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Find video protocols related to scientific articles indexed in Pubmed.
Fungal "colonisation" is Associated with Increased Mortality in Medical Intensive Care Unit Patients with Liver Cirrhosis.
Mycopathologia
PUBLISHED: 07-20-2014
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Patients with liver cirrhosis are at increased risk for fungal infections. However, distinction of fungal colonisation (FC) and invasive mycoses is difficult. Aim of this study was to analyse the impact of FC on mortality of cirrhotic ICU-patients.
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Invasive mycosis in medical intensive care unit patients with severe alcoholic hepatitis.
Mycopathologia
PUBLISHED: 03-05-2014
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Severe alcoholic hepatitis (AH) has a poor short-term prognosis often caused by infections. However, the incidence of invasive mycosis in patients with AH treated with corticosteroids and its impact still remains unknown.
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Clinical aspects of granulomatosis with polyangiitis affecting the head and neck.
Eur Arch Otorhinolaryngol
PUBLISHED: 02-20-2014
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There are many controversies in head and neck granulomatosis with polyangiitis (HN-GPA). Diagnostic/therapeutic regimens vary due to limited knowledge about the special properties of HN-GPA. 28 patients were diagnosed with GPA accordingly. Anti-neutrophil-cytoplasmatic-antibody (ANCA), anti-peroxidase-antibody (anti-PR3) and biopsies were performed for all patients and set into clinical context. 14 patients had sinonasal symptoms. Otological (n = 8) and laryngeal (n = 2) symptoms were usually associated with complex disease activity. Pulmonary and/or renal impairment was present in 14 patients at the time of diagnosis and developed in a further nine patients within 1 year. 21 patients with systemic disease displayed elevated ANCA/anti-PR3. In contrast, those with persistent isolated HN manifestations (n = 6) lacked auto-antibodies. These patients underwent multiple biopsies to diagnose GPA. Interestingly, five patients without clinical HN manifestations but elevated auto-antibodies were identified by nasal "blind" biopsy. Clinical examination, auto-antibody testing, and histology are effective diagnostic tools in HN-GPA. Histological diagnosis remains the gold standard in patients with persistent isolated head and neck manifestations but missing auto-antibodies. Based on our findings, we suggest early and sufficient systemic therapy for all HN-GPA. Nasal mucosal "blind" biopsy should be performed in patients with elevated auto-antibodies but lacking clinical head and neck manifestations.
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Evaluation of a dosing regimen for continuous vancomycin infusion in critically ill patients: an observational study in intensive care unit patients.
J Crit Care
PUBLISHED: 01-25-2014
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We aimed to evaluate a dosing algorithm for continuous vancomycin administration in intensive care unit patients.
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Rheumatic disorders affecting the head and neck: underestimated diseases.
Rheumatology (Oxford)
PUBLISHED: 08-24-2011
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To describe the clinical manifestations of rheumatic disorders with isolated head and neck (H&N) affection and to introduce a novel diagnostic pathway.
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Using TNF-alpha antagonist adalimumab for treatment for multisystem sarcoidosis: a case study.
Rheumatol. Int.
PUBLISHED: 05-22-2011
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We report the usage of the TNF-alpha antagonist adalimumab in patients with progressive multisystem sarcoidosis. Three patients with multisystem sarcoidosis (MSS) were treated with adalimumab for 12 months. All three patients were quickly responded to adalimumab and experienced a nearly complete regression of the symptoms that lead to an intensive immunosuppression. However, some accompanying symptoms of sarcoidosis, such as splenomegalia, did not respond. One patient suffered 18 months later a new unspecified abdominal lymphadenopathy. TNF-alpha antagonists can be helpful agents in the treatment for MSS. However, the experience with TNF-alpha antagonists in patients with sarcoidosis is still limited. Multicenter trials and a comparison of the different agents are needed to validate the safety and efficacy in these patients. Optimal dosage, duration of therapy and long-term toxicity of anti-TNF therapy in patients with refractory sarcoidosis are yet to be determined in prospective trials.
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Hypertension augments cardiac Toll-like receptor 4 expression and activity.
Hypertens. Res.
