Simple triage and rapid treatment protocol for emergency department mass casualty incident victim triage.

OBJECTIVE: Triage plays an essential role in emergency medical care. It is crucial to adopt appropriate triage in a mass casualty incident (MCI) when resources are limited. The simple triage and rapid treatment (START) protocol is commonly used worldwide; however, the effectiveness of the START protocol for emergency department (ED) triage is unclear. This study aimed to examine the accuracy of START for the ED triage of victims following a MCI. METHODS: We retrospectively reviewed the records of victims who presented to our ED during a MCI response after a train crash. The ED nurses applied the START protocol upon patient arrival, and we used a consensus-based standard to determine the outcome-based categories of these same patients. We compared the START protocol and outcome-based categories. In addition, the area under the receiver operating characteristic curve (AUC), sensitivity, and specificity of START in terms of predicting surgery and ED disposition were determined. RESULTS: This study enrolled 47 patients (predominantly women, 68.1%; median age: 39.0years). Most victims were triaged into the START minor category (61.7%) and discharged from the ED (68.1%). Twenty-nine patients had matched START and outcome-based categories, whereas 2 patients were over-triaged and 16 patients were under-triaged. Additionally, the START system had acceptable AUC and sensitivities for predicting surgery and ED disposition (AUC/sensitivity/specificity for surgery: 0.850/100%/69.1%; AUC/sensitivity/specificity for admission: 0.917/93.3%/87.5%; AUC/sensitivity/specificity for intensive care unit (ICU)/ED death: 0.994/100%/97.8%). CONCLUSIONS: This study demonstrated poor agreement between START categories, as determined in the ED, and the consensus-based standard categories. However, the START protocol was acceptable in terms of identifying emergent patients (100% sensitivity for the immediate and deceased categories) and predicting ED disposition (surgery, admission, and ICU/ED mortality). Although START is not perfect, our findings suggest that it could be used for the ED triage of trauma-related MCI victims.

Calycosin alleviates H2 O2 -induced astrocyte injury by restricting oxidative stress through the Akt/Nrf2/HO-1 signaling pathway.

Oxidative stress-induced brain cell damage is a crucial factor in the pathogenesis of reactive oxygen species (ROS)-associated neurological diseases. Further, studies show that astrocytes are an important immunocompetent cell in the brain and play a potentially significant role in various neurological diseases. Therefore, elimination of ROS overproduction might be a potential strategy for preventing and treating neurological diseases. Accumulating evidence indicates that calycosin, a main active ingredient in the Chinese herbal medicine Huangqi (Radix Astragali Mongolici), is a potential therapeutic candidate with anti-inflammation and/or anticancer effects. Here, we investigated the protective effect of calycosin in brain astrocytes by mimicking in vitro oxidative stress using H2 O2 . The results revealed that H2 O2 significantly induced ROS and inflammatory factor (tumor necrosis factor [TNF]-α and interleukin [IL]-1ß) production, whereas post-treatment with calycosin dramatically and concentration-dependently suppressed H2 O2 -induced damage by enhancing cell viability, repressing ROS and inflammatory factor production, and increasing superoxide dismutase (SOD) expression. Additionally, we found that calycosin facilitated nuclear factor erythroid 2-related factor 2 (Nrf2) expression and promoted its nuclear translocation, thereby inducing the expression of antioxidant molecules (heme oxygenase [HO]-1 and SOD) following H2 O2 treatment. Moreover, calycosin did not attenuated H2 O2 -induced astrocyte damage and ROS production in the presence of the ML385 (a Nrf2-specific inhibitor) and following Nrf2 silencing. Furthermore, calycosin failed to increase Akt phosphorylation and mitigate H2 O2 -induced astrocyte damage in the presence of the LY294002 (a selective phosphatidylinositol 3-kinase inhibitor), indicating that calycosin-mediated regulation of oxidative-stress homeostasis involved Akt/Nrf2/HO-1 signaling. These findings demonstrated that calycosin protects against oxidative injury in brain astrocytes by regulating oxidative stress through the AKT/Nrf2/HO-1 signaling pathway.

