Search

Impacts of the Maillard reaction conditions (maltose/parvalbumin weight ratio, reaction temperature and reaction time) on the antigenicity of parvalbumin (PV) were explored using response surface methodology. The model to predict the antigenicity of PVand an optimal reaction condition were obtained. In addition, the antigenicity, immunoglobulin E (IgE) binding ability and amino acid composition of PV-maltose were analysed. The reaction temperature showed a significant effect on the antigenicity of PV. The optimal reaction condition was: maltose/PV weight ratio was 2.04, reaction temperature was 67.15°C and reaction time was 74.25 h. The predicted antigenicity was 0.276 µg mL−1under these conditions, and the test antigenicity was 0.388 µg mL−1. The IgE binding ability of PV-maltose was significantly suppressed after Maillard reaction. Therefore, Maillard reaction was an effective way to control the main allergen of grass carp. [ABSTRACT FROM AUTHOR]

Cyclic GMP‐AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling pathway has emerged as a key DNA‐sensing machinery in innate immunity. Activation of cGAS–STING signaling pathway mediates the production of interferons and proinflammatory cytokines. Although cGAS–STING signaling pathway shows critical function in the maintenance of gut homeostasis, overactive cGAS–STING signaling pathway leads to gastrointestinal (GI) inflammation. Harnessing the effect and mechanism of the cGAS–STING signaling pathway could be beneficial for the development of novel strategies for the treatment of GI diseases. This review presents recent advances regarding the role of cGAS–STING signaling pathway in GI inflammatory disease and cancers and describes perspective therapeutic strategies targeting the signaling pathway. [ABSTRACT FROM AUTHOR]

Idiopathic short stature (ISS) accounts for more than 70% of childhood short stature cases, with an undefined etiology and pathogenesis, leading to limited treatment. However, recent studies have shown that intestinal microbiota may be associated with ISS. This study aimed to characterize the intestinal microbiota in children with ISS, effect of treatment with growth hormones, and association between specific bacterial species and ISS. This study enrolled 55 children, comprising 40 diagnosed with ISS at Jinhua Hospital, Zhejiang University, and 15 healthy controls. The subjects with ISS were divided into the untreated ISS group (UISS group, 22 children who had not been treated with recombinant human growth hormone [rhGH]), treated ISS group (TISS group, 18 children treated with rhGH for 1 year), and control group (NC group, 15 healthy children). High-throughput sequencing was used to determine the intestinal microbiota characteristics. Higher abundances of Bacteroides, Prevotella, Alistipes, Parabacteroides, Agathobacter and Roseburia were found in the UISS and TISS groups than in the control group, whereas Bifidobacterium, Subdoligranulum, and Romboutsia were less abundant. The composition of intestinal microbiota in the UISS and TISS groups was almost identical, except for Prevotella. The TISS group had significantly lower levels of Prevotella than did the UISS group, which were closer to those of the NC group. Receiver operating characteristic curve analysis revealed that the abundances of Prevotella, Bifidobacterium, Bacteroides, and Subdoligranulum were effective in differentiating between the UISS and NC groups. Conclusion: Alterations in intestinal microbiota may be associated with ISS. Specific bacterial species, such as Prevotella, may be potential diagnostic markers for ISS. What is Known: • ISS is associated with the GH-IGF-1 axis. • Recent studies indicated an association between the GH-IGF-1 axis and intestinal microbiota. What is New: • Children with ISS showed alterations in intestinal microbiota, with a relative increase in the abundance of gut inflammation-related bacteria. • The relative abundances of Prevotella, Bacteroides, Bifidobacterium, and Subdoligranulum may serve as potential diagnostic markers. [ABSTRACT FROM AUTHOR]

