A 23-year bibliometric analysis of the development of global research on hereditary renal carcinoma.

Objectives: Medical research continues to be extensively devoted to investigating the pathogenesis and treatment approaches of hereditary renal cancer. By aspect including researchers, institutions, countries, journals, and keywords, we conduct a bibliometric analysis of the literature pertaining to hereditary renal cancer over the last 23 years. Methods: From the Web of Science Core Collection, we conducted a search for publications published between January 1, 2000 and November 28, 2023. Reviews and original articles were included. Results: A cumulative count of 2,194 publications met the specified criteria for inclusion. The studies of the included articles involved a collective of 2,402 institutions representing 80 countries. Notably, the United States exhibited the highest number of published documents, constituting approximately 45.49% of the total. The preeminent institution in this discipline is the National Cancer Institute (NCI), which maintains a publication volume of 8.98%. In addition to being the most prolific author (125 publications), Linehan WM's works received the highest number of citations (11,985). In a comprehensive count, 803 journals have published related articles. In the top 10 most recent occurrences were the terms "hereditary leiomyomatosis" and "fumarate hydratase." Conclusion: This is the first bibliometric analysis of the literature on hereditary renal cancer. This article offers a thorough examination of the present status of investigations concerning hereditary renal cancer during the previous 23 years.

Quantitative susceptibility mapping in the brain reflects spatial expression of genes involved in iron homeostasis and myelination.

Quantitative susceptibility mapping (QSM) is an MRI modality used to non-invasively measure iron content in the brain. Iron exhibits a specific anatomically varying pattern of accumulation in the brain across individuals. The highest regions of accumulation are the deep grey nuclei, where iron is stored in paramagnetic molecule ferritin. This form of iron is considered to be what largely contributes to the signal measured by QSM in the deep grey nuclei. It is also known that QSM is affected by diamagnetic myelin contents. Here, we investigate spatial gene expression of iron and myelin related genes, as measured by the Allen Human Brain Atlas, in relation to QSM images of age-matched subjects. We performed multiple linear regressions between gene expression and the average QSM signal within 34 distinct deep grey nuclei regions. Our results show a positive correlation (p < .05, corrected) between expression of ferritin and the QSM signal in deep grey nuclei regions. We repeated the analysis for other genes that encode proteins thought to be involved in the transport and storage of iron in the brain, as well as myelination. In addition to ferritin, our findings demonstrate a positive correlation (p < .05, corrected) between the expression of ferroportin, transferrin, divalent metal transporter 1, several gene markers of myelinating oligodendrocytes, and the QSM signal in deep grey nuclei regions. Our results suggest that the QSM signal reflects both the storage and active transport of iron in the deep grey nuclei regions of the brain.

Quercetin induces ferroptosis by inactivating mTOR/S6KP70 pathway in oral squamous cell carcinoma.

Although recent studies increasingly suggest the potential anti-cancer effect of quercetin, the exact underlying mechanism remains poorly demonstrated in oral squamous cell carcinoma (oSCC). Therefore, our research explored the impacts of quercetin on the ferroptosis and mTOR/S6KP70 axis in oSCC cell lines. After treating oSCC cells with quercetin or indicated compounds and transfection with SLC7A11- or S6KP70-overexpressing plasmid, cell viability was detected by CCK-8 assay. The level of ferroptosis in oSCC cells was assessed by measuring ROS and GSH levels. The activation of mTOR/S6KP70 axis was assessed by Western blotting. Quercetin promoted ferroptosis in an mTOR/S6KP70-dependent manner to inhibit tumor growth in oSCC cells. Mechanistically, we revealed that quercetin induced lipid peroxidation and reduced GSH levels by repressing SLC7A11 expression in oSCC cells. Specifically, the effects of quercetin on ferroptosis and mTOR and S6KP70 phosphorylation were partially blocked by both mTOR agonist and S6KP70 overexpression. Moreover, mTOR inhibitor promoted ferroptosis in quercetin-treated oSCC cells. Our findings showed that ferroptosis may be a new anti-tumor mechanism of quercetin. Additionally, we identified that quercetin can target mTOR/S6KP70 cascade to inhibit the growth of oSCC cells.

