Periodic changes in spectral scattering and spectral transmission of daylight in tidal water

Seasonal changes in the transmission of certain spectral bands of solar radiation in the inshore waters of the Pacific Northwest were reported by Williams and Utterback (1) for the year 1934 and by tterback and l\1iller (2) for the years 1935 and 1936…

The innate immune response and toll-like receptors in the human endometrium

Includes bibliographical references.The entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.Vita."December 2005"Dissertations, Academic -- University of Missouri--Columbia -- microbiology (Medicine)Thesis (Ph. D.) University of Missouri-Columbia 2005.There are two major divisions of the human immune system: the adaptive and the innate immune systems. The adaptive immune responses are directed against specific pathogens and are essential for control and elimination of pathogens following infection. However, the response requires several days to occur. The innate immune system serves to prevent establishment of infection and protect an individual prior to development of adaptive immune responses. This response is immediate, directed against broad classes of pathogens rather than a specific organism, and is usually sufficient to prevent establishment of infection. Additionally, the nature of the innate immune response will direct and shape adaptive immune responses against invading pathogens. Contact with pathogenic organisms frequently occurs in mucosal tissues lining the body cavities such as the respiratory tract, the gastrointestinal tract, or the reproductive tract. These surfaces are composed of epithelial cells that act as a barrier to pathogen entry into the body and act as sentinel cells, alerting the immune system to the presence of an invading pathogen by initiating innate immune responses to pathogen. The human reproductive tract is exposed to a variety of sexually transmitted pathogens including Human Immunodeficiency Virus (HIV), Herpes Simplex Virus (HSV), and Human Papilloma Virus (HPV). These viruses are the cause of vast global human health and reproductive problems. Currently, there is a need to develop vaccines and treatment strategies to prevent transmission of these viruses. This study examines a cellular protein known as Toll-like receptor 3 (TLR3) that is involved in detecting viral pathogens and initiating innate antiviral immune responses to these viral pathogens. We have found that TLR3 is expressed by endometrial epithelial cells in the human uterus, and that expression levels are altered with progression through the menstrual cycle. TLR3 expression peaked during the secretory phase of the menstrual cycle, when the uterus is prepared for embryo implantation, and was dramatically decreased during menstruation until ovulation, when TLR3 expression levels again begin to increase. Stimulation of TLR3 with its cognitive ligand initiates antiviral responses by endometrial epithelial cells and epithelial cell secretion of natural antimicrobial peptides. These data indicate that antiviral responses in the human uterus can be mediated by TLR3 and may be regulated across the menstrual cycle, indicating that susceptibility to viral infection may be altered at different stages of the menstrual cycle. These results suggest that TLR3 ligands may be utilized in development of treatment and vaccine strategies against viral pathogens of the reproductive tract

The Development of a Speed Monitoring Program for Indiana

From the passage of the National Maximum Speed Limit (NMSL) of 55 mph in 1974 through its repeal in 1995 speed monitoring programs have been mandated by the federal government. The speed-monitoring program was primarily intended to provide reliable data to be included as a part of the State’s annual certification in order to be approved for Federal Aid highway projects. The repeal of the NMSL in 1995 not only authorized states to set their own speed limits, it also allowed states to develop their own speed monitoring programs. The goal of this research is to provide the framework for a speed-monitoring program to meet the needs of agencies and organizations that use speed-monitoring data in the State of Indiana. A proposed speed monitoring plan is developed which distributes speed monitoring stations to highway classes according to three primary criteria: spatial distribution, crash distribution, and distribution of daily vehicle miles traveled. The proposed speed-monitoring program will utilize 38 existing speed, weigh-in-motion, and automated traffic recording stations. The stations will be monitored four times a year for a 24-hour period. Furthermore, the proposed program will monitor speeds based on vehicle length. It is the recommendation of this research that Indiana phase in the proposed speed-monitoring plan developed in the present research, during the 1999 calendar year. The implementation should include a visual inspection of all the WIM, ATR, and speed monitoring stations listed in Appendix A to ensure they are still capable of monitoring speeds by vehicle class and travel direction. If any problems should arise with the existing stations, that station should be substituted for another station within that district and highway class

17beta-estradiol suppresses TLR3-induced cytokine and chemokine production in endometrial epithelial cells

BACKGROUND: The human endometrium is an important site for contact between the host and pathogens ascending the reproductive tract, and thus plays an important role in female reproductive tract immunity. Previous work in our laboratory has suggested that Toll-like receptors (TLRs) are involved in endometrial epithelial recognition of pathogens and that ligation of endometrial TLRs results in the production of cytokines and chemokines important for both immune and reproductive functions of the endometrium. We have also demonstrated cyclic regulation of TLR3 mRNA and protein expression in human endometrium, suggesting that steroid hormones might play a role in the expression and function of TLR3. In this study, the effects of 17beta-estradiol (E2) and progesterone (P) on TLR3 expression and function in endometrial cell lines were investigated. METHODS: Endometrial epithelial cell lines were cultured and examined for the presence of TLR3 and hormone receptors by endpoint RT-PCR. For hormonal studies, cells were pre-treated with ethanol vehicle, 10^(-8) M E2, and/or 10^(-7) M P. For antagonist assays, cells were treated with the ER antagonist, ICI 182, 780, or the PR antagonist, RU486, for two hours prior to treatment with hormones. Following hormone or hormone/antagonist pre-treatment, cells were stimulated with vehicle, the synthetic TLR3 ligand, polyinosinic-polycytidylic acid (Poly I:C), a negative dsDNA control, or a positive control. Cytokine and chemokine production post-stimulation was measured by ELISA. The effects of E2 and P on TLR3 mRNA and protein expression were measured using Real Time RT-PCR and FACS analysis, respectively. RESULTS: Stimulation of TLR3-expressing cells with the synthetic TLR3 ligand, Poly I:C, resulted in the production of cytokines and chemokines important for endometrial function and regulation. Suppression of Poly I:C-induced cytokine and chemokine production by cells treated with 10^(-8) M E2, but not cells treated with 10^(-7) M P, was observed in endometrial epithelial cell lines expressing TLR3 and estrogen receptor alpha (ERalpha). The effects of E2 were not observed on cells which did not express ERalpha or in cells pre-treated with the ER antagonist, ICI 182, 780. Treatment with E2 did not affect TLR3 mRNA or protein expression. However, treatment with E2 did suppress cytokine and chemokine production resulting from TLR3 stimulation with Poly I:C, suggesting that E2 modulates TLR3 function. CONCLUSION: The data presented in this study are the first indication that E2 can markedly alter the innate immune response to dsRNA, providing a previously unreported process by which E2 can alter immune responses

A genome-wide association study identifies four novel susceptibility loci underlying inguinal hernia.

Inguinal hernia repair is one of the most commonly performed operations in the world, yet little is known about the genetic mechanisms that predispose individuals to develop inguinal hernias. We perform a genome-wide association analysis of surgically confirmed inguinal hernias in 72,805 subjects (5,295 cases and 67,510 controls) and confirm top associations in an independent cohort of 92,444 subjects with self-reported hernia repair surgeries (9,701 cases and 82,743 controls). We identify four novel inguinal hernia susceptibility loci in the regions of EFEMP1, WT1, EBF2 and ADAMTS6. Moreover, we observe expression of all four genes in mouse connective tissue and network analyses show an important role for two of these genes (EFEMP1 and WT1) in connective tissue maintenance/homoeostasis. Our findings provide insight into the aetiology of hernia development and highlight genetic pathways for studies of hernia development and its treatment