Combination of Dexmedetomidine and Ketamine for Magnetic Resonance Imaging Sedation

Objectives: The use of dexmedetomidine and ketamine (DEX–KET) combination for magnetic resonance imaging (MRI) sedation has not been evaluated. We investigated the efficacy and safety of DEX–KET for sedation of patients undergoing MRI of the brain.Methods: This quasi-experimental study was conducted to compare the DEX–KET combination and midazolam for MRI sedation. We included 72 patients undergoing brain MRI following bolus injection of midazolam or DEX–KET. In August 1, 2016 a new MRI sedation protocol was implemented. After protocol implementation, bolus doses of DEX–KET were administered (DEX–KET group). Thirty-six patients from the MIDA group and 36 patients from the DEX–KET group underwent MRI sequences and were compared regarding the MRI scan time and sedation-related complications (desaturation, hypotension, cardiorespiratory arrest, and aspiration pneumonia).Results: All MRI sequences were completed for 30 patients (83.3%) from the MIDA group and for 33 patients (91.7%) from the DEX–KET group (P = 0.476). The median MRI scan time was 100.0 min (interquartile range, 87.0–111.5 min) in the MIDA group and 53.5 min (interquartile range, 45.0–60.5 min) in the DEX–KET group (P < 0.001). Complications occurred in 24 (66.7%) and 8 (22.2%) patients of the MIDA and DEX–KET group, respectively (P < 0.001).Conclusions: The efficacy of DEX–KET sedation was comparable to that of midazolam for MRI examination. DEX–KET was related to shorter scan time and lower occurrence of complications compared to midazolam

Brain Microglial Activation in Chronic Pain-Associated Affective Disorder

A growing body of evidence from both clinical and animal studies indicates that chronic neuropathic pain is associated with comorbid affective disorders. Spinal cord microglial activation is involved in nerve injury-induced pain hypersensitivity characterizing neuropathic pain. However, there is a lack of thorough assessments of microglial activation in the brain after nerve injury. In the present study, we characterized microglial activation in brain sub-regions of CX3CR1GFP/+ mice after chronic constriction injury (CCI) of the sciatic nerve, including observations at delayed time points when affective brain dysfunctions such as depressive-like behaviors typically develop. Mice manifested chronic mechanical hypersensitivity immediately after CCI and developed depressive-like behaviors 8 weeks post-injury. Concurrently, significant increases of soma size and microglial cell number were observed in the medial prefrontal cortex (mPFC), hippocampus, and amygdala 8 weeks post-injury. Transcripts of CD11b, and TNF-α, genes associated with microglial activation or depressive-like behaviors, are correspondingly upregulated in these brain areas. Our results demonstrate that microglia are activated in specific brain sub-regions after CCI at delayed time points and imply that brain microglial activation plays a role in chronic pain-associated affective disorders

Cyclooxygenase-2 and p53 Expression as Prognostic Indicators in Conventional Renal Cell Carcinoma

The aim of this study was to investigate the relationship of cyclooxygenase (COX)-2 and p53 expression with prognosis in patients with conventional renal cell carcinoma (RCC). Formalin-fixed, paraffin-embedded tissue sections of conventional RCC from 92 patients, who had undergone radical nephrectomy, were examined for COX-2 and p53 expression by immunohistochemistry and compared with clinicopathological variables. The COX-2 expression significantly correlated only with tumor size (p=0.049), whereas the p53 expression profoundly correlated with the TNM stage (p=0.024), M stage (p=0.001), and metastasis (synchronous or metachronous; p=0.004). The COX-2 overexpression did not significantly associate with p53 positivity (p=0.821). The survival rate of patients correlated with the p53 expression (p<0.0001) but not with the COX-2 expression (p=0.7506). Multivariate analyses indicated that tumor size, M stage, and p53 expression were independent prognostic factors for cancer-specific survival. The COX-2 expression was not an independent factor. These results show that the increased expression of p53 was associated with metastasis and a worse prognosis in conventional RCC, which suggests that p53 might have played an important role in the progression of conventional RCC. The increased expression of COX-2 was associated only with tumor size, but may not be an important prognostic factor in conventional RCC. No association was observed between COX-2 overexpression and p53 positivity in conventional RCC