Walnut-Derived Peptides Ameliorate Scopolamine-Induced Memory Impairments in a Mouse Model via Activation of Peroxisome Proliferator-Activated Receptor γ-Mediated Excitotoxicity.

We investigated the protective effect of walnut peptides and YVPFPLP (YP-7) on scopolamine-induced memory impairment in mice and ß-amyloid (Aß)-induced excitotoxic injury in primary hippocampal neurons, respectively. Additionally, the protective mechanism of YP-7 on neuronal excitotoxicity was explored. Mouse behavioral and hippocampal slice morphology experiments indicate that YP-7 improves the learning and memory abilities of cognitively impaired mice and protects synaptic integrity. Immunofluorescence, western blotting, and electrophysiological experiments on primary hippocampal neurons indicate that YP-7 inhibits neuronal damage caused by excessive excitation of neurons induced by Aß. HT-22 cell treatment with peroxisome proliferator-activated receptor γ (PPARγ) activators and inhibitors showed that YP-7 activates PPARγ expression and maintains normal neuronal function by forming stable complexes with PPARγ to inhibit the extracellular regulated protein kinase pathway. Therefore, YP-7 can ameliorate glutamate-induced excitotoxicity and maintain neuronal signaling. This provides a theoretical basis for active peptides to ameliorate excitotoxicity and the development of functional foods.

A combined in vitro and in silico study of the inhibitory mechanism of angiotensin-converting enzyme with peanut peptides.

Food-derived peptides with low molecular weight, high bioavailability, and good absorptivity have been exploited as angiotensin-converting enzyme (ACE) inhibitors. In the present study, in-vitro inhibition kinetics of peanut peptides, in silico screening, validation of ACE inhibitory activity, molecular dynamics (MD) simulations, and HUVEC cells were performed to systematically identify the inhibitory mechanism of ACE interacting with peanut peptides. The results indicate that FPHPP, FPHY, and FPHFD peptides have good thermal, pH, and digestive stability. MD trajectories elucidate the dynamic correlation between peptides and ACE and verify the specific binding interaction. Noteworthily, FPHPP is the best inhibitor with a strongest binding affinity and significantly increases NO, SOD production, and AT2R expression, and decreases ROS, MDA, ET-1 levels, ACE, and AT1R accumulation in Ang II-injury HUVEC cells.

Identification of idiopathic pulmonary fibrosis hub genes and exploration of the mechanisms of action of Jinshui Huanxian formula.

Idiopathic pulmonary fibrosis (IPF) is a common and heterogeneous chronic disease, and the mechanism of Jinshui Huanxian formula (JHF) on IPF remains unclear. For a total of 385 lung normal tissue samples from the Gene Expression Omnibus database, 37,777,639 gene pairs were identified through microarray and RNA-seq platforms. Using the individualized differentially expressed gene (DEG) analysis algorithm RankComp (FDR < 0.01), we identified 344 genes as DEGs in at least 95 % (n = 81) of the IPF samples. Of these genes, IGF1, IFNGR1, GLI2, HMGCR, DNM1, KIF4A, and TNFRSF11A were identified as hub genes. These genes were verified using quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) in mice with pulmonary fibrosis (PF) and MRC-5 cells, and they were highly effective at classifying IPF samples in the independent dataset GSE134692 (AUC = 0.587-0.788) and mice with PF (AUC = 0.806-1.000). Moreover, JHF ameliorated the pathological changes in mice with PF and significantly reversed the changes in hub gene expression (KIF4A, IFNGR1, and HMGCR). In conclusion, a series of IPF hub genes was identified, and validated in an independent dataset, mice with PF, and MRC-5 cells. Moreover, the abnormal gene expression was normalized by JHF. These findings provide guidance for further exploration of the pathogenesis and treatment of IPF.

Effect of bi-enzyme hydrolysis on the properties and composition of hydrolysates of Manchurian walnut dreg protein.

