Human amniotic epithelial stem cell is a cell therapy candidate for preventing acute graft-versus-host disease.

Graft-versus-host disease (GVHD), an immunological disorder that arises from donor T cell activation through recognition of host alloantigens, is the major limitation in the application of allogeneic hematopoietic stem cell transplantation (allo-HSCT). Traditional immunosuppressive agents can relieve GVHD, but they induce serious side effects. It is highly required to explore alternative therapeutic strategy. Human amniotic epithelial stem cells (hAESCs) were recently considered as an ideal source for cell therapy with special immune regulatory property. In this study, we evaluated the therapeutic role of hAESCs in the treatment of GVHD, based on our previous developed cGMP-grade hAESCs product. Humanized mouse model of acute GVHD (aGVHD) was established by injection of huPBMCs via the tail vein. For prevention or treatment of aGVHD, hAESCs were injected to the mice on day -1 or on day 7 post-PBMC infusion, respectively. We showed that hAESCs infusion significantly alleviated the disease phenotype, increased the survival rate of aGVHD mice, and ameliorated pathological injuries in aGVHD target organs. We demonstrated that hAESCs directly induced CD4+ T cell polarization, in which Th1 and Th17 subsets were downregulated, and Treg subset was elevated. Correspondingly, the levels of a series of pro-inflammatory cytokines were reduced while the levels of the anti-inflammatory cytokines were upregulated in the presence of hAESCs. We found that hAESCs regulated CD4+ subset polarization in a paracrine mode, in which TGFß and PGE2 were selectively secreted to mediate Treg elevation and Th1/Th17 inhibition, respectively. In addition, transplanted hAESCs preserved the graft-versus-leukemia (GVL) effect by inhibiting leukemia cell growth. More intriguingly, hAESCs infusion in HSCT patients displayed potential anti-GVHD effect with no safety concerns and confirmed the immunoregulatory mechanisms in the preclinical study. We conclude that hAESCs infusion is a promising therapeutic strategy for post-HSCT GVHD without compromising the GVL effect. The clinical trial was registered at www.clinicaltrials.gov as #NCT03764228.

Unilateral biportal endoscopy vs. open decompression for lumbar epidural lipomatosis-cohort study using a prospective registry.

Objective: This study aimed to compare the outcomes of unilateral biportal endoscopy, unilateral laminectomy bilateral decompression (UBE-ULBD), and open lumbar decompression (OLD) in patients with lumbar epidural lipomatosis (LEL). Methods: This prospective observational study was conducted from March 2019 to May 2022 and encompassed 33 patients with LEL who underwent lumbar decompression. The study included 15 cases of UBE-ULBD decompression and 18 cases of open decompression, which were followed up for 1 year. The baseline characteristics, initial clinical manifestations, and surgical details [including estimated blood loss (EBL) and preoperative complications] of all patients were recorded. Radiographic evaluation included the cross-sectional area (CSA) of the thecal sac and paraspinal muscles on MRI. Clinical results were analyzed using the Short Form-36 Score (SF-36), the Numeric Pain Rating Scale (NRS) for lumbar and leg pain, creatine kinase, the Roland and Morris Disability Questionnaire (RMDQ), and the Oswestry Disability Index (ODI). Results: The dural sac CSA increased considerably at the 1-year postoperative follow-up in both groups (p < 0.001). The operative duration in the OLD group (48.2 ± 7.2 min) was shorter than that in the UBE-ULBD group (67.7 ± 6.3 min, p < 0.001). The OLD group (97.2 ± 19.8 mL) was associated with more EBL than the UBE-ULBD group (40.6 ± 13.6 mL, p < 0.001). The duration of hospitalization in the OLD group (5.4 ± 1.3 days) was significantly longer compared with the UBE-ULBD group (3.5 ± 1.2 days, p < 0.01). The SF-36, NRS, RMDQ, and ODI scores improved in both groups postoperatively (p < 0.001). Serum creatine kinase values in the UBE-ULBD group (101.7 ± 15.5) were significantly lower than those in the OLD group (330.8 ± 28.1 U/L) 1 day after surgery (p < 0.001). The degree of paraspinal muscle atrophy in the UBE-ULBD group (4.81 ± 1.94) was significantly lower than that in the OLD group (12.15 ± 6.99) at 1 year (p < 0.001). Conclusion: UBE-ULBD and OLD demonstrated comparable clinical outcomes in treating LEL. However, UBE-ULBD surgery was associated with shorter hospital stays, lower rates of incision infection, lighter paravertebral muscle injury, and lower EBL than OLD surgery. Consequently, UBE-ULBD can be recommended in patients with LEL if conservative treatment fails.

