Ceramide (Cer) is a second messenger produced by the degradation of plasma membrane phospholipids in cells. It is an essential lipid mediator for normal cellular function, composed of sphingosine and different chains of fatty acids. Its receptors are widely present in red blood cells, endothelial cells, glial cells, immune cells, and nerve cells, and participate in various pathophysiological processes such as oxidative stress, inflammatory response, signal pathway transduction, and immune regulation. Many studies have confirmed that the increase of Cer level is related to cardiovascular disease, type 2 diabetes and lipid metabolism. Ceramide score can be used as a tool to evaluate the severity and prognosis of cardiovascular events. However, there is limited research on the impact of Cer on acute ischemic stroke (AIS). This article aims to elucidate the role of Cer and its impact on the occurrence, development, and prognosis of AIS.

Ulcerative colitis （UC） is a chronic inflammatory bowel disease with complex etiology. The pathogenesis of this disease， due to a combination of factors， is complex and has not yet been elucidated. Among them， intestinal mucosal barrier damage is the basic pathological change of UC. As a non-destructive response of cells， autophagy regulates intestinal mucosal immunity， inflammation， oxidative stress， and bacterial homeostasis through degradation and reabsorption to actively repair damaged intestinal mucosal barrier， exerting a key role in the occurrence and development of UC. The disease is mainly treated clinically with aminosalicylic acid preparations， glucocorticoids， and immunosuppressants. Western medicine treatment of the disease has a fast onset of effect， and the short-term efficacy is definite， but the long-term application is easy to be accompanied by more adverse reactions. Moreover， some drugs are expensive， bringing great physical and mental pain and economic burden to patients. Therefore， it is urgent to explore new therapies with stable efficacy and mild adverse effects. In recent years， a large number of studies have shown that Chinese medicine can regulate autophagy of the intestinal mucosa with multiple targets and effects and repair the intestinal mucosal barrier function， thereby inhibiting the development of UC. Many experiments have shown that the active ingredient or monomers and compound formulas of Chinese medicine can improve the immunity of the intestinal mucosa， inflammation， oxidative stress， and flora by regulating the level of autophagy to maintain the normal function of the intestinal mucosal barrier to effectively intervene in UC， providing a new measure for the prevention and treatment of UC. However， there is a lack of systematic review of Chinese medicine in regulating the level of autophagy in the intestinal mucosa for the prevention and treatment of UC. Therefore， based on the current research on UC， autophagy process， and Chinese medicine treatment， this article reviewed the relationship of autophagy and its key target proteins with UC to clarify the key role of autophagy in UC production and systematically summarized Chinese medicines targeting the regulation of autophagy to treat UC in recent years to provide new ideas for the treatment and drug development of UC.

Gastric cancer （GC） is a digestive tract tumor that occurs in the epithelial tissues of the gastric mucosa， seriously affecting the life and health of patients， and its mortality rate ranks the third among malignancies. Although medical technology has made great progress in recent years， the progression of GC still cannot be effectively controlled by surgery， chemotherapy， and targeted therapy. The pathogenesis of GC is extremely complex and is closely related to the tumor microenvironment， chronic inflammation， and immune escape， among which the reduction of tumor cell apoptosis is one of the important mechanisms for the occurrence and development of GC. Apoptosis refers to the process of spontaneous termination of cell life caused by genes under specific physiological or pathological conditions， which is of great significance for maintaining the stability of the internal environment. Researchers have found that in the GC state， mitochondrial endogenous apoptosis， endoplasmic reticulum stress， external death receptors， and other apoptosis pathways are regulated by multiple signaling pathways and genes， which together lead to the decline of GC cell apoptosis rate and thus promote the progression of GC. Chinese medicine is advantageous and characterized by multiple components， multiple targets， synergistic effect， and few adverse reactions. A large number of studies have shown that polysaccharide components， as effective components of Chinese medicine， have biological activities such as cancer inhibition， blood sugar control， anti-inflammation， antioxidant damage， and anti-virus， and can effectively inhibit the deterioration of GC by inducing cell apoptosis， gradually becoming a hot spot in GC drug research and development. However， systematic reviews on the apoptosis of GC induced by Chinese medicine polysaccharides are rarely reported. Therefore， this paper analyzed and summarized the studies of Chinese medicine polysaccharides in promoting apoptosis and interfering with GC， in order to provide a theoretical basis for the basic research， new drug development， and clinical application of Chinese medicine polysaccharides in the intervention of GC.

H 1-antihistamines are widely used in the treatment of various allergic diseases, but there are still many challenges in the safe and rational use of H 1-antihistamines in pediatrics, and there is a lack of guidance on the prescription review of H 1-antihistamines for children.In this paper, suggestions are put forward from the indications, dosage, route of administration, pathophysiological characteristics of children with individual difference and drug interactions, so as to provide reference for clinicians and pharmacists.

Anti-seizure medications (ASMs) are the main therapy for epilepsy.There are many kinds of ASMs with complex mechanism of action, so it is difficult for pharmacists to examine prescriptions.This paper put forward some suggestions on the indications, dosage forms/routes of administration, appropriateness of usage and dosage, combined medication and drug interaction, long-term prescription review, individual differences in pathophysiology of children, and drug selection when complicated with common epilepsy, for the reference of doctors and pharmacists.

