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To combat the emergence of drug-resistant bacteria, a locally isolated bacteriophage (HZJ) targeting H5α Escherichia coli was used as an antibacterial agent to make wound dressing samples in this study. The phages were physically embedded within an alginate hydrogel sample so that they could later be released with their tails being free during the infection process, which preserves their lytic activity. The HZJ phage isolated in the study have a 20 min latent period and are stable between pH 6 and pH 9 and at temperatures below 45 °C. The addition of phage to an E. coli culture suppressed over 99% of bacterial growth in 2-h (p 0.001). Phage-embedded hydrogel fibers were used to create porous wound dressing material using three-dimensional (3D) printing. The majority of phage lytic activity (85%-90%) was preserved after encapsulation. After they were embedded in samples, HZJ lysed 57% to 67% of bacteria (p 0.001) within 2 h and the antibacterial effects lasted at least 24 h. The small amount of phage released in 2 h was able to quickly replicate and effectively lysed the majority of the bacterial hosts. Phage-embedded alginate samples released 10% of its incorporated phage particles in 24 h. The SEM micrographs show that, compared to phage-free samples, fewer E.coli cells were observed on phage-embedded samples 2 h after bacteria were exposed to the samples. The phage-embedded sample was not cytotoxic to L929 cells. The presence of HZJ in alginate hydrogel promoted cell growth (p 0.01) and adhesion to the samples. Further, the existence of phage did not alter the tensile strength and modulus of samples (p 0.05). An antibacterial dressing capable of slowly releasing lytic phages and effectively suppressing bacterial growth for up to 24 h was produced in this study. This model represents an attractive means to reduce use of antibiotics and other additives in conventional dressings.

For resectable esophageal cancer (EC), it remains controversial whether to place percutaneous endoscopic gastrostomy (PEG) before the curative surgery to provide nutritional support during the neoadjuvant therapy. To compare surgical outcomes for patients who received preoperative PEG and those without PEG placement (No-PEG) insertion prior to surgery in a potentially operable EC. A comprehensive literature search was conducted to identify randomized and non-randomized studies comparing PEG and No-PEG groups. Four retrospective studies with a total number of 1,027 patients were identified and included in this meta-analysis. The differences in anastomotic leakage, anastomotic stricture, morbidity, pulmonary complications, wound infection, and hospital stay were not statistically significant between the two groups. Operation time was significantly shorter in the PEG group. There was no PEG-related gastric conduit failure and no leak from the PEG site in the PEG group. We conclude preoperative PEG for resectable EC is a safe procedure with no adverse effect on the gastric tube construction and anastomosis, it can be selectively inserted for EC patients with marked weight loss and malnutrition or those at risk of developing malnutrition during neoadjuvant therapy.

Several biological effects of haem oxygenase (HO)‐1, including anti‐inflammatory, antiapoptotic and antioxidative properties were reported; however, the role of HO‐1 in apoptosis is still unclear. In the presence of stimulation by cobalt protoporphyrin (CoPP), an HO‐1 inducer, apoptotic characteristics were observed, including DNA laddering, hypodiploid cells, and cleavages of caspase (Casp)‐3 and poly(ADP) ribose polymerase (PARP) proteins in human colon carcinoma COLO205, HCT‐15, LOVO and HT‐29 cells in serum‐free (SF) conditions with increased HO‐1, but not heat shock protein 70 (HSP70) or HSP90. The addition of 10% foetal bovine serum (FBS) or 1% bovine serum albumin accordingly inhibited CoPP‐induced apoptosis and HO‐1 protein expression in human colon cancer cells. CoPP‐induced apoptosis of colon cancer cells was prevented by the addition of the pan‐caspase inhibitor, Z‐VAD‐FMK (VAD), and the Casp‐3 inhibitor, Z‐DEVD‐FMK (DEVD). N‐Acetyl cysteine inhibited reactive oxygen species‐generated H2O2‐induced cell death with reduced intracellular peroxide production, but did not affect CoPP‐induced apoptosis in human colorectal carcinoma (CRC) cells. Two CoPP analogs, ferric protoporphyrin and tin protoporphyrin, did not affect the viability of human CRC cells or HO‐1 expression by those cells, and knockdown of HO‐1 protein expression by HO‐1 small interfering (si)RNA reversed the cytotoxic effect elicited by CoPP. Furthermore, the carbon monoxide (CO) donor, CORM, but not FeSO4 or biliverdin, induced DNA ladders, and cleavage of Casp‐3 and PARP proteins in human CRC cells. Increased phosphorylated levels of the endoplasmic reticular (ER) stress proteins, protein kinase R‐like ER kinase (PERK), and eukaryotic initiation factor 2α (eIF2α) by CORM and CoPP were identified, and the addition of the PERK inhibitor, GSK2606414, inhibited CORM‐ and CoPP‐induced apoptosis. Increased GRP78 level and formation of the HO‐1/GRP78 complex were detected in CORM‐ and CoPP‐treated human CRC cells. A pro‐apoptotic role of HO‐1 against the viability of human CRC cells via induction of CO and ER stress was firstly demonstrated herein.

It has been a challenge for many clinicians to treat a complicated extended-spectrum-β-lactamase (ESBL) producing Klebsiella Pneumoniae (Kp) and Escherichia coli (E. coli) infection due to widespread antibiotic abuse with renal damage as one of its common side effects. Therefore, this study aimed to assess the antibacterial activity of extracts from several Taiwanese folk medicinal plants against ESBL- Kp and E. coli. with renal protecting ability against lipid peroxidation (LPO) on mice kidney mitochondria. Preliminary antibacterial activities of ethanol extracts from twenty (20) Taiwanese folk medicinal plants were measured by agar-dilution method against standard ESBL strains of E. coli (ATCC 25922, ATCC 35218) and Kp (ATCC 23856, ATCC 700603). Rhus semialata var. roxburghiana DC. (RSR) exerted the most inhibitory effect and then further extracted with n-hexane, ethyl acetate, acetone, ethanol, and water, respectively. Each extract also evaluated against the four standard ATCC microorganisms. Their MIC50, MIC90, and time kill assay were adapted with detecting the maximum inhibitory activities and the antibacterial spectrum range of each extract was measured against twenty-four (24) kinds of microbes. Which were used including gram-positive, gram-negative bacteria and fungus by agar dilution method. Finally, renal protective ability was detected inhibitory effect of ferrous induced lipid peroxidation on mice mitochondria. Among 20 Taiwanese folk medicinal plants tested, Rhus semialata var. roxburghiana DC. (RSR) exhibited maximum inhibition against clinical ESBL-producing Kp and E. coli strains with acetone extracts showing MIC50/MIC90 values at 1000 µg/mL, the course of antimicrobial action was bacteriostatic and with inhibitions to all 24 kinds of microbial including Gram positive and negative bacteria and fungi. Furthermore, result of thiobarbituric acid reactive substances (TBARS) assay from this extract showed high lipid peroxidative (LPO) protective capability on mice kidney mitochondria (IC50: 29.29 ± 0.35µg/mL). RSR acetone extract, with its maximum activity against clinical isolated ESBL-producing Kp and E. coli, antimicrobial effect against other wide spectral range bacteria and relatively high LPO protective ability on mice kidney mitochondria, is a potential source, albeit further studies have yet to be conducted, to develop an antimicrobial drug against ESBL-Kp and E. coli.