A novel fluorescent aptasensor for sensitive and selective detection of environmental toxins fumonisin B1 based on enzyme-assisted dual recycling amplification and 2D δ-FeOOH-NH2 nanosheets.

Fumonisin (FB) is a pervasive hazardous substance in the environment, presenting significant threats to human health and ecological systems. Thus, the selective and sensitive detection of fumonisin B1 (FB1) is crucial due to its high toxicity and wide distribution in corn, oats, and related products. In this work, we developed a novel and versatile fluorescent aptasensor by combining enzyme-assisted dual recycling amplification with 2D δ-FeOOH-NH2 nanosheets for the determination of FB1. The established CRISPR/Cas12a system was activated by using activator DNA (aDNA), which was released via a T7 exonuclease-assisted recycling reaction. Additionally, the activated Cas12a protein was utilized for non-specifically cleavage of the FAM-labeled single-stranded DNA (ssDNA-FAM) anchored on δ-FeOOH-NH2 nanosheets. The pre-quenched fluorescence signal was restored due to the desorption of the cleaved ssDNA-FAM. Due to the utilization of this T7 exonuclease-Cas12a-δ-FeOOH-NH2 aptasensor for signal amplification, the detection range of FB1 was expanded from 1 pg/mL to 100 ng/mL, with a limit of detection (LOD) as low as 0.45 pg/mL. This study not only provides novel insights into the development of fluorescence biosensors based on 2D nanomaterials combined with CRISPR/Cas12a, but also exhibits remarkable applicability in detecting other significant targets.

Silencing of matrix metalloprotease-12 delays the progression of castration-resistant prostate cancer by regulating autophagy and lipolysis.

The complex pathogenesis of castration-resistant prostate cancer (CRPC) makes it challenging to identify effective treatment methods. Matrix metalloproteinase (MMP)-12 can degrade elastin as well as various extracellular matrix (ECM) components, which is associated with cancer progression. However, the relationship between MMP-12 and CRPC progression is poorly understood. In this study, we observed the effect of MMP-12 on the progression of CRPC and further explored its potential mechanism of action. High levels of MMP-12 were observed in patients with CRPC. We therefore developed cell co-culture and mouse models to study the function of MMP-12. Silencing MMP-12 in CRPC cells disrupted lipid utilization and autophagy marker expression via the CD36/CPT1 and P62/LC3 pathways, respectively, leading to reduced CRPC cell migration and invasion. Moreover, animal experiments confirmed that MMP-12-knockdown CRPC xenograft tumors exhibited reduced tumor growth, and the mechanisms involved the promotion of cancer cell autophagy and the inhibition of lipid catabolism. According to our results, MMP-12 played important roles in the progression of CRPC by disrupting adipocyte maturation and regulating cancer migration and invasion via the modulation of autophagy and lipid catabolism pathways.

Silencing of matrix metalloprotease-12 delays the progression of castration-resistant prostate cancer by regulating autophagy and lipolysis

Abstract The complex pathogenesis of castration-resistant prostate cancer (CRPC) makes it challenging to identify effective treatment methods. Matrix metalloproteinase (MMP)-12 can degrade elastin as well as various extracellular matrix (ECM) components, which is associated with cancer progression. However, the relationship between MMP-12 and CRPC progression is poorly understood. In this study, we observed the effect of MMP-12 on the progression of CRPC and further explored its potential mechanism of action. High levels of MMP-12 were observed in patients with CRPC. We therefore developed cell co-culture and mouse models to study the function of MMP-12. Silencing MMP-12 in CRPC cells disrupted lipid utilization and autophagy marker expression via the CD36/CPT1 and P62/LC3 pathways, respectively, leading to reduced CRPC cell migration and invasion. Moreover, animal experiments confirmed that MMP-12-knockdown CRPC xenograft tumors exhibited reduced tumor growth, and the mechanisms involved the promotion of cancer cell autophagy and the inhibition of lipid catabolism. According to our results, MMP-12 played important roles in the progression of CRPC by disrupting adipocyte maturation and regulating cancer migration and invasion via the modulation of autophagy and lipid catabolism pathways.

