Abstract Nanoparticles emerge as alternatives to conventional molecular tags such as fluorophores, owing to their superior optical properties, chemical stability, and long photostability. Herein, we present a fluorescence resonance energy transfer (FRET)-based ratiometric fluorescent probe consisting of nitrogen-doped carbon dots and gold nanoclusters (N-CDs–AuNCs) for the sensitive and selective detection of α-fetoprotein (AFP), a biomarker for early hepatocellular carcinoma. The probe is constructed from a donor–acceptor fluorophore pair, in which blue-emissive N-CDs transfer energy to red-emissive AuNCs, resulting in dual fluorescence at 435 and 710 nm under a single excitation wavelength of 380 nm, enabled by carbodiimide coupling. Blue/red dual-fluorescent nanotags were integrated into a ratiometric fluorescence enzyme-linked immunosorbent assay (RF-ELISA) platform to measure AFP on microplates functionalized with anti-AFP capture antibodies, in combination with a glucose oxidase (GOx)-tagged anti-AFP secondary antibody. After assembly of the sandwich-structured immunocomplex, GOx converted glucose into hydrogen peroxide, thereby quenching the red fluorescence of the AuNCs on the fluorescent nanoprobe. At the same time, the blue emission of the embedded N-CDs remained unchanged, allowing the red/blue fluorescence ratio to serve as a quantitative determination of AFP concentration under optimal conditions. Ratiometric fluorescence at 435:710 nm enabled AFP detection over a concentration range of 0.001 to 45 ng mL–1, with a limit of detection near 1.8 pg mL–1. The method exhibited reliable reproducibility, specificity, and stability. AFP measurements in human serum agreed well with a commercially available ELISA kit.

A highly sensitive and selective electrochemical immunosensor was developed for the detection of the cancer biomarker alpha-fetoprotein (AFP), a key indicator of cancer. This sensor utilizes the enhanced electrochemical current response generated by a composite material consisting of gold nanoparticles (Au NPs) decorated on a metal-organic framework (MOF) containing iron and cobalt (FeCo). The Au NP-decorated FeCo-based MOF labeled with primary antibodies (Ab1) significantly enhances the electrochemical response, enabling accurate detection of AFP. Similarly, HRP-Au nanoprism (Au NPR) nanocomposites were prepared via a one-pot assembly, where horseradish peroxidase (HRP) and the secondary antibody (Ab2) were coimmobilized on Au NPRs to form a stable nanocomposite. The immunosensor was fabricated by assembling Au NPs@ FeCo-MOF and capture antibodies (Ab1) onto a glassy carbon electrode. The MOF served as a conductive matrix, AuNPs enhanced electron transfer, and Ab1 ensured specific antigen recognition. When the AFP antigen is present, labeled Ab2 binds to the Au NP-decorated FeCo-MOF via specific antigen-antibody interactions, leading to enhanced electrochemical signals for sensitive detection. The immunosensor response was measured by differential pulse voltammetry (DPV) in phosphate-buffered solution (PBS) containing hydrogen peroxide (H2O2) and 3,3',5,5'-tetramethylbenzidine (TMB). Under controlled conditions, the immunosensor exhibited a linear response to AFP over the range of 0.0001 to 100 ng mL-1, with a detection limit of 1.2 pg mL-1 (S/N = 3), indicating high sensitivity. The immunosensor's performance was validated by detecting AFP in human serum samples, demonstrating its potential for ultrasensitive detection of AFP and other biomarkers.

