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opencc-by-4.0Oct 2023View details →

FIGURE 1 in Fish injuries resulting from transient operating conditions in a Brazilian hydropower plant: morphological, physiological and biochemical evaluation in Pimelodus maculatus (Siluriformes: Pimelodidae)

FIGURE 1 | Histological gill alterations in Pimelodus maculatus collected during transient operating conditions (magnification: × 400). Arrows indicate the following lesions: A. Aneurysm; B. Epithelium detachment; C. Telangiectasia; and D. Interlamellar hyperplasia.

opencc-by-4.0Oct 2023View details →

FIGURE 2 in Fish injuries resulting from transient operating conditions in a Brazilian hydropower plant: morphological, physiological and biochemical evaluation in Pimelodus maculatus (Siluriformes: Pimelodidae)

FIGURE 2 | Histological alterations in liver and spleen of Pimelodus maculatus collected during transient operating conditions in the tailrace of Machadinho HPP (magnification: × 400). Arrows and asterisks indicate the following lesions: A. Melanomacrophage centers (asterisk) and congested vein (arrow) in the liver; B. Blood cells indicating hepatic hemorrhage (asterisk); C. Melanomacrophage centers in the spleen (asterisk); D. Mononuclear inflammatory infiltrate in the spleen (arrow).

opencc-by-4.0Dec 2005View details →

Fig. 2 in Repaired injuries and shell form in some Palaeozoic pleurotomarioid gastropods

Fig. 2. Schematic drawing of Fig. 1 as a guide to emphasize the location of repaired injuries, here shown in thicker lines. For explanation see Fig. 1 captions and the text. A–F. Turbiniform shells. G–J. Trochiform shells. K, L. Planispiral shells.

Fig. 4 in Unsuccessful predation on Middle Paleozoic plankton: Shell injury and anomalies in Devonian dacryoconarid tentaculites

Fig. 4. The shells of the Recent planktonic gastropod larvae bearing traces of repaired injuries. A. CGU JF819; A1, apical view of cypraeid protoconch with repaired apertural margin; A2, detailed view of specimen A1. B. CGU JF820; B1, detail of view of turrid protoconch; B2, lateral view of turrid protoconch. C. CGU JF821, naticid protoconch with repaired apertural margin. Damaged apertural margins indicated by white arrows. Scale bars 0.1 mm.

Fig. 2 in Unsuccessful predation on Middle Paleozoic plankton: Shell injury and anomalies in Devonian dacryoconarid tentaculites

Fig. 2. The shells of the Early Devonian dacryoconarid tentaculites, with anomalous development of the shell ornament or having repaired injuries. A. The Emsian Homoctenus hanusi Bouček, 1964 (NM L6288) from Daleje−Třebotov Formation, Prague Basin, Holyně locality. Views showing an anomalous development of the shell ornamentation. B. The Pragian Nowakia (Turkestanella) acuaria Richter, 1854 (NM L6291) from Praha Formation, Prague Basin, Bráník locality. Views showing the irregular development of the rings. C. The Emsian Nowakia elegans Barrande, 1867 (CGU PL3970) from the Zlíchov Formation, Prague Basin, Klukovice Locality. Several views demonstrating the damage and the manner of shell repair. All shells illustrated have the same orientation (growth direction is from right to left). Scale bars 1 mm.

Fig. 1 in Unsuccessful predation on Middle Paleozoic plankton: Shell injury and anomalies in Devonian dacryoconarid tentaculites

Fig. 1. Diagrams illustrating the total generic diversity of the Order Dacryoconarida and their turnover rates (relative origination and extinction rates). The generic diversity (including the both genera and subgenera) is defined as the number of generic taxa ranging through the time unit, plus half of the number of those confined to the unit or ranging beyond the time unit, but originating or ending within it. Relative turnover rates (origination or extinction) is defined as the total number of generic level taxa originating or going extinct within the time unit, divided by the total generic diversity. Analysis is based on data of Alberti (1993, 1997a, b, 1998, 2000) and Sepkoski (2002).

Fig. 3 in Unsuccessful predation on Middle Paleozoic plankton: Shell injury and anomalies in Devonian dacryoconarid tentaculites

Fig. 3. Reconstructions of the Emsian tentaculite Nowakia elegans Barrande, 1867. A. Adult shell having normal development. B. Reconstruction of the shell figured here as Fig. 2C.

