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In this paper, numerical Galerkin Finite Element Method (GFEM) is applied for conjugate heat-transfer of a rotating cylinder immersed in Fe 3 O 4 -water nanofluid under the heat-flux and magnetic field. The outer boundaries of the cavity were maintained at low temperatures while beside the cylinder were insulated. It is assumed that the cylinder rotates in both clockwise and counter-clockwise directions. The dimensionless governing equations such as velocity, pressure, and temperature formulation were analyzed by the GFEM. The results were evaluated using the governing parameters such as nanoparticles (NPs) volume fraction, Hartmann and Rayleigh numbers, magnetic field angle and NPs shapes. As a main result, the average Nusselt number increases by increasing the NPs volume fraction, inclination angle and thermal conductivity ratios, while increasing the Hartmann number decreased the Nusselt number. Furthermore, platelet NPs had the maximum average Nusselt number and spherical NPs made the minimum values of Nusselt numbers among examined NPs shapes.

SummaryThe effects of exogenous pulsed electromagnetic field (PEMF) stimulation on T1DM-associated osteopathy were investigated in alloxan-treated rabbits. We found that PEMF improved bone architecture, mechanical properties, and porous titanium (pTi) osseointegration by promoting bone anabolism through a canonical Wnt/β-catenin signaling-associated mechanism, and revealed the clinical potential of PEMF stimulation for the treatment of T1DM-associated bone complications.IntroductionType 1 diabetes mellitus (T1DM) is associated with deteriorated bone architecture and impaired osseous healing potential; nonetheless, effective methods for resisting T1DM-associated osteopenia/osteoporosis and promoting bone defect/fracture healing are still lacking. PEMF, as a safe and noninvasive method, have proven to be effective for promoting osteogenesis, whereas the potential effects of PEMF on T1DM osteopathy remain poorly understood.MethodsWe herein investigated the effects of PEMF stimulation on bone architecture, mechanical properties, bone turnover, and its potential molecular mechanisms in alloxan-treated diabetic rabbits. We also developed novel nontoxic Ti2448 pTi implants with closer elastic modulus with natural bone and investigated the impacts of PEMF on pTi osseointegration for T1DM bone-defect repair.ResultsThe deteriorations of cancellous and cortical bone architecture and tissue-level mechanical strength were attenuated by 8-week PEMF stimulation. PEMF also promoted osseointegration and stimulated more adequate bone ingrowths into the pore spaces of pTi in T1DM long-bone defects. Moreover, T1DM-associated reduction of bone formation was significantly attenuated by PEMF, whereas PEMF exerted no impacts on bone resorption. We also found PEMF-induced activation of osteoblastogenesis-related Wnt/β-catenin signaling in T1DM skeletons, but PEMF did not alter osteoclastogenesis-associated RANKL/RANK signaling gene expression.ConclusionWe reveal that PEMF improved bone architecture, mechanical properties, and pTi osseointegration by promoting bone anabolism through a canonical Wnt/β-catenin signaling-associated mechanism. This study enriches our basic knowledge for understanding skeletal sensitivity in response to external electromagnetic signals, and also opens new treatment alternatives for T1DM-associated osteopenia/osteoporosis and osseous defects in an easy and highly efficient manner.

