BIOCHEMISTS SOLVE ADDRESS PROBLEM IN CELLS THAT LEADS TO LETHAL KIDNEY DISEASE

Research by UCLA biochemists may lead to a new treatment -- or even a cure -- for PH1, a rare and potentially deadly genetic kidney disease that afflicts children. Their findings also may provide important insights into treatments for Parkinson's disease, Alzheimer's disease and other degenerative diseases.

Led by Carla Koehler, a professor of chemistry and biochemistry in the UCLA College, the researchers identified a compound called dequalinium chloride, or DECA, that can prevent a metabolic enzyme from going to the wrong location within a cell. Ensuring that the enzyme -- called alanine: glyoxylate aminotransferase, or AGT -- goes to the proper "address" in the cell prevents PH1.

The findings were published online in the Proceedings of the National Academy of Sciences and will appear later in the journal's print edition.

In humans, AGT is supposed to go to an organelle inside the cell called the peroxisome, but for people with a particular genetic mutation, the enzyme mistakenly goes instead to the mitochondria -- tiny power generators in cells that burn food and produce most of the cells' energy -- which causes PH1.

Koehler's team demonstrated that adding small amounts of DECA, which is FDA-approved, to cells in a Petri dish prevents AGT from going to the mitochondria and sends it to its proper destination, the peroxisome.

"In many mutations that cause diseases, the enzyme doesn't work," Koehler said. "In PH1 the enzyme does work, but it goes to the wrong part of the cell. We wanted to use DECA in a cell model to block AGT from going to the wrong address and send it back to the right address. DECA blocks the mitochondria 'mailbox' and takes it to the peroxisome address instead."

How often did it work?

"All the time," said Koehler, a member of UCLA's Jonsson Comprehensive Cancer Center, Molecular Biology Institute and Brain Research Institute.

For people with the mutation, the correct peroxisome address is present in AGT, but it is ignored because it is accompanied by the address of the mitochondria, which the cell reads first, Koehler said.

Koehler, who also is a member of the scientific and medical advisory board of the United Mitochondrial Disease Foundation, hopes to find out whether a similar "correct address" strategy can slow cancer down. Her laboratory has identified approximately 100 other small molecules, which she calls MitoBloCKs, that she and her colleagues are testing for their ability to combat Parkinson's, Alzheimer's and other diseases.

PH1 -- short for primary hyperoxaluria 1 -- starts at birth and is usually fatal for patients who do not receive both kidney and liver transplants. Approximately half of those with the disease have kidney failure by age 15. Koehler has presented her findings to the Oxalosis and Hyperoxaluria Foundation, which provides support for PH1 patients and their families.

Scientists' ability to diagnose rare diseases has improved in recent years because technological advances in genomics have made it easier to identify more genetic mutations, Koehler said.

According to Koehler, to treat diseases, scientists must first understand how proteins like AGT move inside the cell. Her research, which encompasses biochemistry, genetics and cell biology, studies how mitochondria are assembled and function, how proteins enter the mitochondria and reach the right location inside cells, and how mitochondria communicate with the rest of the cell.

Her laboratory uses model systems that enable them to study the biochemistry in a way that is not possible with humans. Much of the work is conducted in yeast.

"It's exciting that our studies in baker's yeast, a typical laboratory model, might be able to help kids with a complicated disease," Koehler said.

CELL DEATH PROTEINS KEY TO FIGHTINING DISEASE

Melbourne researchers have uncovered key steps involved in programmed cell death, offering new targets for the treatment of diseases including lupus, cancers and neurodegenerative diseases

The research teams from the Walter and Eliza Hall Institute worked together to discover the three-dimensional structure of a key cell death protein called Bak and reveal the first steps in how it causes cell death. Their studies were published in Molecular Celland Proceedings of the National Academy of Sciences.

Programmed cell death, known as apoptosis, occurs naturally when the body has to remove unwanted cells. Chemical signals tell the cell to die by activating the apoptosis proteins Bak and Bax, which break down the 'energy factory' of the cell, known as the mitochondria. When this process goes awry, defective cells such as cancer cells can continue to live, or healthy cells can die unnecessarily, such as occurs in Alzheimer's disease.

