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  • 1
    Electronic Resource
    Electronic Resource
    Abnormal innervation of lower limb epineurial arterioles in human diabetes (1981)
    Springer
    Diabetologia 20 (1981), S. 31-38 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic vascular disease ; diabetes mellitus ; diabetic autonomie neuropathy ; vasomotor nerves ; arterioles ; morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A quantitative ultrastructural analysis was made of the terminal innervation of epineurial arterioles in the sural nerve of 6 diabetic and 6 nondiabetic patients of comparable age (mean±SD: 68 ±9 non-diabetic, 65±16 diabetic) with end stage peripheral vascular disease. The results demonstrated specific differences, identifiable morphometrically, in the pattern of innervation of epineurial vessels of diabetics compared with non-diabetics. The differences were: 1) in the diabetic group the proportion of perivascular axons found less than 7 μm from the nearest smooth muscle cell was significantly less than in the non-diabetic group (p 〈0.001); 2), the mean distance of the axons from their effector sites, the vascular smooth muscle cells, was nearly twice as far in the diabetic group compared with the nondiabetic group (p 〈0.05); and 3) the mean absolute number of axons less than 7 μ from the arteriole in the diabetic group was significantly less than in the non-diabetic group (p 〈0.01). These results demonstrate that the neuropathy associated with diabetes mellitus also involves the autonomic terminal innervation of some blood vessels. In addition, this neuropathy selectively affects the vasomotor nerves closer than 7 μm to the media.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00253813
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Abnormal innervation of lower limb epineurial arterioles in human diabetes (1981)
    Springer
    Diabetologia 21 (1981), S. 31-38 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic vascular disease ; diabetes mellitus ; diabetic autonomic neuropathy ; vasomotor nerves ; arterioles ; morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A quantitative ultrastructural analysis was made of the terminal innervation of epineurial arterioles in the sural nerve of 6 diabetic and 6 nondiabetic patients of comparable age (mean ± SD: 68 ±9 non-diabetic, 65±16 diabetic) with end stage peripheral vascular disease. The results demonstrated specific differences, identifiable morphometrically, in the pattern of innervation of epineurial vessels of diabetics compared with non-diabetics. The differences were: 1) in the diabetic group the proportion of perivascular axons found less than 7 μm from the nearest smooth muscle cell was significantly less than in the non-diabetic group (p〈0.001); 2) the mean distance of the axons from their effector sites, the vascular smooth muscle cells, was nearly twice as far in the diabetic group compared with the nondiabetic group (p〈0.05); and 3) the mean absolute number of axons less than 7 μm from the arteriole in the diabetic group was significantly less than in the non-diabetic group (p〈0.01). These results demonstrate that the neuropathy associated with diabetes mellitus also involves the autonomic terminal innervation of some blood vessels. In addition, this neuropathy selectively affects the vasomotor nerves closer than 7 μm to the media.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01789110
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    Paper (German National Licenses)
    Fulltext
  • 3
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    Nuclear receptor liver receptor homologue 1 (LRH-1) regulates pancreatic cancer cell growth and proliferation [Applied Biological Sciences] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-10-12
    Description: An essential regulator of gene transcription, nuclear receptor liver receptor homologue 1 (LRH-1) controls cell differentiation in the developing pancreas and maintains cholesterol homeostasis in adults. Recent genome-wide association studies linked mutations in the LRH-1 gene and its up-stream regulatory regions to development of pancreatic cancer. In this work, we show that LRH-1 transcription is activated up to 30-fold in human pancreatic cancer cells compared to normal pancreatic ductal epithelium. This activation correlates with markedly increased LRH-1 protein expression in human pancreatic ductal adenocarcinomas in vivo. Selective blocking of LRH-1 by receptor specific siRNA significantly inhibits pancreatic cancer cell proliferation in vitro. The inhibition is tracked in part to the attenuation of the receptor’s transcriptional targets controlling cell growth, proliferation, and differentiation. Previously, LRH-1 was shown to contribute to formation of intestinal tumors. This study demonstrates the critical involvement of LRH-1 in development and progression of pancreatic cancer, suggesting the LRH-1 receptor as a plausible therapeutic target for treatment of pancreatic ductal adenocarcinomas.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Clinical whole-genome sequencing in severe early-onset epilepsy reveals new genes and improves molecular diagnosis (2014)