Walnut dreg (WD) active peptides are an important source of dietary antioxidants; however, the products of conventional hydrolysis have limited industrial output owing to poor flavour and low bioactivity. To this end, in this study, we aimed to employ bvLAP, an aminopeptidase previously identified in our research, as well as commercially available Alcalase for bi-enzyme digestion. The flavour, antioxidant activity, and structures of products resulting from various digestion methods were compared. The results showed that the bi-enzyme digestion products had enhanced antioxidant activity, increased ß-sheet content, and reduced bitterness intensity from 9.65 to 6.93. Moreover, bi-enzyme hydrolysates showed a more diverse amino acid composition containing 1640 peptides with distinct sequences. These results demonstrate that bi-enzyme hydrolysis could be a potential process for converting WD into functional food ingredients. Additionally, our results provide new concepts that can be applied in waste processing and high-value utilisation of WD.

Melatonin attenuates diabetic cardiomyopathy by increasing autophagy of cardiomyocytes via regulation of VEGF-B/GRP78/PERK signaling pathway.

AIMS: Diabetic cardiomyopathy (DCM) is a major cause of mortality in patients with diabetes, and the potential strategies for treating DCM are insufficient. Melatonin (Mel) has been shown to attenuate DCM, however, the underlying mechanism remains unclear. The role of vascular endothelial growth factor-B (VEGF-B) in DCM is little known. In present study, we aimed to investigate whether Mel alleviated DCM via regulation of VEGF-B and explored its underlying mechanisms. METHODS AND RESULTS: We found that Mel significantly alleviated cardiac dysfunction and improved autophagy of cardiomyocytes in type 1 diabetes mellitus (T1DM) induced cardiomyopathy mice. VEGF-B was highly expressed in DCM mice in comparison with normal mice, and its expression was markedly reduced after Mel treatment. Mel treatment diminished the interaction of VEGF-B and Glucose-regulated protein 78 (GRP78) and reduced the interaction of GRP78 and protein kinase RNA -like ER kinase (PERK). Furthermore, Mel increased phosphorylation of PERK and eIF2α, then up-regulated the expression of ATF4. VEGF-B-/- mice imitated the effect of Mel on wild type diabetic mice. Interestingly, injection with Recombinant adeno-associated virus serotype 9 (AAV9)-VEGF-B or administration of GSK2656157 (GSK), an inhibitor of phosphorylated PERK abolished the protective effect of Mel on DCM. Furthermore, rapamycin, an autophagy agonist displayed similar effect with Mel treatment; while 3-Methyladenine (3-MA), an autophagy inhibitor neutralized the effect of Mel on high glucose-treated neonatal rat ventricular myocytes. CONCLUSIONS: These results demonstrated that Mel attenuated DCM via increasing autophagy of cardiomyocytes, and this cardio-protective effect of Mel was dependent on VEGF-B/GRP78/PERK signaling pathway.

Copper-coordinated nanoassemblies based on photosensitizer-chemo prodrugs and checkpoint inhibitors for enhanced apoptosis-cuproptosis and immunotherapy.

Cuproptosis is a recently identified copper-dependent form of nonapoptotic cell death and holds great prospect in cancer treatment. One of the most intriguing aspects of cuproptosis is its ability to synergize with apoptosis-based cancer treatments. Herein, we presented a novel approach using copper-coordinated nanoassemblies (CCNAs) that were constructed by incorporating a photosensitizer Zinc Phthalocyanine (ZnPc)-chemotherapeutic (DOX) prodrug with a thioketal (TK) spacer and an IDO inhibitor (1-methyl tryptophan, 1-MT) as building blocks for Cu2+-coordination self-assembly to achieve combinational apoptosis-cuproptosis and immunotherapy. Upon NIR laser irradiation, the ZnPc component of CCNAs exhibited a photodynamic effect that generated reactive oxygen species (ROS). This triggered the release of DOX, leading to enhanced tumor cell apoptosis. Additionally, the presence of Cu2+ in the CCNAs not only enhanced the photodynamic process by catalyzing oxygen generation but also promoted the aggregation of toxic mitochondrial proteins, leading to cell cuproptosis. Importantly, the intensified cuproptosis-apoptosis effect triggered an immunogenic cell death (ICD) response. The released 1-MT complemented this response by reversing the immunosuppressive tumor microenvironment (ITM), synergistically amplifying anti-tumor immunity and suppressing the growth of primary and distant tumors. The findings of this study provide a new perspective on potential cancer treatments based on cuproptosis-apoptosis synergistic immunotherapy and stimulate further research in the design of advanced metal-coordinated nanomedicines. STATEMENT OF SIGNIFICANCE: The combination of cuproptosis and apoptosis that act with different mechanisms holds enormous potential in cancer treatment. Here, copper-coordinated nanoassemblies (CCNAs) based on photosensitizer-chemo prodrugs and checkpoint inhibitors were constructed for mediating cuproptosis-apoptosis and subsequently promoting cancer immunotherapy. CCNAs not only promoted the photodynamic effect and activation of chemotherapy through catalyzing the generation of oxygen but also induced toxic mitochondrial protein aggregation, leading to cell cuproptosis. These synergistic antitumor effects triggered robust immune responses with the aid of immune checkpoint blockade, almost eradicating primary tumors and inhibiting distant tumors by around 83 % without systemic toxicity.

