Reporting guidelines for traditional Chinese medicine could be improved: a cross-sectional study.

OBJECTIVES: The aim of this study is to identify available reporting guidelines for traditional Chinese medicine (TCM), delineate their fundamental characteristics, assess the scientific rigor of their development process, and evaluate their dissemination. STUDY DESIGN AND SETTING: A search was conducted in Medline (via PubMed), China National Knowledge Infrastructure (CNKI), SinoMed, WANFANG DATA, and the EQUATOR Network to identify TCM reporting guidelines. A preprepared Excel database was used to extract information on the basic characteristics, development process, and dissemination information. The development process quality of TCM reporting guidelines was assessed by evaluating their compliance with the Guidance for Developers of Health Research Reporting Guidelines (GDHRRG). The extent of dissemination of these guidelines was analyzed by examining the number of citations received. RESULTS: A total of 26 reporting guidelines for TCM were obtained from 20 academic journals, with 61.5% of them published in English journals. Among the guidelines, 14 (53.8%) were registered in the EQUATOR Network. On average, the compliance rate of GDHRRG guidelines was reported to be 63.3% ranging from 22.2% to 94.4%. Three steps showed poor compliance, namely guideline endorsement (23.1%), translated guidelines (19.2%), and developing a publication strategy (19.2%). Furthermore, the compliance rate of GDHRRG guidelines published in English journals was higher than that in Chinese journals. In terms of the dissemination, 15.4% of the guidelines had been cited over 100 times, while 73.1% had been cited less than 50 times. CONCLUSION: The development of TCM reporting guidelines still has limitations in terms of regarding scientific rigor and follow-up dissemination. Therefore, it is important to ensure adherence to the scientific process in the development of TCM reporting guidelines and to strengthen their promotion, dissemination, and implementation.

Microplastic-induced NAFLD: Hepatoprotective effects of nanosized selenium.

Polystyrene microplastics (MPs) are persistent environmental pollutants commonly encountered in daily human life. Numerous studies have demonstrated their ability to induce liver damage, including oxidative stress, inflammation, and lipid accumulation. However, limited information exists regarding preventive measures against this issue. In our study, we investigated the potential preventive role of selenium nanoparticles (YC-3-SeNPs) derived from Yak-derived Bacillus cereus, a novel nanobiomaterial known for its antioxidant properties and lipid metabolism regulation. Using transcriptomic and metabolomic analyses, we identified key genes and metabolites associated with oxidative stress and lipid metabolism imbalance induced by MPs. Upregulated genes (Scd1, Fasn, Irs2, and Lpin) and elevated levels of arachidonic and palmitic acid accumulation were observed in MP-exposed mice, but not in those exposed to SeNPs. Further experiments confirmed that SeNPs significantly attenuated liver lipid accumulation and degeneration caused by MPs. Histological results and pathway screening validated our findings, revealing that MPs suppressed the Pparα pathway and Nrf2 pathway, whereas SeNPs activated both pathways. These findings suggest that MPs may contribute to the development of nonalcoholic fatty liver disease (NAFLD), while SeNPs hold promise as a future nanobio-product for its prevention.

Association between primary Sjögren's syndrome and gut microbiota disruption: a systematic review and meta-analysis.

Evidence of gut microbiota disruption for numerous autoimmune diseases has accumulated. Recently, the relationship between the microbiota and primary Sjögren's disease has been increasingly investigated but has yet to be systematically elucidated. Therefore, a meta-analysis of publications dealing on topic was conducted. Case-control studies comparing primary Sjögren's syndrome patients and healthy controls (HCs) were systematically searched in nine databases from inception to March 1, 2023. The primary result quantitatively evaluated in this meta-analysis was the α-diversity. The secondary results qualitatively extracted and analyzed were the ß-diversity and relative abundance. In total, 22 case-control studies covering 915 pSS patients and 2103 HCs were examined. The quantitative analysis revealed a slight reduction in α-diversity in pSS patients compared to HCs, with a lower Shannon-Wiener index (SMD = - 0.46, (- 0.68, - 0.25), p < 0.0001, I2 = 71%), Chao1 richness estimator (SMD = - 0.59, (- 0.86, - 0.32), p < 0.0001, I2 = 81%), and ACE index (SMD = - 0.92, (- 1.64, - 0.19), p = 0.01, I2 = 86%). However, the Simpson index (SMD = 0.01, (- 0.43, 0.46) p = 0.95, I2 = 86%) was similar in the two groups. The ß-diversity significantly differed between pSS patients and HCs. Variations in the abundance of specific microbes and their metabolites and potential functions contribute to the pSS pathogenesis. Notably, the abundance of the phylum Firmicutes decreased, while that of Proteobacteria increased. SCFA-producing microbes including Ruminococcaceae, Lachnospiraceae, Faecalibacterium, Butyricicoccus, and Eubacterium hallii were depleted. In addition to diversity, the abundances of some specific microbes were related to clinical parameters. According to this systematic review and meta-analysis, gut microbiota dysbiosis, including reduced diversity, was associated with proinflammatory bacterium enrichment and anti-inflammatory bacterium depletion in pSS patients. Further research on the relationship between the gut microbiota and pSS is warranted.

