A comparative study of secondary metabolites profiling and biological activity of Smyrnium olusatrum L. leaf, flower and fruit.

Essential oil (EO) composition of Smyrnium olusatrum was characterised by high proportion of furanosesquiterpenes (51.66-69.35%). The leaf methanolic extract composition was found to be rich with Quercetin-O-hexoside (39.78%). Apigenin 6,8-di-Chexoside represent the major component of flower (18.2%) and fruits (18.82%). Flower extract exhibited the highest contents of total phenolic (48.97 mg GAE/g) and flavonoid (52.63 mg RE/g). The ß-carotene and lycopene contents were in the order of 4.55-26.14 mg/100g, and 8.00-49.45 mg/100g, respectively. Methanolic extracts and EOs of different organs were found to possess antioxidant activities, as determined by scavenging effect, chelating activity and ß-carotene-linoleic acid model system. Furthermore, Fruit S. olusatrum EO exhibited a potent inhibitory activity against Acetylcholinesterase, while the methanolic extract showed a weaker activity. The methanolic extract displayed inhibitory effects on α-amylase, whereas the EOs was not as efficient in inhibiting this enzyme. The observed level of biological activities varied depending on the specific extracts and organs studied.

Clinical Features and Outcomes of Acute Kidney Injury in Critically Ill COVID-19 Patients: A Retrospective Observational Study.

BACKGROUND: An alarming number of COVID-19 patients, especially in severe cases, have developed acute kidney injury (AKI). AIM: The study aimed to assess the frequency, risk factors, and impact of AKI on mortality in critically ill COVID-19 patients. METHODS: The study was a retrospective observational study conducted in the MICU. Univariate and multivariate analyses were performed to identify risk factors for AKI and clinical outcomes. RESULTS: During the study period, 465 consecutive COVID-19 patients were admitted to the MICU. The patients' characteristics were median age, 64 [54-71] years; median SAPSII, 31 [24-38]; and invasive mechanical ventilation (IMV), 244 (52.5%). The overall ICU mortality rate was 49%. Two hundred twenty-nine (49.2%) patients developed AKI. The factors independently associated with AKI were positive fluid balance (OR, 2.78; 95%CI [1.88-4.11]; p < 0.001), right heart failure (OR, 2.15; 95%CI [1.25-3.67]; p = 0.005), and IMV use (OR, 1.55; 95%CI [1.01-2.40]; p = 0.044). Among the AKI patients, multivariate analysis identified the following factors as independently associated with ICU mortality: age (OR, 1.05; 95%CI [1.02-1.09]; p = 0.012), IMV use (OR, 48.23; 95%CI [18.05-128.89]; p < 0.001), and septic shock (OR, 3.65; 95%CI [1.32-10.10]; p = 0.012). CONCLUSION: The present study revealed a high proportion of AKI among critically ill COVID-19 patients. This complication seems to be linked to a severe cardiopulmonary interaction and fluid balance management, thus accounting for a poor outcome.

Reinforcing effect of tramadol in the rat.

Tramadol is one of the most commonly prescribed analgesic opioids in various pharmacopeias. Tramadol has been linked to abuse in recent clinical investigations. However, the behavioral effects and neural substrates of the drug have not been well characterized in preclinical studies. As a result, the present study investigated the effects of tramadol on behavioral sensitizations in rats. Its impacts on cellular and molecular alterations in the brain were also investigated. In conditioned place preference (CPP) paradigm, tramadol induced behavioral as well as motor sensitizations. These effects were dramatically reduced by intraperitoneal administration of naltrexone, an opioid receptor antagonist. Tramadol caused changes in several molecular markers (pERK1/2, Δ-FosB, PKCγ, PKMζ GAD67) in the anterior cingulate cortex, which could indicate an increase in excitation within this structure. Tramadol is demonstrated in the present study to be a reinforcing drug in rats, as it increased both behavioral and motor sensitizations. Tramadol's effects are most likely due to the high levels of excitation it causes in the brain, which is mostly caused by the activation of opioid receptors.

Naltrexone promotes mechanical allodynia in humans and rats.

Mechanical allodynia has been studied in chronic naltrexone-treated people (N.T.P.) and rats (N.T.R.). After persistent naltrexone administration, patients acquired static and dynamic mechanical allodynia, as measured by von Frey filament (vFf) and brush stimulations. Pregabalin and levodopa administrations in N.T.P. significantly reduced allodynic behaviour, albeit these molecules did not completely stop it. As evidenced by the deployment of the vFf, subchronic treatment with Naltrexone delivered peripherally or intrathecally induced allodynic behaviour in rats. Increased expressions of two pain markers, pERK1/2 and PKCγ, in the spinal dorsal horn laminae were associated with naltrexone-induced allodynic behaviour. After vFf stimulation, pERK1/2 expression was substantially higher (p < 0.001) in superficial spinal dorsal horn laminae than in non-stimulated or naive non-stimulated rats. In addition, when compared to control rats, N.T.R. showed a substantial (p < 0.001) increase in PKCγ expression. PKCγ expression was found to be strong in lamina IIi and laminae III-IV. A cellular mechanism is proposed for the naltrexone effect. In both people and rats, Naltrexone induces static mechanical allodynia, according to this study.