• ISSN 1674-8301
  • CN 32-1810/R
Articles in press have been peer-reviewed and accepted, which are not yet assigned to volumes /issues, but are citable by Digital Object Identifier (DOI).
To overcome immune tolerance to cancer, the immune system needs to be exposed to a multi-target action intervention. Here, we investigated the activating effect of CpG oligodeoxynucleotides, mesyl phosphoramidate CpG oligodeoxynucleotides, anti-OX40 antibodies, and OX40 RNA aptamers on major populations of immunocompetent cells ex vivo. Comparative analysis of the antitumor effects of in situ vaccination with CpG oligodeoxynucleotides and anti-OX40 antibodies, as well as several other combinations such as mesyl phosphoramidate CpG oligodeoxynucleotides and OX40 RNA aptamers, were conducted. Antibodies against programmed death 1 (PD1) checkpoint inhibitors or corresponding PD1 DNA aptamers were also added to vaccination regimens for analytical purposes. Four scenarios were considered: a weakly immunogenic Krebs-2 carcinoma grafted in CBA mice; a moderately immunogenic Lewis carcinoma grafted in C57Black mice; and an immunogenic A20 B cell lymphoma or an Erlich carcinoma, grafted in BALB/c mice. Adding anti-PD1 antibodies (CpG+αOX40+αPD1) to in situ vaccinations boosts the antitumor effect. When used instead of antibodies, aptamers also possess antitumor activity, although this effect was less pronounced. The strongest effect across all the tumors was observed in highly immunogenic A20 B cell lymphoma and Erlich carcinoma.
This study aims to investigate a suitable adhesive for primary tooth enamel. The shear bond strength (SBS) of primary teeth and the length of resin protrusion were analyzed with one-way ANOVA with Bonferroni multiple comparison tests after etching with 35% H3PO4. SBS and marginal microleakage tests were carried out with Single Bond Universal (SBU)/Single Bond 2 (SB2) adhesives with or without preetching using a nonparametric Kruskal-Wallis test. Clinical investigations were conducted to validate the adhesive for primary teeth restoration using Chi-square tests. The SBS and length of resin protrusion increased significantly with the etching time. The teeth in the SBU with 35% H3PO4 preetching groups had higher bond strength and lower marginal microleakage than those in the SB2 groups. Mixed fractures were more common in the 35% H3PO4 etched 30 seconds + SB2/SBU groups. Clinical investigations showed significant differences between the two groups in the cumulative retention rates at the 6-, 12- and 18-month follow-up evaluations, and in marginal adaptation, discolouration, and secondary caries at the 12- and 18-month follow-up assessments. Together, preetching primary teeth enamel 30 seconds before SBU treatment improved the clinical composite resin restoration, which can provide a suitable approach for restoration of primary teeth.
The erythropoietin-producing human hepatocellular A3 (EphA3) is a member of the largest subfamily of tyrosine kinase receptors—Eph receptors. Previous studies showed that EphA3 is associated with tissue development. Recently, we found that the expression of EphA3 is elevated in the hypothalamus of diet-induced obesity (DIO) mice. However, the role of EphA3 in hypothalamic controlled energy metabolism remains unclear. In this study, we demonstrated that deletion of EphA3 in the hypothalamus by CRISPR/Cas9-mediated gene editing promotes obesity in male mice with high fat diet feeding rather than those with normal chow diet feeding. Moreover, deletion of hypothalamic EphA3 promotes high fat diet-induced obesity by increasing food intake and reducing energy expenditure. Knockdown of EphA3 leads to smaller intracellular vesicles in GT1-7 cells. Our study reveals that hypothalamic EphA3 plays important roles in promoting diet-induced obesity.
