Astragaloside IV attenuates fatty acid-induced renal tubular injury in diabetic kidney disease by inhibiting fatty acid transport protein-2.

BACKGROUND: Renal tubular injury induced by free fatty acid bound to albumin is the key pathological basis for the progression of diabetic kidney disease. However, effective interventions are limited. Astragaloside IV, as a major bioactive component purified from Astragalus membranaceus (Fisch.) Bunge, possesses pharmacological properties of lowering blood glucose and proteinuria, and renal tubular protection in diabetic kidney disease. Further work is needed to understand the underlying molecular mechanisms. PURPOSE: This study was designed to investigate the mechanism of renal tubular protection by astragaloside IV in diabetic kidney disease. METHODS: Rats receiving high-fat diet combined with streptozotocin (30 mg/kg, i.p.) were gavaged with astragaloside IV (10 mg/kg/d or 20 mg/kg/d) or empagliflozin (1.72 mg/kg/d) for 8 weeks. In vitro, the NRK-52E cells were treated with free fatty acid-deleted BSA or palmitic acid-bound BSA in the presence or absence of astragaloside IV (5 µM, 10 µM, 20 µM) or 5 µM of mcc950. The effects of astragaloside IV on mitochondrial function, NLRP3/ASC/IL-18/IL-1ß inflammatory cascade, and renal tubular injury were detected by pathological staining, immunoblotting, MitoSOX Red staining. Next, to investigate the mechanism of renal tubular protection by astragaloside IV, we transfected Fatp2 siRNA into BSA-PA-treated NRK-52E cells and injected lipofermata (a FATP2 inhibitor) intraperitoneally into free fatty acid-bound BSA overloaded rats with concomitant astragaloside IV treatment. RESULTS: Treatment with astragaloside IV for 8 weeks dose-dependently attenuated the blood glucose, ratio of urinary albumin to creatinine, disorder of lipid metabolism, and pathological injury in diabetic kidney disease rats. In addition, astragaloside IV dose-dependently attenuated mitochondrial-derived reactive oxygen species and subsequent inhibiting NLRP3-mediated inflammatory cascade in diabetic kidney disease rats and palmitic acid-bound BSA-treated NRK-52E cells, thereby exerting renal tubular protection. More importantly, the effects of astragaloside IV on restoration of mitochondrial function, inhibition of inflammatory response and amelioration of renal tubular injury in vivo and in vitro were further enhanced when used in combination with Fatp2 siRNA or lipofermata. CONCLUSION: Astragaloside IV exerts antioxidant and anti-inflammatory effects in diabetic kidney disease by inhibiting FATP2-mediated fatty acid transport, thereby attenuating renal tubular injury.

Identifying biochemical changes in the kidney using proton nuclear magnetic resonance in an adenine diet chronic kidney disease mouse model.

This study aimed to investigate the metabolic changes in the kidneys in a murine adenine-diet model of chronic kidney disease (CKD). Kidney fibrosis is the common pathological manifestation across CKD aetiologies. Sustained inflammation and fibrosis cause changes in preferred energy metabolic pathways in the cells of the kidney. Kidney cortical tissue from mice receiving a control or adenine-supplemented diet for 8 weeks (late inflammation and fibrosis) and 12 weeks (8 weeks of treatment followed by 4 weeks recovery) were analysed by 2D-correlated nuclear magnetic resonance spectroscopy and compared with histopathology and biomarkers of kidney damage. Tissue metabolite and lipid levels were assessed using the MestreNova software. Expression of genes related to inflammation, fibrosis, and metabolism were measured using quantitative polymerase chain reaction. Animals showed indicators of severely impaired kidney function at 8 and 12 weeks. Significantly increased fibrosis was present at 8 weeks but not in the recovery group suggesting some reversal of fibrosis and amelioration of inflammation. At 8 weeks, metabolites associated with glycolysis were increased, while lipid signatures were decreased. Genes involved in fatty acid oxidation were decreased at 8 weeks but not 12 weeks while genes associated with glycolysis were significantly increased at 8 weeks but not at 12 weeks. In this murine model of CKD, kidney fibrosis was associated with the accumulation of triglyceride and free lactate. There was an up-regulation of glycolytic enzymes and down-regulation of lipolytic enzymes. These metabolic changes reflect the energy demands associated with progressive kidney disease where there is a switch from fatty acid oxidation to that of glycolysis.

