Functional-structural large-scale brain networks are correlated with neurocognitive impairment in acute mild traumatic brain injury.

Background: This study was conducted to investigate topological changes in large-scale functional connectivity (FC) and structural connectivity (SC) networks in acute mild traumatic brain injury (mTBI) and determine their potential relevance to cognitive impairment. Methods: Seventy-one patients with acute mTBI (29 males, 42 females, mean age 43.54 years) from Nanjing First Hospital and 57 matched healthy controls (HC) (33 males, 24 females, mean age 46.16 years) from the local community were recruited in this prospective study. Resting-state functional magnetic resonance imaging (rs-fMRI) and diffusion tensor imaging (DTI) were acquired within 14 days (mean 3.29 days) after the onset of mTBI. Then, large-scale FC and SC networks with 116 regions from the automated anatomical labeling (AAL) brain atlas were constructed. Graph theory analysis was used to analyze global and nodal metrics. Finally, correlations were assessed between topological properties and neurocognitive performances evaluated by the Montreal Cognitive Assessment (MoCA). Bonferroni correction was performed out for multiple comparisons in all involved analyses. Results: Compared with HC, acute mTBI patients had a higher normalized clustering coefficient (γ) for FC (Cohen's d=4.076), and higher γ and small worldness (σ) for SC (Cohen's d=0.390 and Cohen's d=0.395). The mTBI group showed aberrant nodal degree (Dc), nodal efficiency (Ne), and nodal local efficiency (Nloc) for FC and aberrant Dc, nodal betweenness (Bc), nodal clustering coefficient (NCp) and Ne for SC mainly in the frontal and temporal, cerebellum, and subcortical areas. Acute mTBI patients also had higher functional-structural coupling strength at both the group and individual levels (Cohen's d=0.415). These aberrant global and nodal topological properties at functional and structural levels were associated with attention, orientation, memory, and naming performances (all P<0.05). Conclusions: Our findings suggested that large-scale FC and SC network changes, higher correlation between FC and SC and cognitive impairment can be detected in the acute stage of mTBI. These network aberrances may be a compensatory mechanism for cognitive impairment in acute mTBI patients.

Rich-club reorganization of functional brain networks in acute mild traumatic brain injury with cognitive impairment.

Background: Mild traumatic brain injury (mTBI) is typically characterized by temporally limited cognitive impairment and regarded as a brain connectome disorder. Recent findings have suggested that a higher level of organization named the "rich-club" may play a central role in enabling the integration of information and efficient communication across different systems of the brain. However, the alterations in rich-club organization and hub topology in mTBI and its relationship with cognitive impairment after mTBI have been scarcely elucidated. Methods: Resting-state functional magnetic resonance imaging (rs-fMRI) data were collected from 88 patients with mTBI and 85 matched healthy controls (HCs). Large-scale functional brain networks were established for each participant. Rich-club organizations and network properties were assessed and analyzed between groups. Finally, we analyzed the correlations between the cognitive performance and changes in rich-club organization and network properties. Results: Both mTBI and HCs groups showed significant rich-club organization. Meanwhile, the rich-club organization was aberrant, with enhanced functional connectivity (FC) among rich-club nodes and peripheral regions in acute mTBI. In addition, significant differences in partial global and local network topological property measures were found between mTBI patients and HCs (P<0.01). In patients with mTBI, changes in rich-club organization and network properties were found to be related to early cognitive impairment after mTBI (P<0.05). Conclusions: Our findings suggest that such patterns of disruption and reorganization will provide the basic functional architecture for cognitive function, which may subsequently be used as an earlier biomarker for cognitive impairment after mTBI.

The elephant grass (Cenchrus purpureus) genome provides insights into anthocyanidin accumulation and fast growth.