Sepsis-induced myocardial dysfunction is accompanied primarily by severe sepsis, which is associated with high morbidity and mortality. 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1), a reductase, can convert inactive cortisone into metabolically active cortisol. The role of 11β-HSD1 in sepsis-induced myocardial dysfunction remains poorly understood. This study aimed to investigate the effects of 11β-HSD1 in lipopolysaccharide (LPS)-induced mouse model. LPS(10 mg/kg) was administered to wild-type C57BL/6J mice and 11β-HSD1 global knockout mice. Cardiac function was assessed by echocardiography. Transmission electron microscopy and immunohistochemical staining were performed to analyze myocardial mitochondrial injury and record histological changes. The levels of reactive oxygen species and biomarkers of oxidative stress were determined. Polymerase chain reaction analysis, western blot, and immunofluorescent staining were employed to determine the expression of related genes and proteins, respectively. To investigate the role of 11β-HSD1 in sepsis-induced myocardial dysfunction, LPS was used to induce lentivirus-infected neonatal rat ventricular cardiomyocytes. Knockdown of 11β-HSD1 alleviated LPS-induced myocardial mitochondrial injury, oxidative stress, and inflammation, along with improved myocardial function. Furthermore, depletion of 11β-HSD1 promoted the phosphorylation of adenosine 5'‐monophosphate-activated protein kinase, peroxisome proliferator activated receptor gamma coactivator 1α, and silent information regulator 1 protein levels both in vivo and in vitro. The suppression of 11β-HSD1 may be a viable strategy to improve cardiac function against endotoxemia challenges.
Circulating tumor cells (CTCs) play an important role in tumor metastases, which positively correlates with an increased risk of death. Actin-binding proteins, i.e., cofilin (CFL1), profilin 1 (PFN1), and adenylate cyclase-associated protein 1 (CAP1) are thought to be involved in tumor cell motility and metastasis, specifically in head and neck squamous cell carcinoma (HNSCC). However, there are currently no published studies of CFL1, PFN1, and CAP1 in CTCs and leukocytes in HNSCC patients. We assessed serum levels of CFL1, PFN1, and CAP1 and the number of CTCs and leukocytes containing these proteins in blood from 31 HNSCC patients (T1–4N0–2M0). Analysis was conducted using flow cytometry and an ELISA kit. We found that CAP1+ CTCs and CAP1+ leukocyte subgroups were prevalent in our HNSCC patient samples, while the prevalence rates of CFL1+ and PFN1+ CTCs was relatively low. Patients with stage T2–4N1–2M0 had CFL1+ and PFN1+ CTCs, and with an elevated PFN1 serum level. In general, PFN1 serum level and the relative number of PFN1+CD326+ CTCs could be valuable prognostic markers for HNSCC metastases. This study is the first to obtain data regarding the contents of ABPs in CTCs, and leukocytes in blood from HNSCC patients. This is also the first to assess the relationship between the number of CTCs subgroups and disease characteristics.
Glioblastoma multiforme (GBM) is an essentially incurable brain tumor, which has been explored for approximately a century. Nowadays, surgical resection, chemotherapy, and radiation therapy are still standardized therapeutic options. However, due to the intrinsic invasion and metastasis features and the resistance to chemotherapy, the survival rate of glioblastoma patients remains unsatisfactory. To improve the current situation, much more research needs to be carried out to provide comprehensive knowledge of GBM. In this review, we summarize the latest updates on GBM treatment and invasion. Firstly, we review the traditional and emerging therapies that have been used for GBM treatment. Given the limited efficiency of these therapies, we further discuss the role of invasion in GBM recurrence and progression and present current research progress on the mode and mechanisms of GBM invasion.
Anti-cancer therapy is often a cause of premature ovarian insufficiency and infertility since the ovarian follicle reserve is extremely sensitive to chemotherapy drugs like cisplatin. Various methods have been explored for fertility preservation in women, especially in prepubertal girls undergoing radiotherapy and chemotherapy because of cancer. In recent years, mesenchymal stem cell-derived exosomes (MSC-exos) have been reported to play an important role in tissue repair and treatment of various diseases. In this study, by using exosomes human umbilical cord-derived from mesenchymal stem cells, we observed that human umbilical cord-derived MSC-exos (hucMSC-exos) after short-term culture improved follicular survival and development while receiving cisplatin treatment. Moreover, the intravenous injection of hucMSC-exos improved ovarian function and ameliorated the inflammatory environment within the ovary. The underlying mechanism of hucMSC-exos on fertility preservation was associated with the down-regulation of p53-related apoptosis and their anti-inflammatory function. Taken together, we proposed that HucMSC-derived exosomes might be a potential approach to improve fertility in women diagnosed with cancer.
