Strong Homology Between Colonizing and Bloodstream Carbapenem-Resistant Acinetobacter Spp.: Implications for Empiric Antibiotic Therapy in Hematological Patients.

Objective: This study aimed to assess the impact of colonization status on the outcomes of Acinetobacter spp. bloodstream infection (BSI) and investigate the homology and within-host evolution between colonizing and bloodstream carbapenem-resistant Acinetobacter spp. (CRA) to inform antibiotic therapeutic decisions. Methods: We analyzed clinical outcomes of 46 hematological patients with Acinetobacter spp. BSI and performed whole-genome sequencing on the remaining CRA isolates. Results: Among the patients, 39.1% (n=18) had prior Acinetobacter spp. colonization. Colonized patients had higher rates of polymicrobial BSI (50.0% vs 21.4%, P=0.044) and CRA BSI (72.2% vs 17.9%, P<0.001), resulting in elevated inflammatory markers and increased 30-day mortality. Each of the eight pairs of the remaining respiratory colonizing and bloodstream CRA strains belonged to the same genomospecies. Each pair exhibited definitive agreement in at least 21 of the 22 most representative antibiotic susceptibility tests. The minimum spanning tree based on multilocus sequence typing (MLST) and phylogenetic trees based on MLST and single nucleotide polymorphism (SNP) all indicated that each pair shared the same minimum branch. Very few non-synonymous SNPs in genic regions were identified during the transition from respiratory colonization to bloodstream infection, with minimal changes in virulence genes. Homology analysis suggested that CRA BSI originated from colonizing isolates in the respiratory tract. Conclusion: Strict infection control measures are needed to manage Acinetobacter spp. colonisation in hematological patients. Appropriate empirical therapy can be administered for suspected CRA BSI based on the antimicrobial minimum inhibitory concentration of CRA colonising the respiratory tract.

Is Short-Course Antibiotic Therapy Suitable for Pseudomonas aeruginosa Bloodstream Infections in Onco-hematology Patients With Febrile Neutropenia? Results of a Multi-institutional Analysis.

BACKGROUND: Several studies have suggested that short-course antibiotic therapy was effective in Pseudomonas aeruginosa (PA) bloodstream infections (BSI) in immunocompetent patients. But similar studies in patients with hematological malignancies were rare. METHODS: This cohort study included onco-hematology patients at 2 hematology centers in China. Inverse probability of treatment weighting was used to balance the confounding factors. Multivariate regression model was used to evaluate the effect of short-course antibiotic therapy on clinical outcomes. RESULTS: In total, 434 patients met eligibility criteria (short-course, 7-11 days, n = 229; prolonged, 12-21 days, n = 205). In the weighted cohort, the univariate and multivariate analysis indicated that short course antibiotic therapy had similar outcomes to the prolonged course. The recurrent PA infection at any site or mortality within 30 days of completing therapy occurred in 8 (3.9%) patients in the short-course group and in 10 (4.9%) in the prolonged-course group (P = .979). The recurrent infection within 90 days occurred in 20 (9.8%) patients in the short-course group and in 13 (6.3%) patients in the prolonged-course group (P = .139), and the recurrent fever within 7 days occurred in 17 (8.3%) patients in the short-course group and in 15 (7.4%) in the prolonged-course group (P = .957). On average, patients who received short-course antibiotic therapy spent 3.3 fewer days in the hospital (P < .001). CONCLUSIONS: In the study, short-course therapy was non-inferior to prolonged-course therapy in terms of clinical outcomes. However, due to its biases and limitations, further prospective randomized controlled trials are needed to generalize our findings.

Acinetobacter spp. bloodstream infection in hematological patients: a 10-year single-center study.

