بررسی تغییرات علایم حیاتی مصدومان ترومای مولتیپل دچار شکستگی اندام و یا لگن پس از احیا با توجه به دریافت یا عدم دریافت مسکن وریدی

ntroduction: Trauma is among the injuries associated with a high prevalence of pain and little treatment for it. Pain can change vital signs and especially cause tachycardia due to sympathetic activity. This can distort our assessment of the patient’s shock; therefore, the present study evaluates the effect of prescribing analgesics on vital signs and hydration in trauma patients with extremity or pelvic fractures. Methods: 325 trauma patients over the age of 16 with extremity or pelvic fractures and GCS score of 14 or 15 were evaluated regarding changes in vital signs and receiving crystalloid in 2 groups of with and without analgesic administration. Results: 325 patients were divided into 2 groups of with (263 patients) and without (62 patients) analgesic administration. 80.9% of the patients received analgesics. In the group receiving analgesics, on average heart rate decreased from 103 to 95 (p < 0.001). However, it did not affect blood pressure and the respiratory status of the 2 groups receiving analgesics or not showed a significant difference. The group receiving analgesics received more crystalloids. Conclusion: Pain management in trauma leads to improvement in tachycardia and probably our better understanding of presence or absence of shock in the patient. Therefore, it is recommended to move the evaluation and treatment of acute trauma pain from the secondary survey in trauma to the D phase of the primary survey.مقدمه: تروما از آسیب هایی است که با شیوع بالای درد و درمان کم آن همراه است. درد می تواند موجب تغییر علایم حیاتی و به ویژه تاکی کاردی ناشی از فعالیت سمپاتیک گردد. این امر می تواند ارزیابی ما را از شوک بیمار مختل کند، لذا مطالعه ی حاضر تاثیر تجویز مسکن بر علایم حیاتی و هیدراسیون در بیماران ترومایی دچار شکستگی اندام و یا لگن را بررسی می کند. روش کار: 325 بیمار ترومایی بالای 16 سال دچار شکستگی اندام و یا لگن با معیار کمای گلاسکو 14 و 15 در دو گروه با و بدون دریافت مسکن از نظر تغییرات علایم حیاتی و دریافت کریستالویید ارزیابی شدند. نتایج: 325 بیمار در دو گروه با (263 نفر) و بدون (62 نفر) دریافت مسکن تقسیم شدند. 80.9 درصد بیماران مسکن دریافت کردند. ضربان قلب در گروهی که مسکن گرفتند به طور میانگین از 103 به 95 کاهش یافت (P <0.001). البته این کار تاثیری بر فشار خون نداشت و وضعیت تنفسی دو گروه نیز با و یا بدون دریافت مسکن اختلاف معنادار داشت. گروه با دریافت مسکن، میزان بیشتری از کریستالویید دریافت کردند. نتیجه گیری: کنترل درد در تروما موجب بهبود تاکی کاردی و احتمالا برداشت بهتر ما از وجود یا عدم وجود شوک در بیمار می شود. از این رو پیشنهاد می شود که بررسی و درمان درد حاد تروما از ارزیابی ثانویه (Secondary Survey) در تروما به مرحلهD  از ارزیابی اولیه (Primary Survey) منتقل شود

The Prevalence of Pain and the Role of Analgesic Drugs in Pain Management in Patients with Trauma in Emergency Department

Background: Pain could potentially affect all aspects of patient admission course and outcome in emergency department (ED) when left undertreated. The alleviation of acute pain remains simply affordable but is usually, and sometimes purposefully, left untreated in patients with trauma. This study challenged the conventional emergency department policies in reducing the intensity of acute pain considering the pharmacological treatments.Methods: In this case-control study, the prevalence and intensity of pain in 200 patients were evaluated on admission (T1) and 24 hours later (T2) based on the valid, standardized 10-point numeric rating scale (NRS 0-10) for pain intensity. A group of patients received analgesic drugs and others did not. Changes in pain patterns regarding different aspects of trauma injuries in these two groups were compared.Results: The pain prevalence was high both on admission and 24 hours later. 51.5% of the study population received analgesics and 77.6% of them reported a decrease in the intensity of their pain. Only half of the patients, who did not receive any medication, reported a decrease in their pain intensity after 24 hours. The most beneficial policy to manage the acute pain was a combination therapy of the injury treatment and a supplementary pharmacological intervention.Conclusions: Pharmacological management of pain in patients with trauma is shown to be significantly beneficial for patients as it eases getting along with the pain, and still seems not to affect the diagnostic aspects of the trauma. Pain management protocols or algorithms could potentially minimize the barriers in current pain management of patients with trauma

