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| 1 | 泥炭栽培基质是欧洲可持续园艺业的前提显示文摘过去被当作废物的泥炭今天成为最有前途的栽培基质。在欧洲和其它现代园艺业盛行的国家里,以泥炭为主要成分的栽培基质广泛应用于各种作物栽培。栽培基质作为标准生产资料,和设施农业中计算机自动施肥、小气候控制和杀灭病虫害一样,在实现现代园艺业可持续发展中起着重要的作用。一些欧洲国家已经制定了泥炭栽培基质的国家质量标准,一些公司还制定了自己的企业标准,也有一些公司执行ISO条款。这些产品都在向着CEN标准迈进,并将成为欧洲产品标准。在一些地区和国家,以生活废弃物、工业副产品制成的栽培基质在不断地推向市场的同时,新的标准也在不断地制定。最近起草的一个鼓励利用堆肥的法令中,其中一项就是关于减少泥炭利用的。泥炭业界必须意识到这些发展变化与资源安全息息相关,必须意识到其它替代材料的有利和不利的一面,意识到它们物理、化学、生物性质以及对社会政治和自然环境的利弊影响。 | Gerald Schmeilewski Hartmut Falkenberg 刘永和 | 2002 | 腐植酸2002，，4： | 23 |
| 2 | Novel insight into mechanisms of cholestatic liver injury显示文摘Cholestasis results in a buildup of bile acids in serum and in hepatocytes.Early studies into the mechanisms of cholestatic liver injury strongly implicated bile acidinduced apoptosis as the major cause of hepatocellular injury.Recent work has focused both on the role of bile acids in cell signaling as well as the role of sterile inflammation in the pathophysiology.Advances in modern analytical methodology have allowed for more accurate measuring of bile acid concentrations in serum,liver,and bile to very low levels of detection.Interestingly,toxic bile acid levels are seemingly far lower than previously hypothesized.The initial hypothesis has been based largely upon the exposure of μmol/L concentrations of toxic bile acids and bile salts to primary hepatocytes in cell culture,the possibility that in vivo bile acid concentrations may be far lower than the observed in vitro toxicity has far reaching implications in the mechanism of injury.This review will focus on both how different bile acids and different bile acid concentrations can affect hepatocytes during cholestasis,and additionally provide insight into how these data support recent hypotheses that cholestatic liver injury may not occur through direct bile acid-induced apoptosis,but may involve largely inflammatory cell-mediated liver cell necrosis. | Benjamin L Woolbright Hartmut Jaeschke | 2012 | World Journal of Gastroenterology2012，18，36： | 21 |
| 3 | Response evaluation of chemotherapy in metastatic colorectal cancer by contrast enhanced ultrasound显示文摘AIM:To evaluate whether contrast enhanced ultrasound(CEUS) might also be used for response prediction and early response evaluation in patients receiving bevacizumab based chemotherapy for metastasized colorectal cancer.METHODS:Thirty consecutive patients with non primary resectable liver metastases from colorectal cancer underwent CEUS before treatment(CEUS date 1) and before the second(CEUS date 2) and fourth(CEUS date 3) cycle of bevacizumab based chemotherapy.Three parameters [PEAK,Time to peak(TTP) and RISE RATE]were correlated with radiological response.RESULTS:For neoadjuvant purpose a reduction of tumour mass was required to assume clinical response.Based on these response criteria there was a significant(P < 0.001) correlation in TTP between metastases of responders(9.08 s) and non-responders(14.76 s) archived on CEUS date 1.By calculating a standardized quotient(metastases divided by normal liver tissue) we were able to define a cut off,predicting response with a sensitivity of 92.3 % and a specificity of 100 %.To reflect a palliative intention only those patients with progressive disease were classified as non-responders.In this stetting TTP was also significantly(P < 0.01) different between responders and non-responders.In contrast,Peak and Rise rate did not show any significant difference between responder and non-responder.CONCLUSION:CEUS might serve as a surrogate marker to predict treatment response in patients with metastasized colorectal cancer who receive antiangiogenic therapy. | Ramin Schirin-Sokhan Ron Winograd Christoph Roderburg Jhenee Bubenzer Nicole Cabral do ó Dorothee Guggenberger Hartmut Hecker Christian Trautwein Jens J W Tischendorf | 2012 | World Journal of Gastroenterology2012，18，6： | 16 |
