The cGAS-STING-interferon regulatory factor 7 pathway regulates neuroinflammation in Parkinson's disease

Interferon regulatory factor 7 plays a crucial role in the innate immune response.However,whether interferon regulatory factor 7-mediated signaling contributes to Parkinson's disease remains unknown.Here we report that interferon regulatory factor 7 is markedly up-regulated in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced mouse model of Parkinson's disease and co-localizes with microglial cells.Both the selective cyclic guanosine monophosphate adenosine monophosphate synthase inhibitor RU.521 and the stimulator of interferon genes inhibitor H151 effectively suppressed interferon regulatory factor 7 activation in BV2 microglia exposed to 1-methyl-4-phenylpyridinium and inhibited transformation of mouse BV2 microglia into the neurotoxic M1 phenotype.In addition,si RNA-mediated knockdown of interferon regulatory factor 7 expression in BV2 microglia reduced the expression of inducible nitric oxide synthase,tumor necrosis factorα,CD16,CD32,and CD86 and increased the expression of the anti-inflammatory markers ARG1 and YM1.Taken together,our findings indicate that the cyclic guanosine monophosphate adenosine monophosphate synthase-stimulator of interferon genes-interferon regulatory factor 7 pathway plays a crucial role in the pathogenesis of Parkinson's disease.

Effect of Sishen pill on expression of type Ⅰ and type Ⅲ interferon in acute ulcerative colitis mice model

Objective:To investigate the effects of Sishen pill on the expression of type I interferon(IFN)and type III interferon and their receptors in colonic tissues of mice with acute ulcerative colitis(UC).Methods:Male C57BL/6Cnc mice were randomly divided into control group,model group,sishenwan group and salazosulfapyridine group.The model was made with 0.2 mL 4%dextran sodium sulfate(DSS)for 5 days,and the control group was given 0.2mL normal saline by gavage.On the second day of modeling,sishen pill group was given 0.2mL 1.5 g·kg^(-1) sishen pill,and SASP group was given 0.2mL 0.25 g·kg^(-1) sulfasalazine,twice a day,for 7 days.During the administration period,the disease activity index(DAI)of mice was calculated every day.After administration,the histopathological changes of colon tissues of mice in each group were observed by hematoxylin eosin(HE)staining,and the histological scores were calculated.The expression of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 mRNAs in colon tissues of mice in each group were detected by qRT-PCR.The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 in colon tissues of mice in each group were detected by ELISA.Western blot was used to detect the expression of interferon receptors IFNAR1,IFNAR2 and IFNLR1 in colon tissues of mice in each group.Results:Compared with the control group,the DAI of mice increased significantly(P<0.001)in the model group.The inflammatory cells in colonic tissues infiltrated heavily,lymph nodes enlarged,colonic mucosal structure destroyed,crypt structure lost,inflammation involved a wide range,and the histological score increased significantly(P<0.001).The levels of IFN-α,IFN-βand IFNλ2 mRNA were significantly decreased(P<0.05,P<0.05,P<0.01).The expression levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly decreased(P<0.01,P<0.01,P<0.001,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly decreased(P<0.01,P<0.05,P<0.01).Compared with the model group,the DAI decreased significantly(P<0.001)in Sishen pill group,the infiltration of inflammatory cells in colon tissue were significantly reduced,the structural regeneration of colon mucosa was significantly recovered,the crypt structure was significantly recovered,the lymph nodes were significantly reduced,the range of inflammation involvement was reduced,and the histological score was significantly reduced(P<0.001).The levels of IFN-α,IFN-βand IFN-λ2 mRNA were significantly increased(P<0.01,P<0.001,P<0.001).The levels of IFN-α,IFN-β,IFN-λ2 and IFN-λ3 were significantly increased(P<0.01,P<0.001,P<0.01,P<0.001).The levels of IFNAR1,IFNAR2 and IFNLR1 were significantly increased(P<0.05,P<0.001,P<0.05).Conclusion:Sishen pill may alleviate the symptoms and signs of mice with acute ulcerative colitis by regulating the expression of type I and type III interferon and their receptors in colon tissues.