PURPOSE: This study investigated the clinical and antimicrobial characteristics of Acinetobacter spp. bloodstream infection (BSI) in hematological patients. Risk factors for 30-day mortality and carbapenem-resistant Acinetobacter spp. (CRA) BSI acquisition were also identified. METHODS: We reviewed forty hematological patients with Acinetobacter spp. BSI in a large Chinese blood disease hospital between 2013 and 2022. The remaining CRA isolates were subjected to whole-genome sequencing. RESULTS: The 30-day mortality rate was high at 35%. Hematological patients with Acinetobacter spp. BSI often presented with severe conditions and co-infections at multiple sites. All strains were colistin-susceptible and 40.0% were CR. Multivariate analysis identified several risk factors associated with CRA BSI acquisition, including previous exposure to carbapenems within 30 days and CRA colonization. Very severe aplastic anaemia, tetracycline-resistant Acinetobacter spp. BSI, and unresolved neutropenia after infection were closely associated with 30-day mortality. Non-survivors often presented with higher median PCT and CRP levels and severe complications, such as intracranial infection, cardiac dysfunction, respiratory failure, and severe sepsis or septic shock. Our study also identified inappropriate empirical antibiotic therapy as an independent predictor of 30-day mortality (OR: 11.234, 95% CI: 1.261-20.086, P = 0.030). This study was the first to report A. oleivorans as a human pathogen, and to identify its unique oxacillinase, OXA-325. CONCLUSION: An environment-originated non-pathogenic species can become pathogenic when the body's immunity is compromised. Our results also highlighted the importance of improving neutropenia after infection, treating severe organ dysfunction, and administering appropriate empirical antibiotic therapy to reduce mortality in this patient population.

ConvWin-UNet: UNet-like hierarchical vision Transformer combined with convolution for medical image segmentation.

Convolutional Neural Network (CNN) plays a vital role in the development of computer vision applications. The depth neural network composed of U-shaped structures and jump connections is widely used in various medical image tasks. Recently, based on the self-attention mechanism, the Transformer structure has made great progress and tends to replace CNN, and it has great advantages in understanding global information. In this paper, the ConvWin Transformer structure is proposed, which refers to the W-MSA structure in Swin and combines with the convolution. It can not only accelerate the convergence speed, but also enrich the information exchange between patches and improve the understanding of local information. Then, it is integrated with UNet, a U-shaped architecture commonly used in medical image segmentation, to form a structure called ConvWin-UNet. Meanwhile, this paper improves the patch expanding layer to perform the upsampling operation. The experimental results on the Hubmap datasets and synapse multi-organ segmentation dataset indicate that the proposed ConvWin-UNet structure achieves excellent results. Partial code and models of this work are available at https://github.com/xmFeng-hdu/ConvWin-UNet.

Ultrafast process of microwave-assisted deep eutectic solvent to improve properties of bamboo dissolving pulp.

Viscosity control and reactivity enhancement are critical to produce high-quality cellulose products, such as dissolving pulp, yet remain challenging. In this work, an ultrafast process, namely microwave-assisted deep eutectic solvent (MW-DES), is proposed for this purpose. It is based on the hypothesis that the MW-DES process can deliver an enhanced synergy: a simultaneous fiber swelling and cellulose depolymerization via hydrogen-bonding break-up and acid hydrolysis from the actions of polar and acidic DES further boosted under MW irradiation. Results showed that after the MW-DES (Choline chloride- oxalic acid, ChCl-OA) treatment for only 40 s, the pulp viscosity decreased from 715 to 453 mL/g, and the reactivity increased from 43.0 % to 84.6 %, which is ultrafast in comparison with those reported work. Furthermore, DES in the process shows a high reusability and chemical stability, thus offering a simple, sustainable and effective alternative for upgrading of dissolving pulp, particularly, using non-wood materials of bamboo.

Improving the prognostic ability of PET/CT SUVmax to identify follicular lymphoma with early treatment failure.

Follicular lymphoma (FL) has a high degree of heterogeneity both clinically and molecularly. Early treatment failure (ETF), progression or relapse within 24 months of frontline immunochemotherapy is associated with a poor prognosis in FL. However, the clinical utility of ETF at diagnosis is limited. The maximum standardized uptake value (SUVmax) is a metabolic parameter for positron emission tomography/computed tomography (PET/CT); nevertheless, the relationship between SUVmax and ETF remains unclear. Thus, identifying early biomarkers that incorporate SUVmax and other clinical correlative variables could be helpful in identifying patients at high risk of ETF. A nomogram consisted of three independent variables, including SUVmax ≥ 12, beta-2 microglobulin > 3 mg/L, and Ki67 > 40%, was established to predict ETF in 127 patients with grade 1, 2, or 3a FL from the First Hospital of Jilin University (training cohort) and was validated using data from the Duke University Medical Center (validation cohort, n=95). The nomogram demonstrated prognostic accuracy in predicting ETF (sensitivity 70.8% and specificity 83.5% in the training cohort; sensitivity 84.2% and specificity 68.4% in the validation cohort). The patients were stratified into three groups: low-, intermediate-, and high-risk. In the training cohort, the corresponding 5-year progression-free survival (PFS) rates were 81.7%, 73.4%, and 34.9%, and the 5-year overall survival (OS) rates were 97.4%, 87.4%, and 62.3%, respectively. In the validation cohort, the 5-year PFS rates were 77.7%, 52.9%, and 34.8%, and the 5-year OS rates were 96.4%, 94.1%, and 73.7%, respectively. This was the first study to use a nomogram with SUVmax to predict ETF in FL to identify a subset of patients who might benefit from individualized targeted therapy.

