AAK-2 is one of two ␣ isoforms of the AMP-activated protein kinase in Caenorhabditis elegans and is involved in life span maintenance, stress responses, and germ cell cycle arrest upon dauer entry. We found that AAK-2 was phosphorylated at threonine 243 in response to paraquat treatment and that this phosphorylation depends on PAR-4, the C. elegans LKB1 homologue. Both aak-2 mutation and par-4 knockdown increased the sensitivity of C. elegans worms to paraquat, and the double deficiency did not further increase sensitivity, indicating that aak-2 and par-4 act in a linear pathway. Both mutations also slowed body bending during locomotion and failed to reduce head oscillation in response to anterior touch. Consistent with this abnormal motility and behavioral response, expression of the AAK-2::green fluorescent protein fusion protein was observed in the ventral cord, some neurons, body wall muscle, pharynx, vulva, somatic gonad, and excretory cell. Our study suggests that AMPK can influence the behavior of C. elegans worms in addition to its well known function in metabolic control.

Endothelial cells go through progressive pathophysiologic modification as cellular senescence progresses. In vitro, endothelial cell senescence is accompanied by failure of proliferation and by perturbations in gene and protein expressions. Moreover, this cellular senescence in culture has been proposed to reflect processes that occur in the organism in vivo and free radical theory is accepted to be the most plausible explanation for this process. We have screened proteins involved in both cellular senescence and reactive oxygen species induced condition using 2-D gel analysis and found that ubiquitin carboxyl terminal hydrolase L1, peroxyredoxin 2, peroxyredoxin 4, fatty acid binding proteins (FABPs), and 5'-AMP-activated protein kinase beta-1 subunit were candidate aging-related proteins. To evaluate in vivo function of these proteins, Caenorhabditis elegans (C. elegans) knock-down system using RNA interference was applied. Aging-specific expression of lipofucsin and the lifespan of knocked-down C. elegans were observed to assess the outcome. Interestingly, the inhibition of the genes led to short lifespan and earlier accumulation of lipofucsin with increasing age when compared with the wild type. These results suggest that the above genes may be related to cellular senescence process in determining the longevity in C. elegans and that gene inactivation renders animals susceptible to oxidative stress.

Malakoplakia is a rare granulomatous, inflammatory disease generally manifesting as ulcers of the urogenital tract, especially in the bladder, but it can occur in any part of the body. Because of its varied clinical presentations, malakoplakia is considered for differential diagnosis upon suspicion. The final diagnosis is confirmed by the presence of Michaelis-Gutmann bodies. We report a case of pelvic malakoplakia accompanied by left lower quadrant pain that was misdiagnosed as endometrial cancer with pelvic mass based on imaging studies. The patient underwent dilatation and curettage, and the pathology report revealed no malignancy. Because of persistent pain and septic shock, she underwent a debulking operation to remove the mass. Histopathologic examination revealed malakoplakia. For postoperative management, she received broad-spectrum antibiotics, but abdominal pelvic computerized tomography performed on postoperative day 9 revealed pelvic mass recurrence. To the best of our knowledge, this is the only rare case report of pelvic malakoplakia mimicking endometrial cancer.

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