氧化苦参碱对皮肤创面愈合中PCNA、α-SMA及Type Ⅰ collagen的影响

目的探讨氧化苦参碱对小鼠皮肤创面愈合中血清增殖细胞核抗原(PCNA)、α-平滑肌肌动蛋白(α-SMA)及细胞Ⅰ型胶原蛋白(Type Ⅰ collagen)的影响。方法昆明小鼠背部手术制备1.5 cm×1.5 cm全层皮肤缺损创面模型。自第1 d始,除对照组给予等量生理盐水外,余各组分别按20、40、80 mg/kg给予氧化苦参碱。Van Gieson纤维胶原染色法观察小鼠背部皮肤创面组织胶原纤维的表达;免疫组学法评价创面组织中PCNA、α-SMA及Type Ⅰ collagen的表达。结果Van Gieson纤维胶原染色显示,氧化苦参碱可促进新生肉芽组织、毛细血管及新生纤维胶原生长。免疫组学研究显示,在第7 d时,氧化苦参碱20、40、80 mg/kg使小鼠皮肤创面组织中PCNA表达明显升高(P<0.05);在第9 d、11 d时,氧化苦参碱20 mg/kg使小鼠皮肤创面组织中α-SMA显著增加;氧化苦参碱20 mg/kg在第3 d、11 d,氧化苦参碱40 mg/kg在第3 d,氧化苦参碱80 mg/kg在第3 d、7 d引起Type Ⅰ collagen的表达显著升高(P<0.05)。结论氧化苦参碱能增加皮肤创面愈合中PCNA、α-SMA及Type Ⅰ collagen的表达。

辽东兰花岭地区古元古代Ⅰ型花岗岩类与辽吉A型花岗岩对比研究

辽东半岛是华北克拉通胶-辽-吉古元古代活动带的重要组成部分,古元古代经历了复杂的构造演化过程,并记录了多期岩浆-变质作用,约2.2 Ga的辽吉A型花岗岩和1.89~1.85 Ga的巨斑状花岗岩、正长岩分别标志着辽东古元古代造山作用的开端和结束。最新研究显示,2.20~2.15 Ga的岩浆作用形成了2种不同类型的花岗岩,它们可能具有不同的岩石成因和构造意义。在青城子铅锌矿集区北部采集的兰花岭、白砬子花岗闪长岩和黄泊辉绿岩,锆石U-Pb年龄分别为2177±19 Ma、2129±36 Ma、1876±29 Ma。花岗闪长岩的岩石成因类型、地球化学特征与典型的约2.2 Ga的辽吉A型花岗岩明显不同,属于弱过铝质、低钾钙碱性—碱性岩石,Zr、Hf、Nb、Rb含量较低,K_(2)O/Na_(2)O值、稀土元素总量极低,为典型的Ⅰ型花岗岩类。根据锆石Lu-Hf同位素分析,ε_(Hf)(t)值为-5.1~9.0,二阶段Hf模式年龄t_(DM2)为2089~2817 Ma,岩浆源区为约2.5 Ga的太古宙地壳物质和少量软流圈地幔物质。兰花岭地区花岗闪长岩具备岛弧或活动大陆边缘的地球化学亲缘属性,可能形成于弧岩浆俯冲挤压环境;结合形成于伸展环境的A型条痕状花岗岩特征,认为约2.2 Ga辽东地区古元古代活动带呈现总体伸展、局部挤压的构造环境,为洋壳板块向龙岗地块俯冲碰撞过程中或碰撞后的弧后盆地。

