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| 1 | Impaired contractility and remodeling of the upper gastrointestinal tract in diabetes mellitus type-1显示文摘AIM: To investigate that both the neuronal function of the contractile system and structural apparatus of the gastrointestinal tract are affected in patients with longstanding diabetes and auto mic neuropathy. METHODS: The evoked esophageal and duodenal contractile activity to standardized bag distension was assessed using a specialized ultrasound-based probe. Twelve type-1 diabetic patients with autonomic neuropathy and severe gastrointestinal symptoms and 12 healthy controls were studied. The geometry and biomechanical parameters (strain, tension/stress, and stiffness) were assessed. RESULTS: The diabetic patients had increased frequency of distension-induced contractions (6.0 ± 0.6 vs 3.3 ± 0.5, P < 0.001). This increased reactivity was correlated with the duration of the disease (P = 0.009). Impaired coordination of the contractile activity in diabetic patients was demonstrated as imbalance between the time required to evoke the first contraction at the distension site and proximal to it (1.5 ± 0.6 vs 0.5 ± 0.1, P = 0.03). The esophageal wall and especially the mucosa-submucosa layer had increased thickness in the patients (P < 0.001), and the longitudinal and radial compressive stretch was less in diabetics (P <0.001). The esophageal and duodenal wall stiffness and circumferential deformation induced by the distensions were not affected in the patients (all P > 0.14). CONCLUSION: The impaired contractile activity with an imbalance in the distension-induced contractions likely reflects neuronal abnormalities due to autonomic neuropathy. However, structural changes and remodeling of the gastrointestinal tract are also evident and may add to the neuronal changes. This may contribute to the pathophysiology of diabetic gut dysfunction and impact on future management of diabetic patients with gastrointestinal symptoms. | Jens BrΦndum FrΦkjΦr SΦren Due Andersen Niels EjskjΦr Peter Funch-Jensen AsbjΦrn Mohr Drewes Hans Gregersen | 2007 | World Journal of Gastroenterology2007,13,36: | 8 |
| 2 | Systematic mechanism-orientated approach to chronic pancreatitis pain显示文摘Pain in chronic pancreatitis(CP) shows similarities with other visceral pain syndromes(i.e.,inflammatory bowel disease and esophagitis),which should thus be managed in a similar fashion.Typical causes of CP pain include increased intrapancreatic pressure,pancreatic inflammation and pancreatic/extrapancreatic complications.Unfortunately,CP pain continues to be a major clinical challenge.It is recognized that ongoing pain may induce altered central pain processing,e.g.,central sensitization or pro-nociceptive pain modulation.When this is present conventional pain treatment targeting the nociceptive focus,e.g.,opioid analgesia or surgical/endoscopic intervention,often fails even if technically successful.If central nervous system pain processing is altered,specific treatment targeting these changes should be instituted(e.g.,gabapentinoids,ketamine or tricyclic antidepressants).Suitable tools are now available to make altered central processing visible,including quantitative sensory testing,electroencephalograpy and(functional) magnetic resonance imaging.These techniques are potentially clinically useful diagnostic tools to analyze central pain processing and thus define optimum management approaches for pain in CP and other visceral pain syndromes.The present review proposes a systematic mechanism-orientated approach to pain management in CP based on a holistic view of the mechanisms involved.Future research should address the circumstances under which central nervous system pain processing changes in CP,and how this is influenced by ongoing nociceptive input and therapies.Thus we hope to predict which patients are at risk for developing chronic pain or not responding to therapy,leading to improved treatment of chronic pain in CP and other visceral pain disorders. | Stefan AW Bouwense Marjan de Vries Luuk TW Schreuder Soren S Olesen Jens B Frokjær Asbjorn M Drewes Harry van Goor Oliver HG Wilder-Smith | 2015 | World Journal of Gastroenterology2015,21,1: | 6 |
