Encephalitis caused by Listeria monocytogenes in a healthy adult male in China: A case report.

RATIONALE: Listeria monocytogenes rarely affects immunocompetent adults, and only a few cases of encephalitis caused by L monocytogenes in humans have been reported in China. PATIENT CONCERNS: A 37-year-old male patient presented with headache and fever of 38°C to 39°C for 2 days and dysphoria and dystrophy for 1 day. DIAGNOSIS: The patient was diagnosed as having encephalitis, and his cerebrospinal fluid (CSF) and blood cultures tested positive for L monocytogenes. INTERVENTIONS: The patient was treated with intravenous vancomycin, meropenem, mannitol, methylprednisolone, and enteral nutrition. The computed tomography (CT) scan showed swelling of the brain and hydrocephalus. The patient was treated with emergent surgery, a ventricular drainage tube was inserted, and the CSF was drained daily. OUTCOMES: Despite adequate therapy, the illness was severe and progressed rapidly. The patient died 2 weeks after admission. LESSONS: We report a rare case of L monocytogenes encephalitis in a previously healthy immunocompetent adult in China. The patient's CT scans showed increasing brain swelling and hydrocephalus, and the patient's condition progressively deteriorated.

The value of high-flow nasal cannula oxygen therapy after extubation in patients with acute respiratory failure

OBJECTIVE: To investigate the value of high-flow nasal cannula oxygen therapy after extubation in patients with acute respiratory failure. METHODS: A single-center, prospective, randomized, controlled pilot trial was conducted between January 2013 and December 2014. Sixty enrolled patients were randomized immediately after extubation into either a high-flow nasal cannula group (n=30) or an air entrainment mask group (n=30) at a fixed inspired oxygen fraction (40%). The success rate of oxygen therapy, respiratory and hemodynamic parameters and subjective discomfort (using a visual analogue scale) were assessed at 24h after extubation. RESULTS: The two groups were comparable at extubation. A total of 46 patients were successfully treated including 27 patients in the high-flow nasal cannula group and 19 patients in the air entrainment mask group. Compared to the air entrainment mask group, the success rate of oxygen therapy and the partial pressure of arterial oxygen were significantly higher and the respiratory rate was lower in the high-flow nasal cannula group. In addition, less discomfort related to interface displacement and airway dryness was observed in the high-flow nasal cannula group than in the air entrainment mask group. CONCLUSIONS: At a fixed inspired oxygen fraction, the application of a high-flow nasal cannula after extubation achieves a higher success rate of oxygen therapy and less discomfort at 24h than an air entrainment mask in patients with acute respiratory failure.

Melatonin Attenuates Pain Hypersensitivity and Decreases Astrocyte-Mediated Spinal Neuroinflammation in a Rat Model of Oxaliplatin-Induced Pain.

Neuroinflammatory response in spinal dorsal horn has been demonstrated to be a critical factor in oxaliplatin-induced pain. Melatonin has been shown to have anti-inflammatory and anti-allodynia effects in both preclinical and clinical studies. In the present study, we investigated the role of systemic administration of melatonin on oxaliplatin-induced pain. Intraperitoneal (i.p.) injection with oxaliplatin induced significantly mechanical allodynia and thermal hyperalgesia. Melatonin (i.p.) significantly alleviated mechanical allodynia and thermal hyperalgesia in the oxaliplatin but not sham-treated rats. The attenuation of nociceptive response persisted at least to 3 days after melatonin injection, throughout the entire observing window. Immunohistochemistry showed that oxaliplatin induced a significant increase of glial fibrillary acidic protein (GFAP) immunodensities, which could be suppressed by melatonin. Western blotting showed that GFAP protein levels were significantly elevated in the oxaliplatin-vehicle group. Melatonin significantly decreased oxaliplatin-induced upregulation of GFAP expressions. Oxaliplatin injection also enhanced the messenger RNA (mRNA) expressions of cytokines including interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α) and chemokines including monocyte chemoattractant protein-1 (MCP-1) and monocyte inflammatory protein-1 (MIP-1α) in the spinal dorsal horn, which could be significantly repressed by melatonin. In vitro study showed that mRNA levels of TNF-α, IL-1ß, MCP-1, and MIP-1α in primarily astrocytes were significantly increased after lipopolysaccharide (LPS, 1 µg/ml) stimulation. Melatonin (10 and 100 µM) greatly inhibited synthesis of these inflammatory mediators, in a dose-related manner. Conclusively, our data provide a novel implication of anti-nociceptive mechanism of melatonin in chemotherapy-related pain.

Association between SOD2 C47T polymorphism and lung cancer susceptibility: a meta-analysis.

Lung cancer is one of the most common cancers worldwide, but its etiology is still unclear. Superoxide dismutase 2 (SOD2) plays an essential role in oxidative stress and may be involved in the development of lung cancer. The association between SOD2 C47T polymorphism and lung cancer risk has been widely investigated, but the results of previous studies are contradictory. We conducted a meta-analysis to comprehensively assess the association between SOD2 C47T polymorphism and lung cancer. The association was estimated by odds ratio (OR) with 95 % confidence interval (95 % CI). A total of 10 studies with 5,146 cases and 6,173 controls were identified. The results showed that SOD2 C47T polymorphism was significantly associated with lung cancer (T versus C: OR = 0.88, 95 % CI = 0.83-0.93, P < 0.001; TT versus CC: OR = 0.74, 95 % CI = 0.66-0.83, P < 0.001; TT versus CC/CT: OR = 0.81, 95 % CI = 0.73-0.89, P < 0.001). Subgroup analysis by ethnicity suggested that SOD2 C47T polymorphism was significantly associated with lung cancer in both East Asians and Caucasians. Conclusively, this meta-analysis strongly suggests that SOD2 C47T polymorphism is significantly associated with lung cancer.

