[Efficacy and prognosis of infant kidney transplantation].

Objective: To analyze the effect and prognosis of infant kidney transplantation. Methods: Clinical data of 37 cases of infant kidney transplantation under 3 years old in Tongji Hospital Affiliated to Tongji Medical College of Huazhong University of Science and Technology from June 1, 2017 to July 31, 2022 were retrospectively collected. These 37 cases included 31 primary kidney transplantation and 6 secondary kidney transplantation. Kaplan-Meier method was used to draw the survival curve of the transplanted kidney and the recipient, and the prognosis and complications were analyzed. Median follow-up was 18 months (range: 6-66 months). Results: The recipients were 20 males and 17 females, with a median age of 16 months (range: 2 months, 26 days to 36 months) and a median weight of 8 kg (range: 3.2 to 14.0 kg). The youngest child was only 2 months, 26 days old, and weighed only 3.2 kg. The most common primary disease of recipients was congenital nephrotic syndrome (13 cases, 41.9%). Intra-abdominal transplantation occurred in 19 cases (51.3%) and intra-iliac fossa transplantation occurred in the remaining 18 cases (48.6%). Postoperative renal function recovery was delayed in 7 cases (18.9%), and thrombosis caused renal function loss in 5 cases (13.5%), of which 4 cases received second renal transplantation and were successful. During the follow-up period, there were 11 cases of acute rejection (29.7%) and 6 cases of CMV pneumonia (16.2%). The estimated glomerular filtration rate 1 year after transplantation was higher than that 1 month after surgery [(101.9±22.1) vs (71.1±25.6) ml/(min·1.73m2), P<0.001], and remained constant 2 years after transplantation. Both the 1-year and 2-year survival rates of the transplanted kidney were 85.3%, and both the 1-year and 2-year survival rates of the recipients were 96.8%. Conclusion: Although the implementation of infant kidney transplantation is difficult, it can still achieve relatively satisfactory efficacy and prognosis.

[Technical summary and experiences of urinary reconstruction in mouse kidney transplantation].

The present paper summarizes the methods and technical key points for urinary reconstruction in mouse kidney transplantation. Both bladder patch and ureter implantation techniques are feasible options for urinary reconstruction in mouse kidney transplantation. The dominant complication in bladder patch technique is ischemic necrosis of patch and distal ureter and is associated with donor mouse strains and surgical skills. The most common complication in ureter implantation technique is urine leakage and is related to recipient mouse gender and technical skills. The key technical points for bladder patch method are estimation of blood supply for bladder patch and properly trimming and suturing bladder walls. The key points for ureter implantation method are properly trimming and fixation of the ureter. Comparing with the bladder patch, the ureter implantation technique is faster, its complications are easier to be repaired by secondary surgery, but the risk of urine retention is higher at late time. The timeliness of surgical intervention is a key factor for successfully repairing the early urinary complications.

MicroRNA-130b-5p accelerates the migration and invasion of osteosarcoma via binding to TIMP2.

The article "MicroRNA-130b-5p accelerates the migration and invasion of osteosarcoma via binding to TIMP2, by Z.-H. Cheng, C. Luo, Z.-L. Guo, published in Eur Rev Med Pharmacol Sci 2019; 23 (21): 9267-9276-DOI: 10.26355/eurrev_201911_19419-PMID: 31773678" has been withdrawn from the authors stating that "some data has to be verified by future research". The Publisher apologizes for any inconvenience this may cause. https://www.europeanreview.org/article/19419.

Theoretical Approach for the Calculation of the Pressure Drop in a Multibranch Horizontal Well with Variable Mass Transfer.