A new application of nano-selenium: rescue of CK2 and mitochondria from oxidative stress to prevent cardiac hypertrophy.

Background: Excessive reactive oxygen species (ROS) and subsequent mitochondrial dysfunction are pivotal in initiating cardiac hypertrophy. To explore nano-selenium's (SeNP's) preventive potential against this condition, the authors evaluated chemically synthesized chitosan-SeNPs and biosynthesized Bacillus cereus YC-3-SeNPs in an angiotensin II (Ang II)-induced cardiac hypertrophy model. Methods: This investigation encompassed ROS measurement, mitochondrial membrane potential analysis, transmission electron microscopy, gene and protein expression analyses, protein carbonylation assays, serum antioxidant quantification and histological staining. Results: SeNPs effectively countered Ang II-induced cardiac hypertrophy by reducing ROS, restoring mitochondrial and protein kinase 2α (CK2-α) function, activating antioxidant pathways and enhancing serum antioxidant levels. Conclusion: This finding underscores SeNPs' role in attenuating Ang II-induced myocardial hypertrophy both in vitro and in vivo.

Enlargement of the heart is called cardiac hypertrophy; this is caused by too many reactive oxygen species, which are compounds that damage the mitochondria of cells. The mitochondria provide energy to cells and their disruption can cause a significantly negative effect on cells and the tissues and organs cells make up. Selenium is a type of metal that must be consumed in small amounts to stay healthy; it has antioxidant effects, meaning it can stop reactive oxygen species and potentially prevent cardiac hypertrophy. Nano-selenium (SeNP), consisting of tiny, spherical particles containing selenium, may be a more effective way of delivering selenium as an antioxidant to prevent cardiac hypertrophy. SeNPs were made synthetically and from a type of bacterium called Bacillus cereus; both SeNPs demonstrated antioxidant effects in heart cells taken from chicken embryos and live chickens. These results suggest that SeNPs could be developed into medication to combat cardiac hypertrophy.

Integrated Analysis Identifies Upregulated SAMD9L as a Potential Biomarker Correlating with the Severity of Primary Sjögren's Syndrome.

Background: Primary Sjögren's syndrome (pSS) is an autoimmune disease with lymphocytic infiltration of the salivary and lachrymal glands, whose present disease-specific objective indicators are few and have shortcomings that should be addressed. An integrated analysis of sequencing data from different cohorts has the potential to unveil novel biomarkers in pSS. Methods: We identified 3 GEO datasets, including gene expression data from minor salivary gland (MSG) biopsy samples of 49 patients with pSS and 31 non-pSS and whole blood cells of 30 pSS patients and 30 healthy controls (HCs). Differentially expressed genes (DEGs) involved in pSS were identified from these datasets. Function Enrichment Analyses of common upregulated DEGs and PPI (protein-protein interaction) networks were performed. Furthermore, we have carried out further analysis of these DEGs to explore their potential clinical significance and diagnostic efficacy as a biomarker for pSS. Sterile Alpha Motif Domain Containing 9 Like (SAMD9L), one of the DEGs, has been identified as a promising candidate biomarker that correlates with the severity of pSS. This has been validated by analyzing local clinical samples from 30 pSS and non-pSS patients' MSG biopsies, as well as serum samples of 18 pSS and HC individuals. Finally, we performed correlation analysis to understand the relationship between SAMD9L and infiltrated immune cells. Results: We identified 10 common highly expressed DEGs in pSS of different tissues. These genes were mainly involved in virus infection-related pathways and inferno-related pathways. GEO data and our clinical data showed that SAMD9L increases with disease severity. Public and local cohorts showed that SAMD9L has high diagnostic performance (AUC=0.845-0.867) as a biomarker, and its AUC was comparable to the Focus score when combined with RF or SSA. Conclusion: Up-regulated SAMD9L may serve as a promising novel pSS diagnostic biomarker and have potential value for evaluating the severity of pSS.