Elephant grass (2n = 4x = 28; Cenchrus purpureus Schumach.), also known as Napier grass, is an important forage grass and potential energy crop in tropical and subtropical regions of Asia, Africa and America. However, no study has yet reported a genome assembly for elephant grass at the chromosome scale. Here, we report a high-quality chromosome-scale genome of elephant grass with a total size of 1.97 Gb and a 1.5% heterozygosity rate, obtained using short-read sequencing, single-molecule long-read sequencing and Hi-C chromosome conformation capture. Evolutionary analysis showed that subgenome A' of elephant grass and pearl millet may have originated from a common ancestor more than 3.22 million years ago (MYA). Further, allotetraploid formation occurred at approximately 6.61 MYA. Syntenic analyses within elephant grass and with other grass species indicated that elephant grass has experienced chromosomal rearrangements. We found that some key enzyme-encoding gene families related to the biosynthesis of anthocyanidins and flavonoids were expanded and highly expressed in leaves, which probably drives the production of these major anthocyanidin compounds and explains why this elephant grass cultivar has a high anthocyanidin content. In addition, we found a high copy number and transcript levels of genes involved in C4 photosynthesis and hormone signal transduction pathways that may contribute to the fast growth of elephant grass. The availability of elephant grass genome data advances our knowledge of the genetic evolution of elephant grass and will contribute to further biological research and breeding as well as for other polyploid plants in the genus Cenchrus.

Circulating and Salivary Antibodies to Fusobacterium nucleatum Are Associated With Cystic Pancreatic Neoplasm Malignancy.

Objectives: Intraductal papillary mucinous neoplasms (IPMNs) are cystic precursor lesions to pancreatic cancer. The presence of oral microbes in pancreatic tissue or cyst fluid has been associated with high-grade dysplasia (HGD) and cancer. The present study aims at investigating if humoral immunity to pancreas-associated oral microbes reflects IPMN severity. Design: Paired plasma (n = 109) and saliva (n = 65) samples were obtained from IPMN pancreatic cystic tumor cases and controls, for anti-bacterial antibody analysis and DNA quantification by enzyme-linked immunosorbent assay (ELISA) and qPCR, respectively. Tumor severity was graded by histopathology, laboratory, and clinical data. Circulating plasma and salivary antibody reactivity to a pancreas-associated oral microbe panel were measured by ELISA and correlated to tumor severity. Results: The patient group with high-risk cystic tumors (HGD and/or associated invasive cancer) shows ample circulating IgG reactivity to Fusobacterium nucleatum (F. nucleatum) but not to Granulicatella adiacens (G. adiacens), which is independent of the salivary bacteria DNA levels. This group also shows higher salivary IgA reactivity to F. nucleatum, Fap2 of F. nucleatum, and Streptococcus gordonii (S. gordonii) compared to low-risk IPMN and controls. The salivary antibody reactivity to F. nucleatum and Fap2 are found to be highly correlated, and cross-competition assays further confirm that these antibodies appear cross-reactive. Conclusion: Our findings indicate that humoral reactivity against pancreas-associated oral microbes may reflect IPMN severity. These findings are beneficial for biomarker development.

A preliminary report: genistein attenuates cerebral ischemia injury in ovariectomized rats via regulation of the PI3K-Akt-mTOR pathway.

Stroke is a leading cause of disability and death in the worldwide. Therefore, prevention of stroke is critically important. Genistein, a natural phytoestrogen extracted from soybeans, has been found to be a potential neuroprotective agent for stroke prevention. However, the role of genistein and its underlying mechanism in ovariectomized rats has been rarely evaluated. In this study, ovariectomized rats were treated with genistein (10 mg/kg) or vehicle daily for two weeks before they received middle cerebral artery occlusion (MCAO) and reperfusion. Seventy-two hours after reperfusion, the neurological function was evaluated by Garcia test, infarct volumes were detected by 2,3,5-triphenyltetrazolium chloride staining; and neuronal damage and cell apoptosis were detected by Nissl and Tunel staining in the ischemic penumbra, respectively. In addition, Western blotting was used to detect the activity of PI3K-Akt-mTOR signal pathway in the ischemic penumbra in different groups. And we found that genistein treatment in ovariectomized rats significantly improved neurological outcomes, reduced infarct volumes, decreased neuronal damage and cell apoptosis, and increased the activity of PI3K-Akt-mTOR signal pathway. Our findings indicated that treatment genistein could alleviate neuronal apoptosis induced by cerebral ischemia in ovariectomized rats via promoting the activity of PI3K-Akt-mTOR signal pathway, which provides a new molecular mechanism for the neuroprotective effects of genistein against stroke.

