口服“金双歧”治疗新生儿黄疸32例疗效观察

目的观察双歧杆菌制剂"金双歧”对新生儿黄疸的治疗作用.方法将87例新生儿疸病例随机分为治疗观察组和常规治疗对照组;观察组加用"金双歧”口服.结果2组的黄疸消退的时间分别为(4.0±2.0)d,(5.5±2.5)d(P<0.01).第5天血清总胆红素浓度分别为(45.6±17.34)μmol/L、(82.5±32.6)μmol/L(P<0.01).结论[HTSS〗金双歧对新生儿黄疸有显著的疗效.     

持续性植物状态患者血浆、脑脊液中氨基酸水平的变化

目的：探讨持续性植物状态(PVS)患者脑眷液(CSF)和血浆中氨基酸类物质水平与PVS发病的关系。方法：采用高压液相色谱(HPLC)方法测定。结果:PVS患者血浆中较对照组显著升高的氨基酸有：谷氨酸(Glu)、精氨酸(Arg)。脑眷液中较对照组显著升高的氨基酸有：γ-氨基丁酸(GABA)、丝氨酸(Ser)、酪氨酸(Tyr)、色氨酸(Trp)、赖氨酸(Lys)、胍氨酸(Cit);较对照组显著降低的氨基酸有：胱氨酸(CysT)。结论：CSF中的γ-氨基丁酸、丝氨酸、酪氨酸、色氨酸和赖氨酸等的升高,胱氨酸的降低以及血浆中的谷氨酸、精氨酸的升高可能与PVS的发生和发展过程有关。     

NO对兔窦房结自律性的影响

目的观察外源性NO供体硝普钠(SNP)和吗啉-斯德酮亚胺(SIN-1)对离体兔窦房结起搏细胞(SANC)自律性的影响,并初步探讨其作用机制.方法利用细胞内微电极技术记录SANC动作电位,分析APA(动作电位幅值),Vmax(0期最大除极速率),DD(舒张期除极速率),RPF(起搏细胞放电频率)的变化.结果SNP(10-5-10-2mol/L)增快SANC自发放电频率(RPF)和舒张期除极速率(VDD),并呈浓度依赖性.10-3 mol/LSNP使RPF(beats/min)由163±10.8增至195.0±13.1,DD(mV/s)由50.3±9.6增至70.2±12.1(P<0.01).SIN-1(10-3-10-2mol/L)亦使RPF和VDD增快(P<0.01).鸟苷酸环化酶抑制剂 10-4mol/L甲基美兰(MB)完全阻断了1 mmol/LSNP引起的RPF和VDD增长(P<0.01).If阻断剂2 mmol/L CsCl部分阻断了1 mmol/LSNP引起的正性变时作用和VDD增长(P<0.05).ICa-L阻断剂0.46 μmol/L NIF对于1 mmol/LSNP所致的RPF和VDD的增长无明显影响(P>0.05).结论外源性NO可增快离体兔SANC自律性,此效应通过NO-cGMP途径产生,至少部分与If增强有关,Ca-L对此无显著作用.     

大鼠心肌线粒体L-Arg/ NO系统对线粒体Ca2+转运功能的影响

目的和方法采用大鼠心肌线粒体体外孵育的方法,观察线粒体L-精氨酸/一氧化氮系统对线粒体Ca2+转运功能的影响.结果NO生成的底物L-Arg (10-4 mol/L)、外源性NO供体硝普纳(5×10-7 mol/L)孵育的线粒体NO-2的生成量分别高于对照组66%、89% (P<0.01);钙含量较对照组分别低40%、54% (P<0.01); 线粒体Ca2+的摄入量较对照组分别减少67%、85%(P<0.01), 线粒体Ca2+释放率(11%、8%)降低与对照组(14%)相比差异显著(P<0.05、P<0.01).NO合酶抑制剂左旋硝基精氨酸甲酯(L-NAME, 10-4 mol/L)与相同浓度的L-Arg共同孵育的线粒体,明显抑制了L-Arg对线粒体的效应,与单纯L-Arg组比较,NO2生成减少,线粒体钙含量和反映线粒体45 Ca2+的摄入与释放能力都接近对照组水平.结论心肌线粒体L-精氨酸/一氧化氮系统参与了线粒体对心肌细胞Ca2+浓度的调节,其生理和病理生理意义值得进一步探讨.     