PUBLISHED: 01-20-2011
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Hypertension causes cardiac hypertrophy characterized by low-grade inflammation. Toll-like receptors (TLRs), members of the innate immune system, contribute to cardiac failure. We hypothesized that hypertension is accompanied by enhanced TLR4 expression and activity. Cardiac TLR4 expression was determined in untreated spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY; 4, 8, 16 weeks). Besides, hearts of 8-week-old rats were stimulated with the endogenous TLR4 ligand heparansulfate (HS); the proinflammatory mRNA pattern was assessed (tumor necrosis factor-? (TNF-?), interleukin (IL)-6, monocyte chemotactic protein (MCP)-1). Additionally, we induced hypertension in WKY by L-NAME (N(?)-nitro-L-arginine-methylester hydrochloride). In both hypertension models the effect of ramipril on TLR4 density was assessed. Cardiac TLR4 distribution was investigated by fluorescence-activated cell sorting analysis. Blood pressure (BP) and heart weight/body weight ratio (HW/BW) were elevated in SHR. Constitutive TLR4 expression was augmented in adolescent and adult, but not young SHR compared with WKY. TLR4 staining was pronounced in cardiomyocytes. HS entailed an aggravated TNF-? and IL-6 mRNA response in cardiac tissue, which was significantly pronounced in SHR. Ramipril (10 mg kg(-1) per day) reduced BP, HW/BW and TLR4 expression in SHR. L-NAME also augmented TLR4 expression in WKY. Ramipril (1 mg kg(-1) per day) lowered BP but TLR4 expression remained unaffected. High-dose ramipril (10 mg kg(-1) per day) however decreased TLR4 expression. Starting from adolescence SHR demonstrated enhanced cardiac TLR4 expression. TLR4 was also upregulated in L-NAME induced hypertension. Thus, enhanced TLR4 expression might be linked to the development and maintenance of hypertension. Finally, the antihypertensive, anti-inflammatory action of angiotensin-converting-enzyme inhibition had no effect on TLR4 expression in therapeutic doses but in a high-dose model.
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Treatment of relapsing polychondritis with the TNF-alpha antagonist adalimumab.
Clin. Rheumatol.
PUBLISHED: 03-25-2010
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Relapsing polychondritis (RP) is a rare immune-mediated disease which is associated with inflammation in cartilaginous tissue throughout the body. Especially, the cartilaginous structures of ear, respiratory tract, nose, and joints are affected. Around 30% of the cases are associated with other diseases especially systemic vasculitis. Onset of RP is most likely between the ages of 40-60 years. This case reports the often disguised and similar symptoms of RP to Wegners granulomatosis and the challenge of diagnosis. The relative rarity of RP has not permitted clinical trials to determine the efficacy and safety of different therapies. Current treatment is largely empiric and based on case reports. In this case, we successfully used a treatment with the TNF-alpha antagonist adalimumab.
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If the knee hurts, dont forget the spine!
J Clin Neurosci
PUBLISHED: 02-16-2010
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Calcium pyrophosphate dihydrate crystal-deposits (CPPD) at the spine are rare but the lesions detected with CT scans or MRI are often interpreted as a spondylodiscitis or osteitis. CPPD is a disease of the elderly without major sex predominance. The diagnosis of CPPD requires typical manifestations on a radiograph and/or detection of positively birefringent crystals in the synovial fluid of (peripheral) joints by compensated polarized light microscopy. CPPD crystal deposition at the spine has been associated with clinical manifestations, typically spine stiffness, and is sometimes associated with bony ankylosis or diffuse idiopathic skeletal hyperostosis. The preferred treatment of CPPD in the acute phase is oral non-steroidal anti-inflammatory medication or alternatively oral or intravenous glucocorticoids. CPPD should be considered in patients with non-specific spinal lesions.
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Relapsing polychondritis: An autoimmune disease with many faces.