In this study, the pressure drop obtained from physical experiments and theoretical approaches of a single horizontal wellbore is reviewed and a comprehensive wellbore pressure-drop model is derived for a multibranch well. We propose a new coupling model for fluid flow in multibranch wells and reservoirs. Based on this coupling model, we introduce a theoretical approach for the calculation of the pressure drop in a multibranch horizontal well with variable mass transfer. To facilitate the understanding of the physical model, the entire coupling model was divided into three parts: (1) the pressure-drop model of the wellbore, (2) the reservoir inflow model, and (3) the coupling model. By incorporating the acceleration, friction, mixing, confluence, and gravity pressure drops, a coupling model with a finite-conductivity multibranch horizontal well was developed. Newton-Raphson iterations and Visual Basic programming were employed to solve the coupling model and to obtain the pressure and the inflow rate of the wellbore. The wellbore pressure-drop model was verified by comparing it with different models for the same case study, which has been previously introduced in a different research work. Furthermore, the forecast and sensitivity analysis were conducted, and then the results are discussed. In the proposed new model, several factors are considered, including the wellbore structure, the wellbore completion method, the wellbore, and the fluids and formation properties. The presented approach can be used as a valuable tool to analyze the influence of the pressure drop on the productivity of complex-structured wells and vice versa, and to quantitatively investigate the various pressure drops in wellbores, including the friction, acceleration, mixing, confluence, and gravity pressure losses.

TIR-domain-containing adapter-inducing interferon-ß contributes to TLR3/TLR4 triggered apoptosis and inflammation in nucleus pulposus cells.

The senescence and degeneration of the intervertebral disc are closely related to the reduction of nucleus pulposus (NP) cells caused by apoptosis. TIR-domain-containing adapter-inducing interferon-ß (TRIF) is an adapter for Toll-like receptors 3/4 (TLR3/4), which involves in cell apoptosis. The aim of this study is to detect the role of TRIF in the apoptotic progress of NP cells. The expression of collagen II, aggrecan, TLR3/4, and TRIF were analyzed in different degrees of degenerated human NP samples from patients. NP cells were isolated from mild degenerated tissues and cultured with IL-1ß to accelerate the degradation, and treated with TLR3/4 protein. siRNA was used to silence TRIF gene expression, and TRLF-plasmid was used to upregulate TRLF gene expression. We used flow cytometry assay to analyze cell apoptosis. The expression of collagen II, aggrecan, TLF3/4, TRIF, caspase-8/3, MMP-13, TNF-α was determined by immunofluorescence, Western blot, or RT-PCR. That the expression of collagen II and aggrecan markedly decreased, but TLF3/4, TRIF, caspase-8/3, MMP-3, TNF-α, and IL-1ß were increased in severely degenerated disc tissues. IL-1ß treatment induced NP cell degeneration and TLF3/4, TRIF, caspase-8/3, MMP-3, TNF-α overexpression. TLF3/4 protein treatment promoted NP cell degeneration and apoptosis by upregulation of TRIF, caspase-8/3, MMP-3, and TNF-α. Furthermore, TRIF silencing reversed the negative effect of TLF3/4 overexpression, and TRIF overexpression played the same role in NP cell apoptosis. Based on these results, we believe that TRIF is activated in a degenerated intervertebral disc. TLF3/4 promotes NP cell apoptosis and inflammation through the TRLF adaptor. TRLF expression is positively related to the apoptosis and inflammation in NP cells. These results suggest a therapeutic potential of the TRIF in the treatment of disc degeneration.

MicroRNA-130b-5p accelerates the migration and invasion of osteosarcoma via binding to TIMP2.

OBJECTIVE: To elucidate the potential function of microRNA-130b-5p in the progression of osteosarcoma (OS) and the underlying mechanism. MATERIALS AND METHODS: The relative level of microRNA-130b-5p in OS tissues and cell lines was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between the microRNA-130b-5p level and the pathological characteristics of OS was analyzed by the Chi-square test. The Kaplan-Meier curves were introduced for assessing the survival of OS patients with high expression and low expression of microRNA-130b-5p. The regulatory effects of microRNA-130b-5p on the migratory and invasive abilities of MG63 and U2OS cells were evaluated by the transwell assay. The relative levels of matrix metalloproteinase 2 (MMP2) and MMP9 in OS cells with overexpression or knockdown of microRNA-130b-5p were determined. The binding relationship between microRNA-130b-5p and TIMP2 was verified through the dual-luciferase reporter gene assay. Finally, a series of rescue experiments were performed to uncover the role of microRNA-130b-5p/TIMP2 in the progression of OS. RESULTS: MicroRNA-130b-5p was upregulated in OS tissues and cell lines. The high expression of microRNA-130b-5p indicated a poor prognosis of OS patients. The overexpression of microRNA-130b-5p accelerated OS cells to migrate and invade. Besides, the relative levels of MMP2 and MMP9 were upregulated in OS cells overexpressing microRNA-130b-5p. TIMP2 was the direct target of microRNA-130b-5p, which was negatively regulated by microRNA-130b-5p. The knockdown of TIMP2 reversed the regulatory effect of microRNA-130b-5p on the migratory and invasive abilities of the OS cells. CONCLUSIONS: MicroRNA-130b-5p is upregulated in OS. It accelerates the progression of OS via inhibiting TIMP2 level.