The Mongolian rhubarb—Rheum undulatum L. (RU)—and Rumex crispus L. (RC)—a Taiwanese local rhubarb belonging to the family of Polygonaceae—are principal therapeutic materials in integrative medicine due to their rich quantities of bioactive compounds, however, their phytochemical and antioxidant properties, and anti-cancer activity is poorly investigated. Furthermore, the phytochemical characteristics of both species may be affected by their different geographical distribution and climatic variance. The current study aimed to compare RU with RC extracts in different polarity solvents (n-hexane, ethyl acetate, acetone, ethanol, and water) for their phytochemical contents including the total phenolic content (TPC), total anthraquinone content (TAC), total flavonoid content (TFC), antioxidant and free radical scavenging capacities, and anticancer ability on the HepG2 cell. Except for the n-hexane extract, all of the RU extracts had considerably higher TPCs than RC extracts, ranging from 8.39 to 11.16 mg gallic acid equivalent (GAE) per gram of dry weight, and the TPCs of each extract were also significantly correlated with their antioxidant capacities by ABTS, DPPH, and FRAP assays (p &lt, 0.05). Moreover, there was no remarkable association between the antioxidant capacities and either TACs or TFCs in both the RU and RC extracts. Besides, high-performance liquid chromatography (HPLC) analysis revealed that both the RU and RC extracts contained chrysophanol, emodin, and physcion, and those bioactive compounds were relatively higher in the n-hexane solvent extracts. Additionally, we observed different levels of dose-dependent cytotoxic effects in all the extracts by cell viability assay. Notably, the ethanol extract of RU had a compelling cytotoxic effect with the lowest half-maximum inhibition concentration (IC50-171.94 ± 6.56 µg/mL at 48 h) among the RU extracts than the ethanol extract of RC. Interestingly, the ethanol extract of RU but not RC significantly induced apoptosis in the human liver cancer cell line, HepG2, with a distinct pattern in caspase-3 activation, resulting in increased PARP cleavage and DNA damage. In summary, Mongolian Rhubarb, RU, showed more phytochemical contents, as well as a higher antioxidant capacity and apoptotic effect to HepG2 than RC, thus, it can be exploited for the proper source of natural antioxidants and liver cancer treatment in further investigation.

Hemoptysis, a common symptom of different lung diseases, engenders shortness of breath and increased mortality. Tranexamic acid (TXA), a commonly used antifibrinolytic agent, can control bleeding. However, the effects of its use on pulmonary hemorrhage have rarely been discussed. We conducted this systematic review and meta-analysis of randomized controlled trials (RCTs) of TXA for hemoptysis to investigate its effectiveness in reducing hemoptysis volume and duration. We searched the Cochrane Library, Embase, PubMed (including MEDLINE), and Scopus databases for relevant RCTs. Two of the authors individually assessed study quality by using the Cochrane risk-of-bias (RoB) 2.0 tool, and the pooled results were evaluated using RevMan 5.3. We obtained 617 articles, of which four RCTs met eligibility criteria. The pooled results demonstrated no significant differences in bleeding duration or hemoptysis resolution between the TXA and control groups. Nevertheless, TXA use reduced bleeding volume (mean difference [MD] = − 56.21 mL; 95% CI − 94.70 to − 17.72 mL), further intervention risk (Peto odds ratio = 0.24; 95% CI 0.08–0.67; I2 = 0%), and length of hospital stay (MD = − 1.62 days; 95% CI − 2.93 to − 0.31; I2 = 0%). TXA use was observed to reduce bleeding volume, further intervention risk, and length of hospital stay in patients with hemoptysis; however, our results may have low statistical power because of limited sample size. Additional large-scale RCTs are thus warranted to confirm the effectiveness and safety of TXA use.

Introduction: Spontaneous bacterial peritonitis (SBP) is a fatal infection in patients. It often happens in patients with cirrhosis, cancer or diabetes, and is caused mostly by Enterobacteriaceae. Here we report a rare case of SBP caused by Campylobacter Coli (C coli) infection, which was identified promptly by the matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) and received adequate therapy sooner after. Patient concerns: In the present study, we reported a 46-year-old male with alcoholic liver cirrhosis (Child-Pugh class C) and type 2 diabetes mellitus presented with a 1-day history of fever and abdominal pain. Diagnosis: Based on the clinical examinations, the patient was diagnosed with SBP and the pathogen was quickly identified as C coli by the matrix assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS), a rare causative pathogen of SBP. Interventions: The patient received a 10-day antibiotic treatment with Ciprofloxacin 400 mg every 12 hours, and recovered successfully. Outcomes: The patient had a successful treatment outcome. Conclusion: The study demonstrated a new possible infectious cause of SBP by C Coli, which was rarely seen in liver cirrhosis but mostly found in immunocompromised patients. Thus, it might raise an idea of microorganism screening of broader types that might also induce SBP for immunocompromised patients.

