterocytes, passage of chylomicron from lacteals via lymphatics to liver are all irrelevant.

Other processes in the liver such as cholesterol synthesis are irrelevant as this question is specific and focused on the metabolism of lipoproteins containing apo B-100.


FALSE Statements
  1. This VLDL is major transported [transporter?] of cholesterol [False].
  2. LDL send the phospholipid to cell for cell integrity or to the cell that uses it for the production of energy [False].
  3. VLDL is the major transporter of cholesterol from adipose tissues [False]. 
  4. Lipoproteins are used to generate energy. [False]
  5. Endogenous pathway of lipoprotein metabolism is metabolism of chylomicrons [False].
------
IRRELEVANT Answers

The essay question specifically asked about endogenous pathway (VLDL-IDL-LDL metabolism), which occurs all the time in the body, whether we are fasting or not. There is no need to write about other topics. There is no need to write about carbohydrate metabolism (polysaccharide digestion, glucose and rbc metabolism). There is no need to write about GIT (stomach contents and functions). There is no need to write about lipid digestion and absorption (bile, lipases, micelles, lacteals) Stay focussed on the topic.

(a) Glucose & rbc metabolism
  1. Glucose is converted into pyruvate which will form the cholesterol.
  2. When rbc is damaged, or aged, lipoprotein will metabolised to be store into the body as a source of heat, membrane fluidity.
(b) Lipid digestion and absorption 
  1. So lipoprotein metabolism functions to break down lipid and protein to their respective basic units for better absorption.
  2. Lipid is broken down to its simplest form which are fatty acids and 3 glycerols with the help of ADH for energy.
  3. Lipid will enter lacteals (specialised lymph in the villi) to be utilised by the body again (as chylomicra).
(c) Carbohydrate digestion 
  1. From complex polysaccharide, it is broken down into disaccharide by removal of water. Then disscharide is broken down to amino acids which is the simplest form of protein.
-----
Student Answers on
ENDOGENOUS PATHWAY OF LIPOPROTEIN METABOLISM

