What is hepatitis?

What is hepatitis?

A: Hepatitis is an inflammation of the liver. The condition can be self-limiting or can progress to fibrosis (scarring), cirrhosis or liver cancer. Hepatitis viruses are the most common cause of hepatitis in the world but other infections, toxic substances (e.g. alcohol, certain drugs), and autoimmune diseases can also cause hepatitis. There are 5 main hepatitis viruses, referred to as types A, B, C, D and E. These 5 types are of greatest concern because of the burden of illness and death they cause and the potential for outbreaks and epidemic spread. In particular, types B and C lead to chronic disease in hundreds of millions of people and, together, are the most common cause of liver cirrhosis and cancer.

Hepatitis A and E are typically caused by ingestion of contaminated food or water. Hepatitis B, C and D usually occur as a result of parenteral contact with infected body fluids. Common modes of transmission for these viruses include receipt of contaminated blood or blood products, invasive medical procedures using contaminated equipment and for hepatitis B transmission from mother to baby at birth, from family member to child, and also by sexual contact. Acute infection may occur with limited or no symptoms, or may include symptoms such as jaundice (yellowing of the skin and eyes), dark urine, extreme fatigue, nausea, vomiting and abdominal pain.

Q: What are the different hepatitis viruses?

A: Scientists have identified 5 unique hepatitis viruses, identified by the letters A, B, C, D, and E. While all cause liver disease, they vary in important ways. Hepatitis A virus (HAV) is present in the faeces of infected persons and is most often transmitted through consumption of contaminated water or food. Certain sex practices can also spread HAV. Infections are in many cases mild, with most people making a full recovery and remaining immune from further HAV infections. However, HAV infections can also be severe and life threatening. Most people in areas of the world with poor sanitation have been infected with this virus. Safe and effective vaccines are available to prevent HAV.

Hepatitis B virus (HBV) is transmitted through exposure to infective blood, semen, and other body fluids. HBV can be transmitted from infected mothers to infants at the time of birth or from family member to infant in early childhood. Transmission may also occur through transfusions of HBV-contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use. HBV also poses a risk to healthcare workers who sustain accidental needle stick injuries while caring for infected-HBV patients. Safe and effective vaccines are available to prevent HBV.

Hepatitis C virus (HCV) is mostly transmitted through exposure to infective blood. This may happen through transfusions of HCV-contaminated blood and blood products, contaminated injections during medical procedures, and through injection drug use. Sexual transmission is also possible, but is much less common. There is no vaccine for HCV. Hepatitis D virus (HDV) infections occur only in those who are infected with HBV. The dual infection of HDV and HBV can result in a more serious disease and worse outcome. Hepatitis B vaccines provide protection from HDV infection.

Hepatitis E virus (HEV) is mostly transmitted through consumption of contaminated water or food. HEV is a common cause of hepatitis outbreaks in developing parts of the world and is increasingly recognized as an important cause of disease in developed countries. Safe and effective vaccines to prevent HEV infection have been developed but are not widely available.

http://www.who.int/features/qa/76/en/

New gene discovered that stops spread of deadly cancer

New gene discovered that stops spread of deadly cancer : Scientists identify gene that fights metastasis of a common lung cancer

July 17, 2014 | Source: Salk Institute for Biological Studies

A gene responsible for stopping the movement of cancer from the lungs to other parts of the body has been discovered by researchers, indicating a new way to fight one of the world’s deadliest cancers. By identifying the cause of this metastasis, which often happens quickly in lung cancer and results in a bleak survival rate, scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway may also help researchers understand and treat the spread of melanoma and cervical cancers.

Scientists at the Salk Institute have identified a gene responsible for stopping the movement of cancer from the lungs to other parts of the body, indicating a new way to fight one of the world's deadliest cancers.

By identifying the cause of this metastasis -- which often happens quickly in lung cancer and results in a bleak survival rate -- Salk scientists are able to explain why some tumors are more prone to spreading than others. The newly discovered pathway, detailed today in Molecular Cell, may also help researchers understand and treat the spread of melanoma and cervical cancers.

"Lung cancer, even when it's discovered early, is often able to metastasize almost immediately and take hold throughout the body," says Reuben J. Shaw, Salk professor of molecular and cell biology and a Howard Hughes Medical Institute early career scientist. "The reason behind why some tumors do that and others don't has not been very well understood. Now, through this work, we are beginning to understand why some subsets of lung cancer are so invasive."

Lung cancer, which also affects nonsmokers, is the leading cause of cancer-related deaths in the country (estimated to be nearly 160,000 this year). The United States spends more than $12 billion on lung cancer treatments, according to the National Cancer Institute. Nevertheless, the survival rate for lung cancer is dismal: 80 percent of patients die within five years of diagnosis largely due to the disease's aggressive tendency to spread throughout the body.

