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Bajrović, Fajko F; Sketelj, Janez; Jug, Marko; Gril, Iztok; Mekjavić, Igor B

2002-09-01

Abstract The effect of hyperbaric oxygen treatment (HBO) on sensory axon regeneration was examined in the rat . The sciatic nerve was crushed in both legs. In addition, the distal stump of the sural nerve on one side was made acellular and its blood perfusion was compromised by freezing and thawing. Two experimental groups received hyperbaric exposures (2.5 ATA) to either compressed air (pO2 = 0.5 ATA) or 100% oxygen (pO2 = 2.5 ATA) 90 minutes per day for 6 days. Sensory axon regeneration in the sural nerve was thereafter assessed by the nerve pinch test and immunohistochemical reaction to neurofilament. HBO treatment increased the distances reached by the fastest regenerating sensory axons by about 15% in the distal nerve segments with preserved and with compromised blood perfusion. There was no significant difference between the rats treated with different oxygen tensions. The total number of regenerated axons in the distal sural nerve segments after a simple crush injury was not affected, whereas in the nerve segments with compromised blood perfusion treated by the higher pO2, the axon number was about 30% lower than that in the control group. It is concluded that the beneficial effect of HBO on sensory axon regeneration is not dose-dependent between 0.5 and 2.5 ATA pO2. Although the exposure to 2.5 ATA of pO2 moderately enhanced early regeneration of the fastest sensory axons, it decreased the number of regenerating axons in the injured nerves with compromised blood perfusion of the distal nerve stump.

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Srivastava, R K; Sharma, S; Verma, S; Arora, B; Lal, H

Isoniazid, rifampicin and pyrazinamide during short-course chemotherapy for tuberculosis can result in liver injury. The coexistence of tuberculosis and diabetes is common in patients who receive inadequate treatment. The risk of hepatotoxicity from many toxicants is increased in diabetic rats . Silymarin provides protection against liver injury caused by many hepatotoxicants, including antitubercular drugs (ATDs). In the wake of increased severity of ATD-induced hepatotoxicity in diabetes we report here the results of a study on the influence of diabetes on silymarin hepatoprotection in rats . Rats with diabetes induced via intraperitoneally injected streptozotocin (50 mg/kg), nondiabetic rats and insulin-treated diabetic rats received isoniazid (7.5 mg/kg/day), rifampicin (10 mg/kg/day) and pyrazinamide (35 mg/kg/day) orally (p.o.) with or without silymarin (100 mg/kg/day p.o.) treatment for 45 days. Compared to nondiabetic rats , liver function tests and histological changes of liver revealed exaggerated liver injury in diabetic rats caused by ATDs which was evident by 5- to 8-fold increases in serum levels of marker enzymes (aspartate and alanine aminotransferase, alkaline phosphatase and gamma-glutamyltranspeptidase) and 1- to 2-fold increases in bilirubin accompanied by a 2-fold decrease in total serum proteins, intense fatty and inflammatory infiltrations, necrosis and fibrosis. Coadministration of silymarin provided protection against ATD hepatotoxicity in all animals. However, insulin-treated diabetic animals showed greater silymarin-induced hepatoprotection against ATD-induced liver injury, which was characterized by near normal levels of marker enzymes, an increase in total proteins and normal hepatic structure. These results thus indicate that diabetes exaggerates ATD-induced liver injury and attenuates silymarin-induced hepatoprotection. However, insulin treatment for diabetes offers greater silymarin-induced hepatoprotection against ATD-induced liver

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Ghobadi Pour, Mozhgan; Mirazi, Naser; Alaei, Hojjatollah; Moradkhani, Shirin; Rajaei, Ziba; Monsef Esfahani, Alireza

Silymarin, a mixture of antihepatotoxic flavonolignans used in the treatment of liver diseases, and lactulose, a nonabsorbable synthetic disaccharide, were investigated to analyze their probable synergic and healing effects in a hepatic cirrhotic rat model. Liver damage was induced by the administration and subsequent withdrawal of thioacetamide. The significant decrease in liver enzymes and malondialdehyde levels confirmed the curative effects of silymarin and lactulose. In the silymarin + lactulose group, liver enzyme and malondialdehyde levels were significantly reduced compared with those in the thioacetamide group. All treatments led to liver regeneration and triggered enhanced regeneration . Silymarin and lactulose alone or in combination have potent curative effects and reduce thioacetamide-induced liver damage.

Isolating Lysosomes from Rat Liver .

Pryor, Paul R

2016-04-01

This protocol describes the generation of a fraction enriched in lysosomes from rat liver . The lysosomes are rapidly isolated using density-gradient centrifugation with gradient media that retain the osmolarity of the lysosomes such that they are functional and can be used in in vitro assays. © 2016 Cold Spring Harbor Laboratory Press.

