Bottoms up! The clinical consequence of vodka enemas

2021 ◽  
Author(s):  
Jason T. Hong ◽  
Anshini Jain ◽  
Vinna An ◽  
Alex Wong
Keyword(s):  
Clinical Consequence

scholarly journals Caprine Arthritis Encephalitis Virus Is Associated with Renal Lesions

Viruses ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 1051
Author(s):  
Brian G. Murphy ◽  
Diego Castillo ◽  
Asli Mete ◽  
Helena Vogel ◽  
Dayna Goldsmith ◽  
...  
Keyword(s):  
Renal Injury ◽  
Binding Sites ◽  
Encephalitis Virus ◽  
Clinical Consequence ◽  
Viral Isolate ◽  
Viral Promoter ◽  
Caprine Arthritis Encephalitis Virus ◽  
Renal Lesions ◽  
Cardiac Lesions ◽  
The Central Nervous System

Caprine arthritis encephalitis virus (CAEV) is a monocyte/macrophage-tropic lentivirus that primarily infects goats resulting in a well-recognized set of chronic inflammatory syndromes focused on the joint synovium, tissues of the central nervous system, pulmonary interstitium and mammary gland. Clinically affected animals generally manifest with one or more of these classic CAEV-associated tissue lesions; however, CAEV-associated renal inflammation in goats has not been reported in the peer-reviewed literature. Here we describe six goats with chronic, multisystemic CAEV infections in conjunction with CAEV-associated renal lesions. One of the animals had CAEV antigen-associated thrombotic arteritis resulting in infarction of both the kidney and heart. These goats had microscopic evidence of inflammatory renal injury (interstitial nephritis) with detectable renal immunolabeling for CAEV antigen in three of six animals and amplifiable proviral sequences consistent with CAEV in all six animals. Cardiac lesions (vascular, myocardial or endocardial) were also identified in four of six animals. Within the viral promoter (U3) region, known transcription factor binding sites (TFBSs) were generally conserved, although one viral isolate had a duplication of the U3 A region encoding a second gamma-activated site (GAS). Despite the TFBS conservation, the isolates demonstrated a degree of phylogenetic diversity. At present, the clinical consequence of CAEV-associated renal injury is not clear.

Neuronal regulation of renal function: A model system for nervous system interactions

1992 ◽  
Vol 70 (5) ◽  
pp. 733-734 ◽  
Author(s):  
J. Michael Wyss
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Renal Disease ◽  
Easy Access ◽  
Renal Nerves ◽  
Clinical Consequence ◽  
Nerve Activity ◽  
Renal Nerve ◽  
Renal Nerve Activity

The kidney is the most highly innervated peripheral organ, and both the excretory and endocrine functions of the kidney are regulated by renal nerve activity. The kidney plays a dominant role in body fluid homeostasis, blood ionic concentration, and pH and thereby contributes importantly to systemic blood pressure control. Early studies suggested that the neural-renal interactions were responsible only for short-term adjustments in renal function, but more recent studies indicate that the renal nerves may be a major contributor to chronic renal defects leading to established hypertension and (or) renal disease. The neural-renal interaction is also of considerable interest as a model to elucidate the interplay between the nervous system and peripheral organs, since there is abundant anatomical and physiological information characterizing the renal nerves. The investigator has easy access to the renal nerves and the neural influence on renal function is directly quantifiable both in vivo and in vitro. In this symposium that was presented at the 1990 annual convention of the Society for Neuroscience in St. Louis, Missouri, three prominent researchers evaluate the most recent progress in understanding the interplay between the nervous system and the kidney and explore how the results of these studies relate to the broader questions concerning the nervous system's interactions.First, Luciano Barajas examines the detailed anatomy of the intrarenal distribution of the efferent and afferent renal nerves along the nephron and vasculature, and he evaluates the physiological role of each of the discrete components of the innervation. His basic science orientation combined with his deep appreciation of the clinical consequence of the failure of neural-renal regulation enhances his discussion of the anatomy. Ulla C. Kopp discusses the role of the renorenal reflex, which alters renal responses following stimulation of the contralateral kidney. She also considers her recent findings that efferent renal nerve activity can directly modify sensory feedback to the spinal cord from the kidney. Finally, J. Michael Wyss examines the functional consequences of neural control of the kidney in health and disease. Although the nervous system has often been considered as only an acute regulator of visceral function, current studies into hypertension and renal disease suggest that neural-renal dysfunction may be an important contributor to chronic diseases.Together, these presentations examine most of the recent advances in the area of neural-renal interactions and point out how these data form a basis for future research into neuronal interactions with all visceral organs. The relative simplicity of the neural-renal interaction makes this system an important model with which to elucidate all neural-peripheral and neural-neural interactions.