Azo-Cyanamide Bridged Dinuclear Iron Complexes Exhibiting no Electronic Coupling but Moderate Magnetic Coupling between the two Iron Centers.

To investigate the effect of long-distance organic ligand on electronic coupling between metallic atoms, the mononuclear and dinuclear complexes [Cp(dppe)Fe(apc)] (1), [{Cp(dppe)Fe}2(µ-adpc)] (2), [{CpMe5(dppe)Fe}2(µ-adpc) (3) and their oxidized complexes [Cp(dppe)Fe(apc)][PF6] (1[PF6]), [{Cp(dppe)Fe}2(µ-adpc)][PF6] (2[PF6]2), [{CpMe5(dppe)Fe}2(µ-adpc)][PF6]2 (3[PF6]2) (Cp=1,3-cyclopentadiene, CpMe5=1,2,3,4,5-pentamethylcyclopentadiene, dppe=1,2-bis(diphenylphosphino)ethane), apc-=4-azo(phenylcyanamido)benzene and adpc2-=4,4'-azodi(phenylcyanamido)) were synthesized and characterized by cyclic voltammetry, UV-vis, single-crystal X-ray diffraction and Mössbauer spectra. Electrochemical measurements showed no electronic coupling between the two terminal Fe units, However, the investigation results of the magnetic properties of the two-electron oxidized complexes indicate the presence of moderate antiferromagnetic coupling across 18 Šdistance.

Development of oral health resources and a mobile app for caregivers and autistic children through consensus building.

LAY ABSTRACT: Caregivers of autistic children often lack knowledge regarding oral homecare and when and where to see the dentist. To address this need, we developed a series of information on oral health. An autistic child assisted in developing two social stories to showcase a dental visit. A mobile app was developed to deliver the above mentioned. Other features include creation of customised social stories and visual schedule and an inbox to allow dentists to send messages to parents. The developed information and social stories were reviewed by experts and parents. The app also underwent anonymous and independent testing by parents. Overall the information and app were well received by the experts and parents.

Inhibitory actions of oxyresveratrol on the PI3K/AKT signaling cascade in cervical cancer cells.

The phosphatidyl inositol 3-kinase (PI3K)/AKT signaling plays a critical role in cancer cell proliferation, migration, and invasion. This signal transduction axis in HPV-positive cervical cancer has been proved to be directly activated by E6/E7 proteins of the virus enhancing cervical cancer progression. Hence, the PI3K/AKT pathway is one of the key therapeutic targets for HPV-positive cervical cancer. Here we discovered that oxyresveratrol (Oxy) at noncytotoxic concentration specifically suppressed the phosphorylation of AKT but not ERK1/2. This potent inhibitory effect of Oxy was still observed even when cells were stimulated with fetal bovine serum. Inhibition of AKT phosphorylation at serine 473 by Oxy resulted in a significant decrease in serine 9 phosphorylation of GSK-3ß, a downstream target of AKT. Dephosphorylation of GSK-3ß at this serine residue activates its function in promoting the degradation of MCL-1, an anti-apoptotic protein. Results clearly demonstrated that in association with GSK-3ß activation, Oxy preferentially downregulated the expression of anti-apoptotic protein MCL-1. Furthermore, results from the functional analyses revealed that Oxy inhibited cervical cancer cell proliferation, at least in part through suppressing nuclear expression of Ki-67. Besides, the compound retarded cervical cancer cell migration even the cells were exposed to a potent enhancer of epithelial-mesenchymal transition, TGF-ß1. In consistent with these data, Oxy reduced the expression of ß-catenin, N-cadherin, and vimentin. In conclusion, the study disclosed that Oxy specifically inhibits the AKT/GSK-3ß/MCL-1 axis resulting in reduction in cervical cancer cell viability, proliferation, and migration.

First record of the genus Passiena (Araneae, Lycosidae) from China, with the first description of the male of P.spinicrus Thorell, 1890 from Malaysia.

The genus Passiena is recorded for the first time from China with Passienaduanisp. nov. (♂♀) from Guangxi described here. In addition, the male of P.spinicrus Thorell, 1890 is described for the first time based on a specimen from Malaysia and colour photographs of freshly collected material are also presented. Detailed morphological descriptions, photographs, genital illustrations, and a distribution map for the two species are provided.

