scholarly journals Why Have Detection, Understanding and Management of Kidney Hypoxic Injury Lagged Behind those for the Heart?

2019 ◽  
Vol 8 (2) ◽  
pp. 267 ◽  
Author(s):  
Zaid Abassi ◽  
Seymour Rosen ◽  
Simon Lamothe ◽  
Samuel N. Heyman
Keyword(s):  
Tissue Injury ◽  
Delayed Diagnosis ◽  
Kidney Injury ◽  
Warm Ischemia ◽  
Diagnostic Tools ◽  
Type I ◽  
Ischemia And Reperfusion ◽  
Type Ii ◽  
Hypoxic Injury ◽  
Use Of Models

The outcome of patients with acute myocardial infarction (AMI) has dramatically improved over recent decades, thanks to early detection and prompt interventions to restore coronary blood flow. In contrast, the prognosis of patients with hypoxic acute kidney injury (AKI) remained unchanged over the years. Delayed diagnosis of AKI is a major reason for this discrepancy, reflecting the lack of symptoms and diagnostic tools indicating at real time altered renal microcirculation, oxygenation, functional derangement and tissue injury. New tools addressing these deficiencies, such as biomarkers of tissue damage are yet far less distinctive than myocardial biomarkers and advanced functional renal imaging technologies are non-available in the clinical practice. Moreover, our understanding of pathogenic mechanisms likely suffers from conceptual errors, generated by the extensive use of the wrong animal model, namely warm ischemia and reperfusion. This model parallels mechanistically type I AMI, which properly represents the rare conditions leading to renal infarcts, whereas common scenarios leading to hypoxic AKI parallel physiologically type II AMI, with tissue hypoxic damage generated by altered oxygen supply/demand equilibrium. Better understanding the pathogenesis of hypoxic AKI and its management requires a more extensive use of models of type II-rather than type I hypoxic AKI.

scholarly journals Specific Proteins in Nontuberculous Mycobacteria: New Potential Tools

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Patricia Orduña ◽  
Antonia I. Castillo-Rodal ◽  
Martha E. Mercado ◽  
Samuel Ponce de León ◽  
Yolanda López-Vidal
Keyword(s):  
Nontuberculous Mycobacteria ◽  
Diagnostic Tools ◽  
Type I ◽  
Type Ii ◽  
Diguanylate Cyclase ◽  
Comparative Proteomic Analysis ◽  
Complex Protein ◽  
Specific Proteins ◽  
The Common ◽  
Short Chain Dehydrogenase

Nontuberculous mycobacteria (NTM) have been isolated from water, soil, air, food, protozoa, plants, animals, and humans. Although most NTM are saprophytes, approximately one-third of NTM have been associated with human diseases. In this study, we did a comparative proteomic analysis among five NTM strains isolated from several sources. There were different numbers of protein spots fromM. gordonae(1,264),M. nonchromogenicumtype I (894),M. nonchromogenicumtype II (935),M. peregrinum(806), andM. scrofulaceum/Mycobacterium mantenii(1,486) strains, respectively. We identified 141 proteins common to all strains and specific proteins to each NTM strain. A total of 23 proteins were selected for its identification. Two of the common proteins identified (short-chain dehydrogenase/reductase SDR and diguanylate cyclase) did not align withM. tuberculosiscomplex protein sequences, which suggest that these proteins are found only in the NTM strains. Some of the proteins identified as common to all strains can be used as markers of NTM exposure and for the development of new diagnostic tools. Additionally, the specific proteins to NTM strains identified may represent potential candidates for the diagnosis of diseases caused by these mycobacteria.

scholarly journals Diffusion kurtosis imaging and diffusion-weighted imaging-based classification of acute stroke lesions in the brain: A pilot study

2020 ◽  
Author(s):  
Xin Liu ◽  
Songsen Chen ◽  
Fang Chen ◽  
Lei Wang ◽  
Khan Afsar ◽  
...  
Keyword(s):  
Cerebral Infarction ◽  
Acute Stroke ◽  
Diffusion Weighted Imaging ◽  
Tissue Injury ◽  
Acute Cerebral Infarction ◽  
Diffusion Kurtosis Imaging ◽  
Type I ◽  
Type Ii ◽  
Diffusion Kurtosis