Preparation, characterization, and antioxidant and antiapoptotic activities of biosynthesized nano­selenium by yak-derived Bacillus cereus and chitosan-encapsulated chemically synthesized nano­selenium.

Nano­selenium (SeNPs) is a red elemental selenium with extremely small particles, which can be absorbed by the body and has biological activity. Currently, the most commonly used synthetic methods for SeNPs are biosynthesis and chemical synthesis. In this study, YC-3-SeNPs were biosynthesized by a strain of yak-gut Bacillus cereus YC-3, and meanwhile, CST-SeNPs were chemically synthesized and encapsulated with chitosan. A series of characterizations proved that YC-3-SeNPs and CST-SeNPs are spherical particles with excellent stability, and both have an excellent ability to scavenge free radicals in vitro. The particles of YC-3-SeNPs were encapsulated with polysaccharides, fiber, and protein, and it was less toxic than that of CST-SeNPs. Additionally, YC-3-SeNPs and CST-SeNPs may inhibit H2O2-induced oxidative stress in cardiomyocytes by activating the Keap1/Nrf2/HO-1 signaling pathway thereby scavenging ROS. Meanwhile, they may exert anti-apoptotic activity in cardiomyocytes by stabilizing mitochondrial membrane potential (∆Ψm) and balancing Bax/Bcl-2 protein, thereby reducing the protein expression of Cyt-c and Cleaved-caspase 3. Given the above, YC-3-SeNPs and CST-SeNPs with excellent antioxidant and anti-apoptotic activities may have broad application potential in the field of cardiovascular diseases.

Integrative Bioinformatics Analysis Identifies DDX60 as a Potential Biomarker for Systemic Lupus Erythematosus.

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease with strong heterogeneity, leading to variable clinical symptoms, which makes diagnosis and activity evaluation difficult. Methods: The original dataset of GSE88884 was analyzed to screen differentially expressed genes (DEGs) of SLE and the correlation between DEGs and clinical parameters (SLEDAI, anti-dsDNA, C3, and C4). The result was validated by microarray GSE121239 and SLE patients with RT-qPCR. Next, receiver operator characteristic (ROC) analysis, correlation analysis, and ordinal logistic regression were applied, respectively, to evaluate the capability of diagnosis and prediction of the candidate biomarker. Subsequently, the biological functions of the candidate biomarker were investigated through KEGG and GO enrichment, protein-protein interaction network, and the correlation matrix. Results: A total of 283 DEGs were screened, and seven of them were overlapped with SLE-related genes. DDX60 was identified as the candidate biomarker. Analyses of GSE88884, GSE121239, and SLE patients with RT-qPCR indicated that DDX60 expression level is significantly higher in patients with high disease activity. ROC analysis and the area under the ROC curve (AUC = 0.8818) suggested that DDX60 has good diagnostic performance. DDX60 expression level was positively correlated with SLEDAI scores (r = 0.24). For every 1-unit increase in DDX60 expression value, the odds of a higher stage of activity of SLE disease are multiplied by 1.47. The function of DDX60 mainly focuses on IFN-I-induced antiviral activities, RIG-I signaling, and innate immune. Moreover, DDX60 plays a synergistic role with DDX58, IFIH1, OASL, IFIT1, and other related genes in the SLE pathogenesis. Conclusions. DDX60 is differently expressed in SLE, and it is significantly related to both serological indicators and the disease activity of SLE. We suggested that DDX60 might be a potential biomarker for SLE diagnosis and management.

A new operation for gallstones: Choledochoscopic gallbladder-preserving cholecystolithotomy, a retrospective study of 3,511 cases.