Current capsule endoscopy procedures are ineffective for upper gastrointestinal (GI) tract examination because they do not allow for operator-controlled navigation of the capsule. External controllability of a capsule endoscope with an applied magnetic field is a possible solution to this problem. We developed a novel magnetic-assisted capsule endoscope (MACE) system to visualize the entire upper GI tract. The present study evaluated the safety and feasibility of the MACE system for the examination of the upper GI tract, including the esophagus, stomach, and duodenum. The present open clinical study enrolled ten healthy volunteers. All participants swallowed a MACE, and an external magnetic field navigator was used for magnetic capsule manipulation in the upper GI tract. We assessed the maneuverability of the magnetic capsule and completeness of the MACE examination as well as the safety and tolerability of the procedure. The present study enrolled ten healthy volunteers with a mean age and body mass index of 47.7 years and 25.6 kg/m2, respectively. One volunteer withdrew because of difficulty in swallowing the capsule. In total, nine volunteers underwent the MACE examination. The average examination time was 27.1 min. The maneuverability of the capsule was assessed as good and fair in 55.6 and 44.4% of the participants, respectively. The overall completeness of the examination in the esophagus, stomach, and duodenum was 100, 85.2, and 86.1%, respectively. No severe adverse events occurred during this study. All participants exhibited satisfactory tolerance of the MACE examination. The MACE system has satisfactory maneuverability and visualization completeness with excellent acceptance and tolerance.

Microtubule-targeting agents (MTAs) are widely used in cancer chemotherapy, but the therapeutic responses significantly vary among different tumor types. Protein kinase RNA-like endoplasmic reticular (ER) kinase (PERK) is an ER stress kinase, and the role of PERK in the anticancer effects of MTAs is still undefined. In the present study, taxol (TAX) and nocodazole (NOC) significantly induced apoptosis with increased expression of phosphorylated PERK (pPERK, Tyr980) in four human colon cancer cell lines, including HCT-15, COLO205, HT-20, and LOVO cells. Induction of G2/M arrest by TAX and NOC with increases in phosphorylated Cdc25C and cyclin B1 protein were observed in human colon cancer cells. Application of the c-Jun N-terminal kinase (JNK) inhibitors SP600125 (SP) and JNK inhibitor V (JNKI) significantly reduced TAX- and NOC-induced apoptosis and G2/M arrest of human colon cancer cells. Interestingly, TAX- and NOC-induced pPERK (Tyr980) protein expression was inhibited by adding the JNK inhibitors, SP and JNKI, and application of the PERK inhibitor GSK2606414 (GSK) significantly reduced apoptosis and G2/M arrest by TAX and NOC, with decreased pPERK (Tyr980) and pJNK, phosphorylated Cdc25C, and Cyc B1 protein expressions in human colon cancer cells. Decreased viability by TAX and NOC was inhibited by knockdown of PERK using PERK siRNA in COLO205 and HCT-15 cells. Disruption of the mitochondrial membrane potential and an increase in B-cell lymphoma-2 (Bcl-2) protein phosphorylation (pBcl-2, Ser70) by TAX and NOC were prevented by adding the PERK inhibitor GSK and JNK inhibitor SP and JNKI. A cross-activation of JNK and PERK by TAX and NOC leading to anti-CRC actions including apoptosis and G2/M arrest was first demonstrated herein.

The use of foodstuff as natural medicines has already been established through studies demonstrating the pharmacological activities that they exhibit. Knowing the nutritional and pharmacological significance of foods enables the understanding of their role against several diseases. Among the foods that can potentially be considered as medicine, is sesame or Sesamum indicum L., which is part of the Pedaliaceae family and is composed of its lignans such as sesamin, sesamol, sesaminol and sesamolin. Its lignans have been widely studied and are known to possess antiaging, anticancer, antidiabetes, anti-inflammatory and antioxidant properties. Modern chronic diseases, which can transform into clinical diseases, are potential targets of these lignans. The prime example of chronic diseases is rheumatic inflammatory diseases, which affect the support structures and the organs of the body and can also develop into malignancies. In line with this, studies emphasizing the anti-inflammatory and anticancer activities of sesame have been discussed in this review.

Microtubule-targeting agents (MTAs) are widely used in cancer chemotherapy, but the therapeutic responses significantly vary among different tumor types. Protein kinase RNA-like endoplasmic reticular (ER) kinase (PERK) is an ER stress kinase, and the role of PERK in the anticancer effects of MTAs is still undefined. In the present study, taxol (TAX) and nocodazole (NOC) significantly induced apoptosis with increased expression of phosphorylated PERK (pPERK; Tyr980) in four human colon cancer cell lines, including HCT-15, COLO205, HT-20, and LOVO cells. Induction of G2/M arrest by TAX and NOC with increases in phosphorylated Cdc25C and cyclin B1 protein were observed in human colon cancer cells. Application of the c-Jun N-terminal kinase (JNK) inhibitors SP600125 (SP) and JNK inhibitor V (JNKI) significantly reduced TAX- and NOC-induced apoptosis and G2/M arrest of human colon cancer cells. Interestingly, TAX- and NOC-induced pPERK (Tyr980) protein expression was inhibited by adding the JNK inhibitors, SP and JNKI, and application of the PERK inhibitor GSK2606414 (GSK) significantly reduced apoptosis and G2/M arrest by TAX and NOC, with decreased pPERK (Tyr980) and pJNK, phosphorylated Cdc25C, and Cyc B1 protein expressions in human colon cancer cells. Decreased viability by TAX and NOC was inhibited by knockdown of PERK using PERK siRNA in COLO205 and HCT-15 cells. Disruption of the mitochondrial membrane potential and an increase in B-cell lymphoma-2 (Bcl-2) protein phosphorylation (pBcl-2; Ser70) by TAX and NOC were prevented by adding the PERK inhibitor GSK and JNK inhibitor SP and JNKI. A cross-activation of JNK and PERK by TAX and NOC leading to anti-CRC actions including apoptosis and G2/M arrest was first demonstrated herein.

In this study, we evaluated the ability of Scutellaria baicalensis Georgi to protect lipid-peroxidation (LPO) in lung tissue after free radical-induced injury. We prepared S. baicalensis root (SBR) extracts using different solvents. The total flavonoid and total phenol contents of each extract were measured, and the ROS damage protection was evaluated by analyzing linoleic acid hydroperoxide (LHP)-induced LPO in rat lung mitochondria. Moreover, evaluating diphenylpicrylhydrazyl (DPPH), hydrogen peroxide, superoxide anion radical, and hydroxyl radical scavenging abilities and using metal chelating assays were used to determine in vitro antioxidant activity. The ethyl acetate (EtOAc) extract showed high ROS scavenging ability, and four compounds were subsequently isolated and purified from this extract: baicalin, baicalein, wogonin, and oroxylin A. Baicalein in rat lung mitochondria the most significant LHP-induced LPO inhibition was shown and extracted with EtOAc that contained the highest amount of baicalein. Thus, baicalein and the EtOAc extract of SBR may be efficient in conferring ROS damage protection and inhibiting LHP-induced LPO in rat lung mitochondria. Additional studies are warranted to investigate their use as antioxidant therapy for respiration infections, nutrition supplements, and lead compounds in pharmaceuticals.