Mucosal-associated invariant T cells and oral microbiome in persistent apical periodontitis.

Opportunistic bacteria in apical periodontitis (AP) may pose a risk for systemic dissemination. Mucosal-associated invariant T (MAIT) cells are innate-like T cells with a broad and potent antimicrobial activity important for gut mucosal integrity. It was recently shown that MAIT cells are present in the oral mucosal tissue, but the involvement of MAIT cells in AP is unknown. Here, comparison of surgically resected AP and gingival tissues demonstrated that AP tissues express significantly higher levels of Vα7.2-Jα33, Vα7.2-Jα20, Vα7.2-Jα12, Cα and tumour necrosis factor (TNF), interferon (IFN)-γ and interleukin (IL)-17A transcripts, resembling a MAIT cell signature. Moreover, in AP tissues the MR1-restricted MAIT cells positive for MR1-5-OP-RU tetramer staining appeared to be of similar levels as in peripheral blood but consisted mainly of CD4+ subset. Unlike gingival tissues, the AP microbiome was quantitatively impacted by factors like fistula and high patient age and had a prominent riboflavin-expressing bacterial feature. When merged in an integrated view, the examined immune and microbiome data in the sparse partial least squares discriminant analysis could identify bacterial relative abundances that negatively correlated with Vα7.2-Jα33, Cα, and IL-17A transcript expressions in AP, implying that MAIT cells could play a role in the local defence at the oral tissue barrier. In conclusion, we describe the presence of MAIT cells at the oral site where translocation of oral microbiota could take place. These findings have implications for understanding the immune sensing of polymicrobial-related oral diseases.

Enrichment of oral microbiota in early cystic precursors to invasive pancreatic cancer.

OBJECTIVES: Intraductal papillary mucinous neoplasms (IPMNs) are pancreatic cysts that can progress to invasive pancreatic cancer. Associations between oncogenesis and oral microbiome alterations have been reported. This study aims to investigate a potential intracystic pancreatic microbiome in a pancreatic cystic neoplasm (PCN) surgery patient cohort. DESIGN: Paired cyst fluid and plasma were collected at pancreatic surgery from patients with suspected PCN (n=105). Quantitative and qualitative assessment of bacterial DNA by qPCR, PacBio sequencing (n=35), and interleukin (IL)-1ß quantification was performed. The data were correlated to diagnosis, lesion severity and clinical and laboratory profile, including proton-pump inhibitor (PPI) usage and history of invasive endoscopy procedures. RESULTS: Intracystic bacterial 16S DNA copy number and IL-1ß protein quantity were significantly higher in IPMN with high-grade dysplasia and IPMN with cancer compared with non-IPMN PCNs. Despite high interpersonal variation of intracystic microbiota composition, bacterial network and linear discriminant analysis effect size analyses demonstrated co-occurrence and enrichment of oral bacterial taxa including Fusobacterium nucleatum and Granulicatella adiacens in cyst fluid from IPMN with high-grade dysplasia. The elevated intracystic bacterial DNA is associated with, but not limited to, prior exposure to invasive endoscopic procedures, and is independent from use of PPI and antibiotics. CONCLUSIONS: Collectively, these findings warrant further investigation into the role of oral bacteria in cystic precursors to pancreatic cancer and have added values on the aetiopathology as well as the management of pancreatic cysts.

Small cell lung cancer mimicking lymphoma in CT and 68Ga-DOTA-NOC PET/CT: A case report.

