Evaluation of Surface Structure and Morphological Phenomena of Caucasian Virgin Hair with Atomic Force Microscopy.

Background and Objectives: Atomic force microscopy (AFM) as a type of scanning microscopy (SPM), which has a resolution of fractions of a nanometer on the atomic scale, is widely used in materials science. To date, research using AFM in medicine has focused on neurodegenerative diseases, osteoporosis, cancer tumors, cell receptors, proteins and the DNA mismatch repair (MMR) system. Only a few small studies of hair imaging have been conducted, mostly in biotechnology or cosmetology. Thanks to the possibilities offered by AFM imaging, dermatologists can non-invasively assess the condition of hair and its possible disorders. Our goal was to capture images and microscopically analyze morphological changes in the surface of healthy hair. Materials and Methods: In this study, three to five hairs were collected from each person. Each hair was examined at nine locations (0.5; 1.0; 1.5; 2.0; 3.5; 4.5; 5.5; 6.5 and 7.0 cm from the root). At least 4 images (4-10 images) were taken at each of the 9 locations. A total of 496 photos were taken and analyzed. Metric measurements of hair scales, such as apparent length, width and scale step height, were taken. Results: This publication presents the changes occurring in hair during the natural delamination process. In addition, morphoological changes visualized on the surface of healthy hair (pitting, oval indentations, rod-shaped macro-fibrillar elements, globules, scratches, wavy edge) are presented. A quantitative analysis of the structures found was carried out. Conclusions: The findings of this study can be used in further research and work related to the subject of human hair. They can serve as a reference for research on scalp and hair diseases, as well as hair care.

An estrogen receptor-alpha knock-in mutation provides evidence of ligand-independent signaling and allows modulation of ligand-induced pathways in vivo.

Estrogen-nonresponsive estrogen receptor-alpha (ERalpha) knock-in (ENERKI) mice were generated to distinguish between ligand-induced and ligand-independent ER-alpha actions in vivo. These mice have a mutation [glycine 525 to leucine (G525L)] in the ligand-binding domain of ERalpha, which significantly reduces ERalpha interaction with and response to endogenous estrogens, whereas not affecting growth factor activation of ligand-independent pathways. ENERKI mice had hypoplastic uterine tissues and rudimentary mammary gland ductal trees. Females were infertile due to anovulation, and their ovaries contained hemorrhagic cystic follicles because of chronically elevated levels of LH. The ENERKI phenotype confirmed that ligand-induced activation of ERalpha is crucial in the female reproductive tract and mammary gland development. Growth factor treatments induced uterine epithelial proliferation in ovariectomized ENERKI females, directly demonstrating that ERalpha ligand-independent pathways were active. In addition, the synthetic ERalpha selective agonist propyl pyrazole triol (PPT) and ER agonist diethylstilbestrol (DES) were still able to activate ligand-induced G525L ERalpha pathways in vitro. PPT treatments initiated at puberty stimulated ENERKI uterine development, whereas neonatal treatments were needed to restore mammary gland ductal elongation, indicating that neonatal ligand-induced ERalpha activation may prime mammary ducts to become more responsive to estrogens in adult tissues. This is a useful model for in vivo evaluation of ligand-induced ERalpha pathways and temporal patterns of response. DES did not stimulate an ENERKI uterotrophic response. Because ERbeta may modulate ERalpha activation and have an antiproliferative function in the uterus, we hypothesize that ENERKI animals were particularly sensitive to DES-induced inhibition of ERalpha due to up-regulated uterine ERbeta levels.

Estrogen-dependent and -independent estrogen receptor-alpha signaling separately regulate male fertility.

Estrogen receptor-alpha (ERalpha) plays a critical role in male reproductive tract development and fertility. To determine whether estrogen-dependent and -independent ERalpha mechanisms are involved in male fertility, we examined male estrogen nonresponsive ERalpha knock-in mice. These animals have a point mutation (G525L) in the ligand-binding domain of ERalpha that significantly reduces interaction with, and response to, endogenous estrogens but does not affect growth factor activation of ligand-independent ERalpha pathways. Surprisingly, we found that ligand-independent ERalpha signaling is essential for concentrating epididymal sperm via regulation of efferent ductule fluid reabsorption. In contrast, estrogen-dependent ERalpha signaling is required for germ cell viability, most likely through support of Sertoli cell function. By treating estrogen nonresponsive ERalpha knock-in (ENERKI) mice with the ERalpha selective synthetic agonist propyl pyrazole triol, which is able to bind and activate G525L ERalpha in vivo, we discovered male fertility required neonatal estrogen-mediated ERalpha signaling. Thus, our work indicates both estrogen-dependent and -independent pathways play separable roles in male murine reproductive tract development and that the role of ERalpha in human infertility should be examined more closely.