Fig. 2 in Sublethal injuries in Early Devonian cephalopod shells from Morocco

Fig. 2. Remains of orthoconic nautiloids with minor healed fractures ("forma substructa" of Hölder, 1973; a slightly more extensive fracture in D, F), Tafilalt, Morocco. A. Spyroceras patronus (Barrande, 1866), limestone, with shell, MB.C.9652, bed KMO−I, Pragian, Filon Douce near Taouz, length 38 mm. B. Pseudorthoceratidae indet., limestone, with shell, MB.C.9675, bed KMO−II, Pragian, Filon Douce near Taouz, length 27 mm. C. Orthocycloceras sp., MB.C.9655, bed KMO−II, Pragian, Filon Douce near Taouz, length 33 mm. D. Spyroceras aff. patronus (Barrande, 1866), limestone, with shell, MB.C.9653, bed KMO−I, Pragian, Filon Douce near Taouz, height of displayed detail 11 mm; this specimen and the one in F display two fractures, easily detectable by the course of the ribs after the fracture which gradually changes to the "normal" course, compensating for the shell loss. E. Pseudorthoceratidae indet., limestone, with shell, MB.C.9595, bed KMO−II, Pragian, Filon Douce near Taouz, length 22.9 mm. F. Pseudorthoceratidae indet., PIMUZ 27030, limestone, with shell, latest Pragian or earliest Emsian, Gara Mdouara, length 175 mm. G. Anaspyroceras sp. aff. pseudocalamiteum (Barrande, 1868), limestone, with shell, MB.C.9680, bed KMO−III, Pragian, Filon Douce near Taouz, length 18.25 mm. H. Plagiostomoceras sp., limonitic internal mould, PIMUZ 27031, earliest Emsian, El Atrous, length 14.3 mm. I. Arionoceratidae indet., limestone, with shell, PIMUZ 27032, latest Pragian or earliest Emsian, Gara Mdouara, length 175 mm. The specimens of figures A–C and D–G were collected and photographed by Björn Kröger (Berlin). All specimens were coated with NH4Cl.

Fig. 3 in Sublethal injuries in Early Devonian cephalopod shells from Morocco

Fig. 3. Limonitic internal moulds of Devonobactrites obliquiseptatum (Sandberger and Sandberger, 1852) with minor healed injuries ("forma substructa" of Hölder, 1973) from the early Zlíchovian (early Emsian, Early Devonian) of the Tafilalt (Morocco). A. PIMUZ 7275, Ouidane Chebbi, note the small triangular fracture. B. PIMUZ 7273, Ouidane Chebbi, irregular insertion of ridges after injury. C. PIMUZ 27032, Oum El Jerane. D. PIMUZ 27033, Oum El Jerane; two injuries. E. MB.C.9545, bed EF, Filon Douze; note the deep fracture which extended over approximately one fourth of the body chamber length; at the posterior end of the fracture, two triangles can be seen as in C, reminding of other cephalopod bite−marks. F. PIMUZ 27034, Oum El Jerane; in this case, the mantle was most likely affected, causing the formation of a linear deformation in growth direction. G. PIMUZ 27040, south of Hassi Tachbit, near Ouidane Chebbi. H. PIMUZ 27035, Oum El Jerane; in contrast to most healed injuries, the apical end of the fracture is broad. I. PIMUZ 27036, Oum El Jerane. J. PIMUZ 27042, El Atrous, note the questionable terminal constriction, possibly indicating adulthood and not a malformation. K. PIMUZ 27037, Oum El Jerane. L. PIMUZ 27041, El Atrous; two injuries. M. PIMUZ 27038, Oum El Jerane. N. PIMUZ 27039, Oum El Jerane; like in F, the mantle was also affected, causing the formation of a linear deformation in growth direction. All specimens were coated with NH4Cl. The arrows indicate healed injuries unless otherwise stated.

opencc-by-4.0Aug 2020View details →

Dataset related to article "C3a receptor blockade protects podocytes from injury in diabetic nephropathy"