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Morales-Ruiz, Manuel; Santel, Ansgar; Ribera, Jordi; Jiménez, Wladimiro

The liver is continuously exposed to diverse insults, which may culminate in pathological processes causing liver disease. An effective therapeutic strategy for chronic liver disease should control the causal factors of the disease and stimulate functional liver regeneration . Preclinical studies have shown that interventions aimed at maintaining Akt activity in a dysfunctional liver meet most of the criteria. Although the central function of Akt is cell survival, other cellular aspects such as glucose uptake, glycogen synthesis, cell-cycle progression, and lipid metabolism have been shown to be prominent functions of Akt in the context of hepatic physiology. In this review, the authors describe the benefits of the Akt signaling pathway, emphasizing its importance in coordinating proper cellular growth and differentiation during liver regeneration , hepatic function, and liver disease. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Medicine

Researchers recently discovered certain drugs, including one developed to treat Alzheimer’s, stimulate innate self-repair mechanisms

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For dentists, a cavity is a conundrum—in order to save the tooth they must further damage it. Currently, the primary way to treat a cavity is to excavate the decay and the surrounding area before filling the resulting crater with a durable surrogate material such as metal, plastic or glass cement.

But what if instead of drilling holes into teeth and patching them up with synthetic fillers, dentists could coax our pearly whites to regrow themselves? Recently, Paul Sharpe, a bioengineer at King’s College London, and his colleagues discovered a new way to do exactly this in mice. Last year they published a study describing their innovative techniques in . And since then they have made even more progress that edges this experimental procedure closer to human clinical trials. If the treatment eventually becomes part of the dentist’s standard tool kit, scientists say it would easily be one of the field’s most important advances in 50 years.

Our teeth get damaged all the time. Most of the injuries they endure are due to everyday wear and tear as well as the activity of microbes in the mouth. These organisms coat the surface of each tooth and feed on meal remnants. As they break down particles of food, some of these microbes produce and secrete acids as a by-product. And that acidity degrades enamel—the tooth’s hard outer layer.

Like skin, teeth can usually repair minor mishaps themselves. When our teeth remain uncleaned for too long, however, acid can eat through the enamel and begin dissolving underlying layers of dense, bony tissue called dentin. When dentin is seriously injured, stem cells located in the tooth's soft, innermost layer—the dental pulp—morph into cells called odontoblasts, which secrete new tissue. (Stem cells are capable of becoming virtually any type of cell.) Yet when the injury is too large or deep, that fresh dentin is not sufficient to restore the tooth. The result is often a cavity.

Sharpe suspected he could dramatically boost teeth’s natural healing ability by mobilizing stem cells in the dental pulp. Earlier research had demonstrated the Mules mostaza Clearance Store Cheap Online Sale Shop Offer Choice Cheap Online RWo9hx
—a particular cascade of molecules involved in cell-to-cell communication—is essential for tissue repair and stem cell development in many parts of the body such as the skin, intestines and brain. Sharpe wondered: Could this signaling pathway also be important for self-repair processes in teeth? If so, maybe exposing damaged teeth to drugs that stimulate Wnt signaling would similarly encourage the activity of stem cells in the dental pulp—giving teeth the kind of regenerative superpowers usually seen only in plants, salamanders and starfish.

To test this idea, Sharpe and his fellow researchers drilled holes into the molars of mice, mimicking cavities. They then soaked tiny collagen sponges (which are made from the same protein found in dentin) in various drugs known to stimulate Wnt signaling, including tideglusib, a compound that has been investigated in clinical trials for its potential to treat Alzheimer's and other neurological disorders. The scientists then placed these drug-soaked sponges in the drilled mouse molars, sealed them up and left them for four to six weeks. The teeth treated with these drugs produced significantly more dentin than ones untreated or stuffed with an unsoaked sponge or typical dental fillers. In most cases the technique restored the rodents’ pearly whites to their former intact state. “It was essentially a complete repair,” Sharpe says. “You can barely see the joint where the old and new dentin meet. This could eventually be the first routine pharmaceutical treatment in dentistry.”

David Mooney, a professor or bioengineering at Harvard University who has also investigated new ways to heal teeth but was not involved in the study, says he is “very impressed” by these findings. “This is not just scientifically important, but has significant practical advantages," he says. Adam Celiz, an assistant professor of bioengineering at Imperial College London who was also not involved in the recent research, says this is an important advance in the emerging field of regenerative dentistry. “The materials dentists use could soon be revolutionized,” he says.

Any treatment that recruits the body's native stem cells or adds new stems cells to the body, however, poses a risk of uncontrolled tissue growth. Experimental and unregulated stem cell therapies have resulted in brain tumors, for example, as well as bones growing in eyelids . But in this case, Sharpe says, the amounts of drug used are so tiny that the risk of unwanted growth is minimal. Celiz agrees the danger is small but he says rigorous testing in lab animals and clinical trials should be done to rule out potential side effects.

Since publishing their initial study Sharpe and his colleagues have tested their regenerative technique on rats. (Because those rodents have larger teeth than mice, a drilled rat molar better approximates human tooth decay.) The treatment worked just as well on the rats as it had on the mice, Sharpe says, but the data has not yet been published. Now Sharpe’s team is investigating a larger group of candidate drugs in order to determine whether another medication works better than those already tested, and to determine the optimal dose. They are also developing an alternative delivery system that is more amenable to modern dental practices: The chosen drug will be dissolved in a gel that is injected into a cavity and bathed with ultraviolet light to solidify it—a quick and easy procedure similar to one dentists already use to seal and repair teeth.

In order to formally introduce this treatment to modern dentistry, however, the researchers will need to perform clinical trials with human patients. Such work is at least several years away, Sharpe says. But some of the drugs he might consider are already approved for other uses in humans, which he hopes could expedite the process for eventual approval. "A lot of dental treatments are still in the dark ages," Sharpe says. "It's time to move on."

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