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Background: Although high mobility group box protein 1 (HMGB1) has been researched in relation to cancer in many investigations, a thorough investigation of its role in pan-cancer has yet to be conducted. With the objective of bridging this gap, we delved into the functions of HMGB1 in various tumors. Methods: This investigation employed The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases to examine HMGB1 gene expression differences and correlation with survival across various human tumors. Then, genetic alterations of HMGB1 were analyzed by tool cBioPortal, and immune cell infiltration was assessed. Finally, we gathered clinial samples from 95 patients with various types of solid tumor and performed somatic mutation analysis using panel sequencing. This further highlighted the role of HMGB1 in different solid tumors. Results: There was a notable elevation of HMGB1 gene expression in tumor tissues as opposed to non-cancerous tissues across the bulk of tumor types. Elevated HMGB1 gene expression had a connection with shorter overall survival, progression-free survival, and disease-free survival in specific tumor types. Genetic alterations of HMGB1 suggested that the amplifications and mutations of HMGB1 may impact the prognosis of breast cancer (BRCA) and liver hepatocellular carcinoma (LIHC). Both BRCA and mesothelioma (MESO) displayed a connection between the infiltration of cancer-associated fibroblasts (CAFs) and HMGB1 gene expression. Moreover, HMGB1 co-expression analysis revealed its association with genes involved in RNA splicing, mRNA processing, and modulation of mRNA metabolic processes. Additionally, a pathway analysis by use of the Kyoto Encyclopedia of Genes and Genomes (KEGG) unveiled that HMGB1 was implicated in the pathogenic mechanisms of ''Hepatitis B,'' ''Viral Carcinogenesis,'' and ''Hepatocellular Carcinoma.'' Based on somatic mutation analysis of 95 patients with different solid tumors, we found that the frequency of HMGB1 mutations was higher in Liver cancer patients compared to other solid tumors. This finding is consistent with our in-silico study results. Additionally, we discovered that the frequency of HMGB1 mutations ranked among the top 20 mutated genes in the 95 patients’ data, indicating that HMGB1 plays an important role in the development and prognosis of various solid tumors. Conclusion: This pan-cancer study of HMGB1 underscores its potential as a signature marker and target for the management of various tumor types.

Abstract The methods of QCD sum rules and light-cone sum rules within the framework of heavy quark effective theory have been widely applied to study the singly heavy baryons, and especially, we have applied these methods to predict not only the mass and width of the $$\varXi _b(6087)^0$$ Ξ b ( 6087 ) 0 recently discovered by LHCb, but also its observation channel and its mass difference from the $$\varXi _b(6100)^-$$ Ξ b ( 6100 ) - . We apply the same approach to perform a complete study on the P-wave bottom baryons of the SU(3) flavor $${\bar{\textbf{3}}}_F$$ 3 ¯ F and investigate their fine structure. Besides the $$\varLambda _b(5912)^0$$ Λ b ( 5912 ) 0 , $$\varLambda _b(5920)^0$$ Λ b ( 5920 ) 0 , $$\varXi _b(6087)^0$$ Ξ b ( 6087 ) 0 , and $$\varXi _b(6100)^-$$ Ξ b ( 6100 ) - , our results suggest the existence of the other two $$\varLambda _b$$ Λ b and two $$\varXi _b$$ Ξ b baryons, whose widths are limited. They are the $$\varLambda _b(J^P = 3/2^-)$$ Λ b ( J P = 3 / 2 - ) with the mass and width about $$(5.93^{+0.13}_{-0.13}~\textrm{GeV},\,0.0^{+12.0}_{-~0.0}~\textrm{MeV})$$ ( 5 . 93 - 0.13 + 0.13 GeV , 0 . 0 - 0.0 + 12.0 MeV ) , the $$\varLambda _b(5/2^-)$$ Λ b ( 5 / 2 - ) with $$(5.94^{+0.13}_{-0.13}~\textrm{GeV},\,\approx 0~\textrm{MeV})$$ ( 5 . 94 - 0.13 + 0.13 GeV , ≈ 0 MeV ) , the $$\varXi _b(3/2^-)$$ Ξ b ( 3 / 2 - ) with $$(6.10^{+0.15}_{-0.10}~\textrm{GeV},\, 1.4{^{+11.6}_{-~1.4}}~\textrm{MeV})$$ ( 6 . 10 - 0.10 + 0.15 GeV , 1.4 - 1.4 + 11.6 MeV ) , and the $$\varXi _b(5/2^-)$$ Ξ b ( 5 / 2 - ) with $$(6.11^{+0.15}_{-0.10}~\textrm{GeV},\,1.0{^{+7.4}_{-1.0}}~\textrm{MeV})$$ ( 6 . 11 - 0.10 + 0.15 GeV , 1.0 - 1.0 + 7.4 MeV ) . Their mass splittings are calculated to be $$M_{\varLambda _b(5/2^-)} - M_{\varLambda _b(3/2^-)} = 17\pm 7~\textrm{MeV}$$ M Λ b ( 5 / 2 - ) - M Λ b ( 3 / 2 - ) = 17 ± 7 MeV and $$M_{\varXi _b(5/2^-)} - M_{\varXi _b(3/2^-)} = 14\pm 7~\textrm{MeV}$$ M Ξ b ( 5 / 2 - ) - M Ξ b ( 3 / 2 - ) = 14 ± 7 MeV . All these baryons are explained as the P-wave bottom baryons of the $$\rho $$ ρ -mode, where the orbital excitation is between the two light quarks. However, the existence of this mode is still controversial, so their experimental searches can verify both our approach and the existence of the $$\rho $$ ρ -mode, which can significantly improve our understanding on the internal structure of hadrons.