Visualizing death proteins

Using the Australian Synchrotron, Mr Jason Brouwer, Dr Peter Czabotar, Dr Ruth Kluck and colleagues from the institute's Structural Biology division investigated how the structure of Bak changes in order to initiate cell death. The research was published in Molecular Cell.

"Understanding the way cell death proteins work and what they look like is crucial to finding new ways to treat disease," Dr Czabotar said. "Our research showed how Bak morphs from one shape to another to trigger apoptosis. Once Bak becomes 'activated' within the cell, it couples with another Bak molecule to form a 'dimer', which then goes on to initiate apoptosis."

Dr Czabotar said understanding apoptosis would allow researchers to develop new ways to treat disease. "Knowing the structure of these proteins and how they work in the cell is essential in designing new treatments to fight disease."

Seeking the hole story

Dr Dana Westphal, Dr Kluck, Dr Grant Dewson, Professor Jerry Adams and colleagues from the Molecular Genetics of Cancer and Cell Signalling and Cell Death divisions examined how the Bak and Bax dimers attach to mitochondria and perforate them. The research was published in Proceedings of the National Academy of Sciences.

Dr Kluck said dimers of Bak and Bax break open the mitochondrial surface, but the mechanism remains poorly understood. "A crucial stage of apoptosis is the release of key proteins from within the mitochondria," she said. "Scientists thought this happened by Bak and Bax poking through the mitochondrial membrane to form a hole, but our work has shown this doesn't happen. Instead, these proteins collapse onto the oily surface of the mitochondria and crowd the surface until holes form."

"We and others are now working to discover exactly how these proteins come together to destroy the mitochondria and trigger apoptosis. A deeper understanding of this pivotal event is likely to suggest new ways to regulate apoptosis to combat disease."

 

GINKGO BILOBA FOR ALZHEIMERS DISEASE AND CARDIOVASCULAR DISEASE

Botanical name-Ginkgo biloba Linn

Family- Ginkgoaceae

Common name- Maidenhair tree

Ginkgos are large trees, normally reaching a height of 20–35 m (66–115 ft), with some specimens in China being over 50 m (160 ft). The tree has an angular crown and long, somewhat erratic branches, and is usually deep rooted and resistant to wind and snow damage. Young trees are often tall and slender, and sparsely branched; the crown becomes broader as the tree ages. During autumn, the leaves turn a bright yellow, then fall, sometimes within a short space of time (one to 15 days). A combination of resistance to disease, insect-resistant wood and the ability to form aerial roots and sprouts makes ginkgos long-lived, with some specimens claimed to be more than 2,500 years old.

Leaves: The characteristic greenish-yellow leaves are fan-shaped and composed of two or more distinct lobes; the Latin species name biloba refers to this fact. The common name of maidenhair tree pertains to the similarity of the leaves to those of maidenhair ferns (Adiantum species). In autumn, the leaves of Ginkgo biloba turn a beautiful golden hue before falling to the ground.

Seeds: It takes 20-35 years for maidenhair trees to reach maturity and start bearing seeds. Male and female trees are separate; male trees have pollen-producing catkins while female trees, once fertilised, bear rounded, yellowish seeds with a fleshy outer coat (resembling a plum in appearance). These fall to the ground in the autumn and as the seed coat decays it exudes a rancid butter-like smell

Part used – Leaves

Chemical constituents-- The constituents of primary interest in Ginkgo leaf are ginkgolides and flavonoids. Ginkgolides (ginkgolides A, B, C, J, and M) are diterpenes. Flavonoids present in Ginkgo leaf include flavones, biflavones, flavonols, tannins, and associated glycosides. In general, flavonoids are principally found in the leaves, although they are also present in many other parts of the plant. There are about 20 flavonoid glycosides along with glucosides, quercetin and kaempferol 3-rhamnosides and 3-rutinosides, p-coumaric esters of glucorhamnosides of quercetin, kaempferol and biflavones. The biflavones are amentoflavone, bilobetol, 5-methoxybilobetol, ginkgetin, isoginkgetin, and sciadopitysin, bilobalides. Ginkgo leaves also contain flavan-3-ols, proanthocyanins and poly-isoprenoid - derived betulaprenols in unusually high amounts. Other compounds of interest in the leaf include ginnon, ginnol, 2-hexenal, and bilobalide.

Therapeutic  uses--Ginkgo biloba has been used medicinally for thousands of years. Today, it is one of the top-selling herbs in the United States.