We assessed dynamic changes in visceral hypersensitivity and fecal metabolomics through a mouse model of irritable bowel syndrome (IBS) from childhood to adulthood. A mouse model of IBS was constructed with maternal separation (MS) in early life. Male mice aged 25, 40, and 70 days were used. Visceral sensitivity was assessed by recording the reaction between the abdominal withdrawal reflex and colorectal distension. Metabolomics was identified and quantified by liquid chromatography-tandem mass spectrometry. The visceral sensitivity of the MS group was significantly higher than that of the non-separation (NS) group in the three age groups. The top four fecal differential metabolites in the different age groups were lipids, lipid molecules, organic heterocyclic compounds, organic acids and derivatives, and benzenoids. Five identical differential metabolites were detected in the feces and ileal contents of the MS and NS groups at different ages, namely, benzamide, taurine, acetyl-L-carnitine, indole, and ethylbenzene. Taurine and hypotaurine metabolism were the most relevant pathways at P25, whereas histidine metabolism was the most relevant pathway at P40 and P70. Visceral hypersensitivity in the MS group lasted from childhood to adulthood. The different metabolites and metabolic pathways detected in MS groups of different ages provide a theoretical basis for IBS pathogenesis. [ABSTRACT FROM AUTHOR]

The increasing rates of antibiotic resistance in Helicobacter pylori (H. pylori) are a major concern of the decreasing eradication rate. Large-scale and long-period studies on antimicrobial susceptibility of H. pylori in children are limited. This study aimed to describe the temporal changes of antibiotic resistance among children in southeast China. Gastric biopsies obtained from children were cultured for H. pylori from 2015 to 2020. Susceptibility to clarithromycin (CLA), amoxicillin (AML), metronidazole (MTZ), furazolidone (FZD), tetracycline (TET) and levofloxacin (LEV) was tested. Data from 2012 to 2014 reported previously were obtained for comparing the change in temporal trends of antibiotic resistance. A total of 1638 (52.7%) H. pylori strains were isolated from 3111 children recruited. The resistance rates to CLA, MTZ and LEV were 32.8%, 81.7% and 22.8%, respectively. There were 52.9% strains resistant to single resistance, 28.7% to double resistance, and 9.0% to triple resistance. The total resistance rate and resistance rates to CLA, MTZ, LEV, CLA + LEV and CLA + MTZ + LEV increased annually in a linear manner. All resistant patterns except single resistance increased obviously from 2015 to 2017 and 2018 to 2020 compared to that from 2012 to 2014. Double resistance to CLA + MTZ increased significantly with age. The resistance rate to CLA and triple resistance to CLA, MTZ and LEV increased in children with prior H. pylori treatment than that from children without prior treatment. The antibiotic resistance rates of H. pylori were high in a large pediatric population in southeast China from 2015 to 2020. Individual treatment based on susceptibility test is imperative and optimal regimens should be chosen in H. pylori eradication therapy. [ABSTRACT FROM AUTHOR]

Objectives: Massive fetomaternal hemorrhage (FMH) is a rare but sometimes life-threatening event, and surviving neonates may suffer major neurological complications. Severe neonatal anemia (SNA) affected by massive FMH is less reported in the literature. This study aims to explore the clinical characteristics, laboratory diagnoses, treatments and outcomes of SNA affected by massive FMH.Methods: Data were collected retrospectively from the hospital's electronic medical record system. All neonates born in the hospital and admitted to the neonatal unit diagnosed as SNA affected by massive FMH from 1 January 2013 to 31 June 2017 were included.Results: A total of 8 cases of SNA affected by FMH were identified among 6825 neonates admitted to the neonatal unit. They all presented with pallor but without hydrops at birth. Median gestational age and birthweight were 375/7 (360/7‒401/7) weeks and 2,625 (2300‒3050) g, respectively. Median hemoglobin level was 39.5 (25‒53) g/L at birth and 109.5 (94-127) g/L at discharge. Median maternal serum alpha-fetoprotein (AFP) was 3958.5 (1606‒14,330) ng/mL, which was significantly increased. Three out of eight cases manifested as antenatal decreased fetal movement. Only 1 with the lowest initial hemoglobin 25 g/L manifested as characteristic sinusoidal fetal heart rate tracing and suffered severe neonatal asphyxia and hypovolemic shock. Having experienced resuscitation, he was admitted to the neonatal unit and received twice transfusion of cross-matched red blood cells there. Another case with the initial hemoglobin 45 g/L received positive pressure ventilation and once transfusion. All cases were successfully discharged with a median hospital stay of 8 (5-12) days. Follow-up was available for 6 (75%) of 8 neonates (age range 13 months to 50 months), and all infants were observed to be in good condition with normal neurological status. In our series of eight cases, there were no neonatal deaths.Conclusion: This study strengthens the idea that maternal AFP testing is valuable to confirm massive fetomaternal hemorrhage. Surviving neonates of massive FMH might have a good outcome despite severe anemia at birth. [ABSTRACT FROM AUTHOR]

