Surgical treatment of an old avulsion fracture of the ischial tuberosity and ischial ramus: A case report.

BACKGROUND: Avulsion fracture of the ischial tuberosity is a relatively clinically rare type of trauma that is mainly incurred by adolescents during competitive sports activities. According to previous literature, the most commonly involved sports are soccer, sprinting, and gymnastics, in descending order. Dance-induced avulsion fracture of the ischial tuberosity and ischial ramus is extremely clinically rare. CASE SUMMARY: A case of a neglected avulsion fracture of the ischial tuberosity and ischial ramus was diagnosed in a young female dancer who complained of pain and restricted movement of her right hip. She stated that she had suffered the injury while performing a split leap during a dance performance 9 mo prior. Eventually, she underwent surgery and obtained satisfactory treatment results. CONCLUSION: Early diagnosis of these fractures is important to ensuring early proper treatment towards a quicker recovery. For old fractures with nonunion and chronic buttock pain, surgery is a preferred therapeutic choice with good treatment outcomes.

AZI2 mediates TBK1 activation at unresolved selective autophagy cargo receptor complexes with implications for CD8 T-cell infiltration in breast cancer.

Most breast cancers do not respond to immune checkpoint inhibitors and there is an urgent need to identify novel sensitization strategies. Herein, we uncovered that activation of the TBK-IFN pathway that is mediated by the TBK1 adapter protein AZI2 is a potent strategy for this purpose. Our initial observations showed that RB1CC1 depletion leads to accumulation of AZI2, in puncta along with selective macroautophagy/autophagy cargo receptors, which are both required for TBK1 activation. Specifically, disrupting the selective autophagy function of RB1CC1 was sufficient to sustain AZI2 puncta accumulation and TBK1 activation. AZI2 then mediates downstream activation of DDX3X, increasing its interaction with IRF3 for transcription of pro-inflammatory chemokines. Consequently, we performed a screen to identify inhibitors that can induce the AZI2-TBK1 pathway, and this revealed Lys05 as a pharmacological agent that induced pro-inflammatory chemokine expression and CD8+ T cell infiltration into tumors. Overall, we have identified a distinct AZI2-TBK1-IFN signaling pathway that is responsive to selective autophagy blockade and can be activated to make breast cancers more immunogenic.Abbreviations: AZI2/NAP1: 5-azacytidine induced 2; CALCOCO2: calcium binding and coiled-coil domain 2; DDX3X: DEAD-box helicase 3 X-linked; FCCP: carbonyl cyanide p-triflouromethoxyphenylhydrazone; a protonophore that depolarizes the mitochondrial inner membrane; ICI: immune checkpoint inhibitor; IFN: interferon; NBR1: NBR1 autophagy cargo receptor; OPTN: optineurin; RB1CC1/FIP200: RB1 inducible coiled-coil 1; SQSTM1/p62: sequestosome 1; TAX1BP1: Tax1 binding protein 1; TBK1: TANK binding kinase 1.

Precisely Regulating M2 Subtype Macrophages for Renal Fibrosis Resolution.

Macrophages are central to the pathogenesis of kidney disease and serve as an effective therapeutic target for kidney injury and fibrosis. Among them, M2-type macrophages have double-edged effects regarding anti-inflammatory effects and tissue repair. Depending on the polarization of the M2 subtypes (M2a or M2c) in the diseased microenvironment, they can either mediate normal tissue repair or drive tissue fibrosis. In renal fibrosis, M2a promotes disease progression through macrophage-to-myofibroblast transition (MMT) cells, while M2c possesses potent anti-inflammatory functions and promotes tissue repair, and is inhibited. The mechanisms underlying this differentiation are complex and are currently not well understood. Therefore, in this study, we first confirmed that M2a-derived MMT cells are responsible for the development of renal fibrosis and demonstrated that the intensity of TGF-ß signaling is a major factor determining the differential polarization of M2a and M2c. Under excessive TGF-ß stimulation, M2a undergoes a process known as MMT cells, whereas moderate TGF-ß stimulation favors the polarization of M2c phenotype macrophages. Based on these findings, we employed targeted nanotechnology to codeliver endoplasmic reticulum stress (ERS) inhibitor (Ceapin 7, Cea or C) and conventional glucocorticoids (Dexamethasone, Dex or D), precisely modulating the ATF6/TGF-ß/Smad3 signaling axis within macrophages. This approach calibrated the level of TGF-ß stimulation on macrophages, promoting their polarization toward the M2c phenotype and suppressing excessive MMT polarization. The study indicates that the combination of ERS inhibitor and a first-line anti-inflammatory drug holds promise as an effective therapeutic approach for renal fibrosis resolution.

