The relationship between innate/adaptive immunity and gastrointestinal cancer : a multi-omics Mendelian randomization study.

BACKGROUND: Innate/adaptive immunity is the key to anti-tumor therapy. However, its causal relationship to Gastrointestinal (GI) cancer remains unclear. METHODS: Immunity genes were extracted from the MSigDB database. The Genome-wide association studies (GWAS) summary data of GI cancer were integrated with expression quantitative trait loci (eQTL) and DNA methylation quantitative trait loci (mQTL) associated with genes. Summary-data-based Mendelian randomization (SMR) and co-localization analysis were used to reveal causal relationships between genes and GI cancer. Two-sample MR analysis was used for sensitivity analysis. Single cell analysis clarified the enrichment of genes. RESULTS: Three-step SMR analysis showed that a putative mechanism, cg17294865 CpG site regulating HLA-DRA expression was negatively associated with gastric cancer risk. HLA-DRA was significantly differentially expressed in monocyte/macrophage and myeloid cells in gastric cancer. CONCLUSION: This study provides evidence that upregulating the expression level of HLA-DRA can reduce the risk of gastric cancer.

Dimethyl Fumarate Attenuates Pain Behaviors in Osteoarthritis Rats via Induction of Nrf2-Mediated Mitochondrial Biogenesis.

AIMS: Osteoarthritis (OA), a chronic degenerative disease, leads to pain and loss of function. Existing treatments for OA pain have limited efficacy and show significant side effects. Dimethyl fumarate, a robust nuclear factor erythroid 2-related factor 2 (Nrf2) activator, could alleviate pain behaviors in chronic pain. This study aims to investigate the role of dimethyl fumarate in a rat model of OA and its underlying mechanisms. METHODS: We used von Frey filaments to assess the mechanical allodynia. Weight-bearing apparatus was employed to assess the hindlimb weight distribution. Western blot was employed to investigate the protein expressions of mitochondrial biogenesis markers. RT-qPCR was employed to examine the copy number of mitochondrial DNA (mtDNA). RESULTS: Dimethyl fumarate upregulated mechanical paw withdrawal threshold (MIA + Vehicle, 1.6 ± 0.13g [mean ± SEM]; MIA + DMF, 10.5 ± 0.96g; P ＜ 0.0001). Hindlimb weight distribution was alao upregulated by dimethyl fumarate (MIA + Vehicle, 38.17 ± 0.72g; MIA + DMF, 43.59 ± 1.01g; P ＜ 0.01). Besides, activation of Nrf2 remarkably upregulated the protein levels of PGC-1α (MIA + Vehicle, 0.69 ± 0.07; MIA + DMF, 1.08 ± 0.09; P = 0.0037), NRF1 (MIA + Vehicle, 0.69 ± 0.04; MIA + DMF, 1.00 ± 0.11; P = 0.0114), TFAM (MIA + Vehicle, 0.62 ± 0.11; MIA + DMF, 1.02 ± 0.12; P = 0.0147), and the copy number of mtDNA(MIA + Vehicle, 0.52 ± 0.05; MIA + DMF, 3.81 ± 0.21; P ＜ 0.0001) Conclusions: Taken together, these results show that dimethyl fumarate alleviated pain-related behaviors in a rat model of OA through activation of Nrf2-induced mitochondrial biogenesis.

DKK3 ameliorates neuropathic pain via inhibiting ASK-1/JNK/p-38-mediated microglia polarization and neuroinflammation.

