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Aberrant epigenetic reprogramming contributes to the progression of renal cell carcinoma (RCC). Elucidation of key regulators of epigenetic reprogramming in RCC could help identify therapeutic vulnerabilities to improve treatment. Here, we report upregulation of the nuclear matrix-associated protein, special AT-rich binding protein-2 (SATB2), in RCC samples, which correlated with poor prognosis. SATB2 inhibition suppressed RCC growth and self-renewal capacities. YAP/TEAD4 activated SATB2 expression and depended on SATB2 to enhance cell proliferation. Transcriptome analysis implicated that SATB2 regulates NRF2 downstream targets to suppress oxidative stress without altering NRF2 levels. Integrated chromatin immunoprecipitation sequencing and assay for transposase-accessible chromatin using sequencing analyses demonstrated that SATB2 coordinated with NRF2 to drive enhancer–promoter interactions, amplifying transcriptional activity. SATB2 recruited SWI/SNF complex subunits, including BRD7 or BRG1, to sustain DNA accessibility. Increased SATB2 triggered chromatin remodeling into configurations that rendered RCC more sensitive to SATB2 deficiency. Moreover, SATB2 ablation promoted the sensitivity of RCC to chemotherapy-induced apoptosis. Finally, targeting SATB2 or BRD7 effectively restricted the proliferation of YAP-high tumors in patient-derived xenografts and patient-derived organoids. Together, SATB2 is an oncogenic chromatin organizer in RCC, and targeting SATB2 is an effective strategy to suppress the YAP-high RCC.Significance:A YAP-SATB2-NRF2 regulatory axis amplifies antioxidative stress signaling and provides potential therapeutic targets to enhance response to chemotherapy in renal cell carcinoma.

Cordyceps sinensis (C. sinensis) is a kind of traditional Chinese medicine commonly used to protect renal function and relieve kidney injury. This study aimed to reveal the renal protective mechanism of C. sinensis in renal ischemia–reperfusion injury (RIRI). First, we obtained 8 active components and 99 common targets of C. sinensis against RIRI from public databases. Second, we have retrieved 38 core targets through STRING database analysis. Third, Gene Ontology analysis of 38 core targets is indicated that C. sinensis treatment RIRI may related hormone regulation, oxidative stress, cell proliferation, and immune regulation. Kyoto Encyclopedia of Genes and Genomes enrichment analysis of 38 core targets is indicated that C. sinensis treatment RIRI may involve in PI3K–Akt, HIF-1, and MAPK signaling pathways, as well as advanced glycation end product (AGE)–receptor for AGE (RAGE) signaling pathway in diabetic complications. Lastly, molecular docking was used to detect the binding activity and properties of active components and core target using molecular docking. And the results showed that eight active components of C. sinensis had low affinity with core targets. In conclusion, C. sinensis may improve RIRI by regulating oxidative stress and immunity through PI3K–Akt, HIF-1, and MAPK pathways.