The gastrointestinal tract constantly communicates with the environment, receiving and processing a wide range of information. The contents of the gastrointestinal tract and the gastrointestinal tract generate mechanical and chemical signals, which are essential for regulating digestive function and feeding behavior. There are many receptors here that sense intestinal contents, including nutrients, microbes, hormones, and small molecule compounds. In signal transduction, ion channels are indispensable as an essential component that can generate intracellular ionic changes or electrical signals. Ion channels generate electrical activity in numerous neurons and, more importantly, alter the action of non-neurons simply and effectively, and also affect satiety, molecular secretion, intestinal secretion, and motility through mechanisms of peripheral sensation, signaling, and altered cellular function. In this review, we focus on the identity of ion channels in chemosensing and mechanosensing in the gastrointestinal tract. [ABSTRACT FROM AUTHOR]

Fish is one of the most common sources of food allergens, and grass carp is among the most popular freshwater fish. The objective of this study was to investigate the effects of heat treatment on the antigenicity and allergenicity of white and dark muscle of grass carp. The results showed that the antigenicity of heated white muscle was higher than that of unheated white muscle, while the allergenicity of white muscle was lower than that of unheated muscle when heated at 65°C, and the lowest value was 44.6%. Furthermore, the allergenicity of dark muscle increased for the first 30 min when heated at 65°C, and it increased for the first 60 min and then decreased with the increasing heating time thereafter when heated at 80 and 100°C. In addition, the lowest antigenicity and allergenicity of dark muscle were obtained at 100°C, and the values were 0.447 mg mL−1and 47.0%, respectively. Thus, to decrease the antigenicity and allergenicity of grass carp muscles, it is suggested that heating at 65°C is better than 80 or 100°C for the white muscle, while 100°C is an appropriate heating temperature for the dark muscle. [ABSTRACT FROM AUTHOR]

Nodular gastritis (NG) represents a frequently observed clinical presentation of Helicobacter pylori (H. pylori) infection in pediatric patients. This investigation aimed to explore the microbiota and histological features of the gastric mucosa in children with H. pylori colonized NG. The current investigation examined a sample of 120 children who underwent gastroscopy due to symptoms of gastrointestinal distress, which showed that 64 were patients with H. pylori infection. Endoscopic procedures were conducted to acquire mucosal biopsies for the purpose of DNA extraction and histopathological analysis. The 16S rRNA profiling was utilized to examine the gastric mucosal microbiota. In conjunction with endoscopic evaluation, 26 of 64 patients were diagnosed with NG. The NG group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. The NG group exhibited a significant reduction in the richness levels of the five genera. In terms of the predicted functions, the pathways of synthesis and degradation of ketone bodies and phagosome in the NG group were less abundant compared with the non-NG group, while the Wnt signaling pathway was significantly enriched. NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa. In conclusion, NG group exhibited significant severe inflammation and reduced abundance levels of several bacterial genera compared to the non-NG group. However, individuals with NG did not have a dysregulated microbial community with genotoxic potential. • Nodular gastritis (NG) group had significantly higher inflammation scores and activity scores on histological assessment than the non-NG group. • There was a degree of difference between the two groups in terms of population abundance levels, co-network analysis and functional prediction. • NG does not increase a microbial community that possesses genotoxic potential within the gastric mucosa, suggesting that children with nodular gastritis do not have an increased risk of mucosal carcinogenesis. [ABSTRACT FROM AUTHOR]