Statins, commonly used to lower cholesterol, have been shown to have anti-inflammatory effects in respiratory disease models. Disorders of cholesterol metabolism can cause damage to cells and tissues, and further lead to the development of a variety of diseases. However, the role of cholesterol metabolism in cigarette smoke-induced airway epithelial inflammation is unclear. The present study aims to explore this question. Human bronchial epithelial cells (HBEs) were stimulated with cigarette smoke extract (CSE) and mice were exposed to CS as models. The expression of cholesterol content and cholesterol metabolism-related molecules such as Sterol Regulatory Element-Binding Protein 2 (SREBP2), 3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR), ATP Binding Cassette Transporter A1 (ABCA1), and ATP Binding Cassette Transporter G1 (ABCG1) were detected by cholesterol assay kits and immunohistochemistry (IHC) in vivo, and were detected by cholesterol assay kits, Western blot (WB), and quantitative real-time polymerase chain reaction (Q-PCR) in vitro. Cholesterol metabolism molecules related siRNAs, inhibitors or agonists were used to intervene the Cholesterol levels in HBE. The mRNA level and protein level of interleukin IL-6 and IL-8 were detected by RT-qPCR and enzyme-linked immunosorbent assay (ELISA). Cellular reactive oxygen species (ROS) levels were detected by reactive oxygen species assay kits. We found that cigarette smoke exposure inhibited cholesterol efflux by decreasing the expression of ABCA1, thereby increasing cholesterol accumulation in airway epithelial cells, which promotes the production of reactive oxygen species and promotes the secretion of inflammatory cytokines, ultimately aggravating cigarette smoke-induced airway inflammation. Reducing intracellular cholesterol content by inhibiting intracellular synthesis and promoting increased efflux can reduce the cigarette smoke-induced airway epithelial inflammatory factors secretion. In conclusion, cholesterol accumulation plays an important role in cigarette smoke-induced airway inflammation and may provide new targets in the treatment of this disease in the future.

To investigate the role of B cell receptor associated protein 31 (BAP31) in the pathogenesis of sepsis. Cecal ligation and puncture (CLP)-induced C57BL/6J mice, and LPS-challenged endothelial cells (HUVECs) were established to mimic a sepsis animal model and a sepsis cell model, respectively. Cre/LoxP and shRNA methods were used for BAP31 knockdown in vivo and in vitro respectively. Neutrophils/macrophages-endothelial cocultures were used to evaluate neutrophils or macrophages infiltration and adhesion to endothelial cells. Cox proportional hazards model was used to evaluate the survival time of mice. Western blotting (WB) and Quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect toll-like receptor (TLR) signaling pathway, transforming growth factor β activated kinase 1 (TAK1) signaling pathway and phosphoinositide-3 kinases-protein kinase B (PI3K/AKT) signaling pathway. Deletion of BAP31 reduced CLP-induced mortality of mice, histological damage with less interstitial edema, and neutrophils and macrophages infiltration. IHC and IF showed that BAP31 knockdown significantly decreases the expressions of ICAM1 and VCAM1 both in vivo and in vitro. Coculture showed that LPS-induced neutrophils or macrophages adhesion to endothelial cells was significantly weakened in BAP31 knockdown cells. In addition, BAP31 knockdown of endothelial cells decreased the expression of CD80 and CD86 on the surface of macrophages as well as interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) during sepsis. Mechanistically, LPS-induced the activation of TLR4, MyD88 and TRAF6, and the phosphorylation of TAK1, PI3K, AKT, IκBα and IKKα/β, resulting in activation of nuclear factor kappa B (NF-κB) p65 in endothelial cells. However, BAP31 knockdown significantly reversed the expressions of associated proteins. BAP31 up-regulated the expressions of ICAM1 and VCAM1 in endothelial cells leading to sepsis-associated organ injury. This may be involved in activation of TLR signaling pathway, TAK1 pathway, and PI3K-AKT signaling pathway.

COVID-19 can affect multiple organ systems beyond the respiratory tract, including the gastrointestinal tract, where gastrointestinal symptoms include nausea, vomiting, diarrhea, abdominal pain, and even serious manifestations such as ulcers, perforation, or gastrointestinal bleeding. We report a case of a 45-year-old male patient with small bowel ulcers caused by chronic COVID-19 infection. Initially presenting with fever and transient unconsciousness, he developed ischemic necrosis and required a mid-thigh amputation. Despite treatment with anti-infection therapy, extracorporeal membrane oxygenation, and continuous renal replacement therapy, he experienced persistent abdominal pain and gastrointestinal bleeding. Imaging and colonoscopy confirmed partial small bowel obstruction and inflammation. After treatment with methylprednisolone and enteral nutrition, his symptoms improved. However, he suffered a gastrointestinal perforation requiring emergency surgery and later underwent a successful stoma reversal. The patient was subsequently discharged with improvement and was discharged with a primary diagnosis of \"enterostomal status, perforation of small intestinal ulcer, viral myocarditis, COVID-19 infection, and post right lower extremity amputation\". During the past year of follow-up, the patient has not experienced any recurrence of abdominal pain or rectal bleeding. Although coronavirus pneumonia combined with small bowel ulcers is rare, it requires emergency treatment and has a high mortality rate. This case highlighted the severe gastrointestinal complications induced by COVID-19 infection and the effectiveness of comprehensive management strategies.