Tubular basement membrane immune complex deposition is associated with activity and progression of lupus nephritis: a large multicenter Chinese study.

Tubulointerstitial injury is found frequently in lupus nephritis. Immune complex deposits can occur in the tubular basement membranes (TBMs), although its significance in lupus nephritis patients remains unclear. This study assessed the clinical and prognostic features of lupus nephritis patients with TBM deposits in a large Chinese multicenter cohort. Complete data were collected from 195 patients with renal biopsy-proven lupus nephritis diagnosed in the Peking University First Hospital as the discovery cohort. A total of 102 lupus nephritis patients were enrolled from another four centers as the validation cohort. The status of TBM deposits was retrospectively assessed using electron microscopy, and the associations of the deposits with clinical data, pathological characteristics and renal outcomes were further analyzed. The percentage of positive TBM deposits was nearly 30% in the lupus nephritis patients. Using immuno-gold labeling, we found that 10/10 patients were positive for IgG, 7/10 were C3d positive, 6/10 were C1q positive, and 1/10 were C4d positive. Patients with TBM deposits presented with more active features, including a higher SLEDAI score (SLE Disease Activity Index) ( p < 0.001), higher serum creatinine level ( p = 0.001) and lower serum C3 level ( p < 0.001). These patients also presented with higher scores for most renal pathological indices, including the total activity indices score ( p < 0.001) and total chronicity indices score ( p = 0.001). TBM deposits affected renal outcomes in the univariate Cox hazards regression analysis (HR = 4.2, 95% CI = 1.3-14.3, p = 0.02). In conclusion, TBM deposits were common in lupus nephritis patients and correlated closely with the clinical disease activity and renal outcome.

Phase-field-based multiple-relaxation-time lattice Boltzmann model for incompressible multiphase flows.

In this paper, a phase-field-based multiple-relaxation-time lattice Boltzmann (LB) model is proposed for incompressible multiphase flow systems. In this model, one distribution function is used to solve the Chan-Hilliard equation and the other is adopted to solve the Navier-Stokes equations. Unlike previous phase-field-based LB models, a proper source term is incorporated in the interfacial evolution equation such that the Chan-Hilliard equation can be derived exactly and also a pressure distribution is designed to recover the correct hydrodynamic equations. Furthermore, the pressure and velocity fields can be calculated explicitly. A series of numerical tests, including Zalesak's disk rotation, a single vortex, a deformation field, and a static droplet, have been performed to test the accuracy and stability of the present model. The results show that, compared with the previous models, the present model is more stable and achieves an overall improvement in the accuracy of the capturing interface. In addition, compared to the single-relaxation-time LB model, the present model can effectively reduce the spurious velocity and fluctuation of the kinetic energy. Finally, as an application, the Rayleigh-Taylor instability at high Reynolds numbers is investigated.

Protective effect of icariin on kidney in 5/6 nephrectomized rats and its mechanism.

The aim of this study was to investigate the renal protective effect of icariin in 5/6 nephrectomized rats and the molecular mechanisms involved. Forty male Sprague-Dawley rats were randomly divided into 5 groups: sham-operated group, 5/6 nephrectomy model group, icariin groups (20 and 40 mg/kg), and benazepril group. After 12-weeks treatment, 24-h urine and serum were collected, and urine protein, serum creatinine, and blood urea nitrogen were determined. The rats were then sacrificed and fresh kidney tissues were prepared to obtain single cell suspensions. Cell cycle distribution and cell apoptosis were determined by annexin V-FITC/propidium iodide (PI) double staining using a flow cytometer. mRNA expression of Bcl-2 and Bax was examined using quantitative real-time PCR. After 12-weeks treatment, urinary protein, serum creatinine, and blood urea nitrogen in the icariin-treated group were much lower than in the untreated group compared with 5/6 nephrectomy model. Icariin reduced the percentage of S phase cells, increased the percentage of G0/M phase cells, and inhibited apoptosis in the renal cells. mRNA expression of Bcl-2 and Bax was decreased. In conclusion, icariin has a renal protective effect in 5/6 nephrectomized rats, which may be related mainly to alterations in cell cycle distribution and expression of apoptotic genes.