Nurses' Acceptance of and Satisfaction With the Advanced Cardiac Life Support Electronic Information System in Emergency Departments and Critical Care Units.

Emergency and critical care nurses perform an important role in documenting the resuscitation process. However, paper-based recording is labor intensive and complex and may result in incorrect recording of important parameters, which suggests the need for an appropriate electronic information system for emergency care. This cross-sectional descriptive study explores emergency and critical care nurses' acceptance of, and satisfaction with, the newly developed advanced cardiac life support electronic information system and examines whether paper-based recording and electronic recording approaches differ in the completeness of resuscitation records. Data were collected through a self-designed structured questionnaire and a retrospective review of medical records. Data were analyzed by descriptive statistics, independent sample t test, and one-way analysis of variance. The results indicated that novice nurses were more satisfied with the electronic information system than others. Emergency care nurses were significantly more satisfied than medical and surgical ICU nurses. The electronic information system improved the completeness of resuscitation recording by 23.5%, compared with the paper-based recording approach. Emergency and critical care nurses have a moderate to high degree of acceptance of, and satisfaction with, electronic information systems.

Bioactive dipeptide from potato protein hydrolysate combined with swimming exercise prevents high fat diet induced hepatocyte apoptosis by activating PI3K/Akt in SAMP8 mouse.

Obesity in aged population have surges the occurrence of various metabolic disorders including Nonalcoholic fatty liver disease (NAFLD). Apoptosis in the liver is one of the causative factors for NAFLD-induced liver damage. Plants derived bioactive peptides have been shown as an alternative treatment approach for the treating NAFLD due to its less toxicity. Moderate exercise has been reported to improve cellular physiological function prevent age associated metabolic disorders. In the present study, we evaluate the effects of bioactive dipeptide (IF) derived from alcalase potato-protein hydrolysates and swimming exercise in preventing High Fat Diet (HFD)-induced liver damage in senescence accelerated mouse-prone 8 (SAMP8) mice model. Mouse were fed with HFD for 6 weeks followed by oral IF administration or swimming exercise and both for 8 weeks. HFD induces significant structural changes in liver of HFD fed SAMP8 mouse. Both IF administration and exercise prevent the structural abnormalities induced by HFD, however, combined IF treatment and exercise offer better protection. Combined IF treatment and exercise activate PI3K/Akt cell survival protein and effectively inhibit Fas-FADD-induced apoptosis in HFD fed aged mouse. Oral supplementation of bioactive peptide IF combined with moderate swimming exercise effectively alleviate HFD-induced hepatic injury in aged mice.

Resveratrol enhances therapeutic effect on pancreatic regeneration in diabetes mellitus rats receiving autologous transplantation of adipose-derived stem cells.

Pancreatic damage is the major causative agent in type 1 diabetes mellitus (DM). Several strategies have been suggested to regenerate pancreatic functions, such as stem cell transplantation and administration of active components isolating from natural herbals. This study aims to investigate if the synergistically protective effect on damaged pancreatic tissues can be observed in STZ-induced DM rats with autologous transplantation of adipose-derived stem cells (ADSC) coupling with oral administration of resveratrol. Pathological conditions can be recognized in DM rats with pancreatic damage, including reduction of islet size, suppression of survival markers, downregulation of AMPK/Sirt1 axis, and activation of apoptotic signaling. Autologous transplantation of ADSC slightly improves pancreatic functions, whereas autologous transplantation of ADSC coupling with oral administration of resveratrol significantly improves pancreatic functions in DM rats. We suggest that oral administration of resveratrol may enhance the therapeutic effect on DM patients receiving autologous transplantation of ADSC.

[Using an Information System to Optimize the ACLS Process at the Emergency Department].

