Tetanus Overlooked Due to the Involvement of Multiple Departments: A Case Report.

Tetanus is a fatal disease caused by a neurotoxin produced by the biotrophic anaerobic bacterium Clostridium tetani, which causes muscle hypertonia and autonomic neuropathy. The diagnosis is based on clinical findings and not the result of specific blood and imaging tests; hence, it is very difficult to diagnose at first sight, despite typical initial findings such as lockjaw, muscle spasms, and neck pain and stiffness. This article discusses the case of a 79-year-old woman who first consulted her local doctor because of a lack of jaw opening. Seeing no improvement, she visited our hospital and was suspected of having tetanus after consulting with nine different departments over seven days from the initial visit. In developed countries, tetanus prevalence has declined due to immunization, leading to clinicians' lack of experience in diagnosing it. Furthermore, the increasing specialization in general hospitals poses a risk of missing a tetanus diagnosis when a patient consults multiple departments.

Insulin and glucose infusion could prevent euglycemic diabetic ketoacidosis associated with sodium-glucose cotransporter 2 inhibitors.

Perioperative euglycemic diabetic ketoacidosis (euDKA) is a serious adverse effect of sodium-glucose cotransporter 2 inhibitor (SGLT2i) treatment. We observed perioperative euDKA immediately after discontinuing insulin infusion that was started during surgery in a patient with type 2 diabetes mellitus (T2DM) for whom empagliflozin could not be withdrawn before emergency off-pump coronary artery bypass grafting (OPCAB). Insulin infusion that was started during surgery unexpectedly prevented euDKA until its discontinuation. Therefore, we hypothesized that insulin and glucose infusion initiated at the start of emergency surgery in patients receiving SGLT2is prevents perioperative euDKA. We implemented this strategy during emergency OPCAB in another patient with T2DM who received empagliflozin 2 days before surgery and observed that the patient did not develop perioperative euDKA. With the increasing use of SGLT2is, surgeons may encounter more SGLT2i users who require emergency surgeries. The administration of insulin and glucose infusion in advance emergency surgery can prevent perioperative euDKA.

Flexional distance index: A new prognostic indicator of neurological outcomes at 4 years after cervical laminoplasty for K-line (+) ossification of the posterior longitudinal ligament.

OBJECTIVE: We aimed to investigate whether K-line in the neck flexion (FK-line), flexion angle (FA), or flexion distance index (FDI) could predict the recovery rate of the Japanese Orthopedic Association score (RR-JOA) at 4 years after cervical laminoplasty (LP) for ossification of the posterior longitudinal ligament (OPLL). METHODS: A new index, i.e., the FDI, which is based on the degree of neck flexion and the OPLL size on a lateral radiograph. "Flexional distance" is the distance from C2 to C7 in neck flexion, and "distance to OPLL" is the maximal distance from the line of the flexional distance to OPLL. FDI was defined as follows: FDI = flexional distance/distance to OPLL. Twenty-three patients with K-line (+) OPLL were evaluated at 4 years after LP (follow-up rate, 92%). We investigated the relationships between preoperative radiological factors, including FK-line, FA, and FDI, and RR-JOA at 4 years postoperatively. RESULTS: Preoperative FK-line and FA were significantly related with the RR-JOA at 1 year postoperatively, but not at 4 years postoperatively. Preoperative FDI was significantly positively correlated with the RR-JOA at 1 year and 4 years postoperatively (P = 0.0132, r = 0.504 and P = 0.0183, r = 0.484, respectively). Preoperative FDI < 2.5 was associated with worsening of the RR-JOA at 4 years postoperatively, with a probability of 80% DISCUSSIONS: FDI could predict the RR-JOA at 4 years after LP for OPLL. Decompression with fusion may be recommended for patients with preoperative FDI < 2.5. LEVEL OF EVIDENCE: 4.

Risk factors for delayed elimination of high-dose methotrexate in childhood acute lymphoblastic leukemia and lymphoma.