Abstract Background Williams syndrome is an autosomal dominant multisystem disorder caused by a 1.5–1.8 Mb deletion on chromosome 7q11.23. It is characterized by facial deformations, cardiovascular abnormalities, developmental delays, gastrointestinal manifestations, and endocrine disorders. Case description A 1‐year‐old child presenting with developmental delays, special facial features, gastrointestinal bleeding, renal calcium deposition, and hypotonia was admitted to the hospital for “hypercalcemia and gastrointestinal bleeding.” Genetic testing showed a deletion mutation in the 7q11.23 region. Currently, the child receiving treatment to promote calcium excretion and rehabilitation training, but hypercalcemia has recurred. Conclusion The clinical phenotype of Williams syndrome is complex, and different severities, characterized by developmental delays, facial deformities, cardiovascular abnormalities, gastrointestinal symptoms and endocrine disorders, should be considered in children. The syndrome may require thorough genetic testing for diagnosis and early intervention treatment to improve patient quality of life.

BackgroundRecurrence is considered a vital problem for assessing the prognosis of Henoch–Schonlein purpura (HSP). The objective of this study was to evaluate factors affecting the recurrence in children with HSP.MethodsWe retrospectively reviewed records of 368 patients under the age of 16 years diagnosed with HSP from October 2019 to December 2020 in Beijing Children's Hospital. Patients were divided into a non-recurrence group and a recurrence group according to whether there was a recurrence. Incidence of manifestation, possible cause, age, and treatment were retrospectively analyzed. Univariate and multivariate logistic regression analyses were used to determine the risk factors of recurrence in HSP.ResultsPercentages of patients were 65.2% for the non-recurrence group and 34.8% for the recurrence group. The percentage of patients with renal involvement was significantly higher in the recurrence group (40.6%) than in the non-recurrence group (26.3%). Respiratory tract infection was the most frequent trigger: 67.5% in the non-recurrence group and 66.4% in the recurrence group. Recurrence was more likely to occur in patients aged >6 years (53.3% vs. 71.9%). Logistic regression analysis revealed that hematuria plus proteinuria was an independent risk factor for the recurrence of HSP. Conversely, animal protein, exercise restriction, and age ≤6 years were independent favorable factors for the non-recurrence of HSP.ConclusionThese results suggest that organ involvement, exercise, and diet management during the initial episode of HSP should be strictly monitored for children with HSP. Adequate clinical intervention for these risk factors may limit or prevent HSP recurrence. Moreover, renal involvement is associated with the long-term prognosis of HSP.

