ABSTRACTBackground : Acne vulgaris is a
common skin disease, affecting more than 85% of
adolescents and often continuing into adulthood.
People between 11 and 30 years of age and up to
5% of older adults. For most patients acne remains
a nuisance with occasional flares of unsightly
comedones, pustules and nodules. For other less
fortunate persons, the sever inflammatory response
to Propionibacterium acnes (P.acnes) results in
permanent
Methods: Disfiguring scars. (1, 2) Stigmata of sever
acne cane lead to social ostracism, withdrawal
from society and severe psychologic
depression (1-4).
Result Pathogenesis of acne Traditionally, acne
has been thought of as a multifactorial disease of
the folliculosebaceous unit, involving excess
sebum production, abnormal follicular
hyperkeratinization, overgrowth of
Propionibacterium acnes, and inflammation (Fig
2). Recent laboratory and clinical investigations
into the roles of the innate immune system and
extracellular matrix remodeling proteins have shed
additional light on this pathogenetic process (5-7).
Role of androgens: Activity of type 1 5areductase
enzyme was shown to predominate in
human sebaceous glands and epidermis. This
enzyme is responsible for the conversion of
testosterone to the more potent androgen,
dihydrotestosterone (DHT). DHT in turn is thought
to mediate androgen dependent skin diseases such
as acne, hirsutism and androgenetic alopecia (13)
The enzyme 5a-reductase type 1 has been studied
in those with and without acne and it has been
hypothesized that those with acne might have more
active 5a-reductase type 1 .(2)
Conclusion : The prominent role of hormones in
the pathophysiology of acne has long been
recognized and corroborated by clinical and
experimental observations and therapeutic
experience (14). Although acne is not considered a
primary endocrine disorder, androgens, such as
dihydrotestosterone, dehydroepiandrosterone
sulfate, and testosterone, and growth hormone and
insulin-like growth factors, have all been
implicated in the pathogenesis of acne (15).
Corresponding address to :
Dr. Yasir Mansour Mohamed Al-Ani
Islam Mohammad Nabil El Helou
Apparent molar volume, V?, and viscosity B-coefficient of nicotinc acid in water and in aqueous NaCl solutions have been determined from density and viscosity measurements at (293.15, 298.15, 303.15 and 308.15) K. The experimental density data were evaluated by Masson equation, and the derived, apparent molar volume at infinite dilution, Vo?, and the slope Sv, were interpreted in term of solute-solvent and solute- solute interactions. Transfer apparent molar volumes at infinite dilution of nicotinic acid from water to NaCl solutions at various temperatures have been calculated.The viscosity data have been analyzed using Jones-Dole equation, and the derived parameters, Jones-Dolecoefficient, B,and Falkenhagen coefficient,A, have been also in
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Development of a precise and delicate reaction has been acquired for the determination of vancomycin hydrochloride using batch and cloud point extraction (CPE) methods. The first method is based on the formation of azo dye as a result of diazotized dapsone coupled with vancomycin HCl (VAN) in a basic medium. The sensitivity of this reaction was enhanced by utilizing a nonionic surfactant (Triton X-114) and the cloud point extraction technique (second method). The azo dye formed was extracted into the surfactant-rich phase, dissolved in ethanol and detected at λmax 440 nm spectrophotometrically. The reaction was investigated using both batch and CPE methods (with and without extraction), and a simple comparison between the two
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