Lead (Pb) and furan are toxic agents, and persistent exposure to humans and animals may impair reproductive function. We therefore explored the effect of Pb and furan on male rat hypothalamic-pituitary-gonadal reproductive status, oxidative stress, inflammation, and genomic integrity. We found that co-exposure to Pb and furan reduced the activities of testicular function enzymes, endogenous antioxidant levels, total sulfhydryl group, and glutathione. Sperm abnormality, biomarkers of oxidative stress, inflammation, and p53 expression were increased in a dose-dependent manner by treatment with furan and Pb. Typical rat gonad histoarchitecture features were also damaged. Convincingly, co-exposure to furan—a steroid hormone disruptor; and lead—a toxic metal common in water pipes—induced male reproductive function derangement by decreasing the antioxidant defences in rats, increasing abnormalities in spermatozoa morphology, and reducing reproductive hormone in circulation. These pathophysiological alterations, if persistent, might provide a permissive environment for potentiating reproductive dysfunction and infertility.
An increasing number of studies demonstrated that alcohol vapor chamber is an effective way to model physical signs of alcohol use disorders. Although researchers are developing different exiting vapor chambers to study chronic alcohol exposure model worldwide, few studies build and modify their own vapor chamber in China. Here, we designed and established an alcohol vapor chamber system for small animals. We described a paradigm showing how to control and monitor alcohol concentration in whole system. The vapor chamber system with several advantages including accommodating up to ten standard mouse cages. Furthermore, the system were tested by evaluating the blood alcohol concentration and neuron injury in mice. Importantly, the alcohol withdrawal after vapor exposure caused motor coordination impairment, anxiolytic- and depression-like behavior. Finally, the N-methyl-D-aspartate receptor (NMDAR)-mediated glutamatergic transmissions in medial prefrontal cortex was changed after alcohol vapor exposure-induced behaviors. The frequency and amplitude of spontaneous excitatory postsynaptic currents between control and alcohol groups were not different, suggesting that alcohol exposure-induced behaviors are associated with the change in NMDAR response. Taken together, the new alcohol vapor chamber system was constructed to research the relationship between the stable alcohol exposure and withdrawal behaviors and to study chronic alcohol exposure-induced disorders in China.
Circular RNAs (circRNAs) are characterized by a covalent closed-loop structure with an absent 5′ cap structure and 3′ polyadenylated tail. Numerous studies have found that circRNAs play an important role in various diseases and having a variety of biological regulatory mechanisms, including acting as microRNA sponges, interacting with proteins, modulating the expression of related genes and translating into peptide or protein. CircRNAs have also been used as biomarkers for a number of diseases, which could improve clinical practice. This review summarizes the most recent advances in biogenesis and our knowledge of the biological functions of circRNAs, using up-to-date databases. We specifically describe developments in our understanding of circRNA functions in the field of environmental exposure-induced diseases. Finally, we focus on potential clinical implications of circRNAs to facilitate their clinical transformation into disease treatment.
Acute myocardial infarction (AMI) and sudden cardiac death (SCD), which are associated with acute cardiac ischemia, are one of the leading causes of death of adults in economically developed countries. The development of new approaches for treatment and prevention of AMI, and SCD remains the highest priority for medicine. A study of the cardiovascular effects of chronic hypoxia (CH) could contribute to the development of these methods. Chronic hypoxia exerts both positive and adverse effects. The positive effects are the infarct-reducing, the vasoprotective, and the antiarrhythmic effects, which can lead to the improvement of cardiac contractility in reperfusion. The adverse effects are pulmonary hypertension and right ventricular hypertrophy. This review presents a comprehensive overview of how CH enhances cardiac tolerance to ischemia/reperfusion. It is an in-depth analysis of the published data on the underlying mechanisms which can lead to the development of the cardioprotective effect of CH. A study of the CH-activated protective signaling pathways could contribute to a better understanding of the development of CH as well as could promote the development of new therapeutic approaches in an increase of cardiac tolerance to ischemia/reperfusion.
Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by progressive cognitive defects. The role of the central immune dominated by microglia in the progression of AD has been extensively investigated. However, little is known about the peripheral immune system in AD pathogenesis. Recently, with the discovery of the meningeal lymphatic vessels and glymphatic system, the roles of acquired immunity in the maintenance of central homeostasis and neurodegenerative diseases have attracted increasing attention. T cells not only regulate the function of neurons, astrocytes, microglia, oligodendrocytes and brain microvascular endothelial cells, but also participate in clearance of β-amyloid (Aβ) plaques. Apart from producing antibodies to bind Aβ peptides, B cells affect Aβ-related cascades via a variety of antibody-independent mechanisms. This review systemically summarizes the recent progress in understanding pathophysiological roles of T cells and B cells in AD.
Lupus nephritis (LN) has a high incidence in systemic lupus erythematosus (SLE) patients, but there is a lack of sensitive predictive markers and mechanisms. The purpose of the study was to reveal the association between the CD4+CD8+ double positive T (DPT) lymphocytes and LN. The study included the patients with SLE with no renal impairment (SLE-NRI), LN, nephritic syndrome (NS), or nephritis. Peripheral blood lymphocyte subsets were analyzed by flow cytometry. Biochemical measurements were performed for peripheral blood in accordance with the recommendations proposed by the National Center for Clinical Laboratories. The proportions of DPT cells in LN group were significantly higher than that in SLE-NRI group (t=4.012, P<0.001), NS group (t=3.240, P=0.001), and nephritis group (t=2.57, P=0.011). In LN group, the risk of renal impairment increased significantly in a DPT cells proportion dependent manner. In cases of high proportion of DPT cells, the risk of LN was 5.136 times higher than when the proportion of DPT cells was within the normal range. These findings indicated that the proportion of DPT cells could be a potential marker to evaluate LN susceptibility, and the interference of NS and nephritis could be effectively excluded when assessing the risk of renal impairment during SLE with DPT cells proportion.
Right heart thrombus (RHTh) with concurrent acute pulmonary embolism (PE) is rare and can seriously destabilize hemodynamics, leading to an emergency situation with high mortality. Diagnosis and treatment of RHTh with acute PE are not yet standardized. There are few reports of acute PE concurrent with RHTh and even less is known about patients with a right heart mural thrombus. For physicians, the diagnostic choice and treatment of these patients are particularly difficult due to the lack of knowledge. Here, we report a rare case of partial mural RHTh (type C RHTh) with acute PE. The mural mass in the right heart was initially diagnosed as atrial myxoma according to transthoracic echocardiography (TTE), and both pulmonary embolus and the mural mass were completely absorbed after administering Rivaroxiban. This case suggests that TTE alone is insufficient to identify and diagnoses a right heart mural mass such as this. However, novel oral anticoagulants may be effective at alleviating PE with type C RHTh.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. The major pathological changes in AD progression are the generation and accumulation of amyloid-beta (Aβ) peptides, and the presence of abnormally hyperphosphorylated tau proteins in the brain. Autophagy is a conserved degradation pathway that eliminates abnormal protein aggregates and damaged organelles. Previous studies have suggested that autophagy plays a key role in the production and clearance of Aβ peptides. to maintain a steady-state of Aβ peptides levels. However, a growing body of evidence suggests that autophagy is significantly impaired in the pathogenesis of AD, especially in Aβ metabolisation. Therefore, this article reviews the latest studies concerning the mechanisms of autophagy, the metabolisation of Aβ peptides, and the defective autophagy in the production and clearance of Aβ peptides. Here, we also summarize established and new strategies for targeting autophagy in vivo and through clinical AD trials in order to identify gaps in our knowledge and to generate further questions.
