The discovery of antibiotics has helped to save the lives of an uncountable number of people. Antibiotics have been grouped in different classes based on their origin, structure, and mechanism of action. An intrinsic and acquired mechanism of antimicrobial resistance has been identified in many bacterial strains that are of high clinical importance. This has seriously jeopardized the use of antibiotics and has also caused the spread of microbes that are resistant to effective first-choice, or “first-line” drugs. Thus, sensible use of antibiotics and the search for effective alternative measures are of high importance in order to minimize the effect due to existing and emerging antimicrobial resistant microbes.

Epithelial ovarian tumors appear to arise from the ovarian surface epithelium (OSE), a simple squamous-to-cuboidal mesothelium covering the ovary. Ovarian tumorigenesis is the most frequent cause of cancer death in gynecological malignancies; however the exact mechanism of this disease is not well known. A theory of repeated ovulation which contributes to neoplastic transformation of OSE has been proposed, and the process of healing ruptured OSE may contribute to the disease. Therefore, it can be assumed that endocrine and autocrine factors may have an influence on ovarian carcinogenesis in women. Thus, in this review, we suggest that these endocrine and autocrine factors may play a role in ovarian tumorigenesis in regulation of growth-stimulation or -inhibition and/or apoptosis of normal and neoplastic OSE cells via their specific receptors.

Microbial lipopolysaccharide (LPS) is an endotoxin conveying the surface receptor complex of toll-like receptor 4 (TLR4)-myeloid differentiation 2 (MD-2) in innate immune cells through ancillary proteins such as LPS-binding protein and CD14. However, TLR4 alone is not sufficient for recognition of LPS. MD-2 is essential for sensing the lipid A domain of LPS and for triggering LPS-induced TLR4 activity across the plasma membrane. Therefore, lipid A domain and its binding to MD-2 are potential drug targets for intervention in endotoxemia as well as other disorders associated with LPS etiology. Here, we reviewed MD-2 as a drug target focused on drug candidates-targeting TLRs, transport of microbial LPS into TLR4/MD-2, crystal structure of TLR4/MD-2 alone, crystal structure of TLR4/MD-2 with bound LPS, lipid A derivatives as MD-2 antagonist, non-lipid antagonists of LPS binding to MD-2, and human disorders-implicated with TLR4/ MD-2. This review could be helpful to understanding the biology of TLR4/MD-2, and suggests the importance of MD-2 as a therapeutic target against inflammatory diseases due to infection.

This study was conducted in order to investigate the effect of black sesame oil on hair growth in a shaving animal model of C57BL/6 mice. Five-week-old male mice were acclimated for one week under 22±1 µl room temperature, 50±5% relative humidity, and 12 hours of a light/dark cycle before beginning the experiment. The animals were divided into three groups, including the normal group (saline, N), positive control group (3% MXD, PC), and experimental group (black sesame oil, E) and received topical application of 100 µl once per day, six days per week, for a period of three weeks. Hair regrowth was evaluated by gross and histological examination. In addition, immunohistochemical observation for SCF, the activities of enzymes, including ALP and γ-GT, and the expression quantity of growth factors, including IGF-1 in the skin of mice was performed or evaluated. Topical treatment with black sesame oil and 3% minoxidil for three weeks to dorsal skin resulted in more rapid acceleration of hair regrowth in the E and PC groups than in the N group. Development and elongation of hair follicles were promoted in the E and PC groups, compared with the N group. Serum ALP activity was significantly higher in the E group, compared with the N group within three weeks (p<0.05). Skin ALP activity was significantly higher in the PC group, compared with the N group within two weeks (p<0.05), and higher in the E and PC groups than in the N group within three weeks with no significant differences. Serum γ-GT activity was significantly higher in the PC group, compared with the N group within two weeks (p<0.01), and significantly higher in the E group, compared with the N group within three weeks (p<0.05). Skin γ-GT activity was significantly higher in the PC group, compared with the N group within two weeks (p<0.05), and significantly higher in the PC (p<0.01) and E (p<0.001) groups, compared with the N group within three weeks. IGF-1 expression in the skin was significantly higher in the PC and E groups, compared with the N group (p<0.01). SCF antigens were heavily stained in bulge, stem cells, and dermal papilla and middle stained in inner root sheath, outer root sheath, and epidermis in the E and PC groups. These results indicate that black sesame oil effectively stimulated hair growth in an animal model via several mechanisms and that it can be used practically for hair growth or prevention of hair loss in human beings.

Chronic inflammatory diseases such as Crohn′s disease and ulcerative colitis are associated with increased risk of colon adenocarcinoma. Apoptic induction of colon cancer cells by cytokines and death receptors is an important anti-cancer therapy. We observed that co-administration of TNFα and IFNγ in human colon cancer cell line, HCT116, resulted in cell death and expression of IL-32. Cleavage forms of caspase-3, caspase-9, and PARP were increased in TNFα / IFNγ-treated HCT116. mRNA expression of death receptors, including TNFR1 and Fas were not changed and NO generation was not induced by combination of TNFα and IFNγ. However, mRNA expression of IL-32α, β, and γ was increased in TNFα / IFNγ-treated HCT116. To determine the effect of IL-32 in HCT116 cell apoptosis by TNFα / IFNγ stimulation, IL-32 siRNA-transfected HCT116 cells were cultured with TNFα / IFNγ and cell proliferation was measured. IL-32 siRNA induced slight recovery of cell viability of TNFα / IFNγ-stimulated HCT116. These results suggest that IL-32 is not directly related to apoptosis of HCT116 by TNFα / IFNγ stimulation. However, IL-32 expression by TNFα or TNFα / IFNγ in a colon cancer cell line is very interesting because of the unknown effect of IL-32 in colon cancer. Our study will contribute to development of studies for IL-32 function in human colon cancer and anti-cancer therapies using cytokines.

Cutaneous vasculitis is an inflammatory necrotizing disease of the blood vessel walls. In most cases, the etiology is due to immune-complex disease from type III hypersensitivity. Clinical signs include swelling, erythema, purpura, erythematous plaques, ulceration, and necrosis. Clinical lesions may be localized to distal extremities or areas of less extensive collateral circulation. In this case, history, physical examination, laboratory findings, cytology, histopathologic examination, and immunohistochemistry might aid in differentiation of a clinically similar disease. Consequently, this case was diagnosed as cutaneous vasculitis and treated with ointment containing corticosteroid and antibiotics over a period of two weeks. After treatment, all of the clinical lesions had disappeared.