scholarly journals Clinical consequence of bare metal stent and stent graft failure in femoropopliteal occlusive disease

2013 ◽  
Vol 58 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
Shant M. Vartanian ◽  
Paul C. Johnston ◽  
Joy P. Walker ◽  
Sara J. Runge ◽  
Charles M. Eichler ◽  
...  
Keyword(s):  
Stent Graft ◽  
Graft Failure ◽  
Bare Metal Stent ◽  
Occlusive Disease ◽  
Clinical Consequence ◽  
Bare Metal ◽  
Metal Stent

Is there an exercise duration threshold for exercise-induced troponin elevation in healthy recreational athletes? The NEEDED 2014 advanced heart rate monitor substudy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
M Bjorkavoll-Bergseth ◽  
B Auestad ◽  
O Kleiven ◽  
O Skadberg ◽  
T Eftestol ◽  
...  
Keyword(s):  
Heart Rate ◽  
Clinical Status ◽  
Exercise Duration ◽  
Strenuous Exercise ◽  
Clinical Consequence ◽  
Funding Source ◽  
Recreational Athletes ◽  
National Budget ◽  
Exercise Induced ◽  
Public Grant

Abstract Background/Introduction Following prolonged strenuous exercise there is an exercise-induced troponin (cTn) elevation in healthy individuals. The precise mechanisms and clinical consequence of this cTn elevation remain to be determined. It has recently been demonstrated that exercise intensity, exceeding a heart rate (HR) of 150 bpm, is correlated with exercise-induced cTn elevation. Purpose The present work aims to determine if there is a threshold for exercise duration with a HR exceeding 150 bpm associated with an excessive exercise-induced cTn elevation. Methods A total of 177 healthy subjects were included in the present analysis of HR data obtained from sport watches used during a 91-km recreational mountain bike cycle race. Clinical status, cTnI, ECGs, blood pressure and demographics were obtained 24 h prior to- and at 3 h and 24 h after the race. Results are reported as median and 25th and 75th percentile. We used Tree regression to determine the association between elevated cTnI and exercise duration exceeding a HR of 150 bpm. Results Subjects were 82% (n=146) males, 44 (39–51) years, with a race time of 3.5 (3.1–3.9) h. Baseline cTnI was 1.9 (1.6–3.3) ng/L. There was a cTnI elevation in all study participants at 3 h, cTnI: 60.0 (36.0–99.3) ng/L, with a significant (p<0.001) reduction at 24 hours following exercise, cTnI: 10.9 (6.1–22.4) ng/L. Tree regression identified 168 min of exercise, with a HR exceeding 150 bpm, to be associated with an excessive increase in cTnI both at 3 h, and at 24 h following the race (figure). The median cTn values above and below the threshold are presented in the Table. Conclusion The present analysis suggests that exceeding a specific duration of high intensity exercise may be associated with excessive cTn elevation in susceptible individuals. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): Western Norway Health authoritites.

Minimally Invasive Interventional Management of Gastric Outlet Obstructions

2018 ◽  
Vol 02 (01) ◽  
pp. 025-032
Author(s):  
Wei-Zhong Zhou ◽  
Zheng-Qiang Yang
Keyword(s):  
Stent Placement ◽  
Balloon Dilatation ◽  
Outlet Obstruction ◽  
Covered Stent ◽  
Clinical Consequence ◽  
Endoscopic Stenting ◽  
Stent Patency ◽  
Ulcer Disease ◽  
Recommended Treatment ◽  
Uncovered Stent

AbstractGastric outlet obstruction (GOO) is a clinical consequence of any disease that produces intrinsic or extrinsic obstruction of the pyloric channel or duodenum. The most common symptoms of GOO include nausea, vomiting, abdominal pain, and weight loss. Traditionally, surgery is regarded as the standard treatment modality. However, with the development of mini-invasive technologies, fluoroscopic or endoscopic stenting and balloon dilatation have become the mainstream of the therapies. The initial recommended treatment for malignant GOO is self-expanding metal stent placement. The stent can be classified into covered and uncovered stent according to whether it is coated with a membrane. Covered stent seems to have longer stent patency, while uncovered stent has the advantage of a lower migration rate. Regarding the etiology of benign GOO, peptic ulcer disease and corrosive injury are the two main reasons. Balloon dilatation is a simple and convenient way to treat the benign GOO. Stent placement has recently been reported for the treatment of benign GOO; however, it needs further more studies to verify its effect. This article presents a concise review of current fluoroscopic or endoscopic stenting practice for malignant GOO and balloon dilatation or stenting for benign GOO.

scholarly journals Intracerebral haemorrhage in Down syndrome: protected or predisposed?