| 4 | Structure and composition of the continental crust in East China显示文摘Crustal structures of nine broad tectonic units in China, except the Tarim craton, are derived from 18 seismic refraction profiles including 12 geoscience transects. Abundances of 63 major, trace and rare earth elements in the upper crust in East China are estimated. The estimates are based on sampling of 11 451 individual rock samples over an area of 950 000 km^2, from which 905 large composite samples are prepared and analyzed by 13 methods. The middle, lower and total crust compositions of East China are also estimated from studies of exposed crustal cross sections and granulite xenoliths and by correlation of seismic data with lithologies. All the tectonic units except the Tarim craton and the Qinling orogen show a four-layered crustal structure, consisting of the upper, middle, upper lower, and lowermost crusts. P-wave velocities of the bulk lower crust and total crust are 6.8—7.0 and 6.4—6.5 km/s, respectively. They are slower by 0.2—0.4 km/s than the global averages. The bulk lower crust is | 高山 骆庭川 张本仁 张宏飞 韩吟文 赵志丹 KERN Hartmut | 1999 | Science China Earth Sciences1999，42，2： | 11 |
| 5 | 一株产抑制真菌活性全霉素的胶州湾海洋链霉菌显示文摘目的研究胶州湾海洋链霉菌M095抑菌活性代谢产物及菌株M095的分类。方法采用ESI-MS,EI-MS,1H-NMR,13C-NMR和APTNMR等波谱分析进行结构测定;并根据培养特征、形态特征及16SrDNA序列分析进行分类。结果获得一种对金黄色葡萄球菌和丝状真菌毛霉miehei(Tü284)均有显著抑制作用的化合物,经鉴定其结构与全霉素相同;该菌株可能为球孢类群中的一个变种。结论本文首次报道了全霉素对丝状真菌的抑制作用,拓宽了全霉素的抗菌谱。 | 崔洪霞 李富超 阎斌伦 Khaled Shaaben 秦松 Hartmut Laatsch | 2006 | 中国海洋药物2006，25，1： | 11 |
| 6 | Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury显示文摘We previously found that argon exerts its neuroprotective effect in part by inhibition of the toll-like receptors(TLR)2 and 4.The downstream transcription factors signal transducer and activator of transcription 3(STAT3)and nuclear factor kappa B(NF-κB)are also affected by argon and may play a role in neuroprotection.It also has been demonstrated that argon treatment could mitigate brain damage,reduce excessive microglial activation,and subsequently attenuate brain inflammation.Despite intensive research,the further exact mechanism remains unclear.In this study,human neuroblastoma cells were damaged in vitro with rotenone over a period of 4 hours(to mimic cerebral ischemia and reperfusion damage),followed by a 2-hour post-conditioning with argon(75%).In a separate in vivo experiment,retinal ischemia/reperfusion injury was induced in rats by increasing intraocular pressure for 1 hour.Upon reperfusion,argon was administered by inhalation for 2 hours.Argon reduced the binding of the transcription factors signal transducer and activator of transcription 3,nuclear factor kappa B,activator protein 1,and nuclear factor erythroid 2-related factor 2,which are involved in regulation of neuronal damage.Flow cytometry analysis showed that argon downregulated the Fas ligand.Some transcription factors were regulated by toll-like receptors;therefore,their effects could be eliminated,at least in part,by the TLR2 and TLR4 inhibitor oxidized phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine(OxPAPC).Argon treatment reduced microglial activation after retinal ischemia/reperfusion injury.Subsequent quantitative polymerase chain reaction analysis revealed a reduction in the pro-inflammatory cytokines interleukin(IL-1α),IL-1β,IL-6,tumor necrosis factorα,and inducible nitric oxide synthase.Our results suggest that argon