Abstract Background: We postulated that diffusion kurtosis imaging (DKI) could classify heterogeneous stroke lesions on diffusion-weighted imaging (DWI) and improve our understanding of the characteristics of tissue injury. We aimed to retrospectively study different DKI parameters in patients with acute stroke reported in the literature. Methods: We collected the DWI and DKI data of 41 patients (26 men, 15 women), including 86 cases of acute cerebral infarction in different brain regions. Of them, 20 patients had single infarction, whereas others had multiple infarctions. Acute cerebral infarction lesions were classified into two categories based on DKI and DWI parameters: type I, matched DKI and DWI parameters and type II, mismatched DKI and DWI parameters. Regions of interest (ROIs) were outlined within the most severely infarcted areas of each lesion according to each independent parametric map. In the control groups, same-sized ROIs were located in the corresponding region of the normal contralateral hemisphere. In both categories, DKI and DWI parameters followed a normal Gaussian distribution. We used the independent sample t-test to compare the differences in each group. Results: In type I cases, fractional anisotropy, mean diffusivity, axial diffusivity, radial diffusivity, mean kurtosis (MK), and axial kurtosis (Ka) values were significantly different (P<0.05). In type II cases, only MK and Ka values were significantly different (P<0.05). Conclusions: DKI can provide more information on acute ischemic brain infarction and enrich our understanding of ischemic tissue injury. This DKI and DWI parameters-based classification of acute stroke lesions may confer a renewed understanding of infarction cores.

scholarly journals Type I, but not type II, interferon is critical in liver injury induced after ischemia and reperfusion

Hepatology ◽  
2007 ◽  
Vol 47 (1) ◽  
pp. 199-206 ◽  
Author(s):  
Yuan Zhai ◽  
Bo Qiao ◽  
Feng Gao ◽  
Xiuda Shen ◽  
Andrew Vardanian ◽  
...  
Keyword(s):  
Liver Injury ◽  
Type I ◽  
Ischemia And Reperfusion ◽  
Type Ii

LITIGATION OF MISSED CERVICAL SPINE INJURIES IN PATIENTS PRESENTING WITH BLUNT TRAUMATIC INJURY

Neurosurgery ◽  
2007 ◽  
Vol 60 (3) ◽  
pp. 516-523 ◽  
Author(s):  
Gregory P. Lekovic ◽  
Timothy R. Harrington
Keyword(s):  
Cervical Spine ◽  
Cervical Spine Injury ◽  
Traumatic Injury ◽  
Delayed Diagnosis ◽  
Spine Injury ◽  
Type I ◽  
Type Ii ◽  
Cervical Injury ◽  
Cervical Spine Injuries ◽  
Delays In Diagnosis

Abstract BACKGROUND Approximately 800,000 cervical spines are cleared in emergency departments each year. Errors in diagnosis of cervical spine injury are a potentially huge medicolegal liability, but no established protocol for clearance of the cervical spine is known to reduce errors or delays in diagnosis. METHODS The Lexis-Nexis, Westlaw, and Medline databases were queried for cases of missed cervical injury. Errors were categorized according to a novel system of classification. Type I errors occurred when inadequate or improper tests were ordered. Type II errors occurred when adequate tests were ordered, but were either misread or not read. Type III errors occurred when adequate tests were ordered and read accurately, but the ordered test was not sensitive enough to detect the injury. RESULTS Twenty cases of missed or delayed diagnosis of cervical spine injury were found in 10 jurisdictions. Awards averaged $2.9 million (inflation adjusted to 2002 dollars). Eight cases resulted in verdicts in favor of the defendant, but none of these cases involved an alleged Type II error. CONCLUSION Fear of lawsuits encourages defensive medicine and complicates the process of clearing a patient's cervical spine. This analysis adds medicolegal support for the judicious use of imaging studies in current cervical spine clearance protocols. However, exposure to significant liability suggests that a low threshold for computed tomography is a reasonable alternative.

scholarly journals Positive acute viral infection markers, autoimmune disease and type II mixed cryoglobulinemia: a rare concurrence

2019 ◽  
Vol 12 (11) ◽  
pp. e230492
Author(s):  
Kehua Zhou ◽  
Shumaila Muhammad Iqbal ◽  
Ali Alameri ◽  
Cassandra Zhi ◽  
Ammad Naeem
Keyword(s):  
Viral Infections ◽  
Kidney Injury ◽  
Altered Mental Status ◽  
Mixed Cryoglobulinemia ◽  
Lymphoproliferative Disorders ◽  
Oral Steroid ◽  
Type I ◽  
Type Ii ◽  
Flow Restriction ◽  
Acute Viral Infection

Cryoglobulins are abnormal serum immunoglobulins that tend to precipitate in intravascular compartments at temperatures lower than 37°C causing blood flow restriction to vital organs. They are divided into type I, II and III based on the immunoglobulin subtypes of the cryoprecipitates. Type II cryoglobulinemia is most commonly associated with viral infections, autoimmune diseases and lymphoproliferative disorders. Here, we reported an 80-year-old man who presented with fatigue, acute kidney injury, palpable purpura, anaemia and altered mental status. He was diagnosed with type II cryoglobulinemia with concomitant positive autoimmune markers, varicella IgM antibody and IgM hepatitis B core antibody. The patient responded well to intravenous and oral steroid treatment.

