The Effect of Liraglutide on Axon Regeneration and Functional Recovery after Peripheral Nerve Lesion.

Peripheral nerve injuries inflict severe consequences, necessitating innovative therapeutic strategies. This study investigates the potential of liraglutide, a glucagon-like peptide-1 receptor agonist, in mitigating the consequences of peripheral nerve injury. The existing treatment methods for such injuries underscore the importance of ongoing translational research efforts. Thirty adult Wistar rats underwent sciatic nerve dissection and repair surgery. The nerves were surgically transected using micro scissors at a precise location located 1.5 cm proximal to the trifurcation site. The study included a control group and two experimental groups, one treated with saline (placebo group) and the other with liraglutide (experimental group) for 12 weeks. Motor function, electromyography (EMG), and biochemical and histopathological analyses were performed after 12 weeks of treatment. Electrophysiological assessments revealed that liraglutide improved the compound muscle action potential (CMAP) amplitude and motor function compared to the saline-treated group. Histological and immunohistochemical analyses demonstrated increased NGF expression, total axon number, and diameter and reduced fibrosis in the liraglutide group. Biochemical analyses illustrated liraglutide's antioxidative properties, evidenced by reduced malondialdehyde (MDA) levels. Galectin-3 levels were suppressed and GDF-11 levels were modulated by liraglutide, indicating anti-inflammatory and anti-apoptotic effects. Liraglutide is a promising therapeutic intervention for peripheral nerve injuries, promoting functional recovery and histopathological improvement. Its multifaceted positive impact, beyond glycemic control, suggests constructive effects on the acute and chronic inflammatory processes associated with peripheral neuropathy. These findings warrant further research to elucidate molecular mechanisms and facilitate clinical translation. The study contributes valuable insights to the growing understanding of GLP-1 receptor agonists' neuroprotective properties in the context of peripheral nerve injuries.

Evaluation of the Reparative Effect of Sinomenine in an Acetaminophen-Induced Liver Injury Model.

Due to its rising global prevalence, liver failure treatments are urgently needed. Sinomenine (SIN), an alkaloid from sinomenium acutum, is being studied for its liver-repair properties due to Acetaminophen (APAP) overdose. SIN's effect on APAP-induced hepatotoxicity in rats was examined histologically and biochemically. Three groups of 30 adult male Wistar rats were created: control, APAP-only, and APAP + SIN. Histopathological and biochemical analyses were performed on liver samples after euthanasia. SIN is significantly protected against APAP damage. Compared to APAP-only, SIN reduced cellular injury and preserved hepatocellular architecture. The APAP + SIN Group had significantly lower ALT, MDA, and GSH levels, protecting against hepatocellular damage and oxidative stress. SIN also had dose-dependent antioxidant properties. When examining critical regulatory proteins, SIN partially restored Sirtuin 1 (SIRT1) levels. While BMP-7 levels were unaffected, histopathological evidence and hepatocyte damage percentages supported SIN's liver-restorative effect. SIN protected and repaired rats' livers from APAP-induced liver injury. This study suggests that SIN may treat acute liver damage, warranting further research into its long-term effects, optimal dosage, and clinical applications. These findings aid liver-related emergency department interventions and life-saving treatments.

Intranasal Insulin Eases Autism in Rats via GDF-15 and Anti-Inflammatory Pathways.