Ginkgo is used for the treatment of numerous conditions, many of which are under scientific investigation. Available evidence supports ginkgo for managing dementia, anxiety, schizophrenia, and cerebral insufficiency (insufficient blood flow to brain).

Evidence for other uses is either lacking or mixed. Further research is needed for all uses of ginkgo.

Although ginkgo is generally well tolerated, it should be used cautiously in people with clotting disorders or taking blood thinners, or prior to some surgical or dental procedures, due to reports of bleeding.

HOMOEOPATHIC USES

First time the Homoeopathic proving was done in the year 1933 by Dr. E.A.Maury with the M.T. on seven subjects ( 5 men, 2 women) then six persons and Dr. KORSAKOFF on two men. An auto experimentation was undertaken by Dr. E.G.IVOR of New Zealand in 1971. Homoeopathically proved main symptoms are --- General lameness with chill. Unreasonable fear with rapid flow of words. Suppressed anger. Intellectual weakness.

 Heaviness of the frontal region of head.Vertigo. Sensation of troubles vision with a veil before the eyes.Buzzing in ears.Vesiculous eruptions, burning, prurigious. Great muscular weakness. Asthma

Here, it is interesting to know, that many Homoeopathic pharmaceuticals in India and abroad have spearheaded research on Ginkgo biloba and Ginkgo biloba Mother Tincture is being used globally for Cardio- Vascular disease, neurological problems.

1.       Improves cerebral circulation and pheripheral vascular problems

2.      Improves in age related forgetfulness

3.      Useful in weakness of memory, difficulty in thinking, insomnia, heaviness in frontal region, vertigo, buzzing sensation

4.    Inhibits Prolye endopeptidase (PEP), plays an important role in learning and memory process, depression and senile dementia

5.       Useful in Alzheimer's patients

6.    Inhibits platelet activation factor (PAF), thereby reduces the chances of blood clotting leading to various inflammations and allergic changes

Prion Proteins The Sci Fi Villains Behind Mad Cow Disease And Human Chronic Nerve Problems

Today's post from media.uzh.ch (see link below) may seem light years away from the sorts of neuropathy we experience every day but in fact is much closer than you think. With all these things, you have to continually remind yourself exactly what neuropathy is:- damage to the nerves. There are dozens of causes and dozens of types but nerve damage leads to the symptoms we most frequently feel. This fascinating article brings images from the 90's of cows struggling to stay on their feet under the same general umbrella description as the tingling and burning we suffer from when we report our symptoms to our doctors. Scientists are seemingly just beginning to scratch the surface of the knowledge that concludes that certain proteins can be responsible for all this strange behaviour in our nervous systems. It's fascinating and frightening at the same time but you do get the feeling that we're on the point of huge scientific discoveries regarding neuropathy and that can only be a good thing as we struggle with drug treatments that clearly only work to a limited extent. Worth a read - fascinating stuff!

Impact of prion proteins on the nerves revealed for the first time
News release, 8 August 2016 
 
When prion proteins mutate, they trigger mad cow and Creutzfeldt-Jakob disease. Although they are found in virtually every organism, the function of these proteins remained unclear. Researchers from the University of Zurich and the University Hospital Zurich now demonstrate that prion proteins, coupled with a particular receptor, are responsible for nerve health. The discovery could yield novel treatments for chronic nerve diseases.


Without the prion proteins, the so-called Schwann cells around the sensitive nerve fibers no longer form an insulating layer to protect the nerves. (Image: NatureReview / Neuroscience)

Ever since the prion gene was discovered in 1985, its role and biological impact on the neurons has remained a mystery. “Finally, we can ascribe a clear-cut function to prion proteins and reveal that, combined with particular receptor, they are responsible for the long-term integrity of the nerves,” says Professor Adriano Aguzzi from the Neuropathological Institute at the University of Zurich and University Hospital Zurich. The present study therefore clears up a question that researchers have been puzzling over for 30 years, but ultimately went unanswered.

Prions are dangerous pathogens that trigger fatal brain degeneration in humans and animals. In the 1990s, they were responsible for the BSE epidemic more commonly known as mad cow disease. In humans, they cause Creutzfeldt-Jakob disease and other neurological disorders that are fatal and untreatable. Meanwhile, we know that infectious prions consist of a defectively folded form of a normal prion protein called PrPC located in the neuron membrane. The infectious prions multiply by kidnapping PrPC and converting it into other infectious prions. 