Abstract Background Various stimuli, including Clonorchis sinensis infection, can cause liver fibrosis. Liver fibrosis is characterized by the activation of hepatic stellate cells (HSCs) with massive production of extracellular matrix (ECM). Our previous study showed that the TGF-β1-induced Smad signaling pathway played a critical role in the activation of HSCs during liver fibrosis induced by worm infection; however, the mechanisms that modulate the TGF-β/Smad signaling pathway are still poorly understood. Accumulating evidence demonstrates that miRNAs act as an important regulator of activation of HSCs during liver fibrosis. Methods The target of miR-497 was determined by bioinformatics analysis combined with a dual-luciferase activity assay. LX-2 cells were transfected with miR-497 inhibitor and then stimulated with TGF-β1 or excretory/secretory products of C. sinensis (CsESPs), and activation of LX-2 was assessed using qPCR or western blot. In vivo, the mice treated with CCl4 were intravenously injected with a single dose of adeno-associated virus serotype 8 (AAV8) that overexpressed anti-miR-497 sequences or their scramble control for 6 weeks. Liver fibrosis and damage were assessed by hematoxylin and eosin (H&E) staining, Masson staining, and qPCR; the activation of the TGF-β/Smad signaling pathway was detected by qPCR or western blot. Results In the present study, the expression of miR-497 was increased in HSCs activated by TGF-β1 or ESPs of C. sinensis. We identified that Smad7 was the target of miR-497 using combined bioinformatics analysis with luciferase activity assays. Transfection of anti-miR-497 into HSCs upregulated the expression of Smad7, leading to a decrease in the level of p-Smad2/3 and subsequent suppression of the activation of HSCs induced by TGF-β1 or CsESPs. Furthermore, miR-497 inhibitor delivered by highly-hepatotropic (rAAV8) inhibited TGF-β/smads signaling pathway by targeting at Smad7 to ameliorate CCL4-induced liver fibrosis. Conclusions The present study demonstrates that miR-497 promotes liver fibrogenesis by targeting Smad7 to promote TGF-β/Smad signaling pathway transduction both in vivo and in vitro, which provides a promising therapeutic strategy using anti-miR-497 against liver fibrosis. Graphical Abstract

Abstract Background Microglia activation induced by α-synuclein (α-syn) is one of the most important factors in Parkinson’s disease (PD) pathogenesis. However, the molecular mechanisms by which α-syn exerts neuroinflammation and neurotoxicity remain largely elusive. Targeting metabotropic glutamate receptor 5 (mGluR5) has been an attractive strategy to mediate microglia activation for neuroprotection, which might be an essential regulator to modulate α-syn-induced neuroinflammation for the treatment of PD. Here, we showed that mGluR5 inhibited α-syn-induced microglia inflammation to protect from neurotoxicity in vitro and in vivo. Methods Co-immunoprecipitation assays were utilized to detect the interaction between mGluR5 and α-syn in microglia. Griess, ELISA, real-time PCR, western blotting, and immunofluorescence assays were used to detect the regulation of α-syn-induced inflammatory signaling, cytokine secretion, and lysosome-dependent degradation. Results α-syn selectively interacted with mGluR5 but not mGluR3, and α-syn N terminal deletion region was essential for binding to mGluR5 in co-transfected HEK293T cells. The interaction between these two proteins was further detected in BV2 microglia, which was inhibited by the mGluR5 specific agonist CHPG without effect by its selective antagonist MTEP. Moreover, in both BV2 cells and primary microglia, activation of mGluR5 by CHPG partially inhibited α-syn-induced inflammatory signaling and cytokine secretion and also inhibited the microglia activation to protect from neurotoxicity. We further found that α-syn overexpression decreased mGluR5 expression via a lysosomal pathway, as evidenced by the lysosomal inhibitor, NH4Cl, by blocking mGluR5 degradation, which was not evident with the proteasome inhibitor, MG132. Additionally, co-localization of mGluR5 with α-syn was detected in lysosomes as merging with its marker, LAMP-1. Consistently, in vivo experiments with LPS- or AAV-α-syn-induced rat PD model also confirmed that α-syn accelerated lysosome-dependent degradation of mGluR5 involving a complex, to regulate neuroinflammation. Importantly, the binding is strengthened with LPS or α-syn overexpression but alleviated by urate, a potential clinical biomarker for PD. Conclusions These findings provided evidence for a novel mechanism by which the association of α-syn with mGluR5 was attributed to α-syn-induced microglia activation via modulation of mGluR5 degradation and its intracellular signaling. This may be a new molecular target for an effective therapeutic strategy for PD pathology.

