Статті в журналах: "Tubular injuries"

1

Kato, Takashi, Man Hagiyama, Yasutoshi Takashima, Azusa Yoneshige, and Akihiko Ito. "Cell adhesion molecule-1 shedding induces apoptosis of renal epithelial cells and exacerbates human nephropathies." American Journal of Physiology-Renal Physiology 314, no. 3 (March 1, 2018): F388—F398. http://dx.doi.org/10.1152/ajprenal.00385.2017.

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Chronic kidney disease (CKD) is an important problem throughout the world, associated with the increase of blood urea nitrogen (BUN) and serum creatinine (sCre) and with renal tubular injuries. It is crucial to elucidate the molecular mechanisms of renal injuries to identify the new therapeutics and early diagnostic methods. We focused on cell adhesion molecule-1 (CADM1) protein. CADM1, its isoform SP4, is expressed in the epithelial cells of various tissues, including renal distal tubules, localized on the lateral cell membrane, mediates cell-cell adhesion via trans-homophilic binding, and interacts with various proteins. We previously reported that its expression was downregulated by post-proteolytic cleavage (α- and β-shedding) in pulmonary diseases. To investigate whether CADM1 α-shedding occurs in human nephropathies, we performed Western blotting and immunohistochemical analysis of specimens with arterionephrosclerosis (AS) and diabetic nephropathy (DN) from autopsied kidneys. CADM1 α-shedding was induced in AS and DN kidneys and derived from the decrease in full-length CADM1 (FL-CADM1) and increase of the COOH-terminal fragment (α-CTF). In particular, the reduced FL-CADM1 level was correlated with tubular and tubulointerstitial injuries and the increases in BUN and sCre levels. Apoptosis of renal tubular epithelial cells (TECs) was promoted in both nephropathies, and it was significantly correlated with the decrease in the FL-CADM1. Furthermore, FL-CADM1 knockdown by small interfering RNA downregulated anti-apoptotic Bcl-2 protein and promoted apoptosis of cultured renal TECs. The present study suggests that the reduction of FL-CADM1 leads to renal TEC apoptosis and could exacerbate renal tubular and tubulointerstitial injuries, which contribute to the development of CKD.

2

Guan, Yu, Daisuke Nakano, Lei Li, Haofeng Zheng, Akira Nishiyama, Ye Tian, and Lei Zhang. "Protease-Activated Receptor 1 Contributes to Microcirculation Failure and Tubular Damage in Renal Ischemia-Reperfusion Injury in Mice." BioMed Research International 2021 (February 23, 2021): 1–8. http://dx.doi.org/10.1155/2021/6665714.

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Ischemia-reperfusion- (IR-) induced kidney injury is difficult to avoid during renal transplantation and robot-assisted partial nephrectomy. Renal IR injury is characterized by tubular damage, microcirculation failure, and inflammation, which coordinately augment renal injury; however, no specific treatment is available for these conditions. Protease-activated receptor-1 (PAR-1) and its ligand, thrombin, are involved in coagulation and were shown to be associated with epithelial cell injury. Here, we hypothesized that PAR-1 exaggerated renal IR-induced tubular cell damage and microcirculation failure and that pharmacological inhibition of PAR-1 by Q94 could prevent these injuries. Renal warm IR increased the expression of PAR-1 in the renal tubules. Q94 attenuated renal IR-induced changes and histopathological damage. Microcirculation failure analyzed by congestion in the histopathology and blood cell flow examined by intravital multiphoton microscopy were suppressed by Q94 treatment. Q94 also dramatically increased tubular cell proliferation despite the lower renal damage. Thrombin suppressed cell proliferation and induced apoptosis in the tubules; these effects were prevented by Q94 treatment. Taken together, PAR-1 was associated with renal IR injury. Inhibition of PAR-1 ameliorated injury possibly by improving renal microcirculation and tubular cell survival/proliferation.

3

Hosohata, Keiko, Denan Jin, Shinji Takai, and Kazunori Iwanaga. "Vanin-1 in Renal Pelvic Urine Reflects Kidney Injury in a Rat Model of Hydronephrosis." International Journal of Molecular Sciences 19, no. 10 (October 16, 2018): 3186. http://dx.doi.org/10.3390/ijms19103186.

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Urinary tract obstruction and the subsequent development of hydronephrosis can cause kidney injuries, which results in chronic kidney disease. Although it is important to detect kidney injuries at an early stage, new biomarkers of hydronephrosis have not been identified. In this study, we examined whether vanin-1 could be a potential biomarker for hydronephrosis. Male Sprague-Dawley rats were subjected to unilateral ureteral obstruction (UUO). On day 7 after UUO, when the histopathological renal tubular injuries became obvious, the vanin-1 level in the renal pelvic urine was significantly higher than that in voided urine from sham-operated rats. Furthermore, vanin-1 remained at the same level until day 14. There was no significant difference in the serum vanin-1 level between sham-operated rats and rats with UUO. In the kidney tissue, the mRNA and protein expressions of vanin-1 significantly decreased, whereas there was increased expression of transforming growth factor (TGF)-β1 and Snail-1, which plays a pivotal role in the pathogenesis of renal fibrosis via epithelial-to-mesenchymal transition (EMT). These results suggest that vanin-1 in the renal pelvic urine is released from the renal tubular cells of UUO rats and reflects renal tubular injuries at an early stage. Urinary vanin-1 may serve as a candidate biomarker of renal tubular injury due to hydronephrosis.

4

Huang, Liang-Ti, and Chung-Ming Chen. "Kidney Injuries and Evolution of Chronic Kidney Diseases Due to Neonatal Hyperoxia Exposure Based on Animal Studies." International Journal of Molecular Sciences 23, no. 15 (July 31, 2022): 8492. http://dx.doi.org/10.3390/ijms23158492.

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Preterm birth interrupts the development and maturation of the kidneys during the critical growth period. The kidneys can also exhibit structural defects and functional impairment due to hyperoxia, as demonstrated by various animal studies. Furthermore, hyperoxia during nephrogenesis impairs renal tubular development and induces glomerular and tubular injuries, which manifest as renal corpuscle enlargement, renal tubular necrosis, interstitial inflammation, and kidney fibrosis. Preterm birth along with hyperoxia exposure induces a pathological predisposition to chronic kidney disease. Hyperoxia-induced kidney injuries are influenced by several molecular factors, including hypoxia-inducible factor-1α and interleukin-6/Smad2/transforming growth factor-β, and Wnt/β-catenin signaling pathways; these are key to cell proliferation, tissue inflammation, and cell membrane repair. Hyperoxia-induced oxidative stress is characterized by the attenuation or the induction of multiple molecular factors associated with kidney damage. This review focuses on the molecular pathways involved in the pathogenesis of hyperoxia-induced kidney injuries to establish a framework for potential interventions.

5

Gosling, Peter, and Anne J. Sutcliffe. "Proteinuria following Trauma." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 23, no. 6 (November 1986): 681–85. http://dx.doi.org/10.1177/000456328602300610.

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Thirteen trauma patients admitted to a major injuries unit were classified according to their injury severity. Urinary excretion of total protein, albumin and gamma glutamyl transpeptidase (GGT) activity were assessed over the following 6 days. All patients showed an initial glomerular and tubular proteinuria during the first 24 h which subsided by the second post-trauma day. The excretion of total protein and albumin was positively correlated with injury severity. Those patients with the severest injuries showed a marked recurrent total proteinuria around days 3 to 4 post-trauma which exhibited features of a tubular lesion. The recurrent proteinuria peak coincided with peak levels of serum c-reactive protein (CRP).

6

Duffy, Patrick, Seán McMahon, Xi Wang, Shane Keaveney, Eoin D. O'Cearbhaill, Iban Quintana, Francisco J. Rodríguez та Wenxin Wang. "Synthetic bioresorbable poly-α-hydroxyesters as peripheral nerve guidance conduits; a review of material properties, design strategies and their efficacy to date". Biomaterials Science 7, № 12 (2019): 4912–43. http://dx.doi.org/10.1039/c9bm00246d.

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7

Watanabe, Toru. "Kidney and Urinary Tract Involvement in Kawasaki Disease." International Journal of Pediatrics 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/831834.

