A review of the functional activities of chia seed and the mechanisms of action related to molecular targets.

In recent years, as a functional potential pseudocereal, chia seed (Salvia hispanica L.) has been of great interest for its comprehensive nutritional profile and attractive qualities after ingestion. It is reported that a reasonable dietary supplementation of chia seed (CS) contributes to the prevention and treatment of acute and chronic diseases (inflammation, diabetes, hypertension, obesity, kidney stone, etc.). CS contains a variety of bioactive macromolecular substances, such as oil, protein and gum, which manifest distinguished health-promoting activities in both in vivo and in vitro research studies. This article provides a comprehensive compendium on the functional importance of CS, in the context of biological activities and mechanism of actions of CS. Specifically, CS and its components alleviate inflammation and regulate glucose and fatty acid metabolism by regulating key influencing factors in the adenosine 5'-monophosphate-activated protein kinase (AMPK), mitogen-activated protein kinases (MAPK), nuclear factor kappa B (NF-κB), peroxisome-activated receptor gamma (PPAR-γ) and transforming growth factor-beta (TGF-ß) pathways and the insulin receptor substrate (IRS)-mediated insulin signaling pathway. In the meantime, predictions of metabolic pathways of CS peptides based on the known tracks of newly researched active peptides were proposed, with the aim of emphasizing the enormous research space of CS peptides compared to other functional active peptides.

Comparison of postoperative analgesia in children following ropivacaine and lidocaine surgical field infiltration with epinephrine for cleft palate repair: A double-blinded, randomized controlled trial.

STUDY OBJECTIVE: The study aimed to evaluate the efficacy of ropivacaine in providing postoperative analgesia for children undergoing cleft palate repair. METHODS: A double-blinded, randomized controlled trial was conducted on sixty-four children scheduled for cleft palate repair. The patients received either local infiltration with 1% lidocaine or 0.2% ropivacaine before incision. The primary outcome was the postoperative average pain score, and secondary outcomes included pain scores at various time points, consumption of flurbiprofen and hydromorphone, effectiveness of nurse-controlled analgesia pump, and incidence of bradycardia, vomiting, and respiratory depression. MAIN RESULTS: The results showed that the postoperative average pain score was significantly lower in the ropivacaine group compared to the lidocaine group (1.27±0.28 vs. 1.75±0.29, P<0.001). Pain scores at multiple postoperative time points were also lower in the ropivac:aine group. Additionally, consumption of flurbiprofen and hydromorphone was lower, and ineffective compressions of the nurse-controlled analgesia pump were reduced in the ropivacaine group. The incidence of vomiting, bradycardia, and respiratory depression did not show significant differences between the two groups. CONCLUSION: Local infiltration with ropivacaine effectively provided postoperative analgesia for children undergoing cleft palate repair without major side effects. It was found to be superior to lidocaine in reducing the need for additional rescue analgesia.

Outcomes after natural orifice extraction vs conventional specimen extraction surgery for colorectal cancer: A propensity score-matched analysis.