Effects of Physical Activity on Quality of Life, Anxiety and Depression in Breast Cancer Survivors: A Systematic Review and Meta-analysis.

PURPOSE: Anxiety, depression, and poor quality of life (QOL) were considered important concerns that hindered the rehabilitation of breast cancer survivors. A number of studies have investigated the effects of physical activity, but they have not reached the same conclusions. This review aimed to identify the effects of physical activity on QOL, anxiety, and depression in breast cancer survivors. METHODS: PubMed, Embase, Web of Science, Cumulative Index to Nursing and Allied Health Literature (CINAHL), PsycINFO, SinoMed, CNKI, Vip, and WanFang databases were searched for the time period between January 1, 2012, and April 30, 2022. Studies were included if they were randomized controlled trials of the effects of physical activity on QOL, anxiety, or depression in breast cancer survivors. The tools of the Joanna Briggs Institute were used to assess the quality of the included studies. R software version 4.3.1 was used for meta-analysis. RESULTS: A total of 26 studies, involving 2105 participants, were included in the systematic review. Among these, 20 studies involving 1228 participants were included in the meta-analysis. Compared with the control group, the results indicated that physical activity can significantly improve QOL(Hedges' g = 0.67; 95% CI 0.41-0.92) and reduce anxiety (Hedges' g = -0.28; 95% CI -0.46 to -0.10) in breast cancer survivors. However, the effect of physical activity on depression (Hedges' g = -0.46; 95% CI -0.99 to 0.06) was not statistically significant. CONCLUSIONS: Physical activity was an effective intervention to improve QOL and reduce anxiety in breast cancer survivors, as well as showed positive trends in depression, although without statistical significance. More well-designed studies are required to clarify the effects of different types of physical activities on the QOL, anxiety, and depression among breast cancer survivors. REGISTERED NUMBER ON PROSPERO: CRD42022363094. https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=363094.

Electroacupuncture Inhibits Neuroinflammation Induced by Astrocytic Necroptosis Through RIP1/MLKL/TLR4 Pathway in a Mouse Model of Spinal Cord Injury.

Astrocytic necroptosis plays an essential role in the progression and regression of neurological disorders, which contributes to the neuroinflammation and disrupts neuronal regeneration and remyelination of severed axons. Electroacupuncture (EA), an effective therapeutic efficacy against spinal cord injury (SCI), has been proved to reduce neuronal cell apoptosis, inhibit inflammation, and prompt neural stem cell proliferation and differentiations. However, there have been few reports on whether EA regulate astrocytic necroptosis in SCI model. To investigate the effects of EA on astrocytic necroptosis and the mechanisms involved in the inhibition of astrocytic necroptosis after SCI in mice by EA, 8-week-old female C57BL/6 mice were subjected to SCI surgery and randomly divided into EA and SCI groups. Mice receiving sham surgery were included as sham group. "Jiaji" was selected as points for EA treatment, 10 min/day for 14 days. The in vitro data revealed that EA treatment significantly improved the nervous function and pathological changes after SCI. EA also reduced the number of GFAP/P-MLKL, GFAP/MLKL, GFAP/HMGB1, and Iba1/HMGB1 co-positive cells and inhibited the expressions of IL-6, IL-1ß, and IL-33. The results indicate a significant reduction in inflammatory reaction and astrocytic necroptosis in mice with SCI by EA. Additionally, the expressions of RIP1, MLKL, and TLR4, which are associated with necroptosis, were found to be downregulated by EA. In this study, we confirmed that EA can inhibit neuroinflammation by reducing astrocytic necroptosis through downregulation of RIP1/MLKL/TLR4 pathway in mice with SCI.