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Kawasaki disease (KD) is a systemic vasculitis and can develop multiple organ injuries including kidney and urinary tract involvement. These disorders include pyuria, prerenal acute kidney injury (AKI), renal AKI caused by tubulointerstitial nephritis (TIN), hemolytic uremic syndrome (HUS), and immune-complex mediated nephropathy, renal AKI associated with either Kawasaki disease shock syndrome or unknown causes, acute nephritic syndrome (ANS), nephrotic syndrome (NS), renal tubular abnormalities, renal abnormalities in imaging studies, and renal artery lesions (aneurysms and stenosis). Pyuria is common in KD and originates from the urethra and/or the kidney. TIN with AKI and renal tubular abnormalities probably result from renal parenchymal inflammation caused by T-cell activation. HUS and renal artery lesions are caused by vascular endothelial injuries resulting from vasculitis. Some patients with ANS have immunological abnormalities associated with immune-complex formation. Nephromegaly and renal parenchymal inflammatory foci are detected frequently in patients with KD by renal ultrasonography and renal scintigraphy, respectively. Although the precise pathogenesis of KD is not completely understood, renal vasculitis, immune-complex mediated kidney injuries, or T-cell immune-regulatory abnormalities have been proposed as possible mechanisms for the development of kidney and urinary tract injuries.

8

Futrakul, Narisa, and P. Futrakul. "Renal microvascular and tubular injuries in type II diabetic nephropathy." Kidney International 74, no. 3 (August 2008): 390. http://dx.doi.org/10.1038/ki.2008.173.

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9

Taneda, Sekiko, Kazuho Honda, Kimiko Tomidokoro, Kenta Uto, Kosaku Nitta, and Hideaki Oda. "Eicosapentaenoic acid restores diabetic tubular injury through regulating oxidative stress and mitochondrial apoptosis." American Journal of Physiology-Renal Physiology 299, no. 6 (December 2010): F1451—F1461. http://dx.doi.org/10.1152/ajprenal.00637.2009.

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The present study was designed to elucidate a possible mechanism of hyperglycemia-induced tubular injury and to examine a therapeutic potential of dietary eicosapentaenoic acid (EPA) for the prevention of diabetic kidney disease. Utilizing streptozotocin-induced diabetic mice, the extents of albuminuria and histological injuries were monitored at 2 wk after diabetic induction. Reactive oxygen species (ROS) production, apoptosis, and hypoxia in the kidney were evaluated by immunohistochemistry and Western blotting. An in vitro study was performed using rat proximal tubular cells (NRK-52E) to confirm the protective effect of EPA for methylglyoxal (MG)-induced ROS generation and staurosporine (STS)-induced mitochondrial apoptosis. The extents of albuminuria and histological tubular injuries were significantly lower in EPA-treated diabetic mice compared with untreated diabetic mice. The levels of lipid peroxidation product (4-hydroxy-2-nonenal), oxidative DNA damage (8-hydoxy-deoxyguanosine), and mitochondrial apoptosis (TUNEL, caspase-9, cleaved caspase-3, and cytochrome c release) in the tubular cells were also significantly lower in EPA-treated diabetic mice. Furthermore, hypoxia-inducible factor (HIF)-1α expression was significantly upregulated in the kidney tissues from EPA-treated mice compared with untreated diabetic mice. MG-induced ROS overproduction and STS-induced mitochondrial apoptosis in NRK-52E cells were significantly reduced by EPA treatment in vitro. These results indicated that the ROS generation and mitochondrial apoptosis were involved in hyperglycemia-induced tubular injury and EPA had a beneficial effect by suppressing ROS generation and mitochondrial apoptosis partly through augmentation of an HIF-1α response in diabetic kidney disease.

10

Xiong, Mingxia, Lei Jiang, Yang Zhou, Wenjing Qiu, Li Fang, Rouyun Tan, Ping Wen та Junwei Yang. "The miR-200 family regulates TGF-β1-induced renal tubular epithelial to mesenchymal transition through Smad pathway by targeting ZEB1 and ZEB2 expression". American Journal of Physiology-Renal Physiology 302, № 3 (1 лютого 2012): F369—F379. http://dx.doi.org/10.1152/ajprenal.00268.2011.

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Most chronic kidney injuries inevitably progress to irreversible renal fibrosis. Tubular epithelial-to-mesenchymal transition (EMT) is recognized to play pivotal roles in the process of renal fibrosis. However, a comprehensive understanding of the pathogenesis of renal scar formation and progression remains an urgent task for renal researchers. The endogenously produced microRNAs (miRNAs), proved to play important roles in gene regulation, probably regulate most genes involved in EMT. In this study, we applied microarray analysis to investigate the expression profiles of miRNA in murine interstitial fibrotic kidneys induced by unilateral ureteral obstruction (UUO). It was found that miR-200a and miR-141, two members of the miR-200 family, were downregulated at the early phase of UUO. In TGF-β1-induced tubular EMT in vitro, it was also found that the members of the miR-200 family were downregulated in a Smad signaling-dependent manner. It was demonstrated that the miR-200 family was responsible for protecting tubular epithelial cells from mesenchymal transition by target suppression of zinc finger E-box-binding homeobox (ZEB) 1 and ZEB2, which are E-cadherin transcriptional repressors. The results suggest that downregulation of the miR-200 family initiates the dedifferentiation of renal tubules and progression of renal fibrosis, which might provide important targets for novel therapeutic strategies.

11

Savka, Ivan, Valentyn Malyshev, and Svitlana Savka. "A new sight on the biomechanics of fractures of the lower extremity long tubular bones." Forensic-medical examination, no. 1 (May 29, 2017): 61–65. http://dx.doi.org/10.24061/2707-8728.1.2017.14.

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The main objective of our work is to study of the modern aspects of the biomechanics of fractures of the lower extremity long tubular bones in cases of mechanical trauma. The objects of our studies were 576 samples and 128 expert cases with injuries of the femoral bones, tibia and fibula. The data obtained were statistically processed with the use of multi-factor dispersion analysis. Three grouped hierarchical biomechanical modules have been found to be the most reasonable to apply in detection of mechanical and morphogenesis of fractures of low extremity long tubular bones: elasticity, stiffness and solidity including the most valuable diagnostic morphological signs grouped by the degree of their influence on destructive processes of the given bones. Objective: to study of the modern aspects of the biomechanics of fractures of the lower extremity long tubular bones in cases of mechanical trauma for objective retrospective establishment of the mechanisms of fracture formation. Materials and methods. The material of our study included 576 samples of the femoral bone, tibia and fibula, taken from 16 male and female biomannequins aged from 24 to 70 without their traumatic injuries, visual pathological changes or some mentions about them in the anamnesis. Expert examinations involved also 82 individuals with 128 injures of the lower extremities: femurs – 40 cases, tibia – 46 cases, fibula – 42 cases. The data obtained were statistically processed with the use of multi-factor dispersion analysis. Conclusions: Various portions of long tubular bones of the lower extremity have a number of structural-functional It is presented in macro- and micro-architecture of the bone and influences upon the resistance to external mechanical forces and morphological characteristics of fractures of these bones. Three grouped hierarchical biomechanical modules have been found to be the most reasonable to apply in detection of mechanical and morphogenesis of fractures of low extremity long tubular bones: elasticity, stiffness and solidity including the most valuable diagnostic morphological signs grouped by the degree of their influence on destructive processes of the given Prospects of further studies. The prospects of future studies consists of further comprehensive examination of interrelations between the main structural components of the osseous tissue and regularities of formation of morphological signs in case of fractures of various bones of the human skeleton.

12

Aidarov, R. B. "Treatment of patients with open fractures of long tubular bones with a new external fixation device." Kazan medical journal 68, no. 6 (December 15, 1987): 426–29. http://dx.doi.org/10.17816/kazmj96691.

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The problem of treatment of patients with open metadiaphyseal fractures of long tubular bones is relevant due to the increasing frequency of these injuries and their particular severity.From 1978 to 1983 there were 213 patients with open metadiaphyseal fractures of long tubular bones in the traumatology departments of the emergency hospital. There were 175 (82%) men and 38 (18%) women. The majority (72.7%) were persons of the most employable age, from 21 to 50 years old. There were 45 (21.4%) persons admitted under the influence of alcohol.

13

Igawa, T., K. Matsumoto, S. Kanda, Y. Saito, and T. Nakamura. "Hepatocyte growth factor may function as a renotropic factor for regeneration in rats with acute renal injury." American Journal of Physiology-Renal Physiology 265, no. 1 (July 1, 1993): F61—F69. http://dx.doi.org/10.1152/ajprenal.1993.265.1.f61.

