Effects of acupressure on the childbirth satisfaction and experience of birth: A randomized controlled trial

BackgroundComplementary and alternative medicines have been used to increase comfort and relaxation in mothers during labor. Comforting and preparing the mother in labor can create a positive birth experience. The aim of this study was to evaluate the effect of acupressure on childbirth satisfaction and the experience of giving birth in women with full-term pregnancy, before the onset of labor.MethodsIn 2016, a randomized clinical trial study was conducted in Shahid Akbar Abadi Hospital, Tehran, Iran, enrolling 120 pregnant women at 39–40 gestational weeks with no signs of the onset of labor. They were divided randomly into acupressure, sham acupressure, and control groups. Acupressure points including SP6, BL 60, and BL 32 were pressured bilaterally. Interventions were performed by the researcher, the mother and her relative (husband). Childbirth satisfaction was measured 24 h after delivery. The collected data were analyzed by SPSS software and comparing tests were Chi-squared, Kruskal-Wallis, ANOVA tests (P ≤ 0.05).ResultsThe total childbirth satisfaction did not differ significantly among the three groups (P = 0.460), but the acupressure group had a higher level of satisfaction than the other two groups. Moreover, statistical tests regarding the expectations of the childbirth experience showed a significant difference among the groups (P = 0.033). The actual birth was closest to the expectations of subjects in the acupressure group.ConclusionThis study demonstrated that acupressure may be used as a method in order to attempt to provide a good birth experience and satisfaction of childbirth.     

Oral administration of PEGylated TLR7 ligand ameliorates alcohol-associated liver disease via the induction of IL-22

Effective therapies for alcohol-associated liver disease (ALD) are limited; therefore, the discovery of new therapeutic agents is greatly warranted. Toll-like receptor 7 (TLR7) is a pattern recognition receptor for single-stranded RNA, and its activation prevents liver fibrosis. We examined liver and intestinal damage in Tlr7^−/− mice to determine the role of TLR7 in ALD pathogenesis. In an alcoholic hepatitis (AH) mouse model, hepatic steatosis, injury, and inflammation were induced by chronic binge ethanol feeding in mice, and Tlr7 deficiency exacerbated these effects. Because these results demonstrated that endogenous TLR7 signaling activation is protective in the AH mouse model, we hypothesized that TLR7 activation may be an effective therapeutic strategy for ALD. Therefore, we investigated the therapeutic effect of TLR7 agonistic agent, 1Z1, in the AH mouse model. Oral administration of 1Z1 was well tolerated and prevented intestinal barrier disruption and bacterial translocation, which thus suppressed ethanol-induced hepatic injury, steatosis, and inflammation. Furthermore, 1Z1 treatment up-regulated the expression of antimicrobial peptides, Reg3b and Reg3g, in the intestinal epithelium, which modulated the microbiome by decreasing and increasing the amount of Bacteroides and Lactobacillus, respectively. Additionally, 1Z1 up-regulated intestinal interleukin (IL)-22 expression. IL-22 deficiency abolished the protective effects of 1Z1 in ethanol-induced liver and intestinal damage, suggesting intestinal IL-22 as a crucial mediator for 1Z1-mediated protection in the AH mouse model. Collectively, our results indicate that TLR7 signaling exerts protective effects in the AH mouse model and that a TLR7 ligand, 1Z1, holds therapeutic potential for the treatment of AH.