Mitochondrial injury-triggered podocyte apoptosis is a major risk factor for diabetic nephropathy (DN). However, the detailed relationship between mitochondrial homeostasis and podocyte apoptosis remains unclear. The present study aimed to explore the role and functional mechanism of germacrone in DN in type I diabetes (type I DN). A mouse model of type I DN was established by injecting streptozocin, and a podocyte injury model was constructed using high glucose (HG) induction. Histopathology was detected by hematoxylin and eosin and periodic acid-Schiff staining. Transmission electron microscopy and flow cytometry were used to evaluate the mitochondrial function. Germacrone simultaneously reduced blood glucose, 24 h proteinuria, and other nephrotic symptoms in a type 1 DN mouse model. Moreover, germacrone protected against mitochondrial damage, limited reactive oxygen species (ROS) accumulation, and restored glutathione peroxidase (GPX) activity and GPX4 protein expression, subsequently preventing podocyte apoptosis. Mechanistically, the increased miR-188-3p expression in type I DN mice was reversed in germacrone-challenged DN mice. HG induced miR-188-3p expression and the miR-188-3p antagonist abolished the HG-mediated increase in ROS. Notably, miR-188-3p was found to have a therapeutic effect against DN by aggravating mitochondrial damage and podocyte apoptosis. Germacrone alleviates DN progression in type I diabetes by limiting podocyte apoptosis, which was partly counteracted by miR-188-3p upregulation. The combination of germacrone and miR-188-3p antagonists is expected to be an effective therapeutic strategy for DN. Abbreviations DN: diabetic nephropathy; Type I DN: DN in Type I diabetes; STZ: streptozocin; ROS: reactive oxygen species; NcRNAs: non-coding RNAs; UTR: untranslated regions; NC: negative control; BUN: blood urea nitrogen; BUA: blood uric acid; Ucr: urine creatinine; Scr: serum creatinine; PAS: Periodic Acid-Schiff; IF: Immunofluorescence; FISH: Fluorescence in situ hybridization; TUG1: taurine upregulated gene 1; GPX: Glutathione Peroxidase; GPX4: glutathione peroxidase 4; EMT: epithelial-mesenchymal transition

Aberrant epigenetic reprogramming contributes to the progression of renal cell carcinoma (RCC). Elucidation of key regulators of epigenetic reprogramming in RCC could help identify therapeutic vulnerabilities to improve treatment. Here, we report upregulation of the nuclear matrix-associated protein, special AT-rich binding protein-2 (SATB2), in RCC samples, which correlated with poor prognosis. SATB2 inhibition suppressed RCC growth and self-renewal capacities. YAP/TEAD4 activated SATB2 expression and depended on SATB2 to enhance cell proliferation. Transcriptome analysis implicated that SATB2 regulates NRF2 downstream targets to suppress oxidative stress without altering NRF2 levels. Integrated chromatin immunoprecipitation sequencing and assay for transposase-accessible chromatin using sequencing analyses demonstrated that SATB2 coordinated with NRF2 to drive enhancer–promoter interactions, amplifying transcriptional activity. SATB2 recruited SWI/SNF complex subunits, including BRD7 or BRG1, to sustain DNA accessibility. Increased SATB2 triggered chromatin remodeling into configurations that rendered RCC more sensitive to SATB2 deficiency. Moreover, SATB2 ablation promoted the sensitivity of RCC to chemotherapy-induced apoptosis. Finally, targeting SATB2 or BRD7 effectively restricted the proliferation of YAP-high tumors in patient-derived xenografts and patient-derived organoids. Together, SATB2 is an oncogenic chromatin organizer in RCC, and targeting SATB2 is an effective strategy to suppress the YAP-high RCC.Significance:A YAP-SATB2-NRF2 regulatory axis amplifies antioxidative stress signaling and provides potential therapeutic targets to enhance response to chemotherapy in renal cell carcinoma.

