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Real estate in the Guangdong-Hong Kong-Macao Greater Bay Area (also known as the Greater Bay Area, GBA) - a good representation of China’s advanced and developed urban agglomeration - has received considerable attention from the international community in recent years. However, the real estate market has been under extraordinary stress due to the expansion of COVID-19 in China, the strain on people’s livelihoods brought on by the coronavirus pandemic, and the Chinese government’s series of epidemic preventive initiatives. This study used a combination of qualitative and quantitative techniques, making use of interviews and questionnaires as instruments. It examined China’s GBA real estate market as the pandemic looms. The primary goals are to demonstrate the current state of the GBA’s real estate industry, pinpoint the factors holding back its growth, and estimate when the market might finally experience a breakthrough. Our findings suggested that the impact of COVID-19 on the GBA real estate sector in China is evident, but that it still has a bright future despite the negative externalities. This is because the city has a large population, high purchasing power, and is close to some of the most developed areas in southern China. This study establishes a baseline for studying the impact of China’s “One Belt, One Road” initiative on the GBA real estate market in the future. It also provides valuable resources for China’s GBA’s real estate industry.

To explore the role of nutritional support in nursing practice on postoperative surgical site wound healing in patients undergoing surgery at risk for pressure ulcers. This study adopted a retrospective experimental design and included a total of 60 patients at risk of pressure ulcers, divided into a nutritional support group and a control group, with 30 people in each group. The nutritional support group implemented specific nutritional support measures after surgery, while the control group received standard postoperative care. Outcome measures included redness and swelling scores, edema scores, anxiety assessments, pain scores, bleeding volume, recovery time and incidence of pressure ulcers. The result indicates that patients who received nutritional support exhibited lower postoperative wound redness and swelling scores compared to the control group (3.11 ± 0.45 vs. 4.85 ± 0.74, p < 0.05). Additionally, the nutritional support group showed significantly lower edema scores (2.75 ± 0.37 vs. 3.53 ± 0.62, p < 0.05). Anxiety levels, as measured by the anxiety assessment scale (SAS), were also lower in the nutritional support group (6.52 ± 1.19 vs. 7.60 ± 1.62, p < 0.05). Moreover, the average healing time was shorter for the nutritional support group (7.27 ± 1.36 days) compared to the control group (9.71 ± 1.84 days, p < 0.05). Postoperative pain scores were lower in the nutritional support group (4.13 ± 0.72 vs. 5.43 ± 0.62, p < 0.05), and patient satisfaction scores were higher (9.42 ± 0.76 vs. 7.25 ± 0.81, p < 0.05). Nutritional support has a positive effect on postoperative wound healing at surgical sites in patients at risk of pressure ulcers in nursing practice. It can significantly reduce redness, swelling, edema, anxiety, and pain scores, reduce bleeding, shorten recovery time, and reduce pressure ulcers. incidence rate. [ABSTRACT FROM AUTHOR]

Background: With environmental and lifestyle changes, recent epidemiological studies have shown that the prevalence of Ulcerative Colitis (UC) is on the rise, while treatment options are limited. There is an urgent need to explore the underlying mechanisms of vitamin D (VD) as an effective treatment. Methods: Dextran sulfate sodium-induced mice and lipopolysaccharide-induced HCT116 cells were used to establish the classic UC models in vivo and in vitro, respectively. Typical symbols of inflammation (IL-6, COX-2), oxidative stress (MDA, MPO, GSH), and ferroptosis (ACSL4, GPX4, SLC7A11, and Iron) were analyzed by Western blot, Immunohistochemistry, RT-PCR, and relative assay kits. The inflammation factors and oxidative stress injury of cells transfected with ACSL4+/+ plasmids were tested by Western blot, MDA, and MPO methods. Results: Vitamin D attenuated the levels of COX-2, IL-6, Iron, MDA, and MPO and improved SOD1 and GSH contents in DSS + VD and LPS + VD groups, compared with model groups. Ferrostatin-1 (Fer-1) could relieve the levels of COX-2, IL-6, Iron, MDA, and MPO while increasing the contents of SOD1 and GSH in DSS + Fer-1 and LPS + Fer-1 compared to model groups. VD downregulated the expression of ACSL4 and upregulated GPX4 in tissues and cells. After transfected with ACSL4+/+ plasmids, we found VD's role of downregulating inflammation and oxidative stress was relieved. Conclusions: Vitamin D can relieve UC by inhibiting ferroptosis both in mice and in cells through the negative regulation of ACSL4, providing new insight into the therapeutic function of VD on UC. [ABSTRACT FROM AUTHOR]