Triaging deep vein thrombosis using ultrasonography after lower-extremity orthopedic surgery: analysis of a single-center experience

Purpose This study aimed to stratify risk factors and vein levels for postoperative deep vein thrombosis (DVT) after lower-extremity orthopedic surgery. Methods Ninety-nine patients who underwent Doppler ultrasonography after lower-extremity orthopedic surgery were enrolled. Medical records were reviewed for anesthesia duration, type of surgery, body weight, height, and cardiovascular risk factors (including history of smoking, diabetes mellitus or hypertension, blood pressure, and total cholesterol and high-density lipoprotein [HDL] cholesterol levels), and the DVT treatment. Ultrasound diagnosis of DVT was made according to a routine protocol. The relationships between selected factors and the presence of DVT were assessed using univariate and multivariate regression analyses. Results Thirty-three (33%) patients were found to have calf DVT. The mean age, weight, and height of the non-DVT and postoperative DVT patients were 55.1 years versus 65.4 years, 70.5 kg versus 61.2 kg, and 163.3 cm versus 157.0 cm, respectively. Total cholesterol/HDL levels in the non-DVT and DVT patients were 70.6/20.7 mg/dL and 90.8/26.0 mg/dL, retrospectively. Systolic and diastolic blood pressure in the non-DVT and DVT patients were 133.6/80.2 mm Hg and 132.2/78.1 mmHg, respectively. The mean duration of anesthesia was 173.9 versus 199.9 minutes, and the operative time was 136.4 minutes versus 161.0 minutes. Older age (P=0.005) and lower body weight (P=0.002) were significantly associated with postoperative DVT. No other significant between-group differences were found (P>0.05). The patients with ultrasound-identified DVT received antithrombotic treatment. None of them had distant thromboembolism. Conclusion After lower-extremity orthopedic surgery, the calf veins in elderly patients with low body weight are susceptible to thrombosis; they would most likely benefit from postoperative ultrasonography

Robot-assisted distal gastrectomy for gastric cancer in a situs inversus totalis patient

A 47-year-old man was referred to Seoul National University Bundang Hospital with an ulcerative lesion in the midbody of the stomach. Computed tomography revealed that he was a situs inversus totalis (SIT) patient. Robot-assisted distal gastrectomy with D1+β lymph node dissection and Billroth II anastomosis were performed. With the aid of robotic surgery, the surgeon didn't need to change his position and could perform the surgery without any confusion resulting from the patient's reversed anatomy. The operation took 300 minutes, with no intraoperative complications. The postoperative course was uneventful, and the patient was discharged on postoperative day 8. The final pathologic report was pT3N3a by American Joint Committee on Cancer 7th tumor-node-metastasis staging. We successfully performed robot-assisted distal gastrectomy for gastric cancer in a SIT patient. We believe that this is the first case of robotic surgery reported in a SIT patient with gastric cancer

Clinical outcomes of spontaneous bacterial peritonitis due to extended-spectrum beta-lactamase-producing Escherichia coli and Klebsiella species: A retrospective matched case-control study