Adaptive tracking control for nonlinear systems with uncertain control gains and its application to a TCP/AQM network.

This paper is concerned with the adaptive tracking control problem for nonlinear systems with virtual control coefficients including known and unknown items. The known items are employed for controller design directly, such that more information is utilized to achieve better performance. To deal with the unknown items, a novel real control law is firstly constructed by introducing an auxiliary system. The proposed controller is designed and applied to an uncertain TCP/AQM network system, which guarantees the practical boundedness of all the signals in the closed-loop system. Finally, the effectiveness and practicability of the developed control strategy are validated by simulation results.

Autophagy-dependent expression of osteopontin and its downstream Stat3 signaling contributes to lymphatic malformation progression to lymphangiosarcoma.

Lymphatic malformation (LM) is a vascular anomaly from lymphatic endothelial cells (ECs), and a fraction of the patients could progress to the deadly malignant lymphangiosarcoma (LAS). Using genetic tools to delete an essential autophagy gene Rb1cc1/FIP200 or its mutation specifically blocking its autophagy function, we demonstrated that autophagy inhibition abrogated LM progression to LAS although not affecting LM formation in our recently developed mouse model of LAS. Analysis of the mouse models in vivo and vascular tumor cells in vitro showed that autophagy inhibition reduced vascular tumor cell proliferation in vitro and tumorigenicity in vivo without affecting mTORC1 signaling as an oncogenic driver directly. Transcriptional profiling of autophagy-deficient tumor cells and further mechanistic studies revealed a role for osteopontin (OPN) and its downstream Jak/Stat3 signaling in mediating regulation of vascular tumor cells by autophagy. Together, these results support potential new prophylactic strategies to targeting autophagy and/or its downstream OPN expression to prevent progression of the benign LM to the malignant and deadly LAS.Abbreviations: LM: lymphatic malformation; EC: endothelial cell; LAS: lymphangiosarcoma; OPN: osteopontin; RB1CC1: RB1 Inducible Coiled-Coil 1; FIP200: FAK family-interacting protein of 200 kDa.

A Clinically-Achievable Injectable and Sprayable in Situ Lyotropic Liquid Crystalline Platform in Treating Hormone-Sensitive and Castration-Resistant Prostate Cancer.

When it comes to long-acting injections, lyotropic liquid crystals (LLCs) are considered as an effective and powerful drug delivery technology due to their low manufacturing and injection difficulty, consistent releasing behaviors with low burst, as well as broadly applicable drug loading capacity. However, monoolein and phytantriol, as two widely used LLC-forming materials, may give rise to tissue cytotoxicity and undesired immunological responses, which may hinder the wide application of this technology. In this study, we opted for two ingredients, phosphatidylcholine and α-tocopherol, as carriers on account of their nature-obtainable and biocompatible qualities. By changing the ratios between them, we conducted research on crystalline types, nanosized structures, viscoelastic differences, characteristics of releasing behaviors, and in vivo safety. To fully exploit this in situ LLC platform with both injectability and sprayability, we focused on the treatment of both hormone-sensitive (HSPC) and castration-resistant prostate cancer (CRPC). For HSPC, we found that spraying leuprolide and a cabazitaxel-loaded LLC platform on the tumor bed after resection greatly reduced tumor metastatic rate and prolonged the survival time. Besides, for CRPC, our results demonstrated that although leuprolide (a kind of drug for castration) alone could hardly limit the progression of CRPC with low MHC-I expression, its combination with cabazitaxel in our LLC platform achieved a significantly better tumor-inhibiting and anti-recurrent efficacy than single cabazitaxel-loaded LLC platform, owing to enhanced CD4+ T cell infiltration in tumors and immune-potentiating cytokines. In conclusion, our dual-functional and clinically achievable strategy might provide a treating solution toward both HSPC and CRPC.

Autophagy inhibition prevents lymphatic malformation progression to lymphangiosarcoma by decreasing osteopontin and Stat3 signaling.

