SUMMARYHuman genital infection caused by C hlamydia trachomatis is thought to be immunologically mediated, resulting in local recruitment of lymphocyte subsets and inducing the production of cytokines. Little information is available about the role of lymphocyte recruitment and the regulation of cytokine production in the genital tract of C. trachomatis positive infertile women. We have evaluated the recruitment of lymphocyte subsets in the genital tract and production of Th1/Th2 cytokines in cervical secretions and laparoscopic specimens from the fallopian tubes of C. trachomatis positive infertile women ( n = 17) and compared them with controls, viz. C. trachomatis negative infertile women ( n = 20) using ELISA and flow cytometry. None of these patients were found to be infected either with Candida sps., bacterial vaginosis, Trichomonas vaginalis , Neisseria gonorrhoeae, Mycoplasma hominis or Ureaplasma urealyticum in the cervix. Flow cytometric analysis of cervical secretions in Chlamydia positive women revealed recruitment of both CD4 and CD8 lymphocytes to the genital tract was up-regulated and a variation in the production rates of different cytokines in cervical secretions and fallopian tube was observed. We found that the immune responses in cervical secretions were of Th0 type, since all the analysed cytokines, viz. IFN-g , TNF-a , IL-10 and IL-12 were up-regulated. As, both CD4 and CD8 cells contribute to the production of IFN-g and IL-10, these results suggest that along with CD4 cells, CD8 lymphocytes also may be important for local regulation of Th1/Th2 responses in the genital tract during C. trachomatis infection.

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During the last 2 decades, substantial progress has been made in understanding the relationship between dietary constituents and the development of colon cancer in man. Unlike studies of cancer among smokers and nonsmokers, nutritional epidemiologic studies are confronted with the inherent difficulty of assessing reasonably precise exposures. The lack of consistency between international correlation studies and case-control studies does not necessarily negate a dietary etiology of colon cancer because these inconsistencies may have arisen, at least in part, from methodological limitations. Some of these deficiencies in epidemiological studies of diet and cancer have been corrected; recent case-control studies demonstrated that high dietary fat is a risk factor for colon cancer development and that an overall increase in intake of foods high in fiber might decrease the risk for colon cancer. The results of epidemiologic studies may be assumed to present conservative estimates of the true risk for cancer associated with diet. The populations with high incidences of colon cancer are characterized by high consumption of dietary fat, which may be a risk factor in the absence of factors that are protective, such as whole-grain cereals and of other high fiber. Laboratory-animal model studies have shown that certain dietary lipids and fibers influence tumorigenesis in the colon. The data of metabolic epidemiological and laboratory-animal model studies are sufficiently convincing with respect to the enhancement of colon cancer by type of fat and protection by certain dietary fibers.

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L-subshell ionization cross sections are extracted from measured L␣, L␤, L␥, L␥ 1 , L␥ 23 , and L␥ 44 x-ray production cross sections in thin targets of 75 Re, 78 Pt, and 79 Au bombarded by 4 -8 MeV C 3+ ions. For each projectile energy, using the fluorescence and Coster-Kronig yields recently recommended by Campbell with an amendment for multiple ionization effects, a mutually consistent set of ionization cross sections is extracted from L␣ and six pairs of other L-line x-ray production cross sections. Extracted L 1 -, L 2 -, L 3 -ionization cross sections are compared with the predictions of the ECPSSR theory-which accounts for the energy ͑E͒ loss and Coulomb ͑C͒ deflection of the projectile as well as for perturbed-stationary state (PSS) and relativistic ͑R͒ nature of L subshells-and its modification, ECUSAR-IS. In the ECUSAR-IS theory, the PSS effect is calculated with a united and separated atom (USA) treatment and the intrashell (IS) coupling is accounted for by multiplicative factors of Sarkadi and Mukoyama normalized so that the sum of L-subshell ECUSAR-IS cross sections equals ECUSAR L-shell ionization cross section without the IS correction. Further improvement of this theory to account for better wave functions in its evaluation is made by scaling it with ratios of DiracHartree-Slater cross sections to the screened hydrogenic formulas used in the ECPSSR theory. Very good agreement is obtained with L 2 and L 3 ionization data. For the L 1 subshell, the data are in good agreement with the ECPSSR theory but are by factors of 2 to 3 above the results of its modifications.

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