Effect of 5- AZn-2 '-deoxycytidine on proliferation of human lung adenocarcinoma cell line A549 in vitro.

OBJECTIVE: To explore effect of 5-AZn-2 '-deoxycytidine on proliferation of human lung adenocarcinoma cell line A549 in vitro. METHODS: Superoxide dismutase (SOD) activity was measured by hydroxylamine colorimetric method. Inhibition effect of 5-AZn-2' deoxycytidylic acid at different concentration and different time on growth of A549 cell was determined by MTT assay. Methylene dioxyamphetamine (MDA) was measured by thiobarbituric acid colorimetric method. Effect of 5-AZn-2' deoxycytidylic acid on apoptosis of A549 cell was determined by Hoechst 33258 dyeing detection. RESULTS: 5-AZn-2' deoxycytidylic acid had significant inhibition effect on proliferation of A549 cells in vitro, and the inhibition was notably dependent on time and dosage during 48-72 h; SOD level was significantly lower than those of control group (P<0.05, P<0.01), MDA level was significantly higher than those in the control group (P<0.05, P<0.01). A549 cells began to be in apoptosis after using 5-AZn-2'deoxycytidylic acid. CONCLUSIONS: 5- AZn-2' deoxycytidylic acid has significant inhibition effect on growth of A549 cell, and can lead the change of lipid peroxidation. It indicates that the mechanism has relationship with A549 cell cycle tissue and induction factor of apoptosis.

The disturbance of hippocampal CaMKII/PKA/PKC phosphorylation in early experimental diabetes mellitus.

BACKGROUND: Defining the impact of diabetes and related risk factors on brain cognitive function is critically important for patients with diabetes. AIMS: To investigate the alterations in hippocampal serine/threonine kinases signaling in the early phase of type 1 and type 2 diabetic rats. METHODS: Early experimental diabetes mellitus was induced in rats with streptozotocin or streptozotocin/high fat. Changes in the phosphorylation of proteins were determined by immunoblotting and immunohistochemistry. RESULTS: Our data showed a pronounced decrease in the phosphorylation of Ca(2+) /calmodulin-dependent protein kinase II (CaMKII) in the hippocampi of both type 1 and type 2 diabetic rats compared with age-matched control rats. Unexpectedly, we found a significant increase in the phosphorylation of synapsin I (Ser 603) and GluR1 (Ser 831) in the same experiment. In addition, aberrant changes in hippocampal protein kinase C (PKC) and protein kinase A (PKA) signaling in type 1 and type 2 diabetic rats were also found. Moreover, PP1α and PP2A protein levels were decreased in the hippocampus of type 1 diabetic rats, but significantly up-regulated in type 2 diabetic rats. CONCLUSIONS: The disturbance of CaMKII/PKA/PKC phosphorylation in the hippocampus is an early change that may be associated with the development and progression of diabetes-related cognitive dysfunction.

Myosin light chain kinase is necessary for tonic airway smooth muscle contraction.

Different interacting signaling modules involving Ca(2+)/calmodulin-dependent myosin light chain kinase, Ca(2+)-independent regulatory light chain phosphorylation, myosin phosphatase inhibition, and actin filament-based proteins are proposed as specific cellular mechanisms involved in the regulation of smooth muscle contraction. However, the relative importance of specific modules is not well defined. By using tamoxifen-activated and smooth muscle-specific knock-out of myosin light chain kinase in mice, we analyzed its role in tonic airway smooth muscle contraction. Knock-out of the kinase in both tracheal and bronchial smooth muscle significantly reduced contraction and myosin phosphorylation responses to K(+)-depolarization and acetylcholine. Kinase-deficient mice lacked bronchial constrictions in normal and asthmatic airways, whereas the asthmatic inflammation response was not affected. These results indicate that myosin light chain kinase acts as a central participant in the contractile signaling module of tonic smooth muscle. Importantly, contractile airway smooth muscles are necessary for physiological and asthmatic airway resistance.

CCR3 monoclonal antibody inhibits airway eosinophilic inflammation and mucus overproduction in a mouse model of asthma.

AIM: To explore the effect of a rat anti-mouse CC-chemokine receptor-3 (CCR3) monoclonal antibody (CCR3 mAb) on airway eosinophilia and mucus overproduction in asthmatic mice. METHODS: An asthma model was sensitized and challenged by ovalbumin (OVA) in male C57BL/6 mice. Asthmatic mice were given dual administration (intraperitoneal injection and aerosol inhalation) of CCR3 mAb or nonspecific rat IgG (ns-IgG). The number of total and differential inflammatory cells in the bronchial alveolar lavage fluid (BALF) was counted. Eosinophils number, the goblet cell percentage (GCP) and airway mucus index (AMI) were measured in the lung tissues. Interleukin (IL)-5 levels in the BALF were examined. The expression of MUC5AC and the epidermal growth factor receptor (EGFR) mRNA in the lung tissues was detected by semi-quantitative RT-PCR. The results were compared among the groups. RESULTS: CCR3 mAb significantly suppressed the increased eosinophils in the BALF and lung tissues in OVA-challenged mice compared with ns-IgG-treated mice. IL-5 levels in the BALF in CCR3 mAb and ns-IgG administration mice exhibited no obvious changes relative to OVA-challenged asthmatic mice. CCR3 mAb reduced the increased GCP and AMI after OVA challenge and decreased the enhanced expression of MUC5AC and EGFR mRNA in lung tissues in asthmatic animals. CONCLUSION: CCR3 mAb can significantly inhibit airway eosinophilia and mucus overproduction in asthmatic mice. Blockage of CCR3 may represent a new strategy to asthma therapy.