An electrochemical sandwich immunoassay was fabricated to measure the prostate-specific antigen (PSA) biomarker. The PSA immunosensor was developed by altering the surface of a glassy carbon electrode (GCE) with a nanocomposite comprising carboxyl-functionalized carbon dots that support gold nanoparticles (AuNPs), which were then combined with hydroxylated boron nitride nanosheets (HO-BN). This construction possesses distinctive signal enhancement characteristics and was prepared via a facile method. Considering the high biological affinity of AuNPs for biomolecules, carbon dots (CDs) with carboxyl (COOH) groups make a suitable substrate for electrode modification. This alteration allows for the PSA antibody (Ab1) attachment, resulting in a sandwich-like configuration. Additionally, carbon dot-stabilized AuNPs integrated into HO-BN nanosheet nanocomposites considerably boost the electron transfer rate, leading to remarkable potential in sensor applications. By utilizing horseradish peroxidase (HRP)-conjugated antifree PSA antibody (Ab2), a reduction in hydrogen peroxide (H2O2) was achieved within the electrochemical cell. This reduction led to increased current, attributed to the increased PSA concentration, which is required for the biosensor analysis to perform properly. The developed immunosensor revealed a linear correlation with PSA concentrations ranging from 1.0 to 3500 pg mL-1, achieving a low detection limit of 0.136 pg mL-1. Furthermore, the PSA aptasensor demonstrates excellent selectivity, remarkable stability, and commendable reproducibility, indicating its significant potential for clinical research and diagnostic applications.

The fast, and highly sensitive estimation of cardiac troponin T (cTnT) is crucial for the early identification of acute myocardial infarction (AMI). The electrochemical immunoassay-based (EIB) sensors are highly promising for this purpose, as they offer precise measurements and can be directly assessed in intricate matrices, including blood. To increase sensitivity, EIB sensors use nanomaterials or amplification processes, which can be laborious to develop. With this, we develop an electrochemical immunosensor for the sensitive detection of cardiac troponin T (cTnT). The sensing platform is composed of functionalized triangular carbon quantum dots stabilized gold nanoparticles which are integrated with boron nitride nanosheets (caf-TCQDs@AuNPs on HO-BNNS). Ferrocene carboxylic acid (Fc-COOH) serves as the signal label. The composite was developed and examined using several techniques such as X-ray diffraction (XRD), X-ray photoelectron spectroscopy (XPS), transmission electron microscopy (TEM), cyclic voltammetry, and chronocoulometry. The caf-TCQDs@AuNPs supported on HO-BNNS, have a large surface area and excellent electrical conductivity, and serve as an effective platform for the immobilization of anti-cTnT monoclonal antibodies via carbodiimide coupling. The Fc-COOH, functioning as a signal label through the oxidation process, was integrated with caf-TCQDs@AuNPs on the HO-BNNS platform to establish an electrochemical immunosensor for the detection of cTnT. The electrochemical immunosensor demonstrated excellent performance for the determination of cTnT under optimal conditions, exhibiting a linearity range spanning from 0.0001 to 100 ng mL-1, accompanied by a low detection limit of 0.0013 ng mL-1. Notably, the immunosensor revealed high specificity, as well as excellent levels of reproducibility and reliability for the examination of human serum samples.

A cardiac immunosensor was developed to detect heart attacks (myocardial infarctions) at an early stage. This technique, utilizing carboxylic functionalized triangular carbon dots (caf-TCDs) combined with an antibody anticardiac Troponin T (anti-cTnT), proved to be a quick and sensitive method for detecting cardiac troponin T (cTnT) in both buffer solutions and biological fluids such as serum. The antibody for cardiac Troponin T (cTnT) was chemically linked to amphiphilic caf-TCDs using a carbodiimide coupling reaction. Exfoliated graphene oxide (GO) sheets effectively bind to anti-cTnT labeled caf-TCDs on their surface, resulting in a non-radiative energy transfer process where the fluorescence is suppressed. This interaction between caf-TCDs and GO follows a nonlinear and increasing Stern-Volmer relationship, indicating a combination of static and dynamic quenching. When antigen (cTnT) is present, the interaction between antibodies (anti-cTnT) and the cTnT molecules hinders the energy transfer process. This interaction also affects the positioning of the nano-couple and causes the detachment of CDs from the GO surface. As a result, the energy transfer process is impeded, leading to the restoration of fluorescence intensity. The sensor exhibits high specificity and low sensitivity to non-specific antigens. It shows a linear reaction to cTnT in the range of 0.05-50 ng mL-1, with a detection limit of 0.046 ng mL-1. Therefore, the anti-cTnT-caf-TCD/GO sensor offers a potential platform for detecting cTnT with increased sensitivity.