Lymphatic malformation (LM) is a vascular anomaly originating from lymphatic endothelial cells (ECs). While it mostly remains a benign disease, a fraction of LM patients progresses to malignant lymphangiosarcoma (LAS). However, very little is known about underlying mechanisms regulating LM malignant transformation to LAS. Here, we investigate the role of autophagy in LAS development by generating EC-specific conditional knockout of an essential autophagy gene Rb1cc1/FIP200 in Tsc1iΔEC mouse model for human LAS. We find that Fip200 deletion blocked LM progression to LAS without affecting LM development. We further show that inhibiting autophagy by genetical ablation of FIP200, Atg5 or Atg7, significantly inhibited LAS tumor cell proliferation in vitro and tumorigenicity in vivo. Transcriptional profiling of autophagy-deficient tumor cells and additional mechanistic analysis determine that autophagy plays a role in regulating Osteopontin expression and its down-stream Jak/Stat3 signaling in tumor cell proliferation and tumorigenicity. Lastly, we show that specifically disrupting FIP200 canonical autophagy function by knocking-in FIP200-4A mutant allele in Tsc1iΔEC mice blocked LM progression to LAS. These results demonstrate a role for autophagy in LAS development, suggesting new strategies for preventing and treating LAS.

Recruiting T cells and sensitizing tumors to NKG2D immune surveillance for robust antitumor immune response.

Although recruiting T cells to convert cold tumors into hot can prevent some tumors from evading immune surveillance, tumors have evolved more mechanisms to achieve immune evasion, such as downregulating major histocompatibility complex I (MHC I) molecules expression to prevent T cells from recognizing tumor-antigens, or secreting immune suppression cytokines that disable T cells. Tumor immune evasion not only promotes tumor growth, but also weakens the efficacy of existing tumor immunotherapies. Therefore, recruiting T cells while reshaping innate immunity plays an important role in preventing tumor immune escape. In this study, we constructed a long-acting in situ forming implant (ISFI) based on the Atrigel technology, co-encapsulated with G3-C12 and sulfisoxazole (SFX) as a drug depot in the tumor site (SFX + G3-C12-ISFI). First, G3-C12 could recruit T cells, and transform cold into hot tumors. Furthermore, SFX could inhibit tumor-derived exosomes secretion, reduce the shedding of NKG2D ligand (NKG2DL), repair NKG2D/NKG2DL pathway, reinvigorate natural killer (NK) cells, and evade the effects of MHC I molecules missing. In the humanized cold tumor model, our strategy showed an excellent anti-tumor effect, providing a smart strategy for solving tumor evasion immune surveillance.

Regulation of RB1CC1/FIP200 stability and autophagy function by CREBBP-mediated acetylation in an intrinsically disordered region.

RB1CC1/FIP200 is an essential macroautophagy/autophagy protein that plays an important role in a variety of biological and disease processes through its canonical autophagy-dependent and -independent functions. However, it remains largely unknown whether post-translational modifications could regulate RB1CC1 and its associated autophagy functions. Here, we report acetylation of several lysine residues of RB1CC1 by acetyltransferase CREBBP (CREB binding protein), with K276 as the major CREBBP acetylation site. K276 is also identified as a ubiquitination site by mass spectrometry, and acetylation at this site reduces ubiquitination of RB1CC1 to inhibit its ubiquitin-dependent degradation. We also find that RB1CC1 contains an N-terminal intrinsically disordered region (IDR) capable of forming liquid-liquid phase separation (LLPS) in vitro, which may drive formation of RB1CC1 puncta with LLPS properties in cells independent of SQSTM1/p62 and other autophagy receptors CALCOCO2/NDP52, NBR1, TAX1BP1 and OPTN. Mutational analysis shows that both K276 acetylation and the N-terminal IDR containing it are important for maintaining canonical autophagy function of RB1CC1 in breast cancer cells. Our findings demonstrate regulation of RB1CC1 by a new post-translational mechanism and suggest potential therapeutic application of inducing RB1CC1 degradation through blocking K276 acetylation in the treatment of cancer and other diseases.Abbreviations: Baf-A1: bafilomycin A1; CREBBP/CBP: CREB binding protein; CHX: cycloheximide; EP300/p300: E1A binding protein p300; FRAP: fluorescence recovery after photobleaching; HADCs: histone deacetylases; IDR: intrinsically disordered region; LLPS: liquid-liquid phase separation; KAT2A/GCN5: lysine acetyltransferase 2A; KAT2B/PCAF: lysine acetyltransferase 2B; KAT5/TIP60: lysine acetyltransferase 5; KAT8/MOF: lysine acetyltransferase 8; NAM: nicotinamide; PAS: phagophore assembly site; PEG-8000: polyethylene glycol 8000; RB1CC1/FIP200: RB1 inducible coiled-coil 1; TSA: trichostatin A.