BACKGROUND: Due to the influence of traditional Chinese culture, many cholelithiasis patients refuse to undergo cholecystectomy. This has prompted surgeons to consider a new treatment option for gallstones, which preserves the gallbladder, termed as choledochoscopic gallbladder-preserving cholecystolithotomy. In this study, we reviewed the clinical outcomes of 23 years of single-center application of choledochoscopic gallbladder-preserving cholecystolithotomy. METHODS: A total of 5,451 patients with chronic cholelithiasis were selected from 1992 to 2011 as per the inclusion criteria for the choledochoscopic gallbladder-preserving cholecystolithotomy study, and clinicopathological and follow-up data were collected from 4,340 patients who underwent successful choledochoscopic gallbladder-preserving cholecystolithotomy. The endpoints of the follow-up were recurrence of stones, loss to follow-up, patient death, removal of the gallbladder for other reasons, or end of follow-up in December 2015. RESULTS: All 4,340 cases underwent choledochoscopic gallbladder-preserving cholecystolithotomy with a mean procedure time of 79.6 ± 35.4 minutes, among which 3,511 (80.9%) received at least 1 follow-up. The recurrence rate of gallstones gradually increased with increasing follow-up duration, with a recurrence rate of 0.83% within 1 year after surgery and a maximal cumulative recurrence rate of 7.94% at 23 years. The 5-year cumulative recurrence rate of gallstones in the age group ≤20 years was 16.80%, which was significantly higher than those of other age groups, and the 5-year recurrence rate in the single gallstone group was 2.87%, which was significantly lower than that in the multiple gallstone group. Age and number of gallstones were independent risk factors for gallstone recurrence after choledochoscopic gallbladder-preserving cholecystolithotomy. CONCLUSION: The recurrence rate of gallstones after choledochoscopic gallbladder-preserving cholecystolithotomy is low, and most patients with recurrence are asymptomatic or have only mild symptoms. Age and number of gallstones were independent risk factors. Choledochoscopic gallbladder-preserving cholecystolithotomy is a safe and effective surgical option for gallstone removal in patients who do not wish to undergo cholecystectomy.

Evaluating the Similarity of Different Collagen-Induced Arthritis Models to the Pre-Clinical Phase of RA in Female Rats.

Since the development of RA is a multistep process, it is critical to take action to prevent RA in the pre-clinical phase. Animal models are currently one of the important methods to study RA, but there are very few animal models for studying the pre-clinical phase of RA (Pre-RA). This study aimed to evaluate the similarity of different collagen-induced arthritis models to Pre-RA in rats. Three types of collagen-induced arthritis (CIA) were as follows: (i) standard collagen-induced group (Std-CIA), injected with 200 µg type II collagen at day 0 and 100 µg type II collagen at day 7; (ii) single collagen-induced group (Mono-CIA), injected with 200 µg type II collagen at day 0; (iii) half-dose collagen-induced group (Half-CIA), injected with 100 µg type II collagen at day 0 and 50 µg type II collagen at day 7. Arthritis score, hind paw swelling, serum antibodies, and inflammatory cytokines were measured every 7 days. Gut microbiota analyses were performed on days 0, 11, 21, 28, and 35. Pain threshold measurement, digital radiography, and joint pathology were also assessed. Both Std-CIA and Mono-CIA could successfully cause RA symptoms, including joint swelling and bone erosion, Half-CIA induced only mild swelling in rats. Serum autoantibodies (anti-CCP and anti-CoII) showed no difference among the three types of CIA models, and so did the pain threshold at day 42. In addition, the pathological changes of joint tissues in the Mono-CIA group were the slightest among the collagen-immunized groups. Gut microbiota analysis demonstrated that Half-CIA could impose similar effects on upregulating genus Prevotella as Std-CIA, but Mono-CIA was weaker than them in rats. According to the characteristics of pre-RA, the Half-CIA model is the best suitable animal model for pre-RA among three types of CIA models in rats and can be a valuable model for pre-RA research.

Hexavalent Chromium Causes Apoptosis and Autophagy by Inducing Mitochondrial Dysfunction and Oxidative Stress in Broiler Cardiomyocytes.