In this study, we evaluated the ability of Scutellaria baicalensis Georgi to protect lipid-peroxidation (LPO) in lung tissue after free radical-induced injury. We prepared S. baicalensis root (SBR) extracts using different solvents. The total flavonoid and total phenol contents of each extract were measured, and the ROS damage protection was evaluated by analyzing linoleic acid hydroperoxide (LHP)-induced LPO in rat lung mitochondria. Moreover, evaluating diphenylpicrylhydrazyl (DPPH), hydrogen peroxide, superoxide anion radical, and hydroxyl radical scavenging abilities and using metal chelating assays were used to determine in vitro antioxidant activity. The ethyl acetate (EtOAc) extract showed high ROS scavenging ability, and four compounds were subsequently isolated and purified from this extract: baicalin, baicalein, wogonin, and oroxylin A. Baicalein in rat lung mitochondria the most significant LHP-induced LPO inhibition was shown and extracted with EtOAc that contained the highest amount of baicalein. Thus, baicalein and the EtOAc extract of SBR may be efficient in conferring ROS damage protection and inhibiting LHP-induced LPO in rat lung mitochondria. Additional studies are warranted to investigate their use as antioxidant therapy for respiration infections, nutrition supplements, and lead compounds in pharmaceuticals.

Hepatocellular carcinoma (HCC) ranks as the fourth leading cause of cancer-related deaths worldwide. Sorafenib was the only U.S. Food and Drug Administration (FDA) approved drug for treating advanced HCC until recently, so development of new target therapy is urgently needed. In this study, we established a zebrafish drug screening platform and compared the therapeutic effects of two multiple tyrosine kinase inhibitors, 419S1 and 420S1, with Sorafenib. All three compounds exhibited anti-angiogenesis abilities in immersed fli1:EGFP transgenic embryos and the half inhibition concentration (IC50) was determined. 419S1 exhibited lower hepatoxicity and embryonic toxicity than 420S1 and Sorafenib, and the half lethal concentration (LC50) was determined. The therapeutic index (LC50/IC50) for 419S1 was much higher than for Sorafenib and 420S1. The compounds were either injected retro-orbitally or by oral gavage to adult transgenic zebrafish with HCC. The compounds not only rescued the pathological feature, but also reversed the expression levels of cell-cycle-related genes and protein levels of a proliferation marker. Using a patient-derived-xenograft assay, we found that the effectiveness of 419S1 and 420S1 in preventing liver cancer proliferation is better than that of Sorafenib. With integrated efforts and the advantage of the zebrafish platform, we can find more effective and safe drugs for HCC treatment and screen for personalized medicine.

Early detection is important for improving the survival rate of patients with gastric cancer (GC). Serum tumor markers have been widely used for detecting GC. However, their clinical values remain controversial. This study aims to investigate the role of serum cancer antigen 72-4 (CA72-4) in the diagnosis of GC in a healthy population. A total of 7757 adults who underwent upper gastrointestinal endoscopy and serum CA72-4 level measurement in multicenters in Taiwan from January 2006 to August 2016 were recruited in this retrospective study. Risk factors for GC, serum tumor markers, and esophagogastroduodenoscopy (EGD) findings were evaluated. High serum levels of CA72-4 were found in 7.2% of healthy adults. CA72-4 level showed lower sensitivity (33.3%) but higher specificity (92.8%), however, the positive predictive value was quite low (0.18%). After adjustment of clinical risk factors for GC using EGD findings, gastric ulcer (adjusted odds ratio (aOR) = 2.11), gastric polyps (aOR = 1.42), and atrophic gastritis (aOR = 1.27) were significantly associated with high serum CA72-4 levels. Furthermore, both age (OR = 1.01) and Helicobacter pylori infection (OR = 1.44) exhibited a significant association with high serum CA72-4 levels. These results indicate that routine screening of CA72-4 levels for diagnosing GC in asymptomatic patients may be ineffective due to low sensitivity and low positive predictive value. The clinical utility of EGD findings along with serum CA72-4 level for screening healthy individuals with GC is warranted.

Hispolon (HIS) is an active polyphenol compound derived from Phellinus linteus (Berkeley & Curtis), and our previous study showed that HIS effectively inhibited inflammatory responses in macrophages [Yang, L.Y., S.C. Shen, K.T. Cheng, G.V. Subbaraju, C.C. Chien and Y.C. Chen. Hispolon inhibition of inflammatory apoptosis through reduction of iNOS/NO production via HO-1 induction in macrophages. J. Ethnopharmacol. 156: 61–72, 2014]; however, its effect on neuronal inflammation is still undefined. In this study, HIS concentration- and time-dependently inhibited lipopolysaccharide (LPS)- and lipoteichoic acid (LTA)-induced inducible nitric oxide (NO) synthase (iNOS)/NO production with increased heme oxygenase (HO)-1 proteins in BV-2 microglial cells. Accordingly, HIS protected BV-2 cells from LPS- or LTA-induced apoptosis, characterized by decreased DNA ladder formation, and caspase-3 and poly(ADP ribose) polymerase (PARP) protein cleavage in BV-2 cells. Similarly, the NOS inhibitor, N-nitro-L-arginine methyl ester (NAME), inhibited LPS- or LTA-induced apoptosis of BV-2 cells, but neither NAME nor HIS showed any inhibition of NO production or cell death induced by the NO donor, sodium nitroprusside (SNP), indicating the involvement of NO in the inflammatory apoptosis of microglial cells. Activation of c-Jun N-terminal kinase (JNK) and nuclear factor (NF)-[Formula: see text]B contributed to LPS- or LTA-induced iNOS/NO production and apoptosis of BV-2 cells, and that was suppressed by HIS. Additionally, HIS possesses activity to induce HO-1 protein expression via activation of extracellular signal-regulated kinase (ERK) in BV-2 cells, and application of the HO inhibitor, tin protoporphyrin (SnPP), or knockdown of HO-1 protein by HO-1 small interfering (si)RNA significantly reversed HIS inhibition of NO production and cell death in BV-2 cells stimulated by LPS. Results of an analysis of the effects of HIS and two structurally related chemicals, i.e. dehydroxy-HIS (D-HIS) and HIS-methyl ester (HIS-ME), showed that HIS expressed the most potent inhibitory effects on iNOS/NO production, JNK activation, and apoptosis in BV-2 microglial cells activated by LPS with increased HO-1 protein expression. Overall these results suggested that HIS possesses inhibitory activity against LPS- or LTA-induced inflammatory responses including iNOS/NO production and apoptosis in BV-2 microglial cells and that the mechanisms involve upregulation of the HO-1 protein and downregulation of JNK/NF-[Formula: see text]B activation. A critical role of hydroxyl at position C3 in the anti-inflammatory actions of HIS against activated BV-2 microglial cells was suggested.