In rat models, it is well-documented that chronic administration of propionic acid (PPA) leads to autism-like behaviors. Although the intranasal (IN) insulin approach is predominantly recognized for its effects on food restriction, it has also been shown to enhance cognitive memory by influencing various proteins, modulating anti-inflammatory pathways in the brain, and reducing signaling molecules such as interleukins. This study seeks to explore the potential therapeutic benefits of IN insulin in a rat model of autism induced by PPA. Thirty male Wistar albino rats were categorized into three cohorts: the control group, the PPA-induced autism (250 mg/kg/day intraperitoneal PPA dosage for five days) group, treated with saline via IN, and the PPA-induced autism group, treated with 25 U/kg/day (250 µL/kg/day) insulin via IN. All treatments were administered for 15 days. After behavioral testing, all animals were euthanized, and brain tissue and blood samples were collected for histopathological and biochemical assessments. Following insulin administration, a substantial reduction in autism symptoms was observed in all three social behavior tests conducted on the rats. Moreover, insulin exhibited noteworthy capabilities in decreasing brain MDA, IL-2, IL-17, and TNF-α levels within autism models. Additionally, there is a notable elevation in the brain nerve growth factor level (p < 0.05) and GDF-15 (p < 0.05). The assessment of cell counts within the hippocampal region and cerebellum revealed that insulin displayed effects in decreasing glial cells and inducing a significant augmentation in cell types such as the Purkinje and Pyramidal cells. The administration of insulin via IN exhibits alleviating effects on autism-like behavioral, biochemical, and histopathological alterations induced by PPA in rats. Insulin-dependent protective effects show anti-inflammatory, anti-oxidative, and neuroprotective roles of insulin admitted nasally.

Prognostic Significance of Lactate Clearance in Cardiogenic Pulmonary Edema in the Emergency Department.

Background and Objectives: Acute cardiorespiratory failure disrupts the delicate balance of energy supply, demand, and consumption, with elevated lactate levels and decreased blood pH serving as crucial indicators. Acute cardiogenic pulmonary edema (ACPO), a common cause of acute respiratory failure, poses a substantial mortality risk. Lactate, a byproduct of pyruvate reduction, is a pertinent marker in perfusion assessment. Lactate clearance (LC) has proven prognostic efficacy in various conditions but lacks consensus on its predictive power in acute cardiogenic pulmonary edema. Materials and Methods: This prospective observational study, conducted in a metropolitan area's third-level emergency department, involved patients with cardiogenic pulmonary edema from May 2021 to August 2023. The inclusion criteria specified acute cardiogenic pulmonary edema, excluding patients with incomplete data or other respiratory conditions. Lactate clearance, calculated at presentation and after 6 h, served as the primary outcome predictor. Our data analysis employed logistic regression, the ROC curve, and statistical tests. Results: The cohort of 106 patients revealed that a lactate clearance below 14.29% was significantly associated with mortality. While 51.6% of survivors were discharged, LC's predictive success for discharge was inconclusive. Logistic regression underscored the significance of lactate clearance, with a one-unit increase yielding a 5.55-fold probability of survival. The AUC for LC was 0.759. Conclusions: This study pioneers the exploration of lactate clearance in patients with acute cardiogenic pulmonary edema. LC below 14.29% signifies a poor prognosis, emphasizing its potential as an early treatment initiation marker. While acknowledging this study's limitations, we advocate for further multicenter research to refine the understanding of lactate clearance in this context.

Gallic Acid Protects from Sepsis-Induced Acute Lung Injury.

Sepsis, a leading global cause of morbidity and mortality, involves multiple organ dysfunction syndromes driven by free radical-mediated processes. Uncontrolled inflammation in early sepsis stages can lead to acute lung injury (ALI). Activated leukocytes generate reactive oxygen species, contributing to sepsis development. Gallic acid, a phenolic compound, is known for its antimicrobial properties. This study aims to observe gallic acid's protective and restorative effect on the lungs in an experimental sepsis model. Male Wistar albino rats were subjected to a feces intraperitoneal injection procedure (FIP) to induce sepsis. Four groups were formed: normal control, FIP alone, FIP with saline, and FIP with gallic acid. Gallic acid was administered intraperitoneally at 20 mg/kg/day. Blood samples were collected for biochemical analysis, and computed tomography assessed lung tissue histopathologically and radiologically. Gallic acid significantly decreased malondialdehyde, IL-6, IL-1ß, TNF-α, CRP levels, oxidative stress, and inflammation indicators. Lactic acid levels decreased, suggesting improved tissue oxygenation. Histopathological examinations revealed reduced lung damage in the gallic-acid-treated group. Computed tomography confirmed lower lung density, indicating less severe inflammation. Arterial blood gas analysis demonstrated improved oxygenation in gallic-acid-treated rats. Gallic acid exhibited anti-inflammatory and antioxidant effects, reducing markers of systemic inflammation and oxidative stress. The findings support its potential to protect against ALI during sepsis. Comparable studies underline gallic acid's anti-inflammatory properties in different tissues. Early administration of gallic acid in sepsis models demonstrated protective effects against ALI, emphasizing its potential as an adjunct therapy to mitigate adverse outcomes. The study proposes gallic acid to reduce mortality rates and decrease the need for mechanical ventilation during sepsis-induced ALI.