BACKGROUND: Natural orifice specimen extraction (NOSE) via the anus or vagina replaces conventional transabdominal specimen retrieval via the transabdominal route through a limited mid-line laparotomy or Pfannenstiel incision. Reducing the number of laparoscopic ports further decreases operative abdominal wall trauma. These techniques reduce the surgical wound size as well as the risk of incision-related morbidity. AIM: To compare short-term outcomes following 3-port NOSE surgery with a matched cohort of conventional non-NOSE colorectal cancer surgery. METHODS: Patients who underwent elective 3-port laparoscopic colorectal NOSE surgery between February to October 2021 were identified. Selection criteria for NOSE surgery was adapted from the 2019 International Consensus on Natural Orifice Specimen Extraction Surgery for colorectal cancer. Patients with clinical T4 or N2 tumors on staging computed tomography were also excluded. The propensity score-matched cohort was identified amongst patients who underwent conventional laparoscopic colorectal surgery from January 2019 to December 2020. Matching was performed in the ratio of 1:4 based on age, gender, type of resection, and p - tumor node metastasis staging. RESULTS: Over the eight-month study duration, 14 consecutive cases (nine female, five male) of elective 3-port laparoscopic surgery with NOSE were performed for colorectal cancer. Median age and body mass index were 70 (range 43-82) years and 24.1 (range 20.0-31.7) kg/m2 respectively. Six patients underwent transanal NOSE and eight had transvaginal NOSE. Median operative time, intraoperative blood loss and postoperative length of stay were 208 (range 165-365) min, 30 (range 10-150) mL and 3 (range 2-6) d respectively. Two (14%) suffered minor postoperative compilations not attributable to the NOSE procedure. Median follow-up duration was 12 (range 8-15) mo. No instances of mortality, local or distant disease recurrence were recorded in this cohort. Compared to the conventional surgery cohort of 56 patients, the 3-port NOSE cohort had significantly quicker mean return of bowel function (2.6 vs 1.2 d, P < 0.001), reduced postoperative pain and patient-controlled analgesia use, and decreased length of hospital stay (6.4 vs 3.4 d, P < 0.001). There were no statistical differences in surgical duration and perioperative complication rates between the NOSE and non-NOSE cohorts. CONCLUSION: 3-port laparoscopic colorectal surgery with NOSE is a feasible technique, augmenting the minimally invasive nature of surgery and producing good outcomes. Appropriate patient selection and expertise in conventional laparoscopy are required.

Programmed Intermittent Epidural Bolus in Comparison with Continuous Epidural Infusion for Uterine Contraction Pain Relief After Cesarean Section: A Randomized, Double-Blind Clinical Trial.

Purpose: Programmed intermittent epidural bolus (PIEB) was reported to provide superior maintenance of labour analgesia with better pain relief and less motor block than continuous epidural infusion (CEI). Whether this is also evident for uterine contraction pain relief after cesarean section remains unknown. Patients and Methods: Parturients scheduled for cesarean section were recruited for the study. At the end of the surgery, after a similar epidural loading dose given, patients received either PIEB (6 mL·h-1) or CEI (6 mL·h-1) of 0.1% ropivacaine. The primary outcome was the uterine contraction pain assessed with visual analog scale (VAS-U) at the postoperative 36 h. Secondary outcomes included incision pain at the rest (VAS-R) and in the movement-evoked (VAS-P), and lower extremity motor block (defined as Bromage score > 0). The whole profile of VAS scores between groups was analyzed using linear mixed model. When significant differences were found, the pairwise comparison was done with the Mann Whitney U-test followed by Bonferroni correction. Results: One hundred and twenty parturients were studied (PIEB, 60; CEI, 60). VAS-U at the postoperative 36 h in the PIEB group was lower than in the CEI group (Bonferroni-adjusted P < 0.01). The linear mixed model indicated that VAS-U, VAS-R and VAS-P were lower in the PIEB group compared with the CEI group (all P < 0.01). Motor block was higher in the CEI group than in the PIEB group during the study period except 2 h (all P < 0.05). No differences of adverse events such as hypotension and urinary retention were observed between the two groups. Conclusion: Programmed intermittent epidural bolus provides more effective uterine contraction and incision pain relief and less motor block after cesarean section than continuous epidural infusion without an increased risk of urinary retention and blood pressure instability.

A novel mutation in the STK11 gene causes heritable Peutz-Jeghers syndrome - a case report.

BACKGROUND: Peutz-Jeghers syndrome (PJS) is a rare disorder characterized by multiple gastrointestinal hamartomatous polyps and mucocutaneous pigmentation. STK11 has been identified as a causative gene for this disease. CASE PRESENTATION: Herein we report a Chinese Han kindred with PJS. Onset for the PJS signs in three of the patients was rarely as early as at birth. We identified a novel heterozygous mutation (c.440_441delGT, p.Arg147Leufs*15) in the gene STK11, causing a short frameshift followed by a deletion of 63% of the amino acids in the STK protein. This mutation co-segregated with the PJS phenotype, and was absent in two hundred of unrelated ethnicity-matched controls. The mutation led to expression decrease of unaffected STK11 protein in patients than in controls, as well in PJ polyps than in circulating leucocytes from the patients. Phosphorylation levels of the downstream kinase AMPKα altered according with the expression of STK11. These results indicated the possibility that haploinsufficiency and epigenetic reduction of STK11 contributed to the pathogenesis of the disease. CONCLUSION: This study identifies a novel mutation in the pathogenic gene STK11 leading to PJS.

