Humans can acquire brucellosis by the ingestion of infected food (especially unpasteurized milk), by direct contact with an infected animal (sheep, cattle, or pigs), or by aerosols.1 In humans, brucellosis is a chronic granulomatous infection that is associated with nonspecific, mild clinical symptoms such as fever, fatigue, night sweats, anorexia, and weight loss. It is, therefore,

difficult to diagnose, and screening for Brucella should be performed in the case of fever of unknown origin. Almost every organ and system can be affected, but osteoarticular complications are the most common, with peripheral arthritis, sacroiliitis, and spondylitis occurring.2 Laboratory studies are nonspecific in patients with brucellosis, and white blood cell counts are usually normal GSK-3 inhibitor to low. Although the presence of some degree of hepatitis is frequent, the

click here development of a liver abscess (brucelloma) is rare and occurs in only approximately 1% of patients with brucellosis.3 It most commonly represents a chronic form of the disease that has remained latent. The typical CT scan pattern of liver brucelloma is a rounded or ovoid hypodense area with central calcification5 and is similar to the pattern found in this case. Confirmation of the diagnosis of brucellosis can be achieved by various techniques, including blood cultures, serological tests, and real-time polymerase chain reaction with blood or pus.4 The classic treatment for brucellosis is based on doxycycline and rifampin. In the case of liver abscess, surgery Reverse transcriptase is most often required because the risk of recurrence after conservative management is at least 50%.3 After surgery, which can be performed laparoscopically (as in the present case), a patient’s chance of being cured is extremely good. “
“In a recent report, Choi et al.1 demonstrated that protein arginine methyltransferase-1

(PRMT1)-dependent arginine modification of FoxO1 contributed to the regulation of hepatic glucose production in a mouse model. However, despite presenting the finding of the FoxO1 protein, the investigators failed to discuss another well-defined class of PRMT1 substrates: histones, methylations of which have been identified as key “histone codes” in epigenetic regulation2 and have been shown to regulate hepatic gluconeogenesis under the control of another PRMT in a previous study by Krones-Herzig et al.3 Herein, we compare the two similar studies and suggest that PRMT1-mediated histone arginine methylation should be involved in the network of hepatic glucose metabolism regulation. Both groups found that the PRMTs regulated the same target genes, but methylated different proteins (Table 1). Herzig et al. suggested that PRMT4 contributed to the regulation of hepatic glucose metabolism by methylating histone H3, because methylations of H3 arginines are known to be transcriptional activation markers.