Contamination Status and Serotypes Distribution of Salmonella in Food in Yantai City, China: A 14-Year Continuous Monitoring Study.

Salmonella is a foodborne zoonotic pathogen that threatens food safety and public health. However, few people have conducted long-term and systematic studies on Salmonella contamination in food in Yantai City. In order to investigate the situation of Salmonella contamination in food and improve the ability of early warning and control of foodborne diseases, a total of 3420 samples from 20 categories were collected from 13 monitoring points in Yantai City, from 2010 to 2023. The difference in detection rate and bacterial strain of different monitoring points, different types, and different sources of samples was compared. Of the 3420 samples, 80 were positive with a detection rate of 2.34%. Salmonella detection rates were significantly different for samples collected at different monitoring sites. Salmonella was detected only in meat and meat products and catering food, and none of the other types were detected. The detection rate of Salmonella was higher in raw animal meat and raw poultry. Samples collected at the market stage had the highest detection rate (5.81%), and there was a significant difference in detection rate between samples from different sources (χ2 = 36.93, p < 0.05). Eighty-one strains of Salmonella were detected out of 3420 samples (2 different strains were detected in 1 positive sample). The serological test identified 8 groups and 27 serotypes. The dominant serum groups were group B 30.86% (25/81), group E1 23.46% (19/81), and group D 16.05% (13/81). The main dominant serotypes were Salmonella give 17.28% (14/81), Salmonella enteritidis 16.05% (13/81), and Salmonella derby 13.58% (11/81). Meat and meat products and catering food were the main food products contaminated with Salmonella. The resulting secondary contamination is the hidden threat of foodborne diseases and should be given sufficient attention.

Foodborne Disease Outbreaks Caused by Biotoxins in Yantai City: A 10-Year Spatiotemporal Monitoring Study.

Unsafe food causes 600 million cases of foodborne diseases and 420,000 deaths every year. Meanwhile, biological toxins such as poisonous mushrooms, saponins, and aflatoxin can cause significant damage to humans. Therefore, it is particularly important to study foodborne disease outbreaks caused by biotoxins (FDOB). We collected FDOB in Yantai City from 2013 to 2022 and further established a corresponding database. Statistical analysis was carried out according to time, place, pathogen, and contamination of pathogenic factors. There were 128 FDOB, resulting in 417 patients and 6 deaths. The third quarter was a high season for foodborne disease outbreaks, the number of events, patients and deaths accounted for 65.63% (84/128), 55.88% (233/417), and 100% (6/6) of the total number, respectively. The highest number of outbreaks per 10,000 persons was Qixia (0.41), followed by Zhifu (0.36) and Laiyang (0.33). The top three causes of outbreaks were poisonous mushroom toxin, saponins and hemagglutinin, and Lagenaria siceraria (Molina) Standl. Sixty-five (50.78%) outbreaks were attributed to poisonous mushroom toxin, 18 (14.06%) outbreaks to saponin and hemagglutinin, and 12 (9.38%) outbreaks to L. siceraria (Molina) Standl. The largest number of outbreaks, patients and deaths all occurred in families, accounting for 82.81% (106/128) outbreaks, 66.19% (276/417) patients, and 100% (6/6) deaths, respectively. Followed by catering service establishments, accounting for 14.84% (19/128), 30.22% (126/417), and 0% (0/6), respectively. The main poisoning link of outbreaks was ingestion and misuse, accounting for 72.66% (93/128), followed by improper processing, accounting for 20.31% (26/128). It is necessary to carry out targeted family publicity and education, strengthen the integration of medical and prevention, explore innovative monitoring and early warning mechanisms for foodborne diseases, and reduce the occurrence of underreporting of foodborne disease outbreaks.

Bilateral pulmonary embolism without deep venous thrombosis was observed after knee arthroscopy: a case report.

BACKGROUND: Symptomatic pulmonary embolism (PE) after knee arthroscopy is extremely rare. If the embolism is not treated promptly, the patient may die. Bilateral pulmonary embolism with associated pulmonary infarct without concomitant deep vein thrombosis has never been reported following routine knee arthroscopy. CASE PRESENTATION: A 50-year-old female patient with no other risk factors other than hypertension, obesity, varicose veins in the ipsilateral lower extremities and elevated triglyceride (TG) presented to our ward. She had experienced sudden chest tightness, polypnea and fainting after going to the bathroom the morning of the second postoperative day and received emergency medical attention. Colour ultrasonography of the extremities showed no deep vein thrombosis. Lung computed tomography angiography (CTA) showed multiple embolisms scattered in both pulmonary artery branches. Thus, emergency interventional thrombolysis therapy was performed, followed by postoperative symptomatic treatment with drugs with thrombolytic, anticoagulant and protective activities. One week later, lung CTA showed a significant improvement in the PEs compared with those in the previous examination. Since the aetiology of PE and no obvious symptoms were discerned, the patient was discharged. CONCLUSION: Although knee arthroscopy is a minimally invasive and quick procedure, the risk factors for PE in the perioperative period should be considered and fully evaluated to enhance PE detection. Moreover, a timely diagnosis and effective treatment are important measures to prevent and cure PE after knee arthroscopy. Finally, clear guidelines regarding VTE thromboprophylaxis following knee arthroscopy in patients with a low risk of VTE development are needed.