TangShenWeiNing Formula Prevents Diabetic Nephropathy by Protecting Podocytes Through the SIRT1/HIF-1α Pathway.

Background: Diabetic nephropathy (DN) represents a major complication of diabetes, and podocyte injury has a critical function in DN development. TangShenWeiNing formula (TSWN) has been demonstrated to efficiently decrease proteinuria and protect podocytes in DN. This work aimed to explore the mechanism by which TSWN alleviates DN and protects podocytes. Methods: The major bioactive components of TSWN were detected by mass spectrometry (MS) and pharmacological databases. Eight-week-old male C57BLKS/J db/m and db/db mice were provided pure water, valsartan, low dose TSWN, middle dose TSWN and high dose TSWN by gavage for 12 weeks, respectively. Results: MS and network pharmacology analyses suggested that TSWN might prevent DN through the sirtuin (SIRT)1/hypoxia-inducible factor (HIF)-1α pathway. Diabetic mice showed elevated urinary albumin in comparison with non-diabetic mice, and TSWN decreased urinary albumin in diabetic mice. Histological injury increased in the kidney in diabetic mice, which could be improved by TSWN. Fibrosis and collagen I expression were induced in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney; TSWN alleviated these effects. Apoptosis and cleaved caspase-3 were induced in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney, and TSWN blunted these effects. Podocytes were damaged in the diabetic mouse kidney, which was improved by TSWN. Podocin and nephrin amounts were decreased in the diabetic mouse kidney in comparison with the non-diabetic mouse kidney, and podocalyxin was increased in urine of diabetic animals in comparison with non-diabetic counterparts. After TSWN treatment, podocin and nephrin were raised in the diabetic mouse kidney, and urinary podocalyxin was depressed in diabetic animals. Diabetic mice had lower SIRT1 and higher HIF-1α amounts in kidney specimens in comparison with non-diabetic mice, and TSWN promoted SIRT1 and inhibited HIF-1α in the diabetic mouse kidney. Moreover, co-staining of SIRT1 and podocin revealed that SIRT1 decreased in podocytes from diabetic mice in comparison with those from non-diabetic mice, and TSWN elevated SIRT1 in podocytes. Conclusions: This study indicated that TSWN alleviates DN by improving podocyte injury through the SIRT1/HIF-1α pathway in diabetic mouse kidneys.

The Short-Term Efficacy and Safety of Brentuximab Vedotin Plus Cyclophosphamide, Epirubicin and Prednisone in Untreated PTCL: A Real-World, Retrospective Study.

INTRODUCTION: Brentuximab vedotin (BV) showed high overall remission rates in refractory/relapsed classical Hodgkin's lymphoma (HL) and systemic anaplastic large cell lymphoma (sALCL). Although the efficacy of BV has been reported in clinical trials, its efficacy as a frontline therapy in real world for patients with CD30 positive subtypes of non-Hodgkin's lymphoma (NHL) such as peripheral T-cell lymphoma with T-follicular helper cell (TFH) phenotype (PTCL, TFH), anaplastic large-cell lymphoma (ALCL) and angioimmunoblastic T-cell lymphoma (AITL) in China has not been well documented. METHODS: Analysis of a real-world, observational, retrospective case series in patients suffering from AITL, sALCL and peripheral T-cell lymphoma with T-follicular helper phenotype (PTCL-TFH) and other types of PTCL treated with BV in frontline treatment was conducted. The patients were given treatment from May 2020 till June 28, 2021. All patients were pathologically diagnosed to have PTCL before treatment and expressed CD30. Patients received BV (1.8 mg/kg) combined with CEP (cyclophosphamide, epirubicin, prednisone acetate every 3 weeks). The primary endpoint was objective response rates (ORR), and secondary endpoints were duration of response and incidence of adverse events (AEs). Exploratory endpoints such as progression-free survival (PFS) are discussed even though after such a short period. RESULTS: Nineteen patients completed ≥ 1 cycles of BV-CEP treatment (16 cases completed ≥ 4 cycles, 3 cases only completed 1 cycle). Among them, the ORR reached 89.5% [CR 52.7%; partial response (PR) 36.8%]. In the ALCL group, CR reached 100% with the median duration of response of up to 8 months, while in the AITL group, the ORR was 75% and 2 patients had disease progression after treatment with BV + CEP. We also observed that BV-CEP may extend the PFS compared to traditional chemotherapy such as the CHOEP regimen (BV-CEP: not evaluable, CHOEP: 6.5 months), although the median follow-up was only 6.7 months. Adverse events (AEs), including incidence and severity of febrile neutropenia (26% patients in the BV-CEP group and 30% in the CHOEP group), were similar between groups. There was no incidence of AEs leading to treatment withdrawal or death under BV-CEP treatment. CONCLUSION: BV is a promising treatment in patients with ALCL, AITL and PTCL-TFH in frontline treatment settings.

