Acne treatment

Acne is just annoying. The best advice one can give you, is to go to the dermatologist, isn't it? Yeah, right... Some dermatologists give antibiotics like they are giving candy to a child. Most probably they will start you on a topical cream containing tetracycline/ benzoyl peroxyde/ salycilic acid or similar and some antibiotics. These are said to be wide spectrum antibiotics, meaning that they are effective against a wide variety of bacteria that causes acne and this cure should be effective to most people.  BUT, if it you are resistant to tetracycline, let's say, you are doing this cure for months and getting no results, of course except the side effects of destroying your intestinal flora. Antibiotics are not easy to deal with. You should take them with caution and you should not forget to take probiotics immediately afterwards. 

That's why my advice is not to go to any dermatologist,  but to find a GOOD dermatologist that is responsible. A good dermatologist, versus a dermatologist that is just interested in your pocket, will first ask for your bacteriogram,  which in other words means that they are going to find out to what kind of antibiotics you are sensitive, semi-sensitive and resistant to. This test is very easy to do and not painful at all. It takes just 5 minutes, but it helps a ton, because, after that, the doctor can give you a narrow spectrum antibiotic, that you are actually sensitive to. So, bacteriogram is very important. 

Another important advice that I will give you is that you must take your prescription antibiotics at the same time everyday. Not an hour early or half hour late..Not even 5 minutes late. Just set up your alarm clock or something, because if  you do not take them at the same time everyday the antibiotic's blood level changes and that gives the bacteria the possibility to defend itself, so you became resistant to that kind of antibiotic, which is in your disfavor... 

Again, in combination with antibiotics the dermatologist can give you a cream that contains retinoic acid. These kind of creams are generally very effective, but they are very strong in side effects, too. They peel your skin, make it dry and red, but that's the desired effect from them. If you are using these kind of cream ALWAYS use a cream with a high sunscreen protection factor. 

If your acne is hormonal then the doctor may prescribe to you an oral contraceptive pill that helps in most cases to clear acne with women. Just be cautious if you have cancer history in your family with these kind of pills. Just talk to your doctor and mention that. To find out if your acne is hormonal or not, you will need to get your blood tests done.

If the above methods haven't worked and your acne is coming back again there is always the possibility of Roaccutane (containing isotretionin as the main ingredient). Oh, the famous Roacuttane... 

It does clear up acne and it does have some pretty difficult side effects. If you are thinking of getting pregnant in the next 6 months, you must forget this medicine. Also during the treatment you have to do your blood tests to check the cholesterol levels, because Roaccutane is pretty damaging to your liver. It is said to have also psychological side effects such as depression, anxiety and similar. The most general side effects of this medicine, that in reality is just vitamin A in an excess amount (that's why you should be careful not to eat food containing vitamin A if you are having Roaccutane) are dryness of the skin, lips and mouth, you will have difficulties to see in the dark, your hair will become dry and so on. You will need to moisturize and often... 

This cure is in cycles of 6 months. If you get results from the first cycle yay to you, but if you don't you will have to continue as long as your dermatologist will say. Just don't give up and be patient. I have seen amazing results with Roaccutane. People with severe cystic acne and acne scarring have achieved a baby soft and clear skin. 

The problem with most acne regimes is that they need their time to show results. People tend to get impatient and change the regime before they see the effects. You need to be persistent and not to care a lot about it. Most of people have had acne or will have, at a point in their life, so just relax... It is not the end of the world and it does have some pretty effective acne treatments. 

If your acne is mild you can get use out of the over the counter creams. Just remember that creams containing salycilic acid do enter inside the pore and help to clean it out, so if you want to unblock your pores, clean your blackheads and ease the inflammation get these kind of creams.

If you want a good peeling cream that will help to boost your skin radiance and have anti wrinkle effect get creams containing glycolic acid.

Gosh, this post is getting really long. But I shouldn't forget to mention the OTC creams containing benzoyl peroxyde. Just start from 2,5% and then you can test 5-10%. 

Benzoyl Peroxide kills the bacterium that causes acne by inducing oxygen to the affected area, because the bacterium that causes acne (P. Acnes) is an anaerobe one, meaning it can live only where there is no oxygen. It works as a peeling agent, thus increasing the skin's turnover and clearing pores. It does dry out the skin, a lot... depending on its percentage, that's why you should use a good moisturizer along with it. Some people say they have had good effects combined with jojoba oil. Dermatologists on the other hand say you shouldn't use oils on your face if you have acne prone skin. So give or take... Clean with a mild soap to not irritate your skin and never forget the SPF cream!!!

That's my two cents for today, too. :) I hope I was of any help. Do not neglect a GOOD dermatologist if you have acne problems. It is worth it. 

Stay well!