Tropisetron attenuated the anxiogenic effects of social isolation by modulating nitrergic system and mitochondrial function.

Abstract BACKGROUND: Early social isolation stress (SIS) is associated with the occurrence of anxiety behaviors. It seems interaction between the nitrergic system and mitochondrial function plays a role in mediating the anxiety-like behaviors. In this study, we aimed to investigate the anxiolytic effects of tropisetron in animal model of SIS and we try to illustrate the possible role of nitrergic system and mitochondrial function. METHODS: We applied early social isolation paradigm to male NMRI mice. Animals treated with various doses of tropisetron, nitric oxide agents or their combination and anxiety-like behaviors of animals were assessed using valid behavioral tests including elevated plus maze (EPM), open-field test (OFT) and hole-board test (HBT) in their adulthood. Effects of housing conditions and drug treatments on the mitochondrial function were investigated in the hippocampus by assessing the ATP, GSH, ROS and nitrite levels. RESULTS: Anxiogenic effects of early SIS were assessed in the EPM, OFT, and HBT. Also, SIS disrupted mitochondrial function and caused oxidative stress in the hippocampus of stressed animals. Tropisetron showed an anxiolytic effect in the stressed mice. Also, these effects were mediated by nitrergic system by affecting mitochondrial function and modulating the oxidative stress. L-arginine, a nitric oxide precursor, abolished the anxiolytic effects of tropisetron in the behavioral tasks and blocked the protective effects of it against mitochondrial and oxidative challenge. CONCLUSIONS AND GENERAL SIGNIFICANCE: Our results demonstrated tropisetron attenuated the anxiogenic effects of SIS by mitigation of the negative effects of nitric oxide on mitochondrial functio

Molecular Detection and Genotyping of Intestinal Microspor-idia from Stray Dogs in Iran

Background: Microsporidia as one of the most important pathogens in veterinary and agricultural settings, have emerged in immunocompromised patients in Iran. To date, different Enterocytozoon bieneusi genotypes have been identified in humans and animals, supporting the possibility of zoonotic zoonosis transmission potential. The aim of this study was to evaluate the distribution of E. bieneusi genotypes among overpopulated stray dogs in vicinity of Tehran, the capital city of Iran. Methods: Totally, 75 stool and 75 urine samples were obtained from 75 stray dogs during the time period from Mar 2015 to Oct 2015. DNA extraction was performed on all the samples and specific fragment of small subunit ribosomal RNA gene of E. bieneusi and Encephalitozoon spp. was amplified. Furthermore, specific primers targeting the internal transcribed spacer region of E. bieneusi were applied to determine the genotype of the microorganism. Results: Microsporidia was detected in 5.3% of stool samples, while none of the urine samples was positive for microsporidia species. Overall, 440 bp fragment of E. bieneusi was amplified in all the samples and there was no amplification for Encephalitozoon spp. The results of sequencing of 410 bp fragment of internal transcribed spacer region showed that all the E. bieneusi were genotype D. Conclusion: E. bieneusi was the most prevalent microsporidian species in the stray dogs and all the positive isolates were characterized as genotype D

Morphine modulates the effects of histamine H1 and H3 receptors on seizure susceptibility in pentylenetetrazole-induced seizure model of mice