High-dose methotrexate (HD-MTX) therapy is widely used in patients with acute lymphoblastic leukemia (ALL) and lymphoma. However, some patients experience delayed MTX elimination, which requires treatment suspension or dose reduction to avoid organ damage. This single-center retrospective analysis reviewed the clinical data of 88 children with ALL or non-Hodgkin lymphoma who received a total of 269 courses of HD-MTX therapy between April 2008 and April 2019. HD-MTX was defined as MTX administration at 2.0, 3.0, or 5.0 g/m2 over a 24-h period, and delayed MTX elimination was defined as a serum MTX concentration ≥ 1.0 µmol/L at 48 h after the start of HD-MTX. Clinical factors were compared between courses with and without delayed MTX elimination. MTX elimination was delayed in 21 of the 269 courses (7.8%). Multivariate analysis showed that first HD-MTX course (OR 4.04), lower urine volume per BSA on the first day of HD-MTX administration (< 2,675 mL/m2, OR 5.10), higher total bilirubin (> 0.5 mg/dL, OR 5.11), lower eGFR (< 136 mL/min/1.73 m2, OR 3.90), higher dose of MTX(> 3.0 g/m2, OR 10.8), and lower urine volume per BSA on the next day of starting HD-MTX (< 2,107 mL/m2, OR 3.43) were independent risk factors for delayed MTX elimination.

Prenatal clinical manifestations in individuals with COL4A1/2 variants.

BACKGROUND: Variants in the type IV collagen gene (COL4A1/2) cause early-onset cerebrovascular diseases. Most individuals are diagnosed postnatally, and the prenatal features of individuals with COL4A1/2 variants remain unclear. METHODS: We examined COL4A1/2 in 218 individuals with suspected COL4A1/2-related brain defects. Among those arising from COL4A1/2 variants, we focused on individuals showing prenatal abnormal ultrasound findings and validated their prenatal and postnatal clinical features in detail. RESULTS: Pathogenic COL4A1/2 variants were detected in 56 individuals (n=56/218, 25.7%) showing porencephaly (n=29), schizencephaly (n=12) and others (n=15). Thirty-four variants occurred de novo (n=34/56, 60.7%). Foetal information was available in 47 of 56 individuals, 32 of whom (n=32/47, 68.1%) had one or more foetal abnormalities. The median gestational age at the detection of initial prenatal abnormal features was 31 weeks of gestation. Only 14 individuals had specific prenatal findings that were strongly suggestive of features associated with COL4A1/2 variants. Foetal ventriculomegaly was the most common initial feature (n=20/32, 62.5%). Posterior fossa abnormalities, including Dandy-Walker malformation, were observed prenatally in four individuals. Regarding extrabrain features, foetal growth restriction was present in 16 individuals, including eight individuals with comorbid ventriculomegaly. CONCLUSIONS: Prenatal observation of ventriculomegaly with comorbid foetal growth restriction should prompt a thorough ultrasound examination and COL4A1/2 gene testing should be considered when pathogenic variants are strongly suspected.

Efficacy of liposomal amphotericin against febrile neutropenia in pediatric patients receiving prophylactic voriconazole.

BACKGROUND: The risk factors for invasive fungal infection have gradually become evident for pediatric patients with hematological diseases. Here we analyze the efficacy of liposomal amphotericin (L-AMB) for pediatric patients with febrile neutropenia using prophylactic voriconazole (VRCZ). METHOD: We administered L-AMB (2.5 mg/kg/day) in patients with febrile neutropenia who were receiving prophylactic VRCZ (10 mg/kg/day, orally) and were resistant to second-line antibiotics therapy. Thirteen patients (5 males, 8 females) with 19 febrile neutropenia episodes were targeted in this analysis. The median age of the patients was 14 years (range, 1-19 years). Eighteen out of 19 episodes occurred in patients with acute myeloid leukemia, with the remaining episode occurring in a patient with acute unclassified leukemia. RESULTS: The median period from start of L-AMB administration to resolution of fever was 4 days (1-27 days). In 15 out of 19 episodes, fever resolved within 5 days from commencement of L-AMB administration. Using criteria proposed by T. J. Walsh et al., the success rate of L-AMB for febrile neutropenia was 89.5% in this study. CONCLUSIONS: Although the sample size of our study was small, the extremely high efficacy of L-AMB warrants its administration in patients with febrile neutropenia who are receiving VRCZ.

Severe sepsis caused by Parvimonas micra identified using 16S ribosomal RNA gene sequencing following patient death.