Background: Infected aortic aneurysm is a rel-atively rare disease with significant morbidity and mortality. Because of its deeper position, patients with infected aortic arch aneurysms may present with only fever and other vague symptoms, such as weakness, fatigue, dizziness, anorexia, and functional decline. It is difficult confirm a diagnosis that is based solely on history or physical examination, and it may only be apparent on imaging studies. Case Report: We present a brief case report of a patient presenting to the emergency department with unexplained fever who was di-agnosed with emphysematous salmonella-infected aneurysm of the aortic arch. Why Should an Emergency Physician Be Aware of This?: Infected aortic arch aneurysm is an ex-tremely unusual disease entity that emergency physicians encounter. Because of the high mortality and morbidity of this catastrophic disease, an infected aortic aneurysm should be considered as a possible diagnosis in patients with persis-tent fever and vague symptoms without a specific infection focus. To avoid delayed diagnosis, emergency physicians should be aware of infected aortic arch aneurysm. (c) 2022 Elsevier Inc. All rights reserved.

Material-specific electrocatalytic activity and electrode design are essential factors in evaluating the performance of electrochemical sensors. Herein, the technique described involves electrospinning manganese-based metal-organic frameworks (Mn-MOFs) to develop MnOx nanostructures embedded in carbon nanofibers. The resulting structure features an electrocatalytic material for an enzyme-free glucose sensor. The elemental composition, morphology, and microstructure of the fabricated electrodes materials were characterized by using energy-dispersive X-ray spectroscopy (EDX), field-emission scanning electron microscopy (FESEM), and transmission electron microscopy (TEM). Cyclic voltammetry (CV) and amperometric i-t (current-time) techniques are characteristically employed to assess the electrochemical performance of materials. The MOF MnOx-CNFs nanostructures significantly improve detection performance for nonenzymatic amperometric glucose sensors, including a broad linear range (0 mM to 9.1 mM), high sensitivity (4080.6 μA mM-1 cm-2), a low detection limit (0.3 μM, S/N = 3), acceptable selectivity, outstanding reproducibility, and stability. The strategy of metal and metal oxide-integrated CNF nanostructures based on MOFs opens interesting possibilities for the development of high-performance electrochemical sensors.

Abstract Introduction: Cardiac arrest (CA) often leads to severe brain damage, resulting in neurological disorders and high mortality rates. Hypothermia treatment (HT) is commonly used in clinical practice after CA/cardio-pulmonary resuscitation (CA/CPR) because it has been shown to improve neurological outcomes and increase survival rates. Olanzapine, a medication known to induce hypothermia, has not been extensively studied in the context of CA/CPR. This study aimed to investigate the neuroprotective effects and mechanisms of olanzapine-induced hypothermia (OIH) following ROSC. Male Sprague-Dawley rats were subjected to the following conditions: (i) Sham: no asphyxial CA + saline, (ii) CA: asphyxial CA + saline, and (iii) OCA: asphyxial CA + olanzapine treatment after the return of spontaneous circulation (ROSC). Result CA/CPR resulted in high mortality, severe neurological impairments, and hippocampal neuron damage observed after 5 days in the asphyxia CA group. These pathological complications were ameliorated by olanzapine treatment. OIH also protected the pyramidal neurons in the CA1 region of the hippocampus. The expression of antioxidant factors SOD-1, SOD-2, and CAT were upregulated in the olanzapine-treated group compared to the CA group. Moreover, olanzapine treatment following asphyxial CA reduced the expression of the pro-inflammatory factor COX-2 and the nuclear transcription factor NF-κB, which was sustained for up to 5 days compared to the CA group. OIH provides protection against cerebral injury following ROSC by enhancing the expression of antioxidant and anti-inflammatory factors. Conclusion The results of our study demonstrate that Olanzapine, an atypical antipsychotic medication, induces a noteworthy reduction in body temperature in the asphyxial CA rat model. The effectiveness of hypothermia treatment was evident by its antioxidant and anti-inflammatory mechanisms. Therefore, we suggest olanzapine as a promising therapeutic agent for alleviating cerebral injury via hypothermia in patients with CA.