To become mobile, cancer cells override cellular machinery that typically keeps cells rooted within their respective locations. Deviously, cancer can switch on and off molecular anchors protruding from the cell membrane (called focal adhesion complexes), preparing the cell for migration. This allows cancer cells to begin the processes to traverse the body through the bloodstream and take up residence in new organs.

In addition to different cancers being able to manipulate these anchors, it was also known that about a fifth of lung cancer cases are missing an anti-cancer gene called LKB1 (also known as STK11). Cancers missing LKB1 are often aggressive, rapidly spreading through the body. However, no one knew how LKB1 and focal adhesions were connected.

Now, the Salk team has found the connection and a new target for therapy: a little-known gene called DIXDC1. The researchers discovered that DIXDC1 receives instructions from LKB1 to go to focal adhesions and change their size and number.

When DIXDC1 is "turned on," half a dozen or so focal adhesions grow large and sticky, anchoring cells to their spot. When DIXDC1 is blocked or inactivated, focal adhesions become small and numerous, resulting in hundreds of small "hands" that pull the cell forward in response to extracellular cues. That increased tendency to be mobile aids in the escape from, for example, the lungs and allows tumor cells to survive travel through the bloodstream and dock at organs throughout the body.

"The communication between LKB1 and DIXDC1 is responsible for a 'stay-put' signal in cells," says first author and Ph.D. graduate student Jonathan Goodwin. "DIXDC1, which no one knew much about, turns out to be inhibited in cancer and metastasis."

Tumors, Shaw and collaborators found in the new research, have two ways to turn off this "stay-put" signal. One is by inhibiting DIXDC1 directly. The other way is by deleting LKB1, which then never sends the signal to DIXDC1 to move to the focal adhesions to anchor the cell. Given this, the scientists wondered if reactivating DIXDC1 could halt a cancer's metastasis. The team took metastatic cells, which had low levels of DIXDC1, and overexpressed the gene. The addition of DIXDC1 did indeed blunt the ability of these cells to be metastatic in vitro and in vivo.

"It was very, very surprising that this gene would be so powerful," says Goodwin. "At the start of this study, we had no idea DIXDC1 would be involved in metastasis. There are dozens of proteins that LKB1 affects; for a single one to control so much of this phenotype was not expected."

Right now, there is no specific treatment for cancers harboring LKB1 or DIXDC1 alterations, but those with a deletion of either gene would likely see results from cancer drugs that target the focal adhesions, says Shaw.

"The good news is that this finding predicts that patients missing either gene should be sensitive to new therapies targeting focal adhesion enzymes, which are currently being tested in early-stage clinical trials," says Shaw, who is also a member of the Moores Cancer Center and an adjunct professor at the University of California, San Diego.

"By identifying this unexpected connection between DIXDC1 and LKB1 in certain tumors, we have expanded the potential patient population that may be good candidates for these therapies," adds Goodwin.

Journal Reference: Jonathan M. Goodwin, Robert U. Svensson, Hua Jane Lou, Monte M. Winslow, Benjamin E. Turk, Reuben J. Shaw. An AMPK-Independent Signaling Pathway Downstream of the LKB1 Tumor Suppressor Controls Snail1 and Metastatic Potential. Molecular Cell, 2014; DOI: 10.1016/j.molcel.2014.06.021

SUMMARY

The serine/threonine kinase LKB1 is a tumor suppressor whose loss is associated with increased metastatic potential. In an effort to define biochemical signatures of metastasis associated with LKB1 loss, we discovered that the epithelial-to-mesenchymal transition transcription factor Snail1 was uniquely upregulated upon LKB1 deficiency across cell types. The ability of LKB1 to suppress Snail1 levels was independent of AMPK but required the related kinases MARK1 and MARK4. In a screen for substrates of these kinases involved in Snail regulation, we identified the scaffolding protein DIXDC1. Similar to loss of LKB1, DIXDC1 depletion results in upregulation of Snail1 in a FAK-dependent manner, leading to increased cell invasion. MARK1 phosphorylation of DIXDC1 is required for its localization to focal adhesions and ability to suppress metastasis in mice. DIXDC1 is frequently downregulated in human cancers, which correlates with poor survival. This study defines an AMPK-independent phosphorylation cascade essential for LKB1-dependent control of metastatic behavior.

Why we need evaluation?

Why we need evaluation?

Evaluation is needed every time, when we consider some kind of change. As all sides of education are in a continuous change nowadays, we need to evaluate our educational projects regularly. It is specially true when we'll try to introduce some new learning methodology and after first enthusiastic experiment want to set it on a regular bases, so that this new method becomes well designed, well organised, well run and effective, usable not only by ourselves, but also by our colleagues near and far.