EP45 What’s the chance of precipitation?

Rheumatology ◽  
2020 ◽  
Vol 59 (Supplement_2) ◽  
Author(s):  
Ruth Smith ◽  
Graeme Wild ◽  
Stuart Carter
Keyword(s):  
Renal Disease ◽  
Plasma Exchange ◽  
Laboratory Finding ◽  
Kidney Injury ◽  
The Other ◽  
Type I ◽  
Type Ii ◽  
Hospital Patients ◽  
Clinically Significant ◽  
Cryoglobulinaemic Vasculitis

Abstract Background This project was undertaken to review patients testing positive for cryoglobulins. We wanted to establish the numbers of patients with different types of cryoglobulins, to determine whether there were any shared characteristics and whether there was any consensus on management. Methods Retrospective review of records of Sheffield Teaching Hospital patients testing positive for cryoglobulins January 2014-December 2018. Results 374 cryoglobulin tests were requested. 43 were positive (in 33 patients).There were 9 Type I cryoglobulins, including IgG and IgM lambda and kappa. Titres ranged from 0.07-47.5g/L. All patients had an underlying haematological condition. 2 patients had rash and 1 acute kidney injury (AKI), but there were no other clinical features of cryoglobulinaemia. 1 patient received treatment for cryoglobulinaemia secondary to MGUS with prednisolone, plasma exchange and Velcade/Thalidomide/Dexamethasone. Otherwise the cryoglobulins appear to be a laboratory finding with minimal clinical significance.There were 17 Type II cryoglobulins in 12 patients. The most common pattern was IgM kappa monoclone with polyclonal immunoglobulin (71%). Titres ranged from 0.03-5.4g/L. Patients’ underlying conditions were malignant, infective and inflammatory. 7 patients had rash, 2 arthralgia/arthritis, 4 Raynaud’s, 3 paraesthesia and 2 AKI. The presence of cryoglobulins was not considered significant in 5 patients (titres 0.03-0.39g/L). 3 patients were treated for underlying malignancy or infection and cryoglobulins monitored. 2 patients (titres 0.16 and 1.97g/L) were treated for renal disease in the presence of cryoglobulins with prednisolone and Rituximab in 1 case and prednisolone, Cyclophosphamide and plasma exchange in the other. 2 patients were diagnosed with cryoglobulinaemic vasculitis (titres 0.5g/L and 0.03g/L). 1 was treated with prednisolone and Azathioprine. The other had previously been treated with prednisolone and cyclophosphamide, then azathioprine maintenance therapy; the relapse during this study period was treated with methylprednisolone, plasma exchange and Rituximab.There were 16 Type III cryoglobulins in 14 patients. By definition all had polyclonal immunoglobulins. Titres ranged from 0.06-4.64g/L. Patients’ underlying conditions were malignant, infective and inflammatory. 7 patients had rash, 4 arthralgia/arthritis, 2 paraesthesia and 1 AKI. The presence of cryoglobulins was not thought significant in 5 patients (titres 0.08 to 0.45g/L). 7 patients were treated for underlying infection or rheumatological condition and the cryoglobulins monitored. 1 patient (already reported in the Type II section) was treated for renal disease in the presence of cryoglobulins. 1 patient (titre 0.12g/L) with a diagnosis of cryoglobulinaemic vasculitis was treated with prednisolone and azathioprine, then mycophenolate. Conclusion The study confirms that cryoglobulins are rare and that clinically significant disease related to them is even rarer. Given the small numbers it is difficult to identify strong trends in presentation or treatment. However, it does show that higher cryoglobulin titres do not correlate with higher rates of disease activity in terms of cryoglobulinaemia or cryoglobulinaemic vasculitis. Disclosures: R. Smith: None. G. Wild: None. S. Carter: None.

scholarly journals Clinical Exome Sequencing Enables Congenital Sialidosis Type II Diagnosis in Two Siblings Presenting with Unreported Clinical Features from a Rare Homozygous Sequence Variant p.(Tyr370Cys) in NEU1

