scholarly journals SHROOM3, the gene associated with chronic kidney disease, affects the podocyte structure

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Ryo Matsuura ◽  
Atsuko Hiraishi ◽  
Lawrence B. Holzman ◽  
Hiroki Hanayama ◽  
Koji Harano ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Function ◽  
Genome Wide Association Study ◽  
Kidney Diseases ◽  
Vitro Experiment ◽  
Public Health Burden ◽  
In Vitro Experiment

AbstractChronic kidney disease is a public health burden and it remains unknown which genetic loci are associated with kidney function in the Japanese population, our genome-wide association study using the Biobank Japan dataset (excluding secondary kidney diseases, such as diabetes mellitus) clearly revealed that almost half of the top 50 single nucleotide polymorphisms associated with estimated glomerular filtration rate are located in the SHROOM3 gene, suggesting that SHROOM3 will be responsible for kidney function. Thus, to confirm this finding, supportive functional analyses were performed on Shroom3 in mice using fullerene-based siRNA delivery, which demonstrated that Shroom3 knockdown led to albuminuria and podocyte foot process effacement. The in vitro experiment shows that knockdown of Shroom3 caused defective formation of lamellipodia in podocyte, which would lead to the disruption of slit diaphragm. These results from the GWAS, in vivo and in vitro experiment were consistent with recent studies reporting that albuminuria leads to impairment of kidney function.

In Vitro Experimental Investigation of the Integrity of the Stem–Cement Interface

2013 ◽  
Vol 647 ◽  
pp. 53-56
Author(s):  
Hong Yu Zhang ◽  
Leigh Fleming ◽  
Liam Blunt
Keyword(s):  
Experimental Investigation ◽  
Fluid Flow ◽  
Hip Replacement ◽  
Hip Prosthesis ◽  
Vitro Experiment ◽  
Cement Interface ◽  
In Vitro Experiment ◽  
Mechanical Bonding

The rationale behind failure of cemented total hip replacement is still far from being well understood in a mechanical and molecular perspective. In the present study, the integrity of the stem–cement interface was investigated through an in vitro experiment monitoring fluid flow along this interface. The results indicated that a good mechanical bonding formed at the stem–cement interface before debonding of this interface was induced by physiological loadings during the in vivo service of the hip prosthesis.

scholarly journals The Association between Gut Microbiota and Uremia of Chronic Kidney Disease

2020 ◽  
Vol 8 (6) ◽  
pp. 907 ◽  
Author(s):  
Ji Eun Kim ◽  
Hyo-Eun Kim ◽  
Ji In Park ◽  
Hyunjeong Cho ◽  
Min-Jung Kwak ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Kidney Function ◽  
Kidney Diseases ◽  
Toxin Production ◽  
Positive Interactions ◽  
Uremic Toxin ◽  
Serum Concentrations ◽  
Pyruvate Metabolism

Chronic kidney disease (CKD)-associated uremia aggravates—and is aggravated by—gut dysbiosis. However, the correlation between CKD severity and gut microbiota and/or their uremic metabolites is unclear. We enrolled 103 CKD patients with stage 1 to 5 and 46 healthy controls. We analyzed patients’ gut microbiota by MiSeq system and measured the serum concentrations of four uremic metabolites (p-cresyl sulfate, indoxyl sulfate, p-cresyl glucuronide, and trimethylamine N-oxide) by liquid chromatography–tandem mass spectrometry. Serum concentrations of the uremic metabolites increased with kidney function deterioration. Gut microbial diversity did not differ among the examined patient and control groups. In moderate or higher stage CKD groups, Oscillibacter showed positive interactions with other microbiota, and the proportions of Oscillibacter were positively correlated with those of the uremic metabolites. The gut microbiota, particularly Oscillibacter, was predicted to contribute to pyruvate metabolism which increased with CKD progression. Relative abundance of Oscillibacter was significantly associated with both serum uremic metabolite levels and kidney function. Predicted functional analysis suggested that kidney-function-associated changes in the contribution of Oscillibacter to pyruvate metabolism in CKD may greatly affect the gut environment according to kidney function, resulting in dysbiosis concomitant with uremic toxin production. The gut microbiota could be associated with uremia progression in CKD. These results may provide basis for further metagenomics analysis of kidney diseases.