Juan Jin,* Fengmei Qian,* Danna Zheng, Wenfang He, Jianguang Gong, Qiang He Department of Nephrology, Zhejiang Provincial People’s Hospital and Affiliated People’s Hospital, Hangzhou Medical College, Hangzhou, Zhejiang, 310014, People’s Republic of China*These authors contributed equally to this workCorrespondence: Jianguang Gong; Qiang HeDepartment of Nephrology, Zhejiang Provincial People’s Hospital and Affiliated People’s Hospital, Hangzhou Medical College, 158 Shangtang Road, Xiacheng District, Hangzhou, Zhejiang, 310014, People’s Republic of ChinaEmail gojigu311@163.com; qianghe1973@126.comBackground: Renal fibrosis is a chronic and progressive process affecting kidneys in chronic kidney disease (CKD). Mesenchymal stem cells-derived exosomes (MSCs-Exo) have been shown to alleviate renal fibrosis and injury, but the mechanism of MSCs-Exo-induced renal protection remains unknown.Methods: In this study, MSCs were transfected with let-7i-5p antagomir (anti-let-7i-5p), and then exosomes were isolated from the transfected MSCs to deliver anti-let-7i-5p oligonucleotides to inhibit the level of let-7i-5p in kidney tubular epithelial cells (NRK-52E).Results: In both NRK-52E cells stimulated by TGF-β 1 and the mouse kidneys after unilateral ureteral obstruction (UUO), we demonstrated increased level of let-7i-5p. In addition, MSCs-Exo can deliver anti-let-7i-5p to reduce the level of let-7i-5p in NRK-52E cells and increase the expression of its target gene TSC1. Moreover, exosomal anti-let-7i-5p reduced extracellular matrix (ECM) deposition and attenuated epithelial–mesenchymal transition (EMT) process in transforming growth factor beta 1 (TGF-β 1)-stimulated NRK-52E cells and in the kidneys of UUO-treated mice. Meanwhile, mice received exosomal anti-let-7i-5p displayed reduced renal fibrosis and improved kidney function when challenged with UUO. Furthermore, exosomal anti-let-7i-5p promoted the activation the tuberous sclerosis complex subunit 1/mammalian target of rapamycin (TSC1/mTOR) signaling pathway in vivo and in vitro.Conclusion: In conclusion, exosomal anti-let-7i-5p from MSCs exerts anti-fibrotic effects in TGF-β 1-induced fibrogenic responses in NRK52E cells in vitro as well as in UUO-induced renal fibrosis model in vivo. These results provided a novel perspective on improving renal fibrosis by MSCs-Exo.Keywords: chronic kidney disease, renal fibrosis, mesenchymal stem cells, exosomes and microRNAs

Aim Podocyte injury plays an important role in diabetic nephropathy (DN), yet the underlying molecular mechanisms of podocyte injury in DN is not clear. Here, we investigated the role of activating transcription factor 4 (ATF4) and HO-1 in DN-induced podocyte injury. Methods Protein expression was measured by western blotting (WB) and immunofluorescence. Cellular apoptosis was quantified by flow cytometry. ATF4 siRNA knockdown and HO-1 overexpression in podocyte were employed to evaluate the role of ER stress in DN-induced apoptosis and autophagy response. Urinary protein levels, nephrin expression, serum creatinine and BUN were evaluated and glomerulosclerosis was quantified by Periodic Acid-Schiff staining. Results Expression of ATF4 was increased in podocytes exposed to serum from DN mice. ATF4 knockdown enhanced DN-induced podocyte apoptosis. HO-1 overexpression reduced the decline of DN-induced podocyte autophagy and inhibited apoptosis and the beneficial effects of HO-1 overexpression in DN were blocked by ATF4 knockdown. The diabetic mice were significantly ameliorated by HO-1 agonist hemin treatment. Conclusions ATF4 induces autophagy by enhancing the expression of HO-1, and inhibits podocyte apoptosis in DN. Treatment with the HO-1 agonist reduced proteinuria, apoptosis, and enhanced autophagy response, and thus improved renal function in DN mice.

Growing evidence suggests that mesangial cells (MCs) play a crucial role in the pathogenesis of IgA nephropathy (IgAN) by secreting aIgA1. However, the mechanism by which MCs regulate podocyte injury remains unknown. This study demonstrated that MC-derived exosomes treated with aIgA1 induced podocyte injury in IgA nephropathy. miR-4455, which was significantly upregulated in aIgA1 treatment MC-derived exosomes, can be transferred from MCs to podocytes via exosomes. MC-derived exosomal miR-4455 induced podocyte injury. Mechanistically, exosomal miR-4455 directly targeted ULK2 to regulate LC3II/I and P62 levels, which mediates autophagy homeostasis. This study revealed that MC-derived exosomal miR-4455 is a key factor affecting podocyte injury and provides a series of potential therapeutic targets for treating IgA nephropathy.