Autoimmun Rev
PUBLISHED: 01-17-2010
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Relapsing polychondritis (RPC) is a rare immune mediated disease which is associated with inflammation in cartilaginous tissue throughout the body. Especially the cartilaginous structures of ear, nose, joints and respiratory tract are affected. In around 30% of the cases an association with other diseases especially systemic vasculitis or myelodysplatic syndrome can be detected. The relative rarity of RPC has not permitted clinical trials to determine the efficacy and safety of therapy strategies. Often the medication in current use is largely empiric and based on case reports. Therefore different immunosuppressants such as cyclophosphamide, azathioprine, cyclosporine, mycophenolate mofetil and also new approaches like tumor necrosis factor alpha blockers (TNF-alpha antagonists) have been used for the treatment of severe manifestations of RPC with varying degrees of efficacy. This review gives a close look to clinical manifestation, diagnosis and also therapy options of RPC.
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Mineralocorticoid receptor antagonism and aldosterone synthesis inhibition do not improve glomerulosclerosis and renal interstitial fibrosis in a model of chronic kidney allograft injury.
Kidney Blood Press. Res.
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Chronic allograft injury (CAI) is a major cause of late graft failure with a multifactorial pathogenesis; however, in different experiments an inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor blockers ameliorated the progression of chronic renal disease. Different concepts supposed that aldosterone is involved in development and/or progression of renal diseases via interaction with a non-epithelial mineralocorticoid receptor (MR), e.g. reducing neointima formation. Our examinations therefore targeted on the effects of the aldosterone synthase inhibitor fadrozole and the MR antagonist spironolactone compared to vehicle in an established rat model of CAI. In our model of CAI, neither the aldosterone biosynthesis inhibitor nor a direct MR blockade had a positive effect on renal CAI in rats. Fadrozole- and spironolactone-treated animals demonstrated a higher proteinuria value, pathologically elevated potassium values, higher tubulointerstitial damage and markedly increased heart weight/body weight as compared to vehicle. Our observations also suggest that inhibition of the MR or the biosynthesis itself had a bad influence on the amount of sclerotic glomeruli and tubulointerstitial damage. The positive effects of inhibition of aldosterone as described in cardiac models could not yet be detected in kidney recipients.
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Head and neck sarcoidosis, from wait and see to tumor necrosis factor alpha therapy: a pilot study.
Head Neck
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To suggest treatment modalities with respect to the specific requirements of head and neck sarcoidosis.
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Kidney transplant after preexisting posterior reversible encephalopathy syndrome induced by Goodpastures syndrome.
Exp Clin Transplant
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Posterior reversible encephalopathy syndrome is characterized by varying neurologic symptoms associated with brain vasogenic edema. Posterior reversible encephalopathy syndrome can be associated with severe hypertension (eg, in eclampsia or HELLP syndrome), but it also has been observed without hypertension and in several clinical conditions including infections and autoimmune disorders. The literature offers several reports of posterior reversible encephalopathy syndrome detected or induced after bone-marrow and solid-organ transplant, or induction by immunosuppression. We describe what is, to the best of our knowledge, the first case of man who successfully underwent a kidney transplant with preexisting posterior reversible encephalopathy syndrome induced by Goodpastures syndrome.
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Anti-glomerular basement membrane antibody disease: a rare autoimmune disorder affecting the kidney and the lung.
Autoimmun Rev
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Anti-glomerular basement membrane antibody disease is a rare, but well characterized cause of glomerulonephritis. By definition serum anti-GBM antibody and/or a linear binding of IgG detected by direct immunofluorescence (IF) in a histological specimen of the kidney or the lung have to be detected. These antibodies can lead to acute rapid progressive glomerulonephritis(RPGN) and/or pulmonary hemorrhage (PH) because of collagen similarities in the basement membrane. Principally anti-GBM antibody disease can be divided into two groups: anti-GBM antibody disease without PH was regarded as renal-limited anti-GBM antibody disease and that with PH was defined as Goodpastures syndrome (GPS). The important determinant for the response of therapy and long term diagnosis on anti-GBM disease is early diagnosis to prevent endstage renal disease. Therefore, standard treatment is a combined therapy of plasmapherisis, prednisolone and cyclophosphamide. The aim of this review is an overview of the pathogenesis, clinical presentation, diagnosis and treatment of anti-GBM disease.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

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We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.