Abstract Background Dyslipidemia is a major risk factor for atherosclerotic cardiovascular disease and a leading cause of death worldwide. The clinical utility of commonly used lipid-lowering drugs such as statins and fibrates is sometimes limited by the occurrence of various adverse reactions. Recently, berberine (BBR) has received increasing attention as a safer and more cost-effective option to manage dyslipidemia. Thus, a high-quality randomized controlled trial to evaluate the efficacy and safety of BBR in the treatment of dyslipidemia is deemed necessary. Methods/design This is a randomized, double-blind, and placebo-controlled clinical trial. A total of 118 patients with dyslipidemia will be enrolled in this study and randomized into two groups at a ratio of 1:1. BBR or placebo will be taken orally for 12 weeks. The primary outcome is the percentage of low-density lipoprotein cholesterol reduction at week 12. Other outcome measures include changes in other lipid profiles, high sensitivity C-reactive protein, blood pressure, body weight, Bristol Stool Chart, traditional Chinese medicine symptom form, adipokine profiles, and metagenomics of intestinal microbiota. Safety assessment includes general physical examination, blood and urine routine test, liver and kidney function test, and adverse events. Discussion This trial may provide high-quality evidence on the efficacy and safety of BBR for dyslipidemia. Importantly, the findings of this trial will help to identify patient and disease characteristics that may predict favorable outcomes of treatment with BBR and optimize its indication for clinical use. Trial registration Chinese Clinical Trial Registry ChiCTR1900021361 . Registered on 17 February 2019.

Abstract Extracellular vesicles (EVs), a class of heterogeneous membrane vesicles, are generally divided into exosomes and microvesicles on basis of their origination from the endosomal membrane or the plasma membrane, respectively. EV-mediated bidirectional communication among various cell types supports cancer cell growth and metastasis. EVs derived from different cell types and status have been shown to have distinct RNA profiles, comprising messenger RNAs and non-coding RNAs (ncRNAs). Recently, ncRNAs have attracted great interests in the field of EV-RNA research, and growing numbers of ncRNAs ranging from microRNAs to long ncRNAs have been investigated to reveal their specific functions and underlying mechanisms in the tumor microenvironment and premetastatic niches. Emerging evidence has indicated that EV-RNAs are essential functional cargoes in modulating hallmarks of cancers and in reciprocal crosstalk within tumor cells and between tumor and stromal cells over short and long distance, thereby regulating the initiation, development and progression of cancers. In this review, we discuss current findings regarding EV biogenesis, release and interaction with target cells as well as EV-RNA sorting, and highlight biological roles and molecular mechanisms of EV-ncRNAs in cancer biology.

Abstract The heavy baryon system bounded by the strong interaction has a rich internal structure, so its mass spectra can have the fine structure similar to the line spectra of atom bounded by the electromagnetic interaction. We systematically study the internal structure of P-wave $$\varOmega _b$$ Ωb baryons and calculate their D-wave decay properties. The present study, together with our previous studies on their mass spectra and S-wave decay properties, suggest that all the four excited $$\varOmega _b$$ Ωb baryons recently discovered by LHCb can be well explained as P-wave $$\varOmega _b$$ Ωb baryons, and their beautiful fine structure is directly related to the rich internal structure of P-wave $$\varOmega _b$$ Ωb baryons.

Abstract We use the method of light-cone sum rules to study decay properties of P-wave bottom baryons belonging to the SU(3) flavor $$\mathbf {6}_F$$ 6F representation. In Cui et al. (Phys Rev D 99:094021, 2019) we have studied their mass spectrum and pionic decays, and found that the $$\varSigma _{b}(6097)$$ Σb(6097) and $$\varXi _{b}(6227)$$ Ξb(6227) can be well interpreted as P-wave bottom baryons of $$J^P = 3/2^-$$ JP=3/2- . In this paper we further study their decays into ground-state bottom baryons and vector mesons. We propose to search for a new state $$\varXi _b({5/2}^-)$$ Ξb(5/2-) , that is the $$J^P = 5/2^-$$ JP=5/2- partner state of the $$\varXi _{b}(6227)$$ Ξb(6227) , in the $$\varXi _b({5/2}^-) \rightarrow \varXi _b^{*}\rho \rightarrow \varXi _b^{*}\pi \pi $$ Ξb(5/2-)→Ξb∗ρ→Ξb∗ππ decay process. Its mass is $$12 \pm 5$$ 12±5 MeV larger than that of the $$\varXi _{b}(6227)$$ Ξb(6227) .