Hexavalent chromium (Cr(VI)) is a common environmental pollutant, which has a strong toxic effect on humans and animals. However, the cardiac toxicity of Cr(VI) in broilers remains to be explored. The development of heart disease is often linked to mitochondrial dysfunction especially exposure to toxic substances. In order to investigate the role of mitochondrial dysfunction in apoptosis and autophagy of broiler cardiomyocytes induced by hexavalent chromium, broiler cardiomyocytes were cultured in potassium dichromate of 0 mM, 16 mM, and 32 mM medium for 24 h. The results showed that, compared with the control group, reactive oxygen species (ROS) and apoptosis rate in the Cr(VI) treatment group increased in a dose-dependent manner, the mRNA levels of apoptosis-related genes Bax and p53 were significantly increased, and the mRNA level of Bcl-2 was significantly decreased. Compared with the control group, the mRNA level of autophagy-related genes (LC3-I, LC3-II, and Beclin1) in the Cr(VI) treatment group was significantly increased, the mRNA level of mTOR was significantly decreased, and the protein level of p62/SQSTM1 was significantly decreased. The protein level of Beclin1 and the ratio of LC3-II/LC3-I significantly increased. In addition, compared with the control group, mitochondrial membrane potential decreased in a dose-dependent manner, and mitochondrial dynamics-related genes SIRT1, SIRT3, and Mfn2 mRNA decreased significantly in the Cr(VI) treatment group. In this study, we concluded that Cr(VI) could cause broiler myocardial apoptosis and autophagy by inducing mitochondrial dysfunction and oxidative stress.

Salt-contaminated water inducing pulmonary hypertension and kidney damage by increasing Ang II concentration in broilers.

NaCl is the main component of freshwater salinization. High NaCl concentration in drinking water can cause pulmonary hypertension syndrome (PHS) and kidney damage in broilers. To explore the effect of NaCl in drinking water on broilers' kidneys, this study divided 80 chickens into four groups. With the control group fed with pure water, broiler chickens were fed with fresh water (FW, NaCl 1 g/L), low salt-contaminated water (L-SCW, NaCl 2.5 g/L), and high salt-contaminated water (H-SCW, NaCl 5 g/L). The results show that ascites heart index (AHI) and hematocrit (HCT) of broilers increase in L-SCW and H-SCW, the serum blood urea nitrogen and creatinine of broilers increase significantly, the kidney index increases, the kidney sections show vacuolar degeneration and fibrotic degeneration, and the TUNEL results show that the kidneys possess obvious apoptosis. In addition, the detection of RAAS-related genes (AGT gene in the liver, REN in the kidney, ACE in the lung) demonstrates that after using salt-contaminated water, the transcription levels of AGT, REN, and ACE rise significantly, and the concentration of angiotensin II (Ang II) also increases significantly. In order to verify the effect of Ang II on broiler kidneys, this research used exogenous Ang II to treat chicken embryonic kidney (CEK) cells. The results show that the cell activity of CEK decreased with the increase of the concentration of exogenous Ang II. Meanwhile, the flow cytometry assay shows that Ang II could promote the apoptosis of CEK cells. These results indicate that the salt-contaminated water can aggravate PHS and cause kidney damage. The mechanism may be related to the increase of Ang II.

Nano-selenium alleviating the lipid metabolism disorder of LMH cells induced by potassium dichromate via down-regulating ACACA and FASN.

Chromium (Cr) VI is a common environmental contaminant highly toxic to livers. To explore the protective effect of nano-selenium (NANO-Se) on broiler liver damage caused by Cr (VI), this experiment was conducted with chicken hepatocellular carcinoma cell line (LMH) as the research object, using potassium dichromate (PDC) and NANO-Se gel for culturing cells. The results indicated that: (1) in the PDC-exposure group, LMH cells being treated with 20 µmol/L PDC for 24 h, IC50 (median inhibition concentration) = 23.427 could significantly reduce cell activity (p < 0.01) which decreased over time. PDC markedly increased the concentration of triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) in LMH cells (p < 0.01), which increased over time. In addition, PDC could substantially augment the transcription and protein levels of acetyl-CoA carboxylases alpha (ACACA) and fatty acid synthase (FASN) in LMH cells (p < 0.01). (2) Compared with the PDC-exposure group, the addition of 8 µmol/L NANO-Se after 12 h of PDC treatment could significantly increase the cell viability (p < 0.01) but decreased over time; the levels of TG and LDL-C in LMH cells declined markedly (p < 0.01). In addition, the transcription and protein levels of ACACA and FASN in LMH cells were significantly reduced (p < 0.01). (3) The LMH cells were cultured in advance with 8 µmol/L NANO-Se for 12 h and then with PDC for 24 h. The obtained results were similar to the above. There were no obvious differences in TG and LDL-C levels (p > 0.05). However, significant differences were found in the activity of LMH cells and the expression of genes related to lipid metabolism (p < 0.05).All these results suggest that the exposure to PDC promotes the increase of lipid synthesis in LMH cells and causes disorders in the lipid metabolism. Moreover, NANO-Se can partially attenuate the damage caused by PDC through down-regulating of the lipid metabolism-related genes (ACACA and FASN) in LMH cells.

