Treatment of Umbilical Granuloma in Infants With Topical Application of Common Salt: A Scoping Review

BackgroundCommon salt is a safe, effective and cheap home-made remedy for umbilical granuloma. The aim of this scoping review is to identify and summarize the available evidence and examine the research conducted on salt treatment for umbilical granuloma.MethodsA literature search was performed in the second week of September, 2022 using Google scholar, PubMed, MEDLINE and EMBASE databases using the keywords ‘umbilical granuloma’ and ‘salt treatment’ to identify all English articles pertaining to salt treatment for umbilical granuloma. Tables were made to summarize the methodological characteristics, results and the dosage regimens of salt used by different authors. The Cochrane Collaboration's tool was used for assessing risk of bias in RCTs. The indexing statuses of the journals publishing these studies were also noted. The overall efficacy with the use of common salt was calculated by adding the success rates mentioned in each study.ResultsTwenty-four articles (2 systematic reviews, 6 Randomized Controlled Trials, 11 prospective cohort studies, 1 case control study, 3 retrospective case series and 1 case report) were included. An overall 93.91% success rate (1033/1100) was seen with common salt application, without any reports of complications/recurrences.ConclusionTopical application of common salt for umbilical granulomas is simple, effective and inexpensive. This scoping review provides a broader outlook at the existing level of evidence and may help in planning interventional comparative studies, so that recommendations can be formulated. It also highlights a lack of properly designed randomized controlled trials on this topic.Level of EvidenceI.     

Influence Factors and Prediction Model of Bond Strength of Tunnel Fireproof Coating under Freeze–Thaw Cycles

The freeze–thaw resistant performance of a tunnel fireproof coating (TFC) has an important impact on bonding property and durability. The influence of redispersible emulsion powder, polypropylene fiber and air-entraining agent on TFCs was studied. Transverse fundamental frequency and ultrasonic sound velocity were used to evaluate the damage degree of TFC, and the mechanism was revealed by SEM and pore structure. The results show that the most beneficial effect on bond strength of TFC is redispersible emulsion powder, followed by air-entraining agent, and then polypropylene fiber. After freeze–thaw cycles, the cumulative pore volume of micropores in the TFC increases obviously, while the porosity of macropores does not change significantly. A prediction model was proposed, which can calculate the bond strength from the damage degree of TFC under freeze–thaw cycles. The achievement can promote the application of TFC in cold regions.     

Effect of high salt diet on the renal medullary cyclooxygenase 2 expression

Objective To examine the effect and mechanism of high salt diet on the renal medullary cyclooxygenase 2 (COX2) expression and urinary sodium excretion. Methods Thirty male C57BL/6j mice were divided into four groups: (1) normal salt diet group (0.4%NaCl, n=5); (2) high salt diet group (8% NaCl, n=5); (3) Bortezomib+normal salt diet group (n=10); (4) Bortezomib+high salt diet group (n=10). The different groups were pre-treated with saline or bortezomib，followed by normal salt diet or high salt diet for three days. All the mice were maintained on metabolic cage at the last day and allowed free access to water. Twenty-four hours urine was collected. Body weight, urine volumes were documented. At the end of experiments, mice were sacrificed under anesthesia and the kidneys were harvested for Western blotting and immunohistochemistry. The transgenic mice carrying a luciferase reporter driven by an NF-κB response promoter, HIV long terminal repeat (LTR) (HLL mice) were used to explore the effect of high salt diet on renal medullary NF-κB activity. HLL mice were fed with normal salt diet or high salt diet for 3 days, after which renal medullary luciferase activity was determined using a commercial luciferase assay kit. Luciferase activity was quantified with a luminometer and adjusted for the total amount of proteins. The cellular location of NF-κB was examined using immunohistochemistry of NF-κB p65 staining. Results (1) Western blotting results showed high salt diet significantly increased the COX2 expression in the renal medulla of C57BL/6j mice (P﹤0.05). (2) High salt diet significantly increased NF-κB luciferase reporter activity in the HLL mice renal medullary tissues when compared to normal salt diet (P﹤0.05). The immunohistochemistry of NF-κB p65 showed the expression of NF-κB was mainly in the renal interstitial cells. (3) Western blotting results showed bortezomib inhibited the renal medullar COX2 expression induced by high salt diet (P﹤0.05). (4) Bortezomib decreased the urinary sodium excretion of high salt diet mice (P﹤0.05), but had no change on urine volume. Conclusions High salt diet induce renal medullary COX2 over-expression and activate the activation of NF-κB in renal medullary. Bortezmoib can inhibit the renal medullar COX2 expression induced by high salt diet. The NF-κB pathway activation may involve in the regulation of renal medullar COX2 expression by high salt diet.     