Duck Enteritis Virus Inhibits the cGAS-STING DNA-Sensing Pathway To Evade the Innate Immune Response.

Cyclic GMP-AMP synthase (cGAS), a key DNA sensor, detects cytosolic viral DNA and activates the adaptor protein stimulator of interferon genes (STING) to initiate interferon (IFN) production and host innate antiviral responses. Duck enteritis virus (DEV) is a duck alphaherpesvirus that causes an acute and contagious disease with high mortality in waterfowl. In the present study, we found that DEV inhibits host innate immune responses during the late phase of viral infection. Furthermore, we screened DEV proteins for their ability to inhibit the cGAS-STING DNA-sensing pathway and identified multiple viral proteins, including UL41, US3, UL28, UL53, and UL24, which block IFN-ß activation through this pathway. The DEV tegument protein UL41, which exhibited the strongest inhibitory effect, selectively downregulated the expression of interferon regulatory factor 7 (IRF7) by reducing its mRNA accumulation, thereby inhibiting the DNA-sensing pathway. Ectopic expression of UL41 markedly reduced viral DNA-triggered IFN-ß production and promoted viral replication, whereas deficiency of UL41 in the context of DEV infection increased the IFN-ß response to DEV and suppressed viral replication. In addition, ectopic expression of IRF7 inhibited the replication of the UL41-deficient virus, whereas IRF7 knockdown facilitated its replication. This study is the first report identifying multiple viral proteins encoded by a duck DNA virus, which inhibit the cGAS-STING DNA-sensing pathway. These findings expand our knowledge of DNA sensing in ducks and reveal a mechanism through which DEV antagonizes the host innate immune response. IMPORTANCE Duck enteritis virus (DEV) is a duck alphaherpesvirus that causes an acute and contagious disease with high mortality, resulting in substantial economic losses in the commercial waterfowl industry. The evasion of DNA-sensing pathway-mediated antiviral innate immunity is essential for the persistent infection and replication of many DNA viruses. However, the mechanisms used by DEV to modulate the DNA-sensing pathway remain poorly understood. In the present study, we found that DEV encodes multiple viral proteins to inhibit the cGAS-STING DNA-sensing pathway. The DEV tegument protein UL41 selectively diminished the accumulation of interferon regulatory factor 7 (IRF7) mRNA, thereby inhibiting the DNA-sensing pathway. Loss of UL41 potently enhanced the IFN-ß response to DEV and impaired viral replication in ducks. These findings provide insights into the host-virus interaction during DEV infection and help develop new live attenuated vaccines against DEV.

Duck Enteritis Virus Protein Kinase US3 Inhibits DNA Sensing Signaling by Phosphorylating Interferon Regulatory Factor 7.

The cytosolic DNA sensing pathway mediates innate immune defense against infection by many DNA viruses; however, viruses have evolved multiple strategies to evade the host immune response. Duck enteritis virus (DEV) causes an acute and contagious disease with high mortality in waterfowl. The mechanisms employed by DEV to block the DNA sensing pathway are not well understood. Here, we sought to investigate the role of DEV US3, a serine/threonine protein kinase, in the inhibition of DNA sensing. We found that ectopic expression of DEV US3 significantly inhibited the production of IFN-ß and expression of interferon-stimulated genes induced by interferon-stimulatory DNA and poly(dA-dT). US3 also inhibited viral DNA-triggered IFN-ß activation and promoted DEV replication in duck embryo fibroblasts, while knockdown of US3 during DEV infection enhances the IFN-ß response and suppresses viral replication. US3 inhibited the DNA-sensing signaling pathway by targeting interferon regulatory factor 7 (IRF7), and the kinase activity of US3 was indispensable for its inhibitory function. Furthermore, we found that US3 interacts with the activation domain of IRF7, phosphorylating IRF7, blocking its dimerization and nuclear translocation, and finally leading to the inhibition of IFN-ß production. These findings expand our knowledge on DNA sensing in ducks and reveal a novel mechanism whereby DEV evades host antiviral immunity. IMPORTANCE Duck enteritis virus (DEV) is a duck alphaherpesvirus that causes an acute and contagious disease with high mortality, resulting in substantial economic losses in the commercial waterfowl industry. The evasion of DNA-sensing pathway-mediated antiviral innate immunity is essential for the persistent infection and replication for many DNA viruses. However, the strategies used by DEV to block the DNA-sensing pathway are not well understood. In this study, DEV US3 protein kinase was demonstrated to inhibit the DNA-sensing signaling via binding to the activation domain of interferon regulatory factor 7 (IRF7), which induced the hyperphosphorylation of IRF7 and abolished IRF7 dimerization and nuclear translocation. Our findings provide insights into how duck herpesviral kinase counteracts host antiviral innate immunity to ensure viral replication and spread.