BACKGROUND: Neuropathic pain is a common and severely disabling state that affects millions of people worldwide. Microglial activation in the spinal cord plays a critical role in the pathogenesis of neuropathic pain. However, the mechanisms underlying spinal microglial activation during neuropathic pain remain incompletely understood. Here, we investigated the role of Dickkopf (DKK) 3 and its interplay with microglial activation in the spinal cord in neuropathic pain. METHODS: In this study, we investigated the effects of intrathecal injection of recombinant DKK3 (rDKK3) on mechanical allodynia and microglial activation in the spinal cord after spared nerve injury (SNI) in rats by western blot (WB), immunofluorescence (IF), quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA). RESULTS: We found that SNI induced a significant decrease in the levels of DKK3, Kremen-1 and Dishevelled-1 (DVL-1) and up-regulated the expression of phosphorylated apoptosis signal-regulating kinase 1 (p-ASK1), phosphorylated c-JUN N-terminal kinase (p-JNK), phosphorylated p38 (p-p38) in the spinal cord. Moreover, our results showed that exogenous intrathecal administration of rDKK3 inhibited expression of p-ASK1, p-JNK, p-p38, promoted the transformation of microglia from M1 type to M2 type, and decreased the production of pro-inflammatory cytokines compared to the rats of SNI + Vehicle. However, these effects were reversed by intrathecal administration of Kremen-1 siRNA or Dishevelled-1 (DVL-1) siRNA. CONCLUSIONS: These results suggest that DKK3 ameliorates neuropathic pain via inhibiting ASK-1/JNK/p-38-mediated microglia polarization and neuroinflammation, at least partly, by the Kremen-1 and DVL-1 pathways.

Sestrin2 overexpression attenuates osteoarthritis pain via induction of AMPK/PGC-1α-mediated mitochondrial biogenesis and suppression of neuroinflammation.

BACKGROUND: Our previous study indicated that reactive oxygen species (ROS) are critically involved in chronic pain. Sestrin2 (Sesn2), a novel stress-inducible protein, is evidenced to reduce the generation of ROS. The study examined the role of Sesn2 in osteoarthritis (OA) pain and delineated the underlying molecular mechanisms. METHODS: In the present study, we investigated the impact of Sesn2 on mitochondrial biogenesis in a rat model of OA pain. After adeno-associated viral (AAV)-Sesn2EGFP was injected for 14 days, OA was induced by intra-articular injection of monosodium iodoacetate (MIA). We assessed pain behaviors (weight-bearing asymmetry and paw withdrawal threshold) and explored possible mechanisms in the L4-6 spinal cord. RESULTS: Our results showed that overexpression of Sesn2 in the spinal cord alleviated pain behaviors in OA rats. Moreover, overexpression of Sesn2 increased the activity of AMP-activated protein kinase (AMPK) signaling and significantly restored mitochondrial biogenesis. Besides, Sesn2 overexpression inhibited the activation of astrocytes and microglia, and decreased the production of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the spinal cord of the OA pain rats. These effects were significantly reversed by an AMPK inhibitor. CONCLUSIONS: Collectively, these results suggest that Sesn2 overexpression ameliorates mechanical allodynia and weight-bearing asymmetry in OA rats via activation of AMPK/PGC-1α-mediated mitochondrial biogenesis in the spinal cord. Moreover, Sesn2 overexpression attenuates OA-induced neuroinflammation at least partly by activating AMPK signaling. Sesn2 may become an encouraging therapeutic strategy for OA pain relief and other disorders.

Coupling PEDOT on Mesoporous Vanadium Nitride Arrays for Advanced Flexible All-Solid-State Supercapacitors.

Tailored construction of advanced flexible supercapacitors (SCs) is of great importance to the development of high-performance wearable modern electronics. Herein, a facile combined wet chemical method to fabricate novel mesoporous vanadium nitride (VN) composite arrays coupled with poly(3,4-ethylenedioxythiophene) (PEDOT) as flexible electrodes for all-solid-state SCs is reported. The mesoporous VN nanosheets arrays prepared by the hydrothermal-nitridation method are composed of cross-linked nanoparticles of 10-50 nm. To enhance electrochemical stability, the VN is further coupled with electrodeposited PEDOT shell to form high-quality VN/PEDOT flexible arrays. Benefiting from high intrinsic reactivity and enhanced structural stability, the designed VN/PEDOT flexible arrays exhibit a high specific capacitance of 226.2 F g-1 at 1 A g-1 and an excellent cycle stability with 91.5% capacity retention after 5000 cycles at 10 A g-1 . In addition, high energy/power density (48.36 Wh kg-1 at 2 A g-1 and 4 kW kg-1 at 5 A g-1 ) and notable cycling life (91.6% retention over 10 000 cycles) are also achieved in the assembled asymmetric flexible supercapacitor cell with commercial nickel-cobalt-aluminum ternary oxides cathode and VN/PEDOT anode. This research opens up a way for construction of advanced hybrid organic-inorganic electrodes for flexible energy storage.