Abstract Introduction: Cardiac arrest (CA) often leads to severe brain damage, resulting in neurological disorders and high mortality rates. Hypothermia treatment (HT) is commonly used in clinical practice after CA/cardio-pulmonary resuscitation (CA/CPR) because it has been shown to improve neurological outcomes and increase survival rates. Olanzapine, a medication known to induce hypothermia, has not been extensively studied in the context of CA/CPR. This study aimed to investigate the neuroprotective effects and mechanisms of olanzapine-induced hypothermia (OIH) following ROSC. Male Sprague-Dawley rats were subjected to the following conditions: (i) Sham: no asphyxial CA + saline, (ii) CA: asphyxial CA + saline, and (iii) OCA: asphyxial CA + olanzapine treatment after the return of spontaneous circulation (ROSC). Result CA/CPR resulted in high mortality, severe neurological impairments, and hippocampal neuron damage observed after 5 days in the asphyxia CA group. These pathological complications were ameliorated by olanzapine treatment. OIH also protected the pyramidal neurons in the CA1 region of the hippocampus. The expression of antioxidant factors SOD-1, SOD-2, and CAT were upregulated in the olanzapine-treated group compared to the CA group. Moreover, olanzapine treatment following asphyxial CA reduced the expression of the pro-inflammatory factor COX-2 and the nuclear transcription factor NF-κB, which was sustained for up to 5 days compared to the CA group. OIH provides protection against cerebral injury following ROSC by enhancing the expression of antioxidant and anti-inflammatory factors. Conclusion The results of our study demonstrate that Olanzapine, an atypical antipsychotic medication, induces a noteworthy reduction in body temperature in the asphyxial CA rat model. The effectiveness of hypothermia treatment was evident by its antioxidant and anti-inflammatory mechanisms. Therefore, we suggest olanzapine as a promising therapeutic agent for alleviating cerebral injury via hypothermia in patients with CA.

Carbon dots (CDs) are considered a potential substance for use in biomarker applications due to their exceptional light stability. However, there are several unsolved uncertainties about CD toxicity in vitro and in vivo. In this study, a redesigned derivative of the natural polysaccharide inulin is connected with boron-doped amine-functionalized carbon dots (In@BN-CDs) through carbodiimide coupling to improve the biocompatibility of the nanoformulation. The toxicity and biodistribution of ln@BN-CDs in vivo and in vitro were explored in detail. The In@BN-CDs were tested after a single inhalation dosage of 10, 7, 5, 3, and 1 mg/kg. We explored a dose- and time-dependent technique of collecting blood samples and then centrifuged the blood samples and obtained serum samples, which were then analyzed for fluorescence inspection; findings showed that the fluorescence intensity decreased with time. Similarly, In@BN-CDs were effectively used as in vitro toxicity and fluorescent probes for cellular imaging in living cells due to their biocompatibility and cell membrane accessibility. The biocompatibility and efficacy of In@BN-CDs as fluorescent imaging agents have been demonstrated. The data suggest that the usage of In@BN-CDs in vitro and in vivo should be examined.

