Bloodstream infection caused by Acinetobacter baumannii has become a major clinical concern, especially multidrug-resistant A baumannii (MDRAB). The aim of this study was to identify the risk factors of nosocomial acquired MDRAB bacteremia and to determine the risk factors related to the mortality of patients with MDRAB bacteremia. Patients with nosocomial acquired A baumannii bacteremia were enrolled between January, 2013 and December, 2017 at the First Affiliated Hospital, School of Medicine, Zhejiang University. Medical records were reviewed, and the clinical and microbial characteristics were collected. Among the 338 patients suffering from A baumannii bacteremia, 274 patients were infected with MDRAB bacteremia. Bacteremia-related mortality was 46.4% for the overall sample; 56.2% for MDRAB bacteremia patients, 4.7% for non-MDRAB bacteremia patients. The identified risk factors for developing MDRAB bacteremia were previous exposure to carbapenems [odds ratio (OR) 5.78, P = .005] and penicillins+β-lactamase inhibitors (OR 4.29, P = .009). Primary bacteremia tended to develop non-MDR bacteremia (OR 0.10, P = .002). The risk factors for MDRAB bacteremia-related mortality were old age (OR 1.02, P = .036), a high Pitt bacteremia score (OR 1.32, P < .001), bacteremia occurring after severe pneumonia (OR 8.66, P < .001), while catheter-related infection (OR 0.47, P = .049) and operations for treating infection (OR 0.51, P = .043) may have a better outcome. Patients with MDRAB had a higher mortality rate. Patients with previous carbapenems and penicillins+β-lactamase inhibitor exposure are at an increased risk of MDRAB bacteremia, whereas patients with primary bacteremia tended to develop non-MDR bacteremia. The risk factors for MDRAB bacteremia-related mortality were old age, a high Pitt bacteremia score, and bacteremia occurring after severe pneumonia, whereas catheter-related infection and operations for the treatment of infection may have a better outcome.

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Background EPZ005687 is a selective inhibiter of methyltransferase EZH2. In this article, we investigated the protective role and mechanism of EPZ005687 in transverse aortic constriction-induced pulmonary arterial hypertension in mice. Methods We assigned 15 (6–8 weeks old) male balb/c mice to 3 groups randomly: Sham control + DMSO group, TAC + DMSO group, and TAC + EPZ005687 group (10 mg kg−1, once a week for 4 weeks). On day 28 following TAC operation, the right ventricular systolic blood pressure (RVSBP) was measured, and lung tissues were collected for laboratory examinations (DHE, Western blot, real-time PCR, and ChIP). Results Murine PAH model was successfully created by TAC operation as evidenced by increased RVSBP and hypertrophic right ventricle. Compared with the sham control, TAC-induced PAH markedly upregulated the expression of EZH2 and ROS deposition in lungs in PAH mice. The inhibiter of methyltransferase EZH2, EPZ005687 significantly inhibits the development of TAC-induced PAH in an EZH2-SOD1-ROS dependent manner. Conclusion Our data identified that EZH2 serves a fundamental role in TAC-induced PAH, and administration of EPZ005687 might represent a novel therapeutic target for the treatment of TAC-induced PAH.

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BackgroundVaricella-zoster virus (VZV) is a common and widespread human-restricted pathogen. It is famous for its dermatological manifestations, such as varicella and herpes zoster. Patients with aplastic anemia-paroxysmal nocturnal hemoglobinuria (AA-PNH) syndrome complicated with fatal disseminated varicella zoster virus infection are very rare and in danger.Patient concernsA 26-year-old man with a history of AA-PNH syndrome was receiving cyclosporine and corticosteroid treatment in the hematology department. During his hospitalization in our hospital, he developed fever, abdominal pain, and lower back pain, and his face, penis, trunk, and limbs developed itchy rash. Subsequently, the patient had to undergo cardiopulmonary resuscitation because of sudden cardiac arrest, and be transferred to ICU for treatment. It was presumed that the cause is unknown severe sepsis. The patient’s condition quickly progressed to multiple organ failure, accompanied by liver, respiratory, and circulatory failure, and signs of disseminated intravascular coagulation. Unfortunately, the patient died after 8 h of active treatment. Finally, we collected all the evidence and concluded that the patient died of AA-PNH syndrome combined with poxzoster virus.ConclusionAA-PNH syndrome patients treated with steroids and immunosuppressants are prone to various infections, considering that herpes virus infection with chickenpox and rash as the initial manifestations is characterized by rapid progress and often accompanied by serious complications. It is more difficult to distinguish it from AA-PNH syndrome with skin bleeding points. If it is not identified in time, it may delay the treatment opportunity, make the condition worse, and cause serious adverse prognosis. Therefore, clinicians need to pay attention to it.