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Objective: To analyze the influencing factors of acute gastroenteritis outbreaks caused by norovirus in Beijing from 2014 to 2018. Methods: Data of acute gastroenteritis events caused by norovirus in Beijing from April 2014 to March 2018 were collected. Unconditional logistic regression model was conducted to identify the risk factors of the outbreaks. Results: A total of 765 acute gastroenteritis epidemics caused by norovirus were reported in Beijing, in which 85.88 % (657/765) were cluster events and 14.12 % (108/765) were outbreaks. Among the outbreaks, 70.37 % (76/108) were reported in 2017; 84.26 % (91/108) were reported in winter and spring; 88.89 % (96/108) were reported in kindergartens, primary or secondary schools; 81.48 % (88/108) were through person-to-person transmission; 93.52 % (101/108) were caused by norovirus GⅡ infection. The risk of outbreaks in suburban and out suburb area were 1.84 times (95 %CI : 1.13-3.02) and 3.78 times (95 %CI : 1.62-8.82) as high as that in urban area, respectively. The risks of outbreaks in primary, secondary schools and other institutions were 6.26 times (95 %CI : 3.53-11.10), 14.98 times (95 %CI : 6.23-36.01) and 8.71 times (95 %CI : 3.07-24.71) as high as that in kindergartens, respectively. The risk of outbreak in which patients having lower hospital visiting rate than the median rate of all events was 2.29 times than that in the context of having higher hospital visiting rate (95 %CI :1.42-3.68). The risk of foodborne outbreak was 14.55 times as high as that transmitted through person-to-person (95 %CI : 3.15-67.07). Conclusion: Measures such as strengthening the prevention and control of norovirus outbreaks in suburbs, primary schools, secondary schools and other institutions, promoting patients to visit the hospital actively, improving the management of foodborne events and kitchen workers should be taken to reduce the incidence of acute gastroenteritis outbreaks caused by norovirus.

Objective: To understand the epidemiological and etiological characteristics of outbreaks on acute gastroenteritis caused by sapovirus (SaV) worldwide. Methods: Literature about the outbreaks on acute gastroenteritis caused by SaV were retrieved from the databases including WanFang, CNKI, PubMed and Web of Science after evaluation. Time, geography, setting and population distributions of outbreaks, transmission mode, SaV genotype and clinical characteristics of the patients were analyzed. Results: A total of 34 papers about SaV were included, involving 146 outbreaks occurred between October 1976 and April 2016. In these papers, 138 outbreaks were reported on the related months. All these outbreaks occurred in northern hemisphere. SaV outbreaks occurred all year around, but mainly in cold season, the incidence was highest in December (25 outbreaks) and lowest in in August (2 outbreaks). Most outbreaks were reported by Japan, followed by Canada, the United States of America and the Netherlands. There were 141 outbreaks for which the occurring settings were reported, child-care settings were most commonly reported setting (48/141, 34.04 % ), followed by long-term care facility (41/141, 29.08 % ) and hospital (16/141, 11.35 % ). Clinical symptoms of 1 704 cases in 31 outbreaks were reported, with the most common symptom was diarrhea (1 331/1 704, 78.12 % ), followed by nausea (829/1 198, 69.20 % ), abdominal pain (840/1 328, 63.25 % ), vomiting (824/1 704, 48.36 % ) and fever (529/1 531, 34.53 % ). Genotypes of SaV were determined for 119 outbreaks. GⅠ(51/119, 42.86 % ) and GⅣ (45/119, 37.82 % ) were predominant. The outbreaks of GⅣ SaV increased suddenly in 2007, and the outbreaks of GⅠ SaV mainly occurred in 2008 and during 2011-2013. Conclusions: SaV outbreaks were reported mainly by developed countries, with most outbreaks occurred in cold season, in child-care settings and long term care facility. GⅠ and GⅣ were the most common genotypes of SaV. Prevention and control of SaV outbreak in China seemed relatively weak, and it is necessary to conduct related training and to strengthen the SaV outbreak surveillance in areas where service is in need.