Antagonistic effect of nano-selenium on hepatocyte apoptosis induced by DEHP via PI3K/AKT pathway in chicken liver.

Di-(2-ethylhexyl) phthalate (DEHP) is a common plasticizer which is mainly used as a kind of plastic additive to increase the flexibility of plastic products. Given the widespread use of plastic products, DEHP, as a ubiquitous artificial pollutant, are widely present in the environment. In addition, DEHP could cause biological damage in various organs through oxidative stress. Nano-Selenium, a novel form of selenium, has a wide variety of biomedical applications as an antioxidant, anticancer and anti-inflammatory agent. Nevertheless, researches on the toxicity of DEHP in chicken hepatocyte lines is insufficient. In particular, researches on the interaction between DEHP and nano-selenium is insufficient in chicken cell. Therefore, the innovation of this study is to explore the theoretical mechanism of DEHP toxicity in hepatocytes and the antagonistic effect of nano-selenium on a series of damage in chicken hepatocytes caused by DEHP. Our results showed that, after DEHP exposure, oxidative stress levels in hepatocytes increased, and the mRNA and protein levels of apoptosis-related genes p53, Capsase9, Caspase3 and Bax increased significantly except Bcl-2. The protein levels of apoptosis markers cleaved-Caspase9 and cleaved-Caspase3 also increased significantly. Moreover, the result of TUNEL assay also showed that the level of apoptotic cells increased after DEHP exposure. Meanwhile, the mRNA and protein levels of PI3K, AKT and p-AKT decreased. Therefore, DEHP is able to enhance the degree of oxidative damage and apoptosis of chicken liver cells. Nevertheless, the addition of nano-selenium can reverse the above changes. Experimental results revealed that nano-selenium antagonizes the toxic effects of DEHP via the PI3K/AKT pathway.

Network analysis indicating the pharmacological mechanism of Yunpi-Qufeng-Chushi-prescription in prophylactic treatment of rheumatoid arthritis.

BACKGROUND: Rheumatoid arthritis (RA), is an autoimmune inflammatory disease with increasing global morbidity and high disability. Early treatment is an effective intervention to slow down joint deformation. However, as for early RA and pre-RA patients, it sometimes takes a long time to make a definite diagnosis and few guidelines have made suggestion for these suspected or early phrase individuals. Yunpi-Qufeng-Chushi-Prescription (YQCP) is an optimization of the traditional formula, Cangzhu Fangfeng Tang which is effective for arthromyodynia management. METHODS: In this study, LC-MS identify the main component of YQCP. Ingredients of the 11 herbs were collected from Traditional Chinese Medicine Integrated Database (TCMID). Targets of these ingredients were collected from two source, TCMID and PharmMapper. Microarray of 20 early untreated RA patients and corresponding health control were download from NCBI Gene Expression Omnibus (GEO) database to defined the differential expressed genes. Gene ontology analysis and KEGG enrichment analysis were carried out for the YQCP. Protein-protein interactions (PPIs) networks were constructed to identify the hub targets. At last, molecular docking (MD) were conducted to further verified the the possibility of YQCP for RA therapy. RESULT: The study indicated that by acting on hub targets such as C3, EGFR, SRC and MMP9, YQCP may influence the mature of B cells and inhibit B cell-related IgG production, regulate oxidative stress and modulate activity of several enzymes including peroxidase and metallopeptidase to delay the occurrence and progress of RA and benefit the pre-RA or early RA patients. CONCLUSION: YQCP is a potential effective therapy for prophylactic treatment of RA.

Misdiagnosis of ligamentoid fibromatosis of the small mesenteric: A case report.