• LPS induced depression is accompanied with decline in the numbers of DG-PVIs. • CUMS induced depression is occurring with decrease in PVIs numbers in the vHPC. • Ablation of PVIs from the vDG induced depression-like behavior. • Removal vDG-PVIs induced depression potentially associated with neuroinflammation. Depression is an increasingly common but extremely serve mood disorder that remains poorly understood and inadequately treated. Fast-spiking parvalbumin-positive interneurons (PVIs), a subpopulation of GABAergic interneurons (GABA, g-aminobutyric acid), exhibit a widespread distribution throughout the hippocampus, and has been reported to play an important role in a variety of mental disorders. However, the relationship between depression and hippocampal PVIs remains unclear. Here in this present study, a series of experiments were conducted to clarify the potential relationship. Here, chronic unpredicted mild stress (CUMS) and Lipopolysaccharide (LPS) injection were introduced to induce depression-like behavior in mice, and led to a clear decline in PVIs numbers in the ventral hippocampal (vHPC), particularly in the ventral dentate gyrus (vDG) subfield. After a selectively removal of the PVIs in PV-ires-Cre::Ai14 mice, we confirmed that ablation of PVIs from the vDG induced depression-like behavior. Furthermore, we found that the removal of vDG-PVIs induced depression likely to be accounted for upregulation of neuroinflammation. These findings facilitate us better understand the role of hippocampal PVIs in depression. [ABSTRACT FROM AUTHOR]

Stroke is the second leading cause of death worldwide. Patients who have a stroke are susceptible to many gastrointestinal (GI) complications, such as dysphagia, GI bleeding, and fecal incontinence. However, there are few studies focusing on the GI tract after stroke. The current study is to investigate the changes of intestinal structure and function in mice after ischemic stroke. Ischemic stroke was made as a disease model in mice, in which brain and ileal tissues were collected for experiments on the 1st and 7th day after stroke. Intestinal motility of mice was inhibited, and intestinal permeability was increased after stroke. Hematoxylin-eosin (HE) staining showed the accumulation of leucocytes in the intestinal mucosa. Myeloperoxidase (MPO) activity and inflammatory proteins (nuclear factor kappa-B (NF-κB), inducible nitric oxide synthase (iNOS)) in the small intestine were significantly increased in mice after stroke. The expression of tight junction (TJ) proteins (zonula occludens-1 (ZO-1), occludin, and claudin-1) was downregulated, and transmission electron microscopy (TEM) showed broken TJ of the intestinal mucosa after stroke. Glial fibrillary acidic protein (GFAP) and the apoptosis-associated proteins (tumor necrosis factor (TNF-α), caspase-3, and cleaved caspase-3) were notably upregulated as well. Ischemic stroke led to negative changes on intestinal structure and function. Inflammatory mediators and TNF-α-induced death receptor signaling pathways may be involved and disrupt the small intestinal barrier function. These results suggest that stroke patients should pay attention to GI protection. [ABSTRACT FROM AUTHOR]