IRF family proteins and type I interferon induction in dendritic cells

Dendritic cells （DC）, although a minor population in hematopoietic cells, produce type I interferons （IFN） and other cytokines and are essential for innate immunity. They are also potent antigen presenters and regulate adaptive immunity. Among DC subtypes plasmacytoid DC （pDC） produce the highest amounts of type I IFN. In addition, pro- and anti-inflammatory cytokines such as IL-12 and IL-10 are induced in DC in response to Toll like receptor （TLR） signaling and upon viral infection. Proteins in the IRF family control many aspects of DC activity. IRF-8 and IRF-4 are essential for DC development. They differentially control the development of four DC subsets. IRF-8^-/- mice are largely devoid of pDC and CD8α^＋ DC, while IRF-4^-/- mice lack CD4^＋ DC. IRF-8^-/-, IRF4^-/-, double knock-out mice have only few CD8α CD4^-DC that lack MHC Ⅱ. IRF proteins also control type Ⅰ IFN induction in DC. IRF-7, activated upon TLR signaling is required for IFN induction not only in pDC, but also in conventional DC （cDC） and non-DC cell types. IRF-3, although contributes to IFN induction in fibroblasts, is dispensable in IFN induction in DC. Our recent evidence reveals that type Ⅰ IFN induction in DC is critically dependent on IRF-8, which acts in the feedback phase of IFN gene induction in DC. Type Ⅰ IFN induction in pDC is mediated by MyD88 dependent signaling pathway, and differs from pathways employed in other cells, which mostly rely on TLR3 and RIG-Ⅰ family proteins. Other pro-inflammatory cytokines are produced in an IRF-5 dependent manner. However, IRF-5 is not required for IFN induction, suggesting the presence of separate mechanisms for induction of type Ⅰ IFN and other pro-inflammatory cytokines. IFN and other cytokines produced by activated DC in turn advance DC maturation and change the phenotype and function of DC. These processes are also likely to be governed by IRF family proteins.

Interferon therapy in hepatitis Cleading to chronic type 1 diabetes

AIM: To review the prevalence,clinical data and course of interferon-associated type 1 diabetes in chronic hepatitis C virus(HCV) infection.METHODS: Search of all interferon(INF)-related type 1diabetes mellitus(T1DM) cases published in the English literature from 1992 to December 2013 according to the key words: chronic hepatitis C infection,diabetes mellitus type 1,insulin dependent diabetes mellitus,and interferon treatment.We found 107 cases and analyzed their clinical and laboratory data and long-term followup.Due to the predominance of cases described in Japanese literature,we analyzed separately cases of Caucasian and Japanese origin.In addition we describe a representative case with HCV who developed INFrelated T1 DM.RESULTS: Our data show that INF treatment increases the risk of developing T1 DM by 10-18 fold compared with the corresponding general population and the median age of onset was 43 years(range: 24-66 years) in Caucasians and 52 years(range: 45-63 years) in Japanese.Most patients developed T1 DM during INF treatment,after a median time-period of 4.2 and 5.7 mo in Caucasian and Japanese groups,respectively.The clinical course was characterized by a fulminant course with abrupt severe hyperglycemia or ketoacidosis,a high titer of anti-islet autoantibodies and almost all patients(105/107) permanently required insulin therapy with a follow-up of up to 4 years.A substantial number of patients had evidence for other autoimmune disorders mainly thyroid diseases(25% and 31% in Caucasian and Japanese groups,respectively).CONCLUSION: INF-associated T1 DM in HCV has a fulminant course,often associated with other autoimmune diseases,and results almost inevitably in permanent insulin therapy requirement.

PLP2, a potent deubiquitinase from murine hepatitis virus, strongly inhibits cellular type I interferon production

Infections by coronaviruses such as severe acute respiratory syndrome （SARS） coronavirus （SCoV） and mouse hepatitis virus A59 （MHV-A59） result in very little type I interferon （IFN） production by host cells, which is potentially responsible for the rapid viral growth and severe immunopathology associated with SARS. However, the molecular mechanisms for the low IFN production in cells infected with coronaviruses remain unclear. Here, we provide evidence that Papain-like protease domain 2 （PLP2）, a catalytic domain of the nonstructural protein 3 （nsp3） of MHV-A59, can bind to IRF3, cause its deubiquitination and prevent its nuclear translocation. As a consequence, co-expression of PLP2 strongly inhibits CARDIF-, TBK1- and IRF3-mediated IFNp reporter activities. In addition, we show that wild-type PLP2 but not the mutant PLP2 lacking the deubiquitinase （DUB） activity can reduce IFN induction and promote viral growth in cells infected with VSV. Thus, our study uncovered a viral DUB which coronaviruses may use to escape from the host innate antiviral responses.