Hydrogen-bonded organic frameworks as stationary phase for open-tubular capillary electrochromatography.

BACKGROUND: Capillary electrochromatography (CEC) stationary phases have always been the focus of attention. The selection of excellent stationary phases are the key to realize separate of different compounds. Hydrogen-bonded organic frameworks (HOFs) are porous materials connected by hydrogen bonds between molecules, which have the advantages of renewable, high specific surface area and mild synthesis conditions. At present, HOFs are used in gas adsorption and storage, catalysis and drug delivery. Because of its unique advantages, HOFs have a bright future as CEC stationary phases. RESULTS: Using melamine (MA) and 1,3,6,8-tetra (4-carboxylphenyl)pyrene (H4TBAPy) as reaction monomers, a HOFs named MA/PFC-1 was synthesized by solvent evaporation at room temperature. The inner wall of the capillary column was coated with MA/PFC-1 by chemical bonding. Sulfonamides were used as the target analytes. The effects of pH, phosphate buffer solution concentration, organic additive content and applied voltage on sulfonamides separation were investigated. The MA/PFC-1-coated capillary column had good resolution (>1.5) and reproducibility. The intra-day, inter-day, column-to-column, and inter-batch precision of the retention times were 0.03%-0.09%, 0.04%-0.09%, 0.03%-0.14% and 0.06%-0.09%, respectively. The intra-day, inter-day, column-to-column, and inter-batch precision of the peak areas were 0.11%-0.25%, 0.13%-0.20%, 0.12%-0.15% and 0.08%-0.15%, respectively. The MA/PFC-1-coated capillary column was run 150 consecutive times, and the results showed no noticeable change, which proved that this method had good stability. SIGNIFICANCE: This work applied HOFs to CEC. The results show the that MA/PFC-1-coated capillary column has good separation performance. The MA/PFC-1-coated capillary column has been successfully applied to the determination of sulfamethoxazole in tablets, which has practical application value. To open up the application of HOFs in CEC and provide a new idea for developing new CEC stationary phases.

Skeleton-guided 3D convolutional neural network for tubular structure segmentation.

PURPOSE: Accurate segmentation of tubular structures is crucial for clinical diagnosis and treatment but is challenging due to their complex branching structures and volume imbalance. The purpose of this study is to propose a 3D deep learning network that incorporates skeleton information to enhance segmentation accuracy in these tubular structures. METHODS: Our approach employs a 3D convolutional network to extract 3D tubular structures from medical images such as CT volumetric images. We introduce a skeleton-guided module that operates on extracted features to capture and preserve the skeleton information in the segmentation results. Additionally, to effectively train our deep model in leveraging skeleton information, we propose a sigmoid-adaptive Tversky loss function which is specifically designed for skeleton segmentation. RESULTS: We conducted experiments on two distinct 3D medical image datasets. The first dataset consisted of 90 cases of chest CT volumetric images, while the second dataset comprised 35 cases of abdominal CT volumetric images. Comparative analysis with previous segmentation approaches demonstrated the superior performance of our method. For the airway segmentation task, our method achieved an average tree length rate of 93.0%, a branch detection rate of 91.5%, and a precision rate of 90.0%. In the case of abdominal artery segmentation, our method attained an average precision rate of 97.7%, a recall rate of 91.7%, and an F-measure of 94.6%. CONCLUSION: We present a skeleton-guided 3D convolutional network to segment tubular structures from 3D medical images. Our skeleton-guided 3D convolutional network could effectively segment small tubular structures, outperforming previous methods.

Identification of human-specific amino acid residues governing atenolol transport via organic cation transporter 2.