Evaluation of ABCD2 score during the development of stroke in COVID-19 patients diagnosed with transient ischemic attack in the emergency department.

BACKGROUND: The aim of the present study is to reveal the association between the risk of stroke using ABCD2 score and COVID-19 in patients who presented to our emergency department during the pandemic and were diagnosed with TIA. METHODS: According to the recommendations of the European Stroke Association, patients with an ABCD2 score of <4 were classified as low-risk, and patients with an ABCD2 score of ≥4 were classified as high-risk. Within 90 days of the patient's admission to the emergency room, the development of stroke was tracked and recorded on the system. RESULTS: Stroke occurred in 35.78% of the patients. Regarding COVID-19, 75.34% of stroke patients were positive for COVID-19 and 65.75% had COVID-19 compatible pneumonia on 'thoracic CT'. Regarding mortality, 16.4% of the patients who were positive for COVID-19 and developed a stroke died. The presence of COVID-19 compatible pneumonia on thorax CT, PCR test result and ABCD2 score were determined as independent risk factors for the development of stroke. According to the PCR test results, the probability of having a stroke decreases 0.283 times in patients who are negative for COVID-19. According to the PCR test results, the probability of having a stroke increased 2.7 times in COVID-19 positive patients. CONCLUSIONS: Adding the presence of COVID-19 and the presence of COVID-19 pneumonia to the ABCD2 score, based on the information about the increased risk of stroke in TIA patients, improves the predictive power of the score. More studies are needed in this regard.

The renoprotective effect of Tibolone in sepsis-induced acute kidney injury.

INTRODUCTION: Sepsis-induced acute kidney injury (AKI) remains a major challenge in intensive care, contributing significantly to morbidity and mortality. Tibolone, known for its neuroprotective and hormonal properties, has not been explored for its potential in AKI management. This study investigates the protective effects of Tibolone and its underlying mechanisms involving Sirtuin-1 (SIRT1) and Yes-Associated Protein (YAP) in a rat sepsis model. MATERIALS AND METHODS: Thirty-six female Wistar albino rats underwent cecal ligation and puncture (CLP) to induce sepsis. They were randomly assigned to control, CLP+Saline, and CLP+Tibolone groups. Tibolone was administered intraperitoneally. Biomarkers, including Sirtuin (SIRT1), Yes-associated protein (YAP), Tumor necrosis factor (TNF-α), High mobility group box 1 (HMGB1), malondialdehyde (MDA), creatinine, and urea, were assessed. Histopathological examination evaluated renal damage. RESULTS: Tibolone administration significantly reduced plasma TNF-α, HMGB1, MDA, creatinine, and urea levels compared to the CLP+Saline group. Moreover, Tibolone elevated SIRT1 and YAP levels in kidney tissues. Histopathological examination demonstrated a significant decrease in tubular epithelial necrosis, luminal debris, dilatation, hemorrhage, and interstitial inflammation in Tibolone-treated rats. CONCLUSION: This study unveils the protective role of Tibolone against sepsis-induced AKI in rats. The improvements in inflammatory and oxidative biomarkers and histological evidence suggest Tibolone's potential as a therapeutic intervention in sepsis-associated kidney injury. The upregulation of SIRT1 and YAP indicates their involvement in Tibolone's renoprotective mechanisms. Further investigations are warranted to explore Tibolone's translational potential in human sepsis-induced AKI.

Demonstration of the Protective Effect of Vinpocetine in Diabetic Cardiomyopathy.