Sirtuin 3 (SIRT3), the main family member of mitochondrial deacetylase, targets the majority of substrates controlling mitochondrial biogenesis via lysine deacetylation and modulates important cellular functions such as energy metabolism, reactive oxygen species production and clearance, oxidative stress, and aging. Deletion of SIRT3 has a deleterious effect on mitochondrial biogenesis, thus leading to the defect in mitochondrial function and insufficient ATP production. Imbalance of mitochondrial dynamics leads to excessive mitochondrial biogenesis, dampening mitochondrial function. Mitochondrial dysfunction plays an important role in several diseases related to aging, such as cardiovascular disease, cancer and neurodegenerative diseases. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) launches mitochondrial biogenesis through activating nuclear respiratory factors. These factors act on genes, transcribing and translating mitochondrial DNA to generate new mitochondria. PGC1α builds a bridge between SIRT3 and mitochondrial biogenesis. This review described the involvement of SIRT3 and mitochondrial dynamics, particularly mitochondrial biogenesis in aging-related diseases, and further illustrated the role of the signaling events between SIRT3 and mitochondrial biogenesis in the pathological process of aging-related diseases.
Aging, subjected to scientific scrutiny, is extensively defined as a time-dependent decline in function that involves the majority of organisms. The time-dependent accretion of cellular lesions is generally a universal trigger of aging. Mitochondrial dysfunction is a sign of aging. Dysfunctional mitochondria are identified and removed by mitophagy, a selective form of macroautophagy. Increased mitochondrial damage resulting from reduced biogenesis and clearance may promote the aging process. The primary purpose of this paper is to illustrate in detail the effect of mitophagy on aging and emphasize on the association between mitophagy and other signs of aging including dietary restriction, telomere shortening, epigenetic alterations, and protein imbalance. The evidence regarding the effect of these relationships on aging is still limited, and although the relationship between mitophagy and aging has been long-awaited, analyzing of its details remains the main challenge in aging studies.
Amyotrophic lateral sclerosis (ALS) is known as a progressive paralysis disorder characterized by degeneration of upper and lower motor neurons and has an average survival time of three to five years. Growing evidence has suggested the bidirectional link between gut microbiota and neurodegeneration. Here we aimed to report one female case with ALS who benefited from washed microbiota transplantation (WMT), an improved fecal microbiota transplantation (FMT), through a transendoscopic enteral tube during a 12-month follow-up. Notedly, the accidental scalp trauma the patient suffered later was treated with prescribed antibiotics which caused ALS deterioration. The subsequent rescue WMTs successfully stopped the progression of the disease with quick improvement. The plateaus and reversals occurred during the whole course of WMT. The stool and blood samples from the first WMT to the last were collected for dynamic microbial and metabolomic analysis. We observed the microbial and metabolomic changing trend consistent with the disease status. This case report for the first time shows the direct clinical evidence on using WMT for treating ALS, indicating that WMT may be the novel treatment strategy for controlling this so-called incurable disease.
The Journal of Biomedical Research--2022, 36(6)
Review Article
Acute myocardial infarction (AMI) is one of the main reasons of cardiovascular disease-related death. The introduction of percutaneous coronary intervention to clinical practice dramatically decreased the mortality rate in AMI. Adverse cardiac remodeling is a serious problem in cardiology. An increase in the effectiveness of AMI treatment and prevention of adverse cardiac remodeling is difficult to achieve without understanding the mechanisms of reperfusion cardiac injury and cardiac remodeling. Inhibition of pyroptosis prevents the development of postinfarction and pressure overload-induced cardiac remodeling, and mitigates cardiomyopathy induced by diabetes and metabolic syndrome. Therefore, it is reasonable to hypothesize that the pyroptosis inhibitors may find a role in clinical practice for treatment of AMI and prevention of cardiac remodeling, diabetes and metabolic syndrome-triggered cardiomyopathy. It was demonstrated that pyroptosis interacts closely with apoptosis and autophagy. Pyroptosis could be inhibited by nucleotide-binding oligomerization domain-like receptor with a pyrin domain 3 inhibitors, caspase-1 inhibitors, microRNA, angiotensin-converting enzyme inhibitors, angiotensin Ⅱ receptor blockers, and traditional Chinese herbal medicines.