Absent prion proteins cause nerve diseases

For a long time, it remained unclear why we humans – like most other organisms – have a protein in our neurons that does not perform any obvious function, yet can be extremely dangerous. Aguzzi has spent decades researching this issue and examining the theory that animals without the PrPC gene are resistant to prion diseases. But what are the repercussions for the organism if the prion protein is deactivated?

A few years ago, Aguzzi and his team discovered that mice without the PrPC gene suffer from a chronic disease of the peripheral nervous system. The reason: The so-called Schwann cells around the sensitive nerve fibers no longer form an insulating layer to protect the nerves. Due to this insulating myelin deficit, the peripheral nerves become diseased, potentially resulting in motoric disorders in the motion tract and paralysis.

The researchers have now gone one step further in the lab: In a new study, Alexander Küffer and Asvin Lakkaraju clarify exactly why the peripheral nerves become damaged in the absence of the prion protein PrPC. They discovered how the PrPC produced by the neurons docks onto the Schwann cells: namely via a receptor called Gpr126. If the prion protein and the receptor work together, a particular messenger substance (cAMP) which regulates the chemical interaction in the cells and is essential for the integrity of the nerve’s protective sheath increases. Gpr126 belongs to the large family of “G-protein-coupled receptors”, which are involved in many physiological processes and diseases.

30-year-old research question finally answered

This discovery solves a key question that has long puzzled neuroscientists and points towards future applications in hospitals. “If you want to deactivate the prion protein PrPC fully for potential Creutzfeld-Jakob disease treatments, you need to know the potential side effects on the nerves in the future,” explains Aguzzi. Moreover, the present results on the effect of PrPC at molecular level could yield a new approach for peripheral neuropathy. Currently, there are only extremely limited therapeutic options for these chronic debilitating diseases of the nervous system.
Literature:

Alexander Küffer, Asvin K. K. Lakkaraju, Amit Mogha, Sarah C. Petersen, Kristina Airich, Cédric Doucerain, Rajlakshmi Marpakwar, Pamela Bakirci, Assunta Senatore, Arnaud Monnard, Carmen Schiavi, Mario Nuvolone, Bianka Grosshans, Simone Hornemann, Frederic Bassilana, Kelly R. Monk & Adriano Aguzzi. The prion protein is an agonistic ligand of the G-protein-coupled receptor Gpr1/Adgrg6. Nature, 8 August 2016. doi:10.1038/nature19312

http://www.media.uzh.ch/en/Press-Releases/2016/Prion-Proteine.html

COULD FREE MOBILE APPS SCREENS FOR LIVER DISEASE

In a small study, researchers from the Johns Hopkins Children's Center report they have verified the ability of a free smartphone app to accurately read, interpret and record the color of a newborn's poop as a possible early symptom of biliary atresia (BA) -- a rare disorder that accounts for nearly half of pediatric end-stage liver disease in the United States.

For the vast majority of parents using the program, aptly named PoopMD, the results should provide reassurance that their newborn's stool color is normal, the investigators say. But for the one in 14,000 newborns with BA -- about 400 babies each year in the United States -- parents using the app can rely on it to help detect the symptomatic pale yellow to chalky grey stools that mean urgent medical assessment is needed. PoopMD is free and available for Apple and Android smartphone users.

"Days matter in diagnosing BA," says Douglas Mogul, M.D., M.P.H., a pediatric gastroenterologist at the Johns Hopkins Children's Center and lead author of the study published July 29 in PLOS ONE.

That's because babies with BA treated within the first two months of life have the best outcomes and are far less likely to need a liver transplant later. The first line of treatment involves surgery to repair bile ducts and restore bile flow to prevent irreversible liver damage.

Sadly, the 60-day window is all too often missed, with the average time to diagnosis in the United States standing at 70 days.

"PoopMD does what it says it will do," says Mogul, who worked with HCB Health to create the app, first released in 2014. Among more than 100,000 medical health apps currently available, he says, only a few have been rigorously tested to see if they deliver the benefits they promise.

