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| 1 | Birth defects in pregestational diabetes:Defect range,glycemic threshold and pathogenesis显示文摘Currently,60 million women of reproductive age(18-44 years old) worldwide,and approximately 3 million American women have diabetes mellitus,and it has been estimated that this number will double by 2030.Pregestational diabetes mellitus(PGD) is a significant public health problem that increases the risk for structural birth defects affecting both maternal and neonatal pregnancy outcome.The most common types of human structural birth defects associated with PGD are congenital heart defects and central nervous system defects.However,diabetes can induce birth defects in any other fetal organ.In general,the rate of birth defects increases linearly with the degree of maternal hyperglycemia,which is the major factor that mediates teratogenicity of PGD.Stringent prenatal care and glycemic control are effective means to reduce birth defects in PGD pregnancies,but cannot reduce the incidence of birth defects to the rate of that is seen in the nondiabetic population.Studies in animal models have revealed that PGD induces oxidative stress,which activates cellular stress signalling leading to dysregulation of gene expression and excess apoptosis in the target organs,including the neural tube and embryonic heart.Activation of the apoptosis signalregulating kinase 1(ASK1)-forkhead transcription factor 3a(Fox O3a)-caspase 8 pathway causes apoptosis in the developing neural tube leading to neural tube defects(NTDs).ASK1 activates the c-Jun-N-Terminal kinase 1/2(JNK1/2),which leads to activation of the unfolded protein response and endoplasmic reticulum(ER) stress.Deletion of the ASK1 gene,the JNK1 gene,or the JNK2 gene,or inhibition of ER stress by 4-Phenylbutyric acid abrogates diabetes-induced apoptosis and reduces the formation of NTDs.Antioxidants,such as thioredoxin,which inhibits the ASK1-Fox O3a-caspase 8 pathway or ER stress inhibitors,may prevent PGD-induced birth defects. | Rinat Gabbay-Benziv E Albert Reece Fang Wang Peixin Yang | 2015 | World Journal of Diabetes2015，6，3： | 10 |
| 2 | Acinar cell injury induced by inadequate unfolded protein response in acute pancreatitis显示文摘Acute pancreatitis (AP) is an inflammatory disorder of pancreatic tissue initiated in injured acinar cells. Severe AP remains a significant challenge due to the lack of effective treatment. The widely-accepted autodigestion theory of AP is now facing challenges, since inhibiting protease activation has negligible effectiveness for AP treatment despite numerous efforts. Furthermore, accumulating evidence supports a new concept that malfunction of a self-protective mechanism, the unfolded protein response(UPR), is the driving force behind the pathogenesis of AP. The UPR is induced by endoplasmic reticulum(ER) stress, a disturbance frequently found in acinar cells, to prevent the aggravation of ER stress that can otherwise lead to cell injury. In addition, the UPR's signaling pathways control NFκB activation and autophagy flux, and these dysregulations cause acinar cell inflammatory injury in AP, but with poorly understood mechanisms. We therefore summarize the protective role of the UPR in AP, propose mechanistic models of how inadequate UPR could promote NFκB's pro-inflammatory activity and impair autophagy's protective function in acinar cells, and discuss its relevance to current AP treatment. We hope that insight provided in this review will help facilitate the research and management of AP. | Kaylene Barrera Albert Stanek Kei Okochi Zuzanna Niewiadomska Cathy Mueller Peiqi Ou Devon John Antonio E Alfonso Scott Tenner Chongmin Huan | 2018 | World Journal of Gastrointestinal Pathophysiology2018，9，2： | 9 |