We and other groups have demonstrated that exposure to nickel nanoparticles (Nano-Ni) results in severe and persistent lung inflammation and fibrosis, but the underlying mechanisms remain unclear. Here, we propose that miR-21 may play an important role in Nano-Ni-induced lung inflammation, injury, and fibrosis. Our dose- and time-response studies demonstrated that exposure of C57BL/6J (WT) mice to Nano-Ni resulted in upregulation of miR-21, proinflammatory cytokines, and profibrotic mediators. Histologically, exposure to Nano-Ni caused severe pulmonary inflammation and fibrosis. Based on the dose- and time-response studies, we chose a dose of 50 µg of Nano-Ni per mouse to compare the effects of Nano-Ni on WT with those on miR-21 KO mouse lungs. At day 3 post-exposure, Nano-Ni caused severe acute lung inflammation and injury that were reflected by increased neutrophil count, CXCL1/KC level, LDH activity, total protein concentration, MMP-2/9 protein levels and activities, and proinflammatory cytokines in the BALF or lung tissues from WT mice, which were confirmed histologically. Although Nano-Ni had similar effects on miR-21 KO mice, the above-mentioned levels were significantly lower than those in WT mice. Histologically, lungs from WT mice exposed to Nano-Ni had infiltration of a large number of polymorphonuclear (PMN) cells and macrophages in the alveolar space and interstitial tissues. However, exposure of miR-21 KO mice to Nano-Ni only caused mild acute lung inflammation and injury. At day 42 post-exposure, Nano-Ni caused extensive pulmonary fibrosis and chronic inflammation in the WT mouse lungs. However, exposure of miR-21 KO mice to Nano-Ni only caused mild lung fibrosis and chronic lung inflammation. Our results also showed that exposure to Nano-Ni caused upregulation of TGF-β1, phospho-Smad2, COL1A1, and COL3A1 in both WT and miR-21 KO mouse lungs. However, levels were significantly lower in miR-21 KO mice than in WT mice, except TGF-β1, which was similar in both kinds of mice. Decreased expression of Smad7 was observed in WT mouse lungs, but not in miR-21 KO mice. Our results demonstrated that knocking out miR-21 ameliorated Nano-Ni-induced pulmonary inflammation, injury, and fibrosis, suggesting the important role of miR-21 in Nano-Ni-induced pulmonary toxicity. [ABSTRACT FROM AUTHOR]

Objective The use of IVIG plus high- or low-dose aspirin for the initial treatment of Kawasaki disease remains controversial. The aim of this study was to evaluate the efficacy of IVIG plus high-dose aspirin compared with IVIG plus low-dose aspirin in the treatment of Kawasaki disease. Methods Studies related to aspirin therapy for Kawasaki disease were selected by searching the databases of Medline (PubMed), Embase and the Cochrane Library before March 2019. Statistical analyses were performed by using a Review Manager Software package and STATA v.15.1. Results Eight retrospective cohort studies, characterizing 12 176 patients, were analysed. Overall, no significant difference was found in the incidence of coronary artery abnormalities between the high- and low-dose aspirin groups [relative risk (RR) 1.15; 95% CI: 0.93, 1.43; P = 0.19; random-effects model]. The patients treated with high-dose aspirin had slightly faster resolution of fever [mean difference (MD) −0.30; 95% CI: −0.58, −0.02; P = 0.04; random-effects model]. but the rates of IVIG resistance (RR, 1.26; 95% CI: 0.55, 2.92; P = 0.59; random-effects model) and days in hospital (MD, 0.22; 95% CI: −0.93, 1.37; P = 0.71; random-effects model) were similar between the two groups. Conclusion Low-dose aspirin plus IVIG might be as effective as high-dose aspirin plus IVIG for the initial treatment of Kawasaki disease. Considering that high-dose aspirin may cause more adverse reactions than low-dose aspirin, low-dose aspirin plus IVIG should be recommended as the first-line therapy in the initial treatment of Kawasaki disease. [ABSTRACT FROM AUTHOR]