Studies have shown that teachers’ wellbeing has a positive effect on teachers’ learning quality and learners’ performance. Nevertheless, teaching is a stressful and exhausting profession at all academic level with special difficulties about the nature of language education. Tension and fear are still classic challenges in learning, though the concepts such as hope and optimism are core issues in assisting teachers to feel happy during instruction and work longer. The present review makes efforts to provide the most current confirmation on the interface of hope and optimism with educational issues since they are progressively documented as significant emotional capitals for educational success, job growth, and presentation. It is worth mentioning that the current review of research can benefit educational administrations, and other stakeholders and officials in the educational community to contemplate the functions of constructive emotions in the process of learning to decrease and even diminish stress and apprehension that consequently lead to flourishing.

Abstract Background Celiac disease (CD) is characterized histologically by inflammation and villous atrophy. Villous atrophy is thought to result from a disruption of epithelial cellular proliferation and death. Epithelial cells in intestinal mucosa normally proliferate in the crypts and migrate towards the lumen, eventually dying. Apoptotic bodies in crypts are usually abnormal and are associated with certain disease states. The presence of crypt apoptosis in celiac disease has not been thoroughly examined by routine histologic assessment of crypt apoptotic body count (ABC). Methods We quantified the ABC in duodenal biopsies from celiac patients before and after initiation of a gluten-free diet (GFD). We examined twenty-three duodenal biopsies from adult patients with celiac disease at diagnosis and following GFD and determined the maximum ABC in 10 consecutive crypts. Fourteen biopsies from heartburn patients served as controls. Results Mean duration between paired biopsies was 2.9 (0.5–8.5) years. Mean maximum ABC in active celiac disease was 5.44 per crypt and decreased to 2.60 with GFD (p =

Abstract We apply the method of QCD sum rules to study the structure X newly observed by the BESIII Collaboration in the $$\phi \eta ^\prime $$ ϕη′ mass spectrum in 2.0–2.1 GeV region in the $$J/\psi \rightarrow \phi \eta \eta ^\prime $$ J/ψ→ϕηη′ decay. We construct all the $$s s {\bar{s}} {\bar{s}}$$ sss¯s¯ tetraquark currents with $$J^{PC} = 1^{+-}$$ JPC=1+- , and use them to perform QCD sum rule analyses. One current leads to reliable QCD sum rule results and the mass is extracted to be $$2.00^{+0.10}_{-0.09}$$ 2.00-0.09+0.10 GeV, suggesting that the structure X can be interpreted as an $$s s {\bar{s}} {\bar{s}}$$ sss¯s¯ tetraquark state with $$J^{PC} = 1^{+-}$$ JPC=1+- . The Y(2175) can be interpreted as its $$s s {\bar{s}} {\bar{s}}$$ sss¯s¯ partner having $$J^{PC} = 1^{--}$$ JPC=1-- , and we propose to search for the other two partners, the $$s s {\bar{s}} {\bar{s}}$$ sss¯s¯ tetraquark states with $$J^{PC} = 1^{++}$$ JPC=1++ and $$1^{-+}$$ 1-+ , in the $$\eta ^\prime f_0(980)$$ η′f0(980) , $$\eta ^\prime K {\bar{K}}$$ η′KK¯ , and $$\eta ^\prime K {\bar{K}}^*$$ η′KK¯∗ mass spectra.

Mice with different genetic backgrounds have various susceptibilities to infection with Clonorchis sinensis, although the mechanisms underlying are largely unknown. Toll-like receptor 4 (TLR4) as one of the most important pattern recognition receptors (PPRs) is essential for the invasion, survival, pathogenesis, and elimination of worms. The roles played by TLR4 in C. sinensis infection may vary due to the different genetic backgrounds of mice. In the present study, a relatively resistant mouse strain-C57BL/10 to C. sinensis was used for investigation on the possible roles of TLR4 in the biliary injuries and peribiliary fibrosis. TLR4 wild type (TLR4wild) and TLR4 defective (TLR4def) mice were orally infected with 45 metacercariae of C. sinensis, and all C. sinensis-infected mice and non-infected groups were anesthetized on day 28 post-infection. The liver and serum from each mouse were collected for assessment of the biliary injuries and biliary fibrosis. Meanwhile, hepatic leukocytes were isolated and detected for the activation of M1 or M2 macrophage using flow cytometry. The hepatic type 1 immune response and type 2 immune responses -relative molecules were also evaluated using ELISA and quantitative PCR. The data showed that TLR4def aggravated liver inflammatory cell infiltrations, bile duct proliferation, biliary and hepatocellular injuries, and ECM deposition in C. sinensis-infected mice, compared with TLR4wild mice when they were intragastrically administered with the same amounts of C. sinensis metacercaria. Furthermore, the M2-like macrophages and type 2 immune responses were significantly predominant induced in TLR4def mice, compared with that of TLR4wild mice following C. sinensis infection. But the type 1 immune response were significantly decreased in TLR4def mice, compared with TLR4wild mice after C. sinensis infection. These data demonstrate that TLR4 deficiency exacerbates biliary injuries and peribiliary fibrosis caused by C. sinensis in C57BL/10 strain mice, which is contributed by augments of type 2 immune responses and decrease pro-inflammatory responses.

