Draft genome sequence analysis of a high carbapenem-resistant Klebsiella quasipneumoniae subsp. quasipneumoniae strain isolated from an HIV-positive patient with pneumonia.

OBJECTIVES: The rapid spread of Klebsiella spp. is recognised as a major threat to public health owing to a rise in the number both of healthcare- and community-acquired infections. Here we report the draft genome sequence of a high carbapenem-resistant Klebsiella quasipneumoniae subsp. quasipneumoniae strain (Cln185) isolated from a human immunodeficiency virus (HIV)-positive patient with pneumonia. METHODS: Classical microbiological methods were applied to isolate and identify the strain. Genomic DNA was sequenced using an Illumina HiSeq platform and the reads were de novo assembled into contigs using CLC Genomics Workbench. The assembled contigs was annotated and whole-genome sequencing (WGS) was performed. RESULTS: WGS analysis revealed that the genome comprised a circular chromosome of 5 406 774bp with a GC content of 57.73%. Three important antimicrobial resistance genes (blaIMP-38, blaOKP-B-6 and blaDHA-1) were detected. In addition, genes conferring resistance to aminoglycosides, ß-lactams, fluoroquinolones and tetracycline were also identified. CONCLUSION: The draft genome sequence reported here will lay the foundation for future research on antimicrobial resistance and pathogenic mechanisms in K. quasipneumoniae subsp. quasipneumoniae and also will promote comparative analysis with genomic features among different sources of clinically important multidrug-resistant strains.

Acute Massive Gastrointestinal Bleeding in the Elderly.

An 82-year patient presented with nausea, coffee-ground emesis, melena and hematochezia on July 10, 2011. The patient received blood transfusion on July 11, and continued to bleed from July 12 to 17. The patient underwent upper gastrointestinal endoscopy on July 16. There were no abnormalities in the esophagus, stomach and duodenum. Then the patient presented with shortness of breath, extreme fear, fatigue, hypotension, sweating, and cold limbs. Dopamine, as well as pressurised infusion of packed red blood cells and fresh frozen plasma were given to the patient to maintain blood pressure. CT angiography (CTA) revealed no aortic fistula, and enteroscopy revealed active bleeding in the vicinity of the ligament of Treitz. The retrograde exploration of gastroscopy revealed a 5×4 cm diverticulum on the posterior wall of the duodenum under the ligament of Treitz. Active bleeding of the small artery in the diverticulum was observed via incision of the duodenal wall, and the diverticulum was isolated. Hemostasis was achieved after ligation of blood vessels, and diverticulectomy was performed. Enteroscopy is important for the diagnosis of duodenal and upper small intestinal diseases. Repeated endoscopic exploration of multiple sites in the small intestine revealed the cause of the bleeding. The multidisciplinary team finally found the cause of the bleeding and its proper management.

Cardiac-specific overexpression of metallothionein attenuates myocardial remodeling and contractile dysfunction in l-NAME-induced experimental hypertension: Role of autophagy regulation.

Hypertension is an independent risk factor for heart disease and is responsible for the increased cardiac morbidity and mortality. Oxidative stress plays a key role in hypertensive heart diseases although the precise mechanism remains unclear. This study was designed to examine the effect of cardiac-specific overexpression of metallothionein, a cysteine-rich antioxidant, on myocardial contractile and intracellular Ca(2+) anomalies in N(G)-nitro-l-arginine methyl ester (l-NAME)-induced experimental hypertension and the mechanism involved with a focus on autophagy. Our results revealed that l-NAME treatment (14 days) led to hypertension and myocardial anomalies evidenced by interstitial fibrosis, cardiomyocyte hypertrophy, increased LV end systolic and diastolic diameters (LVESD and LVEDD) along with suppressed fractional shortening. l-NAME compromised cardiomyocyte contractile and intracellular Ca(2+) properties manifested as depressed peak shortening, maximal velocity of shortening/relengthening, electrically-stimulated rise in intracellular Ca(2+), elevated baseline and peak intracellular Ca(2+). These l-NAME-induced histological and mechanical changes were attenuated or reconciled by metallothionein. Protein levels of autophagy markers LC3B and p62 were decreased and increased, respectively. Autophagy signaling molecules AMPK, TSC2 and ULK1 were inactivated while those of mTOR and p70s6K were activated by l-NAME, the effects of which were ablated by metallothionein. Autophagy induction mimicked whereas autophagy inhibition nullified the beneficial effect of metallothionein against l-NAME. These findings suggested that metallothionein protects against l-NAME-induced myocardial anomalies possibly through restoration of autophagy.

