The plasmid-eliminated strains had completely lost resistance to carbapenem and some other b-lactams, including ceftazidime, cefotaxime, and cefepime. The presence of carbapenem hydrolyzing class D b-lactamases is the most important factor mediating carbapenem resistance in Acinetobacter spp. Conjugation experiments by co-cultivation of the A. calcoaceticus strain with E. coli DH5a:pBR322 in vitro and in vivo in mice showed that the plasmid carrying the blaNDM-1 gene was successfully transferred to the recipient DH5a:pBR322 in vitro and in vivo. The minimum bacteriostatic concentration of meropenem for transduced bacteria was greatly increased, but was less than that of strain XM1570, suggesting that the degree of resistance was also dependent on physiological metabolic properties of the bacteria or by the contribution of additional genes to beta-lactam resistance, e.g. blaADC. NDM-1 can efficiently hydrolyze a broad range of b-lactams, but not monobactams, such as aztreonam. In our study, after successful transfer of the blaNDM-1-carrying plasmid, E. coli strain DH5a:pBR322 remained susceptible to aztreonam. The plasmidcured strain maintained resistance to aztreonam. An increasing number of reports have focused on Acinetobacter-derived cephalosporinases, which are common among Acinetobacter spp.. Some ADC b-lactamases had lower MICs of cefotaxime and aztreonam as well. Aztreonam is a weak inducer and weak substrate, but it can be hydrolyzed if sufficient amounts of ADC blactamases are produced. Some ADC b-lactamases can hydrolyze high levels of ceftazidime, cefepime, and aztreonam, which encouraged the classification of this enzyme as an extendedspectrum AmpC. Because of the insertional inactivation of blaOXA-417, we speculated that blaADC-72 conferred resistance to aztreonam, cefazolin, and ampicillin in the plasmidcured strain. This is the first report of NDM-1 -positive A. calcoaceticus from China. Our study provides molecular evidence for the emergence and dissemination of multidrug-resistant bacteria. blaNDM-1 in A. calcoaceticus XM1570 located on a highly mobile plasmid of indeterminable replicon type, further underlining the wide spread of that resistance trait. The results of this study also suggest a potential treatment strategy that may help in controlling NDM-1 bacterial infection and transmission. T Mycophenolic acid lymphocytes respond to pathogens by differentiating to effector subpopulations that mediate the protective immune response. Effector T cells strikingly increase their cellular uptake of multiple nutrients including glucose, amino acids and transferrin. They also swap from metabolising glucose primarily through oxidative phosphorylation to become highly glycolytic. The changes in 
effector T cell metabolism are important as judged by the consequences of inhibiting key metabolic regulators. For example, the serine/threonine kinase mTORC1 integrates inputs from nutrients, antigen and cytokine receptors to link T cell metabolism and T cell differentiation. mTORC1 thus controls expression of cytolytic effector molecules, chemokine and adhesion receptors in effector T cells and controls effector-memory cell transition. One other regulator of T cell differentiation is the adenosinemonophosphate -activated protein kinase. AMPK is phosphorylated and activated by liver kinase B1 in response to energy stress and Echinatin functions to enforce quiescence to restore energy balance in cells. In T lymphocytes, AMPK is important for the transition of effector T lymphocytes to memory T cells during the contraction phase of the immune response.