Photodynamic Therapy

Dermatologists, physicists, and scientists conducted a workshop of UVA treatment, and the workshop’s findings are presented in the New England Journal of Medicine. A previous president of the American Academy of Dermatology wrote an article titled “UVA1 is Often A1” to discuss their findings. The workshop found that medium or high-dose UVA1 works well with morphea, urticarial pigmentosa, atopic dermatitis, dyshydrotic dermatitis, subacute pruigo, and systemic lupus erythematosus. These diseases are treated by UVA rays because the wavelength is longer, which means there is less energy delivered to the skin and the greater penetration of photons (Dahl, 2012). Dermatologists even use sunbeds with higher intensity than regular tanning beds in their offices. For example, Windsor Dermatology uses four different types of light therapy to treat the skin condition psoriasis. One type of light therapy is that of UVA. The anti-inflammatory properties of ultraviolet light aid in slowing the growth of psoriasis effected skin

Exposure to abnormally high frequencies of light can potentially alter the DNA of a cell and turn it cancerous, the resulting cancerous cells are known as skin cancer. The most common cause is ultraviolet light emitted by the sun although it has been known to be caused by tanning booths, unusually high levels of x-rays, exposure to some chemicals and in rare cases the abnormal genes that cause skin cancer can be inherited by children from their parents.

First, a light-sensitive drug is given. For skin cancers, it may be a cream. For internal cancers, it may be an injection into a vein, or rarely a drink. You then wait a few hours to a few days before the next step. This allows time for the drug to concentrate in the cancer cells. Next, a special light (usually a laser) is shone onto the cancer. The light activates the drug to treat the tumour. If the cancer is internal, an ultrasound or scan may be used to guide the light source to the tumour. The side effects can vary depending on where treatment is given, what drugs are used, and how you react. You may become sensitive to light for a time, and will need to take care in the sun, or other bright

The antagonistic effect of glutamine on Azide – 1 mediated light production was tested by increasing the glutamine concentration from 0.1 to 5mM. The results show a dose – dependent inhibition of BLI signal by L – glutamine in HT1080 – luc2 and HepG2 – luc2 cells. This reduction confirms the signal obtained by Azide – 1 was due to the competitive interference with glutamine uptake. However, a fall in the light intensity could not be observed in 4T1 – RLR cells. This outcome does not mean that Azide – 1 did not compete with L – glutamine for the transporter mediated uptake. The reason of no effect observed is because 4T1 – RLR which is a more glucose dependent cell line doesn’t have a good affinity for L – glutamine (Fig. 7A), but binds well

The technique consists in a chemical process carried out by light (photochemistry therapy): the light is absorbed by a photosensitive substance, with the formation of ROS (reactive oxygen species which destroy the cell within which it is formed). Consequently, the pre-neoplastic cell dies. The photosensitive substance - or photosensitizer - is applied on the skin, penetrates and identifies diseased cells. These substances are medicines that, in presence of the light gets activated, triggering the photochemical reaction that leads to the death of the diseased cells (in this case affected by actinic keratosis).

There are various challenges that should be considered in the future prospects such as developing new targeted photosensitizer (PS) in order to provide more

To evaluate the effectiveness of ant cancer treatment, first it is important to understand the difference between normal cells and cancer cells, as well as the effect of cancer cells have on a healthy individual. Normal cells grow and divide as the body needs them. As a cell grows, genetically it is programmed to perform a certain task. As a cell matures abd eventally dies, the body produces new cells. This is an ongoing process, which if not interrupted, will keep the body healthy and functioning well. Normal cells are stimulated by growth signals. Because of this, the cells know when to divide and when to stop. Cancer occurs when there is an imbalance or change in the normal cell production. As a result, there is an overgrowth of abnormal

One of the topics we have studied in Physics 108 is light. Ultraviolet (UV) light is something that most people try to avoid. There are countless sources and almost common knowledge that UV light may be a cause of skin cancer. I am a Physical therapist Assistant and in the field of physical therapy UV light has some therapeutic effects if used within proper parameters.