Risk factors for recurrence after keloid surgery with electron radiotherapy.

The aim of this study was to investigate the effect of postoperative electron radiotherapy (RT) on local control for keloids and to identify risk factors for recurrence. The clinical data of 82 patients treated at our institution from January 2015 to October 2019 were collected. The data included the general condition of the patients, clinical characteristics of the keloids, treatment plan, local control, and treatment side effects. A total of 82 patients (129 keloids) were included. The study included 23 men (28%) and 59 females (72%). The median patient age was 32 years (range, 18-67 years). Twenty-six recurrences were observed, and the 1-, 3-, and 5-year local control rates were 93%, 81%, and 73%, respectively. Univariate analysis revealed that age (P = .03), hypertension (P = .04), scar shape (P < .001), primary site (P = .02), maximum lesion diameter (P < .001), pain and itching (P = .005), local tension (P = .005), and infection (P < .001) were risk factors for local recurrence. Multivariable analysis revealed that maximum lesion diameter (P < .001), infection (P < .001), interval between surgery and RT (P = .02), and previous treatment (P = .02) were independent risk factors. Complete excision of keloids combined with electron RT is safe and seemingly effective. For keloids with a high risk of recurrence, more aggressive treatment should be chosen, and further prospective studies are needed to explore the optimal treatment.

Experiences of breast cancer survivors with exercise rehabilitation: qualitative systematic review and meta-synthesis.

PURPOSE: This study aimed to synthesize and evaluate the available qualitative literature on posttreatment participation in exercise rehabilitation among breast cancer survivors. METHODS: This systematic review followed the Joanna Briggs Institute (JBI) meta-aggregation approach guided by ENTREQ, graded according to the ConQual approach, and evaluated using the JBI Qualitative Assessment and Review Instrument (JBI-QARI). We searched qualitative or mixed methods studies related to the experiences of exercise rehabilitation among breast cancer survivors conducted until April 13, 2023, in nine English and Chinese databases. The selected studies were reviewed independently, and the data were collaboratively synthesized into core themes. RESULTS: A total of 24 studies were included, and 88 findings resulted in five synthesis findings: (a) benefits of participating in exercise rehabilitation, (b) facilitators of participation in exercise rehabilitation, (c) obstacle factors for participating in exercise rehabilitation, (d) evaluation of the exercise program, and (e) recommendations. CONCLUSION: Breast cancer survivors need exercise to recover physically and mentally and to transition from cancer treatment to a normal life. The factors affecting exercise participation in breast cancer survivors are complex. Breast cancer survivors require timely and continuous effective exercise intervention forms, including online, offline, instrumental, and emotional support from others, especially healthcare providers and family members. Moreover, multidisciplinary collaboration is required to develop more effective and convenient exercise interventions.

Revision and psychometric evaluation of a fertility intention scale for young women with breast cancer in Chinese Mainland.

Objective: Neglected fertility intentions affect the quality of life of young women with breast cancer. The purpose of this study was to revise the Taiwanese version of the Fertility Intention Scale and validate its psychometric properties among young women with breast cancer in Chinese Mainland. Methods: We performed a cross-sectional survey with young women with breast cancer at a Chinese cancer hospital to evaluate the psychometric properties of the Revised Fertility Intention Scale. A two-phase study was conducted: (1) revision of the scale and (2) evaluation of the scale's reliability and validity. Results: Six new items and one new dimension were added to the original 15 items and four dimensions, reliability and validity of the 21-item Revised Fertility Intention Scale were verified in a sample of 436 women in Chineses Mainland with breast cancer who were aged 18-40 years. The content validity index, results of factor analysis, convergent validity, and known-groups validity were acceptable, and the Cronbach's alpha and intraclass correlation coefficients supported the revised scale. Conclusions: The 21-item Revised Fertility Intention Scale has satisfactory reliability and validity for assessing fertility intentions among young women with breast cancer in Chinese Mainland. In clinical practice, nurses can use the scale to identify fertility intentions and associated factors in young women with breast cancer and develop feasible and effective oncofertility care measures.