F1000Research ◽  
2016 ◽  
Vol 5 ◽  
pp. 876 ◽  
Author(s):  
Lewis Buss ◽  
Elizabeth Fisher ◽  
John Hardy ◽  
Dean Nizetic ◽  
Jurgen Groet ◽  
...  
Keyword(s):  
Down Syndrome ◽  
Intracerebral Haemorrhage ◽  
Early Onset ◽  
Epidemiological Data ◽  
Haemorrhagic Stroke ◽  
Brain Parenchyma ◽  
Chromosome 21 ◽  
Clinical Consequence ◽  
Increased Risk ◽  
The Central Nervous System

Down syndrome (DS), which arises from trisomy of chromosome 21, is associated with deposition of large amounts of amyloid within the central nervous system. Amyloid accumulates in two compartments: as plaques within the brain parenchyma and in vessel walls of the cerebral microvasculature. The parenchymal plaque amyloid is thought to result in an early onsetAlzheimer’s disease (AD) dementia, a phenomenon so common amongst people with DS that it could be considered a defining feature of the condition. The amyloid precursor protein (APP) gene lies on chromosome 21 and its presence in three copies in DS is thought to largely drive the early onset AD. In contrast, intracerebral haemorrhage (ICH), the main clinical consequence of vascular amyloidosis, is a more poorly defined feature of DS. We review recent epidemiological data on stroke (including haemorrhagic stroke) in order to make comparisons with a rare form of familial AD due to duplication (i.e. having three copies) of the APP region on chromosome 21, here called ‘dup-APP’, which is associated with more frequent and severe ICH. We conclude that although people with DS are at increased risk of ICH, this is less common than in dup-APP, suggesting the presence of mechanisms that act protectively. We review these mechanisms and consider comparative research into DS and dup-APP that may yield further pathophysiological insight.

Calciphylaxis: Clinical Consequence of Rapid Weight Loss.

2010 ◽  
pp. P2-237-P2-237
Author(s):  
A Chandrasekhar ◽  
M Schaefer ◽  
G Gopalakrishnan
Keyword(s):  
Weight Loss ◽  
Clinical Consequence ◽  
Rapid Weight Loss

scholarly journals A post mortem assessment of a 25-year-old man with ascending aortic dissection and a novel MYLK variant

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Katelyn Hodge ◽  
Katherine G. Spoonamore ◽  
Christopher B. Griffith ◽  
David D. Weaver ◽  
Patricia B.S. Celestino-Soper ◽  
...  
Keyword(s):  
Genetic Testing ◽  
Aortic Aneurysm ◽  
Aortic Dissection ◽  
Thoracic Aortic Aneurysm ◽  
Aortic Rupture ◽  
Clinical Consequence ◽  
Post Mortem ◽  
Variant Of Uncertain Significance ◽  
Pathogenic Variants ◽  
Aortic Aneurysm And Dissection

We report on the process of <em>post mortem</em> evaluation and genetic testing following the death of a 25-year-old man due to ascending aortic dissection leading to aortic rupture. Following the negative clinical testing of a 12- gene thoracic aortic aneurysm and dissection panel, research testing revealed a novel c.5732A&gt;T (p.E1911V) variant in exon 34 of the MYLK gene (NM_053025). Two likely pathogenic variants in this gene have been reported previously in individuals with familial thoracic aortic aneurysm and dissection. Given the unclear clinical consequence of the variant found in our proband, we have classified this change as a variant of uncertain significance. In addition to discussing the complexity involved in variant interpretation, we recognize the need for additional research for more accurate <em>MYLK</em> interpretation. Finally, we comment on the unique challenges of <em>post mortem</em> genetic testing.

scholarly journals U2AF1 and EZH2 Mutations Are Associated with Non-Immune Hemolytic Anemia in Myelodysplastic Syndromes