reduced the extent of inflammation in retinal neurons after ischemia/reperfusion injury by suppression of transcription factors crucial for microglial activation.Argon has no known side effects or narcotic properties;therefore,therapeutic use of this noble gas appears ideal for treatment of patients with neuronal damage in retinal ischemia/reperfusion injury.The animal experiments were approved by the Commission for Animal Care of the University of Freiburg(approval No.35-9185.81/G14-122)on October 19,2012. | Ulrich Goebel Stefanie Scheid Sashko Spassov Nils Schallner Jakob Wollborn Hartmut Buerkle Felix Ulbrich | 2021 | Neural Regeneration Research2021，16，1： | 8 |
| 7 | Mitochondrial dysfunction as a mechanism of drug-induced hepatotoxicity:current understanding and future perspectives显示文摘Mitochondria are critical cellular organelles for energy generation and are now also recognized as playing important roles in cellular signaling.Their central role in energy metabolism,as well as their high abundance in hepatocytes,make them important targets for drug-induced hepatotoxicity.This review summarizes the current mechanistic understanding of the role of mitochondria in drug-induced hepatotoxicity caused by acetaminophen,diclofenac,anti-tuberculosis drugs such as rifampin and isoniazid,anti-epileptic drugs such as valproic acid and constituents of herbal supplements such as pyrrolizidine alkaloids.The utilization of circulating mitochondrialspecific biomarkers in understanding mechanisms of toxicity in humans will also be examined.In summary,it is well-established that mitochondria are central to acetaminophen-induced cell death.However,the most promising areas for clinically useful therapeutic interventions after acetaminophen toxicity may involve the promotion of adaptive responses and repair processes including mitophagy and mitochondrial biogenesis,In contrast,the limited understanding of the role of mitochondria in various aspects of hepatotoxicity by most other drugs and herbs requires more detailed mechanistic investigations in both animals and humans.Development of clinically relevant animal models and more translational studies using mechanistic biomarkers are critical for progress in this area.Relevance for patients:This review focuses on the role of mitochondrial dysfunction in liver injury mechanisms of clinically important drugs like acetaminophen,diclofenac,rifampicin,isoniazid,amiodarone and others.A better understanding of the mechanisms in animal models and their translation to patients will be critical for the identification of new therapeutic targets. | Anup Ramachandran Luqi Duan Jephte Y.Akakpo Hartmut Jaeschke | 2018 | Journal of Clinical & Translational Research2018，4，1： | 8 |
| 8 | 海洋链霉菌S007次生代谢产物的分离鉴定(英文)显示文摘采用柱层析、制备薄层层析等方法从海洋链霉菌S007的发酵液提取物中分离得到了9个化合物,经波谱分析确定为嘧啶(1),吡咯-2-羧酸(2),卡拉霉素(3),3-吲哚丙酸(4),吲哚-3-羧酸(5),N-乙酰基酪胺(6),2'-胸腺嘧啶脱氧核苷(7),N-β-乙酰色胺酸(8)和三乙胺盐酸盐(9)。其中三乙胺盐酸盐是首次从链霉菌中得到;海虾致死实验结果显示:化合物3在40μg/mL浓度下对丰年虾的致死率为86.5%,表明卡拉霉素对丰年虾表现出很强的毒性作用。 | 张宏宇 秦梅 李富超 LAATSCH Hartmut 王宏鹏 秦松 | 2011 | 天然产物研究与开发2011，23，3： | 7 |
| 9 | 毛细管区带电泳法快速分离硝基酚和除草剂显示文摘运用毛细管区带电泳法 ,通过在缓冲溶液中添加多阳离子化合物改变电渗流方向的方法 ,快速分离了 11种一取代、二取代和三取代硝基酚及 4种在德国常用的除草剂Bromoxynil,DNOC ,Dinoterb和Ioxynil。使用UV检测 ,这些化合物的检测限在 0 5mg/L~ 1 1mg/L。为满足环境样品分析的要求 ,使用固相萃取方法对样品进行了预处理 ,使硝基酚的检测限达到 1μg/L以下 ,并对实际样品进行了分析。 | 刘学良 王进防 王俊德 商振华 Hartmut FRANK | 2001 | 色谱2001，19，2： | 7 |