The file contains raw data related to the article "C3a receptor blockade protects podocytes from injury in diabetic nephropathy", available from <a href="https://insight.jci.org/articles/view/131849">https://insight.jci.org/articles/view/131849</a>. <ul> <li>Raw data vivo 1: evaluations of complement protein renal expression in vivo</li> <li>Raw data vivo 2: evaluations of systemic and laboratory parameters in vivo</li> <li>Raw data vivo 3: histological evaluation of glomerular damage in vivo</li> <li>Raw data vivo 4: histological evaluation of podocyte and mitochondrial dysfunction in vivo</li> <li>Raw data vitro 1: evaluations of mitochondrial functional integrity in cultured podocytes</li> <li>Raw data vitro 2: western blot analyses of mitochondrial proteins in cultured podocytes</li> <li>Raw data vitro 3: evaluations of mitochondrial bioenergetic changes in cultured podocytes</li> <li>Raw data vitro 4: evaluations of the effect of SS-31 in cultured podocytes</li> </ul>   Abstract of the manuscript: Renal activation of the complement system has been described in patients with diabetic nephropathy (DN), although its pathological relevance is still ill-defined. Here, we studied whether glomerular C3a, generated by uncontrolled complement activation, promotes podocyte damage, leading to proteinuria and renal injury in mice with type 2 diabetes. BTBR ob/ob mice exhibited podocyte loss, albuminuria, and glomerular injury accompanied by C3 deposits and increased C3a and C3a receptor (C3aR) levels. Decreased glomerular nephrin and α-actinin4 expression, coupled with integrin-linked kinase induction, were also observed. Treatment of DN mice with a C3aR antagonist enhanced podocyte density and preserved their phenotype, limiting proteinuria and glomerular injury. Mechanistically, ultrastructural and functional mitochondrial alterations, accompanied by downregulation of antioxidant superoxide dismutase 2 (SOD2) and increased protein oxidation, occurred in podocytes and were normalized by C3aR blockade. In cultured podocytes, C3a induced cAMP-dependent mitochondrial fragmentation. Alterations of mitochondrial membrane potential, SOD2 expression, and energetic metabolism were also found in response to C3a. Notably, C3a-induced podocyte motility was inhibited by SS-31, a peptide with mitochondrial protective effects. These data indicate that C3a blockade represents a potentially novel therapeutic strategy in DN for preserving podocyte integrity through the maintenance of mitochondrial functions.

openmit-licenseNov 2022View details →

Immune checkpoint molecule TIGIT regulates kidney T cell functions and mediates acute kidney injury

This dataset includes the single cell RNA-seq data associated with the publication listed in the title (abstract below). CellRanger.zip contains the raw transcript counts as produced by CellRanger. There is one folder per sample. The samples are indicated by the folder name (e.g. KO_Ctrl).  We have also included .h5ad files that contain of cells that passed quality control, as described in the manuscript. adTIGIT_raw_031422.h5ad contains all passing cells and the raw counts, as well as cell annotations ('celltype') adTIGIT_Tonly_091421.h5ad contains only T cells, .X contains the normalized data and T-cell sub-type ('cluster'). Abstract: T cells mediate pathologic and reparative processes during acute kidney injury (AKI) but exact mechanisms regulating kidney T cell functions are unclear. This study identified upregulation of the novel immune checkpoint molecule, TIGIT, on mouse and human kidney T cells following AKI. TIGIT-expressing kidney T cells produced proinflammatory cytokines and had effector and central memory phenotype. Kidney Tregs were predominantly TIGIT+ and reduced after ischemia reperfusion (IR) injury. TIGIT deficient mice had protection from both ischemic and nephrotoxic AKI. Single cell RNA sequencing led to discovery of possible downstream targets of TIGIT.  TIGIT mediates AKI pathophysiology, is a promising target for developing AKI therapy, and is being increasingly studied in human cancer therapy trials.

opencc-by-4.0Dec 2022View details →

Text-fig. 4. Taphonomic features of the studied localities of ammonoids. a: Sandstone slab with fragmentary remains of productid and spiriferid brachiopods, orthocerids, coiled nautiloids and ammonoids (stratigraphic level No. 3). b: Shell debris cluster and fragment of crushed ammonoid conch (stratigraphic level No. 1). c: Epibionts on the surface of an ammonoid conch (stratigraphic level No. 5). d: Cluster of bivalves, gastropods and cephalopods remains in a siderite nodule (stratigraphic level No. 5). e: Fragment of an ammonoid conch (stratigraphic level No. 3). f: Fragment of an ammonoid conch (?) with terminal aperture and brachiopod valve (stratigraphic level No. 3). g: Specimen of?Anthracoceratites sp. with conch injuries (shown by arrows) (stratigraphic level No. 8). h, i: Bioerosion trace fossils Cyclopuncta girtyi ELIAS, 1958 on the fragments of cephalopod conchs (stratigraphic level No. 5). j: Limonitized conchs of the ammonoid (stratigraphic level No. 7). k: Fragment of an ammonoid conch (stratigraphic level No. 5). Scale bars 10 mm. in Late Bashkirian Ammonoids From The Mospyne Formation Of The Donets Basin, Ukraine

Text-fig. 4. Taphonomic features of the studied localities of ammonoids. a: Sandstone slab with fragmentary remains of productid and spiriferid brachiopods, orthocerids, coiled nautiloids and ammonoids (stratigraphic level No. 3). b: Shell debris cluster and fragment of crushed ammonoid conch (stratigraphic level No. 1). c: Epibionts on the surface of an ammonoid conch (stratigraphic level No. 5). d: Cluster of bivalves, gastropods and cephalopods remains in a siderite nodule (stratigraphic level No. 5). e: Fragment of an ammonoid conch (stratigraphic level No. 3). f: Fragment of an ammonoid conch (?) with terminal aperture and brachiopod valve (stratigraphic level No. 3). g: Specimen of?Anthracoceratites sp. with conch injuries (shown by arrows) (stratigraphic level No. 8). h, i: Bioerosion trace fossils Cyclopuncta girtyi ELIAS, 1958 on the fragments of cephalopod conchs (stratigraphic level No. 5). j: Limonitized conchs of the ammonoid (stratigraphic level No. 7). k: Fragment of an ammonoid conch (stratigraphic level No. 5). Scale bars 10 mm.