Bifunctional NiFe layered double hydroxide@Ni3S2 heterostructure as efficient electrocatalyst for overall water splitting.

The tailored construction of non-noble metal bifunctional electrocatalysts for high-efficiency oxygen/hydrogen evolution reactions (OER/HER) is vital for the development of electrochemical energy conversion. Herein, we report a powerful combined wet chemical method to fabricate a novel binder-free NiFe layered double hydroxide@Ni3S2 (NiFe LDH@Ni3S2) heterostructure as an efficient bifunctional electrocatalyst for overall water splitting. The hydrothermal-synthesized NiFe LDH nanosheets are uniformly coated on the Ni3S2 nanosheet skeleton forming 3D porous heterostructure arrays. By virtue of its synergistic advantages, including its binder-free characteristics, increased catalysis sites and structural stability, the as-obtained NiFe LDH@Ni3S2/NF electrode exhibits low overpotentials of 184 and 271 mV at 20 mA cm-2 for HER and OER in 1 M KOH, respectively. Notably, a low operation potential of 1.74 V at a current density of 20 mA cm-2 is achieved for overall water splitting with a stable cycling life. In addition, the intimate composite structure and sensitive interface of NiFe LDH@Ni3S2 are responsible for the good electrocatalytic activity with a low Tafel slope, fast reaction kinetics and high stability. The versatile fabrication protocol and heterostructure interface engineering provide a new way to construct other bifunctional and cost-effective electrocatalysts for electrocatalysis.

The Association of D-dimer and Spontaneous Hemorrhagic Ascites with Outcomes in Cirrhosis: a Retrospective Study.

BACKGROUND: Cirrhotic patients with hemorrhagic ascites have significant morbidity and mortality. This study aims to determine the relationship between D-dimer values and hemorrhagic ascites in cirrhotic patients and analyze its predictive value. METHODS: This retrospective study screened 572 consecutive cirrhotic patients with ascites and hemorrhagic ascites (defined as red blood cells (RBC) in ascitic fluid ≥ 10,000/µL) during a 72-month period. The overall patient survival rate was measured by Kaplan-Meier analysis method. The relationship between D-dimer and hemorrhagic ascites was also examined. A multivariate Cox proportional hazard analysis was performed to assess the indepen-dent risk factors related to mortality. RESULTS: Both control group and hemorrhagic ascites patients had obvious hepatic dysfunction as determined by Model for End-Stage Liver Disease (MELD) scores of 6.37 ± 1.05 and 11.82 ± 2.86, respectively (p < 0.001). There was a higher prevalence of patients with significant ascites in those with spontaneous hemorrhagic ascites than in the control group (p = 0.003). There were significant differences in D-dimer levels between both groups (9.44 ± 5.11 vs. 26.83 ± 5.35, p < 0.001). Hemorrhagic ascites was significantly and positively correlated with D-dimer levels (r = 0.692, p < 0.0001). The area under the receiver operating characteristic (ROC) curve was 0.9838. Using Cox proportional hazard model for multivariate prognostic analysis, MELD, D-dimer and presence of spontaneous hemorrhagic ascites were independent predictors of 3-year mortality. CONCLUSIONS: Patients with hemorrhagic ascites had a significantly higher MELD score, D-dimer, and mortality than patients with ascites alone. D-dimer was associated with the appearance of hemorrhagic ascites and was found to be a marker of advanced liver disease and poor outcomes.

Images of Anomalous Origin of The Right Coronary Artery From the Pulmonary Artery.

Anomalies of the coronary arteries -- especially their abnormal origin from the pulmonary artery (ARCAPA) trunk -- are among the least common. They're also the most dangerous of congenital heart defects with an incidence of 0.002% in the general population [Williams 2006]. The diagnosis exceedingly is difficult because anatomical abnormalities of the coronary arteries are subtle. We present a case of an anomalous origin of the right coronary artery.

Comparison of Totally Thoracoscopic and Traditional Sternotomy Approaches for Mitral Valve Replacement.