Background and Aims: Helicobacter pylori (HP) culture for diagnosing HP infection is time‐consuming and technologically complex. This study evaluated the clinical significance of gastric mucosal gene chip technology in the rapid diagnosis of HP infection and detection of drug resistance in children. Methods: Patients (between the age of 2.5 and 16.0 years old) manifesting gastrointestinal symptoms were enrolled in this study. HP culture of gastric mucosa and drug sensitivity test were performed. A gene chip of gastric mucosa was used to detect the presence of HP infection, some single nucleotide polymorphisms in HP drug resistance genes, or associated gene mutation. DNA sequencing was investigated and compared with the gene chip test results. Results: Out of 267 cases, HP culture was positive in 169 cases and negative in 98 cases. HP detection by the gene chip method was positive in 208 cases and negative in 59 cases. The sensitivity, specificity, and accuracy of the gene chip technology for diagnosing HP infection were 96.1, 85.0, and 93.6%, respectively. HP resistance gene locus using the gene chip showed the main mutation locus of clarithromycin to be 2143A/G, levofloxacin at locus GyrA 91 and GyrA 87, and amoxicillin at PBP1 556ser. Concordance rates between gene chip and DNA sequencing for VacA‐S/M, 16S rRNA, 23S rRNA, and GyrA were greater than 95%, and that of PBP1 was greater than 82%. Conclusion: Gastric mucosal gene chip technology can be used for rapid diagnosis and drug resistance detection of HP infection in children. [ABSTRACT FROM AUTHOR]

Background and Aim: Upper gastrointestinal bleeding is a rare and potentially life‐threatening condition in children. Herein, clinical features and risk factors in children with upper gastrointestinal bleeding were analyzed, and a clinical scoring system was constructed to assess severity. Methods: This retrospective cohort study involved 224 children hospitalized with upper gastrointestinal bleeding between January 2012 and April 2018. Demographic data, clinical information, and laboratory test results on admission were statistically examined. Results: Out of 224 upper gastrointestinal bleeding cases, 76 were diagnosed as severe and 148 as mild cases according to the rate of blood loss and severity. Severe group was significantly different from mild group in 23 items including age, number of patients aged more than 7 years, and so forth (P < 0.01 or P < 0.05). Positive detection rate of bleeding etiology was gradually decreased (P < 0.01) in relation to delay in timing of endoscopy. Analysis of logistic regression evinced five independent risk factors for severe cases to be associated with poor consciousness, hemoglobin < 80 g/L, hemoglobin drop of > 20 g/L, hematochezia, and anemic appearance (P < 0.01 or P < 0.05). Using these five parameters, a number of scoring models were tested. The most predictive resulted in a scoring system constructed with a total of 16 and a cutoff for intervention of 8. Conclusions: Amalgamation of risk factors with the scoring system plays an important role in assessing upper gastrointestinal bleeding severity in children. [ABSTRACT FROM AUTHOR]

Abstract: Background: The decreasing eradication rate of Helicobacter pylori is mainly because of the progressive increase in its resistance to antibiotics. Studies on antimicrobial susceptibility of H. pylori in children are limited. This study aimed to investigate the resistance rates and patterns of H. pylori strains isolated from children. Materials and Methods: Gastric mucosa biopsy samples obtained from children who had undergone upper gastrointestinal endoscopy were cultured for H. pylori, and susceptibility to six antibiotics (clarithromycin, amoxicillin, gentamicin, furazolidone, metronidazole, and levofloxacin) was tested from 2012‐2014. Results: A total of 545 H. pylori strains were isolated from 1390 children recruited. The total resistance rates of H. pylori to clarithromycin, metronidazole, and levofloxacin were 20.6%, 68.8%, and 9.0%, respectively. No resistance to amoxicillin, gentamicin, and furazolidone was detected. 56.1% strains were single resistance, 19.6% were resistant to more than one antibiotic, 16.7% for double resistance, and 2.9% for triple resistance in 413 strains against any antibiotic. And the H. pylori resistance rate increased significantly from 2012‐2014. There was no significant difference in the resistance rates to clarithromycin, metronidazole, and levofloxacin between different gender, age groups, and patients with peptic ulcer diseases or nonulcer diseases. Conclusions: Antibiotic resistance was indicated in H. pylori strains isolated from children in Hangzhou, and it increased significantly during the 3 years. Our data strongly support current guidelines, which recommend antibiotic susceptibility tests prior to eradication therapy. [ABSTRACT FROM AUTHOR]