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Hepatocyte growth factor (HGF), a potent mitogen for mature hepatocytes, possesses mitogenic and morphogenic activities for renal epithelial cells. To examine the renotropic function of HGF, we investigated the expression of HGF mRNA and HGF activity in the rat kidney after acute renal failure. When acute renal failure was induced by ischemia or by HgCl2 administration, a DNA synthesis occurred predominantly in the renal tubular cells located in the outer medulla with a peak at 48 h after the treatments. In both renal injuries, HGF mRNA in the kidney increased markedly, reaching a maximum 6 to 12 h after the treatments. HGF activity in the kidney also increased to three- to fourfold higher level than the normal level at 12 h after ischemic treatment or HgCl2 administration. In situ hybridization and immunohistochemical analysis indicated that both HGF mRNA and HGF protein were expressed in renal interstitial cells, presumably endothelial cells and macrophages, but not in tubular epithelial cells. In addition, HGF activity in the plasma of rats with renal ischemia or HgCl2 administration rapidly increased, reaching a maximum at 6 h after the treatment. One week after these injuries, HGF mRNA and HGF activity reverted to normal levels, and renal tubular cell regeneration ceased. Moreover, intravenous injection of human recombinant HGF into mice with acute renal failure caused by HgCl2 administration stimulated DNA synthesis of renal tubular cells in vivo.(ABSTRACT TRUNCATED AT 250 WORDS)

14

Skryabin, Evgeny G., and Mikhail A. Akselrov. "Fractures of long tubular bones in newborns: mechanisms of injuries, methods of diagnosis, and treatment." Pediatric Traumatology, Orthopaedics and Reconstructive Surgery 6, no. 4 (December 28, 2018): 70–76. http://dx.doi.org/10.17816/ptors6470-76.

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Background. Medical information on the provision of emergency trauma care to newborns with fractures of tubular bones is scarce. Aim. This scientific review aimed to inform children's orthopedic traumatologists regarding the main mechanisms of injury, methods of diagnosis, and treatment of fractures of long tubular bones in newborns. Material and methods. The article presents a systematic analysis of 60 scientific works of domestic and foreign authors on topical aspects of fractures of long tubular bones in newborns from 1986 to 2018. For writing the literature review, we used modern electronic databases of medical information: PubMed, MEDLINE, Ulrich’s Periodicals Directory, DOAJ, Cyberleninka, and еLibrary. Results and discussion. Similarly from the analysis of scientific publications, the main mechanism of fractures of limb segments in newborns is intranatal trauma, in which the child can receive both during birth through the birth canal and during cesarean section. The predisposing factors for obtaining bone fractures are intrauterine osteopenia, congenital diseases of the digestive system, and prematurity. Fractures are diagnosed on the basis of clinical examination and results of ultrasound and X-ray studies of the injured limb. In the treatment of limb bone fractures, both conservative and surgical methods are used. In recent years, a tendency has been clearly observed in scientific publications, highlighting the ever-widening introduction into clinical practice of operational methods for stabilizing fractures of long tubular bones in newborns, including using the techniques of transosseous osteosynthesis. Conclusion. The presented article fills the existing gap of summarizing scientific publications on the treatment of fractures of limbs in newborns.

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CODEA, Razvan Andrei, Mircea MIRCEAN, Sidonia Alina BOGDAN, Andras Laszlo NAGY, Alexandra BIRIS, Orsolya SARPATAKI, Ionut IONUT, et al. "Urinary N-Acetyl-Beta-D-Glucosaminidase Activity in Rat Experimental Ischemic and Toxic Models of Acute Kidney Injury." Bulletin of University of Agricultural Sciences and Veterinary Medicine Cluj-Napoca. Veterinary Medicine 74, no. 1 (May 18, 2017): 105. http://dx.doi.org/10.15835/buasvmcn-vm:12618.

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The identification of a suitable prevention method which facilitates limiting the deleterious effects of acute kidney injuries is highly required. In order to identify a proper treatment for acute kidney injuries, a suitable experimental model that replicates the structural, metabolic and inflammatory lesions that occur in the natural acute injured kidney is highly necessary. Intense urinary NAG activity can be found in a variety of renal disease such as toxic nephropathies, ischemic renal injury following cardiac surgery or renal transplantation but also in glomerular disease especially in diabetic nephropathy. Rises in urinary NAG enzyme activity strongly suggests tubular cell damage and support NAG enzyme as a biomarker of renal tubular injury. The aim of this paper is to obtain a stable in vivo acute kidney injury experimental model, in Wistar, rats and to evaluate the urinary activity of N-acetyl-Î²-D-glucosaminidase (NAG) enzyme, blood levels of urea and creatinine and microstructural renal alterations induced by ischemia/reperfusion injury respectively gentamicin nephrotoxicity. For this purpose we have used a rat experimental model. Adult male Wistar rats weighing 250-300 g were randomly divided into 3 groups with 8 rats in each group. Group 1 served as a model for the renal ischemia/reperfusion injury experiment, group 2 served for toxic kidney injury experimental model and group 3 served as control group. All individuals in both groups 1 and 2 presented marked elevations in blood urea and creatinine at the moment of euthanasia (day 3 for group 1 and day 9 for group 2) compared to the control group where biochemical values remained within normal limits. Urine analysis of both group 1 and 2 showed marked urinary NAG index activity which suggests acute tubular injury, suggestion confirmed by histological evaluation of the renal parenchyma sampled from this subjects

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Nishida, Yuzo, Yuuta Ito, and Takahiro Satoh. "Origin of Renal Proximal Tubular Injuries by Fe(III)-nta Chelate." Zeitschrift für Naturforschung C 62, no. 7-8 (August 1, 2007): 608–12. http://dx.doi.org/10.1515/znc-2007-7-825.

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Interaction between apo-transferrin and several iron(III) chelates has been investigated in terms of the capillary electrophoresis method. Based on the results, it has been clarified that (i) a binuclear iron(III) unit with an oxo-bridge is necessary for the facile transfer of an iron atom from the iron(III) chelate to apo-transferrin, and (ii) the renal proximal tubular injuries by Fe(III)-nitrilotriacetate (Fe-nta) should be due to the unique binuclear structure of this complex, which gives a peroxide adduct of the binuclear Fe-nta in the presence of glutathione cycle and oxygen

17

Yu, Xiao, Wei-long Li, Qing-jiang Pang, and Rong-li Zhou. "Finite element analysis of locking plate and 1/4 tubular plate for first tarsometatarsal joint fracture-dislocation." Journal of International Medical Research 45, no. 5 (July 31, 2017): 1528–34. http://dx.doi.org/10.1177/0300060517707114.

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Objective The optimal plate for fixation of tarsometatarsal joint injuries is controversial. The objective of this study was to compare the biomechanical characteristics between a locking plate and 1/4 tubular plate for first tarsometatarsal joint fracture-dislocation. Method Finite element analysis was used after establishment of a first tarsometatarsal joint fracture-dislocation model. Two implant simulations using a locking plate and five-hole 1/4 tubular plate were designed to simulate fixation of the fracture-dislocation. The displacement of the first tarsometatarsal articular surface and the stress distribution in the implants were calculated. Results A 700-N load was applied to both models. The minimum displacement of the articular surface in the locking plate and 1/4 tubular plate model was 0.6471 mm and 0.3833 mm, respectively. The maximum principal stress in the locking plate and 1/4 tubular plate was 1.212 × 103 MPa and 1.107 × 103 MPa, respectively. Conclusion Use of a 1/4 tubular plate is recommended for fixation of first tarsometatarsal joint fracture-dislocation after consideration of other factors such as economical issues.

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Gordienko, Ivan Ivanovich, Semen Aleksandrovich Borisov, and Natalya Aleksandrovna Tsap. "The antibiotic prophylaxis algorithm for open hand injuries in children. Experimental study." Journal of Experimental and Clinical Surgery 12, no. 3 (June 3, 2019): 187–92. http://dx.doi.org/10.18499/2070-478x-2019-12-3-187-192.

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Relevance. The rapid development of new technologies in surgery has opened up broad horizons for the implementation of complex surgical interventions. At the same time, the duration of operations was reduced, the invasiveness decreased, and broad operational approaches began to go into the past. However, the infectious process in the area of operative action remains an acute problem of surgery today. Infections of the surgical area (OSIW) are infections that develop within 30 days after surgery or within a year after installing the prosthesis (heart valves, blood vessels or joint).Aim. Develop an algorithm for perioperative antibiotic prophylaxis for open tubular fractures based on experimental research.Methods. An experimental study was conducted on 60 adult guinea pigs, which created a model of an open femur fracture. All animals were divided into 3 groups depending on the timing of the introduction of antibacterial drugs. The degree of local manifestations was assessed according to the developed scale from 0 to 2 points, where 0 is the total absence of inflammatory manifestations, and 2 points is their maximum manifestation. The signs of inflammation were also evaluated in the general clinical blood test.Results. During the experiment it was revealed that the introduction of antibacterial drugs for open fractures of tubular bones is necessary for prophylactic purposes. An increase in the timing of the introduction of antibiotics to three days or more is not rational, since there are no significant differences compared with a shorter course of antibiotic prophylaxis. Conclusions. Experimental perioperative antibiotic prophylaxis (PAP) on the model of an open fracture of the tubular bone indicated the possibility of introducing the PAP algorithm for open hand injuries in children.