The host type I interferon response to viral and bacterial infections

Type I interferons (IFN) are well studied cytokines with anti-viral and immune-modulating functions. Type I IFNsare produced following viral infections, but until recently, the mechanisms of viral recognition leading to IFN productionwere largely unknown. Toll like receptors (TLRs) have emerged as key transducers of type I IFN during viral infectionsby recognizing various viral components. Furthermore, much progress has been made in defining the signaling path-ways downstream of TLRs for type I IFN production. TLR7 and TLR9 have become apparent as universally importantin inducing type I IFN during infection with most viruses, particularly by plasmacytoid dendritic cells. New intracellularviral pattern recognition receptors leading to type I IFN production have been identified. Many bacteria can also inducethe up-regulation of these cytokines. Interestingly, recent studies have found a detrimental effect on host cells if type IIFN is produced during infection with the intracellular gram-positive bacterial pathogen, Listeria monocytogenes. Thisreview will discuss the recent advances made in defining the signaling pathways leading to type I IFN production.

A functional type I interferon pathway drives resistance to cornea herpes simplex virus type 1 infection by recruitment of leukocytes

Type I interferons are critical antiviral cytokines produced following herpes simplex virus type-1 （HSV-1） infection that act to inhibit viral spread. In the present study, we identify HSV-infected and adjacent uninfected corneal epithelial cells as the source of interferon-a. We also report mice deficient in the A1 chain of the type I IFN receptor （CDl18-/） are extremely sensitive to ocular infection with low doses （100 PFU） of HSV-1 as seen by significantly elevated viral titers in the cornea Compared to wild type （WT） controls. The enhanced susceptibil- ity correlated with a loss of CD4＋ and CD8＋ T cell recruitment and aberrant chemokine production in the cornea despite mounting an adaptive immune response in the draining mandibular lymph node of CDll8/ mice. Taken together, these results highlight the importance of IFN production in both the innate immune response as well as eliciting chemokine production required to facilitate adaptive immune cell trafficking.

Effects of Icariin on Expression of OPN mRNA and Type ⅠCollagen in Rat Osteoblasts in Vitro

To study the effects of Icariin on expression of osteopontin （OPN） mRNA and type Ⅰ collagen in rat osteoblasts in vitro and to explore its possible mechanisms in preventing osteoporosis. OB was isolated from calvaria of new-born new-born fetal Sprague-Dawley （SD） rats by means of modified sequential collagenase digestion and incubated in MEM medium and the cell morphology was observed under inverted phase contrast microscope, OB was identified by alkaline phosphatase （ALP） staining. Different concentration （0.1μg/mL, 1.0 μg/mL, 10 μ/mL） of Icariin was added to the OB and incubated. The effect of Icariin on the proliferation and osteogenesis of OB was monitored by MTT analysis. The expression of type l collagen was estimated with immunohistochemistry techniques. The expression levels of mRNA of OPN in the cells in every group were examined by reverse-transcriptase ploymerase chain reaction （RT-PCR）. The expression of OPN mRNA and type Ⅰ collagen was strengthened gradually with the increase of Icariin concentration and peaked with 10 μg/mL Icariin on the 5th day. Icariin could significantly promote the expression of OPN mRNA and type Ⅰ collagen in rat osteoblasts in vitro. The levels of expression of OPN mRNA and type Ⅰ collagen were changed with different concentration of Icariin. Icariin could effectively prevent and treat osteoporosis and promote the bone formation.

Features and imbibition mechanisms of Winsor Ⅰ type surfactant solution in oil-wet porous media

The relationship between NaCl concentration and the phase change behavior of microemulsion of anionic surfactant was characterized by the salinity scan experiments.The wettability of WinsorⅠtype surfactant solution(WⅠsolution)and the effect of NaCL concentration on phase change behavior of WⅠsolution and imbibition in oil-wet porous media were investigated by microfluidic experiments in this study.The WⅠsolution and WinsorⅠtype microemulsion are similar in wetting phase with stronger wettability than other phases.Two main mechanisms of WⅠsolution enhancing imbibitions recovery in oil wet porous media are the wetting phase drive and residual oil solubilization.Under the salinity condition of WinsorⅠtype microemulsion,the NaCl concentration has strong impact on the imbibition mechanism of WⅠsolution,the higher the NaCl concentration,the complex the imbibition process and the higher the imbibition efficiency will be.The NaCl concentration has strong impact on the solubilization ability to oil of the WⅠsolution,the higher the NaCl concentration,the stronger the solubility of the WⅠsolution to residual oil will be.