Chronic kidney disease (CKD) in clinical is defined as a gradual loss of kidney function for more than 3 months. The pathologic course of CKD is characterized by extensive renal fibrosis; thus, preventing renal fibrosis is vital for the treatment of CKD. It has been reported that microRNA (miR)-374a-5p was under-expressed in renal venous blood samples from patients with CKD. In addition, it exhibited anti-apoptotic effects in renal tissues suggesting that miR-374a-5p may play an important role in CKD. However, it is not clear whether miR-374a-5p could be delivered to renal cells by exosomes and exerts anti-renal fibrosis effects. To mimic renal fibrosis in vitro, human renal tubular epithelial cell lines (HK-2 cells) were treated by transforming growth factor-β (TGF-β) 1. Reverse transcription-quantitative polymerase-chain reaction (RT-qPCR) or Western blot was carried out to evaluate the mechanism by which miR-374a-5p regulated the development of renal fibrosis. Next, exosomes were isolated using with ultracentrifugation method, and the relationship between miR-374a-5p and MAPK6 was evaluated using dual-Luciferase a reporter assay system. The results indicated TGF-β1 significantly down-regulated the expression of miR-374a-5p in HK-2 cells and miR-374a-5p agomir remarkably inhibited the progression of fibrosis in vitro. In addition, exosomal miR-374a-5p could be internalized by HK-2 cells and obviously enhanced the level of miR-374a-5p in HK-2 cells. Furthermore, exosomal miR-374a-5p prevented the progression of renal fibrosis in vivo by regulating MAPK6/MK5/YAP axis. In conclusion, exosomal miR-374a-5p inhibited the progression of renal fibrosis by regulating MAPK6/MK5/YAP axis.

Background: Antineutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV) is the most common reason caused rapidly progressive glomerulonephritis worldwide. But the molecular mechanisms of ANCA - associated nephritis (AAN) have not been thoroughly expounded. So that，we aim to seek the potential molecular pathogenesis of AAN by bioinformatic.Result: Finally, four hub genes, PBK, CEP55, CCNB1 and BUB1B, were identified. These four hub geneswas verified higher in AAN than normal.Conclusion: Those four genes identified by integrated bioinformatics analysis may play a critical role in AAN. May offering a new insights and potential therapeutic to the AAN

Patients with ulcerative colitis (UC) are at an increased risk of developingThis study included 89 patients: 30 healthy controls (HC group), 29 with UC alone (UCN group), and 30 with UC and CDI (UCP group). None of the participants has been exposed to antibiotic treatments during the 3 months before stool collection. Stool samples were analyzed using 16S rRNA gene sequencing of the V3-V4 region and gas chromatography tandem time-of-flight mass spectrometry.The UCN group displayed lower diversity and richness in gut microbiota and a higher relative abundance of the phylum Proteobacteria than the HC group. There were no significant differences between the UCN and UCP groups in the α-diversity indices. The UCP group contained a higher relative abundance of the generaOur study identified 11 differential genera and 16 perturbed metabolites in patients with UC and CDI compared to those with UC alone. These findings may guide the design of research on potential mechanisms and specific treatments for CDI in patients with UC.

Background Currently, several specific antigens, M-type receptor for secretory phospholipase A2(PLA2R1), thrombospondin type-1 domain-containing 7A(THSD7A), and neural epidermal growth factor-like 1 protein (NELL-1), are discovered associated with the onset of idiopathic membranous nephropathy (IMN). But the pathomechanisms of IMN still need to be further claried. Understanding the mechanisms of IMN is required to improve its diagnosis and treatment. Methods In this study, we constructed miRNA regulatory networks to investigate IMN development. Moreover, miRNAs and mRNAs that were differentially expressed between Idiopathic Membranous Nephropathy (IMN) patients and normal controls were examined using the GSE115857 dataset and our previous sequence study. DE miRNA target genes were determined based on the FUNRICH software, starBase, miRDB, and miRWalk, and an miRNA-mRNA network was designed using DE-mRNAs that were negatively correlated with DE-miRNAs. The miRNA-mRNA network contained 228 miRNA-mRNA pairs. Thereafter, we conducted KEGG pathway, GO functional annotation, immune-related gene screening, protein interaction networks, and potential hub gene analyses. Furthermore, 10 miRNAs and 10 genes were determined and preliminarily validated using the validation dataset from GEO. Finally, we identified which pair may offer more accurate diagnosis and therapeutic targets for IMN. Results Two miRNA-mRNA pairs, miR-155-5p-FOS and miR-146a-5p-BTG2, were differentially expressed in IMN, indicating that these genes may affect IMN through immune processes. These findings may offer more accurate diagnoses and therapeutic targets for IMN.