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Ji, Linlin, Qingzhu Wang, Fengjuan Huang, Tingting An, Feng Guo, Yanyan Zhao, Yang Liu, Yanyan He, Yi Song, and Guijun Qin. "FOXO1 Overexpression Attenuates Tubulointerstitial Fibrosis and Apoptosis in Diabetic Kidneys by Ameliorating Oxidative Injury via TXNIP-TRX." Oxidative Medicine and Cellular Longevity 2019 (March 6, 2019): 1–14. http://dx.doi.org/10.1155/2019/3286928.

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Objective. The generation of hyperglycemia-induced reactive oxygen species (ROS) is a key event in diabetic nephropathy (DN) development. Since forkhead box class O1 (FOXO1) is associated with oxidative stress and shows a positive effect on DN, its role on renal function and the underlying mechanism is still unclear. Methods. We examined the role of FOXO1 in vivo (in a transgenic diabetic mouse model overexpressing Foxo1) and in vitro (in human HK-2 cells with FOXO1 knockin (KI) and knockout (KO) cultured under high glucose). Results. Renal proximal tubular cells of kidney biopsies from patients with DN showed tubulointerstitial fibrosis and apoptosis. Accordingly, these proximal tubular injuries were accompanied by the increase of ROS generation in diabetic mice. Tissue-specific Foxo1 overexpression in transgenic mice had a protective effect on the renal function and partially reversed tubular injuries by attenuating the diabetes-induced increase in TXNIP and decrease in the TRX levels. FOXO1 knockin and knockout HK-2 cells were constructed to identify the associations between FoxO1 and TXNIP-TRX using CRISPR/CAS9. Similarly, the effects of FOXO1 KI and KO under high glucose were significantly modulated by the treatment of TRX inhibitor PX-12 and TXNIP small interfering RNA. In addition, TXNIP and TXN were identified as the direct FOXO1 transcriptional targets by chromatin immunoprecipitation. Conclusion. The regulatory role of FOXO1/TXNIP-TRX activation in DN can protect against the high glucose-induced renal proximal tubular cell injury by attenuating cellular ROS production. Modulating the FOXO1/TXNIP-TRX pathway may be a new therapeutic target in DN.

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Watanabe, Hirofumi, Robert L. Paxton, Matthew R. Tolerico, Vidya K. Nagalakshmi, Shinji Tanaka, Mark D. Okusa, Shin Goto, et al. "Expression of Acsm2, a kidney-specific gene, parallels the function and maturation of proximal tubular cells." American Journal of Physiology-Renal Physiology 319, no. 4 (October 1, 2020): F603—F611. http://dx.doi.org/10.1152/ajprenal.00348.2020.

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The acyl-CoA synthetase medium-chain family member 2 ( Acsm2) gene was first identified and cloned by our group as a kidney-specific “ KS” gene. However, its expression pattern and function remain to be clarified. In the present study, we found that the Acsm2 gene was expressed specifically and at a high level in normal adult kidneys. Expression of Acsm2 in kidneys followed a maturational pattern: it was low in newborn mice and increased with kidney development and maturation. In situ hybridization and immunohistochemistry revealed that Acsm2 was expressed specifically in proximal tubular cells of adult kidneys. Data from the Encyclopedia of DNA Elements database revealed that the Acsm2 gene locus in the mouse has specific histone modifications related to the active transcription of the gene exclusively in kidney cells. Following acute kidney injury, partial unilateral ureteral obstruction, and chronic kidney diseases, expression of Acsm2 in the proximal tubules was significantly decreased. In human samples, the expression pattern of ACSM2A, a homolog of mouse Acsm2, was similar to that in mice, and its expression decreased with several types of renal injuries. These results indicate that the expression of Acsm2 parallels the structural and functional maturation of proximal tubular cells. Downregulation of its expression in several models of kidney disease suggests that Acms2 may serve as a novel marker of proximal tubular injury and/or dysfunction.

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Lee, Wen-Chin, You-Ying Chau, Hwee-Yeong Ng, Chiu-Hua Chen, Pei-Wen Wang, Chia-Wei Liou, Tsu-Kung Lin, and Jin-Bor Chen. "Empagliflozin Protects HK-2 Cells from High Glucose-Mediated Injuries via a Mitochondrial Mechanism." Cells 8, no. 9 (September 14, 2019): 1085. http://dx.doi.org/10.3390/cells8091085.

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Empagliflozin is known to retard the progression of kidney disease in diabetic patients. However, the underlying mechanism is incompletely understood. High glucose induces oxidative stress in renal tubules, eventually leading to mitochondrial damage. Here, we investigated whether empagliflozin exhibits protective functions in renal tubules via a mitochondrial mechanism. We used human proximal tubular cell (PTC) line HK-2 and employed western blotting, terminal deoxynucleotidyl transferase dUTP nick end labelling assay, fluorescence staining, flow cytometry, and enzyme-linked immunosorbent assay to investigate the impact of high glucose and empagliflozin on cellular apoptosis, mitochondrial morphology, and functions including mitochondrial membrane potential (MMP), reactive oxygen species (ROS) production, and adenosine triphosphate (ATP) generation. We found that PTCs were susceptible to high glucose-induced mitochondrial fragmentation, and empagliflozin ameliorated this effect via the regulation of mitochondrial fission (FIS1 and DRP1) and fusion (MFN1 and MFN2) proteins. Empagliflozin reduced the high glucose-induced cellular apoptosis and improved mitochondrial functions by restoring mitochondrial ROS production, MMP, and ATP generation. Our results suggest that empagliflozin may protect renal PTCs from high glucose-mediated injuries through a mitochondrial mechanism. This could be one of the novel mechanisms explaining the benefits demonstrated in EMPA-REG OUTCOME trial.

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Bernard, A. M., A. A. Vyskocil, P. Mahieu, and R. R. Lauwerys. "Assessment of urinary retinol-binding protein as an index of proximal tubular injury." Clinical Chemistry 33, no. 6 (June 1, 1987): 775–79. http://dx.doi.org/10.1093/clinchem/33.6.775.

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Abstract The urinary excretion of retinol-binding protein (RBP), beta 2-microglobulin (beta 2-m), and beta-N-acetyl-D-glucosaminidase was monitored in patients with renal tubular damage secondary to multiple injuries, rhabdomyolysis, antibiotic treatment, or poisoning by various chemicals such as solvents, heavy metals, or pesticides. In almost all cases, RBP proved to be a more sensitive index of renal tubular damage than was beta-N-acetyl-D-glucosaminidase and, being more stable in acid urine, a more practical analyte to measure than was beta 2-m. We corroborated this finding by studying the relationships between these three analytes in more than 150 patients. On the average, an increase in the urinary excretion of beta-N-acetyl-D-glucosaminidase becomes detectable when urinary RBP already exceeds the normal value by 50- to 100-fold. In urines with pH greater than 6, RBP and beta 2-m concentrations are well correlated (r = 0.93, n = 150), beta 2-m tending to be more frequently positive (i.e., greater than 311 micrograms/L). But in urines with pH less than 6 (about 30-40% of the samples), the RBP/beta 2-m concentration ratio increases as pH decreases, up to 500 in some patients with massive tubular injury. Because the renal uptake of proteins involves a saturable process, the urinary excretion of RBP, like that of beta 2-m, specifically reflects the reabsorption capacity of proximal tubules only when the glomerular filtration rate is normal or slightly impaired (i.e., serum creatinine less than 20 mg/L). Under these conditions the determination of RBP protein in urine appears the most appropriate test when early detection of tubular injury is desirable.

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Mou, Shan, Qin Wang, Beili Shi, Leyi Gu, and Zhaohui Ni. "Hepatocyte growth factor ameliorates progression of interstitial injuries in tubular epithelial cells." Scandinavian Journal of Urology and Nephrology 44, no. 2 (December 9, 2009): 121–28. http://dx.doi.org/10.3109/00365590903449340.

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Verzola, Daniela, Maria T. Gandolfo, Franco Ferrario, Maria P. Rastaldi, Barbara Villaggio, Francesco Gianiorio, Massimo Giannoni, et al. "Response to ‘Renal microvascular and tubular injuries in type II diabetic nephropathy’." Kidney International 74, no. 3 (August 2008): 390–91. http://dx.doi.org/10.1038/ki.2008.178.