Rationale: Sodium nitrite is a potent oxidizing agent that impairs oxygen transport and delivery through methemoglobin formation. Clinical manifestations are known to induce methemoglobinemia, dysrhythmia, hypotension, and even death. While accidental intoxication of sodium nitrite by contaminated water and food has previously occurred, there has been a substantial upsurge in suicide intoxication in recent years. Patient concerns: We present case reports of 2 patients who attempted suicide by sodium nitrite after ordering a “suicide powder” on the internet market. They were brought to the emergency department after attempting suicide by ingesting sodium nitrite. They experienced dyspnea, cyanosis, and mild nausea. Diagnosis: Based on their history and blood tests, methemoglobinemia was initially diagnosed. Interventions and outcomes: The patients received methylene blue antidotal therapy in the emergency department. The patients were discharged after neuropsychiatric evaluation and treatment for mental illness, suicidal ideation, and suicide attempts. They informed us of how simple and easy it was for them to buy sodium nitrite for suicidal purposes. Lessons: With widely shared information on the usage of sodium nitrite for suicide and the absence of proper regulation, the incidence of acute poisoning will increase. This increases physicians’ chances of encountering unexplained cyanosis and methemoglobinemia. Clinical suspicion of sodium nitrite intoxication is warranted in cases of unexplained cyanosis or methemoglobinemia. We want to highlight how simple and easy it is to buy sodium nitrite for suicidal purposes.

Although multi-organ dysfunction is associated with the survival rate following cardiac arrest (CA), the majority of studies to date have focused on hearts and brains, and few studies have considered renal failure. The objective of the present study, therefore, was to examine the effects of therapeutic hypothermia on the survival rate, pathophysiology and antioxidant enzymes in rat kidneys following asphyxial CA. Rats were sacrificed one day following CA. The survival rate, which was estimated using Kaplan-Meier analysis, was 42.9% one day following CA. However, hypothermia, which was induced following CA, significantly increased the survival rate (71.4%). In normothermia rats with CA, the serum blood urea nitrogen level was significantly increased one day post-CA. In addition, the serum creatinine level was significantly increased one day post-CA. However, in CA rats exposed to hypothermia, the levels of urea nitrogen and creatinine significantly decreased following CA. Histochemical staining revealed a significant temporal increase in renal injury after the normothermia group was subjected to CA. However, renal injury was significantly decreased in the hypothermia group. Immunohistochemical analysis of the kidney revealed a significant decrease in antioxidant enzymes (copper-zinc superoxide dismutase, manganese superoxide dismutase, glutathione peroxidase and catalase) with time in the normothermia group. However, in the hypothermia group, these enzymes were significantly elevated following CA. Collectively, the results revealed that renal dysfunction following asphyxial CA was strongly associated with the early survival rate and therapeutic hypothermia reduced renal injury via effective antioxidant mechanisms.

Introduction. This study aimed to establish a predictive model that includes physiological parameters and identify independent risk factors for severe injuries in bicycle rider accidents. Methods. This was a multicenter observational study. For four years, we included patients with bicycle rider injuries in the Emergency Department-Based Injury In-depth Surveillance database. In this study, we regarded ICD admission or in-hospital mortality as parameters of severe trauma. Univariate and multivariate logistic regression analyses were performed to assess risk factors for severe trauma. A receiver operating characteristic (ROC) curve was generated to evaluate the performance of the regression model. Results. This study included 19,842 patients, of whom 1,202 (6.05%) had severe trauma. In multivariate regression analysis, male sex, older age, alcohol use, motor vehicle opponent, load state (general and crosswalk), blood pressure, heart rate, respiratory rate, and Glasgow Coma Scale were the independent factors for predicting severe trauma. In the ROC analysis, the area under the ROC curve for predicting severe trauma was 0.848 (95% confidence interval: 0.830–0.867). Conclusion. We identified independent risk factors for severe trauma in bicycle rider accidents and believe that physiologic parameters contribute to enhancing prediction ability.

