Modulation of inflammatory responses after global ischemia by transplanted umbilical cord matrix stem cells.

Rat umbilical cord matrix (RUCM) cells are stem-cell-like cells and have been shown to reduce neuronal loss in the selectively vulnerable brain regions after cardiac arrest (CA). Here, we investigate whether this protection is mediated by the RUCM cells' modulation of the postischemia inflammation responses, which have long been implicated as a secondary mechanism of injury following ischemia. Brain sections were examined immunohistochemically for glial fibrillary acidic protein (GFAP), vimentin, and nestin as markers for astroglia and reactive astrogliosis, Ricinus Communis Agglutinin-1 (RCA-1) as a marker for microglia, and Ki67 as a marker for cell proliferation. Rats were randomly assigned to six experimental groups: (1) 8-minute CA without treatment, (2) 8-minute CA pre-treated with culture medium injection, (3) 8-minute CA pre-treated with RUCM cells, (4) sham-operated CA, (5) medium injection without CA, and (6) RUCM cell transplantation without CA. Groups 1-3 have significantly higher Ki67(+) cell counts and higher GFAP(+) immunoreactivity in the hippocampal Cornu Ammonis layer 1 (CA1) region compared to groups 4-6, irrespective of treatment. Groups 1 and 2 have highly elevated GFAP(+), vimentin(+), and nestin(+) immunoreactivity, indicating reactive astrogliosis. Strikingly, RUCM cell treatment nearly completely inhibited the appearance of vimentin(+) and greatly reduced nestin(+) reactive astrocytes. RUCM cell treatment also greatly reduced RCA-1 staining, which is found to strongly correlate with the neuronal loss in the CA1 region. Our study indicates that treatment with stem-cell-like RUCM cells modulates the inflammatory response to global ischemia and renders neuronal protection by preventing permanent damage to the selectively vulnerable astrocytes in the CA1 region. Disclosure of potential conflicts of interest is found at the end of this article.

[Combined use of the airway scope and fiberoptic bronchoscopy for tracheal intubation in a patient with a large epiglottic cyst].

A 26-year-old man was scheduled for surgical extraction of a large epiglottic cyst. Mask ventilation was possible under propofol anesthesia without muscle relaxant. It was difficult to see the glottis using either a Macintosh laryngoscope or by fiberoptic bronchoscopy. When the AWS laryngoscope (Hoya, Tokyo Japan) with a part of the blade removed, was inserted orally, it became possible to see the glottis with a part of the epiglottic cyst. A reinforced tube was inserted nasally, and a fiberoptic bronchoscope was passed through the tube into the trachea. The tube was then passed over the fiberscope into the trachea. We believe that the Pentax AWS laryngoscope may lift the epiglottis and its cyst atraumatically, and may facilitate nasal fiberoptic intubation in a patient with a large epiglottic cyst.

Impact of hydroxyethyl starch 70/0.5 on acute kidney injury after gastroenterological surgery.

BACKGROUND: Previous studies reported a higher mortality risk and a greater need for renal replacement therapy in patients administered hydroxyethyl starch (HES) rather than other fluid resuscitation preparations. In this study, we investigated the association between 6% HES 70/0.5 use and postoperative acute kidney injury (AKI) in gastroenterological surgery patients. METHODS: We conducted retrospective full-cohort and propensity-score-based analyses of patients who underwent gastroenterological surgery between June 2011 and August 2013 in a Japanese university hospital. The study sample comprised 66 AKI and 2,152 non-AKI patients in the full-cohort analysis and 35 AKI and 1,269 non-AKI patients in the propensity-score-based analysis. Propensity scores were calculated using an ordered logistic regression model in which the dependent variable comprised three groups based on HES infusion volumes (0, 1-999, and ≥ 1,000 ml). The association between HES groups and postoperative AKI incidence was analyzed using multiple logistic regression models. Other candidate independent variables included patient characteristics and intraoperative measures. RESULTS: In the full-cohort analysis, 40 (60.6%) AKI patients were diagnosed as "risk", 15 (22.7%) as "injury," and 11 (16.7%) as "failure". In the propensity-score-based analysis, the corresponding values were 22 (62.9%), 8 (22.9%), and 5 (14.3%). There was no significant association between total infused HES and postoperative AKI incidence in either the full-cohort or the propensity-score-based analysis (P = 0.168 and P = 0.42, respectively). CONCLUSIONS: AKI incidence was not associated with clinical 6% HES 70/0.5 administration in gastroenterological surgery patients treated at a single center.