PPAR-α Agonist Fenofibrate Prevented Diabetic Nephropathy by Inhibiting M1 Macrophages via Improving Endothelial Cell Function in db/db Mice.

Background: Diabetic nephropathy (DN) is one of the major diabetic microvascular complications, and macrophage polarization plays a key role in the development of DN. Endothelial cells regulate macrophage polarization. Peroxisome proliferator-activated receptor (PPAR)-α agonists were demonstrated to prevent DN and improve endothelial function. In this study, we aimed to investigate whether PPAR-α agonists prevented DN through regulating macrophage phenotype via improving endothelial cell function. Methods: Eight-week-old male C57BLKS/J db/m and db/db mice were given fenofibrate or 1% sodium carboxyl methylcellulose by gavage for 12 weeks. Results: Db/db mice presented higher urinary albumin-to-creatinine ratio (UACR) than db/m mice, and fenofibrate decreased UACR in db/db mice. Fibrosis and collagen I were elevated in db/db mouse kidneys compared with db/m mouse kidneys; however, they were decreased after fenofibrate treatment in db/db mouse kidneys. Apoptosis and cleaved caspase-3 were enhanced in db/db mouse kidneys compared to db/m mouse kidneys, while fenofibrate decreased them in db/db mouse kidneys. Db/db mice had a suppression of p-endothelial nitric oxide synthase (eNOS)/t-eNOS and nitric oxide (NO), and an increase of angiopoietin-2 and reactive oxygen species (ROS) in kidneys compared with db/m mice, and fenofibrate increased p-eNOS/t-eNOS and NO, and decreased angiopoietin-2 and ROS in db/db mouse kidneys. Hypoxia-inducible factor (HIF)-1α and Notch1 were promoted in db/db mouse kidneys compared with db/m mouse kidneys, and were reduced after fenofibrate treatment in db/db mouse kidneys. Furthermore, the immunofluorescence staining indicated that M1 macrophage recruitment was enhanced in db/db mouse kidneys compared to db/m mouse kidneys, and this was accompanied by a significant increase of tumor necrosis factor (TNF)-α and interleukin (IL)-1ß in kidneys and in serum of db/db mice compared with db/m mice. However, fenofibrate inhibited the renal M1 macrophage recruitment and cytokines associated with M1 macrophages in db/db mice. Conclusions: Our study indicated that M1 macrophage recruitment due to the upregulated HIF-1α/Notch1 pathway induced by endothelial cell dysfunction involved in type 2 diabetic mouse renal injury, and PPAR-α agonist fenofibrate prevented DN by reducing M1 macrophage recruitment via inhibiting HIF-1α/Notch1 pathway regulated by endothelial cell function in type 2 diabetic mouse kidneys.

Ferroptosis Enhanced Diabetic Renal Tubular Injury via HIF-1α/HO-1 Pathway in db/db Mice.

