Following preliminary calculations that revealed the need to consider electron correlation and to avoid the basis set superposition error, MP2/6-311+G* calculations were carried out in order to determine the energy of intermolecular interaction for 336 configurations of dimeric acetonitrile, to which an analytic potential function was fitted. The minimum of the function (−20.8 kJ mol-1) corresponds to an antiparallel geometry with C 2 h symmetry where the C−H bonds in the symmetry plane are oriented toward the nitrogen atom of the other molecule. Rotating the methyl group 60° affords a transition state with an energy 1.7 kJ mol-1 above the minimum. Several minima for the trimer and tetramer were also characterized that revealed a tendency of the molecules to retain the antiparallel arrangement.

Repeated implantation failure in some oocyte recipients is associated with an intrinsic defect in the expression of multiple genes in their endometrium. Significantly decreased levels of several transcripts in endometria without manifest abnormalities is demonstrated for the first time and shown to be associated with implantation failure.

Ab initio HF/3-21G* and CIS/3-21G* calculations for the ground and the S1 excited singlet states, respectively, of 2-(2‘-hydroxyphenyl)benzothiazole (HBT) and 2-(2‘-hydroxyphenyl)benzimidazole (HBI) were carried out. Geometric structures at the stationary points, including transition states, were investigated along with harmonic frequencies and hydrogen-bonding characteristics. A topological analysis of the density function, ρ, for the S0 and S1 states of the enol (N and N*) forms in the HBX series (X = −O−, −S−, and −NH−) provided some insight concerning the nature and trends of hydrogen bond interactions. The analysis of some parameters related to the intramolecular proton transfer suggests a qualitative relationship between the barrier height of the process and its exergonicity, consistent with principles of Leffler−Hammond and Bell−Evans−Polanyi and that changes in these two parameters are mainly determined by the strength of the hydrogen bond and to some extent by the electronegativity of X. Preliminary calculations carried out using continuum and specific models showed the important role of the specific effects of the solvent. Finally, some comments about dynamics were included.

Following infection withThe female reproductive tract is an immunologically unique site which must respond to a diverse array of sexually transmitted pathogens and must also be tolerant to allogeneic sperm and to conceptuses. Pelvic inflammatory disease (PID) is an acute clinical syndrome associated with the ascending spread of microorganisms through the female reproductive tract (80). PID encompasses a multitude of inflammatory conditions of the upper reproductive tract organs, with the majority of proven cases of PID being caused by Chlamydia trachomatis and Neisseria gonorrhoeae (gonococcus) (32), and coinfection with both pathogens is common.Neisseria gonorrhoeae is the etiologic agent of gonorrhea, and the organism infects the mucosal epithelia of the male urethra and the lower genital tracts (vagina/cervix) of women. Localized infection with gonococci leads to a mucopurulent cervicitis in women, but it is also frequently asymptomatic. However, in approximately 10 to 25% (7,26,70) of untreated individuals, infection may ascend into the upper reproductive tract to involve the endometrium, ovaries, myometrium, parametrium, and Fallopian tubes (FT) (32, 46). The host response to this ascending infection is manifested as endometritis, pelvic (tubal or ovarian) peritonitis, tubal abscess, and salpingitis in the FT, and all of these inflammatory conditions encompass the clinical syndrome of PID. Long-term sequelae that develop in individuals presenting with PID, such as chronic pelvic pain, tubal damage, and ectopic pregnancy (7,26,70), are recognized as important public health problems worldwide (32,46).The FT is essentially a muscular organ whose lumen is lined by columnar ciliated cells and secretory cells with microvilli (68), and it plays a critical role in mammalian reproduction, functioning as a channel and storage organ for spermatozoa, a collecting vessel for oocytes released from the ovaries, the site of fertilization and zygote formation, and a means for transporting the early embryo to the uterus (54, 68). It is recognized that salpingitis induced by gonococcal infection causes significant tissue damage in the FT, which is resolved by a process of repair by infiltrating fibroblasts that leads to scarring. These events cause functional impairment of the tubes and irreversible infertility (80). However, little is known of the molecular mechanisms involved in the early stages of infection of the FT by ascending gonococci that initiate the inflammatory response. Studying the pathogenesis of gonococcus-induced salpingitis has relied on the use of ex vivo human FT organ tube

Infection of the Fallopian tubes (FT) byNeisseria gonorrhoeae can lead to acute salpingitis, an inflammatory condition, which is a major cause of infertility. Challenge of explants of human FT with gonococci induced mRNA expression and protein secretion for the proinflammatory cytokines interleukin (IL)-1␣, IL-1␤, and tumor necrosis factor alpha (TNF-␣) but not for granulocyte-macrophage colony-stimulating factor. In contrast, FT expression of IL-6 and of the cytokine receptors IL-6R, TNF receptor I (TNF-RI), and TNF-RII was constitutive and was not increased by gonococcal challenge. These studies suggest that several proinflammatory cytokines are likely to contribute to the cell and tissue damage observed in gonococcal salpingitis.