| 3 | Acute pancreatitis in aging animals:Loss of pancreatitis-associated protein protection?显示文摘AIM:To investigate the effect of age on severity of acute pancreatitis(AP) using biochemical markers,histology and expression of the protective pancreatitisassociated proteins(PAPs).METHODS:AP was induced via intraductal injection of 4% sodium taurocholate in young and old rats.Sera and pancreata were assayed at 24 h for the parameters listed above;we also employed a novel molecular technique to assess bacterial infiltration using polymerase chain reaction to measure bacterial genomic ribosomal RNA.RESULTS:At 24 h after induction of AP,the pancreata of older animals had less edema(mean ± SE histologic score of young vs old:3.11 ± 0.16 vs 2.50 ±-0.11,P < 0.05),decreased local inflammatory response(histologic score of stromal infiltrate:3.11 ± 0.27 vs 2.00 ± 0.17,P < 0.05) and increased bacterial infiltration(174% ± 52% increase from sham vs 377% ± 4%,P < 0.05).A decreased expression of PAP1 and PAP2 was demonstrated by Western blotting analysis and immunohistochemical staining.There were no differences in serum amylase and lipase activity,or tissue myeloperoxidase or monocyte chemotactic protein-1 levels.However,in the most-aged group,serum C-reactive protein levels were higher(young vs old:0.249 ± 0.04 mg/dL vs 2.45 ± 0.68 mg/dL,P < 0.05).CONCLUSION:In older animals,there is depressed PAP expression related to a blunted inflammatory response in AP which is associated with worsened bacterial infiltration and higher C-reactive protein level;this may explain the more aggressive clinical course. | Sophia Fu Albert Stanek Cathy M Mueller Nefertti A Brown Chongmin Huan Martin H Bluth Michael E Zenilman | 2012 | World Journal of Gastroenterology2012，18，26： | 5 |
| 4 | 用Agilent G1888顶空进样器/6890N气相色谱/5975inert MSD检测系统测定药品中的残留溶剂显示文摘用配置AgilentG1888顶空进样器(HS)和安捷伦5975inert质谱检测器(MSD)的安捷伦6890N气相色谱系统(GC)检测药品中受法规限制的残留溶剂。标准样品混合物的水溶液配制成接近或低于发表的允许溶剂残留水平的不同浓度以评价系统性能。本文的分析包括了国际协调委员会(ICH)指南(包含美国药典方法467中列出的溶剂)中一类和二类溶剂。MSD进行同步选择离子检测/全扫描模式采集选择离子检测与全全扫描的数据,从而对各个被测成组分别进行鉴定与定量。测定了27种不同溶剂的方法检出限。 | Roger L Firor Albert E Gudat | 2005 | 卫生研究2005，34，5： | 4 |
| 5 | Pancreaticβ-cell dysfunction in type 2 diabetes:Implications of inflammation and oxidative stress显示文摘Insulin resistance and pancreaticβ-cell dysfunction are major pathological mechanisms implicated in the development and progression of type 2 diabetes(T2D).Beyond the detrimental effects of insulin resistance,inflammation and oxidative stress have emerged as critical features of T2D that defineβ-cell dysfunction.Predominant markers of inflammation such as C-reactive protein,tumor necrosis factor alpha,and interleukin-1βare consistently associated withβ-cell failure in preclinical models and in people with T2D.Similarly,important markers of oxidative stress,such as increased reactive oxygen species and depleted intracellular antioxidants,are consistent with pancreaticβ-cell damage in conditions of T2D.Such effects illustrate a pathological relationship between an abnormal inflammatory response and generation of oxidative stress during the progression of T2D.The current review explores preclinical and clinical research on the pathological implications of inflammation and oxidative stress during the development ofβ-cell dysfunction in T2D.Moreover,important molecular mechanisms and relevant biomarkers involved in this process