Cross-diffusive flow of MHD micropolar nanofluid past a slip stretching plate.

As a novel fluid of functional material, magnetohydrodynamic (MHD) micropolar fluid has the special properties of light, heat, magnetic and so on. It is of highly practical significance. The characteristics of flow, heat and mass transfer in MHD micropolar nanofluid boundary layer past a stretching plate are investigated based on the micropolar fluid theory in the present numerical work. In the presence of magnetic field, viscous dissipation and the cross-diffusion caused by Dufour effect and Soret effect are considered. First order slip velocity condition is employed. Mathematical models are built based on the assumptions. Collocation spectral method (CSM) via matrix multiplication is adopted to solve the two-dimensional dimensionless nonlinear partial governing equations. The program codes based on CSM is developed, validated and employed. The coupled effects of microrotation, Dufour effect, Soret effect, magnetic field as well as first order slip velocity boundary condition on the flow, heat and mass transfer are revealed. Besides, the variation trends of local Nusselt number and Sherwood number are analyzed in detail. The numerical results indicate that the fluid flow can be suppressed obviously in the consideration n of slip condition and magnetic field. As slip parameter δ and magnetic parameter M rise, the velocity in the boundary layer becomes lower gradually; further, both temperature and concentration increase. On the other hand, the opposite trend can be noticed with the effect of material parameter K. Moreover, Ec and Df augment the temperature; while, Sr leads to an upsurge in concentration. The temperature rises by about 79.73% with Dufour effect and Sh enlarges by a factor of about 38.15% with Soret effect. The concentration boundary layer decreases by about 37.50% is when K=5.0.

Overlapping infection of Nocardia farcinica and Aspergillus fumigatus in a child with X-linked chronic granulomatous disease: a case report.

BACKGROUND: Chronic granulomatous disease (CGD) is a rare inherited primary immunodeficiency syndrome, manifested as recurrent infections and inflammatory complications. Although prophylactic treatment with antibiotics and antifungals improved the outcome of CGD patients, infections remain the major cause of mortality. CASE PRESENTATION: A boy aged 3 years and 8 months was admitted to hospital complaining of lip swelling with fever for half a month and neck abscess for 11 days. After a thorough examination, severe pneumonia, respiratory failure, oral and maxillofacial space infection, and perianal abscess were confirmed. However, his condition didn't improve after initial comprehensive therapy. Subsequently, overlapping infections of Nocardia farcinica and Aspergillus fumigatus were identified by metagenomic next-generation sequencing. He was treated with imipenem, linezolid, and voriconazole intravenously, plus taking oral compound sulfamethoxazole. Later, his condition improved. Through whole-exome sequencing, the child was ultimately diagnosed as X-linked chronic granulomatous disease (X-CGD) caused by CYBB gene mutation. Allogeneic hematopoietic stem cell transplantation was the potential sanative approach but there were no available human leukocyte antigen compatible donors for the child. The family requested to transfer to a superior hospital for further treatment. Two months later, we followed up the child's family. Unfortunately, the child had expired due to severe infection. CONCLUSION: To our knowledge, this is the first case of overlapping infection of Nocardia farcinica and Aspergillus fumigatus identified by metagenomic next-generation sequencing in a child with X-CGD from China. For infectious pathogens that are hard to diagnosis by traditional detection methods, metagenomic next-generation sequencing is recommended as an adminicle or indispensable approach for microbial identification. Patients with X-CGD have poor prognosis, early diagnosis and intervention of X-CGD may reduce the mortality.

The role of miR-199b-3p in regulating Nrf2 pathway by dihydromyricetin to alleviate septic acute kidney injury.

The pathophysiology of septic acute kidney injury (AKI) is very complex and the fatality is high. Nrf2 is crucial for septic AKI, and dihydromyricetin (DMY) has a protective effect on LPS-induced AKI. We aimed to explore whether DMY could affect Nrf2 pathway by regulating miR-199b-3p and played a protective role in septic AKI. The mouse model was induced by cecal ligation and puncture (CLP) and the cell model was stimulated by LPS. Enzyme-linked immunosorbent assay was conducted to examine MDA, SOD, LDH, GSH, TNF-α, kidney injury molecule 1 (KIM-1), and IL-6 levels. The pathological changes were observed by hematoxylin-eosin staining. The targeted relationship between miR-199b-3p and Nrf2 was verified by a dual-luciferase reporter assay. Levels of SOD, GSH, NQO-1, Nrf2, and HO-1 were decreased, MDA, LDH, TNF-α, IL-6, and KIM-1, and miR-199b-3p were increased in the CLP group and LPS-induced HK-2 cells, while the effect was reversed after DMY treatment. There existed renal tubule cell edema and necrosis, inflammatory cell infiltration in the CLP group, the situation was partially improved by DMY. MiR-199b-3p bound to Nrf2. Nrf2 levels were increased, TNF-α, IL-6, and KIM-1 were decreased after transfected with miR-199b-3p inhibitor, these effects were reversed when co-transfected with si-Nrf2. TNF-α, IL-6, KIM-1, and miR-199b-3p levels were increased; Nrf2, NQO-1, and HO-1 levels were decreased in the LPS + DMY + mimics-miR group. MiR-199b-3p was increased in septic AKI models, DMY might alleviate septic AKI by regulating miR-199b-3p to affect the Nrf2 pathway.