Acute kidney injury (AKI) poses a severe threat to human health. MicroRNAs (miRNAs/miRs) are known to be involved in the progression of AKI; however, the function of miR‑1184 in AKI remains unclear. Thus, the aim of the present study was to examine the role of this miRNA in kidney injury. In order to mimic AKI in vitro, HK‑2 cells were treated with cisplatin. Bioinformatics analysis was performed to explore the differentially expressed miRNAs in AKI. A Cell Counting Kit‑8 assay and flow cytometry were performed to examine cell viability and apoptosis, respectively. mRNA expression levels were detected via reverse transcription‑quantitative PCR, and protein levels were investigated by western blot analysis. ELISA was performed to examine the levels of IL‑1β and TNF‑α in the cell supernatants. The results revealed that miR‑1184 expression was downregulated in AKI. Exosomes derived from miR‑1184 agomir‑treated mesenchymal stem cells (MSCs) significantly reversed cisplatin‑induced cell growth inhibition by inhibiting apoptosis. Moreover, forkhead box O4 (FOXO4) was found to be the direct target of miR‑1184, and exosomes expressing miR‑1184 notably inhibited cisplatin‑induced inflammatory responses in HK‑2 cells via the mediation of IL‑1β and TNF‑α. Furthermore, exosomes derived from miR‑1184 agomir‑treated MSCs significantly induced G1 phase arrest in HK‑2 cells via the regulation of FOXO4, p27 Kip1 and CDK2. In conclusion, the present study demonstrated that exosomal‑miR‑1184 derived from MSCs alleviates cisplatin‑associated AKI. Thus, the findings presented herein may shed new light onto the exploration of novel strategies for the treatment of AKI.

AIM As renin angiotensin system inhibitors (RASi) are widely used in the clinic, early worsening of kidney function (EWKF) after RASi therapy deserves attention, as its clinical significance is unknown. The aim was to evaluate the relationship between EWKF and long-term outcomes including all-cause mortality, kidney and cardiovascular events, in all the patients treated with RASi. METHODS We searched PubMed, Embase, and the Cochrane databases for controlled trials that compared the outcomes of patients with and without EWKF after RASi treatment. Our primary outcome was all-cause mortality, and secondary outcomes were kidney and cardiovascular events. We pooled data using a random effects model. RESULTS A total of ten studies were enrolled, of which eight were randomized trials (including 33 454 patients) and two were observational studies (including 148 144 patients). Of the eight randomized trials, 4996 patients with type 2 diabetes, 19 118 with heart failure (HF), and 9340 with atherosclerotic vascular disease and diabetes with end-organ damage. Both observational studies investigated all kinds of patients with initial RASi treatment. In patients with RASi, the EWKF group had a higher risk of all-cause mortality than the no-EWKF group in the randomized studies (n = 13 581; RR, 1.22; 95% CI, 1.04-1.42; P = .02) and in observational studies (n = 148 144; OR, 1.70; 95% CI, 1.43-2.01; P

Oxidative stress (OxS) is a wildly described cause of damage to macromolecules, resulting in abnormal physiological conditions. In recent years, a few studies have shown that oxidation/antioxidation imbalance plays a significant role in developing diseases involving different systems and organs. However, the research on the circular RNA (circRNA) roles in OxS is still in its very infancy. Therefore, we hope to provide a comprehensive overview of the recent research that explored the function of circRNAs associated with OxS and its role in the pathogenesis of different diseases that affect different body systems like the nervous system, cardiovascular system, kidneys, and lungs. It provides the possibilities of using these circRNAs as superior diagnostic and therapeutic options for OxS associated with these disease conditions.