Blood ◽  
2020 ◽  
Vol 136 (Supplement 1) ◽  
pp. 35-36
Author(s):  
Rami S. Komrokji ◽  
Najla Al Ali ◽  
Mohammad O Hussaini ◽  
David A. Sallman ◽  
Dana Elise Rollison ◽  
...  
Keyword(s):  
Myelodysplastic Syndromes ◽  
Research Funding ◽  
Somatic Mutations ◽  
Hot Spot ◽  
Clinical Consequence ◽  
Intermediate Risk ◽  
Serum Haptoglobin ◽  
Immune Hemolytic Anemia ◽  
Allele Specific ◽  
Baseline Characteristics

Introduction Hemolysis is a well-recognized clinical observation in a subset of myelodysplastic syndromes (MDS) patients (pts). However, the clinical consequence of hemolysis and the associated molecular phenotype in MDS is not well described in the literature. Nonimmune hemolysis in MDS is often attributed to ineffective intramedullary erythropoiesis or acquired hemoglobinopathies that have been described in rare cases of MDS. In this study, we report the prevalence of hemolysis among MDS pts, their clinical and genomic characteristics and its impact on outcomes. Methods We identified all pts in our institutional MDS database who had serum haptoglobin measured at time of diagnosis or referral. We considered serum haptoglobin &lt; 10 mg/dl as a surrogate marker for intravascular hemolysis. We compared the baseline characteristics, response to treatment, and overall survival (OS) in those with hemolysis (haptoglobin &lt; 10 mg/dl) to those in the non-hemolysis group. Further, we explored the mutational landscape among pts with hemolysis compared to the non-hemolysis group. Results Among 519 pts in our database with a known serum haptoglobin at first referral or diagnosis, 54 pts (10%) had serum haptoglobin &lt; 10 mg/dl (the hemolysis group). The baseline characteristics were similar among the two groups except for a slightly younger age and lower platelets count in the hemolysis group. Other laboratory markers associated with hemolysis such as total bilirubin and LDH were significantly increased in the hemolysis groups. However, no difference was seen in coombs test results. Only 13% versus 9% were Coombs positive suggesting that hemolysis in MDS is typically not immune mediated (table 1). The median OS was 31 months versus 39 months among pts with hemolysis and no hemolysis respectively, (p=.98). There was a trend of inferior survival among pts with hemolysis in the low and intermediate risk revised IPSS (R-IPSS) risk groups. The median OS was 44 months with hemolysis compared to 89 months with no hemolysis in low risk R-IPSS (p=.2) and 19 months versus 34 months in intermediate risk group. (p=.7) The hematological improvement (HI) rate using erythroid stimulating agents (ESA) was 16% (3/19 pts) in the hemolysis group compared to 30% (39/130 pts) in the non-hemolysis group. (p=.2) The HI+ best response with hypomethylating agent (HMA) was 70% (22/31) compared to 45% (127/280) among hemolysis and non-hemolysis groups respectively, (p=.05). Table-2 summarizes the somatic mutations landscape between the hemolysis and non-hemolysis groups. U2AF1 and EZH2 hotspot mutations were statistically significantly more common among hemolysis group. Out of the 16 pts with U2AF1 mutations, 15 (94%) harbored a mutation at serine 34 (S34) in the hemolysis group while only 22 of 55 (40%) cases with U2AF1 mutation had an S34 hot spot mutation in the non-hemolysis group suggesting that the association between U2AF1 and hemolysis is allele specific. (p .0001) Conclusion Non immune hemolysis was observed in 10% of MDS patients. Inferior survival trends were observed among lower risk MDS patients with hemolysis. A decreased response rate to ESA and higher responses to HMA were also observed in the hemolysis group. U2AF1 mutation was observed in 30% of patients with hemolysis and occurred almost exclusively at the S34 hot spot. Our data suggest that nonimmune hemolysis is associated with allele specific somatic mutations and associated with key clinical outcomes. Future work will explore the contribution of altered splicing to these acquired hemoglobinopathies. Disclosures Komrokji: BMS: Honoraria, Speakers Bureau; Novartis: Honoraria; Incyte: Honoraria; JAZZ: Honoraria, Speakers Bureau; AbbVie: Honoraria; Agios: Honoraria, Speakers Bureau; Acceleron: Honoraria; Geron: Honoraria. Sallman:Celgene, Jazz Pharma: Research Funding; Agios, Bristol Myers Squibb, Celyad Oncology, Incyte, Intellia Therapeutics, Kite Pharma, Novartis, Syndax: Consultancy. Padron:Novartis: Honoraria; Incyte: Research Funding; Kura: Research Funding; BMS: Research Funding.

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