| 3 | Pain and chronic pancreatitis: A complex interplay of multiple mechanisms显示文摘Despite multiple theories on the pathogenesis of pain in chronic pancreatitis,no uniform and consistently successful treatment strategy exists and abdominal pain still remains the dominating symptom for most patients and a major challenge for clinicians.Traditional theories focussed on a mechanical cause of pain related to anatomical changes and evidence of increased ductal and interstitial pressures.These observations form the basis for surgical and endoscopic drainage procedures,but the outcome is variable and often unsatisfactory.This underscores the fact that other factors must contribute to pathogenesis of pain,and has shifted the focus towards a more complex neurobiological understanding of pain generation.Amongst other explanations for pain,experimental and human studies have provided evidence that pain perception at the peripheral level and central pain processing of the nociceptive information is altered in patients with chronic pancreatitis,and resembles that seen in neuropathic and chronic pain disorders.However,pain due to e.g.,complications to the disease and adverse effects to treatment must not be overlooked as an additional source of pain.This review outlines the current theories on pain generation in chronic pancreatitis which is crucial in order to understand the complexity and limitations of current therapeutic approaches.Furthermore,it may also serve as an inspiration for further research and development of methods that can evaluate the relative contribution and interplay of different pain mechanisms in the individual patients,before they are subjected to more or less empirical treatment. | Jakob Lykke Poulsen Sφren Schou Olesen Lasse Paludan Malver Jens Brφndum Frφkjr Asbjφrn Mohr Drewes | 2013 | World Journal of Gastroenterology2013,19,42: | 5 |
| 4 | Nutrition in chronic pancreatitis显示文摘The pancreas is a major player in nutrient digestion.In chronic pancreatitis both exocrine and endocrine insufficiency may develop leading to malnutrition over time.Maldigestion is often a late complication of chronic pancreatic and depends on the severity of the underlying disease.The severity of malnutrition is correlated with two major factors:(1)malabsorption and depletion of nutrients(e.g.,alcoholism and pain)causes impaired nutritional status;and(2)increased metabolic activity due to the severity of the disease.Nutritional deficiencies negatively affect outcome if they are not treated.Nutritional assessment and the clinical severity of the disease are important for planning any nutritional intervention.Good nutritional practice includes screening to identify patients at risk,followed by a thoroughly nutritional assessment and nutrition plan for risk patients.Treatment should be multidisciplinary and the mainstay of treatment is abstinence from alcohol,pain treatment,dietary modifications and pancreatic enzyme supplementation.To achieve energy-end protein requirements,oral supplementation might be beneficial.Enteral nutrition may be used when patients do not have sufficient calorie intake as in pylero-duodenalstenosis,inflammation or prior to surgery and can be necessary if weight loss continues.Parenteral nutrition is very seldom used in patients with chronic pancreatitis and should only be used in case of GI-tract obstruction or as a supplement to enteral nutrition. | Henrik Hφjgaard Rasmussen φivind Irtun Sφren Schou Olesen Asbjφrn Mohr Drewes Mette Holst | 2013 | World Journal of Gastroenterology2013,19,42: | 4 |