RATIONALE: Small cell lung cancer accounts for 15-20% of all lung cancers and is the most common pulmonary neuroendocrine neoplasm. Most small cell lung cancers arise from lobar or main bronchi, the most common manifestations of small cell lung cancer is a large mass centrally located within the lung parenchyma or a mediastinal mass involving the hilus. Small cell lung cancer is easily ignored by clinicians without lung parenchyma and hilus involvement. Here, we report a case of small cell lung cancer, which was misdiagnosed as the lymphoma in contrast enhanced CT and Ga-DOTA-NOC PET/CT imagings. PATIENT CONCERNS: A 49-year-old male with chief complaint of discontinuous cough for 1 month. DIAGNOSES: Small cell lung cancer. INTERVENTIONS: Radiotherapy and chemotherapy were given thereafter. OUTCOMES: The case had multiple enlarged lymph nodes due to tumor progression. LESSONS: Small cell lung cancer is a malignant and progressive disease, and easy to be ignored in clinical. The case of small cell lung cancer without parenchyma and hilus involvement has never been reported before. Here, we report it and hope it provides a differential diagnosis for clinicians in the following similar cases.

The Formation Mechanism of Hydrogels.

Hydrogels are degradable polymeric networks, in which cross-links play a vital role in structure formation and degradation. Cross-linking is a stabilization process in polymer chemistry that leads to the multi-dimensional extension of polymeric chains, resulting in network structures. By crosslinking, hydrogels are formed into stable structures that differ from their raw materials. Generally, hydrogels can be prepared from either synthetic or natural polymers. Based on the types of cross-link junctions, hydrogels can be categorized into two groups: the chemically cross-linked and the physically cross-linked. Chemically cross-linked gels have permanent junctions, in which covalent bonds are present between different polymer chains, thus leading to excellent mechanical strength. Although chemical cross-linking is a highly resourceful method for the formation of hydrogels, the cross-linkers used in hydrogel preparation should be extracted from the hydrogels before use, due to their reported toxicity, while, in physically cross-linked gels, dissolution is prevented by physical interactions, such as ionic interactions, hydrogen bonds or hydrophobic interactions. Physically cross-linked methods for the preparation of hydrogels are the alternative solution for cross-linker toxicity. Both methods will be discussed in this review.

Combined Counterclockwise Maxillomandibular Advancement and Uvulopalatopharyngoplasty Surgeries for Severe Obstructive Sleep Apnea.

As the most effective surgical technique maxillomandibular advancement (MMA) has been used to treat severe obstructive sleep apnea (OSA) in adults, particularly for those who are intolerant of continuous positive airway pressure. Yet for large-scale advancement, it is faced with esthetic problems with marked skeletal protrusion especially for people with convex facial profile. In this study, the authors performed counterclockwise MMA combined with quantified uvulopalatopharyngoplasty (UPPP) surgeries on Chinese adult patients with severe OSA, in order to initially explore the efficacy of these procedures on Chinese populations and provide evidence for esthetic advantages. As the primary procedure counterclockwise MMA was applied on 10 patients, achieving a forward distance of the mandible and the maxilla for 10.6 and 6.7 mm, respectively, and the occlusion plane rotated counterclockwise of 6.2°. After a follow-up of beyond 12 months, polysomnography results showed the apnea-hypopnea index (AHI) significantly decreased from 64.3 to 11.0 per hour, achieving surgical success of 90%. Upper airway measurements demonstrated that the retropalatal and retrolingual spaces got enlarged greatly, resulting in significant AHI reduction and oxygen saturation elevation. More importantly, cephalometric analysis revealed that SNA and SNB were enlarged but in well control without visual abnormalities. Follow-up results showed large-scale advancement of the maxilla and mandible were stable in treating severe OSA. Quantified UPPP surgeries guaranteed no functional insufficiency in pronouncing and swallowing and played auxiliary role in enlarging the upper airway. Thus, procedures of counterclockwise MMA combined with quantified UPPP surgeries might find more application especially in patients with severe OSA with convex facial profile in future.

Individualized therapy for treating obstructive sleep apnea in pediatric Crouzon syndrome patients.