Hairstyle trick

There is no need for words I think. :) In this way you can get rid of that nasty bump that forms under your bun. ;) It is a pretty easy trick, isn't it?  

Cancer nanotechnology, challenges and achievements

Cancer is one of the world’s most life threatening diseases, with millions of new cases every year. The war against this disease is going on strong. Some battles have been won and others lost, but the weapons that this disease uses are really powerful. They are heterogenity, adaption and resistance. The scientific community has been actively researching on the development of new and improved weapons to overcome and finally win the battle against cancer. Here we will talk about the current approaches against this life threatening disease. 

It is widely known that current cancer treatments include: 

1. Surgical intervention 

2. Radiation 

3. Chemotherapeutic drugs, which often also kill healthy cells and cause toxicity to the patient. 

Unfortunately the effectiveness of current cancer treatments depends on the early diagnosis and the type of cancer. It is therefore needed to develop chemotherapeutics that can either passively or actively target cancerous cells and eliminate them effectively. 

In summary 'passive targeting' investigates the characteristic features of tumur biology that allows nanocarriers to accumulate in the tumor site by the Enhanced Permeability and Retention (EPR) effect. 

The EPR effect is a unique phenomenon of solid tumors related to their anatomical and pathophysiological differences from healthy tissues. Angiogenesis, which is a physiological process involving the growth of new blood vessels from pre-existing vessels, leads to high vascular density in solid tumors. Large gaps exist between endothelial cells in tumor blood vessels, and tumor tissues show selective extravasation and retention of macromolecular drugs, which is the desired effect in order to see the therapeutic efficacy and the shrinkage or elimination of tumors.

Impaired reticuloendothelial/ lymphatic clearance of macromolecules from tumor, or lack of such clearance, is another unique characteristic of tumors, resulting in intratumor retention of macromolecular drugs thus delivered. 

It has been found that the effective pore size in the endothelial lining of blood vessels in most peripheral human tumors ranges from 200 to 600 nm in diameter, and the EPR effect allows for passive targeting to tumors based on the cut-off size of leaky vasculature. 

But on the other hand there are a lot of limitations to the passive targeting, and one way to overcome these limitations is to program the nanocarriers so that they actively bind to specific cells after extravasation. 

This binding may be achieved by attaching targeting agents such as ligands, which are molecules that bind to specific receptors on the cell surface, to the surface of the nanocarrier by a variety of conjugation chemistries. 

Nanocarriers will recognize and bind to target cells through ligand–receptor interactions, and bound carriers are internalized before the drug is released inside the cell. In general, when using a targeting agent to deliver nanocarriers to cancer cells, it is imperative that the agent binds with high selectivity to molecules that are uniquely expressed on the cell surface, so that it minimizes the undesired and strong side effects of the cancer therapy. This is otherwise known as active targeting. 

But what are nanocarriers? Why are they important in cancer diagnosis and therapy? Why not just use the traditional chemotherapeutic drugs? What are their advantages over the current approved cancer treatments? How many types of nanocarriers have been discovered and what is the future perspective? If you want to know more specifics on nanocarriers you can read my other post on this topic entitled 'Nanocarriers for cancer therapy'. 

To simply define, a nanocarrier is nanomaterial composite, used as a transport mean for another substance, such as a drug or an imaging agent, which can be monitored by a specific machine. Such carriers should be targeted to the pathological area to provide maximum therapeutic efficacy while also providing diagnostic imaging. 

The family of nanocarriers includes polymer conjugates, polymeric nanoparticles, lipid-based carriers such as liposomes and micelles, dendrimers, carbon nanotubes, and gold nanoparticles, including nanoshells and nanocages. 

Several therapeutic nanocarriers have been approved for clinical use. However, to date, there are only a few clinically approved nanocarriers that incorporate molecules to selectively bind and target cancer cells. Cancer has been the most often investigated among the many potential targets for these nanocarriers. 

Integration of diagnostic imaging capability with therapy may be key to overcoming the challenges of cancer heterogeneity and adaption. In addition, codelievery of imaging contrast agent and chemotherapeutic drugs can provide real-time validation of the targeting strategy, resulting in an another step forward for individual-based therapy. 

If molecular targets became unavailable, imaging can be used to map out alternative targets. The advantage of this approach is that it can provide early feedback of therapeutic efficacy before detection by means of traditional diagnosis, such as tumor shrinkage. 

That is why “theranostic” was originally used as a term to describe a treatment platform that combines a diagnostic test with targeted therapy and which monitors response to therapy. We will talk more in deep about 'theranostics' in another post, because it is a fascinating and a very promising topic. 