[F] = False statement
[?] = examiner's query


(a) Students' understanding of the different lipoprotein pathways
  1. There are 2 pathway(s) involved in lipoprotein mechanism which are through endogenous pathway and exogenous pathway
  2. Endogenous pathway is about VLDL
  3. Endogenous pathway of lipoprotein is when it is synthesis from cholesterol inside the liver.
  4. Endogenous Pathway is occur within circulation. Endogenous Pathway of lipoprotein metabolism consist of VLDL-LDL metabolism, LDL metabolism and LDL-mediated receptor (uptake).
(b) Ambiguous statements written by students
  1. Lipoprotein metabolism occur in liver. It is combination of lipid and protein.[Abstract writing!]
  2. Cholesterol is transported from the GIT to the liver in both estercifed [esterified] and free form in the liver. [Meaning?]
  3. Cholesterol under go oxidation estirification and compannded with protiens Apo proteins to form lipoproteins which are sent to the bloodstream as VLDL. [Meaning?]
(c) Lipoprotein structure
  1. Lipid basic structure and triglyceride and fatty acids
  2. For proteins, its amino acids
  3. Cholesterol combines with apolipoprotein
  4. Cholesterol, apolipoprotein, phospholipid and triglyceride will form VLDL and also empty HDL
  5. Lipoprotein is constituent of both lipid and protein.
  6. Triglyceride has about 60% in VLDL [This is better written as VLDL contains approximately 60% triglycerides.]
  7. VLDL has Apo B-100 molecule [This is better written as Each VLDL has an apo B-100 molecule.]
  8. IDL is high in cholesterol
(d) Classes of lipoproteins
  1. There are 2 lipoprotein(s) that (are) present in (the) body which are high density lipoprotein (HDL) and low density lipoprotein (LDL). [False] [There are 4 major classes of lipoproteins.]
  2. The last one is HDL(?)
(e) Function of lipoproteins
  1. LDL is described as bad cholesterol
  2. LDL is major transporter of cholesterol. It send the cholesterol (to) the cell of adipose and liver to be stored.
  3. HDL is described as good cholesterol
  4. The function of HDL is to transport excess cholesterol to the liver to be metabolised. The HDL is the could be recycle for the next  use.
(f) Lipoprotein conversions
  1. In lipoprotein metabolism, chylomicron is converted into very low density lipoprotein (VLDL) [F]. VLDL in then convert into intermediate low density lipoprotein (ILDL) [F]. ILDL will form low density lipoprotein (LDL) which then converted into high density lipoprotein (HDL) [F].
  2. Chylomicron will bind to Apo E and C to become high density lipoprotein [F]. Then it become  intermediate density lipoprotein, low density lipoprotein and very low density lipoprotein [F]. 
  3. After the VLDL will converted into IDL or LDL
  4. Triglyceride in VLDL is further dehydrolysed leads to conversion of VLDL to IDL.
  5. Very low density lipoprotein (VLDL) is degraded by IDL [F]. [VLDL is degraded by LPL to IDL.] Then, forming Low density lipoprotein (LDL) and exocytosed [endocytosed?] either via (scavenger) receptor-mediated or via hepatic (receptors). Then, LDL is taken up to the hepatocytes [taken up by hepatocytes?]. LDL converted to free cholesterol in liver.
(g) Lipoprotein movements
  1. Lipid (from circulation) will flow into the liver to (be) metabolised.
  2. VLDL will transport cholesterol from tissue to liver for excretion and HDL will transport cholesterol from liver to tissue [F]. [What does VLDL transport?]
  3. When it enters the blood circulation, VLDL attaches to Apo C and Apo E
  4. Upon entering the circulation, Apo CII activates lipoprotein lipase (LPL). Lipoprotein lipase hydrolyses triglyceride into free fatty acid and glycerol
  5. IDL is taken up by the hepatic cells. This is because hepatic cell recognise Apo E on IDL. Apo C and Apo E is retained from IDL [retained with IDL?]. IDL is hydrolysed [to what?]
(h) Products of lipoprotein hydrolysis by LPL
  1. Free fatty acid is used for energy, milk lactating
  2. Glycerol is needed in glucogenesis and gluconeogenesis
(i) Lipoprotein uptake
  1. Macrophages engulfing lipoprotein becomes foam cell
(j) Depth of students' understanding of the topic asked
  1. LDL is low density lipoprotein which collects cholesterol from liver to body
  2. HDL is good cholesterol which collects cholesterol from body to the liver
  3. Liver will produce VLDL with attachment of Apolipoprotein B-100 which is produced by hepatocyte
  4. VLDL will combine with Apo E and Apo CII
  5. CII will activate lipoprotein lipase to breakdown triglyceride into fatty acid and glycerol
  6. Fatty acid can be used in synthesis of lipid, energy storage, production of milk fat in mammary gland
  7. The breakdown of triglyceride reduce the VLDL into IDL (VLDL remnant)
  8. IDL will transport into the hepatocyte by binding of Apo E on the surface of liver (LDL receptor)
  9. IDL will also degrade into LDL with the help of HTL (hepato ... lipase) [HTL or HTGL is hepatic triglyceride lipase.]
  10. LDL is more dense and reduce in size [Meaning?] [LDL is smaller and denser than IDL.]
  11. It contain more cholesteryl ester
  12. LDL can enter the liver by binding of Apo B-100 at the LDL receptor. [Meaning?] [Where is apo B-100 located?] [LDL apo B-100 binds to LDL receptors present on hepatocytes. OR LDL binds to LDL receptors via its apo B-100.]

--------
CORRECT answers attempted by students (10 marks)
Text only. Associated diagrams are not included here.

Example 1
  1. VLDL (very low density lipoprotein) is synthesized in the liver and consist of triglycerides and Apo B-100. [F] [VLDL contains 4 lipid classes and apo B-100.]
  2. Then, VLDL is goes out of the liver into blood circulation.
  3. Inside the circulation, it receives two apolipoprotein from HDL which is apo C and apo E.
  4. Then, VLDL is hydrolysed by lipoprotein lipase which hydrolyse the triglycerides in(to) fatty acids and monoglycerides.
  5. This make VLDL size and density decrease [F].[VLDL size is reduced, but its density increases after lipolysis by LPL.]
  6. Before transported back into liver, apo C return back to HDL and VLDL remnants diffuse into liver by lipoprotein receptor and by endocytosis. [Diffuse into liver or taken up by liver?]
  7. The VLDL remnants become IDL but IDL does not remain for a long time before it converted into LDL (low density lipoprotein). [IDL exists transiently in blood.]

Example 2
  1. VLDL (very light density lipoprotein) is form(ed) endogenously in liver. 
  2. It consist(s) of free amino acid, cholesterol, cholesteryl ester, phospholipid, triacylglycerol and apo B-100. [VLDL cannot contain free amino acids! Apo B-100 is a large protein!]
  3. It is released into circulation.
  4. It then take up apo C and apo E from HDL (High density lipoprotein).
  5. Apo C will activate Lipoprotein lipase in cappilary epithelium to break down triacylglycerol in VLDL into fatty acid and glycerol. [It should be capillary endothelium.]
  6. Now VLDL decrease in volume increase in density and now convert to IDL (intermediate density lipoprotein).
  7. IDL bind to lipoprotein receptor at hepatocyte  via apo E through endocytosis. [IDL are internalized by endocytosis.]
  8. In the hepatocyte, triacylglycerol in IDL (undergo) further break down by hepatic lipase.
  9. Now the compound is increase in density and rich in cholesterol.
  10. It is now LDL (low density lipoprotein).
  11. It will (be) released by the hepatocyte.
  12. After that LDL (is) either absorb(ed) by the liver or posthepatic tissues to (be) further metabolize(d).

