(3.3%), and Pseudomonas spp. (1.9%). Gram-negative bacteria represented 92.44% of the isolates. E. coli showed maximum resistance towards co-trimoxazole (78.75%) followed by cefuroxime (77.5%) & ciprofloxacin (72.5%). Klebsiella pneumoniae showed the highest resistance against co-trimoxazole (23.75%) and ciprofloxacin (23.75%). CONCLUSIONS The present study gives an idea about the common trend of antibiotic resistance of uropathogens in this region. The findings in our study will help in the formulation of antibiotic policy and determination of empirical treatment of UTI in this region. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.Photodynamic therapy (PDT) is a cancer therapy involving the systemic injection of a Photosensitizer (PS) that localizes to some extent in a tumor. After an appropriate time (ranging from minutes to days) the tumor is irradiated with red or near-infrared light either as a surface spot or by interstitial optical fibers. The PS is excited by the light to form a long-lived triplet state that can react with ambient oxygen to produce Reactive Oxygen Species (ROS) such as singlet oxygen and/or hydroxyl radicals, that kill tumor cells, destroy tumor blood vessels, and lead to tumor regression and necrosis. It has long been realized that in some cases, PDT can also stimulate the host immune system, leading to a systemic anti-tumor immune response that can also destroy distant metastases and guard against tumor recurrence. The present paper aims to cover some of the factors that can affect the likelihood and efficiency of this immune response. The structure of the PS, drug-light interval, rate of light delivery, mode of cancer cell death, expression of tumor-associated antigens, and combinations of PDT with various adjuvants can all play a role in stimulating the host immune system. Considering the recent revolution in tumor immunotherapy triggered by the success of checkpoint inhibitors, it appears that the time is ripe for PDT to be investigated in combination with other approaches in clinical scenarios. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Phosphoinositide-Dependent Kinase 1 (PDK1) is now widely studied in malignant solid tumors. We as well as other researchers have previously revealed that targeting PDK1 could be thought of as a promising anticancer treatment strategy. The aim of this study was designed to evaluate the anticancer activity of GSK-470, a novel and highly specific inhibitor of PDK1, in Pheochromocytoma (PCC) tumor model. METHODS PC12 cells were xenografted into nude mice to build PCC tumor model. Animals were treated with GSK-470 vs vehicle. Mean tumor volume was calculated and compared across groups. TUNEL was used to detect apoptosis. The effects of PDK1 inhibitor GSK-470 on activation of the Akt signaling and its downstream Akt/mTOR pathway in xenotransplant tumor tissues were examined by western bolt. RESULTS The mean tumor volume in GSK-470 group was significantly less than that in control group. TUNEL results found that cell apoptosis were markedly increased in GSK-470 gourp compared with control group. The western bolt analysis showed that the phosphorylation of Akt at threonine 308 was significantly reduced in GSK-470 group. Also, GSK-470 strong inhibited phosphorylation of mTOR on Ser2448, a marker for mTORC1 activity, as well as phosphorylation of p70S6K, the best characterized targets of mTOR. CONCLUSION Our results showed that GSK-470 exhibited potent anticancer activity in PC12 tumor-bearing mice. Also, we found that this effect appeared to be mediated by inhibition of the Akt/mTOR pathway. The present study once again provides new insights into the therapeutic effects of inhibiting PDK1 in treatment of malignant PCC. Therefore, we propose that GSK-470 might be an effective therapeutic agent for the treatment of malignant PCC. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Oxadiazoles, triazoles, and their respective precursors have been shown to exhibit various pharmacological properties, namely antitumour activities.  https://www.selleckchem.com/products/mlt-748.html  Cytotoxic activity was reported for these compounds in various cancer cell lines. AIM AND OBJECTIVES In this study, we aim at investigating the mechanism of apoptosis by N-(4-chlorophenyl)-2-(4-(3,4,5-trimethoxybenzyloxy)benzoyl)-hydrazinecarbothioamide, a triazole precursor, henceforth termed compound P7a, in breast cancer cell line, MCF-7. We first screen a series of analogues containing (3,4,5-trimethoxybenzyloxy)phenyl moiety in breast cancer cell lines (MCF-7 and MDA-MB-231) to select the most cytotoxic compound and demonstrate a dose- and time-dependent cytotoxicity. Then, we unravel the mechanism of apoptosis of P7a in MCF-7 as well as its ability to cause cell cycle arrest. METHODS Synthesis was performed as previously described by Kareem and co-workers. Cytotoxicity of analogues containing (3,4,5-trimethoxybenzyloxy)phenyl moiety against MCF-7addition, cell cycle analysis showed that cell proliferation was arrested at the G1 phase in the MCF-7 cell line. Furthermore, upon treatment, the MCF-7 cell line showed increased activity of caspase-3/7, and caspase-9. Lastly, the western blot analysis showed the up-regulation of pro-apoptotic proteins along with up-regulation of caspase-7 and caspase-9, indicating that an intrinsic pathway of apoptosis was induced. CONCLUSION The results suggest that compound P7a could be a potential chemotherapeutic agent for breast cancer. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.BACKGROUND Breast cancer, the most leading cause of death with 49.9% of crude incidence rate and 12.9% of crude mortality rate. Natural resources have been extensively used throughout history for better and safer treatment against various diseases. OBJECTIVES The present study was aimed to investigate the antioxidant and anticancer potential of a tropical lichen Dirinaria consimilis (DCME) and its phytochemical analysis. METHODS The DCME was preliminarily evaluated for ROS, and RNS scavenging potential. Further, DCME was evaluated for in vitro anticancer activity through cell proliferation assay, cell cycle analysis, annexin V/PI staining, morphological analysis, and western blotting study. Finally, the HPLC and LC-MS analysis was done to identify probable bioactive compounds. RESULTS The in vitro antioxidant studies showed the promising ROS, and RNS scavenging potential of DCME. Also, the in vitro antiproliferative study bared the cytotoxic nature of DCME towards MCF-7 (IC50 - 98.58 ± 6.82µg/mL) and non-toxic towards WI-38 (IC50 - 685.