| 10 | 非清髓性骨髓移植诱导异基因受者小鼠免疫耐受的实验研究显示文摘本研究通过非清髓性预处理方案联合髓腔内骨髓移植(IBMBMT)建立异基因小鼠免疫耐受模型,并探讨其诱导耐受的机理。受鼠为雌性C57BL/6(H2b,B6)小鼠,于第0天接受60Coγ线全身照射(TBI),4小时内输注雄性BALB/c(H2d)小鼠来源的骨髓细胞(BMC),2天后腹腔注射环磷酰胺(CTX)。通过皮肤移植、混合淋巴细胞反应(MLR)检测耐受状态,并通过体外过继转移实验、IL2逆转实验等探讨免疫耐受的机制。结果显示,经骨髓移植的B6小鼠对BALB/c小鼠的皮肤移植物平均存活时间(MST)>150天,较对照组明显延长(P<0.01);骨髓移植后第90天,受鼠(黑色)表型开始呈现供鼠(白色)颜色特征。MLR结果证明,B6小鼠获得供体特异性耐受,该耐受可以被IL2逆转且可被过继转移;所有受鼠均未出现GVHD表现。结论:非清髓预处理联合髓腔内骨髓移植可以有效地诱导异基因小鼠免疫耐受,克隆无能、抑制细胞存在及嵌合体产生均参与耐受的形成。 | 陈宝安 毕延智 丁家华 张琰 高冲 孙耘玉 赵钢 王骏 程坚 孙雪梅 Michael Schmitt Hartmut Dhner | 2005 | 中国实验血液学杂志2005，13，6： | 7 |
| 11 | Chlorpromazine protects against acetaminophen-induced liver injury in mice by modulating autophagy and c-Jun N-terminal kinase activation显示文摘Background and aim:Overdose of acetaminophen(APAP)leads to liver injury,which is one of the most common causes of liver failure in the United States.We previously demonstrated that pharmacological activation of autophagy protects against APAP-induced liver injury in mice via removal of damaged mitochondria and APAP-adducts(APAP-ADs).Using an image-based high-throughput screening for autophagy modulators,we recently identified that chlorpromazine(CPZ),a dopamine inhibitor used for anti-schizophrenia,is a potent autophagy inducer in vitro.Therefore,the aim of the present study is to determine whether CPZ may protect against APAP-induced liver injury via inducing autophagy.Methods:Wild type C57BL/6J mice were injected with APAP to induce liver injury.CPZ was administrated either at the same time with APAP(co-treatment)or 2 h later after APAP administration(post-treat-ment).Hemotoxyline and eosin(H&E)staining of liver histology,terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick end labeling(TUNEL)staining of necrotic cell death as well as serum levels of alanine aminotransferase(ALT)were used to monitor liver injury.Results:We found that CPZ markedly protected against APAP-induced liver injury as demonstrated by decreased serum levels of ALT,liver necrotic areas as well as TUNEL-positive cells in mice that were either co-treated or post-treated with CPZ.Mechanistically,we observed that CPZ increased the number of autolysosomes and decreased APAP-induced c-Jun N-terminal kinase activation without affecting the metabolic activation of APAP.Pharmacological inhibition of autophagy by chloroquine partially weak-ened the protective effects of CPZ against APAP-induced liver injury.Conclusions:Our results indicate that CPZ ameliorates APAP-induced liver injury partially via activating hepatic autophagy and inhibiting JNK activation. | Yuan Li Hong-Min Ni Hartmut Jaeschke Wen-Xing Ding | 2019 | Liver Research2019，3，1： | 7 |
| 12 | Lipids in liver transplant recipients显示文摘Hyperlipidemia is very common after liver transplantation and can be observed in up to 71% of patients. The etiology of lipid disorders in these patients is multifactorial, with different lipid profiles observed depending on the immunosuppressive agents administered and the presence of additional risk factors, such as obesity, diabetes mellitus and nutrition. Due to recent improvements in survival of liver transplant recipients, the prevention of cardiovascular events has become more important, especially as approximately 64% of liver transplant recipients present with an increased risk of cardiovascular events. Management of dyslipidemia and of other modifiable cardiovascular risk factors, such as hypertension, diabetes and smoking, has therefore become essential in these patients. Treatment of hyperlipidemia after liver transplantation consists of life style modification, modifying the dose or type of immunosuppressive agents and use of lipid lowering agents. At the start of administration of lipid lowering medications, it is important to monitor drugdrug interactions, especially between lipid lowering agents and immunosuppressive drugs. Furthermore, as combinations of various lipid lowering drugs can lead to severe side effects, such as myopathies and rhabdomyolysis, these combinations should therefore be avoided. To our knowledge, there are no current guidelines targeting the management of lipid metabolism disorders in liver transplant recipients. This paper therefore recommends an approach of managing lipid abnormalities occurring after liver transplantation. | anna hüsing iyad kabar hartmut h schmidt | 2016 | World Journal of Gastroenterology2016，22，12： | 6 |