TypeⅠinositol 1, 4, 5-triphosphate receptors increase in kidney of mice with fulminant hepatic failure

AIM： To delineate the mechanisms of renal vasoconstriction in hepatorenal syndrome （HRS）, we investigated the expression of type I inositol 1, 4, 5-triphosphate receptors （IP3R I） of kidney in mice with fulminant hepatic failure （FHF）. METHODS： FHF was induced by lipopolysaccharide （LPS） in D-galactosamine （GAIN） sensitized BALB/c mice. There were 20 mice in normal saline （NS）-treated group, 20 mice in LPS-treated group, 20 mice in GaIN- treated group, and 60 mice in GalN/LPS-treated group （FHF group）. Liver and kidney tissues were obtained at 2, 6, and 9 h after administration. The liver and kidney specimens were stained with hematoxylin-eosin for studying morphological changes under light microscope. The expression of IP3R I in kidney tissue was tested by immunohistochemistry, Western blot and reverse transcription （RT）-PCR. RESULTS： Kidney tissues were morphologically normal at all time points in all groups. IP3R I proteins were found localized in the plasma region of glomerular mesangial cells （GMC） and vascular smooth muscle cells （VSMC） in kidney by immunohistochemical staining. In kidney of mice with FHF at 6 h and 9 h IP3R I staining was upregulated. Results from Western blot demonstrated consistent and significant increment of IP3R I expression in mice with FHF at 6 h and 9 h （t = 3.16, P 〈 0.05; t = 5.43, P 〈 0.01）. Furthermore, we evaluated IP3R I mRNA expression by RT-PCR and observed marked upregulation of IP3R I mRNA in FHF samples at 2 h, 6 h and 9 h compared to controls （t = 2.97, P 〈 0.05; t = 4.42, P 〈 0.01; t = 3.81, P 〈 0.01）. CONCLUSION： The expression of IP3R I protein increased in GMC and renal VSMC of mice with FHF, possibly caused by up-regulation of IP3R I mRNA.

Novel electrospun poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits for repair of peripheral nerve injury

Recent studies have shown the potential of artificially synthesized conduits in the repair of peripheral nerve injury. Natural biopolymers have received much attention because of their biocompatibility. To investigate the effects of novel electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits(biopolymer nanofiber conduits) on the repair of peripheral nerve injury, we bridged 10-mm-long sciatic nerve defects with electrospun absorbable biopolymer nanofiber conduits, poly(ε-caprolactone) or silicone conduits in Sprague-Dawley rats. Rat neurologica1 function was weekly evaluated using sciatic function index within8 weeks after repair. Eight weeks after repair, sciatic nerve myelin sheaths and axon morphology were observed by osmium tetroxide staining, hematoxylin-eosin staining, and transmission electron microscopy.S-100(Schwann cell marker) and CD4(inflammatory marker) immunoreactivities in sciatic nerve were detected by immunohistochemistry. In rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits, no serious inflammatory reactions were observed in rat hind limbs, the morphology of myelin sheaths in the injured sciatic nerve was close to normal. CD4 immunoreactivity was obviously weaker in rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits than in those subjected to repair with poly(ε-caprolactone) or silicone. Rats subjected to repair with electrospun absorbable biopolymer nanofiber conduits tended to have greater sciatic nerve function recovery than those receiving poly(ε-caprolactone) or silicone repair. These results suggest that electrospun absorbable poly(ε-caprolactone)/type Ⅰ collagen nanofiber conduits have the potential of repairing sciatic nerve defects and exhibit good biocompatibility. All experimental procedures were approved by Institutional Animal Care and Use Committee of Taichung Veteran General Hospital, Taiwan, China(La-1031218) on October 2, 2014.