For the study of the app, which builds on an earlier "color card" that is distributed to new parents, the team first gathered the medical opinions of seven expert pediatricians who looked at 34 photographs of pale-colored stool. Twenty-seven of the pictures were determined to be of normal stool, and seven were deemed acholic, or bile deficient, signaling high risk for BA.

Next, one expert and three laypeople were asked to use the app on Apple and Android devices to look at and analyze the same pictures under a variety of lighting conditions and using a variety of smartphone models. "These individuals were essentially asked to take a picture of the stool photograph and determine if the app identifies the photo as normal or pale," Mogul says, "but in normal use, a parent just takes pictures of the contents of a diaper."

Even with the picture of the picture, the researchers say, the app correctly identified all of the acholic stool samples and correctly identified 24 of the 27 normal stools, while three normal stools were mislabeled "indeterminate."

"That means the app never identified a normal stool as pale, a type of false positive that could cause unnecessary anxiety for a parent or other app user," says Mogul.

Once downloaded on a smartphone, parents or caregivers use the app by taking a picture of the baby's stool and identifying the part of the picture that has a stool color of concern. The app then immediately identifies whether the stool color matches those associated with gastrointestinal illnesses or problems with the liver, including BA.

The app can store results for future and comparative reference, and parents can email a photo to a pediatrician directly from the app. The app also reminds parents to check their newborn's stool color every two weeks.

"Four out of five adults in the U.S. ages 18-35 -- the age of young parents -- have a smartphone, and that's independent of income level," says Mogul, "so the app gives us a great opportunity to distribute interactive content that helps young parents pay attention to educational advice."

Beyond the health and lifesaving benefits of early diagnosis and treatment of BA, Mogul says, the potential cost savings from diagnosing BA early enough are enormous, Mogul says, including avoiding a liver transplant (approximately $150,000) and ongoing immunosuppression (approximately $25,000/year) to keep the child's body from rejecting the new organ.

Mogul, who also conducted a cost-effectiveness study of the stool color cards, says widespread use of PoopMD is likely to improve medical outcomes and lower costs.

Role of Physiotherapy In Pelvic Inflammatory Disease

Pelvic Inflammatory Disease(PID) 
Pelvic inflammatory disease (PID) may be the inflammation of the upper genital tract relating to the fallopian tubes as well as the ovaries. The soreness is often bilateral because most from the PID is caused by the ascending or blood borne infection and also the close anatomic association from the ovaries with the fallopian tubes favors the bilateral involvement, though one tube might be more affected compared to other. The Pelvic inflammatory disease treatment aims to lessen this inflammation and stop further damage to the organs.
Pelvic inflammatory disease causes
The most typical cause of PID is std's (STD)
Most common being gonococcal and chlamydial infections
60-75% of PID is brought on by STD, of which gonorrhea accounts for about 30% within the developed countries
Gonoccoci and Chlamydia travel in the genital tract across the mucous membrane to reach the fallopian salpingo-oophoritis
Other organisms directly ascend across the lining of the genital tract
Other organisms that create PID include mycoplasma, tubercular bacillus, viruses and E. coli. Both aerobes and anaerobes are implicated in PID
Pelvic inflammatory disease Pathology Acute Salpingitis
The fallopian tube is swollen, edematous and hyperaemic with visible dilated vessels around the peritoneal surfaces.
The sure manifestation of salpingitis (inflammation of the fallopian tube) may be the discharge of seropurulent fluid in the fimbrial end of the tube.
The inflammatory exudate is discharged in to the lumen of the tube resulting in adhesions and tubal blockage or narrowing from the lumen which may be the cause of ectopic pregnancy or infertility.
Pelvic abscess might be formed due to pus collection within the pelvic cavity.
The ovaries are participating and a tubo ovarian abscess or mass may result.
In rare cases the problem may spread upwards to result in generalized peritonitis, paralytic ileus and even sub diaphragmatic and perinephric abscess.
In PID following postabortal and puerperal infection, the problem spreads through the cervix via lymphatics towards the cellular tissue causing cellulitis. The fallopian tube is affected externally and the mucous membrane last but not least.
Pelvic inflammatory disease treatment within the acute stage helps limit the problem and prevent long term harm to the fallopian tube and ovaries resulting in adhesions formation, infertility etc. In early stage pelvic inflammatory disease treatment may require administration from the antibiotics but in the later stage surgical drainage from the abscess and adhesions breakdown may be required.