Organic cation transporter 2 (OCT2/SLC22A2) is predominantly localized on the basolateral membranes of renal tubular epithelial cells and plays a crucial role in the renal secretion of various cationic drugs. Although variations in substrate selectivity among renal organic cation transport systems across species have been reported, the characteristics of OCT2 remain unclear. In this study, we demonstrated that atenolol, a ß1-selective adrenergic antagonist, is transported almost exclusively by human OCT2, contrasting with OCT2s from other selected species. Using chimeric constructs between human OCT2 (hOCT2) and the highly homologous monkey OCT2 (monOCT2), along with site-directed mutagenesis, we identified non-conserved amino acids Val8, Ala31, Ala34, Tyr222, Tyr245, Ala270, Ile394, and Leu503 as pivotal for hOCT2-mediated atenolol transport. Kinetic analysis revealed that atenolol was transported by hOCT2 with a 12-fold lower affinity than MPP+, a typical OCT2 substrate. The inhibitory effect of atenolol on MPP+ transport was 6200-fold lower than that observed for MPP+ on atenolol transport. Additionally, we observed weaker inhibitory effects on MPP+ transport compared to atenolol transport with ten different OCT2 substrates. Altogether, this study suggests that eight hOCT2-specific amino acids constitute the low-affinity recognition site for atenolol transport, indicating differences in OCT2-mediated drug elimination between humans and highly homologous monkeys. Our findings underscore the importance of understanding species-specific differences in drug transport mechanisms, shedding light on potential variations in drug disposition and aiding in drug development.

P4HB regulates the TGFß/SMAD3 signaling pathway through PRMT1 to participate in high glucose-induced epithelial-mesenchymal transition and fibrosis of renal tubular epithelial cells.

BACKGROUND: Diabetic nephropathy (DN) is a common complication of diabetes mellitus, and Prolyl 4-Hydroxylase Subunit Beta (P4HB) expression is increased in high glucose (HG)-induced renal tubular epithelial cells (TECs). But it's role in HG-induced TECs remains to be elucidated. METHODS: The HK-2 cells were induced using HG and transfected with SiRNA-P4HB. DCFH-DA staining was utilized for the detection of cellular levels of ROS. WB and immunofluorescence were utilized to detect the expression of P4HB, epithelial-mesenchymal transition (EMT), fibrosis, and TGFß/SMAD3-related proteins in HK-2 cells. Online databases were utilized for predicting the interaction target of P4HB, and immunoprecipitation (IP) experiments were employed to validate the binding of P4HB with the target. SiRNA and overexpression vectors of target gene were used to verify the mechanism of action of P4HB. RESULTS: HG induced an increase in the expression of P4HB and TGFß, p-SMAD3, and ROS in HK-2 cells. Furthermore, HG downregulated the expression of E-cadherin and upregulated the expression of N-cadherin, Vimentin, α-SMA, Fibronectin, Collagen IV, SNAIL, and SLUG in HK-2 cells. Interfering with P4HB significantly reversed the expression of these proteins. Database predictions and IP experiments showed that P4HB interacts with PRMT1, and the expression of PRMT1 was increased in HG-induced HK-2 cells. Interfering with PRMT1 inhibited the changes in expression of EMT and fibrosis related proteins induced by HG. However, overexpression of PRMT1 weakened the regulatory effect of P4HB interference on the EMT, fibrosis, and TGFß/SMAD3-related proteins in HK-2 cells. CONCLUSION: P4HB regulated the TGFß/SMAD3 signaling pathway through PRMT1 and thus participates in HG-induced EMT and fibrosis in HK-2 cells.

Perioperative outcomes of 105 cases of ABO-incompatible live donor kidney transplantation: a retrospective single-center observational study.

Background: ABO-incompatible (ABOi) kidney transplantation poses significant challenges in achieving successful outcomes. This study aimed to investigate the impact of various interventions and techniques on improving the success rates of ABOi kidney transplantation. Methods: We conducted a retrospective observational analysis of patients who underwent ABOi kidney transplantation from November 2012 to March 2023. The study included a total of 105 patients. We collected and analyzed data on patient demographics, preoperative assessments, surgical details, and postoperative outcomes. Results: The mean ages of the donors and recipients were 50.52±10.32 and 36.63±11.61 years, respectively. The majority of recipients were male (81.9%), while most donors were female (89.5%). The most common blood group among recipients was O (69.5%), and among donors, it was B (46.7%). The median durations of chronic kidney disease and dialysis were 12 months (interquartile range [IQR], 7-28 months) and 6 months (IQR, 2-12 months), respectively. Baseline antibody titers (anti-A and anti-B) ranged from 64.0 to 256.0, while on the day of surgery, they were ≤8. Perioperative complications included hypotension (10.5%), acute tubular necrosis (5.7%), delayed graft function (3.8%), and reexploration (3.8%) due to hematoma. Conclusions: ABOi kidney transplantation is a viable option for recipients lacking available donors with an ABO-compatible match. Perioperative concerns, including hypoalbuminemia, heightened risk of infections, coagulopathies, aseptic precautions, and immunological surveillance, must be carefully addressed.