狂犬病病毒强、弱毒株糖蛋白调节Ⅰ型干扰素作用的差异分析

【目的】狂犬病(Rabies)是由狂犬病病毒(Rabies virus,RABV)引起的一种高致死性人兽共患传染病。Ⅰ型干扰素(IFN-I)通路在抵抗RABV感染中发挥重要作用。RABV可通过磷蛋白及核蛋白的功能逃逸IFN-I的抗病毒作用,本研究旨在探讨对RABV的致病性有重要影响的糖蛋白(Glycoprotein,G)在调节IFN-I通路方面扮演怎样的角色。【方法】将RABV弱毒株Hep-Flury的G基因替换成致病株CVS-11的G基因,拯救得到重组病毒HepG,分析Hep-Flury、CVS-11和HepG这3种毒株在体内和体外感染对IFN-I通路激活和调控的差别,比较它们在神经细胞中对抗IFN-I抗病毒作用的差异性。【结果】替换了CVS-11的G基因后,重组病毒HepG致病力增强,能够100%致死小鼠,在鼠脑中的增殖水平显著高于亲本株Hep-Flury。在感染鼠脑早期及体外神经细胞时,弱毒株Hep-Flury能够较快地激活IFN-I通路相关基因的表达,重组病毒HepG的激活能力介于HepFlury和CVS-11之间。利用Poly(I:C)激活神经细胞的IFN-I通路后,Hep-Flury的增殖被显著抑制,CVS-11和HepG的复制几乎不受影响,表现出一定的抵抗能力。【结论】RABV的G蛋白在调节和抵抗IFN-I通路方面发挥重要功能,为进一步探究RABV致病毒株的G蛋白如何协助病毒在中枢神经系统中逃逸IFN-I提供了线索和依据。

Lentinula edodes extract inhibits matrix metalloproteinase expression and increases typeⅠprocollagen expression via the p38 MAPK/c-Fos signaling pathway in ultraviolet A and B-irradiated HaCaT keratinocytes

Objective:To determine the effect of Lentinula edodes extract on ultraviolet(UV)A and UVB-induced changes in matrix metalloproteinase(MMP)and type I procollagen expression using human immortalized HaCaT keratinocytes.Methods:Lentinula edodes ethanol extract(LEE)was obtained by extraction with 80%ethanol for 4 h at 80℃.Effect of LEE on UVinduced alteration on the expression and production of MMPs and type I procollagen in keratinocytes was investigated using ELISA,RT-PCR,and Western blotting assay.To determine the underlying mechanism of LEE-mediated effects,mitogen-activated protein kinase(MAPK)and activator protein 1 signaling pathways were analysed by Western blotting assay.Results:LEE significantly inhibited the expression of MMP-1 and MMP-9 and increased the expression of type I procollagen in UVA and UVB-irradiated HaCaT keratinocytes.The phosphorylation levels of p38 were significantly inhibited by LEE whereas it did not affect c-Jun N-terminal kinase and extracellular signal-regulated kinase phosphorylation.Suppression of p38 phosphorylation was also accompanied by downregulation of UVA and UVB-induced increase in c-Fos.Conclusions:LEE effectively inhibits the expression of MMP-1 and MMP-9 and increases type I procollagen production through the p38 MAPK/c-Fos signaling pathway in UVA and UVB-irradiated HaCaT keratinocytes.This findings suggest that Lentinula edodes may be developed as a cosmetic material to suppress UV exposuremediated skin aging.

Synthesis and high temperature thermoelectric transport properties of Si-based type-Ⅰ clathrates

N-type Si-based type-Ⅰ clathrates with different Ga content were synthesized by combining the solid-state reaction method,melting method and spark plasma sintering （SPS） method.The effects of Ga composition on high temperature thermoelectric transport properties were investigated.The results show that at room temperature,the carrier concentration decreases, while the carrier mobility increases slightly with increasing Ga content.The Seebeck coefficient increases with increasing Ga content. Among all the samples,Ba7.93Ga17.13Si28.72exhibits higher Seebeck coefficient than the others and reaches -135μV·K^-1 at 1000 K.The sample prepared by this method exhibits very high electrical conductivity,and reaches 1.95x 10^5 S·m^-1 for Ba8.01Ga16.61Si28.93 at room temperature.The thermal conductivity of all samples is almost temperature independent in the temperature range of 300-1000 K,indicating the behaviour of a typical metal.The maximum ZT value of 0.75 is obtained at 1000 K for the compound Ba7.93Ga17.13Si28.72.