Phase-field-based lattice Boltzmann model for axisymmetric multiphase flows.

In this paper, a phase-field-based lattice Boltzmann (LB) model is proposed for axisymmetric multiphase flows. Modified equilibrium distribution functions and some source terms are properly added into the evolution equations such that multiphase flows in the axisymmetric coordinate system can be described. Different from previous axisymmetric LB multiphase models, the added source terms that arise from the axisymmetric effect contain no additional gradients, and therefore the present model is much simpler. Furthermore, through the Chapmann-Enskog analysis, the axisymmetric Chan-Hilliard equation and Navier-Stokes equations can be exactly derived from the present model. The model is also able to deal with flows with density contrast. A variety of numerical experiments, including planar and curve interfaces, an elongation field, a static droplet, a droplet oscillation, breakup of a liquid thread, and dripping of a liquid droplet under gravity, have been conducted to test the proposed model. It is found that the present model can capture accurate interface and the numerical results of multiphase flows also agree well with the analytical solutions and/or available experimental data.

Two novel mutations in the Spastin gene of Chinese patients with hereditary spastic paraplegia.

BACKGROUND AND PURPOSE: Hereditary spastic paraplegia (HSP) is a clinically and genetically heterogeneous group of neurodegenerative diseases. Mutations in the spastin (SPG4) gene are responsible for approximately 40% of autosomal dominant HSP (AD-HSP) and 6.5-18% of sporadic cases. METHODS: Spastin mutations were screened in 11 AD-HSP families and 11 sporadic cases by direct sequencing and MLPA assay. Novel mutations were detected in 100 healthy controls by PCR-RFLP. RESULTS: We identified seven different spastin mutations in five probands and one sporadic patient. Two of seven mutations were novel. The c.458delT was a pathogenic mutation, but the effect of c.1724 G>T remained unknown. CONCLUSIONS: This study allowed us to estimate the frequency of the SPG4 mutations in Chinese at 45% (5/11) in families with AD-HSP and 9% (1/11) in sporadic cases. In addition, our data showed p.T614I was not associated with congenital arachnoid cysts.

Simultaneous incorporation of mass and force terms in the multi-relaxation-time framework for lattice Boltzmann schemes.

This paper presents an analysis of the simultaneous incorporation of force and mass source terms into the multi-relaxation-time (MRT) collision operator. MRT force incorporation was obtained through Chapman-Enskog analysis. The numerical scheme was tested on different benchmark problems, including the decay of a shear wave with different bulk and kinematic viscosities and axisymmetric flow.

A population-based survey of multiple sclerosis in Shanghai, China.

OBJECTIVE: To conduct a large population-based survey on multiple sclerosis (MS) prevalence in Shanghai, China. METHODS: We established a network of physicians, mainly neurologists, for identifying prevalent patients with MS and systematically checked inpatient registers at each hospital in the study area for patients with a diagnosis of MS, neuromyelitis optica, or other demyelinating disorders. MS diagnosis in patients was validated by senior neurologists according to the McDonald criteria. RESULTS: In total, 123 patients with a validated MS diagnosis from the study population, 8.86 million inhabitants with permanent residence in Shanghai, were alive on the prevalence day. The crude MS prevalence rate was 1.39 cases per 100,000 inhabitants (95% CI: 1.16 to 1.66 cases) in the study population in Shanghai. There were 79 female and 44 male patients with MS, a female-to-male ratio of 1.8. Nearly all (96%) of the patients with validated MS had been examined by MRI. CONCLUSION: Multiple sclerosis prevalence in Shanghai is in line with that reported for other Asian populations.

Lattice Boltzmann method for incompressible flows with large pressure gradients.