Pelvic inflammatory disease symptoms and signs
The most typical symptom of acute PID is gloomier pelvic pain. Pain is bilateral and limited to lower abdomen.
Pain spreads upwards if general peritonitis ensues.
Pain is severe in acute stage and it is followed by a high temperature. Vomiting could also follow.
Discharge from the vagina and dysuria also occur.
Menstrual irregularity if any, is a result of preceding endometritis in case of ascending infection in order to the antecedent abortion or delivery.
The patient may develop uterine bleeding at any given time when menstruation isn't expected and the bleeding is usually profuse and prolonged.
In case of pelvic abscess, the individual develops severe diarrhea because of rectal irritation.
Investigations in Pelvic inflammatory disease
Haemoglobin, leucocyte count and ESR.
Cervical and vaginal swab culture for both aerobic and anaerobic organisms.
Blood culture if bacteraemia takes hold. C reactive protein distinguishes between infective and non infective mass.
Ultrasound: Tubo-ovarian abscess appears around the ultrasound.
Computed tomography shows a spherical or tubular structure having a low attenuation center.
Pelvic inflammatory disease treatment
Pelvic inflammatory disease treatment aims to lessen the inflammatory process thereby arresting the development of the organisms resulting in the disease. Since 60-75% of PID come from Sexually transmitted diseases, treatment consists of pharmacological therapy (antibiotics) to eradicate the causative organisms together with supportive therapy for the control over other symptoms. Surgical treatment are usually necesary in case of extensive damage.
Pelvic inflammatory disease treatment in Acute stage:
 Pelvic inflammatory disease treatment within the acute stage includes removal of the causative organisms by proper administration from the antibiotics.
 Mild cases are treated at home with antibiotics.
 Moderate and severe cases of Pelvic inflammatory diseases may require hospitalization.
Hospital management includes:
Rest
Intravenous fluids within the presence of dehydration or vomiting and correction of electrolytic imbalance.
Antibiotics are mandatory to become instituted at the earliest for the pelvic inflammatory disease treatment before the diagnosis is made. Initially, intravenous route is resorted to, however when the infection settles down, oral therapy might be started.
Antibiotics like tetracycline, erythromycin, doxycycline, clindamycin work against both aerobic and anaerobic bacteria. Newer antibiotics include cefoxitin, cefotetan, doxycycline etc can be utilized for the pelvic inflammatory disease treatment. Surgical treatment may be required in the following conditions:
Drainage of the pelvic abscess.
Dilatation and evacuation of septic products of conception or for haemorrhage in postabortal sepsis.
Acute spreading peritonitis and intestinal obstruction.
Physiotherapy management within the acute pelvic inflammatory disease aims to lower the pain and inflammation combined with the pharmacological therapy. In mild and moderate cases of Pelvic inflammatory disease in which the patient does not need hospitalization, pain relieving modality like short wave diathermy could be given.
Short wave diathermy is really a deep heating modality, produces heat both in deep and superficial tissues. Within the acute stage very mild or pulsed short wave diathermy can be used to promote healing and lower pain.
For the Pelvic inflammatory disease treatment short wave diathermy could be given for 5-10 minutes for a time of three days a week while using cross- fire method of diathermy. Cross-fire method involves moving the electrodes to some position at right angles for their previous position midway through the treatment. Half the Pelvic inflammatory disease treatment is offered antero-posteriorly through the pelvis using the patients in the lying position and 2nd half in the side lying using the legs curled up or perhaps in sitting position and also the electrodes placed over the pelvic outlets and also the lumbo-sacral area of the spine.
Pelvic inflammatory disease treatment in Chronic stage: 
Physiotherapy control over the pelvic inflammatory disease within the chronic stage is aimed at:-
Relieving pain.
Promote healing round the area.
Treat existing musculoskeletal dysfunction or prevent further musculoskeletal dysfunction.
Increase function.
Pelvic inflammatory disease treatment modalities contain:-
Short wave diathermy: it's widely known that short wave diathermy may be used to reduce pain and swelling, accelerate the soreness process and promote healing in tissues with chronic inflammation. It results in increased circulation round the area by vasodilatation resulting in better healing. Additionally, it increases the metabolic activity from the area leading to more nutrients, more cellular activity and healing and increasing collagen extensibility. It will help in the repair of pelvic microcirculation, thus enabling lysis of scar tissues, relaxation of contracted muscles within the pelvis and pelvic floor.
For the pelvic inflammatory disease treatment within the chronic stage short wave diathermy is offered for 15-30 minutes, two times a day for thrice per week using the cross-fire method of treatment.
Electrical stimulation as Transcutaneous electrical nerve stimulation (TENS) towards the low back for the symptomatic elimination of low back pain can be given. TENS works at both spinal-cord level and higher brain centres to inhibit the transmission of nocioceptors thus relieving the thought of pain.
Moist hot pack could be given the low back to alleviate pain in the back.
The pelvic floor muscles in females in the chronic PID might be in the hypertonic state because of pain, delayed healing, scarring adhesions or generalized spasm through the pelvic floor tissues. Pelvic floor rehabilitation is suggested for the pelvic inflammatory disease treatment such patients.
Teaching control and relaxation from the pelvic floor musculature is important during these patients. Biofeedback including surface EMG may be used to induce relaxation during these muscles.
For strengthening the pelvic floor musculature instruct the individual to tighten the pelvic floor as though attempting to stop the the flow of urine. Hold for 3-5 seconds and relax. Repeat Ten times per session. These exercises are through with empty bladder.
Elevator exercises : instruct the girl to visually imagine traveling in an elevator. As the elevator goes in one floor to the other, contract the muscles a bit more. Relax the muscles gradually, as though the elevator were descending one floor at any given time.
For treating a woman with hypertonus, boost the rest time between your pelvic floor contractions and sets. Focus on relaxation is equally important for weight training in these clients. Utilization of surface EMG for feedback is invaluable for enhancing understanding of holding patterns and resting tone.
Instruct the girl to contract the pelvic floor as with the strengthening exercises then allow total voluntary release and relaxation from the pelvic floor muscles. This activity could be coordinated with breathing. Instruct the girl to concentrate on a slow deep breath slowly and allow the pelvic floor to totally relax.