Alcohol-associated liver disease (ALD) is caused by chronic and excessive consumption of alcohol. The disease ranges from alcohol-associated fatty liver to alcoholic hepatitis (AH), fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) (1). Alcohol-associated fatty liver is considered reversible and nonprogressive. Nearly 35% of heavy alcohol drinkers develop AH, and up to 40% of severe AH patients die within 6 mo (2). AH patients who survive may progress to alcohol-associated cirrhosis. Treatment options for AH involve the use of corticosteroids and have remained largely unchanged since the early 1970s. Unfortunately, not all patients respond to corticosteroids, and the benefits are temporary in responders (1, 2). Early liver transplant has been shown to be superior to medical management for severe AH, but it still has limitations and can only be considered in a highly selective group of patients (1, 2). Thus, the identification of a better molecular therapeutic target for ALD is a significantly unmet medical need for the development of effective therapies for AH.Previous studies have demonstrated the involvement of Toll-like receptors (TLRs), including TLR2, TLR4, and TLR9, in the development of ALD (3–8). In addition to the direct effect of alcohol and its metabolite, acetaldehyde, in hepatocytes, ethanol intake affects the function of the intestinal epithelial barrier. Chronic alcohol consumption disrupts intestinal tight junction integrity and increases gut permeability, resulting in elevated bacterial lipopolysaccharide (LPS) concentrations in the portal and systemic circulation (4). Translocated LPS activates resident hepatic macrophages, known as Kupffer cells, via TLR4, thereby promoting ALD (1, 2, 7, 8). Other TLRs, such as TLR2 and TLR9, recognize gram-positive bacterial components and bacterial CpG-DNA, respectively (3, 4). Furthermore, TLR2, TLR9, and MyD88 are required for the development of the preclinical AH murine model (5), whereas TLR4 and TLR9 exert protective effects against intestinal inflammation (9, 10).TLR7 signaling has been shown to be protective against liver fibrosis in mice (11). Tlr7^−/− mice exhibit augmented cholestasis and carbon tetrachloride (CCl₄)-induced liver fibrosis (11). TLR7 signaling also induces IFN-α production in dendritic cells (DCs), followed by interleukin (IL)-1 receptor antagonist (IL-1Ra) induction in Kupffer cells. IL-1Ra suppresses IL-1-induced hepatic stellate cell (HSC) activation, resulting in inhibition of liver fibrosis (11). Among the TLRs, TLR3 and TLR7 activation has been reported to ameliorate some liver diseases (11, 12). However, a major disadvantage of the currently available synthetic ligands for TLR3 and TLR7, such as poly I:C, imiquimod, and R848, is the excessive induction of proinflammatory cytokines (3, 4). Thus, developing agents without undesirable adverse effects is of great clinical interest.IL-22 is a hepatoprotective cytokine produced by T helper (Th) 17 cells, Th22 cells, γδ T cells, natural killer (NK) T cells, and innate lymphoid cells (ILCs) (13). Exogenous administration of IL-22 has a profound effect on tissue repair following liver injury via the promotion of proliferation and inhibition of apoptosis in hepatocytes of mouse models of AH (14), liver fibrosis, and drug- and LPS-induced liver injury. Also, IL-22 promotes tissue repair in the intestines and is protective against intestinal epithelial damage and inflammation (13). These findings suggest that IL-22 may suppress ALD via the maintenance of intestinal barrier function, thereby preventing increased intestinal permeability and bacterial translocation due to intestine-derived microbial products that promote ethanol-induced liver injury (15, 16).Here, we have developed a synthetic TLR7 ligand, 1Z1, that possesses antiinflammatory effects via IL-22 induction and that is devoid of systemic toxicity after oral administration (17–19). Treatment with 1Z1 has already been reported to be effective for allergic encephalomyelitis, arthritis, dextran sodium sulfate (DSS)-induced colitis, and type I diabetes in mice (17–20). We hypothesize that targeting TLR7 activation may be an effective treatment strategy for ALD. Our experimental results demonstrate that 1Z1 oral administration inhibits ethanol-induced liver and intestinal damage and that these beneficial effects are due to intestinal IL-22 induction in an AH murine model.     

Marginal Adaptation of CAD/CAM All‐Ceramic Crowns Made by Different Impression Methods: A Literature Review

All‐ceramic crowns for teeth are widely used for restoring teeth. Stone casts have been made from conventional impression methods; however, newer techniques have made this process easier and faster for both the patient and the practitioner. Laboratory CAD/CAM technology mainly involves scanning the die stone, while other systems permit impression or intraoral scanning; however, one major concern remaining is the marginal fit of the restorations made using different methods for recording the prepared teeth. This study aims to review studies evaluating the marginal fit of all‐ceramic crowns manufactured by CAD/CAM systems using different extra‐ and intra‐oral scanners compared to conventional impressions.     