| 13 | 温度、光强和pH对条斑紫菜孢子体和配子体类囊体膜上光系统活性的影响显示文摘光合作用研究中,对于个体发育过程中类囊体膜蛋白结构和功能的变化所知甚少,其中的一个限制因素是能否纯化得到大量高活性的稳定且均一的膜蛋白。作者以条斑紫菜(Porphyra yezoensis)2个不同发育阶段(孢子体和配子体)作为研究对象,分离得到了孢子体和配子体的类囊体膜,在不同的温度、光强和pH下,对其类囊体膜上的光系统活性进行了研究。结果表明,孢子体和配子体的PSI活性均随温度和光强的升高而呈现一个先升高后降低的趋势,在温度18℃,光强为2 320 lx时具有最高的PSI活性。而孢子体和配子体的PSII活性随温度和光强的变化趋势不明显,孢子体PSII活性在温度18℃,光强为2 320 lx 时最高,配子体PSII活性在温度13℃,光强为2 800 lx时最高。孢子体PSI在酸性条件下较活跃,在pH 5.4时具有最高的PSI活性,配子体PSI在碱性条件下较活跃,PSI活性在pH 10.4时最高;孢子体PSII活性随pH的升高呈现一个先升高后降低的趋势,配子体PSII活性随pH变化趋势不明显,但都在pH 8.0处活性最高。 | 梁军 张海霞 Guenter Fritzsch Hartmut Michel 彭国宏 | 2005 | 海洋科学2005，29，9： | 6 |
| 14 | 利用无机抗菌剂研制抗菌自酸蚀处理剂的初步研究显示文摘目的评价利用无机抗菌剂研制抗菌自酸蚀处理剂的初步可行性。方法将6种无机抗菌剂以0.5% w/v和2.5% w/v的浓度分别加入自行研制的实验自酸蚀处理剂ESP中,进行变形链球菌体外药敏试验。并应用添加了抗菌剂的ESP制备黏结样本,测试无机抗菌剂的添加对材料固化后抗菌活性的影响。结果 ESP本身就具有一定的抗菌作用,在其中添加龙贝无机抗菌粉体或氧化锌晶须复合抗菌剂AT-83可使液体状态下ESP的最小抑菌浓度和最小杀菌浓度显著降低;加入受试的无机抗菌剂使材料固化后的抗菌活性显著增强,其中添加氧化锌晶须复合抗菌剂AT-83的效果最为显著。结论从抗菌性能方面证实了利用受试的无机抗菌剂研制抗菌自酸蚀处理剂的初步可行性。 | 方明 Christel Neut 陈吉华 刘奕 赵三军 Hartmut F Hildebrand | 2007 | 北京口腔医学2007，15，1： | 6 |
| 15 | Mechanisms of acetaminophen hepatotoxicity and their translation to the human pathophysiology显示文摘Acetaminophen(APAP)overdose is the most common cause of acute liver failure in the United States and mechanisms of liver injury induced by APAP overdose have been the focus of extensive investigation.Studies in the mouse model,which closely reproduces the human condition,have shown that hepatotoxicity is initiated by formation of a reactive metabolite N-acetyl-p-benzoquinone imine(NAPQI),which depletes cellular glutathione and forms protein adducts on mitochondrial proteins.This leads to mitochondrial oxidative and nitrosative stress,accompanied by activation of c-jun N-terminal kinase(JNK)and its translocation to the mitochondria.This then amplifies the mitochondrial oxidant stress,resulting in translocation of Bax and dynamin related protein 1(Drp1)to the mitochondria,which induces mitochondrial fission,and ultimately induction of the mitochondrial membrane permeability transition(MPT).The induction of MPT triggers release of intermembrane proteins such as apoptosis inducing factor(AIF)and endonuclease G into the cytosol and their translocation to the nucleus,causing nuclear DNA fragmentation and activation of regulated necrosis.Though these cascades of events were primarily identified in the mouse model,studies on human hepatocytes and analysis of circulating biomarkers from patients after APAP overdose,indicate that a number of mechanistic events are identical in mice and humans.Circulating biomarkers also seem to be useful in predicting the course of liver injury after APAP overdose in humans and hold promise for significant clinical use in the near future.Relevance for patients:This review focuses on the mechanisms behind APAP-induced hepatotoxicity and the relevance of these to the human pathophysiology.Current investigations on various biomarkers which may be useful in clinical management of APAP overdose patients are also discussed. | Anup Ramachandran Hartmut Jaeschke | 2017 | Journal of Clinical & Translational Research2017，3，1： | 6 |