生物活性玻璃预处理对牙本质粘接界面耐久性的影响

目的:研究生物活性玻璃(bioactive glass, BG)预处理对维持牙本质粘接界面耐久性的作用。方法:选取30颗无龋坏第三磨牙,去除冠部釉质制备牙本质平面,随机均分对照组、BG组、三偏磷酸钠(sodium trimetaphosphate, STMP)-聚丙烯酸(polyacrylic acid, PAA)-BG组(S-P-BG组)。各组均使用35%(质量分数)磷酸酸蚀牙本质样本,BG组再使用0.5 g/L BG涂擦酸蚀后的牙本质样本;S-P-BG组先使用5%(质量分数)STMP、5%(质量分数)PAA浸泡酸蚀后的牙本质样本1 min,再使用0.5 g/L BG涂擦牙本质样本。各组样本使用3M Single Bond 2粘接剂及3M Z350XT复合树脂粘接,并制备微拉伸柱状样本,每颗牙的柱状样本按时间随机分为24 h、1个月、3个月组。各组样本保存在37 ℃人工唾液(artificial saliva, AS)中相应时间后,进行微拉伸粘接强度测试,并使用单因素方差分析及LSD法进行统计学分析,扫描电镜下观察粘接断裂界面形貌。另选取27颗无龋坏第三磨牙制备牙本质平面,随机分为对照组、BG组、S-P-BG组,并按上述分组处理牙本质样本,再使用含0.1%(质量分数)罗丹明B的3M Single Bond 2粘接剂完成粘接。去除样本牙根暴露髓腔,并保存在 37 ℃ AS中24 h、1个月、3个月后,髓腔内放置0.1(质量分数)荧光素钠溶液染色1 h,激光共聚焦显微镜观察粘接界面形态及混合层微渗漏。结果:AS中浸泡24 h、1个月后,3组微拉伸粘接强度间的差异无统计学意义(P>0.05);浸泡3个月后,S-P-BG组微拉伸粘接强度为(36.91±7.07) MPa,高于对照组粘接强度(32.73±8.06) MPa,且差异有统计学意义(P=0.026);对照组、BG组3个月的微拉伸粘接强度较24 h呈下降趋势,且差异有统计学意义(对照组P=0.017,BG组P=0.01);S-P-BG组3个月微拉伸粘接强度较24 h粘接强度[(37.99±7.98) MPa]下降,但差异无统计学意义(P>0.05)。扫描电镜观察24 h粘接断裂面,3组均未见明显矿化;1个月、3个月后,BG组、S-P-BG组的粘接界面可见矿物质形成,S-P-BG组无明显胶原暴露。激光共聚焦显微镜观察对照组、BG组与S-P-BG组树脂突形成的形态及数量无明显差异;3组样本粘接24 h后粘接界面混合层均有渗漏,3个月后对照组微渗漏增加,BG组和S-P-BG组混合层微渗漏减少。结论:BG预处理牙本质粘接界面能够在粘接界面形成矿物质,减少粘接混合层微渗漏;STMP、PAA 与BG共同预处理牙本质粘接界面,可能在一定程度上维持牙本质粘接修复的耐久性。     

Interacting with α7 nAChR is a new mechanism for AChE to enhance the inflammatory response in macrophages

Acetylcholine (ACh) regulates inflammation via α7 nicotinic acetylcholine receptor (α7 nAChR). Acetylcholinesterase (AChE), an enzyme hydrolyzing ACh, is expressed in immune cells suggesting non-classical function in inflammatory responses. Here, the expression of PRiMA-linked G4 AChE was identified on the surface of macrophages. In lipopolysaccharide-induced inflammatory processes, AChE was upregulated by the binding of NF-κB onto the ACHE promotor. Conversely, the overexpression of G4 AChE inhibited ACh-suppressed cytokine release and cell migration, which was in contrast to that of applied AChE inhibitors. AChEmt, a DNA construct without enzymatic activity, was adopted to identify the protein role of AChE in immune system. Overexpression of G4 AChEmt induced cell migration and inhibited ACh-suppressed cell migration. The co-localization of α7 nAChR and AChE was found in macrophages, suggesting the potential interaction of α7 nAChR and AChE. Besides, immunoprecipitation showed a close association of α7 nAChR and AChE protein in cell membrane. Hence, the novel function of AChE in macrophage by interacting with α7 nAChR was determined. Together with hydrolysis of ACh, AChE plays a direct role in the regulation of inflammatory response. As such, AChE could serve as a novel target to treat age-related diseases by anti-inflammatory responses.     

Excess salt intake promotes M1 microglia polarization via a p38/MAPK/AR-dependent pathway after cerebral ischemia in mice

A high salt diet (HSD) is among the most important risk factors for many diseases. One mechanism by which HSD aggravates cerebral ischemic injury is independent of blood pressure changes. The direct role of HSD in inflammation after cerebral ischemia is unclear. In this research, after twenty-one days of being fed a high salt diet, permanent focal ischemia was induced in mice via operation. At 12 h and 1, 3 and 5 days postischemia, the effects of HSD on the lesion volume, microglia polarization, aldose reductase (AR) expression, and inflammatory processes were analyzed. We report that in mice, surplus dietary salt promotes inflammation and increases the activation of classical lipopolysaccharide (LPS)-induced microglia/macrophages (M1). This effect depends on the expression of the AR protein in activated microglia after permanent middle cerebral artery ligation (pMCAL) in HSD mice. The administration of either the AR inhibitor Epalrestat or a p38-neutralizing antibody blocked the polarization of microglia and alleviated stroke injury.In conclusion, HSD promotes polarization in pro-inflammatory M1 microglia by upregulating the expression of the AR protein via p38/MAPK, thereby exacerbating the development of ischemia stroke.     

Constructing an In Silico Three-Class Predictor of Human Intestinal Absorption With Caco-2 Permeability and Dried-DMSO Solubility

Absorption of drugs is the first step after dosing, and it largely affects drug bioavailability. Hence, estimating the fraction of absorption (Fa) in humans is important in the early stages of drug discovery. To achieve correct exclusion of low Fa compounds and retention of potential compounds, we developed a freely available model to classify compounds into 3 levels of Fa capacity using only the chemical structure. To improve Fa prediction, we added predicted binary classification results of membrane permeability measured using Caco-2 cell line (Papp) and dried–dimethyl sulfoxide solubility (accuracy, 0.836; kappa, 0.560). The constructed models can be accessed via a web application.