Background and aim: Systemic inflammatory response syndrome (SIRS) has to do with how the body reacts to injury. Herein, we analyzed the clinical features of acute pancreatitis (AP) in children with SIRS complication and investigated the role of SIRS score combined with C-reactive protein (CRP) level in assessing AP severity in children. Methods: This retrospective cohort study involved 111 children hospitalized with AP at the Children's Hospital of Zhejiang University School of Medicine between January 2012 and August 2017. Presence of SIRS, demographic data, clinical information and laboratory test results on admission were statistically examined. Results: Out of the 111 AP cases, 45 were diagnosed with SIRS. Differences in CRP, interleukin-6 (IL-6), age, temperature, heart rate (HR), white blood cell (WBC), neutrophil count (NC), body mass index (BMI), duration of onset of disease symptoms as well as cases requiring intensive care unit (ICU) treatment were significantly higher in patients with SIRS than those without SIRS (p < .01 or p < .05). Logistic regression analyses evinced two independent risk factors for SIRS to be coexisted diseases (odds ratio (OR) = 4.871, p = .02) and fever (OR = 3.56, p = .007). SIRS was an independent predictor for AP severity (OR = 10.820, p = .005). The optimal cut-off value of CRP was 27.5 mg/L for severe AP classification according to receiver operating characteristic (ROC) (area under curve was 0.733). Conclusion: Amalgamation of SIRS criterion with CRP level potentially plays an important role in assessing AP severity in children. [ABSTRACT FROM AUTHOR]

The effects of heat treatment on the antigenicity and potential allergenicity of α-Lactalbumin (α-LA), β-Lactoglobulin (β-LG), α-casein (α-CN), and β-casein (β-CN) in milk protein concentrates (MPCs) were investigated at temperatures in the range of 65–100°C for times from 10 to 30 min. The antigenicity and potential allergenicity of α-LA decreased significantly. The antigenicity of β-LG was sharply increased throughout the heat treatment, while the potential allergenicity decreased significantly only at 85°C and 100°C for 25 min. The antigenicity of α-CN and β-CN showed fluctuated changes, but were all lower than untreated sample. The α-CN potential allergenicity decreased when heated at 65°C and 70°C for 25 min. Compared with untreated sample, the potential allergenicity of β-CN increased sharply after heat treatment. The results showed that different proteins in the MPCs showed different sensitivities under heat treatment. [ABSTRACT FROM PUBLISHER]

Zinc oxide nanoparticles (Nano-ZnO) are widely used in sunscreens, clothes, medicine and electronic devices. However, the potential risks of human exposure and the potential for adverse health impacts are not well understood. Previous studies have demonstrated that exposure to Nano-ZnO caused liver damage and hepatocyte apoptosis through oxidative stress, but the molecular mechanisms that are involved in Nano-ZnO-induced hepatotoxicity are still unclear. Endoplasmic reticulum (ER) is sensitive to oxidative stress, and also plays a crucial role in oxidative stress-induced damage. Previous studies showed that ER stress was involved in many chemical-induced liver injuries. We hypothesized that exposure to Nano-ZnO caused oxidative stress and ER stress that were involved in Nano-ZnO-induced liver injury. To test our hypothesis, mice were gavaged with 200 mg/kg or 400 mg/kg of Nano-ZnO once a day for a period of 90 days, and blood and liver tissues were obtained for study. Our results showed that exposure to Nano-ZnO caused liver injury that was reflected by focal hepatocellular necrosis, congestive dilation of central veins, and significantly increased alanine transaminase (ALT) and aspartate transaminase (AST) levels. Exposure to Nano-ZnO also caused depletion of glutathione (GSH) in the liver tissues. In addition, our electron microscope results showed that ER swelling and ribosomal degranulation were observed in the liver tissues from mice treated with Nano-ZnO. The mRNA expression levels of ER stress-associated genes (grp78, grp94, pdi-3, xbp-1) were also up-regulated in Nano-ZnO-treated mice. Nano-ZnO caused increased phosphorylation of RNA-dependent protein kinase-like ER kinase (PERK) and eukaryotic initiation factor 2α (eIF2α). Finally, we found that exposure to Nano-ZnO caused increased ER stress-associated apoptotic protein levels, such as caspase-3, caspase-9, caspase-12, phosphorylation of JNK, and CHOP/GADD153, and up-regulation of pro-apoptotic genes (chop and bax). These results suggest that oxidative stress and ER stress-induced apoptosis are involved in Nano-ZnO-induced hepatotoxicity in mice. [ABSTRACT FROM AUTHOR]