| 16 | High frequency of the c.3207C>A (p.H1069Q) mutation in ATP7B gene of Lithuanian patients with hepatic presentation of Wilson's disease显示文摘AIM: To investigate the prevalence of the ATP7B gene mutation in patients with hepatic presentation of Wilson's disease (WD) in Lithuania. METHODS: Eleven unrelated Lithuanian families, including 13 WD patients were tested. Clinically WD diagnosis was established in accordance to the Leipzig scoring system. Genomic DNA was extracted fromwhole venous blood using a salt precipitation method. Firstly, the semi-nested polymerase chain reaction (PCR) technique was used to detect the c.3207C>A (p.H1069Q) mutation. Patients not homozygous for the c.3207C>A (p.H1069Q) mutation were further analyzed. The 21 exons of the WD gene were amplified in a thermal cycler (Biometra T3 Thermocycler, G?ttingen, Germany). Direct sequencing of the amplified PCR products was performed by cycle sequencing using fluorescent dye terminators in an automatic sequencer (Applied Biosystems, Darmstadt, Germany). RESULTS: Total of 13 WD patients (mean age 26.4 years; range 17-40; male/female 3/10) presented with hepatic disorders and 16 their first degree relatives (including 12 siblings) were studied. Some of WD patients, in addition to hepatic symptoms, have had extrahepatic disorders (hemolytic anemia 3; Fanconi syndrome 1; neurophsychiatric and behavioural disorder 2). Liver biopsy specimens were available in all of 13 WD patients (8 had cirrhosis; 1-chronic hepatitis; 3-acute liver failure, 1-liver steatosis). Twelve of 13 (92.3%) WD patients had the c.3207C>A (p.H1069Q) mutation, 6 of them in both chromosomes, 6 were presented as compound heterozygotes with additional c.3472-82delGGTTTAACCAT, c.3402delC, c.3121C>T (p.R1041W) or unknown mutations. For one patient with liver cirrhosis and psychiatric disorder (Leipzig score 6), no mutations were found. Out of 16 first degree WD relatives, 11 (68.7%) were heterozygous for the c.3207C>A (p.H1069Q) mutation. Two patients with fulminant WD died from acute liver failure and 11 are in full remission under penicillamine or zinc acetate treatment. Three women with WD successfully delivered healthy babies. CONCLUSION: The c.3207C>A (p.H1069Q) missense mutation is the most characteristic mutation for Lithuanian patients with WD. Even 92.3% of WD patients with hepatic presentation of the disease are homozygous or compound heterozygotes for the p.H1069Q mutation. | Laimutis Kucinskas Jolanta Jeroch Astra Vitkauskiene Raimundas Sakalauskas Vitalija Petrenkiene Vaidutis Kucinskas Rima Naginiene Hartmut Schmidt Limas Kupcinskas | 2008 | World Journal of Gastroenterology2008，14，38： | 5 |
| 17 | 银杏内生菌Chaetomium globosum ZY-22次生代谢产物分离鉴定(英文)显示文摘采用柱层析方法从银杏叶内生真菌Chaetomium globosum ZY-22的培养菌丝体提取物中分离得到脑苷脂B(1)、脑苷脂C(2)、尿囊素(3)、9(11)-去氢麦角甾醇过氧化物(4)以及4,6,8,22-四烯-3-酮-麦角甾烷(5)和球毛壳甲素(6)共6个次生代谢物;经波谱分析确定了6个化合物的结构,其中脑苷脂B、脑苷脂C和尿囊素是首次从内生真菌中得到;海虾致死试验结果显示,化合物1~6在10μg/mL浓度下对丰年虾的致死率分别为1.6%、4.2%、7.4%、16.9%、12.8%、83.6%、表明球毛壳甲素对海虾表现出很强的毒性作用. | 秦建春 白莉 李晓明 张雅梅 高锦明 Hartmut laatsch | 2009 | 西北植物学报2009，29，6： | 5 |
| 18 | 跟骨关节内骨折——手术治疗显示文摘这些研究没有证明何种方法是治疗跟骨关节内移位骨折的最佳手术方法。应该对比较性临床研究进行探讨,尤其是不同治疗方法与潜在的风险因素如骨折类型的相关性。 | Tim Pohlemann David Ring Hartmut R.Siebert 陈国奋 顾立强 | 2004 | 中华创伤骨科杂志2004，6，8： | 5 |
| 19 | Mechanisms of reperfusion injury after warm ischemia of the liver显示文摘 | Hartmut Jaeschke | 1998 | Journal of Hepato - Biliary - Pancreatic Surgery1998，，4： | 4 |
| 20 | Analysis of the Vibrissa Parametric Resonance Causing a Signal Amplification during Whisking Behaviour显示文摘 | Tatiana Volkova Igor Zeidis Hartmut Witte Manuela Schmidt Klaus Zimmermann | 2016 | Journal of Bionic Engineering2016，13，2： | 4 |
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