Surgical treatment might be indicated in the chronic pelvic inflammatory disease in which the extent of damage is much more. Tubal damage may require tuboplasty. Laproscopic breaking of adhesions is indicated when the tubal blockage is due to external adhesions. Overall surgery depends on the age and parity from the patient, the symptoms and pelvic pathology.For prevention against Pelvic inflammatory disease, delivery should be conducted in the hospitals, contraceptive devices like barrier methods can be used to prevent sexually transmitted diseases and also the young women should be educated concerning the risk of STDs and its prevention.

IMMUNE CELLS IN LIVER DRIVE FATTY LIVER DISEASE LIVER CANCER

Fatty liver disease -- alongside fatty liver due to massive alcohol consumption -- is mainly caused by excessive consumption of fat and sugar combined with a lack of exercise or a sedentary life style. This is referred to as non-alcoholic fatty liver disease (NAFLD). If NAFLD becomes chronic -- e.g. through the constant uptake of high lipids and high sugar combined with lack of excercise a chronic inflammatory response is triggered in the liver tissue in addition. This can lead to non-alcoholic steatohepatitis (NASH) -- a liver disease with clear detectable pathologic alteratons of the tissue.

These liver diseases (NAFLD and NASH), along with chronic viral infections, are the most common causes of liver cancer, or hepatocellular carcinoma (HCC). In the United States, about 90 million people suffer from NAFLD. In Europe, the figure is more than 40 million, and even in threshold countries like India and China, the number of people affected is rising due to increasingly unhealthy lifestyles. More worrying, in all of the above mentioned states the numbers of NAFLD and NASH patients is constantly increasing. Consequently, the incidence of HCC resulting from NASH and NAFLD is also rising worldwide. In the United States, HCC is the fastest-growing form of cancer at the moment. No efficient causal therapy exists for HCC patients of which approximately 800,000 die every year.