Original Article
Diet/sugar-free soft drinks are considered to be healthier than regular soft drinks. However, few studies have examined the relationship between the types of soft drinks (regular and diet/sugar-free) and lung cancer (LC)/all-cancer (AC) risk. In this study, we comprehensively assessed the influence of the type of soft drink consumption on LC/AC risk based on the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. Multivariable Cox proportional hazards and competing risks Fine-Gray regression models adjusted for relevant confounders were used to estimate hazard ratios (HRs) and subdistribution HRs for different types of soft drink consumption. In the PLCO population, female subgroup, and the ever/current smoker subgroup, consumption of both regular and diet soft drinks was associated with a significantly reduced risk of LC compared with no soft drinks at all. For the non-lung cancer (NLC) risk, consumption of only diet soft drinks had a significant positive association for the total population and female subgroup. Based on our findings, it was suggested that partial replacement of regular soft drinks with diet soft drinks might be beneficial to LC prevention, especially for females and ever/current smokers. Additionally, completely replacing regular soft drinks with diet soft drinks might be detrimental to NLC prevention, especially for females.
The superior vena cava (SVC) is the main component of non-pulmonary vein (PV) ectopy in patients with atrial fibrillation (AF). Researchers have found that epicardial adipose tissue (EAT) volume is related to the AF substrate, which can be defined by the low voltage area (LVA). This study aimed to investigate the relationship between SVC-EAT and SVC-AF. Twenty-six patients with SVC-AF triggers were identified as the SVC-AF group. Other three groups were defined and included as the LVA-AF group (LVA>5%), non-LVA-AF group (LVA<5%), and physical examination (PE) group. EAT around left atrium (LA-EAT) and SVC-EAT volumes were obtained using a cardiac risk assessment module. According to the SVC/LA-EAT ratio, there are significant differences between the SVC-AF group and the three control groups (the SVC-AF group 0.092±0.041 vs. the LVA-AF group 0.054±0.026, the non-LVA-AF group 0.052±0.022, and the PE group 0.052±0.019, all P<0.001). Receiver operating characteristic curve analysis suggests the optimal cut-off point of SVC/LA-EAT ratio is 6.8% for detecting SVC-AF patients, with 81.1% sensitivity, 73.1% specificity, and an area under the curve of 0.83 (95% confidence interval, 0.75–0.91). Those with SVC-AF have a higher SVC/LA-EAT ratio and empirical SVC isolation could be considered if the SVC/LA-EAT ratio was over 6.8%.
In this paper, we propose a framework based deep learning for medical image translation using paired and unpaired training data. Initially, a deep neural network with an encoder-decoder structure is proposed for image-to-image translation using paired training data. A multi-scale context aggregation approach is then used to extract various features from different levels of encoding, which are used during the corresponding network decoding stage. At this point, we further propose an edge-guided generative adversarial network for image-to-image translation based on unpaired training data. An edge constraint loss function is used to improve network performance in tissue boundaries. To analyze framework performance, we conducted five different medical image translation tasks. The assessment demonstrates that the proposed deep learning framework brings significant improvement beyond state-of-the-arts.
Liver diseases with the central pathogenetic mechanism of oxidative stress are one of the main causes of mortality worldwide. Therefore, dihydroquinoline derivatives, which are precursors of hepatoprotectors and have antioxidant activity, are of interest. We have previously found that some compounds in this class have the ability to normalize redox homeostasis under experimental conditions. Here, we initially analyzed the hepatoprotective potential of the dihydroquinoline derivative 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline (BHDQ) for carbon tetrachloride (CCl4)-induced liver injury in rats. Results suggested that BHDQ normalized the alanine aminotransferase, aspartate aminotransferase, and gamma-glutamyl transpeptidase in serum. We also observed an improvement in liver tissue morphology related to BHDQ. Animals with CCl4-induced liver injuries treated with BHDQ had less oxidative stress compared to animals with CCl4-induced liver injury. BHDQ promoted activation changes in superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, and glutathione transferase on control values in animals with CCl4-induced liver injury. BHDQ also activated gene transcription in Sod1 and Gpx1 via nuclear factor erythroid 2-related factor 2 and forkhead box protein O1 factors. Therefore, the compound of concern has a hepatoprotective effect by inhibiting the development of necrotic processes in the liver tissue, through antioxidation.