The best first-aid treatment for cardiac arrest patients is advanced cardiac life support (ACLS) in terms both of saving lives and of reducing the incidence of sequelae. The American Heart Association (AHA) published updated ACLS guidelines for care in 2015. These updated guidelines emphasized the importance of teamwork in resuscitation, noting that, in addition to standard procedures, team members should be familiar with their distinct roles and should cooperate together during emergent situations. Implementing ACLS is not easy due to stress and unfamiliarity with the process and thus often achieves less-than-optimal results in practice. However, ACLS is a standard approach that uses the same procedures to address different cardiac arrest situations. Therefore, we wanted to use an information system to assist the medical team to fully implement the ACLS process. The information system helps the medical team perform resuscitation actions more intensively and precisely while avoiding problems and mistakes due to forgetfulness / unfamiliarity, facilitating an optimal resuscitation effort. Concurrently, electronic medical and nursing records are completed automatically, avoiding the need for medical staff to compile these records afterwards. This information system helps save time and effort and improves precision. Furthermore, data analysis is more convenient, which facilitates the effective management and supervision of resuscitation quality. The information system performs timing, prompting, and guidance in accordance with the ACLS process and records the procedures that will used in emergency treatment (i.e., chest compression frequency, establishment of intravenous route, placement of endotracheal tubes, electric shock, drug type, dose) with a simple click of a mouse. Finally, the associated medical record is completed and logged as soon as the automatically generated file is uploaded. All hospital staffs may use this information system to assist in the implementation of advanced CPR. The system improves the quality of the first aid measures applied in life support, reduces the burden on clinics and medical staff, and streamlines the preparation and submission of medical records.

Activating transcription factor 3 protects against pressure-overload heart failure via the autophagy molecule Beclin-1 pathway.

Activating transcription factor 3 (ATF3), a cAMP response element-binding protein/ATF family transcription factors member, has been implicated in the cardiovascular and inflammatory system and is rapidly induced by ischemic-reperfusion injuries. We performed transverse aortic banding (TAB) experiments using ATF3 gene-deleted mice (ATF3(-/-)) and wild-type (WT) mice to determine what effect it might have on heart failure induced by pressure overloading. Compared with the WT mice, ATF3(-/-) mice were found by echocardiography to have decreased left ventricular contractility with loss of normal cardiac hypertrophic remodeling. The ATF3(-/-) mice had greater numbers of terminal deoxynucleotidyl transferase-mediated digoxigenin-deoxyuridine nick-end labeling-positive cells and higher levels of activated caspase-3, as well as more apoptosis. Restoration of ATF3 expression in the heart of ATF3(-/-) mice by adenovirus-induced ATF3 treatment significantly improved cardiac contractility after TAB. The results from molecular and biochemical analyses, including chromatin immune-precipitation and in vitro /in vivo promoter assays, showed that ATF3 bound to the ATF/cAMP response element of the Beclin-1 promoter and that ATF3 reduced autophagy via suppression of the Beclin-1-dependent pathway. Furthermore, infusion of tert-butylhydroquinone (tBHQ), a selective ATF3 inducer, increased the expression of ATF3 via the nuclear factor erythroid 2-related transcriptional factor, inhibited TAB-induced cardiac dilatation, and increased left ventricular contractility, thereby rescuing heart failure. Our study identified a new epigenetic regulation mediated by the stress-inducible gene ATF3 on TAB-induced cardiac dysfunction. These findings suggest that the ATF3 activator tBHQ may have therapeutic potential for the treatment of pressure-overload heart failure induced by chronic hypertension or other pressure overload mechanisms.

Exosomal ATF3 RNA attenuates pro-inflammatory gene MCP-1 transcription in renal ischemia-reperfusion.

Transcriptional repressor activating transcription factor 3 (ATF3) is induced by various stress stimuli, including inflammation-induced renal injury. In addition, ATF3 also down-regulates adhesion molecules like intercellular adhesion molecule (ICAM), vascular cell adhesion molecule (VCAM), and monocyte chemotactic protein-1 (MCP-1). However, the relation between up-regulated ATF3 after renal ischemia/reperfusion (I/R) injury and MCP-1 is not completely understood. In this study, we demonstrated that, in renal I/R induced inflammation, induction of adhesion molecules (interleukin-6, P-selectin, E-selectin, ICAM, VCAM, and MCP-1) was higher in ATF3-knockout mice than in wild-type animals. Molecular and biochemical analyses revealed that ATF3 binds to the ATF/CRE sites in the MCP-1 promoter and inhibits the secretion of MCP-1 from renal epithelial cells after I/R injury. Urinary exosome containing ATF3 RNA was 60-fold higher in patients with acute kidney injury than in normal controls, but no difference in total urinary ATF3 RNA levels was found. In addition, in vitro study showed that exosome containing ATF3 RNA derived from epithelial cells also inhibits MCP-1 expression in the epithelial cells and macrophage migration. Furthermore, direct administration of the epithelium-derived exosomal ATF3 RNA attenuates I/R induced kidney injury. Together, our studies reveal a novel regulatory mechanism of MCP-1 expression mediated by the exosomal ATF3 RNA under renal I/R insult and suggest a potential targeted therapy for I/R induced acute kidney injury.