Cadmium Chloride Induces Memory Deficits and Hippocampal Damage by Activating the JNK/p66Shc/NADPH Oxidase Axis

2020 ◽  
Vol 39 (5) ◽  
pp. 477-490
Author(s):  
Attalla Farag El-kott ◽  
Ali S. Alshehri ◽  
Heba S. Khalifa ◽  
Abd-El-karim M. Abd-Lateif ◽  
Mohammad Ali Alshehri ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Cadmium Chloride ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Male Rats ◽  
Hippocampal Damage ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
In Vivo Experiment

This study investigated whether the mechanism underlying the neurotoxic effects of cadmium chloride (CdCl2) in rats involves p66Shc. This study comprised an initial in vivo experiment followed by an in vitro experiment. For the in vivo experiment, male rats were orally administered saline (vehicle) or CdCl2 (0.05 mg/kg) for 30 days. Thereafter, spatial and retention memory of rats were tested and their hippocampi were used for biochemical and molecular analyses. For the in vitro experiment, control or p66Shc-deficient hippocampal cells were treated with CdCl2 (25 µM) in the presence or absence of SP600125, a c-Jun N-terminal kinase (JNK) inhibitor. Cadmium chloride impaired the spatial learning and retention memory of rats; depleted levels of glutathione and manganese superoxide dismutase; increased reactive oxygen species (ROS), tumor necrosis factor α, and interleukin 6; and induced nuclear factor kappa B activation. Cadmium chloride also decreased the number of pyramidal cells in the CA1 region and induced severe damage to the mitochondria and endoplasmic reticulum of cells in the hippocampi of rats. Moreover, CdCl2 increased the total unphosphorylated p66Shc, phosphorylated (Ser36) p66Shc, phosphorylated JNK, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, cytochrome c, and cleaved caspase-3. A dose–response increase in cell death, ROS, DNA damage, p66Shc, and NADPH oxidase was also observed in cultured hippocampal cells treated with CdCl2. Of note, all of these biochemical changes were attenuated by silencing p66Shc or inhibiting JNK with SP600125. In conclusion, CdCl2 induces hippocampal ROS generation and apoptosis by promoting the JNK-mediated activation of p66Shc.

scholarly journals A Pilot Study of a Natural Food Supplement as New Possible Therapeutic Approach in Chronic Kidney Disease Patients

2020 ◽  
Vol 13 (7) ◽  
pp. 148 ◽  
Author(s):  
Annalisa Noce ◽  
Alessio Bocedi ◽  
Margherita Campo ◽  
Giulia Marrone ◽  
Manuela Di Lauro ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
High Performance ◽  
Glutathione Transferase ◽  
Food Supplement ◽  
Array Detector ◽  
Natural Food ◽  
Inflammatory Status

The identification of natural bioactive compounds, able to counteract the abnormal increase of oxidative stress and inflammatory status in chronic degenerative non-communicable diseases is useful for the clinical management of these conditions. We tested an oral food supplement (OFS), chemically characterized and evaluated for in vitro and in vivo activity. Vitamin C, analyzed by High Performance Liquid Chromatography-Diode Array Detector (HPLC-DAD), was 0.19 mg/g in rosehip dry extract and 15.74 mg/capsule in the OFS. The identification of polyphenols was performed by HPLC-DAD; the total antioxidant capacity was assessed by Folin–Ciocalteu test. Total polyphenols were 14.73 mg/g gallic acid equivalents (GAE) for rosehip extract and 1.93 mg/g GAE for OFS. A total of 21 chronic kidney disease (CKD) patients and 10 healthy volunteers were recruited. The evaluation of routine laboratory and inflammatory parameters, erythrocyte glutathione transferase (e-GST), human oxidized serum albumin (HSAox), and assessment of body composition were performed at two different times, at baseline and after 5 weeks of OFS assumption. In the study, we highlighted a significant decrease of traditional inflammatory biomarkers (such as C-reactive protein, erythrocyte sedimentation rate, platelet to lymphocyte ratio) and other laboratory parameters like e-GST, azotaemia, and albuminuria after OFS treatment in CKD patients. Moreover, we demonstrated a lipid profile improvement in CKD patients after OFS supplementation.