Prognostic value of preoperative P-CRP in patients with osteosarcoma: A retrospective study of 101 cases.

This study aimed to investigate the value of the product of peripheral blood platelet and serum C-reactive protein (P-CRP), an inflammatory indicator, for the prognosis of patients with osteosarcoma. Patients with osteosarcoma who were diagnosed and treated at the First Affiliated Hospital of Guangxi Medical University, China, between January 2012 and December 2019 were included in this retrospective study. Receiver operating characteristic curves were used to calculate the optimal cut-off values for inflammatory indicators such as P-CRP, the C-reactive protein/albumin ratio (CRP/Alb), the neutrophil-lymphocyte ratio (NLR), and the platelet-lymphocyte ratio (PLR) in the peripheral blood of patients before treatment. Based on the cut-off values, the patients were divided into high P-CRP and low P-CRP groups, high CRP/Alb and low CRP/Alb groups, high NLR and low NLR groups, and high NLR and low NLR groups; the Kaplan-Meier method was used to compare the overall survival (OS) rates and OS times of the above groups. Univariate and multivariate Cox regression models were used to analyze the effects of various factors on the prognosis of osteosarcoma and to determine the independent influencing factors. The Kaplan-Meier survival analysis results suggested that the OS rate of the high P-CRP group was significantly lower than that of the low P-CRP group (14.0% vs 67.2%, P < .001). The univariate analysis results suggested that tumor volume, tumor stage, NLR, PLR, P-CRP and CRP/Alb were factors that affected the prognosis of patients with osteosarcoma, and the differences were statistically significant (P < .05). The multivariate analysis results showed that tumor volume (hazard ratio [HR] = 1.061; 95% CI, 1.001-1.125; P = .046) and preoperative P-CRP (HR, 1.037; 95% CI, 1.024-1.050; P < .01) were independent prognostic factors affecting the OS rate after osteosarcoma surgery. The results of our study showed that P-CRP is a novel and promising prognostic indicator for patients with osteosarcoma. The higher the P-CRP level in the peripheral blood of patients is before treatment, the worse the prognosis might be.

Isolated cryptococcal osteomyelitis of the ulna in an immunocompetent patient: A case report.

BACKGROUND: Cryptococcal osteomyelitis is a bone infection caused by cryptococcus. As an opportunistic infection, bone cryptococcosis usually occurs in patients with immunodeficiency diseases or in those undergoing immunosuppressive therapy and often displays characteristics of disseminated disease. Isolated cryptococcal osteomyelitis is extremely unusual in immunocompetent person. The pathogenic fungus often invades vertebrae, femur, tibia, rib, clavicle, pelvis, and humerus, but the ulna is a rare target. CASE SUMMARY: A 79-year-old woman complaining of chronic pain, skin ulceration and a sinus on her right forearm was admitted, and soon after was diagnosed with cryptococcal osteomyelitis in the right ulna. Unexpectedly, she was also found to have apparently normal immunity. After treatment with antifungal therapy combined with surgery debridement, the patient's osteomyelitis healed with a satisfactory outcome. CONCLUSION: Although rare, cryptococcal osteomyelitis should be considered in the differential diagnosis of osteolytic lesions even in immunocompetent patients, and good outcomes can be expected if early definitive diagnosis and etiological treatment are established.

The Characterization of a Subependymal Giant Astrocytoma-Like Cell Line from Murine Astrocyte with mTORC1 Hyperactivation.