Calycosin Enhances Heat Shock Related-Proteins in H9c2 Cells to Modulate Survival and Apoptosis against Heat Shock.

Heat shock proteins (HSPs), which function as chaperones, are activated in response to various environmental stressors. In addition to their role in diverse aspects of protein production, HSPs protect against harmful protein-related stressors. Calycosin exhibits numerous beneficial properties. This study aims to explore the protective effects of calycosin in the heart under heat shock and determine its underlying mechanism. H9c2 cells, western blot, TUNEL staining, flow cytometry, and immunofluorescence staining were used. The time-dependent effects of heat shock analyzed using western blot revealed increased HSP expression for up to 2[Formula: see text]h, followed by protein degradation after 4[Formula: see text]h. Hence, a heat shock damage duration of 4[Formula: see text]h was chosen for subsequent investigations. Calycosin administered post-heat shock demonstrated dose-dependent recovery of cell viability. Under heat shock conditions, calycosin prevented the apoptosis of H9c2 cells by upregulating HSPs, suppressing p-JNK, enhancing Bcl-2 activation, and inhibiting cleaved caspase 3. Calycosin also inhibited Fas/FasL expression and activated cell survival markers (p-PI3K, p-ERK, p-Akt), indicating their cytoprotective properties through PI3K/Akt activation and JNK inhibition. TUNEL staining and flow cytometry confirmed that calycosin reduced apoptosis. Moreover, calycosin reversed the inhibitory effects of quercetin on HSF1 and Hsp70 expression, illustrating its role in enhancing Hsp70 expression through HSF1 activation during heat shock. Immunofluorescence staining demonstrated HSF1 translocation to the nucleus following calycosin treatment, emphasizing its cytoprotective effects. In conclusion, calycosin exhibits pronounced protective effects against heat shock-induced damages by modulating HSP expression and regulating key signaling pathways to promote cell survival in H9c2 cells.

Adiponectin ameliorates iron-overload cardiomyopathy through the PPARα-PGC-1-dependent signaling pathway.

Adiponectin is a circulating adipose-derived cytokine that may act as an antioxidative and anti-inflammatory protein. Although adiponectin has been reported to exert cytoprotective effects in acute cardiac diseases, its effects on chronic heart failure are less clear. Therefore, we aimed to investigate whether adiponectin would have a beneficial effect in iron-induced chronic heart failure and to elucidate its regulation in cardiomyocytes. Mice were first treated with iron dextran for 4 weeks to induce iron-overload cardiomyopathy. They exhibited decreased survival with impaired left ventricle contractility and decreased serum adiponectin levels. In vivo cardiac adiponectin gene (ADIPOQ) overexpression with adenoassociated virus (AAV)-ADIPOQ ameliorated cardiac iron deposition and restored cardiac function in iron-overloaded mice. In addition, AAV-ADIPOQ-treated iron-overload mice had lower expression of inflammatory markers, including myeloperoxidase activity, monocyte chemotactic protein-1, tumor necrosis factor-α, interleukin-6, and intercellular adhesion molecule-1, than iron-overloaded mice not treated with AAV-ADIPOQ. Our in vitro study showed that adiponectin induced heme oxygenase-1 (HO-1) expression through the peroxisome proliferator-activated receptor (PPAR)α-HO-1 signaling pathway. Furthermore, the adiponectin-mediated beneficial effects were PPARα-dependent as the adiponectin-mediated attenuation of iron deposition was abolished in PPARα-knockout mice. Finally, PPARα-HO-1 signaling involved PPARα and peroxisome proliferator-activated receptor gamma coactivator-1 (PGC-1) binding and nuclear translocation, and their levels were increased by adiponectin therapy. Together, these findings suggest that adiponectin acts as an anti-inflammatory signaling molecule and induces the expression of HO-1 through the PPARα-PGC-1 complex-dependent pathway in cardiomyocytes, resulting in the attenuation of iron-induced cardiomyopathy. Using adiponectin for adjuvant therapies in iron-overload cardiac dysfunction may be an option in the future.