肾上腺髓质素对大鼠损伤性心肌肌浆网功能的改善

通过观察下述五个指标,评价肾上腺髓质素(adrenomedullin,Adm)对大鼠损伤性心肌肌浆网功能的改善程度左心室压力最大变化速率(±dp/dtmax)、肌浆网钙摄取和释放及钙泵活性.皮下注射异丙肾上腺素(isoproterenol,ISO,69μmol/kg体重)制备大鼠心肌损伤坏死模型.摘取心脏后用Adm灌流,观察左心室压力最大变化速率(±dp/dtmax);制备并提纯心肌肌浆网(sarcoplasmicreticulum,SR)膜,测定SRCa2+摄取和释放速率、SR钙泵活性和钙通道蛋白～3H-ryanodine受体的最大结合量.结果发现,5×10-5mol/LAdm灌流能使ISO损伤的大鼠心脏左室±dp/dtmax分别增加16.9%(2?135±281vs1?980±302)和29.2%(1?375±267vs1?064±355,均P<0.05);SRCa2+摄取和释放率分别增加23.0%(15.0±1.4vs12.2±1.2)和43.5%(6.6±1.0vs4.6±0.6,均P<0.01);SRCa2+-ATPase活性和～3H-ryanodine受体最大结合量(Bmax)分别增加24.2%(P<0.01)和42.2%(P<0.05).提示Adm对ISO诱导的大鼠心肌损伤具有保护作用,其机制可能与Adm增加SRCa2+-ATPase活性、增加～3H-ryanodine所致SRCa2+摄取和释放升高有关.外源性给予Adm对损伤心肌可能具有临床治疗作用.     

哮喘患者外周血单核细胞血红素氧合酶-1表达水平的研究

目的探讨血红素氧合酶-1(HO-1)在哮喘患者外周血单核细胞(PBMC)的表达及与肺通气功能的关系.方法应用免疫组织化学和逆转录聚合酶链反应技术分析18例哮喘患者PBMC的 HO-1蛋白及mRNA水平的表达,测定全血一氧化碳血红蛋白(COHb)的百分比含量、血清总IgE含量、肺通气功能,并与18名健康正常者的结果进行比较.结果哮喘组PBMC中HO-1表达阳性的细胞百分比41.7%±7.44%与正常对照组10.5%±4.36%比较,差异有显著性(P<0.01),哮喘组PBMC HO-1 mRNA表达的平均吸光度值(26.05±4.14)与正常对照组(10.82±4.26)比较,差异亦有显著性(P<0.01),HO-1染色阳性细胞的百分比与FEV1占预计值%、PEFR和MEFR50%均呈显著负相关(r值分别为-0.89,-0.56,-0.51,均P<0.01),与全血COHb的百分比含量及血清总IgE含量呈显著正相关(r值分别为0.80, 0.48, 均P<0.05).HO-1 mRNA的表达水平与1s用力呼气容积(FEV1)占预计值%、顶峰呼气流速(PEFR)和50%肺活量时的最大呼气流速(MEFR50%)均呈显著负相关(r 值分别为-0.89,-0.65,-0.67, 均P<0.01),与全血COHb的百分比含量和血清总IgE含量呈显著正相关(r分别为 0.85和0.62, 均P＜0.01).结论哮喘患者PBMC 的HO-1表达水平显著增加,提示HO-1可能参与了哮喘的发病过程,HO-1表达的变化与哮喘患者的病情程度有一定关系.     

复方中药对大鼠力竭运动与恢复过程中端脑神经递质含量的影响

目的：探讨复方中药对运动大鼠中枢神经递质含量的影响,进一步认识中药提高运动能力和促进运动性疲劳恢复的作用机理。方法：选8周龄大鼠64只,随机分成服药组和对照组,服药组灌服中药煎剂8周。然后,每组再分成4个亚组分别于不同状态下断头处死,测其中枢递质含量。结果：服药组大鼠力竭运动时间极显著长于对照组（P〈0．01）;安静时,除谷氨酸（GLU）含量服药组极显著高于对照组（P〈0．01）外、其余各指标无组间显著性差异;定量负荷后,服药组5-羟色胺（5-HT）、5-羟吲哚乙酸（5-HIAA）、弘氨基丁酸（GABA）、多巴胺（DA）含量和5-HT／5-HIAA显著低于对照组,GLU、GLU／GABA和DA／5-HT明显高于对照组;力竭即刻,服药组5-HT、GABA含量和5-HT／5-mAA显著低于对照组（P〈0．05）,GLU含量、DA／5-HT和GLU／GABA显著高于对照组（P〈0．05）;恢复12h。服药组5-HT含量和5-HT／5-HIAA极显著低于对照组（P〈0．01）,GLU、DA、GABA含量和DA／5-HT明显高于对照组（P〈0．05）。结论：在大鼠运动至力竭性的过程中,复方中药制剂有明显抑制5-HT、5-HIAA、DA、GABA生成和促进GLU中枢递质合成的作用,其综合效应表现为兴奋性递质相对显著增多,使中枢神经兴奋性增强、明显延长大鼠运动时间和促进中枢疲劳的恢复。     