Objective: Atherosclerosis is a chronic cardiovascular disease associated with oxidative stress damage, which is caused by excessive oxidation of low-density lipoprotein (ox-LDL). The role of microRNA miR-34a-5p on oxidative stress in ox-LDL–treated macrophages was investigated in this study. Methods: Flow cytometry was prepared for assessing THP1-derived macrophage apoptosis. The protein and expression levels of miR-34a-5p and MDM4 were examined by Western blot and RT-qPCR, respectively. We also measured the levels of total cholesterol (TC) and triglyceride to determine the lipid accumulation. Subsequently, the activities of superoxide dismutase, malondialdehyde, and reactive oxygen species revealed the level of oxidative stress injury after miR-34a-5p and MDM4 knockdown. Results: After ox-LDL treatment, cell apoptosis of macrophages increased in a dose-dependent and time-dependent manner. With the increase of ox-LDL treatment and the prolongation of treatment time, the expression level of miR-34a-5p was upregulated. Next, interfering with miR-34a-5p inhibited lipid accumulation and oxidative stress injury in ox-LDL–stimulated macrophages. MDM4 was a target gene of miR-34a-5p and was upregulated in ox-LDL–stimulated macrophages. With the increase of ox-LDL treatment and the prolongation of treatment time, the expression level of MDM4 was downregulated. Importantly, MDM4 knockdown partially counteracted the inhibitory effect of miR-34a-5p on oxidative stress injury. Conclusion: MicroRNA miR-34a-5p knockdown suppressed oxidative stress injury via MDM4 in ox-LDL–treated macrophages. [ABSTRACT FROM AUTHOR]

Hyperhomocysteinemia (HHcy) is an independent risk factor for cardiovascular and cerebrovascular diseases where the plasma homocysteine (Hcy) concentration exceeds 15 µmol/L. HHcy is affected by vitamins B12, B6, and folic acid (fol); however, its relationship with other nutrients is not fully understood. We investigated the nutritional and genetic factors associated with HHcy and the possible dose–response relationships or threshold effects in patients in Northeast China. Genetic polymorphisms and micronutrients were tested with polymerase chain reaction and mass spectrometry, respectively. This trial was registered under trial number ChiCTR1900025136. The HHcy group had significantly more males and higher body mass index (BMI), methylenetetrahydrofolate reductase (MTHFR 677TT) polymorphism proportion, and uric acid, Zn, Fe, P, and vitamin A levels than the control group. After adjusting for age, sex, BMI, vitamin B12, fol, and MTHFR C677T, the lowest Zn quartile reduced the odds ratio of HHcy compared with the highest Zn quartile. The dose–response curves for the association between plasma Zn and HHcy were S-shaped. High plasma Zn concentrations were significantly correlated with high HHcy odds ratios, and the curve leveled off or slightly decreased. Most importantly, HHcy risk decreased with decreasing plasma Zn concentration; the threshold was 83.89 µmol/L. Conclusively, individuals residing in Northeast China, especially those with the MTHFR 677TT polymorphism, must pay attention to their plasma Zn and Hcy levels. [ABSTRACT FROM AUTHOR]

The booming development of 3D virtual technology provides the basis for the innovation of teaching mode of clinical medicine. Integrating 3D virtual technology into the clinical education teaching of medical students can help medical students learn clinical expertise more intuitively, enrich practical experience, improve hands-on ability, and make up for the shortcomings of traditional medical teaching. However, the traditional 3D modeling method has the problems of sparse and insufficient accuracy of output results, which greatly limits the specific application of 3D virtual technology in clinical teaching. Therefore, this paper addresses the shortcomings of previous 3D virtual technology in 3D modeling of organs, introduces deep learning, and then proposes a pyramidal shape perception network with the ability to generate samples on point clouds. Experimental results show that the proposed model not only has a large improvement in accuracy but also shows a high degree of confidence in providing real-time feedback of local image attributes. [ABSTRACT FROM AUTHOR]