Vernacular building spaces are key elements in adjusting thermal environment of buildings and thermal adaptation of residents. This paper analyzed the comprehensive influence of building spaces on the thermal environment, thermal adaptation behaviors and thermal responses of residents. Regarding the indoor and semi-open spaces of vernacular buildings in arid climate areas of Turpan, China, a one-year survey of building thermal environment and residents' thermal comfort was conducted. It was found that the thermal environment of indoor and semi-open spaces is substantially different, which provides comfortable living spaces for residents at different times. And the thermal adaptation behaviors were closely related to the building spaces. In addition, residents have different thermal comfort in indoor and semi-open spaces, including the neutral temperature, the acceptable temperature and preferred temperature. Among them, the neutral temperature differences in transitional seasons and summer were 1.1 °C and 0.9 °C, respectively. The differences in the value of 80% acceptable temperature were 2.2 °C and 2.7 °C, respectively; and the difference in preferred temperature was 1.6 °C in summer. Further analysis showed that the thermal environment of vernacular buildings in Turpan affected residents' thermal adaptation behavior and thermal comfort. The results indicated that the diverse spaces of vernacular buildings in Turpan can create different thermal environmental conditions for buildings and can stimulate thermal adaptation behaviors of residents, thereby improving residents’ thermal comfort and thermal adaptability.

The adsorption of cobalt (II) by 3-aminopropyltriethoxysilane (APTS) modified halloysite nanotubes (HNTs) was studied. The modified halloysite was characterized by Fourier transform infrared spectroscopy (FT-IR), X-Ray diffraction (XRD) and thermogravimetry (TG). In addition, a batch method was used to study the adsorption behavior and the mechanism of removal Co (II) by modified HNTs; the effective factors influencing the adsorption process including adsorbent concentration, contact time, initial pH, temperature and the initial concentration of Co (II) have been investigated. The results showed that the APTS was successfully grafted on the HNTs surface. The modified HNTs exhibited rapid adsorption speed, which reached the adsorption equilibrium within 30 min. The adsorption capacity of the adsorbent increased significantly with the increase of pH. The adsorption data of Co (II) on the modified HNTs are well consistent with the Langmuir model and the pseudo-second-order kinetic model.

In this study the Mg-Fe-Al trimetal composite was successfully synthesized by an easy co-precipitation method and used as the adsorbent for fluoride removal from aqueous solutions. Synthetic conditions such as Mg/Fe/Al molar ratio and calcination temperature were studied to optimize the adsorbent. The adsorbents were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS), and Fourier transform infrared (FTIR). Batch adsorption studies were conducted under various conditions, such as different fluoride concentration, contact time, temperature, initial solution pH, and coexisting anions. Results indicated that the adsorbent obtained the maximum adsorption capacity of 92.85 mg/g for fluoride with a Mg/Fe/Al molar ratio of 30:1:4, calcined at 500 °C, at near-neutral pH and room temperature (25 °C). The adsorption data were fitted well with the Langmuir isotherm model and the pseudo-first order kinetic model. The adsorption mechanism involved electrostatic interaction on the surface, ion exchange interaction, and reconstruction of original layered structure by rehydration of mixed metal oxides. All results indicated that the Mg-Fe-Al trimetal composite can be a very promising material, has potential application in the removal of fluoride in water treatment, and has positive effects on human health.

