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Green analytical chemistry (GAC) primary goal is to develop environmental and health-friendly analytical methods by reduction or replacement of hazardous substances from analytical procedures. In this research, the application of GAC to quantify five β-lactams antibiotics (cefuroxime sodium, cefaclor, ertapenem sodium, ampicillin sodium and sulbactam sodium) by high-performance liquid chromatography (HPLC) using photodiode arrays (PDA) detector was developed. To achieve this, ethanol was used as a green replacement for methanol and acetonitrile, common solvents in chromatographic procedures. Several chromatographic conditions were investigated to accomplish the optimal conditions. The method validation followed the ICH Q2 (R1) guideline, and the developed method was successfully applied for quantifying some pharmaceutical products. [ABSTRACT FROM AUTHOR]

Carbapenem antibiotics are the most effective antimicrobials for the treatment of infections caused by the most resistant bacteria. They belong to the category of β-lactams that include the penicillins, cephalosporins, monobactams and carbapenems. This class of antimicrobials has a broader spectrum of activity than most other beta-lactams antibiotics and are the most effective against Gram-positive and Gram-negative bacteria. All β-lactams antibiotics have a similar molecular structure: the carbapenems together with the β-lactams. This combination gives an extraordinary stability to the molecule against the enzymes inactivating the β-lactams. They are safe to use and therefore widespread use in many countries has given rise to carbapenem resistance which is a major global public health problem. The carbapenem resistance in some species is intrinsic and consists of the capacity to resist the action of antibiotics with several mechanisms: for the absence of a specific target, or an intrinsic difference in the composition of cytoplasmatic membrane or the inability to cross the outer membrane. In addition to intrinsic resistance, bacteria can develop resistance to antibiotics with several mechanisms that can be gathered in three main groups. The first group includes antibiotics with poor penetration into the outer membrane of bacterium or antibiotic efflux. The second includes bacteria that modify the target of the antibiotics through genetic mutations or post-translational modification of the target. The third includes bacteria that act with enzyme-catalyzed modification and this is due to the production of beta-lactamases, that are able to inactivate carbapenems and so called carbapenemases. In this review, we focus on the mode of action of carbapenem and the mechanisms of carbapenem resistance.

Over the last few decades, β-lactams are the most widely used and favored antimicrobials worldwide, because of their efficacy, broad spectra and low toxicity. They inhibit the bacterial penicillin-binding proteins (PBPs), which are the enzymes that catalyze the final cross-linking of the bacterial cell wall polymer, peptidoglycan. However, due to heavy use of β-lactams antibiotics, bacteria developed various mechanism of resistance. Modification or substitution of the PBPs is important mechanism in gram-positive cocci, while production of β-lactamases is main cause of resistance among gram-negative bacilli. Mostly plasmid harbors the resistance gene and therefore, is crucial in disseminating resistance into previously susceptible species. Throughout the 1960s and 1970s there was a relentless rise in reports of resistance to β-lactams as a consequence of the selection of bacteria that produce β-lactamases. [ABSTRACT FROM AUTHOR]

Carbapenem antibiotics are the most effective antimicrobials for the treatment of infections caused by the most resistant bacteria. They belong to the category of β-lactams that include the penicillins, cephalosporins, monobactams and carbapenems. This class of antimicrobials has a broader spectrum of activity than most other beta-lactams antibiotics and are the most effective against Gram-positive and Gram-negative bacteria. All β-lactams antibiotics have a similar molecular structure: the carbapenems together with the β-lactams. This combination gives an extraordinary stability to the molecule against the enzymes inactivating the β-lactams. They are safe to use and therefore widespread use in many countries has given rise to carbapenem resistance which is a major global public health problem. The carbapenem resistance in some species is intrinsic and consists of the capacity to resist the action of antibiotics with several mechanisms: for the absence of a specific target, or an intrinsic difference in the composition of cytoplasmatic membrane or the inability to cross the outer membrane. In addition to intrinsic resistance, bacteria can develop resistance to antibiotics with several mechanisms that can be gathered in three main groups. The first group includes antibiotics with poor penetration into the outer membrane of bacterium or antibiotic efflux. The second includes bacteria that modify the target of the antibiotics through genetic mutations or post-translational modification of the target. The third includes bacteria that act with enzyme-catalyzed modification and this is due to the production of beta-lactamases, that are able to inactivate carbapenems and so called carbapenemases. In this review, we focus on the mode of action of carbapenem and the mechanisms of carbapenem resistance. [ABSTRACT FROM AUTHOR]

Glutamate is the primary excitatory neurotransmitter in the mammalian central nervous system, which plays an important role in many aspects of normal brain function such as neural development, motor functions, learning and memory etc. However, excessive accumulation of glutamate in the extracellular fluid will induce excitotoxicity which is considered to be a major mechanism of cell death in brain ischemia. There is no enzyme to decompose the glutamate in extracellular fluid, so extracellular glutamate homeostasis within the central nervous system is mainly regulated by the uptake activity of excitatory amino acid transporters. Among the five excitatory amino acid transporters, glial glutamate transporter-1 (GLT-1) is responsible for 90% of total glutamate uptake. Thus, GLT-1 is essential for maintaining the appropriate level of extracellular glutamate, and then limiting excitotoxicity of glutamate in central nervous system. Therefore, the regulation of GLT-1 might be a potential therapeutic target for ischemic brain injury. This review summarizes recent advances including our findings in the methods or medicine that could protect neurons against brain ischemic injury via upregulation of GLT-1 and discuss the possible application of these strategies., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.)