BACKGROUND: We aimed to investigate the feasibility and safety of mitral valve replacement using a totally thoracoscopic approach in comparison with traditional median sternotomy. METHODS: Between January 2016 and December 2017, 94 consecutive patients who underwent mitral valve replacement were divided into two groups: A thoracoscopic group (43 cases) and a traditional group (51 cases). For the thoracoscopic group, all patients underwent total thoracoscopic procedures with femoral arterial and venous cannulation to cardiopulmonary bypass, transthoracic aortic cross-clamp, and antegrade cardioplegia. Three intercostal ports in the right chest were used for access in the thoracoscopic group. The operation was performed completely under two-dimensional video. For the traditional group, all operations were done with traditional median sternotomy. RESULTS: All the operations were successfully performed. The thoracoscopic group had longer aortic cross-clamping and cardiopulmonary bypass times compared with the traditional group (62.30 ± 8.17 minutes versus 44.90 ± 12.00 minutes, P < .001; 92.33 ± 12.03 minutes versus 74.22 ± 14.72 minutes, P < .001). The two groups did not show statistically significant differences with respect to operative times (184.26 ± 32.49 minutes versus 181.47 ± 23.31 minutes, P = .631). In addition, the postoperative mechanical ventilation, ICU stay, and postoperative hospital stay times and postoperative drainage were 10.14 ± 2.21 hours and 11.35 ± 2.58 hours (P = .016), 21.40 ± 3.15 hours and 29.12 ± 6.59 hours (P < .001), 8.70 ± 2.52 days and 10.04 ± 3.11 days (P = .023), and 325.71 ± 97.11 mL and 396.57 ± 121.50 mL (P < .001), respectively. Major postoperative complications occurred in three (6.98%, P = .873) cases of the thoracoscopic group. Four (7.84%) cases of the traditional group had postoperative complications. CONCLUSIONS: Despite the disadvantages such as long cross-clamp and cardiopulmonary bypass times, totally thoracoscopic mitral valve replacement is feasible and safe. More importantly, one of the principal advantages with three intercostal ports over standard sternotomy is avoiding retrosternal adhesion, thus lowering the risk of needing to redo a cardiac procedure in the future.

Structure and mechanism of the uracil transporter UraA.

The nucleobase/ascorbate transporter (NAT) proteins, also known as nucleobase/cation symporter 2 (NCS2) proteins, are responsible for the uptake of nucleobases in all kingdoms of life and for the transport of vitamin C in mammals. Despite functional characterization of the NAT family members in bacteria, fungi and mammals, detailed structural information remains unavailable. Here we report the crystal structure of a representative NAT protein, the Escherichia coli uracil/H(+) symporter UraA, in complex with uracil at a resolution of 2.8 Å. UraA has a novel structural fold, with 14 transmembrane segments (TMs) divided into two inverted repeats. A pair of antiparallel ß-strands is located between TM3 and TM10 and has an important role in structural organization and substrate recognition. The structure is spatially arranged into a core domain and a gate domain. Uracil, located at the interface between the two domains, is coordinated mainly by residues from the core domain. Structural analysis suggests that alternating access of the substrate may be achieved through conformational changes of the gate domain.

Rutin attenuates neuroinflammation in spinal cord injury rats.

BACKGROUND: Neuroinflammatory responses involve the activation of the interleukin (IL) -1ß and IL-18. Processing and activation of the pro-inflammatory IL require NLRP3 inflammasome activation. Rutin can protect spinal cord against damage, but the potential mechanisms underlying remain unknown. Here, we investigated the molecular mechanisms of rutin-mediated neuroprotection in a rat model of spinal cord injury (SCI). MATERIALS AND METHODS: One hundred twenty female Sprague-Dawley rats were randomly assigned to four groups: sham group, SCI group, SCI + Rutin50 group, and the SCI + Rutin100 group. The influences of rutin on inflammatory marker levels, histologic alterations, and locomotion scale were analyzed. RESULTS: SCI significantly increased the expression of the NLRP3, ASC, IL-1ß, IL-18, and tumor necrosis factor-alpha. Rutin significantly reduced the levels of reactive oxygen species, malondialdehyde, NLRP3, ASC, caspase-1, IL-1ß, IL-18, and tumor necrosis factor-alpha. Furthermore, rutin administration significantly attenuated histologic alteration and improved locomotion recovery. CONCLUSIONS: Our data provide clear evidence that rutin attenuates tissue damage and improves locomotion recovery, and the mechanism may be related to the alleviation of inflammation and oxidative stress.