BACKGROUND: Ligamentoid fibromatosis is a rare borderline tumor that occurs in the muscles, fascia, and aponeurosis. It is a kind of soft tissue tumor of fibrous origin, also known as invasive fibromatosis, desmoid fibroma, neurofibromatosis, etc. The tumor is between benign and malignant tumors and rarely has distant metastasis. Its characteristics are mainly local invasion, destruction and growth and easy recurrence. The World Health Organization defines it as a fibroblast cloning value-added lesion originating from deep soft tissue, which causes local invasion and growth leading to tissue reconstruction, extrusion and destruction of important structures and organs. The incidence rate accounts for 0.03% of all tumors and less than 3% of all soft tissue tumors. Definite diagnosis mainly depends on postoperative pathology. Surgical resection is still the main way to treat the disease, and a variety of nonsurgical treatment methods are auxiliary. Combined treatment can effectively reduce the risk of postoperative recurrence. CASE SUMMARY: The patient is a 57-year-old female. One week ago, she accidentally found a mass in the left upper abdomen while lying flat. There was no abdominal pain and abdominal distention, no fever, no black stool and blood in the stool and no nausea and vomiting. She had a 10-year history of glaucoma on the left side, underwent hysterectomy for uterine fibroids 5 years ago, had no hypertension, heart disease, diabetes, hepatitis or tuberculosis, had no history of smoking and had been drinking for 20 years. CONCLUSION: Accurate preoperative diagnosis is difficult, surgical resection is the main treatment, and a variety of nonsurgical treatment methods are auxiliary. Combined treatment can effectively reduce the risk of postoperative recurrence. The prognosis is still good, and the risk of recurrence of secondary surgery is greatly increased.

Antagonistic effects of nano-selenium on broilers hepatic injury induced by Cr(VI) poisoning in AMPK pathway.

Cr (chromium, with common valence states of III and VI) is one of the common broiler feed additives. Liver injury and metabolic disorders could be caused by Cr(VI) (hexavalent chromium) poisoning in broilers. Oxidative damage and metabolic disorders of organisms caused by heavy metals could be antagonized by nano-Se (nano-selenium). Nano-Se was chosen to study the antagonism of Cr(VI) poisoning in broilers. AMPK (Adenosine 5,-monophosphate-activated protein kinase) is known as a "cell energy regulator" and plays a key regulatory role in carbohydrate and lipid metabolism. AMPK pathway and ACACA/CPT1A two genes were selected to study the prevention and treatment of nano-Se on Cr(VI) poisoning in broilers and its molecular mechanism. For this purpose, 180 1-day-old AA (Arbor Acres) broilers were selected and randomly divided into 6 groups (n = 30) for further testing. After feeding as planned for 35 days, the livers of such broilers were taken for further examination including histopathological examination, differential gene expression analysis, and further validation on both mRNA and protein levels using related techniques like RT-qPCR, western blot, and immunohistochemistry (IHC). The histopathological examination suggested that the liver cells of the Cr(VI) poisoning group were more severely injured than the nano-Se addition group. RT-qPCR results showed that the relative expression of ACACA gene in the Cr(VI) poisoning group was significantly increased (P < 0.05), while the CPT1A gene's expression was significantly decreased (P < 0.01). Those results were reversed in the nano-Se addition group. Western blot results were consistent with RT-qPCR and both suggested antagonism of nano-Se on Cr(VI). Through morphological and histopathological observation, as well as the measurement of the mRNA and protein expression levels of ACACA and CPT1A genes in AMPK pathway, it was confirmed that nano-Se has certain preventive and protective effects on Cr(VI) poisoning in broiler chickens. Furthermore, the adverse effects of Cr(VI) on carbohydrate and lipid metabolism in broilers can be antagonized by nano-Se through AMPK pathway. A new method and experimental basis were provided to the future study of Cr(VI) poisoning in broilers.

Effect of selenium nanoparticles against abnormal fatty acid metabolism induced by hexavalent chromium in chicken's liver.