Closed thoracostomy is a procedure commonly performed by emergency physicians throughout their working duties. Re-expansion pulmonary edema (REPE) is a relatively rare complication that occurs in < 1% of chest-tube drainages or thoracocenteses, with mortality rates as high as 20%. REPE can occur when the lung has been rapidly re-expanded after passive collapse by large pleural effusion, atelectasis, or pneumothorax (1). The precise pathophysiology of REPE has not been fully elucidated, but alterations in pulmonary microvasculature permeability and mechanical stress placed on the rapidly re-expanding lung are thought to be involved.

A 33-year-old male presented to the emergency department with sudden and painless left infraorbital swellings immediately after forceful nose blowing. Approximately 2 hours before the onset of symptoms, he was doing laundry and hit his left cheek on a laundry machine. Following the event, he said that he felt discomfort in the cheek area without swelling. However, 2 hours after the hit, the patient blew his nose out with hands and immediately felt like a balloon had popped around his left eye. On admission, there was nontender left periorbital swelling, with crepitus on palpation (Figure 1). His optical examination was normal, including extraocular motion, visual acuity, and funduscopic examination (Figure 2). Facial computed tomography was performed (Figures 3, 4, and 5). The patient was treated conservatively and discharged in stable condition, with the expectation that the issue might resolve spontaneously. Surgical repair and decompression were not performed. The patient was instructed to avoid blowing his nose, sneezing, vomiting or performing any other activities that may lead to increased pressure in the nasal cavity, including diving or flying. An orbital blowout fracture is a traumatic deformity of the orbital wall, typically resulting from the impact of a blunt object with a diameter exceeding the bony margins of the orbit. Cases of spontaneous orbital emphysema with nontraumatic causes are very rare.1 A rapid increase in pressure in the upper airways while sneezing, coughing, and blowing one's nose is related to barotrauma, which very rarely leads to orbital wall fracture. The pressure evoked by forceful nose blowing is estimated to rise to 66 mm Hg. Sneezing with the oral and nasal passages blocked may evoke a pressure of up to 176 mm Hg.2 Orbital emphysema without complication is not a medical emergency and usually resolves spontaneously within 2 weeks.

The present study aimed to investigate the renoprotective effect of therapeutic hypothermia (TH) on renal ischemia-reperfusion injury (RI/RI) induced by asphyxial cardiac arrest (CA) in rats. A total of 48 male rats were randomly divided into five groups: i) Sham (n=6); ii) Normothermia + CA (Normo.) (n=14); iii) Normo. and 2 h of TH after return of spontaneous circulation (ROSC) (n=12); iv) Normo. and 4 h of TH after ROSC (n=9); and v) Normo. and 6 h of TH after ROSC (n=7). All rats except the Sham group underwent asphyxia CA and were sacrificed 1 day after ROSC. The survival rate increased from 42.8% in the Normo. group to 50, 66.6 and 85.7% in the groups with 2, 4 and 6 h of TH after CA, respectively. TH attenuated the histopathological changes of the renal tissues following ROSC and the levels of blood urea nitrogen, serum creatinine and malondialdehyde in renal tissues. On immunohistochemistry, the relative optical density of nuclear erythroid-related factor-2 (Nrf2) and heme oxygenase (HO-1) expression in renal tissues increased in the Normo. group compared with that in the Sham group and exhibited further significant increases at 6 h of TH after ROSC. In conclusion, TH attenuated renal injury and increased the expression of Nrf2 and HO-1 in a TH treatment time-dependent manner.