Gastroprotective effects of Pikad Tri-phol-sa-mut-than herbal remedy on multiple gastric ulcer models in rats.

In Thai traditional medicine, Pikad Tri-phol-sa-mut-than has long been used to alleviate gastrointestinal symptoms, renal disease, inflammation-related disorders, and severe malady. This recipe is composed of dried fruits of Morinda citrifolia L., Coriandrum sativum L., and Aegle marmelos (L.) Corrêa. The aim of this study was to assess the anti-gastric ulcer property of the water extract of Pikad Tri-phol-sa-mut-than (TS), using various animal models with different inducers, including restraint water immersion stress, indomethacin, and ethanol/hydrochloric acid (EtOH/HCl). Its mechanisms of anti-gastric ulcer actions were also elucidated using both in vitro and in vivo experiments. When compared with the control groups, the oral pretreatment of TS at the doses of 150, 300 and 600 mg/kg significantly reduced the gastric ulcer formation in all models. It was also found that TS at the dose of 600 mg/kg could increase gastric wall mucus in rats but could not produce the significant reduction of the gastric volume or total acidity of gastric content. Results from hematoxylin and eosin (H&E) and Periodic acid-Schiff (PAS) staining examinations of gastric tissues confirmed that TS visibly reduced gastric mucosal damage, while immunohistochemistry revealed that TS remarkably suppressed the protein expression of Bcl-2-associated X (BAX), a regulator of apoptosis, compared to those of the control group. The DPPH, ABTS, and FRAP assays showed antioxidant effects of TS. All of these findings demonstrated that TS has gastroprotective effects, which may be related to the increase in the gastric wall mucus secretion, not anti-secretory activity, as well as its antioxidant and antiapoptotic activities.

Lampshade web spider Ectatosticta davidi chromosome-level genome assembly provides evidence for its phylogenetic position.

The spider of Ectatosticta davidi, belonging to the lamp-shade web spider family, Hypochilidae, which is closely related to Hypochilidae and Filistatidae and recovered as sister of the rest Araneomorphs spiders. Here we show the final assembled genome of E. davidi with 2.16 Gb in 15 chromosomes. Then we confirm the evolutionary position of Hypochilidae. Moreover, we find that the GMC gene family exhibit high conservation throughout the evolution of true spiders. We also find that the MaSp genes of E. davidi may represent an early stage of MaSp and MiSp genes in other true spiders, while CrSp shares a common origin with AgSp and PySp but differ from MaSp. Altogether, this study contributes to addressing the limited availability of genomic sequences from Hypochilidae spiders, and provides a valuable resource for investigating the genomic evolution of spiders.

Examining the expression and correlation of trip13 and angpt1 in small cell lung cancer: a professional exploration with an analogy to football players

This professional exploration delves into the intricate realm of thyroid hormone receptor interactor 13 (TRIP13) and angiopoietin-1 (ANGPT1) within the context of small cell lung cancer (SCLC). Drawing parallels to the precision and teamwork exemplified by football players on the field, we meticulously investigate the expression patterns and correlations of these molecular players in the complex landscape of SCLC. Our study encompassed a cohort of 78 SCLC patients treated at our institution between January 2015 and April 2017. Through rigorous immunohistochemical staining, we scrutinized the expression profiles of TRIP13 and ANGPT1 within tumor tissues, seeking to unravel their associations with clinicopathological characteristics and progression-free survival. Noteworthy findings emerged from our analysis. We observed significantly elevated positive expression rates of TRIP13 in SCLC tissues with lower differentiation levels and liver metastases, highlighting the analogy to football players' precise maneuvers. Similarly, ANGPT1 exhibited markedly increased positive expression rates in cases with larger tumor diameters, lower differentiation, and liver metastases, akin to a coordinated football team's collective effort. Our professional exploration uncovered a compelling positive correlation between the expression levels of TRIP13 and ANGPT1 in SCLC, akin to the synergy seen among football players on the field. This molecular partnership shed light on an intriguing aspect of SCLC's pathophysiology. The impact on progression-free survival time further emphasized the clinical relevance of TRIP13 and ANGPT1 in SCLC. Patients expressing both TRIP13 and ANGPT1 or either molecule alone experienced significantly shorter mean progression-free survival times, akin to the swift tactics and strategies employed by football players in a high-stakes game. (AU)

The phenolic profile of walnut meal protein isolate and interaction of phenolics with walnut protein.