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Mangare, Vivek Kumar, and Rakesh Kumar Punia. "Histo-pathological changes in kidneys in autopsies of flame burns at a tertiary care center in North Western India: an autopsy based study at SMS medical college Jaipur (2015-2016)." International Journal of Research in Medical Sciences 5, no. 8 (July 26, 2017): 3659. http://dx.doi.org/10.18203/2320-6012.ijrms20173581.

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Background: Burn injury is associated with an intricate patho-physiological response with rapid involvement of various organ systems and which in turn impact the patient with multisystem disruption. These damages can be attributed to the alteration occurring at the tissue and cellular level leading to the histological changes in the renal tissue.Methods: The main aim of this study was to document the histo-pathological changes in kidneys of fatal cases of flame burns. This study was hospital based observational descriptive study carried out at mortuary of SMS medical college and attached hospitals, Jaipur, Rajasthan, India to study and document the histo-pathological changes in the fatal cases due to flame burns.Results: In this study, most common histo-pathological finding in kidneys was cloudy degeneration followed by congestion. Acute tubular necrosis of proximal convoluted necrosis was most commonly observed during 3 to 7 days of mortality (18 cases) followed by mortality during 0 to 48 hours. Acute tubular necrosis of distal convoluted tubules was most commonly observed during 3 to 7 days followed by mortality during 0 to 48 hours.Conclusions: This study revealed that cloudy degeneration and acute tubular necrosis were the hallmark changes in burn patients which were most prominent at 3-7 days after sustaining burn injuries. This reflects the role of immediate management provided to the patient during this period with timely and effective fluid restoration and it possibly will change the prognosis of patients.

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Agarwal, A., J. Balla, G. Balla, A. J. Croatt, G. M. Vercellotti, and K. A. Nath. "Renal tubular epithelial cells mimic endothelial cells upon exposure to oxidized LDL." American Journal of Physiology-Renal Physiology 271, no. 4 (October 1, 1996): F814—F823. http://dx.doi.org/10.1152/ajprenal.1996.271.4.f814.

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In protein-uric states, renal tubular epithelial cells are exposed to diverse macromolecules, including low-density lipoproteins (LDL), normally excluded from the urinary space. Oxidized LDL (LDLox) is incriminated in atherogenesis and glomerulosclerosis. Since urine is prooxidant, we considered whether LDLox injuries renal tubular epithelial cells (LLC-PK1). We demonstrate that the cytotoxicity of LDLox on LLC-PK1 cells resembles its toxicity to human umbilical vein endothelial cells (HUVEC) in that oxidized but not native LDL is injurious. Pretreatment of LLC-PK1 cells and HUVEC with antioxidants markedly reduced the cytotoxicity of LDLox. Pretreatment of LDL with antioxidants, prior to oxidation of LDL, vitiated its cytotoxicity. That LDLox is prooxidant was supported by expression of heme oxygenase, a redox-sensitive enzyme. LDLox induced heme oxygenase mRNA and enzyme activity. Pretreatment of LDL with antioxidants prior to oxidation attenuated heme oxygenase mRNA induction in LLC-PK1 and HUVEC. An iron chelator prevented cytotoxicity and heme oxygenase expression induced by LDLox. Based on these effects of LDLox, we draw an analogy between tubulointerstitial disease and atherogenesis and speculate that LDLox contributes to tubulointerstitial disease in proteinuric states.

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Sakaguchi, Yusuke, Takayuki Hamano, Isao Matsui, Tatsufumi Oka, Satoshi Yamaguchi, Keiichi Kubota, Karin Shimada, Ayumi Matsumoto, Nobuhiro Hashimoto, and Yoshitaka Isaka. "Low magnesium diet aggravates phosphate-induced kidney injury." Nephrology Dialysis Transplantation 34, no. 8 (December 7, 2018): 1310–19. http://dx.doi.org/10.1093/ndt/gfy358.

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Abstract Background Magnesium is known to protect against phosphate-induced tubular cell injuries in vitro. We investigated in vivo effects of magnesium on kidney injuries and phosphate metabolism in mice exposed to a high phosphate diet. Methods Heminephrectomized mice were maintained on a high phosphate/normal magnesium diet or a high phosphate/low magnesium diet for 6 weeks. We compared renal histology, phosphaturic hormones and renal α-Klotho expression between the two diet groups. Results High phosphate diet–induced tubular injuries and interstitial fibrosis were remarkably aggravated by the low-magnesium diet. At 1 week after high phosphate feeding when serum creatinine levels were similar between the two groups, the low magnesium diet suppressed not only fecal phosphate excretion but also urinary phosphate excretion, resulting in increased serum phosphate levels. Parathyroid hormone (PTH) levels were not appropriately elevated in the low magnesium diet group despite lower 1,25-dihydroxyvitamin D and serum calcium levels compared with the normal magnesium diet group. Although fibroblast growth factor 23 (FGF23) levels were lower in the low magnesium diet group, calcitriol-induced upregulation of FGF23 could not restore the impaired urinary phosphate excretion. The low magnesium diet markedly downregulated α-Klotho expression in the kidney. This downregulation of α-Klotho occurred even when mice were fed the low phosphate diet. Conclusions A low magnesium diet aggravated high phosphate diet–induced kidney injuries. Impaired PTH secretion and downregulation of renal α-Klotho were likely to be involved in the blunted urinary phosphate excretion by the low magnesium diet. Increasing dietary magnesium may be useful to attenuate phosphate-induced kidney injury.

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Almayang, Diaz, Saebani Saebani, Tuntas Dhanardhono, Endang Ambarwati, and Ika Pawitra Miranti. "THE DIFFERENCE OF HISTOPATHOLOGICAL IMAGE OF THE WISTAR RAT’S KIDNEY ADMINISTERED WITH GRADUAL DOSAGE OF PYRETHROID." DIPONEGORO MEDICAL JOURNAL (JURNAL KEDOKTERAN DIPONEGORO) 10, no. 2 (March 31, 2021): 132–37. http://dx.doi.org/10.14710/dmj.v10i2.29537.

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Background: Pyrethroid pesticide poisoning cases in developed and developing countries have a high incidence every year. One of the active substances in pyrethroid widely used is cypermethrin. The effects of cypermethrin intoxication on the kidneys, especially in humans, are little to be studied. This study aims to determine the difference in the histopathological image of the Wistar rat’s kidney.Method: The experimental research of the post-test only control group design involved 24 male Wistar rats divided into 4 groups randomly, the control (not given cypermethrin), treatments of 125 mg/kgBW, 250 mg/kgBW, and 500 mg/kgBW. Cypermethrin are given orally for 14 days. After the rats were terminated, the kidney were processed to be paraffin-embedded tissues and stained with HE. Tubular injuries were examined using 400x magnification of light microscope and focused on closure of tubular lumen as well as proteinaceous cast inside the lumens.Results: The results of this study showed that the means of histopathological damage to the kidneys increased from control group to 500 mg/kgBW treatment group. Statistical analysis with One way ANOVA showed significant differences (p<0.001), continued with Post hoc games Howell test, there was a significant differences between control group with 250 mg/kgBW treatment group and 500 mg/kgBW treatment group, and between 125 mg/kgBW treatment group with 250mg/kgBW treatment group and 500 mg/kgBW treatment group. There was no significant difference between the control group with 125 mg/kgBW group and 250 mg/kgBW treatment group with 500 mg/kgBW treatment group.Conclusion: There is a significant difference in renal histopathological image due to exposure to pyrethroid (cypermethrin) in gradual doses. The image of kidney damages can result in tubules injury which include: albuminous degeneration with narrowing of the tubular lumen and hyaline cast. The means of tubular injury rate will increase with increasing dose of pyrethroid.

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Umanah IN, Akhiwu W, Tanimowo MO, and Ochang A. "fatal wrist incised wound: A case of homicide mimicking suicide." Ibom Medical Journal 4, no. 1 (June 1, 2011): 22–25. http://dx.doi.org/10.61386/imj.v4i1.90.

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Crime scene staging is uncommon in Africa. A 26 year old male was found dead on the outskirts of a market with cuts on both hands. There were no other sharp force injuries or features of blunt trauma. The autopsy revealed acute tubular necrosis of the kidneys indicative of ante mortem hemorrhage and prolonged survival of the victim. We report a case of homicide by wrist incision simulating suicide.Distinction between murder and suicide may be impossible by an examination of the body alone. The purpose of this paper is to emphasize that in every case with fatal sharp weapon injuries, differentiation between suicide and homicide is always required.

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Kwiatkowska, Ewa, Leszek Domański, Violetta Dziedziejko, Anna Kajdy, Katarzyna Stefańska, and Sebastian Kwiatkowski. "The Mechanism of Drug Nephrotoxicity and the Methods for Preventing Kidney Damage." International Journal of Molecular Sciences 22, no. 11 (June 6, 2021): 6109. http://dx.doi.org/10.3390/ijms22116109.