Conventional lattice Boltzmann Bhatnagar-Gross-Krook (LBGK) models can simulate incompressible flows correctly only if the Mach number M and the density variation deltarho are negligibly small. However, the equation of state p=RTrho resulting from the conventional models limits their application to incompressible flows with a rather small pressure gradient. In this paper, based on the Enskog equation, we propose a finite difference lattice BGK model for isothermal incompressible flows with the resulting equation of state and transport properties suitable for nonideal fluids. We validated this model by simulating the plane Poiseuille flow, the two dimensional Womersley flow, and the backward-facing step flow and found that the numerical results obtained by the proposed model are more accurate than those by the conventional LBGK models when the pressure gradient imposed on the flows increases.

Thermal lattice Bhatnagar-Gross-Krook model for flows with viscous heat dissipation in the incompressible limit.

In this paper, by introducing a different distribution function and starting from the Boltzmann equation as well as the Maxwell-Boltzmann distribution, we obtain a Boltzmann Bhatnagar-Gross-Krook (BGK) equation for thermal flows with viscous heat dissipation in the incompressible limit. The continuous thermal BGK model is then discretized over both time and phase space to form a lattice BGK model, which is shown to be consistent with some existing double distribution function lattice BGK models based on macroscopic governing equations. We have also demonstrated that the lattice BGK model derived theoretically in this work can be used to simulate laminar incompressible convention heat transfer with/without viscous heat dissipation.

Activation of nitric oxide-producing neurons in the brain stem during cardiac sympathoexcitatory reflexes in the cat.

Our previous studies have shown that selective inhibition of nitric oxide in the brain reduces pressor responses to activation of cardiac sympathetic afferents, thus suggesting that nitric oxide is involved in central regulation of cardiac-cardiovascular sympathoexcitatory reflexes. Central neural regions in which nitric oxide-producing neurons are activated during these reflexes have not been well characterized. In the present study, we located nitric oxide-producing neurons in the brain stem activated by the input from cardiac sympathetic afferents by detecting colocalization of c-Fos immunoreactivity with nitric oxide synthesizing neurons. Expression of c-Fos has been used as a marker of activated neurons. Nitric oxide-producing neurons were identified by histochemical labeling of nicotine adenine dinucleotide phosphate-diaphorase (NADPH-d). In anesthetized cats with bilateral barodenervation and cervical vagotomy, bradykinin (1-10 microg in 0.1 ml; n=6) was applied to the anterior surface of the left ventricle six times every 20 minutes. Repetitive application of bradykinin consistently increased blood pressure, while the vehicle for bradykinin (0.9% saline, n=5) produced no responses. A substantial fraction (6-27%) of NADPH-d positive neurons displayed Fos immunoreactivity in the nucleus of the solitary tract, caudal and rostral ventral lateral medulla, lateral tegmental field, locus coeruleus and parabrachial nucleus in the bradykinin-treated cats. However, either no or rare (1-4%) double-labeled cells were found in these regions in control animals. Thus, nitric oxide-producing neurons are activated in several regions in the brain stem during stimulation of cardiac sympathetic afferents by bradykinin. Our data suggest that nitric oxide functions as a neurotransmitter/modulator in these areas to regulate the cardiac sympathoexcitatory reflexes.

Central pathways in the pons and midbrain involved in cardiac sympathoexcitatory reflexes in cats.

Activation of cardiac sympathetic afferents elicits pain and excitatory cardiovascular reflexes including acute hypertension and tachyarrhythmias. Our previous studies have shown that specific regions in the medulla, such as the nucleus of solitary tract and ventrolateral medulla, are involved in central regulation of cardiac sympathoexcitatory reflexes. However, the contributions of supramedullary nuclei to these reflexes have not been characterized. In the present study, we located activated neurons in the pons and midbrain induced by inputs from cardiac sympathetic afferents by detecting their c-Fos immunoreactivity. In anesthetized cats with bilateral carotid denervation and cervical vagotomy, epicardial application of bradykinin (1-10 microg, in 0.1 ml; n=7) was performed on the anterior surface of the left ventricle six times, every 20 min. Repetitive application of bradykinin caused consistent excitatory cardiovascular reflexes characterized by increases in blood pressure and heart rate. No responses were evoked by the vehicle for bradykinin (0.9% saline, n=7). Compared to control cats, c-Fos immunoreactive cells were significantly increased (P<0.05) in the rostral pons, caudal and intermediate midbrain in the bradykinin-treated cats. The specific areas activated include the parabrachial nucleus, Kölliker-Fuse nucleus, locus coeruleus, dorsal nucleus of raphe, and dorsal, lateral and ventrolateral periaqueductal gray. From these results we suggest that cardiovascular-related regions in the pons and midbrain form part of a long loop in central integration of cardiac sympathoexcitatory reflexes.