Thromboxane A2 mediates iron-overload cardiomyopathy in mice through calcineurin-nuclear factor of activated T cells signaling pathway.

BACKGROUND: Recent studies demonstrated that iron overload could enhance the production of arachidonic acid and prostanoid, suggesting a causal connection between these signals and iron-overload cardiomyopathy. However, information regarding the downstream signaling is limited. Because thromboxane A2 (TXA2) and prostacyclin are the 2 major prostanoids in the cardiovascular system, and TXA2 plays a major role in vascular atherosclerosis and has pro-inflammatory characteristics, we intended to elucidate the role of TXA2 in iron-overload cardiomyopathy. METHODS AND RESULTS: A 4-week iron loading protocol was instituted for both TXAS gene-deleted (TXAS(-/-)) mice and wild-type (WT) mice, with less severe cardiac fibrosis and preserved normal left ventricular contraction in the TXAS(-/-) mice. Inflammatory profiles, including MCP-1, TNF-α, IL-6, ICAM-1, and myeloperoxidase activity were also lower in the TXAS(-/-) as compared with WT littermates. TXAS supplement to the iron-injured TXAS(-/-) mice re-aggravated cardiac inflammation. Using a TXA2 analog, U46619, for NFAT reporter luciferase activity on cardiomyoctes, and intraperitonal injection of U46619 into nuclear factor of activated T cells (NFAT)-luciferase transgenic mice demonstrated that U46619 increase NFAT expression, and this expression, as well as TNF-α expression, can be blocked by TXA2 receptor antagonist (SQ29548), NFAT-SiRNA, calcineurin inhibitor, or calcium chelator. Finally, intraperitoneal injection of the TNF-α antibody, infliximab, into iron-injured mice decreased TXAS expression and attenuated cardiac fibrosis. CONCLUSIONS: TXA2 mediates iron-overload cardiomyopathy through the TNF-α-associated calcineurin-NFAT signaling pathway.

MicroRNA-494 reduces ATF3 expression and promotes AKI.

MicroRNA-494 mediates apoptosis and necrosis in several types of cells, but its renal target and potential role in AKI are unknown. Here, we found that microRNA-494 binds to the 3'UTR of activating transcription factor 3 (ATF3) and decreases its transcription. In mice, overexpression of microRNA-494 significantly attenuated the level of ATF3 and induced inflammatory mediators, such as IL-6, monocyte chemotactic protein-1, and P-selectin, after renal ischemia/reperfusion, exacerbating apoptosis and further decreasing renal function. Activation of NF-κB mediated this proinflammatory response. In this ischemia/reperfusion model, urinary levels of microRNA-494 increased significantly before the rise in serum creatinine. In humans, urinary microRNA-494 levels were 60-fold higher in patients with AKI than normal controls. In conclusion, upregulation of microRNA-494 contributes to inflammatory or adhesion molecule-induced kidney injury after ischemia/reperfusion by inhibiting expression of ATF3. Furthermore, microRNA-494 may be a specific and noninvasive biomarker for AKI.

Epidemiological investigation of the first locally acquired case of COVID-19 identified by influenza surveillance-Taiwan, February 2020.