Objective: To understand the seasonal distribution of the clustering of fever and diarrhea. Methods: Concentration degree and circular distribution methods were used to analyze the seasonal distribution of the clustering of fever and diarrhea in Beijing from 2009 to 2015. The information were collected from the Infectious Disease Surveillance Information System of Beijing. Results: The M values of the clustering of fever and diarrhea were 0.57 and 0.47. Circular distribution results showed that the clustering of fever and diarrhea angle dispersion index R values were 0.57 and 0.46 respectively, the sample average angle of Rayleigh' s test Z values were 414.14, 148.09 respectively (all P <0.01). The clustering of fever and diarrhea had seasonality. The incidence peak of fever was on October 13, and the epidemic period was during August 13-December 14. The incidence peak of diarrhea was on July 31, and the epidemic period was during May 20-October 11. Conclusion: The clustering of fever had obvious seasonality in Beijing, which mainly occurred in autumn and winter. The cluster of diarrhea had certain seasonality, which mainly occurred in summer and autumn.

Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening syndrome involving a final common pathway of hypercytokinemia, in which tumor necrosis factor (TNF)-α, interferon (IFN)-γ, and soluble interleukin 2-receptor-alpha (sIL-2Rα) are the key cytokines. Pre-B-cell colony-enhancing factor (PBEF) is an inflammatory cytokine involved in several inflammatory diseases. However, its role in HLH is unknown. In this study, we examined the role of PBEF in HLH. Plasma was collected from 22 children with HLH and 14 healthy children. The concentrations of plasma PBEF, TNF-α, IFN-γ, and sIL-2Rα were determined using an enzyme-linked immunosorbent assay. All clinical data were derived from medical records. In the acute phase, children with HLH had much higher PBEF, TNF-α, IFN-γ, and sIL- 2Rα levels than did healthy children (P < 0.05). After treatment, 13 HLH children improved and PBEF, TNF-α, and IFN-γ levels decreased to normal levels (P < 0.05); sIL-2Rα levels also decreased (P < 0.05), but remained above the normal level (P < 0.05). Two patients were lost to follow-up, while 7 patients showed a bad response to therapy and eventually died, showing high PBEF levels above those of the survivors (P < 0.01). PBEF level was significantly positively correlated with TNF-α, IFN-γ, sIL-2Rα, serum ferritin, and triglycerides (all P < 0.05), and was negatively correlated with fibrin (P < 0.05). PBEF appears to be involved in the inflammatory process of HLH, and elevated PBEF is related to disease activity. We are currently evaluating the role of PBEF as a marker for the diagnosis and management of patients.

1. A novel 31-bp indel polymorphism in intron 3 of the chicken paired box 7 (PAX7) gene was identified and genotyped in an F2 resource population of Gushi chicken crossed with Anka broiler to analyse its associations with chicken growth, carcass and meat quality traits. 2. Results showed that the 31-bp indel was significantly associated with body weight at 4, 6, 8, 10, 12 weeks of age and body size indices including shank length, shank girth, body slanting length at 8 and 12 weeks of age. Significant associations were found for carcass weight, semi-evisceration weight, evisceration weight, breast muscle fibre diameter, leg muscle fibre diameter, breast muscle fibre density, while no significant association with leg muscle fibre density was observed. 3. It was concluded that the 31-bp indel in intron 3 of the PAX7 gene was associated with chicken growth, carcass and meat quality traits where the 31-bp deletion had a negative effect on chicken growth and carcass traits and positive effect on meat quality traits.

This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at (http://www.elsevier.com/locate/withdrawalpolicy., (Copyright © 2010. Published by Elsevier Ltd.. All rights reserved.)