Tough Cortical Bone-Inspired Tubular Architected Cement-Based Material with Disorder.

Cortical bone is a tough biological material composed of tube-like osteons embedded in the organic matrix surrounded by weak interfaces known as cement lines. The cement lines provide a microstructurally preferable crack path, hence triggering in-plane crack deflection around osteons due to cement line-crack interaction. Inspired by this toughening mechanism and facilitated by a hybrid (3D-printing/casting) process, the study engineers architected tubular cement-based materials with the stepwise cracking toughening mechanism, that enables a non-brittle fracture. Using experimental and theoretical approaches, the study demonstrates the competition between tube size and shape on stress intensity factor from which engineering stepwise cracking can emerge. Two competing mechanisms, both positively and negatively affected by the growing tube size, arise to significantly enhance the overall fracture toughness by up to 5.6-fold compared to the monolithic brittle counterpart without sacrificing the specific strength. This is enabled by crack-tube interaction and engineering the tube size, shape, and orientation, which promotes rising resistance-curves (R-curve). "Disorder" curves and statistical mechanics parameters are proposed for the first time to quantitatively characterize the degree of disorder for describing the representation of the architected arrangement of materials in lieu of otherwise inadequate "periodicity" classification and misperceived disorder parameters (perturbation and Voronoi tessellation methods).

Renal tubular epithelial cell quality control mechanisms as therapeutic targets in renal fibrosis.

Renal fibrosis is a devastating consequence of progressive chronic kidney disease, representing a major public health challenge worldwide. The underlying mechanisms in the pathogenesis of renal fibrosis remain unclear, and effective treatments are still lacking. Renal tubular epithelial cells (RTECs) maintain kidney function, and their dysfunction has emerged as a critical contributor to renal fibrosis. Cellular quality control comprises several components, including telomere homeostasis, ubiquitin-proteasome system (UPS), autophagy, mitochondrial homeostasis (mitophagy and mitochondrial metabolism), endoplasmic reticulum (ER, unfolded protein response), and lysosomes. Failures in the cellular quality control of RTECs, including DNA, protein, and organelle damage, exert profibrotic functions by leading to senescence, defective autophagy, ER stress, mitochondrial and lysosomal dysfunction, apoptosis, fibroblast activation, and immune cell recruitment. In this review, we summarize recent advances in understanding the role of quality control components and intercellular crosstalk networks in RTECs, within the context of renal fibrosis.

Cylindromatosis lysine 63 deubiquitinase (CYLD) suppress TLR3-mediated CCL5 expression in human renal proximal tubular epithelial cells.

BACKGROUND: One of the causes of tubulointerstitial nephritis is viral infection, with innate immune responses affecting its pathogenesis. Toll-like receptor 3 (TLR3) recognizes viral infections and acts antivirally by activating signaling to produce inflammatory cytokines/chemokines, including C-C motif chemokine ligand 5 (CCL5) and interferon-ß (IFN-ß). Although cylindromatosis lysine 63 deubiquitinase (CYLD) is known to be associated with tubulointerstitial nephritis and renal function, its role in the antiviral innate immune response in tubular epithelial cells remains unknown. In this study, we investigated the association between CYLD and TLR3-mediated CCL5 production in cultured human renal proximal tubular epithelial cells (hRPTECs). METHODS AND RESULTS: Polyinosinic-polycytidylic acid (poly IC), a synthetic TLR3 ligand, was used to stimulate hRPTECs. mRNA expression was measured using reverse transcription-quantitative polymerase chain reaction. Protein expression was assayed using western blotting or an enzyme-linked immunosorbent assay. Knockdown of IFN-ß, nuclear factor-kappa B (NF-κB) p65, and CYLD was performed by transfecting cells with specific small interfering RNAs. The intracellular localization of CYLD in hRPTECs was analyzed using immunofluorescence. Poly IC induced CCL5 expression in a time- and concentration-dependent manner, and knockdown of either IFN-ß or p65 reduced poly IC-induced CCL5 expression. CYLD knockdown increased the poly IC-induced CCL5, phosphorylated IκB kinase α/ß (IKK complex), and phosphorylated p65 expression. The CYLD protein was localized in the cytoplasm, and poly IC did not alter its expression. CONCLUSION: CYLD may prevent excessive inflammation due to an antiviral innate immune response by suppressing IKK complex and NF-κB activation downstream of TLR3 in hRPTECs.