Platelet Storage Media Change the Expression Characteristics of the Platelet-Derived Microparticles

Activated platelets shed microparticles in vivo and definitely in vitro upon aging under storage. Studies about the platelet-derived microparticles (PMPs) produced in different storage media of PC were very limited. The aim of this research was to compare some surface molecules of these microvesicles in dissimilar microenvironments; plasma and the candidate medium for the platelet concentrate, Composol. Thirty units of PCs were prepared from Iranian Blood Transfusion Organization. Each unit was divided into two portions. In one of the portions, plasma was replaced with Composol using a connecting device instrument. MPs were isolated from PC and the levels of PS exposure (the annexin-binding capacity) and binding to vWF were surveyed on their surface using ELISA and flow cytometry techniques. The levels of PS exposure were increased on MPs during 7 days storage in the both media but the differences were not significant (P value >0.05). In addition, binding of PMP to vWF was declined during storage. The binding capabilities of PMP were significantly higher in Composol than that of plasma at the day 4 or 7 of storage (P value = 001). It seemed that the binding of PMPs to vWF was affected from the storage media of PC (plasma and Composol) but PS exposure was not affected from the type of storage media.     

Synthesis,functionalization, and isolation of planar-chiral pillar[5]arenes with bulky substituents using a chiral derivatization agent

Bulky perneopentyloxy-pillar[5]arene (Pillar-1) was synthesized and its conformational mobility was investigated using variable-temperature ¹H NMR spectroscopy. The host–guest interactions between Pillar-1 and n-octyltrimethylammonium hexafluorophosphate (OMA) were investigated, and the formation of a 1 : 1 complex was revealed via¹H NMR. Planar-chiral isomers were synthesized via the reaction of a hydroxy-functionalized pillar[5]arene with chiral derivatization agent (S)-(+)-MTPA-Cl. The (Sp, R)-and (Rp, R)-forms of the pillar[5]arene diastereomers were isolated by HPLC, and their structures were analyzed by ¹⁹F NMR. HPLC measurements indicated that racemization did not take place at 40 °C for 72 h.

Bulky perneopentyloxy-pillar[5]arene was synthesized. Complexation behavior and conformational mobility were investigated using ¹H NMR spectroscopy. Isolation of planar-chiral pillar[5]arenes using a chiral derivatization agent were carried out.     

A new series of Schiff base derivatives bearing 1,2,3‐triazole: Design,synthesis, molecular docking,and α‐glucosidase inhibition

A series of new Schiff bases bearing 1,2,3‐triazole 12a ? o was designed, synthesized, and evaluated as α‐glucosidase inhibitors. All the synthesized compounds showed promising inhibition against α‐glucosidase and were more potent than the standard drug acarbose. The kinetic study on the most potent compound 12n showed that this compound acted as a competitive α‐glucosidase inhibitor. The docking study revealed that the synthesized compounds interacted with the important residues in the active site of α‐glucosidase.     

Evaluation of the Incidence of Chronic Thromboembolic Pulmonary Hypertension 1 Year After First Episode of Acute Pulmonary Embolism: A Cohort Study

Purpose

Chronic thromboembolic pulmonary hypertension (CTEPH) is an important complication after acute pulmonary embolism (PE) with considerable morbidity and mortality. The aim of this study was to estimate the CTEPH incidence in a cohort after the first occurrence of PE.

Methods

We conducted a 1-year follow-up cohort study between 2015 and 2018 to assess the incidence of CTEPH in 474 patients with their first acute episode of PE. For the diagnosis of CTEPH, patients with unexplained persistent dyspnea during follow-up underwent transthoracic echocardiography, right heart catheterization, ventilation-perfusion lung scanning, and CT pulmonary angiography.

Results

Overall, 317 patients were included in the study. The mean age of the patients was 56.5 ± 16 years. One hundred and three patients (32%) had exertional dyspnea at the 1-year follow-up. Patients with evidence of pulmonary hypertension (PH) on echocardiography underwent right heart catheterization. Eleven patients (18%) had no PH (mPAP < 25 mmHg); 47 patients (81%) had mPAP > 25 mmHg. Fifteen patients had PAWP > 15 mmHg, including those with underlying left heart problems or valvular diseases. There were 32 patients with PAH (mPAP > 25 mmHg and PVR > 3 WU) undergoing CTEPH studies; 22 patients (6.9%) had multiple segmental defects suggesting CTEPH on a perfusion scan.

Conclusion

The incidence of CTEPH observed in this study 1 year after the first episode of acute PE was approximately 6.9%. This incidence seems to be high in our population, and diagnostic and therapeutic strategies for the early identification of CTEPH are needed.