Example 3
  1. In the lipoprotein metabolism, it consist the exogenous pathway, endogenous pathway and the reverse metabolism pathway. [F] [There is no such thing as reverse metabolism pathway! There is reverse cholesterol transport.]
  2. During the endogenous pathway it is started in the liver.
  3. From the very low density lipoprotein (VLDL) which is present inside our body will produce in the liver, 
  4. It is function to bring the cholesterol to the tissue cell for storage.
  5. When it enter the circulation it will undergo lypolysis and converted into the Intermediate density lipoprotein (IDL). 
  6. This IDL is appear in the blood just for a while. [Transient]
  7. Next the IDL will undergo the lipolysis and then being the low density lipoprotein (LDL).
  8. This LDL will deposit into our tissue.
  9. Plus the LDL is very anthrogenic [atherogenic], thus LDL will lead into the formation of the atherosclerotic plaque and lead to other disease.
  10. This plaque prone to forming more at the abdominal aorta than the thoracic aorta.
  11. This LDL that deposit inside the tissue will be taken up back into the liver via the high density lipoprotein (HDL) during the reverse lipoprotein pathway. [Reverse cholesterol transport]
  12. The LDL serve as the bad cholesterol inside our body.
  13. {Diagram}

-----------
WRONG answers attempted by students (0 marks)

Example 1
  1. Chylomicrons are found in intestinal mucosa from dietary lipid. 
  2. During the endogenous pathway, high density lipoprotein (HDL) serves as reservoir for apo-C and apo E. [F] [Chylomicron metabolism is exogenous pathway.]
  3. The apo-C and apo-E will bind to chylomicrons.
  4. As chylomicrons enters the blood circulatory system, lipoprotein lipase (LPL) will hydrolyse the triglycerides into free fatty acid and glycerol.
  5. As the triglycerides are broken down, the size of chylomicrons decreases, becomes smaller but its density increases.
  6. The Apo-I in chylomicrons will restore back to high density lipoprotein before reaching liver  while the apo-E will stay with the chylomicrons. [Which apolipoproteins go where?]
  7. The remnants of chylomicrons reach liver, and will be metabolized as source of energy, heat energy. [F] [What do chylomicron remnants contain?]

Example 2
  1. Endogenous pathway of lipoprotein metabolism begins with the absorption of chylomicrons. [F]
  2. The chylomicron binds with Apo B-II. [F] [There is no such thing as Apo B-II.]
  3. The chylomicron then travels through the lymphatic system while being metabolised by lipoprotein lipase .
  4. After a few stages of digestion, the chylomicron enters the liver.

--------------
WRONG answers mixed with correct answers

Example 1 (2 marks)
  1. Endogenous pathway.
  2. The lipoprotein is transported as VLDL. [1 mark]
  3. Then, it changes into LDL. [1 mark]
  4. The LDL form chylomicron. [F]
  5. Chylomicron is absorb(ed) by lacteal. [irrelevant]
  6. Then it moves into blood. [irrelevant]

Example 2 (4 marks)
  1. When dietary lipids and cholesterol enter intestine, they (are) converted to tryglyceride, monoglyceride  and fatty acids by intestinal lipase. [The correct spelling is triglyceride.]
  2. They are absorbed into intestinal cells which (are) then converted into tryglyceride by golgi apparatus [Golgi apparatus].
  3. Tryglyceride, cholesterol will be bind forming chylomicrons (CM). 
  4. Chylomicrons are too big to enter blood vessels so it will enter lacteals which then enter blood vessels.
  5. CM are utilised by lipase that (are) present in blood vessels forming smaller lipids to be transported to muscle cells for energy and to liver for storage,
  6. CM are then transported to liver.
  7. Cholesterol will bind to Apo B to form very low density lipoprotein (VLDL). [1 mark]
  8. VLDL will be transported in blood vessels where it  (is) utilised by tissues converting it to Intermediate density lipoprotein (IDL). [1 mark]
  9. IDL (is) transported to liver forming Low density lipoprotein (LDL). [1 mark]
  10. LDL is then again circulated in blood to be utilised by tissues for energy. [1 mark]

End