Various integration events from simple to complex have been found in transgenic elite rice varieties, which were co-transformed with bar and cecropin B gene by particle bombardment after system studies of the structure and expression of the transgene. It was displayed that there were one to seven insertion loci and one to ten copies of transgene in different transformants. No absolute correlation was found between the numbers of transgene copies and the gene expression. Different level expression of transgenes with similar insertion mode was also discovered. The expression cassette integrity and transcription frequency of selectable bar gene were more than non-selectable cecropin B gene, whereas gene silence in plants integrated with intact bar gene was found and higher expression level of cecropin B gene with 0.6 kb fragments degraded in terminator was deduced.

The insulin receptor signaling pathway is present in beta-cells and is believed to be important in beta-cell function. We show here that insulin directly regulates beta-cell function in isolated rodent islets. Long-term insulin treatment caused a sustained increase in [Ca(2+)](i) and enhanced glucose-stimulated insulin secretion in rat islets, but failed to increase insulin content. Chronic activation of insulin receptor signaling by IRS-1 overexpression in the beta-cell inhibited gene expression of SERCA3, an endoplasmic reticulum Ca(2+)-ATPase. Insulin gene transcription was stimulated by insulin receptor signaling and insulin mimetic compound (L-783 281) in a glucose- and Grb2-dependent manner. Thus, beta-cell SERCA3 is a target for insulin regulation, which implies that beta-cell Ca(2+) homeostasis is regulated in an autocrine feedback loop by insulin. This study identifies a novel regulatory pathway of insulin secretion at the molecular level with two main components: (1) regulation of intracellular Ca(2+) homeostasis via SERCA3 and (2) regulation of insulin gene expression.

We have studied Ca2+ homeostasis in a unique model of human neurons, the NT2N cell, which differentiates from a human teratocarcinoma cell line, NTera2/C1.D1 by retinoic acid treatment. When perifused with Krebs-HEPES buffer containing 2.5 mM CaCl2, fura-2 loaded NT2N cells produced spontaneous cytosolic Ca2+ oscillations, or Ca2+ transients. These cytosolic Ca2+ transients were not blocked by antagonists of glutamate (6-cyano-7-nitroquinoxaline-2,3-dione and D(-)-2-amino-5-phosphonopentanoic acid) or muscarinic (atropine) receptors. Omission of extracellular Ca2+ completely abolished Ca2+ oscillations and decreased the average Ca2+ level from 106 +/- 14 nM to 59 +/- 8 nM. Addition of the L-type Ca2+ channel blocker nifedipine (1 or 10 microM) or of the N-type inhibitor omega-conotoxin GVIA (5 microM) significantly, although incompletely, suppressed Ca2+ oscillations, while omega-conotoxin MVIIC (5 microM), a selective antagonist of P- and Q-channels, had no effect. Ni2+, at 100 microM, a concentration selective for T-type channels, did not inhibit Ca2+ transients. Non-specific blockage of Ca2+ channels by higher concentrations of Ni2+ (2-5 mM) or Co2+ (1 mM) abolished Ca2+ oscillations completely. The endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin (1 microM), slightly decreased Ca2+ oscillation frequency, and induced a small transitory increase in the average cytosolic Ca2+ concentration. The mRNAs of L- (alpha1D subunit) and N-type (alpha1B subunit) Ca2+ channel were present in NT2N cells, while that of a T-type Ca2+ channel (alpha1-subunit) was not present in the NT2N cells as shown by reverse transcription-polymerase chain reaction. In conclusion, NT2N neuronal cells generate cytosolic Ca2+ oscillations mainly by influx of extracellular Ca2+ through multiple channels, which include L- and N-type channels, and do not require activation of glutamate or muscarinic receptors.