    Oxford University Press
    Details
    Publication Date: 2014-05-23
    Description: In severe early-onset epilepsy, precise clinical and molecular genetic diagnosis is complex, as many metabolic and electro-physiological processes have been implicated in disease causation. The clinical phenotypes share many features such as complex seizure types and developmental delay. Molecular diagnosis has historically been confined to sequential testing of candidate genes known to be associated with specific sub-phenotypes, but the diagnostic yield of this approach can be low. We conducted whole-genome sequencing (WGS) on six patients with severe early-onset epilepsy who had previously been refractory to molecular diagnosis, and their parents. Four of these patients had a clinical diagnosis of Ohtahara Syndrome (OS) and two patients had severe non-syndromic early-onset epilepsy (NSEOE). In two OS cases, we found de novo non-synonymous mutations in the genes KCNQ2 and SCN2A. In a third OS case, WGS revealed paternal isodisomy for chromosome 9, leading to identification of the causal homozygous missense variant in KCNT1 , which produced a substantial increase in potassium channel current. The fourth OS patient had a recessive mutation in PIGQ that led to exon skipping and defective glycophosphatidyl inositol biosynthesis. The two patients with NSEOE had likely pathogenic de novo mutations in CBL and CSNK1G1 , respectively. Mutations in these genes were not found among 500 additional individuals with epilepsy. This work reveals two novel genes for OS, KCNT1 and PIGQ . It also uncovers unexpected genetic mechanisms and emphasizes the power of WGS as a clinical tool for making molecular diagnoses, particularly for highly heterogeneous disorders.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 5
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    Global Protease Activity Profiling Provides Differential Diagnosis of Pancreatic Cysts (2017)
    The American Association for Cancer Research (AACR)
    Details
    Publication Date: 2017-08-16
    Description: Purpose: Pancreatic cysts are estimated to be present in 2%–3% of the adult population. Unfortunately, current diagnostics do not accurately distinguish benign cysts from those that can progress into invasive cancer. Misregulated pericellular proteolysis is a hallmark of malignancy, and therefore, we used a global approach to discover protease activities that differentiate benign nonmucinous cysts from premalignant mucinous cysts. Experimental Design: We employed an unbiased and global protease profiling approach to discover protease activities in 23 cyst fluid samples. The distinguishing activities of select proteases was confirmed in 110 samples using specific fluorogenic substrates and required less than 5 μL of cyst fluid. Results: We determined that the activities of the aspartyl proteases gastricsin and cathepsin E are highly increased in fluid from mucinous cysts. IHC analysis revealed that gastricsin expression was associated with regions of low-grade dysplasia, whereas cathepsin E expression was independent of dysplasia grade. Gastricsin activity differentiated mucinous from nonmucinous cysts with a specificity of 100% and a sensitivity of 93%, whereas cathepsin E activity was 92% specific and 70% sensitive. Gastricsin significantly outperformed the most widely used molecular biomarker, carcinoembryonic antigen (CEA), which demonstrated 94% specificity and 65% sensitivity. Combined analysis of gastricsin and CEA resulted in a near perfect classifier with 100% specificity and 98% sensitivity. Conclusions: Quantitation of gastricsin and cathepsin E activities accurately distinguished mucinous from nonmucinous pancreatic cysts and has the potential to replace current diagnostics for analysis of these highly prevalent lesions. Clin Cancer Res; 23(16); 4865–74. ©2017 AACR .