Human herpes virus 8-unrelated primary effusion lymphoma-like lymphoma in a patient with hepatitis B virus-related liver cirrhosis: A case report.

This study describes a rare case of Human Immunodeficiency Virus and Human Herpes Virus 8 (HHV-8) negative primary effusion lymphoma (PEL)-like lymphoma in a patient with hepatitis B virus-related liver cirrhosis, diagnosed in a 66-year-old male who rapidly progressed to a sense of abdominal fullness. Cytological analysis of the pleural effusion demonstrated large atypical lymphoid cells with rounded nuclei, prominent nucleoli, and abundant cytoplasm. Immunocytochemistry of the pleural effusion detected atypical CD20(+) lymphoid cells. The patient was hospitalized, and died following sepsis and multi-organ failure. Our case highlights that HHV-8-unrelated PEL-like lymphoma patients have different pathogenetic mechanisms of causality at the biological level, immunophenotype, clinical behavior, and prognosis.

Full-Endoscopic Transforaminal Debridement and Decompression for Brucellar Thoracic Spinal Epidural Abscess: A Minimally Invasive Alternative to Open Surgery.

OBJECTIVE: Thoracic spinal epidural abscess (SEA) is a rare but dangerous condition, and traditional surgical methods are accompanied by extensive trauma and approach-related complications. Here we introduce the technique of full-endoscopic transforaminal debridement and decompression and evaluate its feasibility for treating brucellar thoracic SEA. METHODS: We performed thoracic full-endoscopic transforaminal decompression and debridement on two patients with neurological deficits caused by brucellar SEA, which is mainly composed of granulation tissue rather than pus. Postoperative MRI was conducted to confirm the presence of any residual abscess compressing the nerves. Frankel grading was employed to assess the recovery of neurological function, and complications were documented. RESULTS: There were no occurrences of dural tear, postoperative hematoma, or pulmonary complications. Their neurological function had significantly improved after surgery, and postoperative MRI confirmed no residual abscess compressing the spinal cord. During the 2-year follow-up, one patient achieved complete recovery (from Frankel-C to Frankel-E), while another patient improved from Frankel-A to Frankel-D. Neither patient experienced infection recurrence, instability, nor kyphotic deformity. CONCLUSION: We described the novel application of transforaminal endoscopic surgery in brucellar thoracic granulomatous SEA and preliminarily indicated the feasibility of this technique as a minimally invasive alternative to open surgery.

Interleukin-17: A Putative Novel Pharmacological Target for Pathological Pain.

Pathological pain imposes a huge burden on the economy and the lives of patients. At present, drugs used for the treatment of pathological pain have only modest efficacy and are also plagued by adverse effects and risk for misuse and abuse. Therefore, understanding the mechanisms of pathological pain is essential for the development of novel analgesics. Several lines of evidence indicate that interleukin-17 (IL-17) is upregulated in rodent models of pathological pain in the periphery and central nervous system. Besides, the administration of IL-17 antibody alleviated pathological pain. Moreover, IL-17 administration led to mechanical allodynia which was alleviated by the IL-17 antibody. In this review, we summarized and discussed the therapeutic potential of targeting IL-17 for pathological pain. The upregulation of IL-17 promoted the development of pathological pain by promoting neuroinflammation, enhancing the excitability of dorsal root ganglion neurons, and promoting the communication of glial cells and neurons in the spinal cord. In general, the existing research shows that IL-17 is an attractive therapeutic target for pathologic pain, but the underlying mechanisms still need to be investigated.

Rational engineering S1' substrate binding pocket to enhance substrate specificity and catalytic activity of thermal-stable keratinase for efficient keratin degradation.