There are always many components in the educational process: students, teacher, school organisation and environment, social culture of the region and country, parents, etc. What we have to do differently to get better learning results in our project based collaborative effort? How to plan and run evaluation of different sides of our project to succeed next time even better than this time? Do we know how successful was our project this time at all? How different participant perceived it? How to analyze - is the project my colleagues ran last year applicable to me, to my class? How do I have to change it according to my circumstances? This site is created to answer these questions.
How to proceed further?

If you are teacher and want to understand, what you have to do before your project, during the project and after it - look at our "For teachers" pages.
If you need some new tool to to evaluate your own project - look at our evaluation tools pages, where more that 10 tools are described and blueprints, how to implement them, are presented.
If you want to look how other teachers have successfully used different evaluation tools to evaluate their own projects - look at "Examples" page.
If you want to understand, why evaluation is important - please read further.
What is evaluation and why we have to evaluate our collaborative e-projects?

Evaluation is an activity with which every teacher is familiar with. But in different schools and different countries different terms can be used and every school has its own culture and attitude to evaluation. This page is to explaine, how terms are used in our ECOLE site. Evaluation has to answer several questions, like: Does it work? How does it work? Why does it work? Who makes it work? With whom it does it work? Can it be replicated? Can it be transferred? Can it be adapted? Can it be scaled? Adaptation of technical innovation is social problem and many social laws have been discovered during last fifty years. One of them is Innovation adoption curve of Rogers, which divides innovation adapters into 5 categories: innovators, early adapters, early majority, late majority and laggards. This curve is explained in the web page of Value Based Management net's Innovation Management Curve page . In those pages we'll try to offer Teacher's Professional continuum for evaluation.
Conceptual model of the evaliuation.
Evaluation process consists of many steps.
Choose tools for evaluation.
Develop evaluation questions.
Collect data.
Analyze data.
Our aim: to make easier for teachers to develop useful, high quality evaluation. We can evaluate our project only on the bases of information we have at hand. And quality of our evaluation depends strughtforward of the quality of this information.

SHAMBA ge kanaba

SHAMBA
Botanical Name: Oroxylum indicum.
Place- Found in Manipur, mostly in Langthabal and Koirengai area.
Parts Used:
1: Seed.
@Medicinal information
*Disease Name: Mumps, Tonsilitis
*Uses: The seed is purgative.
2: Root .
@Medicinal information
*Disease Name: Jaundice, High Blood Pressure, Fever, Cancer, Asthma, Diarrhoea, Dysentery.
*Uses: The root bark is used in stomachache,High Blood Pressure, Weakness due to B.P., Blood purification. Root can be taken as appetiser, in liver congestion,Inflammation, Leucoderma, vomiting, and is anthelmintic.
3: Leaf [ Constituents]
Medicinal information
*Disease Name: Epilepsy,Headache
**Uses: The leave decoction is used in muscular pains and general weakness,stomachache and rheumatism. The leaves are applied externally applied for enlarged spleen.

Common Names of Manipuri Food Plants.

Common Names of Manipuri Food Plants.
Local Name - Common Name

1. Thangjing - Water Fox nut/Gorgon Plant/ Prickly Water lily
2. Komprek - Dropwort / Water Parsley
3. Yaipan - East Indian Arrowroot
4. Yendem - Taro
5. Kolamni - Water Spinach
6. Sougri - Kenaf leaves/ Gongura( telugu)
7. Peruk - Centella
8. Yelang - Jointweed
9. Yongchak - Petai / Stink / Bitter /tree bean
10. Yensin - Woodsorrel
11. Nungshi hidak - Mint
12. Maroi napaakpi - Hooker chives
13. Maroi naakuppi - Chinese chives
14. Awaa phadigom - Mexican coriander/Culantro
15. Mayang-ton - Lemon Basil
16. Toning-khok - Chameleon plant
17. Phakpai - Vietnamese coriander
18. Chantruk - Wavy Bittercress
19. Heikak - Water Chestnut
20. Heikak Yeli / Yena - Trapa natans

Source: SM

Ha Ema Ema O

"Ha Ema EmaO
Eisu lakke EmaO
Nong chuiye lakkano
Yenpak tuptuna Marakke
Lambi nalle lakkano
Cheisu suduna Marakke............................................

Ha Ema Ema O
Hayeng Nong chaoba yangol faraga
Samba pangal chaoraga, sanjel thonggi thongyaida Emabu oklarage.. emaO

-----------Wahathok--------------
Ha Ema EmaO----> Meetei Meeyamna Ema Ema haina kouba, Pukfabi, Naoyok Naukon fabi chareina Khwasetnaribi, ware koubada haidabi, Kangleibu Pokpi Ema Mahak adune.