Beneficial effects of creatine phosphate sodium for the treatment of Henoch-Schönlein purpura in patients with early renal damage detected using urinary kidney injury molecule-1 levels.

Henoch-Schönlein purpura (HSP) is a small-vessel disease in children that is often accompanied by kidney damage. Despite many efforts to improve the early assessment of renal injury in HSP patients, effective markers are still lacking. In recent years, the relationship between kidney injury molecule-1 (KIM-1) and tubulointerstitial injury has drawn much attention, especially regarding the diagnostic potential of serum and urinary KIM-1 levels. However, the diagnostic value of KIM-1 for detecting urinary kidney injury in HSP patients is still elusive. Furthermore, the treatment of Henoch-Schönlein purpura nephritis (HSPN) relies on the clinician's experience without performing renal biopsy, so it is important to find an effective biomarker and therapy. In the present study, we investigated the diagnostic value of urinary KIM-1 for early renal injury in HSP patients enrolled in a prospective, single-center study. Urinary KIM-1 levels were measured in 27 patients with HSP, 32 patients with HSPN (21 HSPN patients had undergone renal biopsy), and 16 healthy donors, as normal controls. The HSPN patients were randomly divided to receive either routine therapy (n = 13) or routine treatment combined with creatine phosphate sodium (CP) (n = 19). Urinary KIM-1 levels were significantly greater in the HSP and HSPN groups than those in the healthy control group (P < 0.01), and were significantly greater in the HSPN group than in the HSP group (P < 0.01). The urinary KIM-1 levels decreased significantly after 10-14 days of treatment with CP compared with conventional therapy (P < 0.05). CONCLUSION: Our results demonstrate the diagnostic value of KIM-1 and the therapeutic potential of CP for early renal damage in HSP patients. WHAT IS KNOWN: Urine kidney injury molecule-1 (KIM-1) is a sensitive biomarker for tubulointerstitial injury. Henoch-Schonlein purpura (HSP) usually presents with renal damage. WHAT IS NEW: Our results suggest that the urinary KIM-1 level is a sensitive and specific biomarker for the detection of early renal damage in HSP and may predict the severity of HSP and HSPN. The administration of creatine phosphate sodium (CP) may reduce urinary KIM-1 levels and thus correct the hypoxic condition of the kidney. Preconditioning with CP may also be a useful adjunct for preventing early renal damage in HSPN patients.

[Significance of serum cholesterol and fibrinogen in evaluating the risk of glomerulosclerosis in children with nephrotic syndrome].

OBJECTIVE: To investigate the significance of serum cholesterol and fibrinogen (Fib) in evaluating the risk of glomerulosclerosis in children with nephrotic syndrome. METHODS: Sixty-three children with primary nephrotic syndrome were divided into two groups according to their pathological types: minimal change glomerulopathy (MCG) (n=39) and focal segmental glomerulosclerosis (FSGS) groups (n=24). Serum levels of total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), non-HDL-C and Fib and 24-hour urinary protein excretion were retrospectively analyzed. RESULTS: Serum levels of TC, non-HDL-C, and LDL-C were significantly higher in the FSGS group than in the MCG group (P<0.05), but there were no significant differences in HDL-C, Fib and 24-hour urinary protein excretion between the two groups (P>0.05). According to the results of logistic regression analysis, high levels of LDL-C, non-HDL-C and TC were risk factors for FSGS (P<0.05). In patients whose proteinuria did not disappear after taking enough glucocorticoid for 4 weeks, the level of non-HDL-C was significantly higher in the FSGS group than in the MCG group (P<0.05); there were no significant differences in TC, LDL-C, HDL-C, and Fib between the MCG and FSGS groups (P>0.05). CONCLUSIONS: Serum cholesterol, especially non-LDL-C, is of great significance in evaluating the risk of glomerulosclerosis in children with nephrotic syndrome. There is no sufficient evidence to support serum Fib as a marker for predicting glomerulosclerosis in these children.