This study reports the rational engineering of the S1' substrate-binding pocket of a thermally-stable keratinase from Pseudomonas aeruginosa 4-3 (4-3Ker) to improve substrate specificity to typical keratinase (K/C > 0.5) and catalytic activity without compromising thermal stability for efficient keratin degradation. Of 10 chosen mutation hotspots in the S1' substrate-binding pocket, the top three mutations M128R, A138V, and V142I showing the best catalytic activity and substrate specificity were identified. Their double and triple combinatorial mutants synergistically overcame limitations of single mutants, fabricating an excellent M128R/A138V/V142I triple mutant which displayed a 1.21-fold increase in keratin catalytic activity, 1.10-fold enhancement in keratin/casein activity ratio, and a 3.13 °C increase in half-inactivation temperature compared to 4-3Ker. Molecular dynamics simulations revealed enhanced flexibility of critical amino acid residues at the substrate access tunnel, improved global protein rigidity, and heightened hydrophobicity within the active site likely underpinned the increased catalytic activity and substrate specificity. Additionally, the triple mutant improved the feather degradation rate by 32.86 % over the wild-type, far exceeding commercial keratinase in substrate specificity and thermal stability. This study exemplified engineering a typical keratinase with enhanced substrate specificity, catalytic activity, and thermal stability from thermally-stable 4-3Ker, providing a more robust tool for feather degradation.

Targeting the JAK2/STAT3 signaling pathway for chronic pain.

Chronic pain is a notable health concern because of its prevalence, persistence, and associated mental stress. Drugs targeting chronic pain with potent abirritation, and minimal side effects remain unidentified. Substantial evidence indicates that the Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway plays a distinct and critical role in different stages of chronic pain. Aberrant activation of the JAK2/STAT3 signaling pathway is evident in multiple chronic pain models. Moreover, an increasing number of studies have demonstrated that the downregulation of JAK2/STAT3 can attenuate chronic pain in different animal models. In this review, we investigated the mechanism and role of the JAK2/STAT3 signaling pathway in modulating chronic pain. The aberrant activation of JAK2/STAT3 can trigger chronic pain by interacting with microglia and astrocytes, releasing proinflammatory cytokines, inhibiting anti-inflammatory cytokines, and regulating synaptic plasticity. We also retrospectively reviewed current reports on JAK2/STAT3 pharmacological inhibitors that demonstrated their significant therapeutic potential in different types of chronic pain. In summary, our results provide strong evidence that the JAK2/STAT3 signaling pathway is a promising therapeutic target for chronic pain.

Matrix metalloproteinases as attractive therapeutic targets for chronic pain: A narrative review.

Chronic pain constitutes an abnormal pain state that detrimentally affects the quality of life, daily activities, occupational performance, and stability of mood. Despite the prevalence of chronic pain, effective drugs with potent abirritation and minimal side effects remain elusive. Substantial studies have revealed aberrant activation of the matrix metalloproteinases (MMPs) in multiple chronic pain models. Additionally, emerging evidence has demonstrated that the downregulation of MMPs can alleviate chronic pain in diverse animal models, underscoring the unique and crucial role of MMPs in different stages and types of chronic pain. This review delves into the mechanistic insights and roles of MMPs in modulating chronic pain. The aberrant activation of MMPs has been linked to neuropathic pain through mechanisms involving myelin abnormalities in peripheral nerve and spinal dorsal horn (SDH), hyperexcitability of dorsal root ganglion (DRG) neurons, activation of N-methyl-d-aspartate receptors (NMDAR) and Ca2+-dependent signals, glial cell activation, and proinflammatory cytokines release. Different MMPs also contribute significantly to inflammatory pain and cancer pain. Furthermore, we summarized the substantial therapeutic potential of MMP pharmacological inhibitors across different types of chronic pain. Overall, our findings underscore the promising therapeutic prospects of MMPs targeting for managing chronic pain.

Photodissociation of gaseous CH3COSH at 248 nm by time-resolved Fourier-transform infrared emission spectroscopy: observation of three dissociation channels.