Psoriasis is an inflammatory disease linked to gut microbiome dysbiosis. However, the mechanisms underlying gut microbiome changes caused by dietary habits in psoriasis remain unclear. We performed a case-control study including 64 psoriasis patients and 64 age-, sex-, and body mass index (BMI)-matched controls. Stool samples were collected for metagenomics sequencing. The differential abundance analysis was performed to identify differentially abundant taxa between psoriasis and control groups. The dietary intake frequency information of each included subject was obtained through face-to-face interviews. Mediation analysis was used to identify potential mediators of the gut microbiome alterations in psoriasis. The gut microbiome of psoriasis patients was significantly alterated when compared to controls. Anaerostipes Hadrus, Blautia Wexlerae, and the other six species may be beneficial to psoriasis. However, Prevotella Copri and Eggerthellaceae could be pathogenic bacteria. The study also identified correlations between specific dietary habits and psoriasis, with the largest correlation observed between poultry consumption and psoriasis (OR=0.735, P=0.001), followed by red meat (OR=0.784, P=0.007) and fresh vegetables (OR=0.794, P=0.028). Mediation analysis revealed that Anaerostipes hadrus, Dorea longicatena, and Eggerthella lenta mediated the association between poultry and psoriasis. The characteristics of intestinal flora in psoriasis patients were significantly different from controls. Intestinal flora mediated the association between diet and psoriasis to some extent. This study provides new insights for adjuvant treatments of psoriasis through dietary and intestinal microbiota interventions.

. In this paper, the physical effect of a variable magnetic field on a nanofluid-based concentrating parabolic solar collector (NCPSC) is demonstrated. A section of reservoir is modeled as a semi-circular cavity under the solar radiation with the magnetic source located in the center or out of the cavity and the governing equations were solved by the FlexPDE numerical software. The effect of four physical parameters, i.e. , Hartmann Number (Ha), nanoparticles volume fraction ( φ , magnetic field strength ( γ and magnetic source location ( b , on the Nusselt number is discussed. To find the interaction of these parameters and its effect on the heat transfer, a central composite design (CCD) is used and analysis is performed on the 25 experiments proposed by CCD. Analysis of variance (ANOVA) of the results reveals that increasing the Hartmann number decreases the Nusselt number due to the Lorentz force resulting from the presence of stronger magnetic field.

Summary The present study was the first report demonstrating that pulsed electromagnetic field (PEMF) could partially prevent bone strength and architecture deterioration and improve the impaired bone formation in streptozotocin-induced diabetic rats. The findings indicated that PEMF might become a potential additive method for inhibiting diabetic osteopenia or osteoporosis. Introduction Diabetes mellitus (DM) can cause various musculoskeletal abnormalities. Optimal therapeutic methods for diabetic bone complication are still lacking. It is essential to develop more effective and safe therapeutic methods for diabetic bone disorders. Pulsed electromagnetic field (PEMF) as an alternative noninvasive method has proven to be effective for treating fracture healing and osteoporosis in non-diabetic conditions. However, the issue about the therapeutic effects of PEMF on diabetic bone complication has not been previously investigated. Methods We herein systematically evaluated the preventive effects of PEMF on diabetic bone loss in streptozotocin-treated rats. Two similar experiments were conducted. In each experiment, 16 diabetic and eight non-diabetic rats were equally assigned to the control, DM, and DM + PEMF group. DM + PEMF group was subjected to daily 8-h PEMF exposure for 8 weeks. Results In experiment 1, three-point bending test suggested that PEMF improved the biomechanical quality of diabetic bone tissues, evidenced by increased maximum load, stiffness, and energy absorption. Microcomputed tomography analysis demonstrated that DM-induced bone architecture deterioration was partially reversed by PEMF, evidenced by increased Tb.N, Tb.Th, BV/TV, and Conn.D and reduced Tb.Sp and SMI. Serum OC analysis indicated that PEMF partially prevented DM-induced decrease in bone formation. In experiment 2, no significant difference in the bone resorption marker TRACP5b was observed. These biochemical findings were further supported by the dynamic bone histomorphometric parameters BFR/BS and Oc.N/BS. Conclusions The results demonstrated that PEMF could partially prevent DM-induced bone strength and architecture deterioration and improve the impaired bone formation. PEMF might become a potential additive method for inhibiting diabetic osteoporosis.