Supplemental Digital Content is available in the text, Rationale: Scrotal swelling is a rare complication of acute pancreatitis. It had been explained by fluid accumulation in scrotum originated from abdomen. Here we demonstrated a case of recurrent pancreatitis with hydrocele caused by impaired testicular venous drainage. Patient concerns: A 53-year-old man presented with sudden onset epigastric pain after an alcohol binge. Recurrent acute pancreatitis was confirmed by medical history, physical examination, elevated lipase level and abdominal computed tomography (CT) scan. Right scrotal swelling was noticed on the next day. Diagnosis: The scrotal ultrasonography demonstrated fluid accumulation around the testis and varicocele consistent with scrotal hydrocele. CT scans of the abdomen and pelvis showed encasement of the right testicular vein by pancreatic phlegmon. Interventions: The patient was subject to Nulla per os, hydration, and opioid analgesics for pancreatitis. No intervention was performed for scrotal swelling. Outcomes: Hydrocele gradually resolved along with acute pancreatitis. Lessons: Pancreatic phlegmon compromised testicular venous return which led to scrotal hydrocele and posed a threat to fertility. The study has provided a novel pathologic linkage. This complication should be taken into account.

Nilotinib (AMN) induces apoptosis in various cancer cells; however the effect of AMN on human ovarian cancer cells is still unclear. A reduction in cell viability associated with the occurrence of apoptotic characteristics was observed in human SKOV-3 ovarian cancer cells under AMN but not sorafenib (SORA) or imatinib (STI) stimulation. Activation of apoptotic pathway including increased caspase (Casp)-3 and poly(ADP-ribose) polymerase 1 (PARP1) protein cleavage by AMN was detected with disrupted mitochondrial membrane potential (MMP) accompanied by decreased Bcl-2 protein and increased cytosolic cytochrome (Cyt) c/cleaved Casp-9 protein expressions was found, and AMN-induced cell death was inhibited by peptidyl Casp inhibitors, VAD, DEVD and LEHD. Increased phosphorylated c-Jun N-terminal kinase (JNK) protein expression was detected in AMN- but not SORA- or STI-treated SKOV-3 cells, and the JNK inhibitors, SP600125 and JNKI, showed slight but significant enhancement of AMN-induced cell death in SKOV-3 cells. The intracellular peroxide level was elevated by AMN and H2O2, and N-acetylcysteine (NAC) prevented H2O2- but not AMN-induced peroxide production and apoptosis in SKOV-3 cells. AMN induction of apoptosis with increased intracellular peroxide production and JNK protein phosphorylation was also identified in human A2780 ovarian cancer cells, cisplatin-resistant A2780CP cells, and clear ES-2 cells. The evidence supporting AMN effectively reducing the viability of human ovarian cancer cells via mitochondrion-dependent apoptosis is provided.

Background The occurrence rate and severity of gastroesophageal reflux disease with erosive esophagitis (EE) in patients after converting nasogastric tube (NGT) feeding to percutaneous endoscopic gastrostomy (PEG) are not well-known. The aim of this study was to determine the influence of PEG placement on the occurrence and severity of EE in patients with long-term PEG feeding. Methods This retrospective study included patients with NGT feeding who were converted to PEG feeding and received pre- and post-PEG endoscopy between January 2000 and June 2013. Factors predictive of the occurrence of EE after PEG were analyzed. Results One-hundred and twenty patients with NGT feeding were converted to PEG, and 47 patients were included. Before PEG, 21 (44.7%) NGT-feeding patients had EE. The mean follow-up time was 45.7 months (range, 6–147 months). Erosive esophagitis occurred in nine (19.1%) patients after PEG. The occurrence rate (p

Background Early clinical exposure (ECE) is viewed as a way to provide contexts of basic science and highlight its relevance to medical practice. However, very few studies have specifically looked into how the ECE experience contributes to students’ academic performance. The purpose of this study was to investigate whether ECE experiences (external cause) or students’ learning attitudes (internal cause) more closely correlated with medical students’ academic performance. Methods Subjects who participated in the study comprised 109 s-year students at Taipei Medical University. Fifty of the 109 study participants were enrolled in an elective ECE program. The dependent variable in this study was the test score of a systems-based basic sciences (SBBS) course. Independent variables of the study included students’ attitudes and test anxiety towards the SBBS course, engagement/length of time spent in ECE, and the ECE learning environment. Data of students’ engagement in ECE, levels of their motivational beliefs and test anxiety, differences in the ECE learning environment, and the SBBS final test scores of these 109 respondents were collected for hierarchical multiple regression (HMR) analyses. Results Results of the HMR analyses revealed that students’ test anxiety towards basic science and also the learning environment of the ECE had significant positive predictive power on their SBBS test scores. Conculsion This study discovers that medical students’ academic performance in basic science correlates not only with their anxiety to testing, but even more so with the clinical environment they are exposed to. Hence we suggest including further investigations about different learning environments on ECE experiences in future studies. Electronic supplementary material The online version of this article (10.1186/s12909-019-1612-0) contains supplementary material, which is available to authorized users.

