, Elaeagnus angustifolia L., Eucalyptus tereticornis L., Ficus carica L., Fraxinus excelsior L., Melia azadirach L., Morus alba L., Morus nigra L., Pistacia vera L., Prunus armeniaca L., Punica granatum L., Robinia pseudo acacia L., Rosa indica L. and Vitis vinifera L. grown AZD9291 in
the urban (polluted site) and peri-urban (non-polluted) sites of Quetta. Results showed that all plant species exhibited significant (p<0.05) reduction at polluted site in their leaf length, width, area and petiole length when compared with the same plant species of non-polluted site. These plant species also showed significant variation in the growth of morphological parameters from season to season. Results also showed that the overall reduction % in leaf length, width, area and length of petiole during different seasons at polluted sites with respect to those of non-polluted sites were found maximum during summer (33.91, 36.61, 37.08 and 46.17 %), followed by autumn and lowest was recorded during spring season (28.39, 23.50. 32.49 and 26.34 %), respectively. Results also deciphered that minimum decrease in
leaf length (19.86%), leaf width (17.81%), leaf area (22.66%) and petiole length (02.56%) was observed in Vitis vinefera L., Pistacia vera L., Ficus carica L. and Pistacia vera L. Whereas, maximum decrease 72.59, 50.58, 57.98 and 65.48% for the same attributes were noted in Punica 4SC-202 inhibitor granatum L., Elaeagnus angustifolia L., Rosa indica L. and Eucalyptus tereticornis L., respectively. Results further indicated that as the plants get ages, the reduction % of various leaf attributes of polluted plants also increased as compared with non-polluted plant species. This could be mainly due to maximum exposure of plants to air pollutants come from various auto emission sources.”
“Constitutive expression of Kruppel-like factor 3 (KLF3, BKLF) increases marginal zone (MZ) B cell numbers, a phenotype shared
with mice lacking KLF2. Ablation of KLF3, known to interact with serum response factor (SRF), or SRF itself, results in fewer MZ PF-00299804 purchase B cells. It is unknown how these functional equivalences result. In this study, it is shown that KLF3 acts as transcriptional repressor for the leukocyte-specific integrin beta(7) (Itgb7, Ly69) by binding to the beta(7) promoter, as revealed by chromatin immunoprecipitation. KLF2 overexpression antagonizes this repression and also binds the beta(7) promoter, indicating that these factors may compete for target sequence(s). Whereas beta(7) is identified as direct KLF target, its repression by KLF3 is not connected to the MZ B cell increase because beta(7)-deficient mice have a normal complement of these and the KLF3-driven increase still occurs when beta(7) is deleted. Despite this, KLF3 overexpression abolishes lymphocyte homing to Peyer’s patches, much like beta(7) deficiency does. Furthermore, KLF3 expression alone overcomes the MZ B cell deficiency when SRF is absent. SRF is also dispensable for the KLF3-mediated repression of beta(7).