[Anesthesia for cesarean section in a patient with cor triatriatum].

Cor triatriatum is a rare congenital cardiac anomaly, in which left ventricular filling is impeded by obstructive membrane in the left atrium. We administered spinal anesthesia for cesarean section in a patient with cor triatriatum (type III A1) with congestive heart failure. We optimized hemodynamics with the aid of pulmonary artery cathter. In general, cor triatriatum involves similar hemodynamic profiles to mitral stenosis and thus tachycardia should be avoided during anesthesia. However, in our patient, increasing the heart rate to 80-90 beats x min(-1) was beneficial in maintaining adequate systemic blood pressure and cardiac output. Spinal anesthesia could be a method of choice for cesarean section in a patient with cor triatriatum when adequate hemodynamic monitoring is available.

Edaravone, a free radical scavenger, mitigates both gray and white matter damages after global cerebral ischemia in rats.

Recent studies have shown that similar to cerebral gray matter (mainly composed of neuronal perikarya), white matter (composed of axons and glias) is vulnerable to ischemia. Edaravone, a free radical scavenger, has neuroprotective effects against focal cerebral ischemia even in humans. In this study, we investigated the time course and the severity of both gray and white matter damage following global cerebral ischemia by cardiac arrest, and examined whether edaravone protected the gray and the white matter. Male Sprague-Dawley rats were used. Global cerebral ischemia was induced by 5 min of cardiac arrest and resuscitation (CAR). Edaravone, 3 mg/kg, was administered intravenously either immediately or 60 min after CAR. The morphological damage was assessed by cresyl violet staining. The microtubule-associated protein 2 (a maker of neuronal perikarya and dendrites), the beta amyloid precursor protein (the accumulation of which is a maker of axonal damage), and the ionized calcium binding adaptor molecule 1 (a marker of microglia) were stained for immunohistochemical analysis. Significant neuronal perikaryal damage and marked microglial activation were observed in the hippocampal CA1 region with little axonal damage one week after CAR. Two weeks after CAR, the perikaryal damage and microglial activation were unchanged, but obvious axonal damage occurred. Administration of edaravone 60 min after CAR significantly mitigated the perikaryal damage, the axonal damage, and the microglial activation. Our results show that axonal damage develops slower than perikaryal damage and that edaravone can protect both gray and white matter after CAR in rats.

Potential treatment of cerebral global ischemia with Oct-4+ umbilical cord matrix cells.

Potential therapeutic effects of Oct-4-positive rat umbilical cord matrix (RUCM) cells in treating cerebral global ischemia were evaluated using a reproducible model of cardiac arrest (CA) and resuscitation in rats. Animals were randomly assigned to four groups: A, sham-operated; B, 8-minute CA without pretreatment; C, 8-minute CA pretreated with defined media; and D, 8-minute CA pretreated with Oct-4(+) RUCM cells. Pretreatment was done 3 days before CA by 2.5-microl microinjection of defined media or approximately 10(4) Oct-4(+) RUCM cells in left thalamic nucleus, hippocampus, corpus callosum, and cortex. Damage was assessed histologically 7 days after CA and was quantified by the percentage of injured neurons in hippocampal CA1 regions. Little damage (approximately 3%-4%) was found in the sham group, whereas 50%-68% CA1 pyramidal neurons were injured in groups B and C. Pretreatment with Oct-4(+) RUCM cells significantly (p < .001) reduced neuronal loss to 25%-32%. Although the transplanted cells were found to have survived in the brain with significant migration, few were found directly in CA1. Therefore, transdifferentiation and fusion with host cells cannot be the predominant mechanisms for the observed protection. The Oct-4(+) RUCM cells might repair nonfocal tissue damage by an extracellular signaling mechanism. Treating cerebral global ischemia with umbilical cord matrix cells seems promising and worthy of further investigation.