Histamine regulates release of neurotransmitters such as dopamine, serotonin, gamma-aminobutyric acid (GABA), glutamate and also is involved in several functions in central nervous system (CNS). It has been shown that histamine participates in disorders like seizure. It has been well documented that morphine dose-dependently induces anti or proconvulsant effects. In the current study, we firstly showed that morphine (1 mg/kg) exerts anticonvulsant effects which significantly reversed by naltrexone administration. Secondly, we determined seizure threshold for H1 and H3 receptors agonists and antagonists in mouse model of pentylenetetrazole (PTZ)-induced clonic seizures. Our results showed that activation of H1 receptors by 2-(2-Pyridyl)-ethylamine exerts anticonvulsant properties while inhibition of H1 receptors by pyrilamine maleate induced proconvulsant effects. Furthermore, we showed that immepip dihydrobromide, a H3 receptor agonist, increased seizure susceptibility to PTZ whereas thioperamide, a H3 receptor antagonist increased seizure threshold. We also revealed that pretreatment with morphine potently reversed the effects of histaminergic system on seizure threshold suggesting the involvement of opioid system in alteration of seizure threshold by histaminergic drug

Downregulation of Autophagy-related Genes in Macrophages from Patients with Behcet's Disease

Objective: Overwhelming inflammatory chemokines and cytokines characterize the immunological profile and inflammatory settings of Behcet disease (BD). The connection between autophagy-related genes (ATGs) and various perspectives of innate and adaptive immunobiology such as antigen presentation, immune tolerance, lymphocyte development and differentiation, cytokine signaling, and inflammation have been implicated. The aim of this study was to evaluate the mRNA expression profile of ATGs in macrophages of patients with BD. Materials and Methods: Whole blood samples were obtained from 10 BD patients and 10 healthy controls. Monocytes were isolated from the blood samples and then differentiated to macrophages using macrophage colony-stimulating factor (M-CSF). After total RNA extraction and cDNA synthesis, quantitative analysis of ATGs including ATG5, ATG7, ATG12, LC3b, mTOR, RAPTOR, and RICTOR was conducted by SYBR Green master mix and real-time polymerase chain reaction (PCR). Results: mRNA expression of all ATGs was downregulated in macrophages of BD patients compared with healthy controls. It is worth to note that the downregulation of ATG12 and LC3b mRNAs in macrophages of BD patients was statistically significant in comparison to that of healthy control group (P = 0.007 and 0.021, respectively). Conclusion: Considering the role of autophagy in initiation of immune responses and then clearance of dead cells as well as its participation in the development and differentiation of immune cells, downregulation of ATGs in macrophages of BD patients may be involved in uncontrolled immune response and overproduction of inflammatory cytokines

Experiencing neonatal maternal separation increased the seizure threshold in adult male mice: Involvement of the opioid system

Experiencing early-life stress has been considered as a potent risk factor for the development of many of brain disorders, including seizures. Intervening mechanisms through which neonatal maternal separation (MS) alters the seizure susceptibility in adulthood have not been well studied. In the current study, by applying 180 min of MS stress (PND 2–14), we determined the seizure susceptibility and considered the role of the opioid system. Maternal separation increased the seizure threshold, and administration of anticonvulsant/proconvulsant doses of morphine (1 and 30 mg/kg, respectively) reversed the impact of MS. Using tail flick and hot plate tests, we exposed animals to 30 min Restraint stress (RS) and found that MS decreased the pain threshold, suggesting the hyporesponsiveness of the opioid system. These results supported the abnormal seizure activity observed in the MS mice and suggested that abnormalities in the opioid system following MS alter seizure susceptibility in later life

Tropisetron suppresses colitis-associated cancer in a mouse model in the remission stage