    Print ISSN: 1078-0432
    Electronic ISSN: 1557-3265
    Topics: Medicine
    Published by The American Association for Cancer Research (AACR)
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  • 6
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    Clinical Outcomes of Carotid Endarterectomy in Patients With Carotid Artery Tandem Lesions [Brief Reports] (2014)
    American Heart Association (AHA)
    In: Stroke
    Details
    Publication Date: 2014-10-28
    Description: Background and Purpose— When carotid artery tandem lesions are present, the benefits of carotid endarterectomy (CEA) to reduce recurrent stroke remain uncertain. The present retrospective cohort study aimed to determine the clinical outcomes of CEA for carotid artery tandem stenosis that was diagnosed by contrast-enhanced magnetic resonance angiography. Methods— Six hundred forty-seven consecutive patients underwent CEA between January 2001 and December 2010. Tandem stenosis, defined as a significant carotid bifurcation stenosis and identifiable stenosis of ≥50% of any downstream distal cerebral artery, was identified in 92 patients (14.2%) by contrast-enhanced magnetic resonance angiography. Patients with and without tandem stenosis were compared in terms of CEA outcomes. The primary end point was the composite of any stroke, myocardial infarction, or death during the periprocedural period or ipsilateral stroke within 4 years after CEA. Results— Tandem stenosis did not associate with ipsilateral stroke during postoperative follow-up. The 2 groups did not differ in terms of estimated 4-year primary end point rates (8.7% versus 3.8%; P =0.07) or ipsilateral stroke-free ( P =0.56), any stroke-free ( P =0.89), or overall survival ( P =0.41) rates. Conclusions— After diagnosis by contrast-enhanced magnetic resonance angiography, patients with and without tandem stenosis had similar rates of stroke and death.
    Keywords: Carotid endarterectomy
    Print ISSN: 0039-2499
    Electronic ISSN: 1524-4628
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 7
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    LKB1 deletion causes early changes in atrial channel expression and electrophysiology prior to atrial fibrillation (2015)
    Oxford University Press
    Details
    Publication Date: 2015-09-17
    Description: Aims Liver kinase B1 (LKB1) is a protein kinase that activates the metabolic regulator AMP-activated protein kinase (AMPK) and other related kinases. Deletion of LKB1 in mice leads to cardiomyopathy and atrial fibrillation (AF). However, the specific role of the LKB1 pathway in early atrial biology remains unknown. Thus, we investigated whether LKB1 deletion altered atrial channel expression and electrophysiological function in a cardiomyocyte-specific knockout mouse model. Methods and results We performed a systematic comparison of αMHC-Cre LKB1 fl/fl and littermate LKB1 fl/fl male mice. This included analysis of gene expression, histology, and echocardiography, as well as cellular and tissue-level electrophysiology using patch-clamp recordings in vitro , optical mapping ex vivo , and ECG recordings in vivo . At postnatal day 1, atrial depolarization was prolonged, and Na v 1.5 and Cx40 expression were markedly down-regulated in MHC-Cre LKB1 fl/fl mice. Inward sodium current density was significantly decreased in MHC-Cre LKB1 fl/fl neonatal atrial myocytes. Subsequently, additional alterations in atrial channel expression, atrial fibrosis, and spontaneous onset of AF developed by 2 weeks of age. In adult mice, abnormalities of interatrial conduction and bi-atrial electrical coupling were observed, likely promoting the perpetuation of AF. Mice with AMPK-inactivated hearts demonstrated modest overlap in channel expression with MHC-Cre LKB1 fl/fl hearts, but retained normal structure, electrophysiological function and contractility. Conclusions Deletion of LKB1 causes early defects in atrial channel expression, action potential generation and conduction, which precede widespread atrial remodelling, fibrosis and AF. LKB1 is critical for normal atrial growth and electrophysiological function.
    Print ISSN: 0008-6363
    Electronic ISSN: 1755-3245
    Topics: Medicine
    Published by Oxford University Press
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  • 8
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    A Drosophila LexA Enhancer-Trap Resource for Developmental Biology and Neuroendocrine Research (2016)
    Genetics Society of America (GSA)
    Details
    Publication Date: 2016-10-14
    Description: Novel binary gene expression tools like the LexA-LexAop system could powerfully enhance studies of metabolism, development, and neurobiology in Drosophila . However, specific LexA drivers for neuroendocrine cells and many other developmentally relevant systems remain limited. In a unique high school biology course, we generated a LexA-based enhancer trap collection by transposon mobilization. The initial collection provides a source of novel LexA-based elements that permit targeted gene expression in the corpora cardiaca, cells central for metabolic homeostasis, and other neuroendocrine cell types. The collection further contains specific LexA drivers for stem cells and other enteric cells in the gut, and other developmentally relevant tissue types. We provide detailed analysis of nearly 100 new LexA lines, including molecular mapping of insertions, description of enhancer-driven reporter expression in larval tissues, and adult neuroendocrine cells, comparison with established enhancer trap collections and tissue specific RNAseq. Generation of this open-resource LexA collection facilitates neuroendocrine and developmental biology investigations, and shows how empowering secondary school science can achieve research and educational goals.