Chemotherapy and radiation treatments are commonly used as treatment options against cancer; however, one of the negative consequences is the possibility of incomplete tumor removal due to partial tumor penetration. Furthermore, these anticancer treatments lack targeting; chemotherapy and radiation will harm healthy tissue surrounding the cancer site, in addition to targeting malignant tissue. As a result of partial penetration and lack of malignant tissue targeting, the possibility exists that cancer will reoccur within the patient.

PDT does not describe a single technique but instead a series of related protocols involving a photosensitizer, that when excited by light irradiation triggers an oxidative reaction. The light sensitive drug does not become active until it is exposed to a certain type of light. Photosensitizers have been shown to favorably accumulate within tumour cells, allowing for targeted, PDT-induced cytotoxicity of malignant cancer cells. Therefore, PDT may be a viable treatment option in treatment of brain tumours (Quirk et al., 2015, Stylli and Kaye, 2006).

It is a type of laser therapy that is non-thermal. It is used to activate the medication that has been given intravenously. This procedure is used to close off the abnormal blood vessels and reduce leaking of the blood behind the retina.

Mature melanocytes have long projections that are in contact with 30-40 neighbouring keratinocytes thus making up the epidermal-melanin unit (Tsatmali, Ancans, & Thody, 2002). In order for melanin to play its role in photoprotection, the mature melanosomes are transported into the cytoplasm of the keratinocytes via the melanocyte’s long projections. Inside the keratinocytes, melanosomes form a cap around the nucleus. The melanin inside the melanosomes absorbs the UVR emitted from the sun thus reducing the amount of UVR reaching the nucleus (Tsatmali et al., 2002; Videira et al., 2013). This process of photoprotection is illustrated in Figure 1. This photoprotection is necessary as UVR can damage DNA causing mutations leading to cancer (Videira et al., 2013). In addition, melanosomes are not only found in the skin but can also be found in several other tissues such as the central nervous system, cardiovascular system, the uvea of the eye, cochlea and adipose tissues (D’Mello, Finlay, Baguley, & Askarian-Amiri,

Photodynamic Therapy is a treatment that uses drugs called Photosensitizing Agents and light to kill cancerous cells and treat certain skin disorders.

Photolabile nucleobase protection has been used to achieve exquisite control over biological processes through light regulation, also referred as photocaging. The concept was introduced by Engels (Engels and Schlaeger, 1977; Engels and Reidys, 1978) and independently by Hofmann (Kaplan et al., 1978). Watson–Crick base pairing is blocked by caging groups, completely preventing oligonucleotide duplex formation. Duplex formation is restored when irradiated by light at a specfic wavelength. Photolabile groups when introduced at specific locations render the molecule inactive; however, upon irradiation with light at a particular wavelength, the molecules can be activated (See detailed review by Shao and Xing, 2010; Tang et al. 2013; Liu and Deiters, 2014). Caging groups can also be introduced at phosphate, 2′-OH, and nucleobases (Tang et al., 2013); however, nucleobase caging has been of particular interest.

Vertebrate melanopsin phototransduction shares similarities with invertebrate-type opsin, which responds to light via activating a Gq protein (Gq)/ phospholipase C (PLC) signaling cascade5. Previous studies demonstrated a solar ultraviolet radiation (UVR)-sensitive phototransduction pathway in human epidermal melanocytes6,7,8,9. Specifically, UVR triggered a Gαq/11/PLCβ signaling pathway, which led to phosphatidylinositol (4,5)-bisphosphate (PIP2) hydrolysis to create diacylglycerol (DAG) and inositol 1, 4, 5-trisphosphate (IP3), and thus activated the transient receptor potential ankyrin 1 (TRPA1). The influx of Ca2+ and Na2+ depolarized the cell9. The recent discovered light-sensitive DRG neurons also innervate the skin and exhibit non-image-forming light responses. It’s likely that opsin X has a downstream signal cascade similar to the pathway characterized in opsin of human epidermal melanocytes and in non-image-forming melanopsin in retinal ganglion cells. Therefore, the current study is to characterize the G-protein pathway that is responsible for light transduction as well as to determine whether the light-sensitive DRG shares a similar pathway as human epidermal melanocytes. This project will test the central hypothesis that light stimulation activates the Gα /PLC signaling pathway, and then opens the TRP channel as well as depolarizes the cell.