Background: Diabetic cardiomyopathy (DCM) poses a significant risk for heart failure in individuals with diabetes, yet its underlying mechanisms remain incompletely understood. Elevated blood sugar levels initiate harmful processes, including apoptosis, collagen accumulation, and fibrosis in the heart. Vinpocetine, a derivative of Vinca minor L., has demonstrated diverse pharmacological effects, including vasodilation, anti-inflammatory properties, and enhanced cellular metabolism. This study aims to investigate Vinpocetine's protective and remodeling effects in diabetic cardiomyopathy by evaluating biochemical and histopathological parameters. Methods: Twenty-one adult male Wistar rats were induced with diabetes using streptozocin and divided into Diabetes and Diabetes + Vinpocetine groups. Histopathological analyses, TGF-ß1 immunoexpression, and measurements of plasma markers (TGF-ß, pro-BNP, Troponin T) were performed. Biochemical analyses included HIF-1 alpha and neuregulin-1ß quantification and evaluation of lipid peroxidation. Results: Vinpocetine significantly reduced cardiac muscle thickness, TGF-ß1 expression, and plasma in diabetic rats. HIF-1 alpha and neuregulin-1ß levels increased with Vinpocetine treatment. Histopathological observations confirmed reduced fibrosis and structural abnormalities in Vinpocetine-treated hearts. Conclusions: This study provides comprehensive evidence supporting the protective effects of Vinpocetine against diabetic cardiomyopathy. Vinpocetine treatment improved cardiac morphology, immunohistochemistry, and modulation of biochemical markers, suggesting its potential as a therapeutic intervention to attenuate the negative impact of diabetes on heart function.

Caffeine mitigates tamoxifen-induced fatty liver in Wistar rats.

PURPOSE: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats. METHODS: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration. RESULTS: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001). CONCLUSIONS: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.

Hydroxychloroquine attenuates sepsis-induced acute respiratory distress syndrome in rats.

BACKGROUND: This study investigates the effects of hydroxychloroquine (HCQ) on a sepsis-induced acute respiratory distress syndrome (ARDS) model in rats, initiated by a fecal intraperitoneal injection procedure (FIP). METHODS: Three groups were established: control (n=8), FIP + saline (n=7), and FIP + HCQ (20 mg/kg/day) (n=9). Blood samples were collected for arterial blood gas and biochemical analyses, and bilateral pneumonectomy was performed for histopathologic examination. RESULTS: In the FIP + saline group, PaO2 decreased and PaCO2 increased, whereas these levels normalized in the FIP + HCQ group compared to the control (p<0.001 and p<0.05, respectively). Histopathological scores for alveolar congestion, perivascular/interstitial edema, hemorrhage in alveolar tissue, leukocyte infiltration or aggregation in air spaces/vascular walls, and alveolar wall/hyaline membrane thickness increased in the FIP + saline group compared to the control group (p<0.01). These scores decreased in the FIP + HCQ group compared to the FIP + saline group (p<0.01). HCQ reversed the sepsis-induced increase in malondialdehyde, tumor necrosis factor-alpha, interleukin-6, and lactic acid. CONCLUSION: HCQ may be an effective and safe option to mitigate the severe progression of ARDS.

Oxytocin: A Shield against Radiation-Induced Lung Injury in Rats.

BACKGROUND: Radiation-induced lung injury (RILI), a serious side effect of thoracic radiotherapy, can lead to acute radiation pneumonitis (RP) and chronic pulmonary fibrosis (PF). Despite various interventions, no effective protocol exists to prevent pneumonitis. Oxytocin (OT), known for its anti-inflammatory, antiapoptotic, and antioxidant properties, has not been explored for its potential in mitigating RILI. MATERIALS AND METHODS: This study involved 24 female Wistar albino rats, divided into three groups: control group, radiation (RAD) + saline, and RAD + OT. The RAD groups received 18 Gy of whole-thorax irradiation. The RAD + OT group was treated with OT (0.1 mg/kg/day) intraperitoneally for 16 weeks. Computerizing tomography (CT) imaging and histopathological, biochemical, and blood gas analyses were performed to assess lung tissue damage and inflammation. RESULTS: Histopathological examination showed significant reduction in alveolar wall thickening, inflammation, and vascular changes in the RAD + OT group compared to the RAD + saline group. Biochemical analysis revealed decreased levels of TGF-beta, VEGF, and PDGF, and increased BMP-7 and prostacyclin in the RAD + oxytocin group (p < 0.05). Morphometric analysis indicated significant reductions in fibrosis, edema, and immune cell infiltration. CT imaging demonstrated near-normal lung parenchyma density in the RAD + oxytocin group (p < 0.001). CONCLUSION: Oxytocin administration significantly mitigates radiation-induced pneumonitis in rats, implying that is has potential as a therapeutic agent for preventing and treating RILI.