[Value of color Doppler ultrasound in the examination of prethrombotic state].

OBJECTIVE: To explore the clinical value of color Doppler ultrasound in patients with prethrombotic state (PTS). METHODS: From October 2011 to November 2012, a total of 201 patients were diagnosed with PTS. There were 95 males and 106 females with an average age of 52 years (range: 15-78). They were divided into intervention and observation groups on the basis of drug intervention. And the relevant literatures were reviewed and the images of color Doppler ultrasound before and after treatment compared. RESULTS: Before treatment, blood flow peak rates of common femoral, popliteal and calf intermuscular veins were (0.16 ± 0.03), (0.14 ± 0.03) and (0.13 ± 0.02) m/s; after treatment, (0.19 ± 0.03), (0.17 ± 0.03) and (0.15 ± 0.01) m/s respectively. The peak flow increased and sluggish flow decreased or disappeared in 152 PS patients. It indicated a relief or an obvious resolution of hypercoagulable state. And the symptom of lower extremity soreness was greatly relieved. Among 49 patients without drug intervention, severe full-lumen storm floating occurred in 12 cases. And 8 of them suffered deep vein thrombosis within 2 weeks. The incidence of thrombus was 66.7%. CONCLUSION: Color Doppler ultrasound may detect and assess PTS effectively so as to guide effective interventions.

Inhibition of CYP2E1 attenuates chronic alcohol intake-induced myocardial contractile dysfunction and apoptosis.

Alcohol intake is associated with myocardial contractile dysfunction and apoptosis although the precise mechanism is unclear. This study was designed to examine the effect of the cytochrome P450 enzyme CYP2E1 inhibition on ethanol-induced cardiac dysfunction. Adult male mice were fed a 4% ethanol liquid or pair-fed control diet for 6weeks. Following 2weeks of diet feeding, a cohort of mice started to receive the CYP2E1 inhibitor diallyl sulfide (100mg/kg/d, i.p.) for the remaining feeding duration. Cardiac function was assessed using echocardiographic and IonOptix systems. Western blot analysis was used to evaluate CYP2E1, heme oxygenase-1 (HO-1), iNOS, the intracellular Ca(2+) regulatory proteins sarco(endo)plasmic reticulum Ca(2+)-ATPase, Na(+)Ca(2+) exchanger and phospholamban, pro-apoptotic protein cleaved caspase-3, Bax, c-Jun-NH(2)-terminal kinase (JNK) and apoptosis signal-regulating kinase (ASK-1). Ethanol led to elevated levels of CYP2E1, iNOS and phospholamban, decreased levels of HO-1 and Na(+)Ca(2+) exchanger, cardiac contractile and intracellular Ca(2+) defects, cardiac fibrosis, overt O(2)(-) production, and apoptosis accompanied with increased phosphorylation of JNK and ASK-1, the effects were significantly attenuated or ablated by diallyl sulfide. Inhibitors of JNK and ASK-1 but not HO-1 inducer or iNOS inhibitor obliterated ethanol-induced cardiomyocyte contractile dysfunction, substantiating a role for JNK and ASK-1 signaling in ethanol-induced myocardial injury. Taken together, these findings suggest that ethanol metabolism through CYP2E1 may contribute to the pathogenesis of alcoholic cardiomyopathy including myocardial contractile dysfunction, oxidative stress and apoptosis, possibly through activation of JNK and ASK-1 signaling.