Novel Tubeimoside I liposomal drug delivery system in combination with gemcitabine for the treatment of pancreatic cancer.

Aim: To evaluate the anti-pancreatic cancer effect of novel Tubeimoside I multifunctional liposomes combined with gemcitabine.Methods: Liposomes were prepared through the thin film hydration method, with evaluations conducted on parameters including encapsulation efficiency (EE%), particle size, polydispersity index (PDI), zeta potential (ZP), storage stability, and release over a 7-day period. The cellular uptake rate, therapeutic efficacy in vitro and in vivo and the role of immune microenvironment modulation were evaluated.Results: The novel Tubeimoside I multifunctional liposomal exhibited good stability, significant anti-cancer activity, and immune microenvironment remodeling effects. Furthermore, it showed a safety profile.Conclusion: This study underscores the potential of Novel Tubeimoside I multifunctional liposomal as a promising treatment option for pancreatic cancer.

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EP300-mediated H3 acetylation elevates MTHFD2 expression to reduce mitochondrial dysfunction in lipopolysaccharide-induced tubular epithelial cells.

Sepsis represents an organ dysfunction resulting from the host's maladjusted response to infection, and can give rise to acute kidney injury (AKI), which significantly increase the morbidity and mortality of septic patients. This study strived for identifying a novel therapeutic strategy for patients with sepsis-induced AKI (SI-AKI). Rat tubular epithelial NRK-52E cells were subjected to lipopolysaccharide (LPS) exposure for induction of in-vitro SI-AKI. The expressions of E1A binding protein p300 (EP300) and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) in NRK-52E cells were assessed by western blot and qRT-PCR, and their interaction was explored by chromatin immunoprecipitation performed with antibody for H3K27 acetylation (H3K27ac). The effect of them on SI-AKI-associated mitochondrial dysfunction of tubular epithelial cells was investigated using transfection, MTT assay, TUNEL staining, 2',7'-Dichlorodihydrofluorescein diacetate probe assay, Mitosox assay, and JC-1 staining. MTHFD2 and EP300 were upregulated by LPS exposure in NRK-52E cells. LPS increased the acetylation of H3 histone in the MTHFD2 promoter region, and EP300 suppressed the effect of LPS. EP300 ablation inhibited the expression of MTHFD2. MTHFD2 overexpression antagonized LPS-induced viability reduction, apoptosis promotion, reactive oxygen species overproduction, and mitochondrial membrane potential collapse of NRK-52E cells. By contrast, MTHFD2 knockdown and EP300 ablation brought about opposite consequences. Furthermore, MTHFD2 overexpress and EP300 ablation counteracted each other's effect in LPS-exposed NRK-52E cells. EP300-mediated H3 acetylation elevates MTHFD2 expression to reduce mitochondrial dysfunction of tubular epithelial cells in SI-AKI.

Fanconi syndrome and renal tubular necrosis in patients following ingestion of potentially contaminated red yeast rice supplement: Two case reports.