Background: Ferroptosis is a recently identified iron-dependent form of cell death as a result of increased reactive oxygen species (ROS) and lipid peroxidation. In this study, we investigated whether ferroptosis aggravated diabetic nephropathy (DN) and damaged renal tubules through hypoxia-inducible factor (HIF)-1α/heme oxygenase (HO)-1 pathway in db/db mice. Methods: Db/db mice were administered with or without ferroptosis inhibitor Ferrostatin-1 treatment, and were compared with db/m mice. Results: Db/db mice showed higher urinary albumin-to-creatinine ratio (UACR) than db/m mice, and Ferrostatin-1 reduced UACR in db/db mice. Db/db mice presented higher kidney injury molecular-1 and neutrophil gelatinase-associated lipocalin in kidneys and urine compared to db/m mice, with renal tubular basement membranes folding and faulting. However, these changes were ameliorated in db/db mice after Ferrostatin-1 treatment. Fibrosis area and collagen I were promoted in db/db mouse kidneys as compared to db/m mouse kidneys, which was alleviated by Ferrostatin-1 in db/db mouse kidneys. HIF-1α and HO-1 were increased in db/db mouse kidneys compared with db/m mouse kidneys, and Ferrostatin-1 decreased HIF-1α and HO-1 in db/db mouse kidneys. Iron content was elevated in db/db mouse renal tubules compared with db/m mouse renal tubules, and was relieved in renal tubules of db/db mice after Ferrostatin-1 treatment. Ferritin was increased in db/db mouse kidneys compared with db/m mouse kidneys, but Ferrostatin-1 reduced ferritin in kidneys of db/db mice. Diabetes accelerated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived ROS formation in mouse kidneys, but Ferrostatin-1 prevented ROS formation derived by NADPH oxidases in db/db mouse kidneys. The increased malondialdehyde (MDA) and the decreased superoxide dismutase (SOD), catalase (CAT), glutathione peroxidases (GSH-Px) were detected in db/db mouse kidneys compared to db/m mouse kidneys, whereas Ferrostatin-1 suppressed MDA and elevated SOD, CAT, and GSH-Px in db/db mouse kidneys. Glutathione peroxidase 4 was lower in db/db mouse kidneys than db/m mouse kidneys, and was exacerbated by Ferrostatin-1 in kidneys of db/db mice. Conclusions: Our study indicated that ferroptosis might enhance DN and damage renal tubules in diabetic models through HIF-1α/HO-1 pathway.

Association between decreased thyroid stimulating hormone and hyperuricemia in type 2 diabetic patients with early-stage diabetic kidney disease.

BACKGROUND: Serum uric acid (SUA) is associated with the development of diabetic kidney disease (DKD). Thyroid hormones can regulate metabolism and insulin resistance. The relationship between SUA and thyroid function in patients with DKD is still uncertain. In current study, we aimed to investigate the association between thyroid stimulating hormone (TSH) and SUA in type 2 diabetic patients with early-stage DKD. METHODS: Two hundred fifty-four type 2 diabetic patients with early-stage DKD were enrolled in current study and were further classified as high SUA group (SUA level > 420 µmol/L in males or > 360 µmol/L in females, n = 101) and normal SUA group (SUA level ≤ 420 µmol/L in males or ≤ 360 µmol/L in females, n = 153). Eighty-five control subjects were recruited as control group. The clinical characteristics were obtained via face-to-face surveys and medical records. RESULTS: Compared with normal SUA group and control group, high SUA group exhibited the increased SUA level, and the decreased TSH level (P < 0.017 for all), and no significant difference was detected in SUA and TSH between normal SUA group and control group. TSH was negatively associated with SUA (r = - 0.35, P < 0.001) in type 2 diabetic participants with early-stage DKD. Furthermore, the decreased TSH level was independently correlated with higher SUA level (ß = - 25.69, P < 0.001), and retained a significant association with hyperuricemia (odds ratio = 1.73, P = 0.002) after adjusting for confounding factors in type 2 diabetic patients with early-stage DKD. CONCLUSIONS: TSH is negatively correlated with SUA, and decreased TSH is an independent risk factor for hyperuricemia in type 2 diabetic patients with early-stage DKD. These results indicate that thyroid hormones, TSH in particular, might participate in regulating uric acid metabolism in patients with early-stage DKD.

Integrating phosphotungstic acid-assisted prerefining with cellulase treatment for enhancing the reactivity of kraft-based dissolving pulp.