Evaluation of the effects of the pandemic period on cirrhosis patients.

Introduction: Cirrhosis is a common liver disease, which is characterized by life-limiting complications. In cirrhosis, liver ACE2 mRNA levels were 34-times upregulated, ACE2 protein 97-times upregulated, and ACE2 receptors increased in 80% of hepatocytes. Increased ACE2 receptor sensitizes hepatocytes to COVID-19. Aim: To evaluate the applications of cirrhosis patients to the Emergency Department before and after the pandemic. Material and methods: The study was conducted retrospectively in a single centre on cirrhotic patients who applied to the Emergency Department in a 2-year period. The obtained data were compared with the laboratory values of the patients: the severity of cirrhosis, the reasons for applying to the Emergency Department, hospitalization/discharge status, and pre-pandemic and pandemic period values. The mortality of the patients was recorded. Results: The biochemical values, CTP score, and complications of cirrhosis patients deteriorated during the pandemic period, which contributed to the increase in mortality and that the CTP score and its complications worsened, which contributed to the increase in mortality. COVID-19 positivity contributes to the progression of the CTP score, but it is not directly associated with mortality. Conclusions: We think that new treatment protocols should be included in the guidelines to minimize the effects of this type of viral infection on the liver.

Have Chest Imaging Habits Changed in the Emergency Department after the Pandemic?

The rate of patients undergoing tomography in the emergency department has increased in the last two decades. In the last few years, there has been a more significant increase due to the effects of the pandemic. This study aimed to determine the rate of patients who underwent chest imaging in the emergency department, the preferred imaging method, and the demographic characteristics of the patients undergoing imaging during the pre-pandemic and post-pandemic periods. This retrospective cross-sectional study included patients admitted to the emergency department between January 2019 and March 2023. The number of female, male, and total emergency admissions, the rate of patients who underwent chest X-ray (CXR) and chest computed tomography (CCT), and the age and gender distribution of the cases who underwent chest imaging were compared according to the pre-pandemic (January 2019-February 2020), pandemic (March 2020-March 2022), and post-pandemic (April 2022-March 2023) periods. Total emergency admissions were similar in the pre-pandemic and post-pandemic periods (pre-pandemic period: 21,984 ± 2087; post-pandemic period: 22,732 ± 1701). Compared to the pre-pandemic period, the CCT rate increased (pre-pandemic period: 4.9 ± 0.9, post-pandemic period: 7.46 ± 1.2), and the CXR rate decreased (pre-pandemic period: 16.6 ± 1.7%, post-pandemic period: 13.3 ± 1.9%) in the post-pandemic period (p < 0.001). The mean age of patients who underwent chest imaging (CXR; Pre-pandemic period: 56.6 ± 1.1 years; post-pandemic period: 53.3 ± 5.6 years. CCT; Pre-pandemic period: 68.5 ± 1.7 years; post-pandemic period: 61 ± 4.0 years) in the post-pandemic period was lower than in the pre-pandemic period (p < 0.001). Chest imaging preferences in the emergency department have changed during the post-pandemic period. In the post-pandemic period, while younger patients underwent chest imaging in the emergency department, CCT was preferred, and the rate of CXR decreased. It is alarming for public health that patients are exposed to higher doses of radiation at a younger age.