PURPOSE: Pediatric patients with Crouzon syndrome have great possibilities of suffering from obstructive sleep apnea (OSA), which is mainly due to midfacial hypoplasia and facial deformities. For most patients, a multidisciplinary and sequential treatment plan is necessary to make for Crouzon syndrome often has different phenotypes of different severity in OSA and facial deformities. Typical patients were selected in this paper to illustrate the necessity of individualized therapy for treating OSA. METHODS: In this paper, we have introduced four Crouzon syndrome children of different severity in suffering from OSA and maxillofacial deformities. Detailed information was given including clinical manifestations, radiological findings, and polysomnography detections. Based on the above findings, different but effective treatment options for these children's OSA problems were adopted, either by surgeries including distraction osteogenesis and craniomaxillofacial surgeries with or without tonsillectomy or by noninvasive continuous positive airway pressure (CPAP) therapy. RESULTS: Follow-up studies for more than 1 year showed problems of OSA and nocturnal hypoxia of those four patients were all alleviated greatly, as well as maxillofacial deformities. Combined with pre-operative and post-operative orthodontics, one patient also got optimal results in better facial profile and dental occlusion. CONCLUSION: Thus, based on adequate clinical evaluations and patients' conditions including age, disease severity, and esthetic considerations, individualized therapy should be made and performed carefully to obtain optimized results in treating OSA for pediatric Crouzon syndrome patients.

The Role of Intravoxel Incoherent Motion MRI in Predicting Early Treatment Response to Chemoradiation for Metastatic Lymph Nodes in Nasopharyngeal Carcinoma.

INTRODUCTION: Pilot studies have suggested potential clinical applications for intravoxel incoherent motion (IVIM) magnetic resonance imaging (MRI) in head and neck cancers. This study aimed to characterize metastatic lymph nodes using IVIM MRI, and to evaluate the role of IVIM MRI in the prediction of the early treatment response of lymph node metastasis from nasopharyngeal carcinoma (NPC). METHODS: A total of 122 patients with metastatic lymph nodes from NPC underwent two MRI examinations, pre-treatment and post-treatment (at 4 weeks and at ≥2 years from the end of chemoradiotherapy). Treatment response was assessed using the Response Evaluation Criteria in Solid Tumors version 1.1. Differences in the initial IVIM parameters [pure molecular diffusion (D), pseudo-diffusion coefficient (D*), and perfusion fraction (f)] between nodes with a partial response (PR) and a complete response (CR) were analyzed in 102 patients after the exclusion of 20. RESULTS: The initial D*, D, and apparent diffusion coefficient (ADC) did not reveal a significant difference between nodes showing a PR or a CR. The mean initial f value was significantly higher in patients with a PR relative to patients with a CR (p = 0.003), and its sensitivity and specificity in predicting treatment response to chemoradiotherapy were 86.7% and 100%, respectively. CONCLUSIONS: The present study indicated that the initial f value may be more accurate than the initial D*, D, and ADC in the early prediction of treatment response to chemoradiotherapy for metastatic lymph nodes in patients with NPC.

Short-Term Side Effects after Radioiodine Treatment in Patients with Differentiated Thyroid Cancer.

OBJECTIVES: I-131 therapy for differentiated thyroid cancer (DTC) could induce adverse effects. The purpose of this study was to report and analyze symptoms after I-131 treatment within the hospitalization and present relevant medical intervention. METHODS: I-131 doses ranging from 3.7 to 9.25 GBq (100-250 mCi) were administrated for thyroid remnant ablation or treating DTC metastases. 117 patients with DTC for I-131 therapy were monitored through the video and intercommunicating with standardized questionnaire at different time points after I-131 oral administration. Adverse effects were recorded and relevant clinical factors were analyzed. RESULTS: Among all the 117 patients, 55 cases complained of neck's pain or swelling and 79 cases presented with gastrointestinal symptoms. Pain or swelling of salivary gland occurred in 15 patients, headache and vertigo in 10, insomnia in 9, vocal cord paralysis in 6, fatigue or general malaise in 6, and foreign body sensation in 5. Body numbness and urinary symptoms were observed in only 1 case, respectively. Those side effects were related with sex, pre-I-131 treatment TSH levels, frequency of I-131 therapy, and lymph node metastases. CONCLUSIONS: Short-term side effects after I-131 therapy for DTC patients varied individually; severe symptoms were not uncommon but generally did not need emergent medical intervention.