Oxidative stress or excessive antioxidant levels-caused redox imbalance can alter apoptotic responses, and N-acetyl-L-cysteine (NAC) was able to inhibit H2O2-mediated cell death, but unable to prevent apoptosis induced by other chemicals such as etoposide. We now demonstrate that 10 and 20 mM NAC, non-toxic concentrations, can enhance fisetin (FIS)-mediated apoptosis in colon cancer cells COLO205. Compared to treatment with FIS alone, combination treatment with NAC increased the expression of cleaved caspase-3 and PAPR protein, and produced greater density of DNA ladders. NAC reduced the mitochondrial membrane potential of FIS-treated COLO205 cells with induction of caspase 9 protein cleavage. DNA ladders induced by FIS + NAC were diminished by adding the caspase 3 inhibitor, DEVD-FMK, and the caspase 9 inhibitor, YVAD-FMK. Combinatorial treatment COLO205 cells with NAC and FIS showed potent inhibition on ERK protein phosphorylation, compared with those from FIS or NAC-treated groups by Western blotting using specific antibodies. Addition of the chemical ERK inhibitors, PD98059 and U0126, significantly inhibited ERK protein phosphorylation, accompanied by induced DNA ladder formation, cleavage of caspase 3 and PARP protein in COLO205 cells. Furthermore, NAC showed an enhancement on a FIS-related chemical chrysin-induced apoptosis of COLO205 cells, and NAC sensitization of colon cancer cells to FIS-induced apoptosis was also identify in colonic cancer cells HCT-116, HT-29, and HCT-15 cells. The evidence to support NAC sensitizing human colon cancer cells to FIS-induced apoptosis was provided, and application of NAC and FIS as a strategy to treat colonic cancer deserved for further in vivo study. © 2013 Wiley Periodicals, Inc.

We revealed the cytotoxic effect of the flavonoid, fisetin (FIS), on human COLO205 colon cancer cells in the presence and absence of the HSP90 inhibitors, geldanamycin (GA) and radicicol (RAD). Compared to FIS treatment alone of COLO205 cells, GA and RAD significantly enhanced FIS-induced cytotoxicity, increased expression of cleaved caspase-3 and the PAPR protein, and produced a greater density of DNA ladder formation. GA and RAD also reduced the MMPs with induction of caspase-9 protein cleavage in FIS-treated COLO205 cells. Increased caspase-3 and -9 activities were detected in COLO205 cells treated with FIS+GA or FIS+RAD, and the intensity of DNA ladder formation induced by FIS+GA was reduced by adding the caspase-3 inhibitor, DEVD-FMK. A decrease in Bcl-2 but not Bcl-XL or Bax protein by FIS+GA or FIS+RAD was identified in COLO205 cells by Western blotting. A reduction in p53 protein with increased ubiquitin-tagged proteins was observed in COLO205 cells treated with FIS+GA or FIS+RAD. Furthermore, GA and RAD reduced the stability of the p53 protein in COLO205 cells under FIS stimulation. The evidence supports HSP90 inhibitors possibly sensitizing human colon cancer cells to FIS-induced apoptosis, and treating colon cancer by combining HSP90 inhibitors with FIS deserves further in vivo study.

Aims and objectives. This study aimed to explore the correlation between fatigue and physical activity in patients with liver cirrhosis. Background. Many patients with liver cirrhosis perceive lower physical functioning and more fatigue than non-cirrhotic individuals. To date, however, few studies have examined the relationship between fatigue and physical activity in this patient population. Design. This study used a correlation design. Participants were patients with liver cirrhosis recruited from the gastroenterology clinic of a teaching medical centre in Taiwan. Methods. Data were collected using a structured questionnaire, consisting of a fatigue scale and a seven-day Physical Activity Recall scale. spss version 13.0 software was used to analyse the data through statistical methods, including one-way analysis of variance, independent t-test and Pearson’s correlations. Results. Patients participating in this study suffered from moderate-to-severe fatigue, and their engagement in physical activity of moderate or higher intensity was decreased. On average, fatigue had a moderate level of influence on physical activity. A significant negative correlation was found between the fatigue level and average seven-day physical activity level. Conclusions. Patients with liver cirrhosis can experience severe fatigue, which may reduce their level of physical activity. Relevance to clinical practice. Early evaluation of the fatigue level and physical activity constraints in patients with liver cirrhosis should be conducted in the clinic or community. Individualised instructions for patient’s physical activity should be provided.

Colon cancer is the third most common malignancy worldwide. Recently, some interesting associations between ghrelin and cancer were reported, and it may participate in colon cancer development. In the present report, we explored the role of the growth hormone secretagogue receptor (GHS-R), Ras, phosphatidylinositol 3-kinase (PI3K), Akt, and mammalian target of rapamycin (mTOR) pathways in the ghrelin-induced proliferation of human colon cancer cells. Ghrelin-caused HT-29 proliferation was reduced by [D-Lys3]-GHRP-6 (a GHS-R inhibitor). We also found that a dominant negative mutant of Ras (Ras DN), a PI3K inhibitor (LY 294002), an Akt DN, and an mTOR inhibitor (rapamycin) attenuated ghrelin-caused colon cancer cell proliferation. We found that ghrelin induced time-dependent increases in Ras activity. Moreover, ghrelin-mediated Akt Ser473 phosphorylation was attenuated by a Ras DN and LY 294002. Furthermore, a Ras DN, LY 294002, and an Akt DN all inhibited ghrelin-caused mTOR Ser2448 phosphorylation. These results indicate that the Ras/PI3K/Akt/mTOR cascade plays a critical role in ghrelin-induced colon cancer cell proliferation.

Background Evodiamine (EVO; 8,13,13b,14-tetrahydro-14-methylindolo[2′3′-3,4]pyrido[2,1-b]quinazolin-5-[7H]-one derived from the traditional herbal medicine Evodia rutaecarpa was reported to possess anticancer activity; however, the anticancer mechanism of EVO against the viability of human ovarian cancer cells is still unclear. Purpose A number of studies showed that chemotherapeutic benefits may result from targeting the endoplasmic reticular (ER) stress signaling pathway. The objective of the study is to investigate the mechanism by which ER stress protein PERK plays in EVO-induced apoptosis of human ovarian cancer cells. Methods Cell death analysis was performed by MTT assay, DNA fragmentation assay, and Giemsa staining. DiOC6 staining was used for mitochondrial membrane potential measurement. Protein levels were analyzed by Western blotting. Pharmacological studies using MAPK inhibitors and PERK inhibitor GSK2606414 were involved. Results The viability of human ovarian cancer cells A2780, A2780CP, ES-2, and SKOV-3 was inhibited by EVO at various concentrations in accordance with increases in the percentage of apoptotic cells, DNA ladders, and cleavage of caspase 3 and poly(ADP ribose) polymerase (PARP) proteins. Decreased viability of cells was reversed by adding caspase inhibitors VAD and DEVD in SKOV-3 and A2780CP cells, and incubation of cells with JNK inhibitor SP600125 (SP) and JNKI, but not other MAPK and AKT inhibitors including PD98059, SB203580, significantly prevented the apoptosis elicited by EVO in human ovarian cancer cells. Furthermore, increased expression of phospho-eIF2α (peIF2α) and phospho-PERK (pPERK) proteins was detected in EVO-treated human ovarian cancer cells, and that was inhibited by adding JNK inhibitors SP600125 and JNKI. Application of a PERK inhibitor GSK2606414 showed a significant protection of human ovarian cancer cells A2780 and A2780CP from EVO-induced apoptosis. EVO disruption of mitochondrial membrane potential (MMP) was also inhibited by adding JNK or PERK inhibitors. The structure-activity relationship study indicated that the alkyl group at position 14 in EVO is important for apoptosis induction via activation of JNK and PERK in human ovarian cancer cells. Conclusion Evidence supporting EVO induction of apoptosis via activation of JNK and PERK to disrupt MMP in human ovarian cancer cells is provided, and the alkyl at position 14 is a critical substitution for the apoptotic actions of EVO.