An 83-year-old man visited an orthopedic hospital for his lower back pain. A compression fracture was noted in his second lumbar vertebra. He had taken pain medication for approximately five weeks, but the pain had worsened and he was unable to walk by himself. He was transferred to our hospital and diagnosed with lumbar spondylodiscitis, an iliopsoas abscess, gas gangrene of his left lower limb, and left massive pleural effusion. He was admitted to the intensive care unit. We drained the abscess and pleural effusion, provided continuous hemodiafiltration under ventilator control, and administered intravenous antibiotics. However, he died from sepsis and multiple organ failure three days following admission. Several days after his death, gram-positive cocci were identified in blood culture, pus from the abscess, and pleural exudate; although the causative organism could not be identified. Two weeks subsequent to his death, 16S ribosomal RNA gene sequencing identified Parvimonas micra in specimens taken from his body.

Peripherally Inserted Central Venous Catheter for Pediatric and Young Adult Patients With Hematologic and Malignant Diseases.

BACKGROUND: Long-term venous access is essential when treating malignant diseases. As an alternative to conventional central venous catheters, peripherally inserted central venous catheter (PICC) are now widely used. The aim of this study is to evaluate the safety, efficacy, and reliability of PICCs in comparison with previous reports, and to describe significant complications associated with their use. PATIENTS AND METHODS: From June 2009 to November 2017, PICCs were inserted 258 times in a total of 160 pediatric and young adult patients at our institution. We retrospectively evaluated our data regarding catheter life, a note of caution during insertion, reasons for removal, infection, and other notable complications. RESULTS: The 258 PICCs were placed for a total of 30,901 catheter-days with a median catheter life of 102 days ranging from 2 to 471 days. The most suitable vein for the insertion was a basilic vein. The insertion depth from the cubital fossa to the point of the lower third superior vena cava was found to have a strong correlation with body surface area. Suspected catheter infection requiring catheter removal was observed 30 times (0.97/1000 catheter-days) and catheter-related bloodstream infection was observed 2 times (0.06/1000 catheter-days). All the responsible pathogens were Staphylococcus epidermidis. As notable complications, fibrin sheath formation were seen in 4 patients and catheter tip migration to the thorax in 1 patient. CONCLUSIONS: Our data suggest that PICC is safe and effective in pediatric and young adult patients receiving long-term treatment. However, clinicians should be aware of the possible complications during PICC use.

Pulmonary edema caused by inhalation of vapors from water-soluble paint.

AIM: To report the effects of inhaling vapor from water-soluble paint after a recent encounter with 16 patients treated in our emergency department. METHODS: We examined a series of chest computed tomography (CT) images from the 16 affected patients. Computed tomography was carried out on days 1, 2, 5, and 19 after the inhalation event. RESULTS: Twelve of the patients were found to have pulmonary edema, based on their CT findings. Patients with pulmonary edema were classified as its persisted period. In the severe group, its pulmonary edema persisted over 5 days include, exacerbated edema, delayed-onset edema (during the follow-up), or edema amelioration. One patient had exacerbated edema, three patients had delayed-onset edema, and one patient experienced amelioration of their edema in the severe group. In all cases, the pulmonary edema had disappeared from the CT images by day 19 after the inhalation event. Thirteen of the 16 patients had a fever of ≥37°C. Three kinds of solutes (ethylene glycol, titanium dioxide, and silicon oxide) had been blended in the water-soluble paint. The titanium dioxide was considered the probable cause of the pulmonary edema. CONCLUSION: Inhalation of vapors from water-soluble paints is considered relatively safe. However, our observations suggest that new lesions might develop and existing lesions could worsen, even if the edema is not severe immediately after the exposure. Thus, follow-up imaging is needed for approximately 2 weeks in such cases.

Accuracy of the smaller superior mesenteric vein sign for the detection of acute superior mesenteric artery occlusion.

Aims: The smaller superior mesenteric vein (SMV) sign is a well-known computed tomography (CT) parameter for acute superior mesenteric artery (SMA) occlusion. This CT sign is potentially beneficial for the early diagnosis of acute SMA occlusion; however, few reports have documented this sign. The present study aimed to determine the accuracy of the smaller SMV sign for the detection of acute SMA occlusion. Methods: We retrospectively reviewed CT images from 20 patients with acute SMA occlusion and 1,216 controls. We measured the external diameters of the SMV and SMA, and calculated the SMV/SMA diameter ratio. A ratio ≤1 indicated a positive smaller SMV sign. Results: Of the 20 patients, 14 had the smaller SMV sign, whereas of the 1,216 controls, 88 had the smaller SMV sign. Of the 88 controls with a positive sign, 79 had apparent reasons for the decreased flow in the SMA and nine patients had no reason for the decreased flow. The sensitivity and specificity of the smaller SMV sign for acute SMA occlusion were 70% and 99.2%, respectively. Conclusion: The smaller SMV sign is an accurate and important CT parameter for the detection of acute SMA occlusion.