Viscosity control and reactivity enhancement are of practical importance for high-quality dissolving pulp manufacturing. In this work, we demonstrate a two-step activating process consisting of a phosphotungstic acid (PTA)-assisted prerefining (PTA/R pretreatment), followed by cellulase treatment for this purpose. The cellulase adsorption can increase from 29.1% to 49.7% as a result of PTA/R pretreatment (8000 r at 90 °C). The viscosity of the resultant pulp decreases from 665 to 430 mL/g, while its Fock reactivity increases from 31.5% to 74.4% under a low-loading cellulase treatment (0.5 mg cellulase /g odp), which mainly due to the fact that the PTA/R pretreatment can increase fiber accessibility and viscosity control, thus facilitating cellulase adsorption and reaction efficiency. Moreover, PTA also shows a high recyclability/ reusability (more than 86%) during the PTA/R pretreatment. Therefore, the new proposed two-step activating process provides a green, and efficient pathway for large-scale manufacturing of high-quality dissolving pulp.

SIRT3 Deficiency Sensitizes Angiotensin-II-Induced Renal Fibrosis.

BACKGROUND: Sirtuin 3 (SIRT3) has a crucial role in the cardiovascular diseases. Our previous study revealed that SIRT3 knockout (SIRT3KO) promoted cardiac pericyte-fibroblast transition. In this study, we investigated the involvement of pericyte and iron in angiotensin II (Ang-II)-mediated renal fibrosis in the SIRT3KO mice. METHODS AND RESULTS: NG2-DsRed mice and NG2-DsRed-SIRT3 knockout (SIRT3KO) mice were infused with saline or Ang-II (1000 ng/kg/min) for 4 weeks. Renal fibrosis, iron content and reactive oxygen species (ROS) were measured. Masson's trichrome staining showed that SIRT3KO enhanced Ang-II-induced renal fibrosis. Immunostaining showed that Ang-II treatment increased the number of NG2-DsRed+ cells in the kidney, and SIRT3KO further enhanced NG2-DsRed+ cells. Moreover, SIRT3KO promoted pericyte differentiation into fibroblasts as evidenced by co-staining NG2-DsRed/FSP-1. Furthermore, DsRed/FSP-1+ and DsRed/transforming growth factor-ß1 (TGF-ß1)+ fibroblasts were elevated by SIRT3KO after Ang-II infusion. Ang-II-induced collagen I and TGF-ß1 expression was also enhanced in the SIRT3KO mice. SIRT3KO significantly exacerbated Ang-II-induced iron accumulation. This was accompanied by an increase in acetyl-p53, HO-1 and FPN expression. Further, SIRT3KO sensitized Ang-II-induced upregulation of p47phox and gp91phox together with increased ROS formation in the kidney. CONCLUSION: Our study suggests that SIRT3 deficiency sensitized Ang-II-induced renal fibrosis by the mechanisms involved in promoting differentiation of pericytes into fibroblasts, exacerbating iron overload and accelerating NADPH oxidase-derived ROS formation.

The AC Soft Magnetic Properties of FeCoNixCuAl (1.0 ≤ x ≤ 1.75) High-Entropy Alloys.

High-entropy alloys (HEAs) with soft magnetic properties are one of the new candidate soft magnetic materials which are usually used under an alternating current (AC) magnetic field. In this work, the AC soft magnetic properties are investigated for FeCoNixCuAl (1.0 ≤ x ≤ 1.75) HEAs. The X-ray diffraction (XRD) and scanning electron microscope (SEM) show that the alloy consists of two phases, namely a face-centred cubic (FCC) phase and a body-centred cubic (BCC) phase. With increasing Ni content, the FCC phase content increased. Further research shows that the AC soft magnetic properties of these alloys are closely related to their phase constitution. Increasing the FCC phase content contributes to a decrease in the values of AC remanence (AC Br), AC coercivity (AC Hc) and AC total loss (Ps), while it is harmful to the AC maximum magnetic flux density (AC Bm). Ps can be divided into two parts: AC hysteresis loss (Ph) and eddy current loss (Pe). With increasing frequency f, the ratio of Ph/Ps decreases for all samples. When f ≤ 150 Hz, Ph/Ps > 70%, which means that Ph mainly contributes to Ps. When f ≥ 800 Hz, Ph/Ps < 40% (except for the x = 1.0 sample), which means that Pe mainly contributes to Ps. At the same frequency, the ratio of Ph/Ps decreases gradually with increasing FCC phase content. The values of Pe and Ph are mainly related to the electrical resistivity (ρ) and the AC Hc, respectively. This provides a direction to reduce Ps.

Diffuse Myocardial Injuries are Present in Subclinical Hypothyroidism: A Clinical Study Using Myocardial T1-mapping Quantification.