Ca2+ channel expression and regulation of intracellular Ca2+ homeostasis were studied during retinoic acid (RA)-induced differentiation of the human teratocarcinoma cell line Ntera 2/C1.D1 (NT2- cells) into NT2N neurons, a unique model of human neurons in culture. The cytosolic Ca2+ level of undifferentiated NT2- cells was low (75 +/- 5 nM) and stable under basal conditions, and it was only marginally decreased (by 9%) upon removal of extracellular Ca2+. After 10 microM RA treatment, NT2- cells were irreversibly differentiated into a phenotype of neuron-like NT2N cells. Cytosolic Ca2+ level of NT2N neurons was higher (106 +/- 14 nM) than that of NT2- cells and spontaneously fluctuated (0.208 +/- 0.038 transients/min) under basal conditions. Although K+ increased 86Rb fluxes in both NT2- cells and NT2N neurons, it only increased cytosolic Ca2+ level in NT2N neurons. The K+-induced increase in cytosolic Ca2+ in NT2N neurons was antagonized by 0.1-10 microM nifedipine or verapamil, 5 microM omega-CgTx GVIA, but not by 1 microM omega-agatoxin IVA, 1 microM omega-agatoxin TK, 1 microM FTX-3.3, or 100 microM Ni+ implicating L- and N-type voltage-dependent Ca2+ channels. In L- and N-type channels, but not in P- and Q-types, mRNAs were expressed in NT2N neurons as well as NT2- cells. Quantitative analysis of L- and N-type Ca2+ protein levels showed major differences between NT2- cells and NT2N neurons. In NT2- cells, N-type Ca2+ channels were undetectable while L-type channels levels were fivefold lower compared to NT2N neurons. Our findings show that L- and N-type channels are expressed during differentiation of NT2- cells into neurons, and that these voltage-dependent Ca2+ channels have a major role in regulating intracellular Ca2+ homeostasis and neuronal excitability., (Copyright 1998 Academic Press.)

The effects of synthetic beta-amyloid (A beta1-42) on cell viability and cellular Ca2+ homeostasis have been studied in the human neuron-like NT2N cell, which differentiates from a teratocarcinoma cell line, NTera2/C1.D1, by retinoic acid treatment. NT2N viability was measured using morphological criteria and fluorescent live/dead staining and quantified using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide metabolism. A beta1-42 dose-dependently caused NT2N cell death when it was present in the cell culture for 14 days but had no effect on viability when it was present for 4 days. The lowest effective concentration was 4 microM, and the strongest effect was produced by 40 microM. Control NT2N cells produced spontaneous cytosolic Ca2+ oscillations under basal conditions. These oscillations were inhibited dose-dependently (0.4-40 microM) by A beta1-42 that was present in the cell culture for 1 or 4 days. Ca2+ wave frequency was decreased from 0.21 +/- 0.02 to 0.05 +/- 0.02/min, amplitude from 88 +/- 8 to 13 +/- 4 nM, and average Ca2+ level from 130 +/- 8 to 58 +/- 3 nM. The Ca2+ responses to 30 mM K+ and 100 microM glutamate were not different between control and A beta-treated cells. Thus, the results do not support the hypothesis that cytosolic early Ca2+ accumulation mediates A beta-induced NT2N cell death.

There has been a large amount of recent literature suggesting that omega-3 unsaturated fatty acids found in fish oils should be incorporated into the diet for the purpose of decreasing serum cholesterol levels. Inclusion of these fatty acids in the diet has been shown to decrease total serum cholesterol as well as low-density lipoprotein cholesterol. Some of these trials have been complicated by the fact that many of the subjects are afflicted with non-insulin-dependent diabetes mellitus. Unfortunately, the effects of omega-3 unsaturated fatty acids on insulin secretion have not been well characterized. In this study, we have examined the effect of a common omega-3 unsaturated fatty acid, eicosapentaenoic acid (C20:5), on insulin secretion. Using the beta-TC3 insulinoma cell line as a model system for studying insulin exocytosis, C20:5 selectively potentiated glucose-induced insulin secretion. At the same concentration at which it significantly increased glucose-induced insulin secretion, C20:5 did not affect glucose metabolism or intracellular free calcium concentrations. C20:5 also augmented potassium-induced insulin secretion. These data suggest that C20:5, an abundant omega-3 unsaturated fatty acid, acts to augment insulin secretion in a glucose-dependent manner.