TRPC3 channel confers cerebrovascular remodelling during hypertension via transactivation of EGF receptor signalling.

AIMS: Ionic perturbation in vascular smooth muscle cells contributes to cerebrovascular remodelling in the setting of hypertension, but the role of transient receptor potential (TRP) channel superfamily remains unknown. The present study was conducted to define the contribution of TRP channels to cerebrovascular remodelling. METHODS AND RESULTS: By integrating quantitative PCR, western blotting, patch clamping, and Ca(2+) imaging, we identified TRP channel, subfamily canonical, member 3 (TRPC3) as the channel subtype most considerably elevated in basilar arteries of two-kidney, two-clip stroke-prone hypertensive rats. Importantly, administration of pyrazole 3 (Pyr3), a TRPC3 channel blocker, attenuated cerebrovascular remodelling. During hypertension, epidermal growth factor receptor (EGFR) was transactivated, as evidenced by marked EGFR phosphorylation, increased pro-HB-EGF shedding, and elevated activity of ADAM17 (HB-EGF sheddase). ADAM17 activity was increased owing to enhanced activation rather than elevated expression. Remarkably, Pyr3 treatment suppressed EGFR transactivation in hypertension. In proliferating basilar artery smooth muscle cells or basilar arteries of hypertensive rats, co-immunoprecipitation assay revealed an interaction between TRPC3 and ADAM17 upon Ang II stimulation. CONCLUSION: Collectively, we demonstrated that enhanced EGFR transactivation, due to increased TRPC3 expression and functional coupling of TRPC3/ADAM17, resulted in cerebrovascular remodelling. Therefore, TRPC3-induced EGFR transactivation may be therapeutically exploited to prevent hypertension-induced cerebrovascular remodelling.

Activation of α2 adrenoceptor attenuates lipopolysaccharide-induced hepatic injury.

Sepsis induces hepatic injury but whether alpha-2 adrenoceptor (α2-AR) modulates the severity of sepsis-induced liver damage remains unclear. The present study used lipopolysaccharide (LPS) to induce hepatic injury and applied α2-AR agonist dexmedetomidine (DEX) and/or antagonist yohimbine to investigate the contribution of α2-AR in LPS-induced liver injury. Our results showed that LPS resulted in histological and functional abnormality of liver tissue (ALT and AST transaminases, lactate), higher mortality, an increase in proinflammatory cytokines (IL-1ß, IL-6 & TNF-α), as well as a change in oxidative stress (MDA, SOD). Activation of α2-AR by dexmedetomidine (DEX) attenuated LPS-induced deleterious effects on the liver and block of α2-AR by yohimbine aggravated LPS-induced liver damage. Our data suggest that α2-AR plays an important role in sepsis-induced liver damage and activation of α2-AR with DEX could be a novel therapeutic avenue to protect the liver against sepsis-induced injury.

In Vivo Evaluation of the Ameliorating Effects of Small-Volume Resuscitation with Four Different Fluids on Endotoxemia-Induced Kidney Injury.

Acute kidney injury associated with renal hypoperfusion is a frequent and severe complication during sepsis. Fluid resuscitation is the main therapy. However, heart failure is usually lethal for those patients receiving large volumes of fluids. We compared the effects of small-volume resuscitation using four different treatment regimens, involving saline, hypertonic saline (HTS), hydroxyethyl starch (HES), or hypertonic saline hydroxyethyl starch (HSH), on the kidneys of rats treated with lipopolysaccharide (LPS) to induce endotoxemia. LPS injection caused reduced and progressively deteriorated systemic (arterial blood pressure) and renal hemodynamics (renal blood flow and renal vascular resistance index) over time. This deterioration was accompanied by marked renal functional and pathological injury, as well as an oxidative and inflammatory response, manifesting as increased levels of tumor necrosis factor-α, nitric oxide, and malondialdehyde and decreased activity of superoxide dismutase. Small-volume perfusion with saline failed to improve renal and systemic circulation. However, small-volume perfusion with HES and HSH greatly improved the above parameters, while HTS only transiently improved systemic and renal hemodynamics with obvious renal injury. Therefore, single small-volume resuscitation with HES and HSH could be valid therapeutic approaches to ameliorate kidney injury induced by endotoxemia, while HTS transiently delays injury and saline shows no protective effects.