Abstract Background Despite marked advances in our understanding of the pathophysiology of the coronary slow flow phenomenon (CSFP), the exact mechanism remains unclear. Previous studies have suggested that CSFP might be associated with generalized atherosclerosis, endothelial dysfunction, and low-grade chronic inflammation. High serum alkaline phosphatase (ALP) levels are associated with vascular calcification, atherosclerotic disease, and an increased risk of cardiovascular events. However, the relationship between ALP and CSFP is unclear. Methods We investigated 64 patients with angiographically proven CSFP and 50 with normal coronary flow. Serum ALP levels were measured in all studied individuals. Results Serum ALP levels in patients with CSFP were significantly higher than those in the control group (70.5 ± 17.1 vs. 61.9 ± 16.1 U/L, P = 0.007). A positive association was observed (r = 0.42, P = 0.032) between serum ALP levels and the mean thrombolysis in myocardial infarction frame count (mTFC). Regression analysis showed a high serum ALP level was the only independent predictor of the mTFC (β = 0.309, P 67.5 U/L was a predictor of CSFP (sensitivity = 83.3%, specificity = 84.1%). Conclusions Patients with CSFP show high serum ALP levels, which may be associated with the pathogenesis of CSFP. A high serum ALP level is a predictor of CSFP. Future studies are needed to clarify the role of ALP in patients with CSFP.

Abstract Background Multiple risk factors contribute to the progression of Parkinson’s disease, including oxidative stress and neuroinflammation. Epidemiological studies have revealed a link between higher urate level and a lower risk of developing PD. However, the mechanistic basis for this association remains unclear. Urate protects dopaminergic neurons from cell death induced by oxidative stress. Here, we investigated a novel role of urate in microglia activation in a lipopolysaccharide (LPS)-induced PD model. Methods We utilized Griess, ELISA, real-time PCR, Western blot, immunohistochemistry, and immunofluorescence to detect the neuroinflammation. For Griess, ELISA, Western blot, and immunofluorescence assay, cells were seeded in 6-well plates pre-coated with poly-l-lysine (PLL) and incubated for 24 h with the indicated drugs. For real-time PCR assay, cells were seeded in 6-well plates pre-coated with PLL and incubated for 6 h with the indicated drugs. For animal experiments, rats were injected with urate or its vehicle twice daily for five consecutive days before and after stereotaxic surgery. Rats were killed and brain tissues were harvested after 4 weeks of LPS injection. Results In cultured BV2 cells and rat primary microglia, urate suppressed proinflammatory cytokine production and inducible cyclooxygenase 2 and nitric oxide synthase expression to protect dopaminergic neurons from the toxic effects of activated microglia. The neuroprotective effects of urate may also be associated with the stimulation of anti-inflammatory factors interleukin 10 and transforming growth factor β1. Intracellular urate level was increased in a dose-dependent manner upon co-treatment with urate and LPS as compared with LPS alone, an effect that was abrogated by pretreatment with probenecid (PBN), an inhibitor of both glucose transporter 9 and urate transporter 1 (URAT1). PBN also abolished the anti-inflammatory effect of urate. Consistent with these in vitro observations, the number of tyrosine hydroxylase-positive neurons was decreased and the loss of motor coordination was reversed by urate administration in an LPS-induced rat model of PD. Additionally, increased plasma urate level abolished the reduction of URAT1 expression, the increase in the expression of interleukin-1β, and the number of ionized calcium-binding adaptor molecule 1-positive microglia along with changes in their morphology. Conclusions Urate protects neurons against cytotoxicity induced by microglia activation via modulating urate transporter-mediated intracellular urate level.