Eisu Lakke EmaO----> Wahei pareng Asina Hairi... Chatkhidouraba Ama, Matung ellakke haiba Ama, Anisini.Chatkadouriba Asina Meetei Pokpi Ema Mahak Aduni..... tung ellakke hairiba Asina Meetei Meeyamni. Kanglei pokpi Emana, Ema mahakki maramdam Kangleibu thadoktuna chatlage khallakpa mikupta mapari mamomsingda pukmen paomennabagi matang aduni. Adungei Meetei meeyamna Ramandi Laining louramdai, tangkak ama lakpa matamda Kanglei pokpi Emana meetluda Pirang sintha Kapna chatkhibabu Uba ngamba ChingU Maichousingna Seithabirambani.
Nong Chuiye Lakkano----> Leipak ningthougi Akanba sana yathangna Nong chubagum Chutharaklaba, Miyan Laining Chatrabadi, 'Hare Rama sita rama' sollu, yadrabadi haiduna makhan makhan-gi Akan Akanba Cheirak piganini haibagi Meetei cha khudinggi thamoida Mipaiba, Amangba Akibagi masak fanglaba Nong gi matougum chutharakE haibabuni NONG CHUI haibadi. madugumlaba Ningthougi akanba Yathangdo Endrabadi Awaba tagani haibani.
Yenpak Tuptuna Lakke---> masida Yenpak Haiba ama yaoribasi ``Nong chottananaba Peiyana marol ani naina saraga Warukraka mayaida chapa, Kokki mapada wangkhatna Tumkhatpa, ateina nemthana fandokkhiba potsak'' Adu natte. Masida palliba Yenpak asidi-> Meetei Epa Epusingna thambiramba Laining Laisol, chatna Kanglon, Yumpallon, Enat amadi Feeset Chakcha da amatta wattana thambirambabu, Pakkhre Chaokhare Yelhoungei dagi LeirakE, Yelhoungeidagi pakna chaona sandoktuna leirakE haiba wabu samna Yenpak haibani. Adugumlaba Epana Epuna thambiramlaba YENPAk, haibadi Laining Laisoldu Ngakna chatchage haibabu, Yenpak Tuptuna, Araiba Waheisina Nunggi Lukhraba Waram kayabu Fumduna thambirambani.
Lambi nalli Lakkano---> Nong chukhibagi ( ingthougi Yathang) sit sit nallaba Lambi khong thaduna chatpa yararoidraba Lambi (Sanamahi Laining Lambi) oihanbikhraba....... Ngambadagi ngamba Leipakki Angamba Ningthouna Thingkhibana, kanasu magi maiyokta leppa ngamloi, thadokningdrabasu thadokpa tabani haiba wabuni................
Cheisu suduna Marakke---> asigumlaba ningthougi ka henba sajat pu yaningdraba Meetei meeyamna asaobaga loinana pennakhide, chei thangnarakkhi. Tunggi Meerolnasu Ningthou mabu athiba Waheina Cheinahouragani....Chei cheiduna laknaragani haiba wadubuni Cheisu suduna lakke haibadi. Amaromda Cheisu haibasi Awabasinggi ngaklouni.
Asumna Kanglei Emaga Kainarakpa Chahi Kumsing Yamlakle. Ema mahakna Kapliba, khudang Pifmnana Firuk khum, maru lukna khanglibasi yengduna leingamlibara Kangleichasa. Mikap thokpa matm oidribara Athoubasa. Chaoba Yanggol farakle, samba panggal chaorakle, Sanjenthong wangma landuna chatkhrabi kanglei pokpi Emana hanwairakpa matm yourakle, chongthoraklo athoubasa samu tongduna thoklasi Emabu oklurasi.

Sawombung (Awang Keibi Sawombung)

Thangwai madaimadi awang keipi Sawompung-O koubadi karidagino Hairapati Lairel Meitingu Loinai kouba Thouwanthabana tongcheng phakmanungta yaorou sha tanbada Meidingu Thouwan Thabana [ 1195-1239 faobada pallamba Meidingu Thawanthaba] Lilwai (Eril  Turel) kharangpokpu panchongna tupi meina wotna khousabadi yaorou khuchummu kaipi yek sawom, sawom tharaitang samphabi pamel U kappapu pharammi. Meidingu na punglon thonlamye. yaorou sawom achangbabusung panam kaithang leina sana, punlamye. adu maramgibu lamlen awang kaipi sawom pun-o kou e [thangmeiron].  sawom pun-o haibadagi sawombung haina khangnakhi.