The aim of this study was to interpret the interaction of phenolics with walnut protein and determine their effects on protein functional properties. The phenolic profiles of walnut meal (WM) and walnut meal protein isolate (WMPI) were established using UPLC-Q-TOF-MS. A total of 132 phenolic compounds were detected, including 104 phenolic acids and 28 flavonoids. Phenolic compounds bound to protein via hydrophobic interactions, hydrogen bonds, and ionic bonds were identified in WMPI. They were also present as free forms, but the hydrophobic interactions and hydrogen bonds were the main non-covalent binding forces between phenolics and walnut proteins. The interaction mechanisms were further supported by the fluorescence spectra of WMPI with ellagic acid and quercitrin. In addition, changes in the functional properties of WMPI after removal of phenolic compounds were evaluated. Dephenolization significantly increased water holding capacity, oil absorptive capacity, foaming capacity, foaming stability, emulsifying stability index, and the in vitro gastric digestibility. However, in vitro gastric-intestinal digestibility was not significantly affected. These results provide insights into the interactions between walnut protein and phenolics, which indicates potential strategies for removing phenolics from walnut protein.

Association of solute carrier family 30 A8 zinc transporter gene variations with gestational diabetes mellitus risk in a Chinese population.

Background: The solute carrier family 30 A8 zinc transporter (SLC30A8) plays a crucial role in insulin secretion. This study aimed to investigate the impact of SLC30A8 gene polymorphisms on gestational diabetes mellitus (GDM). Methods: The research objective was to select 500 patients with GDM and 502 control subjects. Rs13266634 and rs2466293 were genotyped using the SNPscan™ genotyping assay. Statistical tests, such as the chi-square test, t-test, logistic regression, ANOVA, and meta-analysis, were conducted to determine the differences in genotypes, alleles, and their associations with GDM risk. Results: Statistically significant differences were observed in age, pregestational BMI, SBP, DBP, and parity between individuals with GDM and healthy subjects (P < 0.05). After adjusting for these factors, rs2466293 remained significantly associated with an increased risk of GDM in overall subjects (GG+AG vs. AA: OR = 1.310; 95% CI: 1.005-1.707; P = 0.046, GG vs. AA: OR = 1.523; 95% CI: 1.010-2.298; P = 0.045 and G vs. A: OR = 1.249; 95% CI: 1.029-1.516; P = 0.024). Rs13266634 was still found to be significantly associated with a decreased risk of GDM in individuals aged ≥ 30 years (TT vs. CT+CC: OR = 0.615; 95% CI: 0.392-0.966; P = 0.035, TT vs. CC: OR = 0.503; 95% CI: 0.294-0.861; P = 0.012 and T vs. C: OR =0.723; 95% CI: 0.557-0.937; P = 0.014). Additionally, the haplotype CG was found to be associated with a higher risk of GDM (P < 0.05). Furthermore, pregnant women with the CC or CT genotype of rs13266634 exhibited significantly higher mean blood glucose levels than those with the TT genotype (P < 0.05). Our findings were further validated by the results of a meta-analysis. Conclusion: The SLC30A8 rs2466293 polymorphism was found to be associated with an increased risk of GDM, while rs13266634 was associated with a decreased risk of GDM in individuals aged ≥ 30 years. These findings provide a theoretical basis for GDM testing.

Artesunate Inhibits Apoptosis and Promotes Survival in Schwann Cells via the PI3K/AKT/mTOR Axis in Diabetic Peripheral Neuropathy.