| 5 | Brain changes in diabetes mellitus patients withgastrointestinal symptoms显示文摘Diabetes mellitus is a common disease and its prevalence is increasing worldwide. In various studies up to 30%-70% of patients present dysfunction and complications related to the gut. To date several clinical studies have demonstrated that autonomic nervous system neuropathy and generalized neuropathy of the central nervous system(CNS) may play a major role. This systematic review provides an overview of the neurodegenerative changes that occur as a consequence of diabetes with a focus on the CNS changes and gastrointestinal(GI) dysfunction. Animal models where diabetes was induced experimentally support that the disease induces changes in CNS. Recent investigations with electroencephalography and functional brain imaging in patients with diabetes confirm these structural and functional brain changes. Encephalographic studies demonstrated that altered insular processing of sensory stimuli seems to be a key player in symptom generation. In fact one study indicated that the more GI symptoms the patients experienced, the deeper the insular electrical source was located. The electroencephalography was often used in combination with quantitative sensory testingmainly showing hyposensitivity to stimulation of GI organs. Imaging studies on patients with diabetes and GI symptoms mainly showed microstructural changes,especially in brain areas involved in visceral sensory processing. As the electrophysiological and imaging changes were associated with GI and autonomic symptoms they may represent a future therapeutic target for treating diabetics either pharmacologically or with neuromodulation. | Anne M Drewes Eirik Søfteland Georg Dimcevski Adam D Farmer Christina Brock Jens B Frøkjær Klaus Krogh Asbjørn M Drewes | 2016 | World Journal of Diabetes2016,7,2: | 4 |
| 6 | Titanium-based composites produced by powder metallurgy 显示文摘 | Wanjara P Yue S Drew R A L | 1997 | Key Eng Mater1997,,: | 2 |
| 7 | Tissue inhibitor of metalloproteinase-2(TIMP-2)binds to the catalytic domain of the cell surface receptor,membrane type-1 matrix metalloproteinase 1(MT-MMP) 显示文摘 | Zucker S Drews M Conner C | 1998 | J Biol Chem1998,273,: | 1 |
| 8 | Multiple paternity in a natural population of a wild tobacco fly, Bactrocera cacuminata (Diptera: Tephritidae), assessed by microsatellite DNA markers 显示文摘 | Song S D Drew R A Hughes J M | 2007 | Molecular Ecology2007,16,11: | 1 |
| 9 | Entropy minimization for shadow removal 显示文摘 | FINLAYSON G D DREW M S LU C | 2009 | International Journal of Computer Vision2009,85,1: | 1 |
| 10 | Tatanium based composites produced by powder metallurgy显示文摘 | Wanjara P Yue S Drew R A L | 1997 | Key Eng Mater1997,,: | 1 |
| 11 | Homologous recombination deficiency and ovarian cancer 显示文摘 | Ledermann J A Drew Y Kristeleit R S | 2016 | Eur J Cancer2016,60,: | 1 |
| 12 | Deriving spectra from colors and rendering light interference 显示文摘 | Sun Y Fracehia F D Calvert T W Drew M S | 1999 | IEEE Computer Graphics and Applications1999,19,4: | 1 |
| 13 | Microvessel density of invasive breast cancer assessed by dynamic Gd-DTPA enhanced MRI显示文摘 | Buckley DL Drew PJ Mussurakis S | 1997 | J Magn Reson Imaging1997,7,3: | 1 |
| 14 | Recent advances in membrane bioreactors (MBRs) : Membrane fouling and membrane material 显示文摘 | MEN(X-F G CHAE S R DREWS A | 2009 | Water Research2009,43,6: | 1 |
| 15 | Fate of antibiotics during municipal water recycling treatment processes显示文摘 | Le-Minh N Khan S J Drewes J E | 2010 | Water Res2010,44,15: | 1 |
| 16 | Fibrino- gen is an important determinant of the metastatie potential of circu- lating tumor cells显示文摘 | PALUMBO J S KOMBRINCK K W DREW A F | 2000 | Blood2000,96,10: | 1 |
| 17 | Tissue inhibitor of metalloproteinase 2 (TIMP-2) binds to the catalytic domain of the cell surface receptor, membrane type 1-matrix metalio proteinase 1 (MT1 MMP)显示文摘 | ZUCKER S DREWS M CONNER C | 1998 | Biol Chem1998,273,2: | 1 |
| 18 | Fate of antibiotics during municipal water recycling treatment processes 显示文摘 | Le-Minh N Khan S J Drewes J E | 2010 | Water Research2010,44,15: | 1 |
| 19 | Methylated A-type proanthoc- vanidins and related metabolites from Cassipourea gummi- flua 显示文摘 | Drewes S E Taylor C W | 1994 | Phytochemistry1994,37,2: | 1 |
| 20 | Comparison of Sensititre microdilutionmethod to other standard methods for susceptibility testing of coagulase-negative staphylococci from paediatric blood cultures 显示文摘 | Drew RJ Paulus S | 2014 | Diagnostic Microbiology and Infectious Disease2014,78,3: | 1 |