The effect of selenium on excessive fatty acid-induced apoptosis and abnormal amino acid metabolism in the liver is well known, because it is an important site in the fatty acid metabolism pathway. However, the protective role of nano-elemental selenium (nano-Se) supplementation against hexavalent chromium (K2Cr2O7)-induced abnormal fatty acid metabolism has not been evaluated yet. Therefore, we conducted chicken experiments with different nano-Se supplementation doses to investigate the role of nano-Se against Cr(VI)-induced adverse effects. For this purpose, a total of 120 1-day-old chicks were randomly divided into control group, Cr(VI)-exposed group, protection group, treatment group, prevention group, and nano-Se control group. The results of RT-qPCR showed that the nano-Se supplementation notably downregulated (P < 0.01) the messenger RNA (mRNA) expression levels of fatty acid synthase (FASN), whereas nano-Se supplementation significantly upregulated (P < 0.01) the mRNA expression level of acyl-coenzyme A oxidase 1 (ACOX1) in chicken's liver at day 35 of the experiment. Similar results were further verified by western blot analysis. Moreover, nano-Se supplementation significantly enhanced and reduced the antibody expression levels of ACOX1 and FASN in immunohistochemical analysis, respectively. Thus, finally, it was concluded that nano-Se can alleviate K2Cr2O7-induced abnormal fatty acid metabolism in chicken's liver.

Metabonomic analysis of the hepatic injury suffer from hexavalent chromium poisoning in broilers.

Chromium is used in daily life and has a wide range of functions. It plays an important role in protein synthesis and carbohydrate and lipid metabolism. Chromium is found in trivalent Cr(III) and hexavalent Cr(VI) form; Cr(III) is relatively stable and intimately participates with many phenomena of metabolisms. Whereas, Cr(VI) is toxic, which results in growth inhibition and leading to changes in components of antioxidant systems as well as secondary metabolites. However, the molecular mechanism that is involved in Cr (VI)-induced hepatotoxicity is still unclear. For this purpose, 40 chickens were randomly assigned into two groups: the normal group (feeding the basic diet and clear water), the chromium group (16%LD50, 74.24 mg/kg/day K2Cr2O7 ). The samples were subjected to pathological examination and UHPLC-QE-MS non-target metabolomics method for metabolomics analysis of broiler liver using principal component analysis (PCA) and partial least squares discriminant analysis (OPLS-DA). The central venous cells of the broiler liver in the chromium poisoning group showed turbidity and flaky necrosis, nuclear condensation, nuclear rupture, and even nuclear dissolution. The differential metabolite analysis between the chromium poisoning and the control group showed that 32 differential metabolites were upregulated and 15 were downregulated in positive ion mode. Whereas,17 differential metabolites were downregulated, and 35 were downregulated in negative ion mode (P ≤ 0.05). The potential marker substances are oleic acidamide, farnesylacetone, betaine, taurine, choline, and galactinol. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways showed that the lipid metabolism, carbohydrate metabolism, nucleotide metabolism, amino acid metabolism, energy metabolism, membrane transport, digestive system, and nervous system were the most important metabolic pathways in the liver. This study provides a theoretical basis for the future understanding of the pathogenesis of chromium poisoning and a new insight of the subsequent molecular mechanism of chromium hepatotoxicity.

Transcriptome analysis reveals the molecular mechanism of hepatic metabolism disorder caused by chromium poisoning in chickens.

Chromium (Cr) is one of the most important environmental pollutants which are released into the environment due to their wide usage in numerous industries. The excess of Cr (VI) can induce hepatotoxicity, while the molecular mechanism that is involved in Cr (VI)-induced hepatotoxicity is unclear. We demonstrated the induction of chromium poisoning model in chickens to identify the differentially expressed genes (DEGs), and their functions were analyzed under different physiological and pathological conditions. Histopathological examination and transcriptome data for chromium-poisoned livers and control livers were annotated with Illumina® HiSeq 2000. The histopathological examination in chromium poisoning groups showed diapedesis, hemolysis, degeneration, nucleus pycnosis, and central phlebectasia in the liver. A total of 334 genes were upregulated and 509 genes were downregulated. The most strongly upregulated genes were HKDC1, DDX4, ACACA, FDFT1, CYYR1, PPP1R3C, and SLC16A14, while the most downregulated genes were MYBPC3, CCKAR, PCK1, and CPT1A. A Gene Ontology (GO) term with the highest enrichment of DEGs is small molecule metabolic process. In cell component domain, the term with the highest enrichment is extracellular matrix. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways showed that glucose metabolism, lipid metabolism, and protein metabolism were the most important metabolic pathways in the liver. The current study first time provides important clues and evidence for identifying the differentially expressed genes in livers due to Cr (VI)-induced liver injury in chickens.