The objective of this study was to evaluate the effects on chemical and microbiological properties of paddy soil of short-term biochar, straw, and chemical fertilizers compared with chemical fertilization alone. Five soil fertilization treatments were evaluated: regular chemical fertilizers (RF), straw+regular chemical fertilizers (SRF), straw biochar+regular chemical fertilizers (SCRF), bamboo biochar (BC)+regular chemical fertilizers (BCRF), and straw biochar+70% regular chemical fertilizers (SC+70%RF). Their effects were investigated after approximately 1.5 years. The soil pH and cation exchange capacity (CEC) were significantly higher in biochar-treated soils. The soil phosphorous (P) and potassium (K) contents increased with biochar application. The soil Colwell P content was significantly increased with the addition of straw biochar in the treatments of SCRF and SC+70%RF. The oxygen (0):carbon (C) ratio doubled in BC picked from the soil. This indicated that BC underwent a significant oxidation process in the soil. The denaturing gradient gel electrophoresis (DGGE) fingerprints of microbial communities differed among the treatments. Soils with added biochar had higher Shannon diversity and species richness indices than soils without biochars. The results suggest that biochar can improve soil fertility.

Mucinous cystic neoplasm (MCN) is characterized by mucinous epithelial lining and subepithelial ovarian-like stroma and is a precursor to invasive carcinoma. Type 1 autoimmune pancreatitis (AIP), on the other hand, is a form of IgG4-related disease (IgG4-RD) and can present as a pancreatic mass. There is no known causal relationship between these two entities in the current literature. Here, we report a case of a middle-aged female patient who was found to have an enlarging pancreatic mass and subsequently underwent a distal pancreatectomy. Gross examination of the pancreatectomy specimen showed a 4.3 cm mass with a central 3.4 cm cystic component, confirmed to be an MCN on microscopy. The immediately adjacent peritumoral tissue showed storiform fibrosis, obliterative phlebitis, and focal IgG4-positive plasma cell–rich infiltrates (≥75/HPF) with an IgG4+/IgG+ ratio of 80%. The background pancreas was histologically normal and these characteristic AIP findings were limited to the pericystic tissue. Clinical workup with CT scan and MRI did not show any evidence of systemic IgG4-RD, nor was the serum IgG4 level ever elevated. To our knowledge, this is only the second reported case of a pancreatic MCN associated with peritumoral AIP-like changes in a patient without systemic IgG4-RD. Awareness of these potential AIP-like changes surrounding pancreatic neoplasms may be helpful in preventing misdiagnosis in needle biopsy and aspiration specimens. Keywords: Type 1 autoimmune pancreatitis, IgG4-related disease, IgG4-RD, IgG4-related pancreatitis, Mucinous cystic neoplasm, MCN, Sclerosing pancreatitis

Objective: To determine the prevalence and genotype distribution of HPV in Guangzhou in last year in order to provide the latest evidence for the prevention and treatment of HPV infection. Methods: HPV types and their correlations with gender, age and HIV were retrospectively analyzed in 3 014 samples from our hospital from January to December, 2018. Results: A total of 3 014 patients, including 730 (24.22%) males and 2 284 (75.78%) females, were included in the analysis. Common types were HPV6, 11, 16, 52 and 58, accounting for 8.36% (252/3014), 7.83% (236/3014), 6.74% (203/3014), 5.97% (180/3014) and 4.64% (140/3014), respectively. In males, 67.81% (495/730) were HPV positive (P0.05). Higher positive rates of HPV were found in age groups of 15~24 and 65~74 years, depicting a trend of "U" shape over age groups. Among 345 out of 3 014 patients with HIV positive, 84.06% (290/345) were HPV positive (P0.05). Conclusions: The most common types of HPV in Guangzhou are HPV 6, 11, 16, 52 and 58 in the last year. The prevalence of HPV is related to gender, age and HIV infection. Strengthening the prevention and treatment of HIV infection are critical for reduction of the HPV infection in Guangzhou.