Background The resistance of Helicobacter pylori ( H. pylori) to antibiotics is increasing worldwide, lowering its efficacy in current eradication therapies. This study evaluated H. pylori resistance to antibiotics in the southeast coastal region of China and suggests appropriate alternatives. Materials and Methods Seventeen thousand seven hundred and thirty one H. pylori strains were collected from eight areas of two provinces in coastal southeast China from 2010 to 2012. The resistance of these strains to six antibiotics was tested using the agar dilution method. Results The resistance rates to clarithromycin, metronidazole, levofloxacin, amoxicillin, gentamicin and furazolidone were 21.5, 95.4, 20.6, 0.1, 0.1 and 0.1%, respectively. Double, triple and quadruple antibacterial resistant percentages were 25.5, 7.5 and 0.1%, respectively. A positive association between the resistance to levofloxacin and to clarithromycin was found, but there was a negative correlation in the resistances to levofloxacin and to metronidazole. Conclusions The prevalence of H. pylori resistance to clarithromycin, metronidazole, levofloxacin and multiple antibiotics in coastal southeast China is high. Choice of therapy should be individualized based on a susceptibility test in this region of the country. [ABSTRACT FROM AUTHOR]

Segmented filamentous bacteria (SFB) are indigenous gut commensal bacteria. They are commonly detected in the gastrointestinal tracts of both vertebrates and invertebrates. Despite the significant role they have in the modulation of the development of host immune systems, little information exists regarding the presence of SFB in humans. The aim of this study was to investigate the distribution and diversity of SFB in humans and to determine their phylogenetic relationships with their hosts. Gut contents from 251 humans, 92 mice and 72 chickens were collected for bacterial genomic DNA extraction and subjected to SFB 16S rRNA-specific PCR detection. The results showed SFB colonization to be age-dependent in humans, with the majority of individuals colonized within the first 2 years of life, but this colonization disappeared by the age of 3 years. Results of 16S rRNA sequencing showed that multiple operational taxonomic units of SFB could exist in the same individuals. Cross-species comparison among human, mouse and chicken samples demonstrated that each host possessed an exclusive predominant SFB sequence. In summary, our results showed that SFB display host specificity, and SFB colonization, which occurs early in human life, declines in an age-dependent manner. [ABSTRACT FROM AUTHOR]

Most anticancer therapies trigger apoptosis to eliminate malignant cells. However, the majority of malignant cancer cells are resistant to apoptosis due to genetic mutations or heterogeneity. Here, we report that opening the pore of the bacterial large conductance mechanosensitivity channel (MscL) provides a novel approach of inducing non-apoptotic cell death. The gain-of-function mutant V23A-MscL and chemically responsive mutant G26C-MscL can be functionally expressed in hepatocellular carcinoma HepG2 cells. V23A-MscL spontaneously opens, and G26C-MscL also responds to its chemical activator MTSET. Opening of the MscL channel causes increased intracellular Ca2+ concentration and suppressed cell growth and viability. MTSET-activated G26C channels induce necrosis, while V23A-MscL expression leads to cytoplasmic vacuolization cell death in HepG2 cells and suppresses tumor growth in a mouse model. We propose that MscL may act as a nanovalve through which intracellular homeostasis suffers a disruption and results in malignant tumor cell damage, leading to a new strategy for cancer therapy. [ABSTRACT FROM AUTHOR]