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Detection of autofluorescence at the skin surface is highly influenced by melanin and hemoglobin. Epidermal absorption and scattering may also be an influencing factor and is represented in this article as a quantitative parameter, epidermal thickness. To examine this parameter we measured the 370 nm fluorescence in vivo after excitation with 330 nm and the 455 nm fluorescence after excitation with 330 and 370 nm. Measurements were performed on sun-exposed skin at the dorsal aspect of the forearm and shoulder and on nonexposed buttock skin. Skin pigmentation and redness of the same body sites were measured by reflectance spectroscopy. The thickness of the stratum corneum and the cellular part of epidermis was quantified by light microscopy of skin biopsies. Multiple regression analysis was used to find correlations between autofluorescence and the potential influencing factors. We found a highly significant correlation of skin autofluorescence with pigmentation and redness for both emission wavelengths (Em). A small but significant correlation to epidermal thickness was found only for excitation wavelength (Ex) 370 nm and Em455 nm if body site was included in the analysis. No correlation between Ex330:Em370 and Ex330:Em455 and thickness of epidermis was found. For practical use, correction of skin autofluorescence for pigmentation is essential, correction for redness is of less importance and correction for epidermal thickness is unnecessary.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12870847&dopt=Abstract [PubMed - in process]

CNS Drugs. 2003;17(10):729-62.
Neuroprotective strategies in Parkinson's disease : an update on progress.

Mandel S, Grunblatt E, Riederer P, Gerlach M, Levites Y, Youdim MB.

Department of Pharmacology, Technion - Faculty of Medicine, Eve Topf and US National Parkinson's Foundation Centers for Neurodegenerative Diseases, Bruce Rappaport Family Research Institute, Haifa, Israel.

In spite of the extensive studies performed on postmortem substantia nigra from Parkinson's disease patients, the aetiology of the disease has not yet been established. Nevertheless, these studies have demonstrated that, at the time of death, a cascade of events had been initiated that may contribute to the demise of the melanin-containing nigro-striatal dopamine neurons. These events include increased levels of iron and monoamine oxidase (MAO)-B activity, oxidative stress, inflammatory processes, glutamatergic excitotoxicity, nitric oxide synthesis, abnormal protein folding and aggregation, reduced expression of trophic factors, depletion of endogenous antioxidants such as reduced glutathione, and altered calcium homeostasis. To a large extent, the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and 6-hydroxydopamine (6-OHDA) animal models of Parkinson's disease confirm these findings. Furthermore, neuroprotection can be afforded in these models with iron chelators, radical scavenger antioxidants, MAO-B inhibitors, glutamate antagonists, nitric oxide synthase inhibitors, calcium channel antagonists and trophic factors.Despite the success obtained with animal models, clinical neuroprotection is much more difficult to accomplish. Although the negative studies obtained with the MAO-B inhibitor selegiline (deprenyl) and the antioxidant tocopherol (vitamin E) may have resulted from an inappropriate choice of drug (selegiline) or an inadequate dose (tocopherol), the niggling problem that still remains is why these drugs, and others, do work in animals while they fail in the clinic. One reason for this may be related to the fact that in normal human brains the number of dopaminergic neurons falls by around 3-5% every decade, while in Parkinson's disease this decline is greater. Brain autopsy studies have shown that by the time the disease is identified, some 70-75% of the dopamine-containing neurons have been lost. More sensitive reliable methods and clinical correlative markers are required to discern between confoundable symptomatic effects versus a possible neuroprotective action of drugs, namely, the ability to delay or forestall disease progression by protecting or rescuing the remaining dopamine neurons or even restoring those that have been lost.A number of other possibilities for the clinical failure of potential neuroprotectants also exist. First, the animal models of Parkinson's disease may not be totally reflective of the disease and, therefore, the chemical pathologies established in the animal models may not cause, or contribute to, the progression of the disease clinically. Second, because of the series of events occurring in neurodegeneration and our ignorance about which of these factors constitutes the primary event in the pathogenic process, a single drug may not be adequate to induce neuroprotection and, as a consequence, use of a cocktail of drugs may be more appropriate. The latter concept receives support from recent complementary DNA (cDNA) microarray gene expression studies, which show the existence of a gene cascade of events occurring in the nigrostriatal pathway of MPTP, 6-OHDA and methamphetamine animal models of Parkinson's disease.Even with the advent of powerful new tools such as genomics, proteomics, brain imaging, gene replacement therapy and knockout animal models, the desired end result of neuroprotection is still beyond our current capability.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12873156&dopt=Abstract [PubMed - in process]

Arch Facial Plast Surg. 2003 Jul-Aug;5(4):310-5.
Nonablative laser resurfacing using the long-pulse (1064-nm) Nd:YAG laser.

Dayan SH, Vartanian AJ, Menaker G, Mobley SR, Dayan AN.

Department of Otolaryngology-Head and Neck Surgery, University of Illinois at Chicago 60657, USA. docdayaol.com

BACKGROUND: Lasers with infrared wavelength ranges have been used in nonablative rejuvenation of skin. In this process, cooling of the epidermis allows for laser energy heat-induced injury to the dermis without ablation of the epidermal layer. This dermal injury is theorized to produce improvements in skin quality. In addition, long-pulse Nd:YAG lasers target melanin less efficiently, allowing safer treatment of patients with all skin types. In this study, we evaluate the use of the 1064-nm Nd:YAG laser for the purpose of rejuvenating the aging face. MATERIALS AND METHODS: Fifty-one patients were enrolled in the study. Patients with Fitzpatrick skin types I through V were included. Standard photographs were taken before the first and after the last treatment. The Nd:YAG laser treatments were initiated with a chilled tip-cooling device. At each treatment session, patients were given self-assessment questionnaires. At completion of the study, 3 physicians performed masked evaluations of patient pretreatment and posttreatment photographs. RESULTS: Thirty-four of 51 patients completed at least 7 treatments, had posttreatment photographs, and were entered into the study. Follow-up ranged from 1 to 6 months. No adverse events were noted. Masked analysis and patient subjective scores demonstrated a subtle improvement in several skin variables. Patient-assigned Fitzpatrick Scale scores declined after 6 treatments for coarse wrinkles (-22.3%; P<.01), skin laxity (-36.3%; P<.01), and overall improvement (-40.6%; P<.01). Physician-graded scores demonstrated decreases in coarse wrinkles (-11.9%; P<.01), skin laxity (-17.3%; P<.01), and overall improvement (-20.0%; P<.01). CONCLUSIONS: Nonablative resurfacing techniques are well suited for patients requesting rejuvenating treatments of the aging face with minimal downtime. Although improvements in photodamaged skin are subtle and gradual, the 1064-nm Nd:YAG laser was well tolerated by patients of all skin types.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12873868&dopt=Abstract [PubMed - in process]

Hair loss is a problem in modern soceity. Examining the factors of hair growth may shed light on how hair loss might occur. How long can hair grow before it stops growing eventually if it does? Given that the hair growth rate is quite uniform and constant, somewhere between 0.3-0.5 millimeters per day, it's believed that the length of anagen, the growth phase, differs among individuals, and this is the major determinant to the maximum hair length. For some individuals, anagen may last ten years. Of course the length of the anagen is governed by genes, and the genetic background of the individuals. Non-genetic factors such as nutritional condition, weather, seasonal changes (hair may grow a bit faster during winter), taking medications, health condition may of course influence the rate of hair growth as well as hair loss. The shape of the hair, straight or curly, is dependent on the shape of the follicle. A circular or round hair follicle would generate straight hair, while the follicle with oval or elliptical shapes (in its cross-section) would produce a curly hair.

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