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Recent advancements in cancer biology, microbiology, and bioengineering have spurred the development of engineered live biotherapeutics for targeted cancer therapy. In particular, natural tumor-targeting and probiotic bacteria have been engineered for controlled and sustained delivery of anticancer agents into the tumor microenvironment (TME). Here, we review the latest advancements in the development of engineered bacteria for cancer therapy and additional engineering strategies to potentiate the delivery of therapeutic payloads. AZD2171 datasheet We also explore the use of combination therapies comprising both engineered bacteria and conventional anticancer therapies for addressing intratumor heterogeneity. Finally, we discuss prospects for the development and clinical translation of engineered bacteria for cancer prevention and treatment.Lung cancer (LC) represents the most commonly diagnosed neoplasm worldwide for both sexes and is the leading cause of cancer mortality. Malnutrition is a comorbidity frequently found in neoplastic patients, but it remains often underestimated and thus undertreated. In this review, we aimed to investigate the incidence of malnutrition among LC patients according to different screening and assessment tools, to evaluate the impact of weight loss and body composition on survival, and to analyze the efficacy of different nutritional interventions in this setting. Although malnutrition, weight loss, and body composition changes can affect survival and other clinical outcomes in LC patients, the role of nutritional interventions is not yet strongly proven, and further studies are recommended. Nevertheless, screening, assessing, and eventually treating malnutrition in LC patients are strongly recommended, according to the most recent nutritional intervention guidelines for oncology patients.
To investigate the effect of cannabidiol (CBD) on sevoflurane minimum alveolar concentration (MAC
) reduction produced by morphine in rats.
Randomized, blinded trial.
A total of 75 male Wistar Han rats weighing 276 ± 23g (mean and standard deviation), aged 3 months.
Cannabidiol (CBD) was prepared in an ethanol-solutol-saline vehicle. Animals were randomly divided into 15 groups and given an intraperitoneal bolus of 1, 3, 5, 6.5, 7.5 or 10mgkg
of CBD alone (CBD1, CBD3, CBD5, CBD6.5, CBD7.5 and CBD10 respectively) or combined with 5mgkg
of morphine (MOR+CBD1, MOR+CBD3, MOR+CBD5, MOR+CBD6.5, MOR+CBD7.5 and MOR+CBD10). While three controls groups MOR+saline, MOR+vehicle and vehicle were given an intraperitoneal bolus of morphine with saline, morphine with vehicle or vehicle alone respectively. The MAC
was determined from alveolar gas samples at the time of tail clamp application. The MAC
reduction was analyzed using a one-way ANOVA followed by Tukey's test. Additionally, Kruskal-Wallis test for non-normally-distributed data was performed. Data are presented as mean ± standard deviation. P < 0.05 RESULTS The mean MAC
was not reduced by the action of CBD administered alone, but the addition of morphine to the different doses of CBD significantly reduced the MAC
. That reduction was greatest in the MOR+CBD1, MOR+CBD7.5 and MOR+CBD10 groups (29 ± 5%, 32 ± 5% and 30 ± 6% respectively), less in MOR+CBD3 and MOR+CBD6.5 groups (24 ± 3% and 26 ± 4% respectively) and least in MOR+CBD5 group (17 ± 2%). However, only the MOR+CBD5 group was statistically significantly different from MOR+CBD1, MOR+CBD7.5 and MOR+CBD10 groups.
MAC
in rat was unaltered by the action of CBD alone, the reduction in MAC
produced by morphine was not enhanced by the addition of CBD at the doses studied.
MACSEV in rat was unaltered by the action of CBD alone, the reduction in MACSEV produced by morphine was not enhanced by the addition of CBD at the doses studied.
To evaluate two transducer and needle handling methods, along the visual axis (AL) and across the visual axis (AC), in non-skilled and skilled clinicians.
Prospective randomized crossover study.
A total of 26 students with no ultrasound locoregional anaesthesia experience (non-skilled group) and six clinicians experienced and familiar with ultrasound locoregional anaesthesia (skilled group) were enrolled. The non-skilled group was asked to perform two tasks the first on a phantom and the second on canine cadavers, whilst the skilled group performed only the second task. The tasks consisted of guiding the tip of the needle to a target point (simulated nerve on the jelly phantom and sciatic nerve on the cadavers) using two different methods of needle handling-AL or AC. All operators performed each task three times for each method. The time to drive the needle to the target for the two methods was analysed with a paired Student t test, and the number of times the needle was not visualized on the screen between the groups was compared using an unpaired Student t test. Data are presented as mean ± standard deviation. Value of p < 0.05 was considered significant.
The AL method, compared with the AC method, resulted in shorter performance time in both skilled (9 ± 5 versus 20 ± 8 seconds for the second task) and non-skilled groups (9 ± 8 versus 17 ± 15 seconds for the first task and 18 ± 11 versus 32 ± 26 seconds for the second task).
In both groups, the AL method significantly reduced the time to complete the task. Results from this study indicate that the AL method should be the preferred method for learning/teaching ultrasound-guided regional anaesthesia.
In both groups, the AL method significantly reduced the time to complete the task. Results from this study indicate that the AL method should be the preferred method for learning/teaching ultrasound-guided regional anaesthesia.
To investigate the pharmacokinetics of carprofen after a single intravenous (IV) dose and multiple oral doses administered to pigs undergoing electroporation of the pancreas.
Prospective experimental study.
A group of eight female pigs weighing 31.74 ± 2.24 kg (mean ± standard deviation).
Carprofen 4 mg kg
was administered IV after placement of a central venous catheter during general anaesthesia with isoflurane. Blood samples were collected 30 seconds before and 5, 10, 20, 30 and 60 minutes and 2, 4, 6, 8, 12 and 24 hours after carprofen administration. Subsequently, the same dose of carprofen was administered orally, daily, for 6 consecutive days and blood collected at 36, 48, 60, 72, 96, 120, 144 and 168 hours after initial carprofen administration. Plasma was analysed using liquid chromatography with mass spectrometry. Standard pharmacokinetic parameters were calculated by compartmental analysis of plasma concentration-time curves. Data are presented as mean ± standard error.
The initial plasma concentration of IV carprofen was estimated at 54.
My Website: https://www.selleckchem.com/products/Cediranib.html
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