Rosmarinic acid exerts anti-inflammatory effect and relieves oxidative stress via Nrf2 activation in carbon tetrachloride-induced liver damage.

Background: Rosmarinic acid (RA) has biological and pharmaceutical properties and shows hepatoprotective potential. However, the hepatoprotective mechanism of RA needs to be further elucidated in vivo and in vitro. Objective: This study was aimed to evaluate the protective effect of RA on carbon tetrachloride (CCl4)-induced liver injury and elucidate the hepatoprotective mechanism of RA in vivo and in vitro. Design: In vivo, the mice were orally administrated with RA (10, 20, and 40 mg/kg bw) daily for 28 consecutive days, and 1% CCl4 (5 mL/kg bw, dissolved in peanut oil) was used to induce liver injury. In vitro, the big rat liver (BRL) hepatocytes were pretreated with RA (0.2, 0.4, and 0.8 mg/mL) for 3 h, and then the hepatocytes were treated with CC14 (final concentration, 14 mM) for 3 h to induce cell injury. The related indexes, including hepatic function, oxidative stress, protein expression of nuclear-factor erythroid 2-related factor 2 (Nrf2) pathway, inflammation, histopathological change, hepatocyte apoptosis, and mitochondrial membrane potential, were evaluated. Results: Oral administration of RA to mice considerably decreased the CCl4-induced elevation of serum alanine aminotransferase (ALT), alkaline phosphatase (ALP), triacylglycerols (TG), total cholesterol (TC), total bilirubin (TBIL), hepatic reactive oxygen species (ROS), malondialdehyde (MDA), nitric oxide (NO), 8-hydroxydeoxyguanosine (8-OHdG), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8). RA also increased the levels of hepatic glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) and the protein expressions of Nrf2, quinine oxidoreductase (NQO1), and heme oxygenease-1 (HO-1). Histopathological examinations indicated that RA (20 and 40 mg/kg bw) alleviated the liver tissue injury induced by CCl4. Moreover, RA inhibited the hepatocyte apoptosis caused by CCl4 based on TUNEL assay. In vitro, RA pretreatment remarkably recovered the cell viability and reduced the CCl4-induced elevation of AST, ALT, lactate dehydrogenase (LDH), ROS, and 8-OHdG. Immunohistochemistry staining demonstrated that pretreatment with RA markedly inhibited the expression of IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and Caspase-3 in CCl4-treated hepatocytes. Additionally, RA pretreatment significantly decreased the elevation of mitochondrial membrane potential in CCl4-treated hepatocytes. Conclusions: RA exerted a protective effect against CCl4-induced liver injury in mice through activating Nrf2 signaling pathway, reducing antioxidant damage, suppressing inflammatory response, and inhibiting hepatocyte apoptosis. RA could attenuate BRL hepatocyte ROS production, DNA oxidative damage, inflammatory response, and apoptosis induced by CCl4 exposure.

Protective effect of free phenolics from Lycopus lucidus Turcz. root on carbon tetrachloride-induced liver injury in vivo and in vitro.

Protective effect of free phenolics from Lycopus lucidus Turcz. root (FPLR) on CCl4-induced hepatotoxicity in vivo and in vitro was first evaluated. Oral administration of FPLR (100 mg/kg bw) to mice significantly reduced the CCl4-induced elevation of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, triacylglycerols, total cholesterol, and total bilirubin. FPLR also increased the hepatic GSH contents and antioxidant enzyme activities of SOD and CAT and decreased the hepatic MDA level. Histopathological examinations further confirmed that the FPLR could protect the liver from CCl4-induced damage. Further research indicated that FPLR prevented the DNA fragmentation caused by CCl4 based on TUNEL assay. Moreover, immunohistochemistry staining demonstrated that pretreatment with FPLR significantly inhibited the elevation of hepatic TNF-α, IL-6, IL-8, iNOS, COX-2, and Caspase-3 in CCl4-treated mice. In vitro experiments showed that FPLR remarkably reduced BRL hepatocyte apoptosis and damage caused by CCl4 treatment. These findings indicate that FPLR could be developed as a functional food or medication for therapeutic purpose and prevention of hepatic injury.