2021 ◽  
pp. 1-8
Author(s):  
Elda Ariadna Flores-Contreras ◽  
José Elías García-Ortiz ◽  
Carla Daniela Robles-Espinoza ◽  
Viviana Zomosa-Signoret ◽  
Luis Eduardo Becerra-Solano ◽  
...  
Keyword(s):  
Exome Sequencing ◽  
Clinical Features ◽  
Molecular Model ◽  
Molecular Diagnostic ◽  
Diagnostic Tools ◽  
Compound Heterozygous ◽  
Sequence Variant ◽  
Sequence Variants ◽  
Type I ◽  
Type Ii

Sialidosis is a rare autosomal recessive disease that presents with progressive lysosomal storage of sialylated glycopeptides and oligosaccharides caused by homozygous or compound heterozygous sequence variants in the neuraminidase 1 (<i>NEU1</i>) gene. These sequence variants can lead to sialidosis type I and II; the latter is the most severe and presents prenatally or at early age. However, sialidosis diagnosis is challenging, especially in those health systems with limited resources of developing countries. Consequently, it is necessary to dip into high-throughput molecular diagnostic tools to allow for an accurate diagnosis with better cost-effectiveness and turnaround time. We report a 4-member pedigree segregating an ultrarare missense variant, c.1109A&#x3e;G; p.Tyr370Cys, in <i>NEU1</i> as detected by whole-exome sequencing. Two short-lived siblings, who presented with previously unreported clinical features from such a homozygous sequence variant, were diagnosed with sialidosis type II. Additionally, we present a novel molecular model exhibiting the consequences of the variant in the sialidase-1 tridimensional structure. This study allowed us to provide a definitive diagnosis for our patients, increase our understanding of this pathogenic variant, and improve genetic counseling.

Heat-Etching with a Bullivant Type II Simple Freeze-Cleave Device

1970 ◽  
Vol 28 ◽  
pp. 106-107 ◽  
Author(s):  
Ronald S. Weinstein ◽  
N. Scott McNutt
Keyword(s):  
New Zealand ◽  
General Hospital ◽  
Massachusetts General Hospital ◽  
Type I ◽  
Type Ii ◽  
Collaborative Effort ◽  
Temperature And Pressure ◽  
The University

The Type I simple cold block device was described by Bullivant and Ames in 1966 and represented the product of the first successful effort to simplify the equipment required to do sophisticated freeze-cleave techniques. Bullivant, Weinstein and Someda described the Type II device which is a modification of the Type I device and was developed as a collaborative effort at the Massachusetts General Hospital and the University of Auckland, New Zealand. The modifications reduced specimen contamination and provided controlled specimen warming for heat-etching of fracture faces. We have now tested the Mass. General Hospital version of the Type II device (called the “Type II-MGH device”) on a wide variety of biological specimens and have established temperature and pressure curves for routine heat-etching with the device.

Labelling of non-A, non-B hepatitis infected chimpanzee hepatocytes with nuclease-gold conjugates

1984 ◽  
Vol 42 ◽  
pp. 250-251
Author(s):  
G. D. Gagne ◽  
M. F. Miller ◽  
D. A. Peterson
Keyword(s):  
Endoplasmic Reticulum ◽  
Experimental Infection ◽  
Uranyl Acetate ◽  
Type I ◽  
Cellular Injury ◽  
Type Ii ◽  
Tubular Structures ◽  
Type Iii ◽  
Type Iv ◽  
Infected Chimpanzee

Experimental infection of chimpanzees with non-A, non-B hepatitis (NANB) or with delta agent hepatitis results in the appearance of characteristic cytoplasmic alterations in the hepatocytes. These alterations include spongelike inclusions (Type I), attached convoluted membranes (Type II), tubular structures (Type III), and microtubular aggregates (Type IV) (Fig. 1). Type I, II and III structures are, by association, believed to be derived from endoplasmic reticulum and may be morphogenetically related. Type IV structures are generally observed free in the cytoplasm but sometimes in the vicinity of type III structures. It is not known whether these structures are somehow involved in the replication and/or assembly of the putative NANB virus or whether they are simply nonspecific responses to cellular injury. When treated with uranyl acetate, type I, II and III structures stain intensely as if they might contain nucleic acids. If these structures do correspond to intermediates in the replication of a virus, one might expect them to contain DNA or RNA and the present study was undertaken to explore this possibility.

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