<p>Abstract</p> <p>Background</p> <p>Clinical outcomes of spontaneous bacterial peritonitis (SBP) due to extended-spectrum β-lactamase-producing <it>Escherichia coli </it>and <it>Klebsiella </it>species (ESBL-EK) have not been adequately investigated.</p> <p>Methods</p> <p>We conducted a retrospective matched case-control study to evaluate the outcomes of SBP due to ESBL-EK compared with those due to non-ESBL-EK. Cases were defined as patients with liver cirrhosis and SBP due to ESBL-EK isolated from ascites. Control patients with liver cirrhosis and SBP due to non-ESBL-EK were matched in a 3:1 ratio to cases according to the following five variables: age (± 5 years); gender; species of infecting organism; Child-Pugh score (± 2); Acute Physiological and Chronic Health Evaluation II score (± 2). 'Effective initial therapy' was defined as less than 72 hours elapsing between the time of obtaining a sample for culture and the start of treatment with an antimicrobial agent to which the EK was susceptible. Cephalosporin use for ESBL-EK was considered 'ineffective', irrespective of the minimum inhibitory concentration. ESBL production was determined according to the Clinical and Laboratory Standards Institute guidelines on stored isolates.</p> <p>Results</p> <p>Of 1026 episodes of SBP in 958 patients from Jan 2000 through Dec 2006, 368 (35.9%) episodes in 346 patients were caused by SBP due to EK, isolated from ascites. Of these 346 patients, twenty-six (7.5%) patients with SBP due to ESBL-EK were compared with 78 matched controls. Treatment failure, evaluated at 72 hours after initial antimicrobial therapy, was greater among the cases (15/26, 58% <it>vs</it>. 10/78, 13%, <it>P </it>= .006); 30-day mortality rate was also higher than in the controls (12/26, 46% <it>vs</it>. 11/78, 15%, <it>P </it>= .001). When the case were classified according to the effectiveness of the initial therapy, 'ineffective initial therapy' was associated with higher 30-day mortality rate (11/18, 61% <it>vs</it>. 1/8, 13%, <it>P </it>= .036).</p> <p>Conclusion</p> <p>SBP due to ESBL-EK had poorer outcomes than SBP due to non-ESBL-EK. Ineffective initial therapy seems to be responsible for the higher rate of treatment failure and mortality in SBP due to ESBL-EK.</p

Anti-apoptotic effects of human placental hydrolysate against hepatocyte toxicity in vivo and in vitro

Apoptosis and oxidative stress are essential for the pathogenesis of acute liver failure and fulminant hepatic failure. Human placental hydrolysate (hPH) has been reported to possess antioxidant and anti-inflammatory properties. In the present study, the protective effects of hPH against D-galactosamine (D-GalN)- and lipopolysaccharide (LPS)-induced hepatocyte apoptosis were investigated in vivo. In addition, the molecular mechanisms underlying the anti-apoptotic activities of hPH against D-GalN-induced cell death in vitro were examined. Male Sprague-D awley rats were injected with D-GaIN/LPS with or without the administration of hPH. Rats were sacrificed 24 h after D-GaIN/LPS intraperitoneal injection, and the blood and liver samples were collected for future inflammation and hepatotoxicity analyses. Changes in cell viability, apoptosis protein expression, mitochondrial mass, mitochondrial membrane potential, reactive oxygen species generation, and the levels of proteins and mRNA associated with a protective mechanism were determined in HepG2 cells pretreated with hPH for 2 h prior to D-GalN exposure. The findings suggested that hPH treatment effectively protected against D-GalN/LPS-induced hepatocyte apoptosis by reducing the levels of alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase, interleukin-6, and tumor necrosis factor-α, and increasing the level of proliferating cell nuclear antigen. It was also found that hPH inhibited the apoptotic cell death induced by D-GalN. hPH activated the expression of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, and catalase, which were further upregulated by the Kelch-like ECH2-associated protein 1-p62-nuclear factor-erythroid 2-related factor 2 pathway, a component of oxidative stress defense mechanisms. Furthermore, hPH markedly reduced cytosolic and mitochondrial reactive oxygen species and rescued mitochondrial loss and dysfunction through the reduction of damage-regulated autophagy modulator, p53, and C/EBP homologous protein. Collectively, hPH exhibited a protective role in hepatocyte apoptosis by inhibiting oxidative stress and maintaining cell homeostasis. The underlying mechanisms may be associated with the inhibition of endoplasmic reticulum stress and minimization of the autophagy progress