BACKGROUND: COVID-19 and influenza have similar clinical presentations that can range from mild to severe disease. The World Health Organization recommends that countries use existing influenza surveillance to monitor COVID-19 transmission in communities. We aim to describe the surveillance and investigation of COVID-19 at the early stage of the pandemic in Taiwan. METHODS: In February 2020, the Taiwan Centers for Disease Control enhanced COVID-19 surveillance through its existing influenza surveillance. We retrospectively tested patients for SARS-CoV-2 who had symptoms of severe complicated influenza but were negative in influenza testing. We conducted an epidemiological investigation and contact tracing for the index patient and secondary cases to prevent virus transmission. RESULTS: We identified the first COVID-19 patient on February 15 through enhanced COVID-19 surveillance. He had no history of traveling abroad and an unclear history of contact with COVID-19 cases. He presented with influenza-like illness on January 27 and was hospitalized from February 3 to 15. We identified 39 close contacts of the index patient, including 11 family members and 28 healthcare workers. In total, four close family contacts of the index patient tested positive for SARS-CoV-2. An additional 84 close contacts of the four secondary cases were identified and traced; none was diagnosed with COVID-19. CONCLUSIONS: We recommend enhancing COVID-19 surveillance by testing patients with influenza-like illness. To prevent the spread of COVID-19, we recommend using appropriate personal protective equipment when in close contact with patients who present with influenza-like illness or when caring for patients with pneumonia of unknown etiology.

Case Report: Clinical Presentation of Toad Venom-Induced Cardiac Intoxication.

Six people made the mistake of eating toad soup, and one of them died before arriving hospital. Five patients presented conscious change, gastrointestinal upset, or bradycardia. We checked their blood and electrocardiography to monitor the cardiac intoxication from toad venom. This experience revealed that the serum level of digoxin does not indicate the severity of intoxication but has the diagnostic value. And, serum potassium level is useful to provide valuable therapeutic information.

Anti-apoptotic effects of diosgenin on ovariectomized hearts.

BACKGROUND: The anti-apoptotic effects of diosgenin, a steroid saponin, on hearts in female with estrogen deficiency have been less studied. This study aimed to evaluate the anti-apoptotic effects of diosgenin on cardiac widely dispersed apoptosis in a bilateral ovariectomized animal model. METHODS: A total of 60 female Wistar rats, aged 6-7 months, were divided into the sham-operated group (Sham), bilateral ovariectomized rats for 2 months, and ovariectomized rats administered with 0, 10, 50, or 100 mg/kg diosgenin daily (OVX, OVX 10, OVX 50, and OVX 100, respectively) in the second month. The excised hearts were analyzed by H&E staining, TUNEL(+) assays and Western Blot. RESULT: Cardiac TUNEL(+) apoptotic cells, the levels of Fas ligand, Fas death receptors, Fas-associated death domain, active caspase-8, and active caspase-3 (FasL/Fas-mediated pathways) as well as the levels of Bax, Bad, Bax/Bcl2, Bad/p-Bad, cytosolic Cytochrome c, active caspase-9, and active caspase-3 (mitochondria-initiated pathway) were increased in OVX compared with Sham group but those were decreased in OVX 50 compared with OVX. CONCLUSION: Diosgenin appeared to prevent or suppress ovariectomy-induced cardiac FasL/Fas-mediated and mitochondria-initiated apoptosis. These findings might provide one of the possible therapeutic approaches of diosgenin for potentially preventing cardiac apoptosis in women after bilateral ovariectomy or women with estrogen deficiency.

Application of acupuncture in the emergency department for patients with ileus: A pilot prospective cohort clinical study.

Acupuncture can be conveniently used for pain control in patients with a variety of conditions, and it has obvious effects on various acute pains. In 2018, we implemented a program for emergency treatment with Chinese medicine to promote the integration of Chinese and Western medicine at the Emergency Department (ED). Ileus is a common cause of abdominal pain among patients in the ED, and it is an indication for emergency treatment with Chinese medicine. This study investigated the efficacy of acupuncture as a traditional Chinese medicine (TCM)-based treatment method for the treatment of patients with ileus in the ED. We analyzed data of patients with ileus, who visited ED between January and December 2019, and compared the length of ED stay between the Western medicine group and the Western medicine plus acupuncture group. Furthermore, pain intensity was measured by a visual analogue scale before and after acupuncture. We found that the length of ED stay was 10.8 hours lesser in the Western medicine plus acupuncture group than in the Western medicine group (P = .04), and the visual analogue scale score decreased by 2.0 on average from before to after acupuncture treatment (P = .02). Acupuncture treatment was effective and rapid in relieving the symptoms and discomfort in patients with ileus and in reducing their length of stay in the ED.

