Therapeutic Effects of Liposome-Enveloped Ligusticum chuanxiong Essential Oil on Hypertrophic Scars in the Rabbit Ear Model

Hypertrophic scarring, a common proliferative disorder of dermal fibroblasts, results from an overproduction of fibroblasts and excessive deposition of collagen. Although treatment with surgical excision or steroid hormones can modify the symptoms, numerous treatment-related complications have been described. In view of this, we investigated the therapeutic effects of essential oil (EO) from rhizomes of Ligusticum chuanxiong Hort. (Umbelliferae) on formed hypertrophic scars in a rabbit ear model. EO was prepared as a liposomal formulation (liposome-enveloped essential oil, LEO) and a rabbit ear model with hypertrophic scars was established. LEO (2.5, 5, and 10%) was applied once daily to the scars for 28 days. On postoperative day 56, the scar tissue was excised for masson's trichrome staining, detection of fibroblast apoptosis, assays of the levels of collagens I and III, and analysis of the mRNA expression of matrix metalloproteinase-1 (MMP-1), caspase-3 and -9, and transforming growth factor beta 1 (TGF-β1). In addition, the scar elevation index (SEI) was also determined. As a result, LEO treatment significantly alleviated formed hypertrophic scars on rabbit ears. The levels of TGF-β1, MMP-1, collagen I, and collagen III were evidently decreased, and caspase -3 and -9 levels and apoptosis cells were markedly increased in the scar tissue. SEI was also significantly reduced. Histological findings exhibited significant amelioration of the collagen tissue. These results suggest that LEO possesses the favorable therapeutic effects on formed hypertrophic scars in the rabbit ear model and may be an effective cure for human hypertrophic scars

Largest ancient fortress of South-West Asia and the western world?:Recent fieldwork at Sasanian Qaleh Iraj at Pishva, Iran

The article presents recent works at Qale Iraj, near Varamin, Iran. My short contribution is on the Middle Persian ostraka found at the site

The role of childhood maltreatment in cortisol in the hypothalamic-pituitary-adrenal (HPA) axis in methamphetamine-dependent individuals with and without depression comorbidity and suicide attempts

Background: The hypothalamic-pituitary-adrenal (HPA) axis dysregulation which was found to have an important role in the pathophysiology of depression, suicide, and substance dependence, may be influenced by childhood maltreatment (CM). The present study aimed to investigate the relationship between CM and cortisol changes in methamphetamine-dependent individuals. Methods: In a cross-sectional study, methamphetamine-dependent individuals (n. = = 195) with or without both comorbid major depressive disorder (MDD) and a history of suicide attempts were selected and completed the Childhood Trauma Questionnaire-Short Form (CTQ-SF), the Beck Scale for Suicide Ideation (BSSI), and the Beck Depression Inventory-II (BDI-II). To assess cortisol levels, saliva samples were collected at six time intervals for two consecutive days. Results: A history of CM significantly predicted wake-up cortisol level, cortisol awakening response (CAR), and diurnal cortisol slope. Methamphetamine-dependent individuals with both MDD and lifetime suicide attempts had higher CM and higher cortisol levels with a blunted diurnal cortisol slope than individuals who were merely methamphetamine-dependent. Individuals with high CM showed higher cortisol levels with a blunted diurnal slope than those with low or without CM. Limitations: Cross-sectional data and use of self-report scales, especially retrospective measurements (e.g., the CTQ-SF), were important limitations of this study. Conclusion: Findings suggest that methamphetamine-dependent individuals with adverse psychological factors such as CM, MDD, and suicide attempts may show dysregulation in biological factors including cortisol level. In addition, CM and its effects on cortisol in the HPA axis may emerge as important factors regarding psychopathological use of methamphetamine

P2-purinergic receptor agonists inhibit the growth of androgen-independent prostate carcinoma cells.

To develop a new approach to the treatment of advanced, hormone-refractory prostate cancer, the signal transductions regulating the growth of human androgen-independent prostate carcinoma cell lines were studied. Agonist-stimulated Ca2+ mobilization, a critical regulatory event in other secretory cell types, was studied as a means of identifying previously undescribed plasma membrane receptors that may transduce a growth inhibitory signal. In all of the cell lines tested, P2-purinergic receptor agonists, including ATP and certain hydrolysis-resistant adenine nucleotides, induced a rapid, transient increase in cytoplasmic free Ca2+ that was detectable at 50 to 100 nM ATP, was maximal at 100 microM ATP, and was inhibited approximately 50% by chelation of extracellular Ca2+. Within 8 s after addition, ATP stimulated accumulation of the polyphosphatidylinositol products inositol (1, 4, 5) trisphosphate, inositol (1, 3, 4) trisphosphate, and inositol tetrakisphosphate. In addition to stimulating phosphatidylinositol turnover and Ca2+ mobilization, ATP and hydrolysis-resistant ATP analogues induced greater than 90% inhibition of the growth of all lines tested. These data demonstrate that human androgen-independent prostate carcinoma cells express functional P2-purinergic receptors linked to phospholipase C, and that agonists of this receptor are markedly growth inhibitory, suggesting a novel therapeutic approach to this common adult neoplasm