We present two cases of middle-aged men who developed Fanconi syndrome and renal dysfunction after consuming "foods with functional claims (FFC)" containing red yeast rice. In the first case, the patient had consumed an FFC for 1 year and another FFC suspected to have contained nephrotoxin for 3 weeks; kidney biopsy performed during the acute phase of renal injury showed severe acute tubular necrosis and tubular cell regeneration. He achieved near-complete recovery 40 days after the FFC was discontinued. In the second case, the patient had consumed FFC for 4 years and stopped 70 days prior to presentation; kidney biopsy revealed significant tubular recovery, persistent tubular injuries, and interstitial fibrosis. Although the manifestations of Fanconi syndrome subsided, mild renal dysfunction persisted. These cases suggest that FFC with nephrotoxins may induce Fanconi syndrome owing to acute tubular necrosis. Recovery is possible after discontinuing the FFC; while short-term ingestion of FFC allows for tubular regeneration, its long-term ingestion may cause irreversible damage and lead to chronic kidney disease. Long-term follow-up is crucial for preventing further renal deterioration.

Paricalcitol prevents renal tubular injury induced by ischemia-reperfusion: Role of oxidative stress, inflammation and AT1R.

The vitamin D receptor (VDR) is associated with antioxidative and anti-inflammatory effects and modulation of the renin-angiotensin-aldosterone system. This study evaluated whether VDR agonist paricalcitol protects renal ischemia-reperfusion (IR) induced tubular injury in rats by evaluating: 1) ATP-dependent tubular Na+ transport; 2) renal redox signaling; 3) renal content of proinflammatory cytokines TNF-α and IL-6; and 4) renal content of renin and angiotensin II receptor type 1 (AT1R). Paricalcitol prevented IR-induced tubular injury, evidenced by the prevention of histopathological changes and renal fibrosis with preservation of the activity of ATP-dependent Na+ transporters in the renal cortex. Paricalcitol decreased renal oxidative stress by reducing NADPH oxidase activity and increasing catalase. Paricalcitol also decreased the renal content of TNF-α, IL-6, and AT1R. The NADPH oxidase inhibitor apocynin did not present additive protection to paricalcitol-induced effects. The protective effects of paricalcitol on tubular injury induced by renal IR may dependent on the modulation of redox and proinflammatory signaling and renal angiotensin II/AT1R signaling.

An Uncommon Cause of Recurrent Dysphagia and Chest Pain in an Adolescent Boy.

An 11-year-old boy was brought to the emergency department with a week-long history of widespread pain in his upper abdomen that worsened with deep breathing and eating, sialorrhea, food impaction sensation, and a recent fever. Ten months prior, he had similar symptoms and was diagnosed with a pharyngeal phlegmon. He was treated with antibiotics and dexamethasone. In the current episode, he presented with mild elevation of inflammatory markers, a slight deviation of the trachea on chest X-ray, and a tubular esophageal duplication was identified on a thoracic CT, with its opening observed during the endoscopic study. The patient was admitted for further treatment with fluids, analgesia, and antibiotics, and showed improvement over the next seven days with no significant incidents. Esophageal duplications are a rare congenital anomaly and their exact cause is unknown. Typically found in the posterior mediastinum and lower esophagus, they can cause symptoms such as pain, dysphagia, regurgitation, and malnutrition. Surgical or endoscopic resection can be a treatment option for these malformations.

Histopathological and Immunohistochemical Study of Acute Tubular Injury in Native Kidney Biopsy.

Background: Acute tubular injury (ATI) is a common diagnosis on renal biopsy. There are no accepted parameters to assess the severity of injury or predict recovery. An objective histologic grading system would be of immense value in clinical practice. The macrophage response to injury involves the MI phenotype which is proinflammatory and M2 which is prorepair. The study of these macrophages could aid in studying the severity and the recovery. Materials and Methods: A total of 58 native kidney biopsies with features of ATI and a minimum follow-up of 12 weeks were graded into mild, moderate and severe, using scores for simplification, sloughing, and mitosis. These scores and the density of macrophages stained with CD68, CD163, and HLA-DR were correlated with serum creatinine at presentation and with recovery. The effect of chronicity index as measured by glomerulosclerosis, tubular atrophy, and interstitial fibrosis and of co-morbidities of age, hypertension, and diabetes on the recovery pattern was also studied. Results: All three histologic scores and the grades of ATI showed positive correlation with the serum creatinine level. The densities of CD 68 + and CD163 + macrophages also showed a significant correlation with serum creatinine level. However, none of these these histological features nor the macrophage densities predicted clinical recovery. Age >60 years, hypertension, diabetes, and chronicity score on biopsy were indicators of partial and delayed recovery. Conclusion: The histopathological semiquantitative scoring system can be used routinely to grade ATI. However none of the studied parameters predicted recovery.