A group of 662 women in our gynecologic OPD were screened for Chlamydia trachomatis with direct immunofluorecence monoclonal antibody (DFA) staining technique. Their age distribution ranged from 16 to 60 years old. The overall positivity rate was 26.3%. Of the 269 pregnant women, 64 cases were found to have Chlamydia trachomatis infection, an infection rate of 23.74%. There was no statistically significant difference of infection rates among age groups. In the positive group, however, the rate of infertility was 25.43%, much higher than that in the negative group (12.88%, P < 0.01). And there was no statistical significance of infection rates between patients taking contraception and those did not. A positive correlation existed between the degree of cervicitis and the Chlamydia trachomatis infection.

Glucose controls insulin release by beta-cells at two sites at least. By controlling the membrane potential, it controls the influx of Ca2+ and the rise in cytoplasmic Ca2+ which triggers exocytosis. At this level, the principal targets of glucose are the K(+)-ATP channels whose activity may be modulated by changes in the ATP/ADP ratio. A second, newly identified, mechanism of regulation is independent of changes in beta-cell membrane potential and of changes in Cai2+. It is not sufficient to induce insulin release, but serves to increase the response. This appears to be achieved through an amplification of the effectiveness of Cai2+ on the secretory process and may also depend on the changes in energy state of beta-cells.

The effects of arginine-vasopressin (AVP) on hormone release by the endocrine pancreas have been studied with incubated islets from normal mice. A wide range of AVP concentrations (1 pM-100 nM) were tested in the presence of various glucose concentrations. AVP did not affect somatostatin release in a glucose-free medium but increased it in the presence of all tested glucose concentrations (3-30 mM). The lowest effective concentration was 1 mM and the effect was not yet maximal at 100 nM AVP. AVP markedly increased glucagon release in the absence of glucose. Its effect was attenuated but not abolished when glucagon release was inhibited by glucose. Surprisingly, the attenuation of the effect of AVP was stronger in 3-10 mM than in 15-30 mM glucose. The lowest effective concentration was 1 nM and the effect was not yet maximal at 100 nM AVP. AVP was ineffective on basal insulin release (0, 3 and 7 mM glucose), but potentiated the effect of 10, 15 and 30 mM glucose. The lowest effective concentration was 0.1-1 nM AVP and the maximal effect was produced by 10-100 nM AVP. The results suggest a direct action of AVP on each of the three islet cell types which display a roughly similar sensitivity to the peptide. This sensitivity is too low to make islet cells a possible target for circulating AVP under physiological conditions. On the other hand, the presence of AVP in the pancreas suggests that it might be involved in the peptidergic control of islet function.

The effects of vanadate (Na3VO4) on pancreatic B-cell function were studied in normal mouse islets. Vanadate did not affect basal insulin release but potentiated the effect of 7-30 mM glucose at concentrations of 0.1-1 mM. This effect was progressive and slowly reversible. It was abolished by omission of extracellular Ca2+ but unaffected by blockers of adrenergic or muscarinic receptors. Comparison of the changes in membrane potential, 86Rb efflux and 45Ca efflux that vanadate and ouabain produced in B-cells made it possible to exclude the hypothesis that vanadate increases insulin release by blocking the sodium pump. Vanadate was also without effect on cAMP levels. On the other hand, it markedly changed the characteristics of the Ca(2+)-dependent electrical activity and of the oscillations of cytoplasmic Ca2+ recorded in B-cells stimulated by 15 mM glucose. In the steady state, Ca2+ influx was increased by vanadate, and this resulted in a rise in cytoplasmic Ca2+. The exact mechanisms underlying these changes could not be established but a blockade of K channels was excluded. In the presence of LiCl, vanadate markedly increased inositol phosphate levels in islet cells. This effect was attenuated but not suppressed by omission of Ca2+. A small increase in inositol bisphosphate was still produced by vanadate in the absence of LiCl. These results suggest that vanadate both stimulates phosphoinositide breakdown and inhibits inositol phosphate degradation. In conclusion, vanadate does not induce insulin release, but markedly potentiates the stimulation by glucose. This property is not due to an inhibition of the sodium pump or to a rise in cAMP concentration. It results from a complex interplay between changes in B-cell membrane potential, phosphoinositide metabolism and Ca2+ handling.

