Renal sinus fat (RSF) crucially influences metabolic regulation, inflammation, and vascular function. We investigated the association between RSF accumulation, metabolic disorders, and nutritional status in obese individuals with hypertension. A cross-sectional study involved 51 obese hypertensive patients from Salamat Specialized Community Clinic (February–September 2022). Basic and clinical information were collected through interviews. Data included anthropometrics, blood pressure, number of antihypertensive medications, body composition (bioelectrical impedance analysis), dietary intake (semi-quantitative 147-item food frequency questionnaire), and blood samples. Renal sinus fat was measured via ultrasonography. Statistical analyses included Pearson correlation, binary logistic regression, and linear regression. RSF positively correlated with abdominal visceral adipose tissue (VAT) area (P = 0.016), systolic blood pressure (SBP) (P = 0.004), and diastolic blood pressure (DBP) (P = 0.005). A strong trend toward a positive association was observed between antihypertensive medications and RSF (P = 0.062). In linear regression, RSF was independently associated with abdominal VAT area, SBP, and DBP after adjusting for confounders. After considering other risk factors, RSF volume relates to prescribed antihypertensive medications, hypertension, and central fat accumulation in obese hypertensive subjects. These findings suggest the need for further investigations into whether RSF promotes metabolic disorders.

Chia seeds have gained attention for their potential anti-inflammatory properties, which may be attributed to their high content of omega-3 fatty acids, dietary fibre, and antioxidants. This study aims to provide an overview of the current understanding regarding the effects of chia seeds on inflammatory markers, specifically C-reactive protein (CRP), interleukin-6 (IL-6), and tumour necrosis factor-alpha (TNF-α). A comprehensive literature search was conducted on PubMed, Scopus, Web of Science, Cochrane, and Google Scholar up to June 2024. Randomized controlled trials (RCTs) assessing the effect of chia seed on CRP or/and IL-6 or/and TNF-α. Data were extracted and analysed using a random-effects model, and reported as weighted mean differences (WMD) with 95% confidence intervals (CI). Subgroup and sensitivity analyses were also performed. Four RCTs involving 210 participants were included in the meta-analysis. The results showed that chia consumption significantly decreased CRP (WMD: –0.64 mg/dl; 95% CI: –1.24, –0.04; P = 0.03). But it had no significant effect on IL-6 (WMD: 0.29 pg/dl; 95% CI: –0.40, 0.98; P = 0.41), and TNF-α (WMD: 0.05%; 95% CI: –0.21 to 0.30; P = 0.72). Chia consumption can significantly decrease CRP, but no significant effect was observed on IL-6 and TNF-α. To prove our findings, more studies with a larger sample size are needed.

Recent development in immunotherapy for cancer treatment has substantiated to be more effective than most of the other treatments. Immunity is the first line of defence of the body; nevertheless, cancerous cells can manipulate immunity compartments to play several roles in tumour progression. Tumour-associated macrophages (TAMs), one of the most dominant components in the tumour microenvironment, are recognized as anti-tumour suppressors. Unfortunately, the complete behaviour of TAMs is still unclear and understudied. TAM density is directly correlated with the progression and poor prognosis of hepatocellular carcinoma (HCC), therefore studying TAMs from different points of view passing by all the factors that may affect its existence, polarization, functions and repolarization are of great importance. Different epigenetic regulations were reported to have a direct relation with both HCC and TAMs. Here, this review discusses different epigenetic regulations that can affect TAMs in HCC whether positively or negatively.

Summary

Background and objectives: Apoptosis occurs after thermal injury and may result from either ischaemic intestinal insult or inflammatory mediators released after burn injury. The aim of the study was to investigate the effects of propofol and ketamine on gut epithelium apoptosis after burn injury. Methods: Sixty male Wistar Albino rats were randomly assigned into four groups. Anaesthesia was induced and maintained with propofol in Groups 1 and 2, and ketamine in Groups 3 and 4 over 12 h. Groups 2 and 4 received 30% total body surface area burn. Groups 1 and 3 had no burn injury. Mean arterial pressure was maintained within 10% of baseline levels in all animals. At 12 h postburn, animals were sacrificed and tissue samples were taken from small intestine for determination of lipid peroxidation, apoptosis and proliferation. Also blood samples were taken for measurement of serum tumor necrosis factor-alpha (TNF-α) levels. Results: Ileal malondialdehyde (MDA) concentration (extent of lipid peroxidation) increased significantly in Group 4 (112.4 ± 10.2 nmol g−1) compared to Group 3 (48.4 ± 5.6 nmol g−1) and Group 2 (59.8 ± 3.2 nmol g−1). The mean TNF-α level in Group 4 (118.9 ± 10.5 pg mL−1) at 12 h postburn was significantly higher than the mean in Group 2 (56.4 ± 4.3 pg mL−1). Group 4 had the highest mean TUNEL index (terminal deoxyuridine nick-end labelling – an index of extent of apoptosis) of all the groups (265/10). Also the mean TUNEL index value in Group 2 (53/10) was higher than that of Group 1 (3/10) and Group 3 (5/10). The proliferating cell nuclear antigen index (extent of proliferation) remained unchanged among groups. Conclusions: Propofol could offer a protection against apoptosis of enterocytes with a stable tissue MDA and serum TNF-α level compared to ketamine anaesthesia in an animal model of burn injury.

Damage to the surface membrane of adult Schistosoma mansoni, and the activity of the excretory system, as shown by resorufin fluorescence, was observed following treatment with praziquantel and incubation with other molecules. Praziquantel treatment induced damage to the surface membrane as measured by the use of a variety of fluorescent compounds. The excretory system of the male worm was inhibited immediately after praziquantel treatment, but fully recovered after culture for 2 h following removal of praziquantel. The excretory system of the female, observed to be minimally active in untreated worm pairs, was often greatly activated in paired females, as shown by intense resorufin labelling, after praziquantel treatment, and this continued during recovery of the male excretory system. In experiments with normal worm pairs, the female could be activated by inhibiting the metabolic rate of the pair by a cooling procedure. The effects on the excretory system of changes in culture conditions (such as changes in pH, concentrations of bacterial lipopolysaccharide, cytokines, reactive oxygen species, compounds which remove cholesterol, such as beta-methyl cyclodextrin, and damaging basic poly-L-lysine) were also assessed. It is concluded that the extensive excretory system of the adult worm is responsive to drug treatment and to certain changes in environmental conditions. Its activity seems to be strongly linked to the integrity of the surface membrane.

Cytokine responses to Leishmania infection begin very early in infection, and differ between susceptible and resistant mice. Susceptibility to chronic Leishmania infection has been associated with increased haematopoiesis. To analyse the effect that acute infection with L. major has on bone-marrow haematopoiesis in susceptible (BALB/c) and resistant (CBA) mice, we enumerated erythroid progenitors and granulocyte-monocyte progenitors 3 days after infection. We found that haematopoiesis was stimulated in BALB/c mice infected with L. major, while haematopoiesis was inhibited in CBA mice. We found that this effect could be partially explained by cytokine production: interleukin-4 was involved in stimulation of BALB/c haematopoiesis and tumour necrosis factor-α was involved in inhibition of CBA haematopoiesis. Our conclusions are that haematopoietic changes occur shortly after L. major infection, and may be related to disease outcome.