Diabetic peripheral neuropathy (DPN) is an early developing complication of diabetes mellitus associated with nerve dysfunction. Artesunate (ART), a natural compound extracted from the herb Artemisia annua L., was reported to benefit neural injury. However, whether ART has a role in preventing DPN is still unknown. In this study, a rat model of DPN with a high fat diet feeding and streptozotocin (STZ) injection was established. The findings indicated that ART treatment significantly ameliorated hyperglycemia-induced hot plate reaction latency (HPRL) decline, cold sensitivity and mechanical allodynia, and nerve injury by inhibiting sciatic nerve apoptosis. Further, ART restored high glucose (HG)-induced elevated apoptosis and deficient survival in rat neuronal Schwann cells, RSC96 cells. We demonstrated that ART promoted protein kinase B (AKT) phosphorylation as well as its downstream factor mammalian target of rapamycin (mTOR) in vivo and in vitro. Of note, the protective effects of ART in RSC96 cells under HG condition could be counteracted by LY294002, a phosphatidylinositol 3-kinase (PI3K) inhibitor. Taken together, ART mitigated hyperglycemia-induced nerve injury by suppressing apoptosis and promoting the viability of Schwann cells via the PI3K/AKT/mTOR signaling pathway.

Nanocomplexes of Biodegradable Anticancer Macromolecules: Prolonged Plasma Half-Life, Reduced Toxicity, and Increased Tumor Targeting.

Anticancer drug resistance is a large contributing factor to the global mortality rate of cancer patients. Anticancer macromolecules such as polymers have been recently reported to overcome this issue. Anticancer macromolecules have unselective toxicity because they are highly positively charged. Herein, an anionic biodegradable polycarbonate carrier is synthesized and utilized to form nanocomplexes with an anticancer polycarbonate via self-assembly to neutralize its positive charges. Biotin is conjugated to the anionic carrier and serves as cancer cell-targeting moiety. The nanoparticles have sizes of < 130 nm with anticancer polymer loading levels of 38-49%. Unlike the small molecular anticancer drug doxorubicin, the nanocomplexes effectively inhibit the growth of both drug-susceptible MCF7 and drug-resistant MCF7/ADR human breast cancer cell lines with low half maximal inhibitory concentration (IC50 ). The nanocomplexes increase the anticancer polymer's in vivo half-life from 1 to 6-8 h, and rapidly kill BT474 human breast cancer cells primarily via an apoptotic mechanism. The nanocomplexes significantly increase the median lethal dose (LD50 ) and reduce the injection site toxicity of the anticancer polymer. They suppress tumor growth by 32-56% without causing any damage to the liver and kidneys. These nanocomplexes may potentially be used for cancer treatment to overcome drug resistance.

Evaluation of Inflammatory Infiltration in the Retroperitoneal Space of Acute Pancreatitis Using Computer Tomography and Its Correlation with Clinical Severity.

This paper investigates the correlation between the degree and severity of CT inflammatory infiltration in the retroperitoneal space of acute pancreatitis (AP). A total of 113 patients were included based on diagnostic criteria. The general data of the patients and the relationship between the computed tomography severity index (CTSI) and pleural effusion (PE), involvement, degree of inflammatory infiltration of retroperitoneal space (RPS), number of peripancreatic effusion sites, and degree of pancreatic necrosis on contrast-enhanced CT at different times were studied. The results showed that the mean age of onset in females was later than that in males; 62 cases involved RPS to varying degrees, with a positive rate of 54.9% (62/113), and the total involvement rates of only the anterior pararenal space (APS); both APS and perirenal space (PS); and APS, PS, and posterior pararenal space (PPS) were 46.9% (53/113), 53.1% (60/113), and 17.7% (20/113), respectively. The degree of inflammatory infiltration in the RPS worsened with the increase in CTSI score; the incidence of PE was higher in the group greater than 48 hours than in the group less than 48 hours; necrosis >50% grade was predominant (43.2%) 5 to 6 days after onset, with a higher detection rate than other time periods (P < 0.05). Thus, when the PPS was involved, the patient's condition can be treated as severe acute pancreatitis (SAP); the higher the degree of inflammatory infiltration in the retroperitoneum, the higher the severity of AP. Enhanced CT examination 5 to 6 days after onset in patients with AP revealed the greatest extent of pancreatic necrosis.

Influencing factors and predictive model of postoperative infection in patients with primary hepatic carcinoma.