Patients with inflammatory bowel disease (IBD) have a high risk for development of colitis-associated cancer (CAC). Serotonin is a neurotransmitter produced by enterochromaffin cells of the intestine. Serotonin and its receptors, mainly 5-HT3 receptor, are overexpressed in IBD and promote development of CAC through production of inflammatory cytokines. In the present study, we demonstrated the in vivo activity of tropisetron, a 5-HT3 receptor antagonist, against experimental CAC. CAC was induced by azoxymethane (AOM)/dextran sodium sulfate (DDS) in BALB/c mice. The histopathology of colon tissue was performed. Beta-catenin and Cox-2 expression was evaluated by immunohistochemistry as well as quantitative reverse transcription-PCR (qRT-PCR). Alterations in the expression of 5-HT3 receptor and inflammatory-associated genes such as Il-1β, Tnf-α, Tlr4 and Myd88 were determined by qRT-PCR. Our results showed that tumor development in tropisetron-treated CAC group was significantly lower than the controls. The qRT-PCR analysis demonstrated that the expression of 5-HT3 receptor was significantly increased following CAC induction. In addition, tropisetron reduced expression of β-catenin and Cox-2 in the CAC experimental group. The levels of Il-1β, Tnf-α, Tlr4 and Myd88 were significantly decreased upon tropisetron treatment in the AOM/DSS group. Taken together, our data show that tropisetron inhibits development of CAC probably by attenuation of inflammatory reactions in the colitis

NMDA receptor antagonists attenuate the proconvulsant effect of juvenile social isolation in male mice

Experiencing psychosocial stress inearly life, suchas social isolationstress (SIS), is knowntohavenegative enduring effects on the development of the brain and behavior. In addition to anxiety and depressive-like behaviors, we previously showed that juvenile SIS increases susceptibility to pentylenetetrazole (PTZ)- induced seizures in mice through enhancing the nitrergic system activity in the hippocampus. In this study, we investigated the possible involvement of N-methyl-d-aspartate (NMDA) receptors in proconvulsant effects of juvenile SIS. Applying 4 weeks of SIS to juvenile male mice at postnatal day 21–23, we observed an increased susceptibility to PTZ as well as anxiety and depressive-like behaviors in adult mice. Intraperitoneal (i.p.) administration of NMDA receptor antagonists, MK-801 (0.05 mg/kg) and ketamine (0.5 mg/kg), reversed the proconvulsant effects of SIS in Isolated (and not social) housed animals. Coadministration of non-effective doses of nitric oxide synthase (NOS) inhibitors, 7NI (25 mg/kg) and L-NAME (10 mg/kg), with NMDA receptor antagonists, MK-801 (0.01 mg/kg) and ketamine (0.1 mg/kg) attenuated the proconvulsant effects of juvenile SIS only in isolated housed mice. Also, using real time RT-PCR, we showed that hippocampal upregulation of NR2B subunit of NMDA receptor may play a critical role in proconvulsant effects of juvenile SIS by dysregulation of NMDA/NO pathway. In conclusion, results of present study revealed that experiencing SIS during adolescence predisposes the co-occurrence of seizure disorders with psychiatric comorbidities and also, alteration of NMDA receptor structure and function in hippocampus plays a role in proconvulsant effects of juvenile SIS through enhancing the NMDA/NO pathwa

Morphine Attenuated the Cytotoxicity Induced by Arsenic Trioxide in H9c2 Cardiomyocytes.

Arsenic trioxide (ATO) is an efficient drug for the treatment of the patients with acute promyelocytic leukemia (APL). Inhibition of proliferation as well as apoptosis, attenuation of migration, and induction of differentiation in tumor cells are the main mechanisms through which ATO acts against APL. Despite advantages of ATO in treatment of some malignancies, certain harmful side effects, such as cardiotoxicity, have been reported. It has been well documented that morphine has antioxidant, anti-apoptotic, and cytoprotective properties and is able to attenuate cytotoxicity. Therefore, in this study, we aimed to investigate the protective effects of morphine against ATO toxicity in H9c2 myocytes using multi-parametric assay including thiazolyl blue tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) generation, caspase 3 activity, nuclear factor kappa B (NF-κB) phosphorylation assay, and expression of apoptotic markers. Our results showed that morphine (1 μM) attenuated cytotoxicity induced by ATO in H9c2 cells. Results of this study suggest that morphine may have protective properties in management of cardiac toxicity in patients who receive ATO as an anti-cancer treatment