SPI1 involvement in malignant melanoma pathogenesis by regulation of HK2 through the AKT1/mTOR pathway.

Spi-1 proto-oncogene (SPI1) plays a vital role in carcinogenesis. Our work aimed to investigate the potential regulatory mechanism of SPI1 in melanoma. The mRNA and protein levels were measured via qRT-PCR and Western blotting. Cell viability was assessed by CCK-8 assay. The target relationship between SPI1 and hexokinase 2 (HK2) was determined using dual-luciferase reporter detection. ChIP was conducted to confirm the targeted relationship between SPI1 and the HK2 promoter. Immunohistochemistry analysis was conducted to measure the positive cell number of SPI1 and HK2 in melanoma tissues. The cell migration abilities were determined using a wound healing assay. Glucose consumption, pyruvate dehydrogenase activity, lactate production and ATP levels were measured to assess glycolysis. SPI1 transcription in melanoma cells and tissues was dramatically higher than that in adjacent normal tissues and epidermal melanocyte HEMa-LP, respectively. Knockdown of SPI1 restrained cell viability, metastasis and glycolysis in melanoma cells. SPI1 directly targeted HK2, and knockdown of SPI1 repressed HK2 expression. Overexpression of HK2 weakened the inhibitory effects of SPI1 knockdown on the viability, metastasis and glycolysis of melanoma cells. The serine-threonine kinase 1 (AKT1)/mammalian target of rapamycin (mTOR) axis is involved in melanoma progression. SPI1 knockdown restrained melanoma cell proliferation, metastasis and glycolysis by regulating the AKT1/mTOR pathway.

The mediating effect of coping styles between self-compassion and body image disturbance in young breast cancer survivors: a cross-sectional study.

BACKGROUND: Young breast cancer survivors with body image disturbance have poor quality of life. Self-compassion and different coping styles can influence their body image. The purpose of the study was to investigate the relationship between self-compassion, coping styles, and body image disturbance, and examined the mediation role of coping styles between self-compassion and body image disturbance among young breast cancer survivors in China. METHODS: In the cross-sectional study, a total of 310 young women with breast cancer were assessed on self-compassion, coping styles, and body image disturbance by self-reported questionnaires in China. Spearman's correlation was used to test the links between variables and to verify the indirect effects between variables by constructing a structural equation model. RESULTS: There were correlations between self-compassion, different coping styles, and body image disturbance. Confrontation, avoidance, and acceptance-resignation coping had significant mediation effects on the association between self-compassion and body image disturbance. The mediation effects of confrontation coping were greater than avoidance, and acceptance-resignation coping. CONCLUSIONS: In this study, different coping styles acted as mediators between self-compassion and body image disturbance, providing support for further understanding the mechanism between self-compassion and body image disturbance, and developing comprehensive interventions for body image disturbance. Oncology nurses should pay attention to the breast cancer survivors' self-compassion and coping styles and encourage them to adopt adaptive coping strategies, which can reduce body image disturbance.

Direct localization and delineation of human pedunculopontine nucleus based on a self-supervised magnetic resonance image super-resolution method.