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Acute kidney injury (AKI) is a global health challenge of vast proportions, as approx. 13.3% of people worldwide are affected annually. The pathophysiology of AKI is very complex, but its main causes are sepsis, ischemia, and nephrotoxicity. Nephrotoxicity is mainly associated with the use of drugs. Drug-induced AKI accounts for 19–26% of all hospitalized cases. Drug-induced nephrotoxicity develops according to one of the three mechanisms: (1) proximal tubular injury and acute tubular necrosis (ATN) (a dose-dependent mechanism), where the cause is related to apical contact with drugs or their metabolites, the transport of drugs and their metabolites from the apical surface, and the secretion of drugs from the basolateral surface into the tubular lumen; (2) tubular obstruction by crystals or casts containing drugs and their metabolites (a dose-dependent mechanism); (3) interstitial nephritis induced by drugs and their metabolites (a dose-independent mechanism). In this article, the mechanisms of the individual types of injury will be described. Specific groups of drugs will be linked to specific injuries. Additionally, the risk factors for the development of AKI and the methods for preventing and/or treating the condition will be discussed.

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Qi, Huiyue, Fei Deng, Yinghuai Wang, Hao Zhang, Yashpal S. Kanwar, and Yingbo Dai. "Myo-Inositol Supplementation Alleviates Cisplatin-Induced Acute Kidney Injury via Inhibition of Ferroptosis." Cells 12, no. 1 (December 21, 2022): 16. http://dx.doi.org/10.3390/cells12010016.

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Myo-inositol, a carbocyclic sugar, is believed to be relevant to renal pathobiology since the kidney is the major site for its catabolism. Its role in acute kidney injury (AKI) has not been fully investigated. Ferroptosis, a unique form of regulated cell death, is involved in various types of renal injuries. The relevance of myo-inositol with respect to the process of ferroptosis has not been explored either. Herein, our current exploratory studies revealed that supplementation of myo-inositol attenuates cisplatin-induced injury in cultured Boston University mouse proximal tubular (BUMPT) cells and renal tubules in vivo. Moreover, our studies unraveled that metabolic parameters pertaining to ferroptosis were disrupted in cisplatin-treated proximal tubular cells, which were seemingly remedied by the administration of myo-inositol. Mechanistically, we noted that cisplatin treatment led to the up-regulation of NOX4, a key enzyme relevant to ferroptosis, which was normalized by the administration of myo-inositol. Furthermore, we observed that changes in the NOX4 expression induced by cisplatin or myo-inositol were modulated by carboxy-terminus of Hsc70-interacting protein (CHIP), an E3 ubiquitin ligase. Taken together, our investigation suggests that myo-inositol promotes CHIP-mediated ubiquitination of NOX4 to decelerate the process of ferroptosis, leading to the amelioration of cisplatin-induced AKI.

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Kito, Naoko, Kosuke Endo, Masahiro Ikesue, Huachun Weng, and Naoharu Iwai. "miRNA Profiles of Tubular Cells: Diagnosis of Kidney Injury." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/465479.

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MicroRNAs (miRNAs) are small noncoding RNAs of 18–23 nucleotides that regulate gene expression. Recently, plasma miRNAs have been investigated as biomarkers for various physiological and pathological conditions. The present study details the conserved miRNA expression profiles of tubular tissues, and discusses whether they could be used to distinguish between proximal tubule injury, diagnose acute kidney injury (AKI), and the early-stage renal tubular dysfunction. miRNA expression was assessed with miRNA array and real-time reverse transcription polymerase chain reaction using the TaqMan system. The expression profiles of miR-200a/b/c, miR-145, miR-192, miR-194, miR-216a/b, miR-217, and miR-449a in human and rat tubular tissues such as the kidneys, lung, small intestine, and various exocrine glands were adequate for discriminating tubular tissues. In the kidney, miR-192 and miR-194 were highly expressed, whereas miR-145 and miR-449a were absent. miR-145 and miR-449a were relatively specifically expressed in small intestine and lung, respectively. Therefore, the combined levels of miR-200a/b/c, miR-192, and miR-194 in plasma were very useful in diagnosing AKI induced by contact freezing in mice. Moreover, urinary miR-200a levels were useful for the diagnosis of renal tubular dysfunction in Dahl salt-sensitive rat with high salt administration. Our results indicate that miRNA expression profiles are useful as biomarkers for identification of various kidney injuries.

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Japaridze, Nino. "Pathological Processes in Oral Cavity at Vitamin D-Resistant Rickets (Family Case Reports)." MODERN ISSUES OF MEDICINE AND MANAGEMENT 24, no. 2 (November 9, 2022): 1–8. http://dx.doi.org/10.56580/geomedi13.

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Vitamin D-resistant rickets of X-linked dominant transmission type is caused by pathology of renal tubular apparatus resulting in impaired absorption of calcium and phosphorus in the small intestine; it proceeds with the injuries of varying severity to skeletal system as well as dental and periodontal complex. The purpose of the study is to describe a family case of vitamin D-resistant rickets.

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Chen, Da-wei, Bing Li, Yun-feng Yang, and Guang-rong Yu. "Torsional Stiffness in Supplemental One-Third Tubular Plate Fixation for Isolated Syndesmosis Injuries." Foot & Ankle International 34, no. 9 (September 2013): 1320. http://dx.doi.org/10.1177/1071100713496225.

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Yousef, Mohamed M., Omayma K. Helal, and Nermeen Adly. "Effect of silymarin on cisplatin-induced renal tubular injuries in adult male rabbits." Egyptian Journal of Histology 34, no. 4 (December 2011): 800–807. http://dx.doi.org/10.1097/01.ehx.0000407698.55603.e7.

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Lin, Hugo Y., Chia-Hung Yen, Yi-Siao Chen, I.-Ya Chen, Jee-Fu Huang, and Tzongshi Lu. "Mechanistic Role of Renal Tubular Mitochondrial AKT1 in Metabolic Syndrome-Induced Renal Injuries." Journal of the American Society of Nephrology 33, no. 11S (November 2022): 672. http://dx.doi.org/10.1681/asn.20223311s1672a.

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LUNDBORG, G., B. ROSÉN, L. DAHLIN, J. HOLMBERG, and I. ROSÉN. "Tubular Repair of the Median or Ulnar Nerve in the Human Forearm: A 5-Year Follow-Up." Journal of Hand Surgery 29, no. 2 (April 2004): 100–107. http://dx.doi.org/10.1016/j.jhsb.2003.09.018.

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The long-term outcome from silicone tube nerve repair was compared with the outcome from routine microsurgical repair in a clinical randomized prospective study, comprising 30 patients with median or ulnar nerve injuries in the distal forearm. Postoperatively, the patients underwent neurophysiological and clinical assessments of sensory and motor function regularly over a 5-year period. After 5 years there was no significant difference in outcome between the two techniques except that cold intolerance was significantly less severe with the tubular technique. In the total group there was ongoing improvement of functional sensibility throughout the 5 years after repair. It is concluded that tubular repair of the median and ulnar nerves is at least as good as routine microsurgical repair, and results in less cold intolerance.

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Kolar, Mallappa K., and Paul J. Kingham. "Regenerative effects of adipose-tissue-derived stem cells for treatment of peripheral nerve injuries." Biochemical Society Transactions 42, no. 3 (May 22, 2014): 697–701. http://dx.doi.org/10.1042/bst20140004.

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Peripheral nerve injuries are a common occurrence affecting the nerves found outside the central nervous system. Complete nerve transections necessitate surgical re-anastomosis, and, in cases where there is a significant gap between the two ends of the injured nerve, bridging strategies are required to repair the defect. The current clinical gold standard is the nerve graft, but this has a number of limitations, including donor site morbidity. An active area of research is focused on developing other techniques to replace these grafts, by creating tubular nerve-guidance conduits from natural and synthetic materials, which are often supplemented with biological cues such as growth factors and regenerative cells. In the present short review, we focus on the use of adipose-tissue-derived stem cells and the possible mechanisms through which they may exert a positive influence on peripheral nerve regeneration, thereby enabling more effective nerve repair.

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Lin, Tien-An, Victor Chien-Chia Wu, and Chao-Yung Wang. "Autophagy in Chronic Kidney Diseases." Cells 8, no. 1 (January 16, 2019): 61. http://dx.doi.org/10.3390/cells8010061.