GABA对大鼠下丘脑正中隆起LHRH释放调节的研究

本研究应用大鼠下丘脑正中隆起(ME),观察 γ-氨基丁酸(GABA)和去甲肾上腺素(NA)对下丘脑促黄体生成激素释放激素(LHRH)神经元末梢分泌作用的影响。结果发现:GABA(10~(-6)mol/L)可显著促进 ME 的 LHRH 和 NA 的释放,即 LHRH 释放量由27.3±2.5pg/100ul 增加至150.4±27.9pg/100μl;NA 释放量由50.9±4.2pg/100μl 增加至105.5±19.1pg/100ul,两者与对照组相比有显著差异(P<0.01)。GABA 这些作用可被受体拮抗剂荷包牡丹碱(Bicuculline)所翻转。当荷包牡丹碱和 GABA(10~(-6)mol/L)同时存在于 ME 的培灌液中,LHRH 的分泌量下降为18.2±1.9pg/100μl,而 NA 分泌量下降为43.9±3.4pg/100μl。在内源性 NA 被利血平耗竭时,LHRH 的释放量仅增加26.5%,而 GABA 能使正常大鼠 LHRH 释放量增加451.9%。本研究提示:GABA 可促进下丘脑 ME 释放 LHRH,这一作用可能通过 NA 中介。     

克伦特罗对大鼠肝脏氮代谢及IGF-I水平的影响

目的探讨克伦特罗(CL)影响机体物质代谢的有关肝脏机制.方法利用大鼠离体肝脏灌流技术测定CL对肝脏灌流液中尿素氮水平,肝组织谷丙转氨酶(GPT)活性以及肝脏胰岛素样生长因子I(IGF-I)合成和分泌的影响.结果CL可使大鼠离体肝脏产生的尿素氮浓度下降,并有一定的剂量效应和时间效应.在给药后灌流的1、2、3、4h内1×10-6 mol/L的CL使大鼠肝脏产生的尿素氮分别下降15.02% (P>0.05)、17.97% (P>0.05)、26.76%(P<0.05)和30.08%(P<0.01),1×10-8mol/L的CL具有类似的效应.CL抑制大鼠肝组织中GPT的活性,×10-6mol/L的CL使得肝组织中GPT活性下降24.65%(P<0.05).CL还影响大鼠离体肝脏IGF-I的生成和分泌,×10-6 mol/L CL使大鼠肝组织内IGF-I的含量比对照组升高19.77%(P<0.05),灌流液中IGF-I的水平也呈增加的趋势.结论CL可通过增加对肝脏氮的储留及增强肝脏IGF-1的合成和分泌而促进机体的物质代谢.     

应激大鼠肾胞液[^3H]醛固酮结合活性的变化及调节机制的初步研究

为探讨烫伤引起病理性应激时大鼠肾胞液醛固酮结合活性的变化及可能的调节机制,以[～3H]-醛固酮为配体,用放射性配基-受体结合分析法测定了正常对照组、轻度烫伤组和重度烫伤组大鼠肾胞液醛固酮结合活性的结合容量(Rt)和表观解离常数(Kd);采用体内注射TNF-α、IL-1β中和抗体和α-促黑色素细胞刺激激素(α-melanocyte-stimulatinghormone,α-MSH)和合成肽KPV(Ac-D-Lys-L-Pro-D-Val)等措施调节其改变.结果发现,肾胞液存在两种不同结合容量、不同亲和力的醛固酮结合活性受体.与正常对照组的Rt(Rt141.6±7.2fmol/mgpro;Rt2317.6±70.0fmol/mgpro)相比,轻烫组的Rt(Rt141.4±5.0fmol/mgpro;Rt2314.8±45.7fmol/mgpro)无显著差异(P>0.05;P>0.05);重烫组的Rt(Rt122.4±5.4fmol/mgpro;Rt2196.3±32.5fmol/mgpro)则显著下降(P<0.01;P<0.01).体内注射TNF-α与IL-1β中和抗体、α-MSH及KPV均能明显提高重烫组Rt值.结果提示,重度烫伤大鼠肾胞浆醛固酮结合活性降低,TNF-α、IL-1β中和抗体、α-MSH及KPV均可防止重度烫伤引起病理性应激时醛固酮结合活性降低.     

Changes in lactate dehydrogenase activity in chicken tissues in hyperthyreosis in ontogenesis

The lactate dehydrogenase activity in reactions of lactate oxidation and synthesis was studied in subfractions of the chicken brain, heart and liver at the embryonal, early postembryonal and adult stages of development after thyroxine administration. It has been shown that during embryogenesis thyroxine predominantly enhanced the rate of lactate oxidation in the mitochondrial tissues. A marked increase in the lactate synthesis was found in cytoplasm of the adult chicken tissues. Specificity of enzyme activity alterations was detected in the chicken brain during ontogenesis after thyroxine administration.     