Surface Changes of Fluoride-Releasing Composites: a Comparison of in Vivo and in Vitro Results

1995 ◽  
Vol 9 (4) ◽  
pp. 348-354 ◽  
Author(s):  
G.E.H.M. Dijkman ◽  
J. De Vries ◽  
W.L. Jongebloed ◽  
J. Arends
Keyword(s):  
Mechanical Properties ◽  
Outer Surface ◽  
Tap Water ◽  
Surface Microhardness ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Over Time ◽  
Surface Changes

Fluoride-releasing composites lose fluoride very slowly over time. An interesting question is the possible change in mechanical properties related to the F release. If this happens, it might be expected that the mechanical properties of the outer surface of a fluoridating composite are affected first. The purpose of this study was to investigate in vivo and in vitro the changes in surface microhardness and surface structure of three fluoride-releasing composites and a non-F-containing control after 28 days. In the in vitro experiment, the composites were stored in tap water at 37°C. The results show that all composites stored in water were significantly softened after 28 days. In vivo, however, a very different picture emerged: The surface microhardness of the fluoride-releasing composites did not change significantly. In vitro, the data indicate that the amount of softening of the fluoridating composites is related to the amount of fluoride released. No relation was found between the amount of F released in one month in vitro and the microhardness changes in vivo. SEM micrographs of fluoridating composites do not reflect the microhardness changes mentioned.

scholarly journals Mitochondrial Targeting of Herbal Medicine in Chronic Kidney Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Qing Li ◽  
Changying Xing ◽  
Yanggang Yuan
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Herbal Medicine ◽  
Mitochondrial Function ◽  
Conventional Medicine ◽  
Treatment Options ◽  
Renal Diseases ◽  
Public Health Issue

Chronic kidney disease (CKD) is a common progressive disease that is typically characterized by the permanent loss of nephrons and an eventual decline in glomerular filtration rate. CKD increases mortality and has a significant impact on the quality of life and the economy, which is becoming a major public health issue worldwide. Since current conventional-medicine treatment options for CKD are not satisfactory, many patients seek complementary and alternative medicine treatments including Traditional Chinese Medicine. Herbal medicine is often used to relieve symptoms of renal diseases in the clinic. The kidney is abundant in the number of mitochondria, which provide enough energy for renal function and metabolism. In recent years, a vital role for mitochondrial dysfunction has been suggested in CKD. Mitochondria have become a new target for the treatment of diseases. A growing number of studies have demonstrated herbal medicine could restore mitochondrial function and alleviate renal injury both in vivo and in vitro. In this review, we sum up the therapeutic effect of herbal medicine in CKD via targeting mitochondrial function. This implies future strategies in preventing CKD.

Abstract 17562: GPCR Gβγ Signaling Mediates Renal Dysfunction and Fibrosis in Heart Failure Mice

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Fadia A Kamal ◽  
Joshua G Travers ◽  
Allison E Schafer ◽  
Qing Ma ◽  
Prasad Devarajan ◽  
...  
Keyword(s):  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Dysfunction ◽  
G Protein ◽  
Kidney Diseases ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Direct Role