Cotransplantation of glial restricted precursor cells and Schwann cells promotes functional recovery after spinal cord injury.

Oligodendrocyte (OL) replacement can be a promising strategy for spinal cord injury (SCI) repair. However, the poor posttransplantation survival and inhibitory properties to axonal regeneration are two major challenges that limit their use as donor cells for repair of CNS injuries. Therefore, strategies aimed at enhancing the survival of grafted oligodendrocytes as well as reducing their inhibitory properties, such as the use of more permissive oligodendrocyte progenitor cells (OPCs), also called glial restricted precursor cells (GRPs), should be highly prioritized. Schwann cell (SC) transplantation is a promising translational strategy to promote axonal regeneration after CNS injuries, partly due to their expression and secretion of multiple growth-promoting factors. Whether grafted SCs have any effect on the biological properties of grafted GRPs remains unclear. Here we report that either SCs or SC-conditioned medium (SCM) promoted the survival, proliferation, and migration of GRPs in vitro. When GRPs and SCs were cografted into the normal or injured spinal cord, robust survival, proliferation, and migration of grafted GRPs were observed. Importantly, grafted GRPs differentiated into mature oligodendrocytes and formed new myelin on axons caudal to the injury. Finally, cografts of GRPs and SCs promoted recovery of function following SCI. We conclude that cotransplantation of GRPs and SCs, the only two kinds of myelin-forming cells in the nervous system, act complementarily and synergistically to promote greater anatomical and functional recovery after SCI than when either cell type is used alone.

Small volume resuscitation with 7.5% hypertonic saline, hydroxyethyl starch 130/0.4 solution and hypertonic sodium chloride hydroxyethyl starch 40 injection reduced lung injury in endotoxin shock rats: comparison with saline.

BACKGROUND: The aim of this study was to investigate the effects of small volume resuscitation with 7.5% hypertonic sodium chloride (HSS), hydroxyethyl starch 130/0.4 solution (HES), and hypertonic sodium chloride hydroxyethyl starch 40 injection (HSH) on endotoxin shock rat lung. METHODS: Thirty Sprague-Dawley (SD) rats were divided randomly into 5 groups ，Group C (negative control group), Group E (lipopolysaccharide, LPS +4 ml/kg saline), Group HSS (LPS +4 ml/kg HSS), Group HES (LPS +4 ml/kg HES) and Group HSH (LPS +4 ml/kg HSH). Endotoxin shock model of rat was produced by injection with LPS. Then small volume resuscitation with different fluids was implemented in each group, respectively. RESULTS: Compared to Group C(negative control group）, lung injury in the other four groups was increased. Compared to Group E(LPS +4 ml/kg normal saline), lung injury of Group HSS(LPS +4 ml/kg HSS), HES(LPS +4 ml/kg HES), and HSH (LPS +4 ml/kg HSH)was lessened. Compared to Group C, oxygenation index in Groups E, HSS, HES, and HSH were decreased (P < 0.01). Compared to Group E, oxygenation indexes in Groups HSS, HES, and HSH were significantly increased (P < 0.01). Data of tumor necrosis factor (TNF)-α of lung tissue had similar results. However, protein concentration of bronchoalveolar lavage fluid and hydrogen sulfide (H(2)S) concentration indicated contrary results. CONCLUSION: Small volume resuscitation with 7.5% hypertonic sodium chloride, hydroxyethyl starch 130/0.4 solution, and hypertonic sodium chloride hydroxyethyl starch 40 injection could lessen lung injury caused by lipopolysaccharide. And this effect had relation to change of TNF-α and H(2)S.