Subclinical hypothyroidism (SHT) is a common disorder that may represent early thyroid dysfunction and is related to adverse cardiovascular events. However, myocardial injuries induced by SHT are difficult to detect. Our previous study demonstrated that the cardiac magnetic resonance (CMR) myocardial longitudinal relaxation time (T1) mapping technique is a useful tool for assessing diffuse myocardial injuries in overt hypothyroidism patients. This study was designed to detect whether diffuse myocardial injuries were present in SHT by using the T1 mapping technique. We found that SHT participants had significantly increased native T1 values within four segments of the left ventricle (all p < 0.01), especially patients with thyroid-stimulating hormone (TSH) levels ≥10 µIU/mL, compared with those in the controls. In addition, the native T1 values were negatively correlated with free thyroxine (FT4) (r = -0.476, p = 0.003) and were positively correlated with TSH (r = 0.489, p = 0.002). Furthermore, left ventricular diastolic function estimated by the peak filling rate (PFR) was significantly lower in patients with TSH levels ≥10 µIU/mL than that in the controls (p < 0.05). In conclusion, diffuse myocardial injuries were present in SHT, and T1 mapping may be a useful tool for evaluating mild myocardial injuries in SHT at an early stage. Our study is the first to confirm myocardial injuries in SHT patients using T1 mapping.

Hexagonal Boron Nitride/Microfibril Cellulose/Poly(vinyl alcohol) Ternary Composite Film with Thermal Conductivity and Flexibility.

Microfibril cellulose (MFC), which is detrimental to soil cultivation and environmental protection, is derived from waste pineapple leaves. Hexagonal boron nitride (h-BN) was modified with polydopamine (PDA)-PDA@h-BN named pBN, and then combined with MFC to prepare a novel hybrid powder. The effect of PDA on h-BN and the binding effect between pBN and MFC were characterized by X-ray photoelectron spectroscopy (XPS), Thermogravimetric (TG), scanning electron microscopy (SEM), and Fourier Transform-Infrared (FT-IR). Poly (vinyl alcohol) (PVA) was used as an eco-friendly polymeric matrix to prepare a pBN-MFC-PVA composite film. The mechanical strength, hydrophobicity, and thermal conductivity of the film were studied and the results confirmed that h-BN was chemically modified with PDA and was uniformly distributed along the MFC. The thermal conductivity of the pBN-MFC-PVA composite film increased with the addition of a pBN-MFC novel powder. MFC acted as "guides" to mitigate the h-BN agglomerate. In addition to the possible usage in the pBN-MFC-PVA composite film itself, the pBN-MFC hybrid powder may be a potential filler candidate for manufacturing thermal interface materials and wearable devices or protective materials.

Hyperhomocysteinemia as a Metabolic Risk Factor for Glucose Intolerance Among High-Risk Groups of Chinese Adults.

BACKGROUND Impaired glucose tolerance (IGT) is characterized by insulin resistance and causes atherosclerosis. Hyperhomocysteinemia is associated with insulin resistance and predicts cardiovascular diseases. In this study, we assessed the possible association between homocysteine and IGT. MATERIAL AND METHODS This was a cross-sectional study of 118 consecutive subjects with IGT (IGT group) and 128 consecutive subjects with normal glucose tolerance (NGT group). Homocysteine and clinical characteristics were measured. RESULTS The IGT group had higher homocysteine than the NGT group [18.00 (14.00, 22.25) vs. 12.50 (9.00, 15.00) µmol/L, p<0.001]. Homocysteine was positively associated with body mass index (BMI) (r=0.178, p=0.005), triglycerides (r=0.306, p<0.001), fasting blood glucose (FBG) (r=0.312, p<0.001), 2-hour postchallenge glucose (2hPG) (r=0.363, p<0.001), fasting insulin (FINS) (r=0.655, p<0.001), and homeostasis model assessment for insulin resistance (HOMA-IR) (r=0.643, p<0.001), and was negatively correlated with high-density lipoprotein cholesterol (HDL-C) (r=-0.250, p<0.001). After controlling for confounders, hyperinsulinemia (ß=7.430, p<0.001) was independently related to hyperhomocysteinemia. In a logistic regression analysis, high triglycerides (OR=1.177, p<0.001) and homocysteine (OR=1.508, p=0.007), and low HDL-C (OR=0.315, p=0.026) were associated with IGT. CONCLUSIONS Patients with IGT have higher homocysteine levels compared with subjects with normal glucose tolerance, and hyperhomocysteinemia might be correlated with IGT.