Climate can greatly affect building design, life style and thermal perception for all groups of people; however, this phenomenon has not yet been rigorously evaluated in China's hot-arid climate. The aim of this paper is to present the results of a thermal comfort survey by evaluating the influence of the hot-arid climate upon the behavioural patterns and thermal comfort responses of 160 residents in 65 traditional vernacular houses in Turfan, China, in 2011. In this survey, there were 206 sets of effective data, and the features of the traditional residential buildings and the human behaviour patterns in Turfan were described and analysed. The results showed that the diversified courtyards and shade spaces were the most obvious features of traditional houses in Turfan. People here typically spend most of their time in one of two spaces for eating, resting, and entertaining. It was found that the preferred temperature was 26.5°C. The preferred air velocity occurred at 0.62m/s. A suitable air velocity range of 0.15-1.24m/s was suggested in Turfan. Moreover, the neutral temperature of the local people was 30.1°C (tg or to). The upper limits of the 80% acceptable zone by using the direct and indirect acceptability method were 32.7 and 33.8°C, respectively. The neutral temperature and upper limit of the acceptable zone in Turfan were higher than those of the adaptive standards. Attention should be paid to the role of thermal comfort in influencing building design by using simple passive cooling strategies. The above results are believed to be potentially valuable for the design and evaluation of residential buildings located in hot-arid climate.

Halloysite nanotubes (HNTs) were modified with Fe3O4 to form novel magnetic HNTs-Fe3O4 composites, and the composites were characterized by X-ray diffraction (XRD), transmission electron microscope (TEM), Fourier transform infrared spectroscopy (FT-IR) and vibrating sample magnetometer (VSM). The as-obtained results indicated that Fe3O4 nanoparticles were successfully installed on the surface of HNTs. The adsorption of UO22+ on HNTs-Fe3O4 was investigated as a function of solid content, contact time, pH, ionic strength and temperature by batch experiments. The consequences revealed that the adsorption of UO22+ onto HNTs-Fe3O4 was strongly dependent on pH and ionic strength. Equilibrium data fitted well with the Langmuir isotherm. The experimental results demonstrated that the adsorbents with HNTs-Fe3O4 had the largest adsorption capacity of 88.32 mg/g for UO22+.

Herein, a relatively rare case is reported in which a knowledge, attitude, and practice (KAP) health education model was applied in a young female patient with metabolic syndrome (MS) and acute pancreatitis (AP), with a satisfactory effect. The purpose of this report is to provide a reference for a viable health education program in clinical practice for intervention of MS with concurrent AP in the absence of clinical trials. The patient’s unhealthy lifestyle led to obesity, diabetes mellitus, severe fatty liver, hyperlipidemia, and AP. We used a KAP health education model in a nursing intervention and evidence-based multidisciplinary cooperation to develop a personalized diet, exercise plan, education plan, and continuous care of the patient after discharge from the hospital. Within 2 months, the patient achieved weight loss, stable blood lipids, controlled blood sugar levels, and decreased glycated hemoglobin level from 9.0% to 5.4%. This KAP-based health education model has clinical importance as an intervention for lifestyle modification in patients with MS and AP. This approach can be adopted to help other patients to effectively control and prevent the recurrence of diseases.

Recently, the construction of energy efficiency buildings has been one of the main objectives of sustainable development, especially for areas with extreme climate. In present study, the adaptive thermal comfort and climate responsive strategies in dry–hot and dry–cold areas were investigated with field measurement and questionnaire in the Turpan basin, China. First, the adaptive thermal comfort model was established to reveal the relationship between indoor thermal comfort conditions and outdoor climate. Then, the climate responsive strategies which helped residents adapt to harsh climate were concluded. The prototype of climate responsive dwellings is proposed. Finally, the effects of these strategies were investigated by field measurement of indoor thermal environment in two demonstration houses and evaluated by the proposed thermal comfort model. The results showed that residents in the Turpan basin exhibited better adaptability to the hot climate than the cold climate with the upper limits of 80% acceptability reaching 34 °C. The heavy structure envelope and constructional patterns based on the thermal adaptive behaviors of residents could improve indoor thermal environment. In summer, semi-basement was the most effective strategy to satisfy human thermal comfort, followed by night ventilation. The indoor air temperature in semi-basement was around 31 °C while outdoor temperature exhibited diurnal variation of 15.7 °C from 28.6 °C to 44.3 °C. In winter, passive solar heating and semi-basement were both effective. The indoor air temperature was higher in the bedroom located at the south semi-basement compared with other rooms. The study can provide new thoughts for designing climate friendly buildings in dry-hot and dry-cold areas.