Background: Atopic dermatitis (AD) is an inflammatory skin disease characterized by chronic recurrent dermatitis with profound itching. Most patients have personal and/or family history of atopic diseases. Several criteria have been proposed for the diagnosis of AD. Although the clinical features of childhood AD have been widely studied, there has been less large-scale study on adult/adolescent AD. The aim of this study was to investigate the clinical features of adult/adolescent patients with chronic symmetrical eczema/AD and to propose Chinese diagnostic criteria for adult/adolescent AD. Methods: A hospital-based study was performed. Forty-two dermatological centers participated in this study. Adult and adolescent patients (12 years and over) with chronic symmetrical eczema or AD were included in this study. Questionnaires were completed by both patients and investigators. The valid questionnaires were analyzed using EpiData 3.1 and SPSS 17.0 software. Results: A total of 2662 valid questionnaires were collected (1369 male and 1293 female). Of all 2662 patients, 2062 (77.5%) patients had the disease after 12 years old, while only 600 (22.5%) patients had the disease before 12 years old, suggesting late-onset eczema/AD is common. Two thousand one hundred and thirty-nine (80.4%) patients had the disease for more than 6 months. One thousand one hundred and forty-four (43.0%) patients had a personal and/or family history of atopic diseases. One thousand five hundred and forty-eight (58.2%) patients had an elevated total serum IgE and/or eosinophilia and/or positive allergen-specific IgE. Based on these clinical and laboratory features, we proposed Chinese criteria for adult/adolescent AD. Of all 2662 patients, 60.3% were satisfied with our criteria, while only 48.2% satisfied with Hanifin Rajka criteria and 32.7% satisfied with Williams criteria, suggesting a good sensitivity of our criteria in adult/adolescent AD patients. Conclusion: Late-onset of eczema or AD is common. The clinical manifestations of AD are heterogeneous. We have proposed Chinese diagnostic criteria for adolescent and adult AD, which are simple and sensitive for diagnosis of adult/adolescent AD.

We study the Λ b ( 6146 ) 0 and Λ b ( 6152 ) 0 recently observed by LHCb using the method of Quantum Chromodynamics (QCD) sum rules within the framework of heavy quark effective theory. Our results suggest that they can be interpreted as D-wave bottom baryons of J P = 3 / 2 + and 5 / 2 + respectively, both of which contain two λ -mode excitations. We also investigate other possible assignments containing ρ -mode excitations. We extract all the parameters that are necessary to study their decay properties when using the method of light-cone sum rules. We predict masses of their strangeness partners to be m Ξ b ( 3 / 2 + ) = 6.26 − 0.14 + 0.11 GeV and m Ξ b ( 5 / 2 + ) = 6.26 − 0.14 + 0.11 GeV with the mass splitting Δ M = m Ξ b ( 5 / 2 + ) − m Ξ b ( 3 / 2 + ) = 4.5 − 1.5 + 1.9 MeV, and propose to search for them in future CMS, EIC, and LHCb experiments.

The paper proposes an analytical framework for evaluating, in the case of interrupted conditions, the effect of bus bridging services on the degree of connectivity of rail networks. The average travel time is used to compare a normal network and an interrupted rail network. Different situations in interrupted rail network are compared with a normal network, namely, making passengers wait for troubleshooting, detouring them to other routes, and the bus bridging service strategy. The study uses ratios of average travel time under various situations to assess the connectivity of interrupted rail transit. The approach is applied to a case study based on the Beijing public transit system and actual travel data. It found that bus bridging is a relatively effective method of enhancing the connectivity of metro network and minimizing delays. In particular, key factors such as the behavior of affected passengers, the willingness to use bus bridging service, and transfer passenger, which influence connectivity of interrupted rail networks with bus bridging services, are provided.

Background and Aim: Patients suspected of Alpha 1-Antitrypsin (A1AT) abnormality based on low serum concentration are routinely confirmed through polymerase chain reaction (PCR) testing of peripheral blood. Genotyping formalin- fixed paraffin-embedded (FFPE) tissue is a novel approach that could aid in detecting variant A1AT. We performed qPCR on FFPE liver explants with Periodic Acid Schiff after Diastase (PASD)- and A1AT-positive globules to confirm and estimate the frequency of A1AT deficiency in transplant cases. Materials and Methods: Eighteen (12.68%) of 142 patients with end-stage liver disease showed PASD/A1AT positive globules. FFPE of the explants was tested through qPCR to detect S and Z alleles. A second age- and sex-matched control group consisting of five liver transplant patients with negative globules was included in the study. Results: qPCR assay was successful with all the samples meeting QC parameters. All patients included in the study elucidated Z allele variants; 2 homozygous (11.1%) and 16 heterozygous (88.9%). The control group demonstrated normal wild-type MM allele. Conclusion: Screening for A1AT deficiency using serum levels is not sufficiently sensitive to detect deficiency, especially in carriers. If A1AT testing was not performed preoperatively and the risk is high based on the PASD/ A1AT-positive globules in the explants, then molecular testing of FFPE tissue can be a viable method for confirming the diagnosis. [ABSTRACT FROM AUTHOR]