Low apoA-I is associated with insulin resistance in patients with impaired glucose tolerance: a cross-sectional study.

BACKGROUND: Low apolipoprotein A-I (apoA-I) is an independent risk factor for atherosclerotic cardiovascular diseases. Insulin resistance predicts the progression of abnormal glucose metabolism, which is the main cause of atherosclerotic cardiovascular disease. In this study, we assessed the potential association between apoA-I levels and insulin resistance in patients with impaired glucose tolerance (IGT) and the possible link between apoA-I and IGT. METHODS: This study evaluated a cross-sectional study of 108 participants with impaired glucose tolerance (IGT group) and 84 controls (control group). ApoA-I and clinical characteristics were measured, and a homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. RESULTS: The IGT group exhibited significantly lower apoA-I and higher HOMA-IR levels than the control group (apoA-I: 1.37 ± 0.36 vs 1.57 ± 0.39 g/L; HOMA-IR: 4.21 ± 1.56 vs 2.15 ± 0.99; P < 0.001 for both). ApoA-I was negatively correlated with HOMA-IR in both the IGT and control groups (IGT group: r = -0.269, P = 0.005; control group: r = -0.262, P = 0.016). Multiple stepwise regression analysis showed that low apoA-I levels (ß = -1.470, P = 0.002) were independently correlated with high HOMA-IR levels in the IGT group. Moreover, logistic regression analysis identified that low apoA-I was an independent influencing factor for IGT (ß = -1.170, OR = 0.310, P = 0.007). CONCLUSIONS: ApoA-I is inversely associated with insulin resistance in patients with impaired glucose tolerance, and low apoA-I is an independent risk factor for impaired glucose tolerance. These results indicate that apoA-I plays an important role in regulating insulin sensitivity and glucose metabolism in patients with IGT.

PPAR-α Agonist Fenofibrate Reduces Insulin Resistance in Impaired Glucose Tolerance Patients with Hypertriglyceridemia: A Cross-Sectional Study.

INTRODUCTION: Peroxisome proliferator-activated receptor-α (PPAR-α) agonists can regulate metabolism and protect the cardiovascular system. This study investigated the effects of PPAR-α agonist fenofibrate on insulin resistance in patients with impaired glucose tolerance (IGT). METHODS: This research evaluated cross-sectional and interventional studies. 191 subjects with IGT were divided into a hypertriglyceridemia group (HTG group, n = 118) and a normal triglyceride (TG) group (NTG group, n = 73). 79 subjects with normal glucose tolerance were recruited as a control group. The HTG group was treated with fenofibrate (200 mg/day) for 12 weeks. The homeostatic model assessment index 2 (HOMA2) and the McAuley index (McA) were calculated. RESULTS: HOMA2 for ß-cell function (HOMA2-%B) was 93.47 ± 26.28, 68.47 ± 21.29, and 79.92 ± 23.15 in HTG, NTG, and control groups, respectively. HOMA2 for insulin sensitivity (HOMA2-%S) was 48.40 (39.70, 68.70), 110.20 (62.55, 141.95), and 101.20 (79.90, 140.10) in HTG, NTG, and control groups, respectively. HOMA2 for insulin resistance (HOMA2-IR) was 2.09 (1.46, 2.52), 0.92 (0.70, 1.61), and 0.99 (0.71, 1.25) in HTG, NTG, and control groups, respectively. McA was 5.05 ± 0.76, 7.99 ± 1.79, and 8.34 ± 1.55 in HTG, NTG, and control groups, respectively. The HTG group had higher HOMA2-%B and HOMA2-IR, and lower HOMA2-%S and McA than NTG and control groups (P < 0.001 for all). Fenofibrate decreased HOMA2-%B and HOMA2-IR and increased HOMA2-%S and McA in the HTG group (HOMA2-%B: from 93.47 ± 26.28 to 89.34 ± 23.53, P = 0.018; HOMA2-%S: from 48.40 (39.70, 68.70) to 56.75 (44.88, 72.53), P < 0.001; HOMA2-IR: from 2.07 (1.46, 2.52) to 1.76 (1.38, 2.30), P < 0.001; McA: from 5.05 ± 0.76 to 9.34 ± 0.88, P < 0.001). CONCLUSION: PPAR-α agonists improve parameters of glucoregulation in IGT patients with hypertriglyceridemia.