Background: Cardiorenal syndrome type 2 (CRS2), the development of chronic kidney disease (CKD) secondary to chronic heart failure (CHF), is clinically associated with increased incidence of organ failure and reduced survival. Heart and kidney damage in CRS2 is greatly caused by chronic stimulation of the adrenergic and endothelin receptors as a result of elevated neurohormonal signaling of the sympathetic nervous system (SNS) and its downstream endothelin (ET) system, respectively. These receptors belong to the superfamily of G protein-coupled receptors (GPCRs). While chronic GPCR stimulation and its associated upregulated interaction between the G-protein βγ subunit (Gβγ), the GPCR-kinase 2 (GRK2) and β-arrestin are known to be central to various cardiovascular diseases, their role in kidney diseases are by far unknown and beg investigation. Objective: CRS2 animal studies utilize combine ischemic cardiac injury and renal injury, which is of poor clinical relevance. Our study investigates: (1) the development of chronic kidney disease (CKD) in a model of non-ischemic CHF without inducing surgical kidney injury, aiming to establish a more clinically relevant CRS2 model. (2) The possible salutary effect of renal GPCR-Gβγ inhibition in CKD developed in the established CRS2 model. Methods and results: We utilized transverse aortic constriction (TAC) as a non-ischemic hypertrophic murine CHF model. Twelve weeks after TAC, mice developed CKD secondary to CHF suggesting a CRS2 model. This was associated with elevated renal GPCR-Gβγ signaling and ET system expression. Importantly, systemic pharmacologic Gβγ inhibition by gallein attenuated these renal pathological changes in parallel with alleviated CHF. A direct effect of gallein on the kidney was subsequently confirmed in a bilateral ischemia reperfusion acute kidney injury (AKI) mouse model where it attenuated renal dysfunction, tissue damage and ET system activation, indicating a direct role for GPCR-Gβγ signaling in AKI. Further, in vitro studies in mouse embryonic fibroblasts showed a key role for ET receptor-Gβγ signaling in fibroblast activation. Conclusion: Our data suggest TAC as a clinically relevant CRS2 model and GPCR-Gβγ inhibition as a novel therapeutic approach for CRS2 and AKI.

scholarly journals Alternative control of post-harvest diseases in Tainung 1 papaya

2018 ◽  
Vol 48 (1) ◽  
pp. 29-35 ◽  
Author(s):  
Andréa Mirne de Macêdo Dantas ◽  
Selma Rogéria de Carvalho Nascimento ◽  
Beatriz Letícia Silva da Cruz ◽  
Fernando Henrique Alves da Silva ◽  
Márcia Michelle de Queiroz Ambrósio ◽  
...  
Keyword(s):  
Essential Oil ◽  
Mycelial Growth ◽  
Vitro Experiment ◽  
In Vitro Experiment ◽  
Post Harvest ◽  
Randomized Design ◽  
Clove Essential Oil

ABSTRACT Controlling post-harvest papaya diseases without using agrochemicals is a challenge for producers. This study aimed at evaluating the effect of clove essential oil, biological fungicide (Trichodermil®), resistance inducer (Cob Sistem®) and chemical fungicide (Imazacure®) on the in vitro control of phytopathogenic fungi isolates from papaya as well as on the post-harvest quality of Tainung 1 papaya. The in vitro experiment was conducted in a complete randomized design, with five fungal species x five treatments and five replications. The in vivo experiment was conducted in a complete randomized design, with five treatments x five storage times, five replications and three fruits per replication. The fruits were stored under refrigeration at 10 ± 2 ºC and 90 ± 5 % of relative humidity and evaluated at 0, 7, 14, 21 and 28 days of storage, plus two shelf life days at 25 ± 2 ºC, to simulate marketing conditions. The inhibition of mycelial growth was evaluated in the in vitro experiment, while the diseases occurrence and post-harvest quality of the fruits were evaluated in the in vivo experiment. The clove essential oil and Trichodermil® were as efficient as Imazacure® in inhibiting the mycelial growth of Alternaria sp., Colletotrichum gloeosporioides and Rhizopus sp. The treatments with clove essential oil, Trichodermil® and Imazacure® were similar in controlling the pathogens up to 21 days of storage. The treatments had no effect on the fruits soluble solid contents.

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