SIRT2 inhibition exacerbates neuroinflammation and blood-brain barrier disruption in experimental traumatic brain injury by enhancing NF-κB p65 acetylation and activation.

Sirtuin 2 (SIRT2) is a member of the sirtuin family of NAD(+) -dependent protein deacetylases. In recent years, SIRT2 inhibition has emerged as a promising treatment for neurodegenerative diseases. However, to date, there is no evidence of a specific role for SIRT2 in traumatic brain injury (TBI). We investigated the effects of SIRT2 inhibition on experimental TBI using the controlled cortical impact (CCI) injury model. Adult male mice underwent CCI or sham surgery. A selective brain-permeable SIRT2 inhibitor, AK-7, was administrated 30 min before injury. The volume of the brain edema lesion and the water content of the brain were significantly increased in mice treated with AK-7 (20 mg/kg), compared with the vehicle group, following TBI (p < 0.05 at 1 day and p < 0.05 at 3 days, respectively). Concomitantly, AK-7 administration greatly worsened neurobehavioral deficits on days 3 and 7 after CCI. Furthermore, blood-brain barrier disruption and matrix metalloproteinases (MMP)-9 activity increased following SIRT2 inhibition. AK-7 treatment increased TBI-induced microglial activation both in vivo and in vitro, accompanied by a large increase in the expression and release of inflammatory cytokines. Mechanistically, SIRT2 inhibition increased both K310 acetylation and nuclear translocation of NF-κB p65, leading to enhanced NF-κB activation and up-regulation of its target genes, including aquaporin 4 (AQP4), MMP-9, and pro-inflammatory cytokines. Together, these data demonstrate that SIRT2 inhibition exacerbates TBI by increasing NF-κB p65 acetylation and activation. Our findings provide additional evidence of an anti-inflammatory effect of SIRT2. SIRT2 is a member of the sirtuin family of NAD+-dependent protein deacetylases. Our study suggests that the SIRT2 inhibitor AK-7 exacerbates traumatic brain injury (TBI) via a potential mechanism involving increased acetylation and nuclear translocation of NF-κB p65, resulting in up-regulation of NF-κB target genes, including aquaporin 4 (AQP4), matrix metalloproteinase 9 (MMP-9), and pro-inflammatory cytokines. Our findings provide additional evidence of an anti-inflammatory effect of SIRT2.

Iron Deposition Is Positively Related to Cognitive Impairment in Patients with Chronic Mild Traumatic Brain Injury: Assessment with Susceptibility Weighted Imaging.

BACKGROUND: This study aimed to evaluate the usability of SWI in assessment of brain iron to detect cognitive dysfunction in patients with chronic mild traumatic brain injury (mTBI). METHODS: 39 patients with mTBI and 37 normal controls were given the Mini-Mental State Examination (MMSE) and underwent SWI scanning at least 6 months after injury. Angle radian values were calculated with phase images. The angle radian values were compared between groups using analysis of covariance, and their association with MMSE scores was analyzed using Spearman correlations. RESULTS: Significantly higher angle radian values (p < 0.05) were found in the head of the caudate nucleus, the lenticular nucleus, the hippocampus, the thalamus, the right substantia nigra, the red nucleus, and the splenium of the corpus callosum (SCC) in the mTBI group, compared to the control group. MMSE scores were negatively correlated with angle radian values in the right substantia nigra (r = -0.685, p < 0.001). CONCLUSIONS: Patients with chronic mTBI might have abnormally high accumulations of iron, and their MMSE scores are negatively associated with angle radian values in the right substantia nigra, suggesting a role of SWI in the assessment of cognitive impairments of these patients.

Recent advances in cell sheet technology for periodontal regeneration.