Body iron levels have recently been shown to be a strong predictor for non-alcoholic fatty liver disease (NAFLD). The aims of this study were to investigate the prevalence of NAFLD in a general adult population, and to investigate the relationship between body iron levels, NAFLD and the metabolic syndrome (MetS). 2186 adults participated in the third National Nutrition and Health Survey in Taiwan (NAHSIT, 2005-2008). The participants underwent anthropometry measurements and phlebotomy after an overnight fast, and those with excessive alcohol intake, iron overload of serum ferritin > 600 ng/ml, hepatitis viral infection and hepatocellular carcinoma were excluded. Suspected NAFLD was diagnosed by three alanine transaminase (ALT) cut-points: cut-point 1: serum ALT > 40 U/l; cut-point 2: ALT ≥ 25 U/l for male and ALT ≥ 17 U/l for female; and cut-point 3: ALT ≥ 35 U/l for male and ALT ≥ 26 U/l for female. The prevalence proportion of suspected NAFLD among Taiwanese adults was 6.6% (cut-point 1), 36% (cut-point 2); and 14.3% (cut-point 3). Body iron levels were significantly higher in individuals with suspected NAFLD compared with those without. Distribution of hemoglobin levels, but not serum ferritin levels, by decade of age showed strong correlation with the prevalence of suspected NAFLD in individuals with MetS. Multivariate adjusted odds ratio (OR) showed that the best predictors for suspected NAFLD with the MetS were hemoglobin [OR 1.43 (1.21-1.68); P < 0.0001] and hyperlipidemia [OR 1.52 (1.19-1.94); P = 0.0007]. In individuals without MetS, the adjusted OR of suspected NAFLD was markedly higher for hemoglobin [OR 1.25 (1.12-1.41); P < 0.0001]. In conclusion, adults with high hemoglobin levels (14.4 μg/dl for male and 13.2 μg/dl for female) are at the greatest risk for developing abnormal liver function. Hemoglobin test should be considered as a part of clinical evaluation for patients with NAFLD.

Objective. Chronic hepatitis C virus (HCV) infection is a serious health problem in Taiwan. The high dropout rate due to side effects limits the efficacy of treatment. The objective of this study is to investigate the effectiveness of telecare for the treatment of chronic hepatitis.Material and Methods. Two hundred and ninety-eight patients randomly chose either of the two support programs. Group 1 was offered public health nurse consultation at outpatient clinic. Group 2 was offered telecare program with 24 hours of consultation services via a health communication center. All patients were treated with standard therapy and followed up for 72 weeks.Results. Normalization of serum biochemistry was noted in both Group 1 (150 patients) and Group 2 (148 patients). The most common types of side effect in both groups were influenza-like symptoms. Patient compliance was 88% (Group 1) and 94.6% (Group 2). Total dropout cases were 18 (12%) in Group 1 and 8 (5.4%) in Group 2. The program costs were 232,632 USD (Group 1) and 112,500 USD (Group 2).Conclusion. Telecare system with health care communication center model is significant in reducing dropout rate and is more effective with easy access.

Evodiamine (EVO; 8,13,13b,14-tetrahydro-14-methylindolo[2′3′-3,4]pyrido[2,1-b]quinazolin-5-[7H]-one derived from the traditional herbal medicine Evodia rutaecarpa was reported to possess anticancer activity; however, the anticancer mechanism is still unclear. In this study, we investigated the anticancer effects of EVO on human colon COLO205 and HT-29 cells and their potential mechanisms. MTT and lactate dehydrogenase (LDH) release assays showed that the viability of COLOL205 and HT-29 cells was inhibited by EVO at various concentrations in accordance with increases in the percentage of apoptotic cells and cleavage of caspase-3 and poly(ADP ribose) polymerase (PARP) proteins. Disruption of the mitochondrial membrane potential by EVO was accompanied by increased Bax, caspase-9 protein cleavage, and cytochrome (Cyt) c protein translocation in COLO205 and HT-29 cells. Application of the antioxidant N-acetyl-L-cysteine (NAC) inhibited H2O2-induced reactive oxygen species (ROS) production and apoptosis, but did not affect EVO-induced apoptosis of COLO205 or HT-29 cells. Significant increases in the G2/M ratio and cyclinB1/cdc25c protein expression by EVO were respectively identified in colon carcinoma cells via a flow cytometric analysis and Western blotting. Induction of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) protein phosphorylation was detected in EVO-treated cells, and the JNK inhibitor, SP600125, but not the ERK inhibitor, U0126, inhibited EVO-induced phosphorylated JNK protein expression, apoptosis, and G2/M arrest of colon carcinoma cells. Data of the structure-activity analysis showed that EVO-related chemicals containing an alkyl group at position 14 were able to induce apoptosis, G2/M arrest associated with increased DNA ladder formation, cleavage of caspase-3 and PARP, and elevated cycB1 and cdc25c protein expressions in COLO205 and HT-29 cells. Evidence supporting JNK activation leading to EVO-induced apoptosis and G2/M arrest in colon carcinoma cells is provided, and alkylation at position 14 of EVO is a critical substitution for treatment of colonic cancer.