are discussed to divulge a pathological link between inflammation and oxidative stress duringβ-cell failure in T2D.Underpinning the clinical relevance of the review,a systematic analysis of evidence from randomized controlled trials is covered,on the potential therapeutic effects of some commonly used antidiabetic agents in modulating inflammatory makers to improveβ-cell function. | Phiwayinkosi V Dludla Sihle E Mabhida Khanyisani Ziqubu Bongani B Nkambule Sithandiwe E Mazibuko-Mbeje Sidney Hanser Albert Kotze Basson Carmen Pheiffer Andre Pascal Kengne | 2023 | World Journal of Diabetes2023，14，3： | 2 |
| 6 | Medical complications of surgical treatment of adult spinal deformity and how to avoid them显示文摘 | Baron E M Albert T J | 2006 | Spine2006，31，19： | 1 |
| 7 | Structural Requirements of the Fructan-Lipid Interaction 显示文摘 | Ingrid J V J Albert van kuik Toon H E | 2003 | Biophysical Journal2003，84，： | 1 |
| 8 | Direct continous method for monitoring biofilm infection in a mouse model显示文摘 | Kadurugamuwa JL Sin L Albert E | 2003 | Infec Immun2003，71，2： | 1 |
| 9 | Pancreatic cancer detection with magnetic resonance cholangiopancreatography and endoscopic retrograde cholangiopancreatography:a prospective controlled study显示文摘 | Adamek H E Albert J Breer H | 2000 | Lancet2000，356，9225： | 1 |
| 10 | CO2 separation with polyolefin membrane contactors and dedicated absorption liquids:performances and prospects 显示文摘 | Paul H M Feron Albert E Jansen | 2002 | Separation and Purification Technology2002，27，： | 1 |
| 11 | Runoff and soil losses as affected by corn and soybean tillage systems显示文摘 | F Ghidey E E Alberts | 1998 | Journal of Soil and Water Conservation1998，53，1： | 1 |
| 12 | Directed evolution of ionizing radiation resistance in Escherichia coli 显示文摘 | Harris D R Pollock S V Wood E A Goiffon R J Klingele A J Cabot E L Schackwitz W Martin J Eggington J Durfee T J Middle C M Norton J E Popelars M C Li H Klugman S A Hamilton L L Bane L B Pennacchio L A Albert T J Perna N T Cox M M Battista J R | 2009 | Journal of Bacteriology2009，191，16： | 1 |
| 13 | Acne scarring : A review and current treatment modalities 显示文摘 | Albert E Rivera | 2008 | J of the Ame Acad of Dermatolo- gy2008，59，： | 1 |
| 14 | Nitrogen and Phosphorted by Eroded Soil Aggregates显示文摘 | Alberts E E Moldenhauer W C | 1981 | Soil Sci Soc A m J1981，45，： | 1 |
| 15 | Screening for depression in hemodialysis patients:associations with diagnosos,treatment,and outcomes in the DOPPS显示文摘 | LOPES A A ALBERT J M YOUNG E W | 2004 | Kideney Int2004，66，5： | 1 |
| 16 | Effect of statin therapy on C reactive protein levels: the pravastatin inflammation/CRP evaluation (PRINCE): a randomized trial and cohort study显示文摘 | Albert MA Danielson E Rifai N | 2001 | JAMA2001，286，1： | 1 |
| 17 | Fiber,sex,and colorectal adenoma:results of a pooled analysis显示文摘 | JACOBS E T LANZA E ALBERTS D S | 2006 | Am J Clin Nutr2006，83，2： | 1 |
| 18 | Effect of statin therapy on creative protein levels: the pravastatin inflammation/CRP evaluation (PRINE): a randomizen trial and cohort study 显示文摘 | Albert MA Danielson E Rifai N | 2001 | JAMA2001，286，： | 1 |
| 19 | Randomized trial ofadjuvant intraperitoneal alpha-interferon in stage 111 ovariancancer patients who have no evidence of disease after primarysurgery and chemotherapy:an intergroup study 显示文摘 | Alberts D S Hannigan E V Liu P Y | 2006 | GynecolOncol2006，100，1： | 1 |
| 20 | Nomenclature for factors of the HLA system显示文摘 | Marsh S G E Albert E D Bodmer W F | 2002 | Human Immunology2002，63，12： | 1 |
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