The pedunculopontine nucleus (PPN) is a small brainstem structure and has attracted attention as a potentially effective deep brain stimulation (DBS) target for the treatment of Parkinson's disease (PD). However, the in vivo location of PPN remains poorly described and barely visible on conventional structural magnetic resonance (MR) images due to a lack of high spatial resolution and tissue contrast. This study aims to delineate the PPN on a high-resolution (HR) atlas and investigate the visibility of the PPN in individual quantitative susceptibility mapping (QSM) images. We combine a recently constructed Montreal Neurological Institute (MNI) space unbiased QSM atlas (MuSus-100), with an implicit representation-based self-supervised image super-resolution (SR) technique to achieve an atlas with improved spatial resolution. Then guided by a myelin staining histology human brain atlas, we localize and delineate PPN on the atlas with improved resolution. Furthermore, we examine the feasibility of directly identifying the approximate PPN location on the 3.0-T individual QSM MR images. The proposed SR network produces atlas images with four times the higher spatial resolution (from 1 to 0.25 mm isotropic) without a training dataset. The SR process also reduces artifacts and keeps superb image contrast for further delineating small deep brain nuclei, such as PPN. Using the myelin staining histological atlas as guidance, we first identify and annotate the location of PPN on the T1-weighted (T1w)-QSM hybrid MR atlas with improved resolution in the MNI space. Then, we relocate and validate that the optimal targeting site for PPN-DBS is at the middle-to-caudal part of PPN on our atlas. Furthermore, we confirm that the PPN region can be identified in a set of individual QSM images of 10 patients with PD and 10 healthy young adults. The contrast ratios of the PPN to its adjacent structure, namely the medial lemniscus, on images of different modalities indicate that QSM substantially improves the visibility of the PPN both in the atlas and individual images. Our findings indicate that the proposed SR network is an efficient tool for small-size brain nucleus identification. HR QSM is promising for improving the visibility of the PPN. The PPN can be directly identified on the individual QSM images acquired at the 3.0-T MR scanners, facilitating a direct targeting of PPN for DBS surgery.

Estrogen ameliorates sepsis-induced vascular hyporeactivity in thoracic aorta of female rats via permissive effect of GRα expression.

OBJECTIVE: Estrogen is correlated to the lower mortality and disease severity of female than that of male, which indicates the potential therapeutic role of estrogen supplement therapy in sepsis. The structure of Daidzein is similar to that of 17ß estradiol (E2), an estrogen in human body, causing the exogenous Daidzein can interact with estrogen receptor as well as E2 in the body. We aim to explore the therapeutic role of estrogen in sepsis-induced vascular dysfunction. Also, we wonder if estrogen regulates blood pressure via glucocorticoid-mediated vascular reactivity. METHODS: Female SD rats received ovariectomy (OVX) to induce estrogen deficiency. After 12 weeks of administration, cecal ligation and puncture (CLP) was used to establish the in vivo model of sepsis. Lipopolysaccharide (LPS) was used to construct the in vitro model of sepsis in vascular smooth muscle cells (VSMCs). E2 and Daidzein were used for estrogen supplement therapy. RESULTS: E2 and Daidzein significantly inhibited inflammation infiltration and histopathological injury in thoracic aorta in the rat model with CLP. E2 and Daidzein improved carotid pressure and vascular hyporeactivity in sepsis rats with OVX. Importantly, E2 and Daidzein promoted glucocorticoid permissive action and increased glucocorticoid receptor α (GRα) expression in thoracic aorta smooth muscle cells. E2 and Daidzein upregulated GRα, and inhibits cytokine production, proliferative phenotype and cell migration in LPS-induced VSMCs. CONCLUSION: Estrogen improved vascular hyporeactivity in thoracic aorta induced by sepsis via permissive effect of GRα expression.

Association of self-compassion and body image disturbance among young breast cancer patients: Mediating effect of body surveillance and body shame.

Objective: To examine whether body surveillance and body shame mediated the association between self-compassion and body image disturbance among young breast cancer patients. Methods: In this cross-sectional descriptive study, a total of 310 young women with breast cancer were recruited by convenience sampling. All of them completed self-report measurements of demographic and clinical characteristics, self-compassion scale, body image self-rating questionnaire for breast cancer and body surveillance scale, and body shame scale between September and December 2021 â€‹at a tertiary cancer hospital in Tianjin, China. Data analysis was performed with correlation analysis and structural equation modeling to verify relationships between key variables. Results: Less self-compassion was significantly associated with greater body image disturbance, while a positive correlation was found between body image disturbance, body surveillance, and body shame. Self-compassion indirectly negative predicted body image disturbance via the chain mediation of body surveillance and body shame. Conclusions: The links of self-compassion and body image disturbance were mediated by body surveillance and body shame. Reducing patients' excessive body surveillance and body shame by improving their ability of self-compassion may be an effective measure to reduce body image disturbance.