Role of cAMP in activation of ischemically sensitive abdominal visceral afferents.

A number of metabolites produced during abdominal ischemia can stimulate and/or sensitize visceral afferents. The precise mechanisms whereby these metabolites act are uncertain. Other studies have shown that the adenylate cyclase-cAMP system may be involved in the activation of sensory neurons. Therefore, we hypothesized that cAMP contributes to the activation of ischemically sensitive abdominal visceral afferents. Single-unit activity of abdominal visceral C fibers was recorded from the right thoracic sympathetic chain in anesthetized cats before and during 7 min of abdominal ischemia. Forty-six percent of ischemically sensitive C fibers responded to intra-arterial injection of 8-bromo-cAMP (0.35-1. 0 mg/kg), an analog of cAMP, with responses during ischemia increasing from 0.50 +/- 0.06 to 0.84 +/- 0.08 impulses/s (P < 0.05, n = 11 C fibers). Conversely, an inhibitor of adenylate cyclase, 2', 5'-dideoxyadenosine (DDA; 0.1 mg/kg iv), attenuated ischemia-induced increase in activity of afferents from 0.66 +/- 0.10 to 0.34 +/- 0. 09 impulses/s (P < 0.05; n = 8). Furthermore, whereas exogenous PGE(2) (3-4 microg/kg ia) augmented the ischemia-induced increase in activity of afferents (P < 0.05, n = 10), treatment with DDA (0.1 mg/kg iv) substantially reduced the increase in discharge activity of afferents during ischemia, which was augmented by PGE(2) (1.45 +/- 0.24 vs. 0.70 +/- 0.09 impulses/s, -DDA vs. +DDA; P < 0.05) in six fibers. A time control group (n = 4), however, demonstrated similar increases in the activity of afferents with repeated administration of PGE(2). These data suggest that cAMP contributes to the activation of abdominal visceral afferents during ischemia, particularly to the action of PGs on activation and/or sensitization of these endings.

Activation of visceral afferents by bradykinin and ischemia: independent roles of PKC and prostaglandins.

We have shown that the cyclooxygenase (COX) and protein kinase C (PKC) systems both contribute to afferent activation in response to bradykinin (BK) and abdominal ischemia. Because the contribution from PKC to C fiber activation may depend, in part, on prostaglandin production, we hypothesized that an intact COX system is required for PKC-induced activation of ischemically sensitive abdominal visceral afferents by BK and abdominal ischemia. Single-unit activity of abdominal visceral C fibers was recorded from the right thoracic sympathetic chain of anesthetized cats. Three repeated injections of BK (1-2 micrograms/kg ia) produced similar increases in afferent activity from the baseline of 1.32 +/- 0.24, 1.37 +/- 0.32, and 1.41 +/- 0.24 impulses/s (n = 5). In another group of animals (n = 5), the second and third BK injections were performed after COX inhibition (indomethacin; 5 mg/kg iv) and then combined COX + PKC inhibition [PKC-(19-36), 20 micrograms/kg iv], respectively. Inhibition of COX reduced (P < 0.05) the afferent response to BK (0.59 +/- 0.12 impulses/s) compared with the unblocked condition (1.14 +/- 0.27 impulses/s), whereas combined COX + PKC inhibition further attenuated the increase from baseline (0.18 +/- 0.09 impulses/s; P < 0.05). Similar results were obtained in a third group of cats when the antagonists were administered in reverse order (n = 7). In a fourth group of cats (n = 9) that were pretreated with indomethacin, ischemia increased afferent activity (0.78 +/- 0.17 impulses/s). However, neural activity was attenuated (0.51 +/- 0.14 impulses/s; P < 0.05) during a second bout of ischemia in the presence of indomethacin + PKC-(19-36). These results suggest that the contribution from PKC to the activation of ischemically sensitive C fibers, particularly by BK, does not require an intact cyclooxygenase system.