Tissue engineering has yielded several successes in early clinical trials of regenerative medicine with grafting therapeutic cells seeded into biodegradable scaffolds. However this conventional cell delivery method has limited the field's progress. In recent decades, we have developed a novel cell transferring method, cell sheet technology that allows for controlled attachment and detachment of cells via simple temperature variations of a surface-intelligent temperatureresponsive polymer:poly (N-isopropylacrylamide). It has been widely applied to create functional tissue sheets with cells derived from various tissues to treat a wide range of diseases. Periodontal cell sheets non-invasively harvested from temperature- responsive culture surfaces have been successfully manufactured, resulting in communicative multilayered constructs. Transplantation of cell sheets onto periodontal defects has improved bone and tissue regeneration in animal models and humans and shows low immunogenicity. In this review, we summarize the recent advances of techniques in cell sheet engineering and its application for periodontal regeneration.

Imaging proliferation in human leukemia-tumor bearing mice with (18)F-FLT: Comparison with (18)F-FDG PET.

Leukemia threatens human life due to its uncontrolled proliferative malignancy. 3'-deoxy-3'-(18)F-fluorothymidine ((18)F-FLT) has been suggested as a new positron emission tomography (PET) tracer for imaging tumor proliferation. The aim of the study was to investigate the usefulness of (18)F-FLT PET for imaging human leukemia-tumor bearing mice, compared with fluorine-18-fluorodesoxyglucose ((18)F-FDG PET). In vitro the experiments of (18)F-FLT and (18)F-FDG uptake were performed in K562 cell lines at various time points and radioactive tracer uptake was measured in a gamma counter. (18)F-FLT and (18)F-FDG PET imaging were performed both in the same mouse when eight tumor-bearing mice models of human chronic myeloid leukemia were established successfully by injecting K562 cells. Regions of interest were drawn over the tumor, the crossed normal tissue was regarded as background and the ratio of tumor to non-tumor counts (T/NT) in tissues was calculated. A higher uptake of (18)F-FLT (15min, 5.73±0.05%; 30min, 5.90±0.06%; 60min, 6.16±0.19%; 120min, 6.32±0.08%) than that of (18)F-FDG (15min, 1.05±0.10%; 30min, 1.11±0.14%; 60min, 1.14±0.37%; 120 min, 1.36±0.25%) was observed in K562 cells in the tracer uptake experiment. Ratios of T/NT of (18)F-FLT PET (0.5h, 5.39±0.42; 1h, 4.88±0.43; 2h, 3.81±0.38) were higher than those of (18)F-FDG PET/CT (0.5h, 0.34±0.12; 1h, 0.21±0.06; 2h, 0.13±0.05) after injection. Both uptake and T/NT differences of (18)F-FLT versus (18)F-FDG were significant (P>0.05). In conclusion, (18)F-FLT and (18)F-FDG quantitative and semi-quantitative uptake measurements resulting from cell lines and PET imaging respectively suggested a promising potential of (18)F-FLT for metabolic imaging of human chronic myeloid leukemia.

Cutaneous Rosai-Dorfman disease recurrence in infraorbital region.

Rosai-Dorfman disease (RDD), also named sinus histiocytosis with massive lymphadenopathy, is a rare, idiopathic, and benign disorder that classically presents as a painless massive bilateral cervical lymphadenopathy. In cases of extranodal presentations, such as cutaneous RDD, it may not involve the classic manifestation. The diagnosis is usually made by histopathologic analysis. Surgery is suggested in the cases of significant cosmetic deformity or when there is fatal or functional obstruction. We reported a case of extranodal RDD that recurred in the infraorbital region postoperatively.

[Effects of lysyl oxidase down-regulation on invasion, migration and E-cadherin protein expression of hypoxic lung cancer cells].