Photovoltaic power generation is greatly affected by weather factors. To improve the prediction accuracy of photovoltaic power generation, complete ensemble empirical mode decomposition with an adaptive noise algorithm (CEEMDAN) is proposed to preprocess the power sequence. Then, the full convolutional network (FCN) model optimized based on the sparrow search algorithm (SSA) is used to predict the short-term photovoltaic power. SSA can more reasonably determine the parameters of FCN and improve the prediction performance of FCN. Therefore, the FCN model optimized by the SSA algorithm is used to establish prediction models for subsequences and predict each subsequence, respectively. Finally, the predicted value of each subsequence is superimposed. Taking the actual data of a photovoltaic power station in Jiangsu province of China as an example, by comparing some different common prediction models, it is proved that the proposed method is reasonable and feasible. [ABSTRACT FROM AUTHOR]

The inhibitory effects of vitamin D on colitis have been previously documented. Global vitamin D receptor (VDR) deletion exaggerates colitis, but the relative anticolitic contribution of epithelial and nonepithelial VDR signaling is unknown. Here, we showed that colonic epithelial VDR expression was substantially reduced in patients with Crohn's disease or ulcerative colitis. Moreover, targeted expression of human VDR (hVDR) in intestinal epithelial cells (IECs) protected mice from developing colitis. In experimental colitis models induced by 2,4,6-trinitrobenzenesulfonic acid, dextran sulfate sodium, or CD[4.sup.+]CD45R[B.sup.hi] T cell transfer, transgenic mice expressing hVDR in IECs were highly resistant to colitis, as manifested by marked reductions in clinical colitis scores, colonic histological damage, and colonic inflammation compared with WT mice. Reconstitution of Vdr-deficient IECs with the hVDR transgene completely rescued Vdr-null mice from severe colitis and death, even though the mice still maintained a hyperresponsive Vdr-deficient immune system. Mechanistically, VDR signaling attenuated PUMA induction in IECs by blocking NF-kB activation, leading to a reduction in IEC apoptosis. Together, these results demonstrate that gut epithelial VDR signaling inhibits colitis by protecting the mucosal epithelial barrier, and this anticolitic activity is independent of nonepithelial immune VDR actions., 10.1172/JCI65842. Introduction Ulcerative colitis (UC) and Crohn's disease (CD) are major chronic inflammatory bowel diseases (IBDs) in humans. Although the etiology and pathogenesis of IBD remain uncertain, it is believed [...]

The intrarenal renin-angiotensin system (RAS) plays a key role in the development of diabetic nephropathy. Recently, we showed that combination therapy with an [AT.sub.1] receptor blocker (ARB) and an activated vitamin D analog produced excellent synergistic effects against diabetic nephropathy, as a result of blockade of the ARB-induced compensatory renin increase. Given the diversity of vitamin D analogs, here we used a pro-drug vitamin D analog, doxercalciferol (1[alpha]-hydroxyvitamin [D.sub.2]), to further test the efficacy of the combination strategy in long-term treatment. Streptozotocin-induced diabetic DBA/2J mice were treated with vehicle, losartan, doxercalciferol (0.4 and 0.6 [micro]g/kg), or losartan and doxercalciferol combinations for 20 wk. Vehicle-treated diabetic mice developed progressive albuminuria and glomerulosclerosis. Losartan alone moderately ameliorated kidney injury, with renin being drastically upregulated. A similar therapeutic effect was seen with doxercalciferol alone, which markedly suppressed renin and angiotensinogen expression. The losartan and doxercalciferol combination most effectively prevented albuminuria, restored glomerular filtration barrier structure, and dramatically reduced glomerulosclerosis in a dose-dependent manner. These effects were accompanied by blockade of intrarenal renin upregulation and ANG II accumulation. These data demonstrate an excellent therapeutic potential for doxercalciferol in diabetic renal disease and confirm the concept that blockade of the compensatory renin increase enhances the efficacy of RAS inhibition and produces synergistic therapeutic effects in combination therapy. renin-angiotensin system; compensatory renin increase; albuminuria; glomerulosclerosis