The mechanisms by which arginine-vasopressin (AVP) affects pancreatic B-cell function were studied in normal mouse islets. AVP produced a dose-dependent (0.1-1000 nM; EC50 approximately 1-2 nM) amplification of glucose-induced insulin release. This amplification was of slow onset and reversibility. AVP was ineffective when the concentration of glucose was less than 7 mM, but was still very effective in 30 mM glucose. The increase in insulin release produced by AVP was accompanied by small accelerations of 86Rb and 45Ca efflux from islet cells. Omission of extracellular Ca2+ accentuated the effect of AVP on 86Rb efflux, attenuated that on 45Ca efflux, and abolished that on release. Under no condition did AVP inhibit 86Rb efflux. AVP did not significantly affect cAMP levels, but increased inositol phosphate levels in islet cells, even in the absence of extracellular Ca2+. AVP did not affect the membrane potential in unstimulated B-cells and augmented glucose-induced electrical activity only slightly. This was not due to a direct action on ATP-sensitive K+ channels as revealed by patch-clamp recordings (whole cell and outside-out patches). In conclusion, AVP is not an initiator of insulin release, but it potently amplifies glucose-induced insulin release in normal mouse B-cells. This effect involves a stimulation of phosphoinositide metabolism, and presumably an activation of protein kinase C, rather than a change in cAMP levels or a direct control of the membrane potential.

A comparison of the effects of magnesium valproate (MV) and sodium valproate (SV) on the action potential of isolated papillary muscle from guinea pigs and dogs was made in this study. The results in both animals were as follows: MV and SV induced a slight reduction of slope plateau of action potential and prolongation of action potential duration (APD). What is more, APD50 and APD90 were prolonged significantly, thus the ratio of APD90/APD25 was increased. The effective refractory period (ERP) was prolonged significantly. MV or SV showed no effects on action potential amplitude, overshoot, resting potential and phase 0 upstroke velocity. The above results suggested that MV and SV might play an antiarrhythmic role and that their effects were analogic. The mechanism of MV and SV inducing significant prolongation of APD50, APD90, and ERP, might be closely related to the slow-down of the velocity of K+ efflux during plateau and repolarization of phase 3 by radical of valproate and the slow-down of velocity of K+ efflux of repolarization of phase 3 in particular. These results showed that there was no difference in SV and MV action on guinea pigs and dogs.

From 1957 to 1980, 151 patients with thyroid cancer were treated by surgery in our hospital. Papillary adenocarcinoma was predominant (53%), followed by undifferentiated (23%) and follicular types (20%). The diagnosis, established only according to the clinical symptoms and 131I scan, gave a high misdiagnosis rate (44%). The misdiagnosis could also be made on the operation. The causes are: 1) limitation of 131I scan in diagnostic specificity; 2) lack of vigilance for thyroid cancer; 3) neglecting the subtle histological changes during the operation; 4) failure in submitting the frozen section. Fine needle aspiration cytology is emphasized in order to improve the preoperative diagnostic accuracy. Lobectomy and modified neck dissection are the most common modalities of operation for papillary and follicular cancers. The 5 year survival rates were 74% and 50% respectively. Modified neck dissection increased the 5 year survival up to 85%. Undifferentiated cancer could be treated, at best, by palliative treatment. The authors believe that a rational radical operation should be performed according to the pathological type, biological behavior and stage of the lesion, followed by adjuvant endocrine and/or isotope therapy, which could improve the treatment result.