A vascular anomaly of the iliac artery in a patient with VATER association.

In patients with VATER association, some have vascular anomaly that makes procedure difficult. Pretreatment CT angiography should be necessary for the patients with VATER association's feature.

Nicotiana benthamiana MAPK-WRKY pathway confers resistance to a necrotrophic pathogen Botrytis cinerea.

MEK2-SIPK/WIPK cascade, a Nicotiana benthamiana mitogen-activated protein kinase (MAPK) cascade, is an essential signaling pathway for plant immunity and involved in hypersensitive response (HR) accompanied by cell death. WRKY transcription factors as substrates of SIPK and WIPK have been isolated and implicated in HR cell death. Here, we show virus-induced gene silencing of WRKY genes compromised constitutively active MEK2-triggered cell death in N. benthamiana leaves. In general, HR cell death enhances susceptibility to necrotrophic pathogens such as Botrytis cinerea. However, the WRKY gene silencing elevated susceptibility to B. cinerea. These findings suggest that downstream WRKYs of MEK2-SIPK/WIPK cascade are required for cell death-dependent and -independent immunities in N. benthamiana.

WRKY Transcription Factors Phosphorylated by MAPK Regulate a Plant Immune NADPH Oxidase in Nicotiana benthamiana.

Pathogen attack sequentially confers pattern-triggered immunity (PTI) and effector-triggered immunity (ETI) after sensing of pathogen patterns and effectors by plant immune receptors, respectively. Reactive oxygen species (ROS) play pivotal roles in PTI and ETI as signaling molecules. Nicotiana benthamiana RBOHB, an NADPH oxidase, is responsible for both the transient PTI ROS burst and the robust ETI ROS burst. Here, we show that RBOHB transactivation mediated by MAPK contributes to R3a/AVR3a-triggered ETI (AVR3a-ETI) ROS burst. RBOHB is markedly induced during the ETI and INF1-triggered PTI (INF1-PTI), but not flg22-tiggered PTI (flg22-PTI). We found that the RBOHB promoter contains a functional W-box in the R3a/AVR3a and INF1 signal-responsive cis-element. Ectopic expression of four phospho-mimicking mutants of WRKY transcription factors, which are MAPK substrates, induced RBOHB, and yeast one-hybrid analysis indicated that these mutants bind to the cis-element. Chromatin immunoprecipitation assays indicated direct binding of the WRKY to the cis-element in plants. Silencing of multiple WRKY genes compromised the upregulation of RBOHB, resulting in impairment of AVR3a-ETI and INF1-PTI ROS bursts, but not the flg22-PTI ROS burst. These results suggest that the MAPK-WRKY pathway is required for AVR3a-ETI and INF1-PTI ROS bursts by activation of RBOHB.

SK2 channels are neuroprotective for ischemia-induced neuronal cell death.

In mouse hippocampal CA1 pyramidal neurons, the activity of synaptic small-conductance Ca(2+)-activated K(+) channels type 2 (SK2 channels) provides a negative feedback on N-methyl-D-aspartate receptors (NMDARs), reestablishing Mg(2+) block that reduces Ca(2+) influx. The well-established role of NMDARs in ischemia-induced excitotoxicity led us to test the neuroprotective effect of modulating SK2 channel activity following cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR). Administration of the SK channel positive modulator, 1-ethyl-benzimidazolinone (1-EBIO), significantly reduced CA1 neuron cell death and improved CA/CPR-induced cognitive outcome. Electrophysiological recordings showed that CA/CPR-induced ischemia caused delayed and sustained reduction of synaptic SK channel activity, and immunoelectron microscopy showed that this is associated with internalization of synaptic SK2 channels, which was prevented by 1-EBIO treatment. These results suggest that increasing SK2 channel activity, or preventing ischemia-induced loss of synaptic SK2 channels, are promising and novel approaches to neuroprotection following cerebral ischemia.