The renin-angiotensin system (RAS) is a major mediator of renal injury in diabetic nephropathy. Our previous studies demonstrated that 1,25-dihydroxyvitamin [D.sub.3] [1,25[(OH).sub.2][D.sub.3]] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. The mechanism whereby 1,25[(OH).sub.2][D.sub.3] transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. Exposure of mesangial cells or podocytes to high glucose (HG; 30 mM) markedly stimulated AGT expression. In mesangial cells, the stimulation was inhibited by 1,25[(OH).sub.2][D.sub.3] (20 nM) or NF-[kappa]B inhibitor BAY 11-7082, suggesting the involvement of NF-[kappa]B in HG-induced AGT expression and the interaction between 1,25[(OH).sub.2][D.sub.3] and NF-[kappa]B in the regulation. Plasmid pNF-[kappa]B-Luc luciferase reporter assays showed that 1,25[(OH).sub.2][D.sub.3] blocked HG-induced NF-[kappa]B activity. EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-[kappa]B binding site at--1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25[(OH).sub.2][D.sub.3] treatment. Overexpression of p65/p50 overcame 1,25[(OH).sub.2][D.sub.3] suppression, and mutation of this NF-[kappa]B binding site blunted 1,25[(OH).sub.2][D.sub.3] suppression of the promoter activity. In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. These data indicate that 1,25[(OH).sub.2][D.sub.3] suppresses hyperglycemia-induced AGT expression by blocking NF-[kappa]B-mediated pathway. vitamin D receptor; renin-angiotensin system; diabetic nephropathy

Recent studies have established that vitamin D plays multiple biological roles beyond calcium metabolism; however, whether vitamin D is involved in energy metabolism is unknown. To address this question, we characterized the metabolic phenotypes of vitamin D receptor (VDR)-null mutant mice. Under a normocalcemic condition, VDR-null mice displayed less body fat mass and lower plasma triglyceride and cholesterol levels compared with wild-type (WT) mice; when placed on a high-fat diet, VDR-null mice showed a slower growth rate and accumulated less fat mass globally than WT mice, even though their food intake and intestinal lipid transport capacity were the same as WT mice. Consistent with the lower adipose mass, plasma leptin levels were lower and white adipocytes were histologically smaller in VDR-null mice than WT mice. The rate of fatty acid [beta]-oxidation in the white adipose tissue was higher, and the expression of uncoupling protein (UCP) 1, UCP2 and UCP3 was markedly upregulated in VDR-null mice, suggesting a higher energy expenditure in the mutant mice. Experiments using primary brown fat culture confirmed that 1,25-dihydroxyvitamin [D.sub.3] directly suppressed the expression of the UCPs. Consistently, the energy expenditure, oxygen consumption, and C[O.sub.2] production in VDR-null mice were markedly higher than in WT mice. These data indicate that vitamin D is involved in energy metabolism and adipocyte biology in vivo in part through regulation of [beta]-oxidation and UCP expression. adipocytes; uncoupling proteins; energy metabolism

Emerging evidence supports a pathological link between vitamin D deficiency and the risk of inflammatory bowel disease (IBD). To explore the mechanism we used the dextran sulfate sodium (DSS)-induced colitis model to investigate the role of the vitamin D receptor (VDR) in mucosal barrier homeostasis. While [VDR.sup.+/+] mice were mostly resistant to 2.5% DSS, [VDR.sup.-/-] mice developed severe diarrhea, rectal bleeding, and marked body weight loss, leading to death in 2 wk. Histological examination revealed extensive ulceration and impaired wound healing in the colonic epithelium of DSS-treated [VDR.sup.-/-] mice. Severe ulceration in [VDR.sup.-/-] mice was preceded by a greater loss of intestinal transepithelial electric resistance (TER) compared with [VDR.sup.+/+] mice. Confocal and electron microscopy (EM) revealed severe disruption in epithelial junctions in [VDR.sup.-/-] mice after 3-day DSS treatment. Therefore, [VDR.sup.-/-] mice were much more susceptible to DSS-induced mucosal injury than [VDR.sup.+/+] mice. In cell cultures, 1,25-dihydroxy-vitamin [D.sub.3] [1,25[(OH).sub.2][D.sub.3]] markedly enhanced tight junctions formed by Caco-2 monolayers by increasing junction protein expression and TER and preserved the structural integrity of tight junctions in the presence of DSS. VDR knockdown with small interfering (si)RNA reduced the junction proteins and TER in Caco-2 monolayers. 1,25[(OH).sub.2][D.sub.3] can also stimulate epithelial cell migration in vitro. These observations suggest that VDR plays a critical role in mucosal barrier homeostasis by preserving the integrity of junction complexes and the heating capacity of the colonic epithelium. Therefore, vitamin D deficiency may compromise the mucosal barrier, leading to increased susceptibility to mucosal damage and increased risk of IBD. tight junction; inflammatory bowel disease; dextran sulfate sodium