一类广义Type Ⅰ函数的多目标优化问题

对于非光滑多目标优化的模型,定义了几种广义Type Ⅰ函数,研究了广义Type Ⅰ函数的多目标优化问题,得到了有效解的最优性条件.

Type Ⅰ kerogen-rich oil shale from the Democratic Republic of the Congo: mineralogical description and pyrolysis kinetics

The Democratic Republic of the Congo holds important reserves of oil shale which is still under geological status.Herein,the characterization and pyrolysis kinetics of typeⅠkerogen-rich oil shale of the western Central Kongo(CK)were investigated.X-ray diffraction,Fourier-transform infrared spectroscopy and thermal analysis(TG/DTA)showed that CK oil shale exhibits a siliceous mineral matrix with a consistent organic matter rich in aliphatic chains.The pyrolysis behavior of kerogen revealed the presence of a single mass loss between 300 and 550°C,estimated at 12.5%and attributed to the oil production stage.Non-isothermal kinetics was performed by determining the activation energy using the iterative isoconversional model-free methods and exhibits a constant value with E=211.5±4.7 kJ mol.1.The most probable kinetic model describing the kerogen pyrolysis mechanism was obtained using the Coats–Redfern and Arrhenius plot methods.The results showed a unique kinetic triplet confirming the nature of kerogen,predominantly typeⅠand reinforcing the previously reported geochemical characteristics of the CK oil shale.Besides,the calculation of thermodynamic parameters(ΔH~*,ΔS~*andΔG~*)corresponding to the pyrolysis of typeⅠkerogen revealed that the process is non-spontaneous,in agreement with DTA experiments.

Type Ⅰ neurofibromatosis with spindle cell sarcoma: A case report

BACKGROUND Neurofibromatosis type Ⅰ(NF1) is the most frequent subtype of neurofibromatosis. Its related tumor-suppressor syndromes are characterized by a predisposition to multiple tumor types and other disorder presentations. In addition, the incidence of tumors is much higher in patients with neurofibromatosis type Ⅰ. However, there are very few reports at home and abroad on this topic. Here, we present a case of NF1 with spindle cell sarcoma.CASE SUMMARY A 50-year-old male was found to have a right axillary mass for 20 years.Specialist examination found cafe-au-lait spots on many parts of the skin,rounded nodules in the skin, a bulge in the right armpit, touching a lump(10 cm× 6 cm, hard, unclear boundary, poor mobility, local tenderness). The anterior side of the thigh felt weakened on the opposite side;in the right groin a swollen lymph node(hard, clear border, good mobility, local tenderness). According to the results of positron emission tomography/computed tomography, puncture pathology and immunohistochemistry, genetic testing, a diagnosis of NF1 with spindle cell sarcoma was confirmed. According to the genetic testing result, the patient was given a targeted treatment with crizotinib.CONCLUSION Surgery, chemotherapy and radiotherapy are the main treatment methods of NF1. However, with the continuous progress of molecular biology research,molecular targeted therapy may bring benefits for patients.

Significance of elevated serum concentration of type Ⅰ collagen metabolites and its correlation with serum interleukin 6 activities in multiple myeloma

In this study, serum concentrations of carboxyterminal propeptide of type Ⅰ collagen(PICP) and carboxyterminal cross-linked telopeptide of type Ⅰ collagen (ICTP), which represent the rates of synthesis and degradation of type Ⅰ collagen, were determined by radioimmunoassay in 56 patients with multiple myeloma (MM) and 22 healthy controls. It was discovered that serum concentrations of both PICP and ICTP were higher in MM than those in healthy controls (P<0. 01 ). With the disease progressing and the number of bone lesions increasing,serum concentration of ICTP elevated while serum concentration of PICP showed no significant change. Neither serum PICP nor ICTP concentration was related to M-component classes. Our results indicated that serum ICTP concentration was a good serological marker to reflect severity of bone lesions in MM and elevated serum PICP concentration might be due to compensatory increase in type Ⅰ collagen synthesis. Moreover, we also found that serum ICTP concentrations in MM correlated with serum interleukin-6 (IL-6) activities (r= 0. 610, P< 0. 01),which confirms the effectiveness of IL-6 as an osteoclast activating factor.