OBJECTIVE: To observe the effects of lysyl oxidase (LOX) down-regulation on invasion, migration and epithelial-mesenchymal transition phenotype molecule E-cadherin protein expression, induced by hypoxia in lung cancer NCI-H460 cells. METHODS: Small interfering RNA against human LOX gene (LOX siRNA) was used to transfect lung cancer cells under normoxia (19%O2). After a 24 h incubation, the cells were plated for 24 h in hypoxic incubator (0.5%O2). Real-time polymerase chain reaction (PCR) was performed to detect the LOX mRNA expression. The protein levels of LOX and E-cadherin were determined by Western blot. And invasion and migration capacities were detected by transwell chamber. RESULTS: Compared with NCI-H460 cells under normoxia (set to 1), hypoxia increased to the levels of LOX mRNA and protein expression up to 26.04 ± 1.78 and 5.57 ± 1.27 respectively (both P < 0.05). Compared with control siRNA group (set to 1), LOX mRNA and protein expression after LOX siRNA transfection were 0.24 ± 0.03 and 0.29 ± 0.03 respectively, cellular invasive and migratory capacities were 0.57 ± 0.03 and 0.49 ± 0.02 respectively, the protein expression of E-cadherin was 2.17 ± 0.21 (all P < 0.05). CONCLUSION: LOX down-regulation reduces invasion and migration potentials of hypoxic human lung cancer cell and potentiates the protein expression of E-cadherin.

A first described chest wall metastasis from colon cancer demonstrated with (18)F-FDG PET/CT.

It is well known that, haematogenous colon cancer metastases are most commonly found in the liver, less likely in the lungs through the paravertebral venous system and rarely in other organs. Sporadic clinical cases of colon cancer metastases to the abdominal wall, the thyroid or the adrenal glands have been reported. Here, we present an uncommon case of chest wall metastasis from colon cancer demonstrated with 2-fluoro [fluorine-18]-2-deoxy-D-glucose ((18)F-FDG) positron emission tomography/computed tomography (PET/CT). A 52 years old female patient was examined after she felt a swelling mass above her left breast. Tumor makers, such as serum cancer embryonic antigen (CEA) 146.22kU/L (normal range:0.00~37.0kU/L) and CA19-9 (258.16µg/L (normal range:0.00~10.0µg/L) and neuron-specific enolase (NSE) 78.2 (normal range: 0.00~17.00) were abnormally high. Chest CT revealed the soft tissue density mass on the left anterior chest wall with invasion of left 4th rib, and CT-guided biopsy showed a poorly differentiated adenocarcinoma of unkown origin. The patient was then referred for the (18)F-FDG-PET scan which was performed one hour after the intravenous injection of 370MBq of (18)F-FDG (Discovery Camera, VCT, GE, USA) and showed in addition to the chest mass, abnormal (18)F-FDG accumulation in both lungs, left supraclavicular and peritoneal lymph nodes. Furthermore, high (18)F-FDG uptake was detected in the sigmoid. Pathology findings from colonoscopy confirmed that this was a sigmoid colon adenocarcinoma. So far, chest wall metastasis from colon cancer as an initial finding has not been reported. Usually, an initial chest wall mass is hardly suspected to be a colon cancer metastasis. Abnormal serum tumor markers such as CEA and CA19-9 supported the diagnosis of a gastrointestinal adenocarcinoma. In our case, we found high serum NSE and normal findings of bowel wall on the CT scan, thus without the positive (18)F-FDG findings, one would probably consider as first diagnosis: chest wall metastasis from lung cancer, or a neuroendocrine tumor. The unusual finding in this case was that on the CT images there was no obvious local density of the intestine, no bowel wall thickening, or suspicious nodular lesions. Segmental (18)F-FDG accumulation seen in the sigmoid colon had early maximum standardized uptake value (SUV(max)) 7.3 and in 1h delayed estimation, 8.1. Colonoscopy showed that the (18)F-FDG-avid area at the colon was circular and thickened. "Hot" lesions found in both lungs, the supraclavicular and retroperitoneal lymph nodes by (18)F-FDG PET/CT scan were considered to be most probably metastases from colon adenocarcinoma. In conclusion, PET as a rather simple procedure and less dependent on bowel preparation diagnosed the primary colon cancer, its metastases and specifically a first described chest wall metastasis, while CT alone did not show the primary tumor.