opencc-by-4.0May 2022View details →

Dataset related to: Shiga Toxin 2 Triggers C3a-Dependent Glomerular and Tubular Injury through Mitochondrial Dysfunction in Hemolytic Uremic Syndrome

The files contain all the dataset included in the manuscript, divided by figure in each tab.   Abstract Shiga toxin (Stx)-producing Escherichia coli is the predominant offending agent of post-diarrheal hemolytic uremic syndrome (HUS), a rare disorder of microvascular thrombosis and acute kidney injury possibly leading to long-term renal sequelae. We previously showed that C3a has a critical role in the development of glomerular damage in experimental HUS. Based on the evidence that activation of C3a/C3a receptor (C3aR) signaling induces mitochondrial dysregulation and cell injury, here we investigated whether C3a caused podocyte and tubular injury through induction of mitochondrial dysfunction in a mouse model of HUS. Mice coinjected with Stx2/LPS exhibited glomerular podocyte and tubular C3 deposits and C3aR overexpression associated with cell damage, which were limited by C3aR antagonist treatment. C3a promoted renal injury by affecting mitochondrial wellness as demonstrated by data showing that C3aR blockade reduced mitochondrial ultrastructural abnormalities and preserved mitochondrial mass and energy production. In cultured podocytes and tubular cells, C3a caused altered mitochondrial fragmentation and distribution, and reduced anti-oxidant SOD2 activity. Stx2 potentiated the responsiveness of renal cells to the detrimental effects of C3a through increased C3aR protein expression. These results indicate that C3aR may represent a novel target in Stx-associated HUS for the preservation of renal cell integrity through the maintenance of mitochondrial function.

opencc-by-4.0Oct 2023View details →

Data from: Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury

This data pertain to the paper titled "Characterisation of GFAP-Expressing Glial Cells in the Dorsal Root Ganglion after Spared Nerve Injury " by Elena A. Konnova, Alexandru-Florian Deftu, Paul Chu Sin Chung, Marie Pertin, Guylène Kirschmann, Isabelle Decosterd and Marc R. Suter. The name of the data files correspond to the for each figure in the study. The data file in .csv format are organized so that they can easily be opened in R or other analysis language. To understand them and how they are labelled, it is advised to open the figure next to them and find the appropriate panel.Here are included:<ul><li>the representative images of immunohistochemistry for GFAP, IBA1, Ki67, NeuN, ATF3, FABP7, GS, Cx43, Kir4.1, MBP, L1CAM in the dorsal root ganglia (DRG) of hGFAP-CFP mice after spared nerve injury (SNI).</li><li>the western blot images of DRG samples and FACS sorted CFP+ cells from the DRG of hGFAP-CFP mice after SNI</li><li>the voltage clamp data of GFAP+ cells from DRG of hGFAP-CFP mice after SNI</li></ul>

closedIPD-NOFeb 2026View details →

Covered CP Stents for the Prevention or Treatment of Aortic Wall Injury Associated With Coarctation of the Aorta

ClinicalTrials.gov study NCT01278303. IPD Sharing: NO. Countries: 1. Publications: 1.

closedIPD-NOFeb 2026View details →

SAFEty Study of Early Infusion of Vitamin C for Treatment of Novel Coronavirus Acute Lung Injury (SAFE EVICT CORONA-ALI)

ClinicalTrials.gov study NCT04344184. IPD Sharing: NO. Countries: 1. Publications: 10.

A Study to Evaluate the Results of Facial Soft Tissue Reconstruction in Patients Who Have Suffered Traumatic Injury

ClinicalTrials.gov study NCT01345591. IPD Sharing: YES. Countries: 1. Publications: 3.

Short-term Atorvastatin's Effect on Acute Kidney Injury Following Cardiac Surgery

ClinicalTrials.gov study NCT00791648. IPD Sharing: YES. Countries: 1. Publications: 3.

Feasibility of Improving Sleep Apnea Treatment Adherence After Brain Injury

ClinicalTrials.gov study NCT04221009. IPD Sharing: YES. Countries: 1. Publications: 1.

Dysport® Treatment of Urinary Incontinence in Adults Subjects With Neurogenic Detrusor Overactivity (NDO) Due to Spinal Cord Injury or Multiple Sclerosis - Study 2

ClinicalTrials.gov study NCT02660359. IPD Sharing: YES. Countries: 16. Publications: 1.