Scurvy in capybaras bred in captivity in Argentine

In order to determine if the absence of vitamin C in the diet of capybaras (Hydrochoerus hydrochaeris) causes scurvy, a group of seven young individuals were fed food pellets without ascorbic acid, while another group of eight individuals received the same food with 1 g of ascorbic acid per animal per day. Animals in the first group developed signs of scurvy-like gingivitis, breaking of the incisors and death of one animal. Clinical signs appeared between 25 and 104 days from the beginning of the trial in all individuals. Growth rates of individuals deprived of vitamin C was considerably less than those observed in the control group. Deficiency of ascorbic acid had a severe effect on reproduction of another population of captive capybaras. We found that the decrease in ascorbic acid content in the diet affected pregnancy, especially during the first stages. The results obtained suggest that it is necessary to supply a suitable quantity of vitamin C in the diet of this species in captivity.     

Role for dopamine in malonate-induced damage in vivo in striatum and in vitro in mesencephalic cultures

Defects in mitochondrial energy metabolism have been implicated in the pathology of several neurodegenerative disorders. In addition, the reactive metabolites generated from the metabolism and oxidation of the neurotransmitter dopamine (DA) are thought to contribute to the damage to neurons of the basal ganglia. We have previously demonstrated that infusions of the metabolic inhibitor malonate into the striata of mice or rats produce degeneration of DA nerve terminals. In the present studies, we demonstrate that an intrastriatal infusion of malonate induces a substantial increase in DA efflux in awake, behaving mice as measured by in vivo microdialysis. Furthermore, pretreatment of mice with tetrabenazine (TBZ) or the TBZ analogue Ro 4-1284 (Ro-4), compounds that reversibly inhibit the vesicular storage of DA, attenuates the malonate-induced DA efflux as well as the damage to DA nerve terminals. Consistent with these findings, the damage to both DA and GABA neurons in mesencephalic cultures by malonate exposure was attenuated by pretreatment with TBZ or Ro-4. Treatment with these compounds did not affect the formation of free radicals or the inhibition of oxidative phosphorylation resulting from malonate exposure alone. Our data suggest that DA plays an important role in the neurotoxicity produced by malonate. These findings provide direct evidence that inhibition of succinate dehydrogenase causes an increase in extracellular DA levels and indicate that bioenergetic defects may contribute to the pathogenesis of chronic neurodegenerative diseases through a mechanism involving DA.     

SSTR5 ablation in islet results in alterations in glucose homeostasis in mice

Somatostatin (SST) peptide is a potent inhibitor of insulin secretion and its effect is mediated via somatostatin receptor 5 (SSTR5) in the endocrine pancreas. To investigate the consequences of gene ablation of SSTR5 in the mouse pancreas, we have generated a mouse model in which the SSTR5 gene was specifically knocked down in the pancreatic beta cells (betaSSTR5Kd) using the Cre-lox system. Immunohistochemistry analysis showed that SSTR5 gene expression was absent in beta cells at three months of age. At the time of gene ablation, betaSSTR5Kd mice demonstrated glucose intolerance with lack of insulin response and significantly reduced serum insulin levels. Insulin tolerance test demonstrated a significant increase of insulin clearance in vivo at the same age. In vitro studies demonstrated an absence of response to SST-28 stimulation in the betaSSTR5Kd mouse islet, which was associated with a significantly reduced SST expression level in betaSSTR5Kd mice pancreata. In addition, betaSSTR5Kd mice had significantly reduced serum glucose levels and increased serum insulin levels at 12 months of age. Glucose tolerance test at an older age also indicated a persistently higher insulin level in betaSSTR5Kd mice. Further studies of betaSSTR5Kd mice had revealed elevated serum C-peptide levels at both 3 and 12 months of age, suggesting that these mice are capable of producing and releasing insulin to the periphery. These results support the hypothesis that SSTR5 plays a pivotal role in the regulation of insulin secretion in the mouse pancreas.     

2018年中国植物科学若干领域重要研究进展

2018年中国植物科学继续呈现快速发展的态势, 我国科学家在国际植物科学主流学术刊物发表论文数量大幅增加, 取得了多项具有重要影响的成果。调控植物生长-代谢平衡实现可持续农业发展入选2018年度中国科学十大进展; 中国被子植物区系进化历史研究入选2018年度中国生命科学十大进展。以水稻为代表的农作物和果蔬等经济作物研究在国际上已呈现出明显的优势, 若干领域已从“追赶”状态跨越到“领跑”地位。该文对2018年中国科学家在植物科学若干领域取得的重要研究成果进行了概括性评述, 旨在全面追踪和报道当前中国植物科学领域的发展前沿和热点, 展示中国科学家所取得的杰出成就。