Although there are ever increasing reports of extraintestinal human infections caused by Aeromonads, in both immunocompromised and immunocompetent patients, respiratory tract infections remain uncommon. We describe a case of aspiration pneumonia in an immunocompetent patient with multiple sclerosis, caused by a community acquired, multidrug resistant strain of Aeromonas hydrophila sensitive only to meropenem. The case highlights the clinical significance of Aeromonas hydrophila as a respiratory pathogen, as well as the community origin of multidrug resistance and the utility of newer carbapenems in such cases.
Adolescent ; *Aeromonas hydrophila/physiology ; Drug Resistance, Microbial ; Drug Resistance, Multiple ; Female ; *Gram-Negative Bacterial Infections/drug therapy ; Human ; Pneumonia, Aspiration/*microbiology ; Thienamycins/therapeutic use

NO Abstract Available
Antitubercular Agents/*pharmacology ; Chromosome Mapping ; Drug Resistance, Bacterial ; Ethambutol/*pharmacology ; Korea ; *Mutation ; Mycobacterium tuberculosis/drug effects/*genetics ; Pentosyltransferases/*genetics

The endoplasmic reticulum (ER) is an important subcellular organelle that is involved in numerous activities required to achieve and maintain functional proteins in addition to its role in the biosynthesis of lipids and as a repository of intracellular Ca²⁺. The inability of the ER to cope with protein folding beyond its capacity causes disturbances that evoke ER stress. Cells possess molecular mechanisms aimed at clearing unwanted cargo from the ER lumen as an adaptive response, but failing to do so navigates the system towards cell death. This systemic approach is called the unfolded protein response. Aging insults cells through various perturbations in homeostasis that involve curtailing ER function by mitigating the expression of its resident chaperones and enzymes. Here the unfolded protein response (UPR) cannot protect the cell due to the weakening of its protective arm, which exacerbates imbalanced homeostasis. Aging predisposed breast malignancy activates the UPR, but tumor cells maneuver the mechanistic details of the UPR, favoring tumorigenesis and thereby eliciting a treacherous condition. Tumor cells exploit UPR pathways via crosstalk involving various signaling cascades that usher tumor cells to immortality. This review aims to present a collection of data that can delineate the missing links of molecular signatures between aging and breast cancer.
Aging* ; Arm ; Breast Neoplasms* ; Breast* ; Carcinogenesis ; Cell Death ; Endoplasmic Reticulum* ; Homeostasis ; Organelles ; Protein Folding ; Unfolded Protein Response*