Autophagy and anti-inflammation ameliorate diabetic neuropathy with Rilmenidine.

PURPOSE: To evaluate the neuroprotective effects of Rilmenidine on diabetic peripheral neuropathy (DPN) in a rat model of diabetes induced by streptozotocin (STZ). METHODS: STZ (60 mg/kg) was administered to adult Sprague-Dawley rats to induce diabetes. On the 30th day after STZ administration, electromyography (EMG) and motor function tests confirmed the presence of DPN. Group 1: Control (n = 10), Group 2: DM + 0.1 mg/kg Rilmenidine (n = 10), and Group 3: DM + 0.2 mg/kg Rilmenidine (n = 10) were administered via oral lavage for four weeks. EMG, motor function test, biochemical analysis, and histological and immunohistochemical analysis of sciatic nerves were then performed. RESULTS: The administration of Rilmenidine to diabetic rats substantially reduced sciatic nerve inflammation and fibrosis and prevented electrophysiological alterations. Immunohistochemistry of sciatic nerves from saline-treated rats revealed increased perineural thickness, HMGB-1, tumor necrosis factor-α, and a decrease in nerve growth factor (NGF), LC-3. In contrast, Rilmendine significantly inhibited inflammation markers and prevented the reduction in NGF expression. In addition, Rilmenidine significantly decreased malondialdehyde and increased diabetic rats' total antioxidative capacity. CONCLUSIONS: The findings of this study suggest that Rilmenidine may have therapeutic effects on DNP by modulating antioxidant and autophagic pathways.

The Effect of Adipose-Derived Mesenchymal Stem Cells on Peripheral Nerve Damage in a Rodent Model.

Peripheral nerve damage is a significant clinical problem with limited therapeutic options. Adipose-derived mesenchymal stem cells (ADSCs) have emerged as a promising therapeutic approach due to their regenerative potential. However, the underlying mechanisms by which ADSCs promote peripheral nerve regeneration remain unclear. In this study, we investigated the role of syndecan-1 and heat shock protein 70 (HSP-70) in mediating the regenerative effects of ADSCs on peripheral nerves. ADSCs were characterized and isolated from the adipose tissue of rats. In vitro experiments were conducted to evaluate the ability of ADSCs to secrete syndecan-1 and HSP-70 in response to stress conditions. To evaluate the therapeutic potential of ADSCs, rats with sciatic nerve injuries were treated with ADSCs and assessed for functional recovery, nerve regeneration, and changes in syndecan-1 and HSP-70 levels. Regeneration was evaluated with Electromyography (EMG) histology. The results showed that ADSCs could secrete syndecan-1 and HSP-70 in response to stress conditions. Furthermore, ADSC treatment significantly improved functional recovery and nerve regeneration and increased syndecan-1 and HSP-70 levels in the injured nerve. On the other hand, ADSCs make improvements histologically through the influence of Nerve growth factor (NGF), Malondialdehyde (MDA), and EMG.

Antifibrotic preventive effect of polyethylene glycol (PEG) 3350 in methotrexateinduced hepatoxicity model.

PURPOSE: Liver damage caused by drugs and other chemicals accounts for about 5% of all cases. Methotrexate (MTX), a folic acid analogue, is a first-line synthetic antimetabolite agent routinely used in the treatment of rheumatoid arthritis and other autoimmune and chronic inflammatory diseases. Polyethylene glycol (PEG) has antioxidant activity. In this study, we evaluated biochemically and histopathologically the antifibrotic effect of PEG 3350 administered intraperitoneally to prevent methotrexate-induced liver damage in rats. METHODS: A total of 30 male rats including 10 rats was given no drugs (normal group), and 20 rats received single-dose 20 mg/kg MTXfor induced liver injury in this study. MTX was given to 20 rats, which were divided in two groups. Group 1 rats was given PEG30 mg/kg/day (Merck) intraperitoneally, and Group 2 rats % 0.9 NaCl saline 1 mL/kg/day intraperitoneally daily for two weeks. RESULTS: Transforming growth factor beta (TGF-ß), plasma malondialdehyde (MDA), liver MDA, serum tumour necrosis factor alpha (TNF-α), alanine aminotransferase and plasma pentraxin-3 levels and, according to tissue histopathology, hepatocyte necrosis, fibrosis and cellular infiltration were significantly better in MTX+PEG group than in MTX+saline group. CONCLUSIONS: PEG 3350 is a hope for toxic hepatitis due to other causes, since liver damage occurs through oxidative stress and cell damage, similar to all toxic drugs.