In theranostic treatments imaging can be used to track nanoparticles systemically, prevalidate appropriate targeting, and track the expression pattern of surface markers for adaptive targeting, as well as provide real-time information on tumor response. It is very important to see how the therapy is going, because the canccer therapy has pretty strong side effects, that may be lethal and if it is controlled that the chemotherapeutic drug is not arriving at its tumore target, the treatment regime can be urgently changed, before the damage happens and shows the symptoms in the organism. The surface properties of the polymeric nanoparticulate drug delivery systems play a key role on the biological behavior that is shown in the organism by the drug delivery system.

Surface modification can be defined as the improvement and replacement of the surface properties of nano-sized drug delivery systems. In the field of pharmaceutical technology, surface modification provides several advantages to improve the physicochemical properties and pharmaceutical activities of many nanosized carriers particularly polymeric nanoparticles. 

By the modification circulation times are prolonged, especially the accumulation in the tumor tissues is improved to higher levels.

On the other hand lipid-based carriers pose several challenges, which represent general issues in the use of other targeted nanocarriers such as polymeric nanoparticles. For example, upon intravenous injection, particles are rapidly cleared from the bloodstream by the reticuloendothelial defence mechanism, regardless of particle composition. 

Moreover, instability of the carrier and burst drug release, as well as non-specific uptake by the mononuclear phagocytic system (MPS), provides additional challenges for translating these carriers to the clinic. 

Several anticancer drugs enter the cells in our body through diffusion method. But there are some integral proteins in the cell membrane that are known as MDR transporters, which transport a variety of anticancer drugs out of the cancer cell and produce resistance against chemotherapy. As a solution to this challenge the delivery of drugs through targeted nanocarriers that are internalized by cells, can provide an alternative route to diffusion of drugs into cells. 

It is very important not to forget that cancer drug resistance is very complex and has been linked to elevated levels of enzymes that can neutralize chemotherapeutic drugs. However, it is more frequently due to the overexpression of MDR transporters that actively pump chemotherapeutic drugs out of the cell and reduce the intracellular drug doses below lethal threshold levels. 

Since fortunately not all cancer cells express the MDR transporters, chemotherapy will kill only drug-sensitive cells that do not or only mildly express MDR transporters, while leaving behind a small population of drug resistant cells that highly express MDR transporters. But with new forming tumors, chemotherapy may fail because residual drug-resistant cells can dominate over the normal cells, resulting in a more aggressive tumor mass.

Among the MDR transporters, the most widely investigated proteins are: P-glycoprotein, the multidrug resistance associated proteins and the breast cancer resistance protein. These proteins have different structures, but they share a similar function of expelling chemotherapy drugs from the cells. 

Combination treatments with targeted nanocarriers for selective delivery of drugs and MDR pump inhibitors will likely address some of the problems posed by resistant tumors in the future.

Do not forget that it is always better to prevent than to cure, so do not neglect the regular check ups at the doctor and if you have familiar history with the cancer disease double them up to twice a year.

Stay well!

References:

1. Couvreur, P. & Vauthier, C. Nanotechnology: Intelligent design to treat complex disease. Pharm. Res.23, 1417–1450 (2006).

2. Alonso, M.J. Nanomedicines for overcoming biological barriers. Biomed. Pharmacother. 58,168–172 (2004).

3. Matsumura, Y. & Maeda, H. A new concept for macromolecular therapeutics in cancer chemotherapy — Mechanism of tumoritropic accumulation of proteins and the antitumor agent smancs. Cancer Res. 46, 6387–6392 (1986).

4. Yuan, F. et al. Vascular-permeability in a human tumor xenograft — Molecular-size dependence and cutoff size. Cancer Res. 55, 3752–3756 (1995).

5. Torchilin, V. P. Recent advances with liposomes as pharmaceutical carriers. Nat. Rev. Drug Discov. 4, 145–160 (2005).

6. Hobbs, S.K. et al. Regulation of transport pathways in tumor vessels: role of tumor type and microenvironment. Proc. Natl Acad. Sci. USA95, 4607–4612 (1998).

7. Gottesman, M. M., Fojo, T. & Bates, S. E. Multidrug resistance in cancer: Role of ATP-dependent transporters. Nat. Rev. Cancer 2, 48–58 (2002).

8. Peer, D. & Margalit, R. Fluoxetine and reversal of multidrug resistance. Cancer Lett. 237, 180–187 (2006).

9. Jain, R.K. Barriers to drug-delivery in solid tumors. Sci. Am. 271, 58–65 (1994).

10. Allen, T.M. Ligand-targeted therapeutics in anticancer therapy. Nat. Rev. Cancer 2, 750–763 (2002).

11. Hong, S. et al. The binding avidity of a nanoparticle-based multivalent targeted drug delivery platform. Chem. Biol. 14, 107–115 (2007).