Purpose To reveal and evaluate the efficacy and safety of intensive statin therapy in older patients (age ≥ 65 years) with coronary heart disease (CHD). Methods Electronic databases were searched for randomized controlled trials (RCTs) that involved intensive statin therapy use in older patients with CHD. Data was extracted and used to calculate risk ratios (RR) by software Revman 5.1. Results Five RCTs and 11,132 patients were included in. Compared with non-intensive statin therapy, intensive statin therapy had significant effect on reducing low density lipoprotein cholesterol (LDL-C) levels (55.4 %) and total cholesterol (TC) and triglyceride (Tg). Although the results showed that intensive statin therapy had no superior effect on reduction of mortality (both all-cause mortality [RR = 0.97, p  = 0.65] and cardiac death [RR = 0.95, p  = 0.57]) and cardiac arrest (RR = 1.09, p  = 0.81), it possessed significant effects on prevention of nonfatal myocardial infarction (MI) (RR = 0.78, p  = 0.008), stroke (RR = 0.72, p  = 0.02) and coronary revascularization (RR = 0.69, p  = 0.007). In terms of side effects, intensive statin therapy was associated with small absolute increase in incidence of drug discontinuation, due to adverse events (3.9 %) and liver enzymes abnormalities (1.7 %). And the occurrence rates of myopathy, rhabdomyolysis and creatine kinase (CK) elevation were very low. Conclusions This results show that intensive statin therapy has excellent effects on reduction of serum lipid level including LDL-C, TC, Tg, and also on prevention of nonfatal MI, stroke and coronary revascularization with small absolute increased risk of side effects. Our analysis supports the use of intensive statin therapy in patients ≥ 65 years old with CHD.

Therapeutic application of natalizumab, an anti-CD49d Ab, in patients with multiple sclerosis (MS) has been associated with increased levels of circulating CD34+ progenitors. We analyzed the frequency, phenotype and functional activity of CD34+ HSC in blood and BM of patients with MS who were treated with natalizumab. Compared with healthy controls and untreated MS patients, natalizumab treatment increased CD34+ cells in the peripheral blood 7-fold and in BM 10-fold. CD34+ cells derived from blood and marrow of natalizumab-treated patients expressed less of the stem cell marker CD133, were enriched for erythroid progenitors (CFU-E) and expressed lower levels of adhesion molecules than G-CSF-mobilized CD34+ cells. The level of surface CXCR-4 expression on CD34+ cells from patients treated with natalizumab was higher compared with that of CD34+ cells mobilized by G-CSF (median 43.9 vs 15.1%). This was associated with a more than doubled migration capacity toward a chemokine stimulus. Furthermore, CD34+ cells mobilized by natalizumab contained more mRNA for p21 and less for matrix metallopeptidase 9 compared with G-CSF-mobilized hematopoietic stem cell (HSC). Our data indicate that G-CSF and CD49d blockade mobilize different HSC subsets and suggest that both strategies may be differentially applied in specific cell therapy approaches.