Upon one-photon excitation at 248 nm, gaseous CH(3)C(O)SH is dissociated following three pathways with the products of (1) OCS + CH(4), (2) CH(3)SH + CO, and (3) CH(2)CO + H(2)S that are detected using time-resolved Fourier-transform infrared emission spectroscopy. The excited state (1)(n(O), π*(CO)) has a radiative lifetime of 249 ± 11 ns long enough to allow for Ar collisions that induce internal conversion and enhance the fragment yields. The rate constant of collision-induced internal conversion is estimated to be 1.1 × 10(-10) cm(3) molecule(-1) s(-1). Among the primary dissociation products, a fraction of the CH(2)CO moiety may undergo further decomposition to CH(2) + CO, of which CH(2) is confirmed by reaction with O(2) producing CO(2), CO, OH, and H(2)CO. Such a secondary decomposition was not observed previously in the Ar matrix-isolated experiments. The high-resolution spectra of CO are analyzed to determine the ro-vibrational energy deposition of 8.7 ± 0.7 kcal/mol, while the remaining primary products with smaller rotational constants are recognized but cannot be spectrally resolved. The CO fragment detected is mainly ascribed to the primary production. A prior distribution method is applied to predict the vibrational distribution of CO that is consistent with the experimental findings.

Use of (18)F-FDG PET/CT to locate primary malignancies in patients with hepatic cirrhosis and malignant ascites.

OBJECTIVE: Ascites in patients with hepatic cirrhosis is caused by cirrhosis in most cases. For most malignant ascites, the primary malignancy could be readily identified using conventional imaging methods, e.g., computed tomography (CT) and magnetic resonance imaging (MRI). However, in a small fraction of the patients, the primary malignancy remains occult even with these examinations. In this retrospective study, we assessed the usefulness of (18)F-FDG PET/CT in patients with hepatic cirrhosis and malignant ascites of otherwise unknown origin. METHODS: Twenty-eight patients with malignant ascites of unknown primary sites after CT, MRI and ultrasound during the period of five years between January 2008 and December 2012 had received (18)F-FDG PET/CT. Medical records of these patients were reviewed and analyzed. RESULTS: Elevated (18)F-FDG absorption was found in 23 of 28 cases in the following sites: gastrointestinal tract (n=10, 43.5%), prostate (n=5, 21.7%), peritoneum (n=4, 13.3%), and ovary (n=4, 13.3%). Cancer was confirmed by pathology in 20 cases after open or laparoscopic surgeries. Five patients were found to have benign ascites, among which, 3 were found to be false positive due to tuberculosis. SUV values were significantly higher for tumors than for benign lesions (mean values, 6.95 vs. 2.94; P=0.005). CONCLUSIONS: The (18)F-FDG PET/CT can be as a powerful imaging tool in identifying tissue origin in liver cirrhosis patients suspected of cancers or with cancers of unknown primary sites.

Ultrasound-guided Jamshidi needle puncture to reduce radiation exposure during percutaneous pedicle screw placement: study protocol for a randomised controlled trial.

INTRODUCTION: Percutaneous pedicle screw placement (PPSP) is a minimally invasive procedure highly dependent on fluoroscopic guidance, which results in increased radiation exposure and prolonged operative time. Ultrasound can image the lumbar paravertebral anatomy and the needle trajectory in real time, which may help reduce the use of fluoroscopy and radiation dose in PPSP. We will conduct a parallel randomised controlled trial to mainly investigate the effect of ultrasound guidance in radiation reduction during PPSP. METHODS AND ANALYSIS: A total of 42 patients will be recruited and randomly assigned to the intervention group and the control group at a 1:1 ratio. In the intervention group, we will use ultrasound in combination with fluoroscopy to guide the insertion of the Jamshidi needles. In the control group, PPSP will be performed under conventional fluoroscopic guidance. The primary outcomes are the cumulative fluoroscopy time (s), radiation dose (mGy) and exposure times of screw placement. The secondary outcomes are insertion time of guidewire, rate of pedicle perforation, rate of facet joint violation, visual analogue scale for back pain, Oswestry Disability Index and complications. The participants, outcome assessors and data analysts will be blinded to allocation. ETHICS AND DISSEMINATION: The trial was approved by the research ethics committee of Shengjing Hospital, China Medical University. The results will be presented at academic seminars and submitted for publication in peer-reviewed journals.This study involves human participants and was approved by Research Ethics Committee of Shengjing Hospital, China Medical University reference number：2022PS704K. Participants gave informed consent to participate in the study before taking part. TRIAL REGISTRATION NUMBER: ChiCTR2200057131.