ABSTRACT Purpose To investigate the role of Nrf2/HO-1 in renal histopathological ailments time-dependently in asphyxial cardiac arrest (CA) rat model. Methods Eighty-eight Sprague Dawley male rats were divided into five groups of eight rats each. Asphyxial CA was induced in all the experimental rats except for the sham group. The rats were sacrificed at 6 hours, 12 hours, one day and two days post-CA. Serum blood urea nitrogen (BUN), creatinine (Crtn) and malondialdehyde from the renal tissues were evaluated. Hematoxylin and eosin and periodic acid-Schiff staining were done to evaluate the renal histopathological changes in the renal cortex. Furthermore, Nrf2/HO-1 immunohistochemistry (ihc) and western blot analysis were performed after CA. Results The survival rate of rats decreased in a time-dependent manner: 66.6% at 6 hours, 50% at 12 hours, 38.1% in one day, and 25.8% in two days. BUN and serum Crtn markedly increased in CA-operated groups. Histopathological ailments of the renal cortical tissues increased significantly from 6 hours until two days post-CA. Furthermore, Nrf2/HO-1 expression level significantly increased at 6 hours, 12 hours, and one day. Conclusions The survival rate decreased time-dependently, and Nrf/HO-1 expression increased from 6 hours with the peak times at 12 hours, and one day post-CA.

The hierarchical three-dimensional nitrogen-doped carbon nanotube anchored bimetallic cobalt copper organic framework (NCNT MOF CoCu) is successfully synthesized by the direct growth approach using the high-temperature carbonization of bimetallic cobalt copper organic framework (MOF CoCu-500). The as-prepared NCNT MOF CoCu nanostructure possesses high-level activity for both glucose and hydrogen peroxide (H2O2) sensing molecules. The cyclic voltammetry (CV) and chronoamperometry (CA) studies demonstrate excellent electrocatalytic performance for the oxidation of glucose with a linear range of 0.05 to 2.5 mM, high sensitivity of 1027 mu A mM(-1)cm(-2), and the lowest detection limit of 0.15 mu M. Similarly, the NCNT MOF CoCu nanostructure showed significantly higher H2O2 activity with a linear range of 0.05 to 3.5 mM, high sensitivity of 639.5 mu A mM(-1)cm(-2), and the lowest detection limit of 0.206 mu M. Thanks to its special hierarchical nanoarchitecture, homogeneous nitrogen-doped carbon nanotubes, and highly graphitized carbon, which may be increased the synergistic effect between bimetallic CoCu and NCNT in the organic framework. The potentially effective fabricated sensor was also used as a suitable probe for the detection of glucose and H2O2 in the analysis of the real samples.

Cardiac arrest (CA) is a sudden interruption in the effective blood flow due to heart failure. The current research aimed to conduct the pathophysiological and histopathological analysis in the kidney in asphyxial cardiac arrest rat model. Cardiac arrest was induced by intravenous injection of vecuronium bromide (2 mg/kg), following stop of mechanical ventilation. Rats were kept on the CA condition for 5 minutes. After that, cardiopulmonary resuscitation (CPR) was done to achieve return of spontaneous circulation (ROSC) following intravenous injection of epinephrine bolus (0.005 mg/kg), sodium bicarbonate (1 mEq/kg) and turn on mechanical ventilation. Then Rats were sacrificed after cardiopulmonary resuscitation (CPR) following asphyxial CA at 6 hrs, 12 hrs, 1 day, 2 days, and 5 days. The intensity of renal injury measured by the serum levels of blood urea nitrogen (BUN), creatinine (Crtn). Moreover, Hematoxylin & eosin, and Periodic Acid Schiff staining in the kidney was done for evaluating the renal histopathological changes. Furthermore, COX-2 immunoreactivity and western analysis were performed in the kidney. Survival rate declined following ROSC compared to the sham group, it showed 80% at 6 hrs and decreased time-dependently to 8% at 5 days. In this study, serum BUN and Crtn levels and renal histopathological scores significantly increased after ROSC in CA. Moreover, COX-2 expression also increased after ROSC in comparison to the sham group with its peak level at 5 days following CA. Renal histological damage score and COX-2 expression were upregulated after ROSC following CA. These results direct that COX-2 takes part in the asphyxial CA-induced ischemic renal injury