T cells involved in the development of fatty liver disease, NASH and HCC

The mechanisms that cause diseases such as fatty liver disease, steatohepatitis and HCC are still not widely understood. However, immune cells, particularly CD8+ T cells and NK T cells seem to play an important role. This finding was made by a team of scientists led by Prof. Mathias Heikenwälder, Prof. Matthias Tschöp, Dr. Kerstin Stemmer, Dr. Kristian Unger, Prof. Ulrike Protzer and the working group of Dr. Hans Zischka from the Helmholtz Zentrum München together with a team headed by Prof. Percy Knolle of the Technische Universität München (TUM), Prof. Achim Weber from Zurich University Hospital and Dr. Monika Wolf, Institute of Surgical Pathology, University Hospital Zurich. The animal model which was used to examine the long-term effects of metabolic syndrome* enabled the scientists to elucidate new mechanisms that cause fatty liver disease and also show how it can develop into liver cancer.

Inflammatory events offer starting point for prevention and treatment

The scientists assume that an existing metabolic imbalance results in the activation and migration of immune cells to the liver. There, the immune cells interact with liver cells and trigger an inflammatory response that damages the liver tissue and also destabilizes the metabolic activity of the liver cells. "Initially it immune cells promote fatty liver degeneration. The inflammation, which is triggered by specific immune cells, encourages the progression of fatty liver pathology and causes NASH to develop. These processes are the basis for liver cell degeneration, which can cause HCC," explains Prof. Heikenwälder, who led the study. "Our results provide completely new insights into the development of these serious liver diseases. Building on this knowledge, we now want to develop new, preventive and therapeutic strategies to combat these diseases." The initial studies are already under way in the preclinical model.

*Metabolic syndrome: a combination of obesity / abdominal adiposity, insulin resistance, raise levels of lipids in the blood and raised blood pressure.

HOMOEOPATHIC REMEDIES FOR PARKINSONS DISEASE

Parkinson's disease is a degenerative disorder of the central nervous system mainly affecting the motor system. The motor symptoms of Parkinson's disease result from the death of dopamine generating cells in the substantia nigra a region of the midbrain. The causes of this cell death are poorly understood. Early in the course of the disease, the most obvious symptoms are movement-related; these include shaking, rigidity, slowness of movement and difficulty with walking and gait. Later, thinking and behavioral problems may arise, with dementia commonly occurring in the advanced stages of the disease, and depression is the most common psychiatric symptom Other symptoms include sensory, sleep and emotional problems. Parkinson's disease is more common in older people, with most cases occurring after the age of 50; when it is seen in young adults, it is called young onset PD (YOPD).

The main motor symptoms are collectively called parkinsonism, or a "parkinsonian syndrome". The disease can be either primary or secondary. Primary Parkinson's disease is referred to as idiopathic (having no known cause), although some atypical cases have a genetic origin, while secondary parkinsonism is due to known causes like toxins. Many risks and protective factors have been investigated: the clearest evidence is for an increased risk of PD in people exposed to certain pesticides and a reduced risk in tobacco smokers. The pathology of the disease is characterized by the accumulation of a protein into Lewy bodies in neurons, and insufficient formation and activity of dopamine in certain parts of the midbrain. Where the Lewy bodies are located is often related to the expression and degree of the symptoms of an individual. Diagnosis of typical cases is mainly based on symptoms, with tests such as neuroimaging being used for confirmation.

HOMOEOPATHIC REMEDIES

AGARICUS MUS. 200-CM- Jerking , trembling and stiffness of  the muscles. Spine cannot even bear to touch

GELSEMIUM  30-CM—There is trembling of the head and other parts of the body. Staggering gait.Trembling is the chief indication for the use of this remedy

ARGENTUM NITRICUM 200-CM- Use it with Gelsemium on alternate days, when the memory is also impaired with spurting diarrhea and flatulence

AVENA SAATIVA  Q- Best tonic for debility after exhausting disease , nervous exhaustion and paralysis agitans. Give 20 drops thrice daily in warm water

CAUSTICUM 200-CM- Unsteadiness of the muscles of forearm and hand. Numbness. Loss of sensation of hands

CURARE 200—Reflexes lessened or abolished in extremities. Weakness of hands and fingers , cannot lift the fingers

HELODERMA 200—Parkinson’s disease affecting the left side mostly with the feeling of prostration and coldness

MAGNESIUM PHOS  1M—Involuntary shaking of the hand. Give it weekly

PHYSOSTIGMA 200- Muscular weakness is felt more on movement and in winter. Palpitation of the heart is felt throughout the body

STRAMONIUM 200- CM—Parkinsonism. Tremor, muscular weaknessd rigidity. Peculiar gait and shaking