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Autophagy is a cellular recycling process involving self-degradation and reconstruction of damaged organelles and proteins. Current evidence suggests that autophagy is critical in kidney physiology and homeostasis. In clinical studies, autophagy activations and inhibitions are linked to acute kidney injuries, chronic kidney diseases, diabetic nephropathies, and polycystic kidney diseases. Oxidative stress, inflammation, and mitochondrial dysfunction, which are implicated as important mechanisms underlying many kidney diseases, modulate the autophagy activation and inhibition and lead to cellular recycling dysfunction. Abnormal autophagy function can induce loss of podocytes, damage proximal tubular cells, and glomerulosclerosis. After acute kidney injuries, activated autophagy protects tubular cells from apoptosis and enhances cellular regeneration. Patients with chronic kidney diseases have impaired autophagy that cannot be reversed by hemodialysis. Multiple nephrotoxic medications also alter the autophagy signaling, by which the mechanistic insights of the drugs are revealed, thus providing the unique opportunity to manage the nephrotoxicity of these drugs. In this review, we summarize the current concepts of autophagy and its molecular aspects in different kidney cells pathophysiology. We also discuss the current evidence of autophagy in acute kidney injury, chronic kidney disease, toxic effects of drugs, and aging kidneys. In addition, we examine therapeutic possibilities targeting the autophagy system in kidney diseases.

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Aubert, Vivien, Jacques Kaminski, François Guillaud, Thierry Hauet, and Patrick Hannaert. "A Computer Model of Oxygen Dynamics in the Cortex of the Rat Kidney at the Cell-Tissue Level." International Journal of Molecular Sciences 20, no. 24 (December 11, 2019): 6246. http://dx.doi.org/10.3390/ijms20246246.

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The renal cortex drives renal function. Hypoxia/reoxygenation are primary factors in ischemia-reperfusion (IR) injuries, but renal oxygenation per se is complex and awaits full elucidation. Few mathematical models address this issue: none captures cortical tissue heterogeneity. Using agent-based modeling, we develop the first model of cortical oxygenation at the cell-tissue level (RCM), based on first principles and careful bibliographical analysis. Entirely parameterized with Rat data, RCM is a morphometrically equivalent 2D-slice of cortical tissue, featuring peritubular capillaries (PTC), tubules and interstitium. It implements hemoglobin/O2 binding-release, oxygen diffusion, and consumption, as well as capillary and tubular flows. Inputs are renal blood flow RBF and PO2 feeds; output is average tissue PO2 (tPO2). After verification and sensitivity analysis, RCM was validated at steady-state (tPO2 37.7 ± 2.2 vs. 36.9 ± 6 mmHg) and under transients (ischemic oxygen half-time: 4.5 ± 2.5 vs. 2.3 ± 0.5 s in situ). Simulations confirm that PO2 is largely independent of RBF, except at low values. They suggest that, at least in the proximal tubule, the luminal flow dominantly contributes to oxygen delivery, while the contribution of capillaries increases under partial ischemia. Before addressing IR-induced injuries, upcoming developments include ATP production, adaptation to minutes–hours scale, and segmental and regional specification.

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Ibragimov, F. I., and N. A. Kasumov. "Surgical treatment of multiple and concomitant injuries." VESTNIK KHIRURGII IMENI I.I.GREKOVA 177, no. 5 (November 23, 2018): 30–35. http://dx.doi.org/10.24884/0042-4625-2018-177-5-30-35.

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The objectiveof the study was to conduct a comparative analysis of the results of traditional and modern methods of surgical treatment of patients with severe concomitant injury, accompanied by fractures of the tubular bones of the limbs.Material and methods. The retro-and prospective analysis of the results of surgical treatment of 1033 patients with severe concomitant injury hospitalized in Baku Clinical Hospital № 3 for the period from 2009 to 2015 is presented. The patients were divided into 2 groups for a comparative evaluation of the results of treatment, depending on the effectiveness of the applied medical tactics. The 1st (main) group consisted of 828 (80.2 %) patients who were treated using the tactics of programmed multi-stage surgical treatment in accordance with the concept of «damage control». The 2nd (comparison group) included 205 (19.8 %) patients, who were treated using the traditional tactics of surgical treatment.Results.In a multi-field General surgical hospital, the introduction of the «damage control» program using the tactics of programmed surgical treatment in patients with severe concomitant and multiple injury allowed to increase surgical activity and reduce the mortality rate from 45.9 to 21.6 %.Conclusion.The application of tactics of stage surgical correction of injuries allows to improve the immediate results of treatment of patients with severe concomitant and multiple injury.

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Savka, Ivan G. "FORENSIC MORPHOLOGICAL SIGNS CHARACTERIZING STABILITY OF THE FEMUR, TIBIA AND FIBULA DURING EFFECT OF EXTERNAL DESTRUCTIVE LOAD." Wiadomości Lekarskie 72, no. 2 (2019): 198–200. http://dx.doi.org/10.36740/wlek201902111.

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Introduction: Fractures of the lower limb bones very often become the subject of forensic expertise when experts have to determine the mechanisms of fracture formation, make retrospective restoration of conditions of their occurrence, solve the issues concerning the possibility of their formation under certain conditions. The aim of study is directed to investigation of morphological signs facilitating solidity of the osseous tissue of the lower limb long tubular bones, and therefore, promoting biochemical processes of their destruction in case of external traumatic impact. Materials and methods: Expert investigations included 128 injuries of the long tubular bones of the lower limb: femoral bone – 40 cases, tibia – 46, fibula – 42. Fractures of every bone were assessed by the three thirds: proximal, middle and distal. All the 29 macroscopic and 8 microscopic morphological signs of the osseous tissue were examined. Control studies were carried out on 576 specimens of the femoral bone, tibia and fibula (192 specimens of each), removed from dead males and females aged from 24 to 70. Results: The most valuable morphological signs forming “modulus of stability” are: length of plastic deformity zones from the site of stretching and compression, deviation angle of sphenoid cracks together with the character of traumatic injury impact. An important value in this respect belongs to the square of the medullar canal, length of the biggest sphenoid crack, number of longitudinal cracks and shape of the medullar canal from the site of compression, total mineral content and the height of the biggest crest in the rupture zone. Conclusions: “Modulus of stability” of the osseous tissue of the long tubular bones of the lower limb most accurately reflects interaction of traumatic mechanical impact with the bone structures during their injuries that should be considered in forensic practice in the process of making expertise.

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Mansano, André Marques, Pedro Thadeu Galvão Vianna, Viciany Erique Fabris, Leopoldo Muniz da Silva, Leandro Gobbo Braz, and Yara Marcondes Machado Castiglia. "Prevention of renal ischemia/reperfusion injury in rats using acetylcysteine after anesthesia with isoflurane." Acta Cirurgica Brasileira 27, no. 4 (April 2012): 340–45. http://dx.doi.org/10.1590/s0102-86502012000400010.

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PURPOSE: To evaluate the effect of N-acetylcysteine, as a renoprotective agent, when administered early after anesthesia induction, against ischemia/reperfusion injury in rats anesthetized with isoflurane. METHODS: Eighteen male Wistar rats weighing > 300g were anesthetized with isoflurane. The internal jugular vein and the left carotid artery were dissected and cannulated. The animals were randomly divided into GAcetyl, receiving intravenous N-acetylcysteine, 300mg/kg, and GIsot, isotonic saline. After 30 minutes, right nephrectomy was performed and the left renal artery was clamped during 45 minutes. The animals were sacrificed after 48 hours and blood samples were taken after anesthetic induction and upon sacrificing of the animals to evaluate blood creatinine. The kidneys were sent for histological analysis. RESULTS: The variation in serum creatinine was 2.33mg/dL ± 2.21 in GAcetyl and 4.38mg/dL ± 2.13 in GIsot (p=0.074). Two animals presented intense tubular necrosis in GAcetyl, compared to 5 in GIsot. Only GAcetyl presented animals free of tubular necrosis (two) and tubular degeneration (one). CONCLUSION: After renal ischemia/reperfusion, the rats which were given N-acetylcysteine presented less variation in serum creatinine and milder kidney injuries than the control group.

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Zalups, R. K., M. K. Robinson, and D. W. Barfuss. "Factors affecting inorganic mercury transport and toxicity in the isolated perfused proximal tubule." Journal of the American Society of Nephrology 2, no. 4 (October 1991): 866–78. http://dx.doi.org/10.1681/asn.v24866.