Tuberous sclerosis complex (TSC) is a genetic disorder caused by inactivating mutations in TSC1 (hamartin) or TSC2 (tuberin), crucial negative regulators of the mechanistic target of rapamycin complex 1 (mTORC1) signaling pathway. TSC affects multiple organs including the brain. The neurologic manifestation is characterized by cortical tubers, subependymal nodules (SEN), and subependymal giant cell astrocytoma (SEGA) in brain. SEGAs may result in hydrocephalus in TSC patients and mTORC1 inhibitors are the current recommended therapy for SEGA. Nevertheless, a major limitation in the research for SEGA is the lack of cell lines or animal models for mechanistic investigations and development of novel therapy. In this study, we generated TSC1-deficient neural cells from spontaneously immortalized mouse astrocytes in an attempt to mimic human SEGA. The TSC1-deficient cells exhibit mTORC1 hyperactivation and characteristics of transition from astrocytes to neural stem/progenitor cell phenotypes. Rapamycin efficiently decreased mTORC1 activity of these TSC1-deficient cells in vitro. In vivo, TSC1-deficient cells could form SEGA-like tumors and Rapamycin treatment decreased tumor growth. Collectively, our study generates a novel SEGA-like cell line that is invaluable for studying mTORC1-driven molecular and pathological alterations in neurologic tissue. These SEGA-like cells also provide opportunities for the development of novel therapeutic strategy for TSC patients with SEGA.

Autophagy mediated lipid catabolism facilitates glioma progression to overcome bioenergetic crisis.

BACKGROUND: Activation of mTORC1 plays a significant role in cancer development and progression. However, the metabolic mechanisms to sustain mTORC1 activation of cancer cells within stressed environments are still under-appreciated. We recently revealed high autophagy activity in tumour cells with mTORC1 hyper-activation. Nevertheless, the functions and mechanisms of autophagy in regulating mTORC1 in glioma are not studied. METHODS: Using glioma patient database and human glioma cells, we assessed the mechanisms and function of selective autophagy to sustain mTORC1 hyper-activation in glioma. RESULTS: We revealed a strong association of altered mRNA levels in mTORC1 upstream and downstream genes with prognosis of glioma patients. Our results indicated that autophagy-mediated lipid catabolism was essential to sustain mTORC1 activity in glioma cells under energy stresses. We found that autophagy inhibitors or fatty acid oxidation (FAO) inhibitors in combination with 2-Deoxy-D-glucose (2DG) decreased energy production and survival of glioma cells in vitro. Consistently, inhibition of autophagy or FAO inhibitors with 2DG effectively suppressed the progression of xenografted glioma with hyper-activated mTORC1. CONCLUSIONS: This study established an autophagy/lipid degradation/FAO/ATP generation pathway, which might be used in brain cancer cells under energy stresses to maintain high mTORC1 signalling for tumour progression.

Evaluation of the Liver Disease Information in Baidu Encyclopedia and Wikipedia: Longitudinal Study.

BACKGROUND: The internet has changed the way of people acquiring health information. Previous studies have shown that Wikipedia is a reasonably reliable medical resource, and it has been ranked higher than other general websites in various search engines. Baidu Encyclopedia is one of the most popular encyclopedia websites in China. However, no studies have shown the quality of the content provided in the Baidu Encyclopedia. OBJECTIVE: This study aimed to evaluate the quality of liver disease information provided by Wikipedia (in English) and Baidu Encyclopedia (in Chinese) and to perform a comparison of the quality and timeliness of the articles published in these two encyclopedias. Moreover, a 3-year follow-up study was conducted to compare if the information in both these websites was updated regularly over this period. METHODS: We searched for information on liver diseases by using the International Statistical Classification of Diseases and Related Health Problems 10th Revision Version 2016 codes on Wikipedia (in English) and Baidu Encyclopedia (in Chinese). The quality of the articles was assessed using the DISCERN instrument, which consists of 3 sections. We recorded the latest editing date of the webpages and calculated the date interval to evaluate the update timeliness of these websites. RESULTS: We found 22 entries on liver diseases in Baidu Encyclopedia and 15 articles in Wikipedia between September 15, 2016, and September 30, 2016, and we found 25 entries in Baidu Encyclopedia and 16 articles in Wikipedia between September 15, 2019, and September 30, 2019. In section 1 of the DISCERN instrument, the mean (SE) scores of Baidu Encyclopedia entries were significantly lower than those of Wikipedia articles. In section 2 and section 3 of the DISCERN instrument, the DISCERN scores of Baidu Encyclopedia entries were lower than those of Wikipedia articles, but the differences were not statistically significant. The total DISCERN scores of Baidu Encyclopedia entries were significantly lower than those of Wikipedia articles. The update interval of the entries in Baidu Encyclopedia was found to be significantly longer than that of the articles in Wikipedia. CONCLUSIONS: This study shows that the quality of articles and the reliability of the research content on liver diseases in Wikipedia are better than those of the entries in Baidu Encyclopedia. However, the quality of the treatment choices provided in both Wikipedia and Baidu Encyclopedia is not satisfactory. Wikipedia is updated more frequently than Baidu Encyclopedia, thereby ensuring that the information presented has the most recent research findings. The findings of our study suggest that in order to find accurate health information, it is important to seek the help of medical professionals instead of looking for a prescription amid the confusing information provided on the internet.