Indoor thermal environment is usually non-uniform in buildings with passive or active radiant surfaces, and strict constraints for thermal homogeneity would increase the difficulty of system design and cause unnecessary energy consumption. In order to explore the thermal comfort response characteristics in non-uniform environments, 20 subjects were recruited in this study to participate in a thermal comfort experiment in two types of non-uniform environments. The two non-uniform environments were created by different combinations of indoor air temperature and radiant temperature. In the first non-uniform environment, all the interior surface temperatures were equal, but the radiant temperature and air temperature were not equal (ANUE). The other type was a single surface non-uniform environment where the surface temperature of one interior surface and the air temperature were not equal (SNUE). Subjects’ physiological parameters were measured and subjective evaluations were obtained by questionnaires. The results showed that in thermal neutral condition, the mean skin temperature was 33.6 °C under ANUE environment, while it was 33.8°C–33.9 °C under SNUE environment. Based on the experimental results, thermal dissatisfied percentage (TDP) models for the two environments were proposed and evaluated by determination coefficient and Bayesian information criterion (BIC). According to the five different TDP levels (5%, 10%, 15%, 20%, 25%), coupling thermal comfort zone of indoor air temperature and surface temperature was classified into five hierarchies. The study has implications for the proper design of comfortable and energy saving non-uniform environments.

To understand the characteristic of human adaptive thermal comfort in the districts with dry-hot and dry-cold climate type, approach of field survey of thermal comfort has been carried out in Turfan of China. Statistical regression analysis has been used to find out the correlation between human thermal sensation and the operative temperature in winter and summer, and adaptive coefficient (λ) proposed in adaptive PMV model (aPMV) has been used to analyze the levels of adaptation of people there. The adaptive coefficient (λ) is -0.48 for winter and 0.62 for summer. The λ for summer varies from Evaluation Standard for indoor thermal environment in civil buildings in China. This indicates that a special evaluation index of λ should be given for those districts with dry-hot climate type which is although in the same climate zone.

BACKGROUND Endothelial dysfunction is an important pathophysiologic feature in many smoke-related diseases. Endothelial progenitor cells (EPCs) are the precursors of endothelial cells and play a fundamental role in the maintenance of endothelial integrity and function. Endothelial nitric oxide synthase (eNOS) is the dominant NOS isoform in the vasculature and plays a central role in the maintenance of endothelial homeostasis. p16(INK4a) is a cyclin-dependent kinase inhibitor and could be regarded as a major dominant senescence gene. The present study aimed to determine whether the expression of eNOS and p16(INK4a) in EPCs is related to EPCs function and the possible epigenetic mechanism, if any. MATERIAL AND METHODS We investigated EPCs capacity for proliferation, adhesion, and secretion, and the expression of eNOS and p16(INK4a) in EPCs which were altered by cigarette smoke extract (CSE) in vitro. Furthermore, Decitabine (Dec), an agent of demethylation, was used to examine whether it could alter the changes induced by CSE. RESULTS The present study demonstrated that EPCs altered by CSE in vitro displayed decreased capacities of proliferation, adhesion, and secretion, which was accompanied by decreased eNOS expression and increased p16(INK4a) expression in EPCs. Furthermore, Dec could alleviate the changes in the expression of eNOS and p16(INK4a), and protect against the EPCs dysfunction caused by CSE. CONCLUSIONS The decreased eNOS expression and increased p16(INK4a) expression was associated with dysfunction of EPCs caused by CSE. The mechanism of methylation, one of the most common epigenetic mechanism, may be involved in the EPCs dysfunction caused by CSE.