[Two cases of preceded aortic valve replacement for severe aortic stenosis before the cancer operations].

We report two cases of aortic valve replacement (AVR) for severe aortic stenosis (AS) before the cancer operations. Severe AS poses a great risk for noncardiac surgery. In the ACC/AHA 2007 Guideline on Perioperative Cardiovascular Evaluation and Care for Noncardiac Surgery, if the AS is symptomatic, elective noncardiac surgery should generally be postponed or canceled. Such patients require AVR before elective noncardiac surgery. On the other hand, in patients with severe AS who refuse cardiac surgery, noncardiac surgery can be performed with a mortality risk of approximately 10%. In our cases, severe AS was found in the preoperative examination. We informed them about necessary AVR before noncardiac surgery, and patients consented to our suggestion. AVR was performed around 7 days after this consent, and cancer operation was performed around 30 days after the AVR. However, there are no clear guidelines for this interval between AVR and cancer operation. In our cases the patients underwent the cardiac surgery and noncardiac surgery in a short period without serious complication in the perioperative management. It is very important to discuss among surgeon, cardiovascular surgeon, cardiologist and anesthesiologist. Especially anesthesiologist should take an important role in organizing these departments for such patients.

Testosterone exacerbates neuronal damage following cardiac arrest and cardiopulmonary resuscitation in mouse.

Male animals exhibit greater neuronal damage following focal cerebral ischemic injury in many experimental injury models, however the mechanism of this is unknown. This study used cardiac arrest and cardiopulmonary resuscitation (CA/CPR) in male mice exposed to physiological vs. pharmacological doses of testosterone and tested the hypothesis that testosterone increases damage following global cerebral ischemia. Analysis of histological damage 72h after resuscitation revealed a complex dose-response curve for testosterone, such that low and high doses of testosterone exacerbated ischemic neuronal damage, while intermediate doses had no effect on neuronal survival. In agreement with these histological observations of neuronal damage, both low and high doses of testosterone increased sensorimotor deficit following CA/CPR compared to vehicle treated animals. Finally, the androgen receptor antagonist flutamide inhibited the increase in neuronal damage and sensorimotor impairment observed in testosterone treated mice. Our data showed that low and supra-physiological levels of testosterone increase neuronal damage following global cerebral ischemia and that blockade of androgen receptors limits this injury. Therefore, this study indicated that testosterone may have a role in determining sex-linked differences in cerebrovascular disease as well as having important health implications in clinical conditions of elevated testosterone.

Estrogen is renoprotective via a nonreceptor-dependent mechanism after cardiac arrest in vivo.

BACKGROUND: Severe ischemia induces renal injury less frequently in women than men. In this study, cardiac arrest and cardiopulmonary resuscitation were used to assess whether estradiol is renoprotective via an estrogen receptor (ER)-dependent mechanism. MATERIALS AND METHODS: Male and female C57BL/6 and ER gene-deleted mice underwent 10 min of cardiac arrest followed by cardiopulmonary resuscitation. Serum chemistries and renal stereology were measured 24 h after arrest. RESULTS: Estrogen did not affect mean arterial pressure, regional renal cortical blood flow, and arterial blood gases. Hence, female kidneys were protected (mean +/- SEM: blood urea nitrogen, 65+/- 21 vs.149+/- 27 mg/dl, P = 0.04; creatinine, 0.14 +/- 0.05 vs. 0.73 +/- 0.16 mg/dl, P = 0.01; volume of necrotic tubules, 7 +/- 1% vs. 10 +/- 0%, P = 0.04). Estrogen also reduced renal injury. In intact females (n = 5), ovariectomized/vehicle-treated (n = 8), and ovariectomized/estrogen-treated (n = 8) animals, blood urea nitrogen was 65 +/- 21, 166 +/- 28, and 50 +/- 14 mg/dl (P = 0.002); creatinine was 0.14 +/- 0.05, 0.74 +/- 0.26, and 0.23 +/- 0.27 mg/dl (P = 0.014); necrotic tubules were 2.5 +/- 0.25%, 12.0 +/- 1.9%, and 5.0 +/- 1.6% (P = 0.004), respectively. In ER-[alpha] and ER-[beta] gene-deleted mice and controls estradiol-reduced functional injury (blood urea nitrogen: estradiol 117 +/- 71, vehicle 167 +/- 56, P = 0.007; creatinine: estradiol 0.5 +/- 0.5, vehicle 1.0 +/- 0.4, P = 0.013), but the effect of estradiol was not different between ER-[alpha] or ER-[beta] gene-deleted mice. Adding ICI 182,780 to estradiol did not alter injury. CONCLUSIONS: In women, kidneys were protected from cardiac arrest through estrogen. Estradiol-mediated renoprotection was not affected by ER deletion or blockade. Estradiol is renoprotective after cardiac arrest. The results indicate that estradiol renoprotection is ER-[alpha] and ER-[beta] independent.

Dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic brain injury in rats.

PURPOSE: Dexmedetomidine has been used for purposes of anesthesia and sedation, and experimental studies have demonstrated its neuroprotective effects. However, it has also been shown that the constriction of cerebral vessels in response to high doses of dexmedetomidine decreases cerebral blood flow. We tested the hypothesis that dexmedetomidine-induced cerebral hypoperfusion exacerbates ischemic cerebral injury. METHODS: The effects of dexmedetomidine on cerebral blood flow and mean arterial blood pressure were studied first. Six rats received intravenous infusions of dexmedetomidine in doses ranging from 0.01 to 10 microg.kg(-1).min(-1). At the end of this phase of treatment, the alpha-2 adrenergic antagonist yohimbine was administered (3 mg.kg(-1) ip). Cerebral blood flow and mean arterial blood pressure were recorded continuously. A second series of experiments was then performed using a rat model of transient middle cerebral artery occlusion. Forty-two rats received 1microg.kg(-1).min(-1) or 10 microg.kg(-1).min(-1) dexmedetomidine with or without pretreatment with either of the alpha-2 adrenergic antagonists yohimbine or rauwolscine. Five days after middle cerebral artery occlusion and reperfusion, the rat brains were removed and the infarct volumes were measured. RESULTS: In the first protocol, increasing the dose of dexmedetomidine significantly decreased cerebral blood flow. Mean arterial blood pressure decreased to 79.9% relative to baseline with a dose of 0.01 microg.kg(-1).min(-1) dexmedetomidine, and increased to 119.9% relative to baseline with a dose of 10 microg.kg(-1).min(-1) dexmedetomidine. In the second protocol, the infarct volume in the control group was 9.5% of the total brain volume; the infarct volume increased to 11.3% in rats treated with 1 microg.kg(-1).min(-1) dexmedetomidine and the volume increased to 24.5% in rats treated with 10 microg.kg(-1).min(-1) dexmedetomidine. Pretreatment with an alpha-2 adrenergic antagonist, either yohimbine or rauwolscine, reduced the size of these high-dose dexmedetomidine-induced infarct volumes. CONCLUSION: Hypertension following the administration of high-dose dexmedetomidine is associated with cerebral hypoperfusion and the exacerbation of ischemic brain injury, possibly through alpha-2-induced cerebral vasoconstriction.

Soluble epoxide hydrolase gene deletion reduces survival after cardiac arrest and cardiopulmonary resuscitation.

The P450 eicosanoids epoxyeicosatrienoic acids (EETs) are produced by cytochrome P450 arachidonic acid epoxygenases and metabolized through multiple pathways, including soluble epoxide hydrolase (sEH). Pharmacological inhibition and gene deletion of sEH protect against ischemia/reperfusion injury in brain and heart, and against hypertension-related end-organ damage in kidney. We tested the hypothesis that sEH gene deletion improves survival, recovery of renal function and pathologic ischemic renal damage following transient whole-body ischemia induced by cardiac arrest (CA) and resuscitation. Mice with targeted deletion of sEH (sEH knockout, sEHKO) and C57Bl/6 wild-type control mice were subjected to 10-min CA, followed by cardiopulmonary resuscitation (CPR). Survival in wild-type mice was 93% and 80% at 10 min and 24 h after CA/CPR (n=15). Unexpectedly, survival in sEHKO mice was significantly lower than WT. Only 56% of sEHKO mice survived for 10 min (n=15, p=0.014 compared to WT) and no mice survived for 24 h after CA/CPR (p<0.0001 versus WT). We conclude that sEH plays an important role in cardiovascular regulation, and that reduced sEH levels or function reduces survival from cardiac arrest.