Case Report
Mast cell activation syndrome (MCAS) includes a group of disorders that result in the inappropriate release of inflammatory mediators from mast cells. These mediators can affect multiple organ systems and lead to significant morbidity, and possible fatality. Although reactions, typically in response to various nonspecific stimuli, are usually mild, they may put those with MCAS at increased risk of anaphylaxis. In this case report, we present two clinical scenarios of MCAS, and identify possible factors triggering mast cell mediator release. We also define a preoperative preventive pathway, outline anesthetic considerations, and discuss the management of immediate hypersensitivity reactions in patients with MCAS. Meticulous preoperative preparation, avoidance of triggers, and development of a plan to treat possible adverse organ responses are paramount of good outcomes.
Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) plays an important role in cancer therapy. However, EGFR is highly expressed in the skin and gives rise to one of the most concerning issues for the EGFR-TKI treatment, namely skin toxicity. Antibiotics and corticosteroids are usually used to treat the EGFR inhibitor-associated skin rash, with prominent side effects over long-time use. Pien Tze Huang (PZH) Unguentum Compositum is a traditional product for external application which is made of traditional Chinese medicine and oil base. Herein, we reported the case of a 50-year-old man who presented with skin rash on the face, head, and back induced by an EGFR-TKI named erlotinib. By using PZH Unguentum Compositum, we observed that the skin rash was mitigated and eventually disappeared. This case report suggests that PZH Unguentum Compositum may be an effective therapy in treating skin rash caused by EGFR-TKI with fewer side effects.
Letter to the Editor
Myocardin in biology and disease
Joseph M. Miano
2015, 29(1): 3-19.   doi: 10.7555/JBR. 29.20140151
+Abstract PDF 5076KB
Exosomes and their role in the micro-/macro-environment: a comprehensive review
Naureen Javeed, Debabrata Mukhopadhyay
2017, 31(5): 386-394.   doi: 10.7555/JBR.30.20150162
+Abstract PDF 185KB
Immune checkpoint inhibitors in cancer therapy
Eika S. Webb, Peng Liu, Renato Baleeiro, Nicholas R. Lemoine, Ming Yuan, Yaohe Wang
2018, 32(5): 317-326.   doi: 10.7555/JBR.31.20160168
+Abstract PDF 275KB
GYY4137 protects against myocardial ischemia and reperfusion injury by attenuating oxidative stress and apoptosis in rats
Guoliang Meng, Jing Wang, Yujiao Xiao, Wenli Bai, Liping Xie, Liyang Shan, Philip K Moore, Yong Ji
2015, 29(3): 203-213.   doi: 10.7555/JBR.28.20140037
+Abstract PDF 2347KB
Platelets in hemostasis and thrombosis: Novel mechanisms of fibrinogen-independent platelet aggregation and fibronectinmediated protein wave of hemostasis
Yan Hou, Naadiya Carrim, Yiming Wang, Reid C. Gallant, Alexandra Marshall, Heyu Ni
2015, 29(6): 437-444.   doi: 10.7555/JBR.29.20150121
+Abstract PDF 610KB
Recent advances in targeting the autotaxin-lysophosphatidate-lipid phosphate phosphatase axis in vivo
Matthew G.K. Benesch, Xiaoyun Tang, Ganesh Venkatraman, Raie T. Bekele, David N. Brindley