Laparoscopic Enucleation of Hepatic Cysts Reduces the Recurrence of Nonparasitic Hepatic Cysts.

Background: Standard treatments for nonparasitic hepatic cysts (NPHCs) include laparoscopic deroofing (LD), percutaneous aspiration, and alcohol sclerotherapy. However, these treatments have limitations. LD and alcohol sclerotherapy, for example, fail to prevent NPHC recurrences, although alcohol sclerotherapy is satisfactorily effective in treating small cysts (diameter <5 cm), which do not usually need treatment. The present study introduces a novel surgical procedure, laparoscopic enucleation with intact cyst (LEIC), which may prevent postoperative cyst recurrence. Materials and Methods: In this study, we enrolled 14 patients, with NPHCs larger than 9 cm in diameter, who underwent LEIC. Dissection and coagulation were performed using the harmonic shear enucleation and bipolar coagulation techniques. We attempted to completely remove the cysts intact. Results: For all patients, symptoms disappeared after complete elimination of the cyst capsule. No complications (hemorrhage or bile leakage) were found during the perioperative period. The mean follow-up period was 19.3 months (range 10-38 months), during which no recurrences or complications were noted. Conclusions: LEIC is a novel surgical approach that shows satisfactory efficacy and safety in patients with large, surficial, and symptomatic NPHCs. LEIC's main advantage is that it can efficiently prevent cyst recurrence and decrease postoperative morbidity. However, its long-term efficacy and safety require further verification, especially with huge cysts.

Recombinant Duck Enteritis Virus-Vectored Bivalent Vaccine Effectively Protects Against Duck Hepatitis A Virus Infection in Ducks.

Duck enteritis virus (DEV) and duck hepatitis A virus (DHAV) are prevalent duck pathogens, causing significant economic losses in the duck industry annually. Using a fosmid-based rescue system, we generated two DEV recombinants, rDEV-UL26/27-P13C and rDEV-US7/8-P13C, in which the P1 and 3C genes from DHAV type 3 (DHAV-3) were inserted into the DEV genome between genes UL26 and UL27 or genes US7 and US8. We inserted a self-cleaving 2A-element between P1 and 3C, allowing the production of both proteins from a single open reading frame. P1 and 3C were simultaneously expressed in infected chicken embryo fibroblasts, with no difference in growth kinetics between cells infected with the recombinant viruses and those infected with the parent DEV. Both recombinant viruses induced neutralizing antibodies against DHAV-3 and DEV in ducks. A single dose of the recombinant viruses induced solid protection against lethal DEV challenge and completely prevented DHAV-3 infection as early as 7 days post-vaccination. These recombinant P1- and 3C-expressing DEVs provide potential bivalent vaccines against DEV and DHAV-3 infection in ducks.

[Advances in clinical diagnosis and treatment of chronic osteomyelitis in adults].

OBJECTIVE: To review the progress of clinical diagnosis and treatment of chronic osteomyelitis in adults. METHODS: The literature related to chronic osteomyelitis in recent years was extensively reviewed, and the clinical diagnosis and treatment methods were summarized. RESULTS: Clinical characteristics and laboratory examination can help to diagnose chronic osteomyelitis in adults. Pathogenic identification is the basis for choosing antibiotics. Diagnostic imaging is specific. The treatment includes systemic treatment and local treatment, and the local treatment is the key to radical cure. CONCLUSION: The diagnosis of chronic osteomyelitis in adults should be made as early as possible. According to the anatomical and physiological classification of the patients, the appropriate treatment plan should be made.