Oxidative stress or excessive antioxidant levels-caused redox imbalance can alter apoptotic responses, and N-acetyl-L-cysteine (NAC) was able to inhibit H2 O2 -mediated cell death, but unable to prevent apoptosis induced by other chemicals such as etoposide. We now demonstrate that 10 and 20 mM NAC, non-toxic concentrations, can enhance fisetin (FIS)-mediated apoptosis in colon cancer cells COLO205. Compared to treatment with FIS alone, combination treatment with NAC increased the expression of cleaved caspase-3 and PAPR protein, and produced greater density of DNA ladders. NAC reduced the mitochondrial membrane potential of FIS-treated COLO205 cells with induction of caspase 9 protein cleavage. DNA ladders induced by FIS + NAC were diminished by adding the caspase 3 inhibitor, DEVD-FMK, and the caspase 9 inhibitor, YVAD-FMK. Combinatorial treatment COLO205 cells with NAC and FIS showed potent inhibition on ERK protein phosphorylation, compared with those from FIS or NAC-treated groups by Western blotting using specific antibodies. Addition of the chemical ERK inhibitors, PD98059 and U0126, significantly inhibited ERK protein phosphorylation, accompanied by induced DNA ladder formation, cleavage of caspase 3 and PARP protein in COLO205 cells. Furthermore, NAC showed an enhancement on a FIS-related chemical chrysin-induced apoptosis of COLO205 cells, and NAC sensitization of colon cancer cells to FIS-induced apoptosis was also identify in colonic cancer cells HCT-116, HT-29, and HCT-15 cells. The evidence to support NAC sensitizing human colon cancer cells to FIS-induced apoptosis was provided, and application of NAC and FIS as a strategy to treat colonic cancer deserved for further in vivo study.

The phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), is a potent stimulator of differentiation in human leukemia cells; however, the effects of arachidonic acid (AA) on TPA-induced differentiation are still unclear. In the present study, we investigated the contribution of AA to TPA-induced differentiation of human leukemia HL-60 cells. We found that treatment of HL-60 cells with TPA resulted in increases in cell attachment and nitroblue tetrazolium (NBT)-positive cells, which were significantly enhanced by the addition of AA. Stimulation of TPA-induced intracellular reactive oxygen species (ROS) production by AA was detected in HL-60 cells via a DCHF-DA analysis, and the addition of the antioxidant, N-acetyl-cysteine (NAC), was able to reduce TPA+AA-induced differentiation in accordance with suppression of intracellular peroxide elevation by TPA+AA. Furthermore, activation of extracellular-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) by TPA+AA was identified in HL-60 cells, and the ERK inhibitor, PD98059, but not the JNK inhibitor, SP600125, inhibited TPA+AA-induced NBT-positive cells. Suppression of TPA+AA-induced ERK protein phosphorylation by PD98059 and NAC was detected, and AA enhanced ERK protein phosphorylation by TPA was in HL-60 cells. AA clearly increased TPA-induced HL-60 cell differentiation, as evidenced by a marked increase in CD11b expression, which was inhibited by NAC and PD98059 addition. Eicosapentaenoic acid (EPA) as well as AA showed increased intracellular peroxide production and differentiation of HL-60 cells elicited by TPA. Evidence of AA potentiation of differentiation by TPA in human leukemia cells HL-60 via activation of ROS-dependent ERK protein phosphorylation was first demonstrated herein.

This study aimed to explore the correlation between fatigue and physical activity in patients with liver cirrhosis.Many patients with liver cirrhosis perceive lower physical functioning and more fatigue than non-cirrhotic individuals. To date, however, few studies have examined the relationship between fatigue and physical activity in this patient population.This study used a correlation design. Participants were patients with liver cirrhosis recruited from the gastroenterology clinic of a teaching medical centre in Taiwan.Data were collected using a structured questionnaire, consisting of a fatigue scale and a seven-day Physical Activity Recall scale. spss version 13.0 software was used to analyse the data through statistical methods, including one-way analysis of variance, independent t-test and Pearson's correlations.Patients participating in this study suffered from moderate-to-severe fatigue, and their engagement in physical activity of moderate or higher intensity was decreased. On average, fatigue had a moderate level of influence on physical activity. A significant negative correlation was found between the fatigue level and average seven-day physical activity level.Patients with liver cirrhosis can experience severe fatigue, which may reduce their level of physical activity.Early evaluation of the fatigue level and physical activity constraints in patients with liver cirrhosis should be conducted in the clinic or community. Individualised instructions for patient's physical activity should be provided.

In this paper, we adopt the Taxes IC BQ2954 to design a switching type battery charger that is very light, high efficiency, and very fast. The charger is able to fully charge a 36V/5.6AH Li-ion battery within 30 minutes.

To investigate the effect of hot water-extracted Lycium barbarum (LBE) and Rehmannia glutinosa (RGE) on cell proliferation and apoptosis in rat and/or human hepatocellular carcinoma (HCC) cells.Rat (H-4-II-E) and human HCC (HA22T/VGH) cell lines were incubated with various concentrations (0-10 g/L) of hot water-extracted LBE and RGE. After 6-24 h incubation, cell proliferation (n = 6) was measured by a colorimetric method. The apoptotic cells (n = 6) were detected by flow cytometry. The expression of p53 protein (n = 3) was determined by SDS-PAGE and Western blotting.Crude LBE (2-5 g/L) and RGE (2-10 g/L) dose-dependently inhibited proliferation of H-4-II-E cells by 11% (P0.05) to 85% (P0.01) after 6-24 h treatment. Crude LBE at a dose of 5 g/L suppressed cell proliferation of H-4-II-E cells more effectively than crude RGE after 6-24 h incubation (P0.01). Crude LBE (2-10 g/L) and RGE (2-5 g/L) also dose-dependently inhibited proliferation of HA22T/VGH cells by 14%-43% (P0.01) after 24 h. Crude LBE at a dose of 10 g/L inhibited the proliferation of HA22T/VGH cells more effectively than crude RGE (56.8% +/- 1.6% vs 70.3% +/- 3.1% of control, P = 0.00030.01). The apoptotic cells significantly increased in H-4-II-E cells after 24 h treatment with higher doses of crude LBE (2-5 g/L) and RGE (5-10 g/L) (P0.01). The expression of p53 protein in H-4-II-E cells was 119% and 143% of the control group compared with the LBE-treated (2, 5 g/L) groups, and 110% and 132% of the control group compared with the RGE -treated (5, 10 g/L) groups after 24 h.Hot water-extracted crude LBE (2-5 g/L) and RGE (5-10 g/L) inhibit proliferation and stimulate p53-mediated apoptosis in HCC cells.