2016, 30(4): 272-284.   doi: 10.7555/JBR.30.20150058
+Abstract PDF 462KB
Statistical analysis for genome-wide association study
Ping Zeng, Yang Zhao, Cheng Qian, Liwei Zhang, Ruyang Zhang, Jianwei Gou, Jin Liu, Liya Liu, Feng Chen
2015, 29(4): 285-297.   doi: 10.7555/JBR.29.20140007
+Abstract PDF 3937KB
Hepatic ischemia-reperfusion injury in liver transplant setting: mechanisms and protective strategies
Rampes Sanketh, Ma Daqing
2019, 33(4): 221-234.   doi: 10.7555/JBR.32.20180087
+Abstract + HTML PDF 1187KB
Deciphering the role of hedgehog signaling in pancreatic cancer
Dongsheng Gu, Kelly E Schlotman, Jingwu Xie
2016, 30(5): 353-360.   doi: 10.7555/JBR.30.20150107
+Abstract PDF 376KB
Autoantibodies in Alzheimer's disease: potential biomarkers, pathogenic roles, and therapeutic implications
Jianming Wu, Ling Li
2016, 30(5): 361-372.   doi: 10.7555/JBR.30.20150131
+Abstract PDF 426KB
Class A scavenger receptor activation inhibits endoplasmic reticulum stress-induced autophagy in macrophage
Hanpeng Huang, Xiaoyu Li, Yan Zhuang, Nan Li, Xudong Zhu, Jin Hu, Jingjing Ben, Qing Yang, Hui Bai, Qi Chen
2014, 28(3): 213-221.   doi: 10.7555/JBR.28.20130105
+Abstract [PDF 11939KB](954)
Dual therapy of rosiglitazone/pioglitazone with glimepiride on diabetic nephropathy in experimentally induced type 2 diabetes rats
Ravi Prakash Rao, Ansima Singh, Arun K Jain, Bhartu Parsharthi Srinivasan
2011, 25(6): 411-417.   doi: 10.1016/S1674-8301(11)60054-7
+Abstract [PDF 1947KB](871)
A clinical perspective on mucoadhesive buccal drug delivery systems
Ritu MGilhotra, Mohd Ikram, Sunny Srivastava, Neeraj Gilhotra
2014, 28(2): 81-97.   doi: 10.7555/JBR.27.20120136
+Abstract [PDF 2323KB](1034)
AEG-1 expression correlates with CD133 and PPP6c levels in human glioma tissues
Jia Guo, Xin Chen, Ruxing Xi, Yuwei Chang, Xuanwei Zhang, Xiaozhi Zhang
2014, 28(5): 388-395.   doi: 10.7555/JBR.28.20140015
+Abstract [PDF 14254KB](944)
Lipoprotein metabolism in nonalcoholic fatty liver disease
Zhenghui Gordon Jiang, Simon C. Robson, Zemin Yao
2013, 27(1): 1-13.   doi: 10.7555/JBR.27.20120077
+Abstract [PDF 1247KB](1200)
ApoB/apoA1 is an effective predictor of coronary heart disease risk in overweight and obesity
Min Lu, Qun Lu, Yong Zhang, Gang Tian
2011, 25(4): 266-273.   doi: 10.1016/S1674-8301(11)60036-5
+Abstract [PDF 4KB](902)
Development of Leishmania vaccines: predicting the future from past and present experience
Joshua Muli Mutiso, John Chege Macharia, Maria Ndunge Kiio, James Maina Ichagichu, Hitler Rikoi, Michael Muita Gicheru
2013, 27(2): 85-102.   doi: 10.7555/JBR.27.20120064
+Abstract [PDF 4KB](1174)
Atrial fibrillation
Thomas M. Munger, Li-Qun Wu, Win K. Shen
2014, 28(1): 1-17.   doi: 10.7555/JBR.28.20130191
+Abstract [PDF 5352KB](1828)
Fracture resistance of posterior teeth restored with modern restorative materials
Ibrahim M. Hamouda, Salah H. Shehata
2011, 25(6): 418-424.   doi: 10.1016/S1674-8301(11)60055-9
+Abstract [PDF 763KB](863)
Maternal risk factors for low birth weight for term births in a developed region in China: a hospital-based study of 55,633 pregnancies
Yihua Bian, Zhan Zhang, Qiao Liu, Di Wu, Shoulin Wang
2013, 27(1): 14-22.   doi: 10.7555/JBR.27.20120046
+Abstract [PDF 4KB](926)