Guidelines for COVID-19 Laboratory Testing for Emergency Departments From the New Diagnostic Technology Team of the Taiwan Society of Emergency Medicine.

COVID-19 tests have different turnaround times (TATs), accuracy levels, and limitations, which emergency physicians should be aware of. Nucleic acid amplification tests (NAATs) can be divided into standard high throughput tests and rapid molecular diagnostic tests at the point of care (POC). The standard NAAT has the advantages of high throughput and high accuracy with a TAT of 3-4 hours. The POC molecular test has the same advantages of high accuracy as standard high throughput PCR, but can be done in 13-45 minutes. Roche cobas Liat is the most commonly used machine in Taiwan, displaying 99%-100% sensitivity and 100% specificity, respectively. Abbott ID NOW is an isothermal PCR-based POC machine with a sensitivity of 79% and a specificity of 100%. A high rate of false positives and false negatives is associated with rapid antigen testing. Antibody testing is mostly used as part of public health surveys and for testing for immunity.

Nerolidol improves cardiac function in spontaneously hypertensive rats by inhibiting cardiac inflammation and remodelling associated TLR4/ NF-κB signalling cascade.

Toll-like receptor 4 (TLR4) is an important mediator of hypertension and AngII induced cardiac inflammation and remodelling. In this study, the potential of nerolidol to ameliorate hypertension induced cardiac injuries and the underlying mechanism of action was explored by using in vitro and in vivo models. The in vitro analysis was performed on AngII challenged H9c2 cells and their ability to overcome cardiac inflammation and cardiac remodelling effects was determined by evaluating TLR4/NF-κB signalling cascade using Western blot analysis and immunofluorescence. The results were further ascertained using in vivo experiments. Eighteen week old male rats were randomly allocated into different groups i.e. Wistar Kyoto (WKY) rats, hypertensive SHRs, SHRs treated with a low-dose (75 mg/kg b.w) and high-dose of nerolidol (150 mg/kg b.w) and SHRs treated with captopril (50 mg/kg b.w) through oral gauge and finally analysed through echocardiography, histopathological techniques and molecular analysis. The results show that nerilodol target TLR4/NF-κB signalling and thereby attenuate hypertension associated inflammation and oxidative stress thereby provides effective cardioprotection. Echocardiography analysis showed that nerolidol improved cardiac functional characteristics including Ejection Fraction and Fractional Shortening in the SHRs. Collectively, the data of the study demonstrates nerolidol as a cardio-protective agent against hypertension induced cardiac remodelling.

Hemorrhagic adrenal myelolipoma after trauma to left adrenal gland: A case report.

Myelolipomas are rare benign tumors comprised of mature adipose tissue and hematopoietic elements. Adrenal myelolipomas associated with traumatic adrenal injury are relatively rare and less common on the left due to the limited size and well-protected position of the gland. A 59-year-old female admitted to the emergency department with intermittent left flank pain radiating to the left abdomen after falling from the bed six hours earlier. Her vital signs were stable, and she had tenderness over the left flank area and left abdomen. Her initial hemoglobin level was 12.9 g/dL. Bedside focused assessment with sonography for trauma revealed unclear left kidney margins. Contrast abdominal computed tomography (CT) revealed a space-occupying mass, 11.6×10.4×8.8 cm in dimension, in the left suprarenal region with active bleeding in the lower pole. Angiography did not reveal any active contrast medium extravasation. The CT-guided biopsy, was well performed concomitantly with angiography. Pathological assessment of the biopsy specimen revealed the presence of mostly adipose tissue with few erythrocytes and leukocytes. She was diagnosed with adrenal myelolipoma and admitted to the urology ward for left adrenalectomy with tumor resection. Traumatic adrenal injury, an unusual presentation of adrenal myelolipoma incidentally found in less than 5% of all abdominal blunt injuries, should be considered in cases of bleeding with trauma to the flank for prompt treatment.