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The effects of cysteine (80 microM), glutathione (80 microM), rabbit albumin (100 microM), and an ultrafiltrate of rabbit plasma on the toxicity and transport of inorganic mercury (Hg2+; 18.4 microM) in isolated perfused S1, S2, and S3 segments of the renal proximal tubule from the rabbit were studied. Cellular and tubular injuries were assessed qualitatively by light microscopy observations and quantitatively by the tubular leak of the volume marker 3H-glucose. The lumen-to-bath transport of inorganic mercury was assessed by measuring both the rate of disappearance of inorganic mercury from the luminal fluid and the rate of appearance of inorganic mercury in the bath. When glutathione was added to the perfusate containing the inorganic mercury, no signs of epithelial cell necrosis or injury were detected in any of the three segments of the proximal tubule. There was also an absence of or a decrease in cellular injury in the epithelium of the same tubular segments when either cysteine or the ultrafiltrate was present in the perfusate. However, when rabbit albumin and inorganic mercury were present in the perfusate, severe degenerative and necrotic changes occurred very rapidly in the epithelium of all three segments of the proximal tubule. In almost every instance where glutathione, cysteine, or the plasma ultrafiltrate were present in the perfusate, the disappearance flux of inorganic mercury from the tubular lumen into the tubular epithelium was lowered. It was concluded that glutathione, cysteine, and the ultrafiltrate of rabbit plasma provide isolated perfused S1, S2, and S3 segments of the proximal tubule varying degrees of protection from the toxic effects of inorganic mercury. This protection appears to be related to a decrease in the movement of inorganic mercury across the luminal membrane of the tubular epithelial cells.

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Yusupalieva, Gulnora Akmalovna, Temur Abdurashidovich Yuldashev, Sherzod Farkhadovich Akhralov, Adiba Rustamovna Manashova, and Umida Asqarovna Umarova. "Complex Radiation Diagnostics of Non-Healed Fractures and Post-Traumatic False Joints of Long Tubular Bones." Advances in Clinical Medical Research 3, no. 1 (March 31, 2022): 05–08. http://dx.doi.org/10.48112/acmr.v3i1.27.

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The dependence of severity, and accordingly, the number of complications and consequences, including false joints, on the mechanism of injury is known. Recently, there has been an increase in the number of injuries resulting from exposure to high kinetic energy (road traffic, firearms), leading to an increase in disability. In this regard, in order to reduce the severity of the social consequences of injuries, specialized assistance to victims, the introduction of new diagnostic and treatment technologies, both at the stage of primary care and at the stage of treatment of consequences, is becoming important. The purpose of the study. To improve the diagnosis of ungrown fractures and post-traumatic false joints of long tubular bones by using complex ultrasound diagnostics. The study of patients was carried out in a supine position or sitting at rest and was carried out both under conditions of plaster immobilization and without it. During plaster immobilization, the sensor was positioned through a "window" in the plaster splint, while control from the healthy limb was carried out in the same position of the sensor as on the affected side.

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Savka, Ivan. "Forensic characteristics of fissures as valuable morphological signs to detect mechanogenesis of fractures of long bones in the lower limbs." Forensic-medical examination, no. 2 (December 17, 2017): 59–62. http://dx.doi.org/10.24061/2707-8728.2.2017.14.

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The objective of our work is to study regularities of formation and spread of cracks of long bone diaphysis in the lower limbs for more profound understanding of biomechanics of fractures. The material of the study was 128 cases with injuries of the femoral, tibia and fibula bones. The data obtained were statistically processed by means of multifactor analysis of variance (MANOVA). Different kinds of cracks were found to possess their own signs by the number and direction reflecting mechanics of fractures of the examined bones. The value of deviation angle of wedge-shaped cracks was found to be of a special diagnostic importance. Detected regularities can be used in forensic medicine practical work in case of retrospective renewal of conditions and circumstances of getting injuries. Objective: to formulate new regularities in the process of formation and spread of diaphysis cracks of long tubular bones in the lower limbs for more comprehensive understanding of biomechanics of their fractures. Materials and methods. The material of the study was based on the expert investigations including 82 persons with 128 injuries of the lower limbs: femoral bones – 40 cases, tibia – 46 cases, fibula – 42 cases. The data obtained were statistically processed by means of multifactor analysis of variance (MANOVA). Conclusions: Different kinds of cracks have their own signs by the number and direction reflecting mechanics of fracture of certain portions in the long tubular bones of the lower limb. Cracks in the rupture area are of more importance to detect the mechanism of The value of deviation angle of wedge- shaped cracks is of a special diagnostic importance. Prospects of further studies. Prospects of further studies assume computed multi-dimensional visualization of crack characteristics of different bones of the human skeleton.

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Bargagli, Matteo, Maria Clarissa Tio, Sushrut S. Waikar, and Pietro Manuel Ferraro. "Dietary Oxalate Intake and Kidney Outcomes." Nutrients 12, no. 9 (September 2, 2020): 2673. http://dx.doi.org/10.3390/nu12092673.

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Oxalate is both a plant-derived molecule and a terminal toxic metabolite with no known physiological function in humans. It is predominantly eliminated by the kidneys through glomerular filtration and tubular secretion. Regardless of the cause, the increased load of dietary oxalate presented to the kidneys has been linked to different kidney-related conditions and injuries, including calcium oxalate nephrolithiasis, acute and chronic kidney disease. In this paper, we review the current literature on the association between dietary oxalate intake and kidney outcomes.

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Tsai, Dong-Ming, Jaw-Jou Kang, Shoei-Sheng Lee, San-Yuan Wang, I.-Lin Tsai, Guan-Yuan Chen, Hsiao-Wei Liao, Li Wei-Chu, Ching-Hua Kuo, and Y. Jane Tseng. "Metabolomic Analysis of Complex Chinese Remedies: Examples of Induced Nephrotoxicity in the Mouse from a Series of Remedies Containing Aristolochic Acid." Evidence-Based Complementary and Alternative Medicine 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/263757.

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Aristolochic acid nephropathy is caused by aristolochic acid (AA) and AA-containing herbs. In traditional Chinese medicine, a principle called “Jun-Chen-Zou-Shi” may be utilized to construct a remedial herbal formula that attempts to mitigate the toxicity of the main ingredient. This study usedBu-Fei-A-Jiao-Tang(BFAJT) to test if the compound remedy based on a principle of “Jun-Chen-Zou-Shi” can decrease the toxicity of AA-containing herbs. We compared the three toxicities of AA standard,Madouling(anAristolochiaherb), and a herbal formula BFAJT. AA standard was given for BALB/c mice at a dose of 5 mg/kg bw/day or 7.5 mg/kg bw/day for 10 days.Madoulingand BFAJT were given at an equivalence of AA 0.5 mg/kg bw/day for 21 days. Nephrotoxicity was evaluated by metabolomics and histopathology. The urinary metabolomics profiles were characterized by1H NMR spectroscopy. The spectral data was analyzed with partial least squares discriminant analysis, and the significant differential metabolites between groups were identified. The result showed different degrees of acute renal tubular injuries, and metabolomics analysis found that the kidney injuries were focused in proximal renal tubules. Both metabolomics and pathological studies revealed that AA standard,Madouling, and BFAJT were all nephrotoxicants. The compositions of the compound remedy did not diminish the nephrotoxicity caused by AA.

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Hidaka, Sumi, Bettina Kränzlin, Norbert Gretz, and Ralph Witzgall. "Urinary clusterin levels in the rat correlate with the severity of tubular damage and may help to differentiate between glomerular and tubular injuries." Cell and Tissue Research 310, no. 3 (December 1, 2002): 289–96. http://dx.doi.org/10.1007/s00441-002-0629-5.

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Yuan, Sheau-Yun, Chi-Rei Yang, Chen-Li Cheng, Shih-Lan Hsu, Jiunn-Wang Liao, Chi-Chen Lin, Ying-Yi Chou, and Ya-Wen Cheng. "Comparative Nephrotoxicity of Aristolochic Acid and Tetrandrine In Vitro and In Vivo." International Journal of Toxicology 30, no. 1 (January 11, 2011): 35–46. http://dx.doi.org/10.1177/1091581810387164.

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Aristolochic acid (AA) and tetrandrine (TET) are the major bioactive components in Chinese herbs used for weight loss. The nephropathy caused by the 2 Chinese herbs has not been simultaneously investigated. The aim of this study was to examine the potential nephrotoxicity of AA and TET using Madin-Darby canine kidney (MDCK) cells and mice. The results showed that TET was more potent than AA in inhibiting MDCK cell growth via inducing apoptosis, as determined by annexin-V staining, 4’, 6’-diamino-2-phenylindole (DAPI) staining, DNA fragmentation, and caspase 3 activity. Mice treated with AA (10 mg/kg) by intraperitoneal administration for 3 months showed nephrotoxicity, elevated blood urea nitrogen, and increased renal tubular injuries. In contrast, mice treated with 50 mg/kg of TET in the same time period had moderate hydropic degeneration of the distal tubules in the kidneys. These results suggest that TET is more cytotoxic than AA in MDCK cells but shows less nephrotoxic than AA in mice.

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