A rare complication of cardiopulmonary resuscitation applied during transportation by ambulance: A case report of flail chest.

Cardiopulmonary resuscitation (CPR) to be applied during patient transfer by ambulance differs from CPR applied in the field or in the hospital in terms of physical condition. Especially the deeper and faster chest compressions recommended in the latest CPR guidelines, when administered during ambulance transport, may result in a further increase in traumatic CPR complications. However, in the current CPR guidelines, there are no clear recommendations regarding additional measures that can be taken to reduce the complications and increase the efficiency of CPR during patient transport. In this study, a case of flail chest that developed after short-term CPR application during ambulance transport is presented. The aim of this study was to evaluate the flail chest complication and solution suggestions that may occur due to chest compressions applied during transportation.

The Evaluation of End Tidal Carbon Dioxide Values in Intubated Patients with COVID-19.

BACKGROUND: The aim of this study is to establish the value of PETCO2 in COVID-19 patients intubated in emergency department, and its effects on mortality.  Objectives: Between May 15, 2020 and January 15, 2021, The patients aged ≥18 years and diagnosed COVID-19, scheduled for urgent intubation in the emergency department were included. METHOD: Single-center, prospective and observational study. Age, gender, vital signs, laboratory findings are recorded. Immediately after intubation as measured by the capnography, the initial PETCO2_1 and at post-ventilation 15 min, PETCO2_2 and first, second arterial blood gas analysis are recorded. RESULTS: The mean age of the 48 patients was 74 years. The PETCO2_1 and PETCO2_2 measurements were statistically significantly different between the patients who survived and those who died (p=0.014, p=0.015). The patients with a high first PETCO2_1 value and a decrease to the normal level survived, but those with a low PETCO2_1 value that could not increase to a normal value died (p=0.038, p=0.031). Increased levels of SpO2, PETCO2_1, PETCO2_2 and PaCO2_2 decreased the risk of mortality, while an increased level of PaO2_2 increased the risk of mortality. CONCLUSION: Capnography is non-invasive and provides continuous measurement. Assessment of changes in PETCO2 value would contribute to patient survival.

Autophagy and anti-inflammation ameliorate diabetic neuropathy with Rilmenidine

Purpose: To evaluate the neuroprotective effects of Rilmenidine on diabetic peripheral neuropathy (DPN) in a rat model of diabetes induced by streptozotocin (STZ). Methods: STZ (60 mg/kg) was administered to adult Sprague-Dawley rats to induce diabetes. On the 30th day after STZ administration, electromyography (EMG) and motor function tests confirmed the presence of DPN. Group 1: Control (n = 10), Group 2: DM + 0.1 mg/kg Rilmenidine (n = 10), and Group 3: DM + 0.2 mg/kg Rilmenidine (n = 10) were administered via oral lavage for four weeks. EMG, motor function test, biochemical analysis, and histological and immunohistochemical analysis of sciatic nerves were then performed. Results: The administration of Rilmenidine to diabetic rats substantially reduced sciatic nerve inflammation and fibrosis and prevented electrophysiological alterations. Immunohistochemistry of sciatic nerves from saline-treated rats revealed increased perineural thickness, HMGB-1, tumor necrosis factor-α, and a decrease in nerve growth factor (NGF), LC-3. In contrast, Rilmendine significantly inhibited inflammation markers and prevented the reduction in NGF expression. In addition, Rilmenidine significantly decreased malondialdehyde and increased diabetic rats' total antioxidative capacity. Conclusions: The findings of this study suggest that Rilmenidine may have therapeutic effects on DNP by modulating antioxidant and autophagic pathways.