Minimally Invasive Resection of a Lumbar Spine Vertebral Osteoid Osteoma: A Case Report.

Introduction: Open surgical resection involves extended recovery and soft-tissue damage, prompting the development and increasing adoption of less invasive techniques. While Mast Quadrant tubular retractors have been used in spine fusion and endoscopic procedures, their application in minimally invasive tumor resections has not been widely discussed. This report showcases the use of a Mast Quadrant tubular retractor for the minimally invasive resection of a lumbar vertebral body osteoid osteoma. Case Report: A 38-year-old Caucasian man, suffering from six years of lumbar pain and refractory osteoid osteoma, underwent resection using a minimally invasive lateral approach with a Mast Quadrant tubular retractor. This came after the failure of less invasive treatment modalities, including facet injections and radiofrequency facet ablation. Conclusion: Vertebral body osteoid osteomas can be resected with no recurrence using a tubular retractor to spare paravertebral muscles and the morbidity of open resection, allowing patients an earlier return to work and activity.

Simulation of anaerobic biodegradation process in a tubular bioreactor with a biofilm layer: Steady-state and unsteady-state conditions.

In this paper, anaerobic biodegradation process in a tubular bioreactor with an inner biofilm layer for steady-state and unsteady-state conditions are simulated. The effects of various parameters including bioreactor diameter, fraction of active biomass transferred to liquid phase, and residence time of the liquid on bioreactor performance are examined. Simulations indicate that decreasing diameter of bioreactor leads to increasing degree of conversion of the substrate in liquid phase and decreasing dimensionless concentration of the substrate in biofilm. With an increase in the fraction of active biomass transferred to liquid, substrate concentrations in liquid and biofilm slightly vary. Increased residence time of the liquid phase results in the degree of conversion of substrate goes up, but substrate concentration in biofilm lowers a little. In addition, it is found that biomass concentration of liquid phase is boosted with decreased bioreactor diameter and increased residence time of liquid. A proportional-integral controller is designed and the tuned parameters of K P = - 0.131 and K I = 0.02 are obtained using genetic algorithm. It is observed that controller regulate well the degree of conversion of the substrate within 120 s for both servo and regulatory modes.

Photoinduced Deoxygenative C2 Arylation of Quinoline N-oxides with Phenylhydrazines to 2-Arylquinolines over Porous Tubular Graphitic Carbon Nitride Semiconductor Photocatalyst.

The photo-induced deoxygenative C2 arylation of quinoline N-oxides to 2-arylquinolines is achieved over a heterogeneous porous tubular graphitic carbon nitride (PTCN) catalyst with phenylhydrazines as arylation reagent. A wide range of quinoline N-oxides can be efficiently transformed into their corresponding 2-arylquinolines under visible light irradiation. Moreover, PTCN catalyst is easily separated and could be reused several times without loss to its original activity.

The influence of insulin and incretin-based therapies on renal tubular transport.

The tubular function of the kidney is very complex and is finely regulated by many factors. These include a variety of hormonal signaling pathways which are involved in the expression, activation and regulation of renal transporters responsible for the handling of electrolytes. Glucose-lowering drugs such as insulin and incretin-based therapies, exert a well-known renal protective role in diabetic kidney disease, mainly acting at the glomerular level. In the literature, several studies have described the effect of insulin and the incretin hormones on tubular transport. Most of these studies focused on the variations in excretion and clearance of sodium but did not extensively and systematically investigate the possible variations that these hormones may induce in the tubular regulation of all the other electrolytes, urea metabolism, acid-base balance and urinary pH. While insulin action on the kidney is very well-described, the renal tubular impact of incretin-based therapies is less consistent and the results available are scarce. To our knowledge, this is the first review summarizing the effects induced on renal tubules by insulin, glucagon-like peptide-1 (GLP-1) receptor agonists and serine protease dipeptidyl peptidase-4 (DPP4) inhibitors in both healthy and diabetic human subjects. This is significant because it highlights the existence of a renal-gut and pancreas axis which also has a direct tubular effect and enables a deeper understanding of renal physiology.