BACKGROUND: The purpose of this study was to explore the risk factors for postoperative infection in patients with primary hepatic carcinoma (PHC), build a nomogram prediction model, and verify the model to provide a better reference for disease prevention, diagnosis and treatment. METHODS: This single-center study included 555 patients who underwent hepatobiliary surgery in the Department of Hepatobiliary Surgery of Tianjin Third Central Hospital from January 2014 to December 2021, and 32 clinical indicators were selected for statistical analysis. In this study, Lasso logistic regression was used to determine the risk factors for infection after liver cancer resection, establish a predictive model, and construct a visual nomogram. The consistency index (C-index), calibration curve, and receiver operating characteristic (ROC) curve were used for internal validation, and decision curve analysis (DCA) was used to analyze the clinical applicability of the predictive model. The bootstrap method was used for intramodel validation, and the C-index was calculated to assess the model discrimination. RESULTS: Among the 555 patients, 279 patients met the inclusion criteria, of whom 48 had a postoperative infection, with an incidence rate of 17.2%. Body mass index (BMI) (P = 0.022), alpha-fetoprotein (P = 0.023), total bilirubin (P = 0.016), intraoperative blood loss (P < 0.001), and bile leakage (P < 0.001) were independent risk factors for infection after liver cancer surgery. The nomogram was constructed and verified to have good discriminative and predictive ability. DCA showed that the model had good clinical applicability. The C-index value verified internally by the bootstrap method results was 0.818. CONCLUSION: Postoperative infection in patients undergoing hepatectomy may be related to risk factors such as BMI, preoperative AFP level, TBIL level, intraoperative blood loss and bile leakage. The prediction model of the postoperative infection nomogram established in this study can better predict and estimate the risk of postoperative infection in patients undergoing hepatectomy.

Decompression via unilateral biportal endoscopy for severe degenerative lumbar spinal stenosis: A comparative study with decompression via open discectomy.

Background: Previous studies have shown that the Unilateral Biportal Endoscopy is an effective and safety surgery for sufficient decompression of degenerative lumbar spinal stenosis. However, data are lacking in terms of its benefits when compared with conventional open lumbar discectomy (OLD), especially in patients with severe degenerative lumbar spinal stenosis (DLSS). Aim: To compare the clini cal outcomes of two types decompressive surgery: unilateral biportal endoscopy-unilateral laminectomy bilateral decompression (UBE-ULBD) and conventional open lumbar discectomy (OLD) in severe degenerative lumbar spinal stenosis (DLSS). Methods: We retrospectively analyzed patients who underwent UBE-ULBD (n = 50, operated at 50 levels; UBE-ULBD group) and conventional open lumbar discectomy (n = 59, operated at 47 levels; OLD group) between February 2019 and July 2021. All patients were diagnosed with severe stenosis based on the Schizas classification (Grade C or D) on MRI. We compared radiographic and clinical outcome scores [including the visual analog scale (VAS), Oswestry Disability Index (ODI), and Zurich Claudication Questionnaire (ZCQ)] between the 2 groups at 1 year of follow-up. The radiographic evaluation included the cross-sectional area (CSA) of the thecal sac and paraspinal muscles on MRI. Fasting blood was drawn before and 1 and 7 days after the operation to detect creatine kinase (CK). Surgical data perioperative complications were also investigated. Results: The baseline demographic data of the 2 groups were comparable, including VAS, ODI and ZCQ scores, the cross-sectional area of the thecal sac and paraspinal muscles and creatine kinase levels. The dural sac CSA significantly increased post -operatively in both groups, which confirmed they benefited from comparable decompressive effects. The operative duration in the OLD group was less than the UBE-ULBD group (43.9 ± 5.6 min vs. 74.2 ± 9.3 min, p < 0.05). The OLD group was associated with more estimated blood loss than the UBE-ULBD group (111.2 ± 25.0 ml vs. 41.5 ± 22.2 ml, P < 0.05). The length of hospital stay (HS) was significantly longer in the OLD group than in the UBE-ULBD group (6.8 ± 1.6 vs. 4.0 ± 1.4 days, P < 0.05). The VAS, ODI, and ZCQ scores improved in both groups after the operation. Serum creatine kinase values in the UBE-ULBD group were significantly lower than in the OLD group at 1 day after surgery (108. 1 ± 11.9 vs. 347.0 ± 19.5 U/L, P < 0.05). The degree of paraspinal muscle atrophy in the UBE-ULBD group was significantly lower than in the OLD group at 1 year (4.50 ± 0.60 vs. 11.42 ± 0.87, P < 0.05). Conclusions: UBE-ULBD and conventional OLD demonstrate comparable short-term clinical outcomes in treating severe DLSS. However, UBE-ULBD surgery was associated with a shorter hospital stay, less EBL and paravertebral muscle injury than OLD surgery.