    Electronic ISSN: 2160-1836
    Topics: Biology
    Published by Genetics Society of America (GSA)
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  • 9
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    Tumor-related leukocytosis is associated with poor radiation response and clinical outcome in uterine cervical cancer patients (2016)
    Oxford University Press
    Details
    Publication Date: 2016-10-29
    Description: Background To evaluate response to radiation and clinical outcome of uterine cervical cancer patients with tumor-related leukocytosis (TRL) at initial diagnosis and during definitive radiotherapy. Patients and methods We retrospectively analyzed 2456 patients with stage IA–IVA uterine cervical cancer who received definitive radiotherapy with (37.4%) or without (62.6%) platinum-based chemotherapy between 1986 and 2012. TRL was defined as two or more occurrences of leukocytosis over 9000/μl at the time of diagnosis and during the course of treatment. Locoregional failure-free survival (LFFS) and overall survival (OS) were compared between patients with or without TRL. Results The median age of all patients was 55 years, and the median follow-up time was 65.1 months. TRL was observed in 398 patients (16%) at initial diagnosis; TRL (+) patients were younger and had larger tumors, advanced stage, and more frequent lymph node metastases (all P 〈 0.05). TRL (+) patients showed a significantly lower rate of complete remission than TRL (–) patients (89.9% versus 96.3%, respectively, P = 0.042). Ten-year LFFS and OS for all patients were 84% and 78%, respectively. LFFS and OS were significantly lower in TRL (+) patients than TRL (–) patients (10-year LFFS: 69% versus 87% respectively, P 〈 0.001; 10-year OS: 63% versus 81% respectively P 〈 0.001). After propensity score matching, LFFS and OS rates in TRL (+) patients remained significantly lower than for TRL (–) patients; this significant difference was also observed on multivariate analysis. Twenty-six percent of patients with locoregional failure ( n = 345) were TRL (+) and had significantly poorer median OS (6 versus 12 months, P = 0.001). Conclusion This study reveals the aggressive nature of cervical cancer with TRL and its poor response to radiation therapy. Given the unfavorable prognosis and higher probability of treatment failure, optimal diagnostic and therapeutic approaches and careful monitoring for early detection of recurrence should be considered for these patients.
    Print ISSN: 0923-7534
    Electronic ISSN: 1569-8041
    Topics: Medicine
    Published by Oxford University Press
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  • 10
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    Attenuation of natural killer cell functions by capsaicin through a direct and TRPV1-independent mechanism (2014)
    Oxford University Press
    Details
    Publication Date: 2014-07-02
    Description: The assessment of the biological activity of capsaicin, the compound responsible for the spicy flavor of chili pepper, produced controversial results, showing either carcinogenicity or cancer prevention. The innate immune system plays a pivotal role in cancer pathology and prevention; yet, the effect of capsaicin on natural killer (NK) cells, which function in cancer surveillance, is unclear. This study found that capsaicin inhibited NK cell-mediated cytotoxicity and cytokine production (interferon- and tumor necrosis factor-α). Capsaicin impaired the cytotoxicity of NK cells, thereby inhibiting lysis of standard target cells and gastric cancer cells by modulating calcium mobilization in NK cells. Capsaicin also induced apoptosis in gastric cancer cells, but that effect required higher concentrations and longer exposure times than those required to trigger NK cell dysfunction. Furthermore, capsaicin inhibited the cytotoxicity of isolated NK cells and of an NK cell line, suggesting a direct effect on NK cells. Antagonists of transient receptor potential vanilloid subfamily member 1 (TRPV1), a cognate capsaicin receptor, or deficiency in TRPV1 expression failed to prevent the defects induced by capsaicin in NK cells expressing functional TRPV1. Thus, the mechanism of action of capsaicin on NK cells is largely independent of TRPV1. Taken together, capsaicin may have chemotherapeutic potential but may impair NK cell function, which plays a central role in tumor surveillance.
    Print ISSN: 0143-3334
    Electronic ISSN: 1460-2180
    Topics: Medicine
    Published by Oxford University Press
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