Antipyretic-analgesics are currently one of the most prescribed drugs in children.The clinical application of antipyretic-analgesics for children in our country still have irrational phenomenon, which affects the therapeutic effect and even poses hidden dangers to the safety of children.In this paper, suggestions were put forward from the indications, dosage form/route, dosage suitability, pathophysiological characteristics of children with individual differences and drug interactions in the symptomatic treatment of febrile children, so as to provide reference for the general pharmacists when conducting prescription review.

Health promoting lifestyle can help patients with chronic diseases to prevent diseases, maintain their health, and reduce or eliminate dangerous behaviors by changing the incorrect lifestyle of chronic diseases. This article reviews the overview, measuring tool, status quo, influencing factors, and interventions of health promotion lifestyle for patients with chronic diseases, and puts forward the corresponding prospects.

OBJECTIVE: To investigate the inhibitory effects of dihydromyricetin on the proliferation and migration of gastric cancer BGC-823 cells and explore the molecular mechanisms. METHODS: BGC-823 cells in routine culture were treated with different concentrations of dihydromyricetin (0, 40, 60, 80, 100, and 120 μg/mL) for 24 h, and the changes in cell viability were detected using CCK-8 assay; colony forming assay and Transwell assay were performed to assess the changes in colonyforming and migration abilities of the cells, respectively. The levels of MMP-2 and MMP-9 in the treated cells were determined using ELISA, and Western blotting was used to detect the expressions of E-cadherin, N-cadherin, cyclin D1, cyclin E1, HSP70 and HMGB1 and the phosphorylation levels of Akt and Stat3. RESULTS: CCK-8 assay showed that dihydromyricetin treatment dose-dependently inhibited the viability of BGC-823 cells ( CONCLUSIONS Dihydromyricetin inhibits the proliferation and migration of BGC-823 cells through suppressing the activation of Akt/stat3 signaling pathways and HMGB1 expression.
Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Flavonols ; HMGB1 Protein/metabolism* ; Humans ; Proto-Oncogene Proteins c-akt/metabolism* ; STAT3 Transcription Factor ; Stomach Neoplasms

Objective: To explore the application of endoscopy and clinical effect of endoscopic resection of benign tumor in infratemporal fossa. Methods: The clinical data of 11 patients with benign tumors in infratemporal fossa admitted to the Department of Otorhinolaryngology Head and Neck Surgery and Skull Base Surgery of the Affiliated Hospital of Qingdao University from January 2016 to September 2018 were retrospectively analyzed. There were 6 males and 5 females, with the age ranging from 11 to 63 years old. The main clinical manifestations were pharyngeal foreign body sensation, submaxillary pain, maxillofacial numbness and tongue numbness. Imaging examination showed that the tumor was round and had a clear boundary with the surrounding tissue. All the patients underwent endoscopic surgery. Appropriate surgical approach was selected according to the location of the tumor and its relationship with the internal carotid artery. The endoscopic surgical approaches included trans-oropharyngeal approach in 7 cases, trans-lateral pterygomandibular raphe approach in 1 case and trans-medial pterygomandibular raphe approach in 3 cases. The pathological results, prognosis, complications and relapse of patients were summarized through descriptive statistics. Results: The tumors were completely resected under endoscope in all patients, and there was no significant complication occurred after surgery. The average pain VAS score was 3.1 after surgery and average hospital stay was 5.9 d. The postoperative pathological diagnoses consisted of 6 cases of pleomorphic adenoma, 4 cases of neurilemmoma and 1 case of basal cell adenoma. All patients were followed up regularly from 6 to 39 months without recurrence of tumor. Conclusion Endoscopic resection of benign tumors in infratemporal fossa has the advantages of minimal damage, rapid recovery, few complications, and definite curative effect, which can be used as an important alternative for surgical treatment of benign tumors.

OBJECTIVE: To investigate the effect of calenduloside E on lipopolysaccharide (LPS)-induced inflammatory response in RAW264.7 cells and explore the underlying molecular mechanism. METHODS: CCK-8 assay was used to examine the effect of different concentrations of calenduloside E (0-30 μg/mL) on the viability of RAW264.7 cells. The release of the pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in RAW264.7 cells in response to pretreatment with 6, 8, and 10 μg/mL calenduloside E for 2 h followed by stimulation with 100 ng/mL LPS was detected using enzyme-linked immunosorbent assay (ELISA). The expression levels of iNOS and COX-2 and the activation of JAK-stats, MAPKs and NF-кB signaling pathways in the treated cells were determined using Western blotting. A reactive oxygen species (ROS) detection kit was used to detect ROS production in the cells, and the nuclear translocation of the transcription factor stat3 was observed by laser confocal microscopy. RESULTS: Calenduloside E below 20 μg/mL did not significantly affect the viability of RAW264.7 cells. Calenduloside E dose-dependently decreased the expression levels of iNOS and COX-2 induced by LPS, inhibited LPS-induced release of TNF-α and IL-1β, and suppressed LPS-induced JAK1-stat3 signaling pathway activation and stat3 nuclear translocation. Calenduloside E also significantly reduced ROS production induced by LPS in RAW264.7 cells. CONCLUSIONS Calenduloside E inhibits LPS-induced inflammatory response by blocking ROS-mediated activation of JAK1-stat3 signaling pathway in RAW264.7 cells.
Animals ; Lipopolysaccharides ; Mice ; NF-kappa B ; Oleanolic Acid ; analogs & derivatives ; RAW 264.7 Cells ; Reactive Oxygen Species ; Saponins ; Signal Transduction