Molecular basis underlying default mode network functional abnormalities in postpartum depression with and without anxiety.

Although Postpartum depression (PPD) and PPD with anxiety (PPD-A) have been well characterized as functional disruptions within or between multiple brain systems, however, how to quantitatively delineate brain functional system irregularity and the molecular basis of functional abnormalities in PPD and PPD-A remains unclear. Here, brain sample entropy (SampEn), resting-state functional connectivity (RSFC), transcriptomic and neurotransmitter density data were used to investigate brain functional system irregularity, functional connectivity abnormalities and associated molecular basis for PPD and PPD-A. PPD-A exhibited higher SampEn in medial prefrontal cortex (MPFC) and posterior cingulate cortex (PPC) than healthy postnatal women (HPW) and PPD while PPD showed lower SampEn in PPC compared to HPW and PPD-A. The functional connectivity analysis with MPFC and PPC as seed areas revealed decreased functional couplings between PCC and paracentral lobule and between MPFC and angular gyrus in PPD compared to both PPD-A and HPW. Moreover, abnormal SampEn and functional connectivity were associated with estrogenic level and clinical symptoms load. Importantly, spatial association analyses between functional changes and transcriptome and neurotransmitter density maps revealed that these functional changes were primarily associated with synaptic signaling, neuron projection, neurotransmitter level regulation, amino acid metabolism, cyclic adenosine monophosphate (cAMP) signaling pathways, and neurotransmitters of 5-hydroxytryptamine (5-HT), norepinephrine, glutamate, dopamine and so on. These results reveal abnormal brain entropy and functional connectivities primarily in default mode network (DMN) and link these changes to transcriptome and neurotransmitters to establish the molecular basis for PPD and PPD-A for the first time. Our findings highlight the important role of DMN in neuropathology of PPD and PPD-A.

Mechanistic Investigations of Thermal Decomposition of Perfluoroalkyl Ether Carboxylic Acids and Short-Chain Perfluoroalkyl Carboxylic Acids.

In this study, we investigated the thermal decomposition mechanisms of perfluoroalkyl ether carboxylic acids (PFECAs) and short-chain perfluoroalkyl carboxylic acids (PFCAs) that have been manufactured as replacements for phased-out per- and polyfluoroalkyl substances (PFAS). C-C, C-F, C-O, O-H, and C═C bond dissociation energies were calculated at the M06-2X/Def2-TZVP level of theory. The α-C and carboxyl-C bond dissociation energy of PFECAs declines with increasing chain length and the attachment of an electron-withdrawing trifluoromethyl (-CF3) group to the α-C. Experimental and computational results show that the thermal transformation of hexafluoropropylene oxide dimer acid to trifluoroacetic acid (TFA) occurs due to the preferential cleavage of the C-O ether bond close to the carboxyl group. This pathway produces precursors of perfluoropropionic acid (PFPeA) and TFA and is supplemented by a minor pathway (CF3CF2CF2OCFCF3COOH → CF3CF2CF2· + ·OCFCF3COOH) through which perfluorobutanoic acid (PFBA) is formed. The weakest C-C bond in PFPeA and PFBA is the one connecting the α-C and the ß-C. The results support (1) the C-C scission in the perfluorinated backbone as an effective PFCA thermal decomposition mechanism and (2) the thermal recombination of radicals through which intermediates are formed. Additionally, we detected a few novel thermal decomposition products of studied PFAS.

Platelet-Rich Fibrin in Fat Grafts for Facial Lipofilling: A Randomized, Controlled Split-Face Clinical Trial.

Objective: Previous studies have reported that platelet-rich fibrin (PRF) may enhance the efficacy of fat grafts in facial lipofilling. However, these studies either lacked objective data or were not randomized, controlled trials. Thus, we aimed to objectively evaluate the efficacy of PRF in facial lipofilling. Methods: A controlled, split-face, randomized trial (January 2018 to May 2019) based on 18 patients who underwent fat grafts for bilateral temple lipofilling was performed. Each patient received a combination of an autologous fat graft and PRF on one side and a fat graft combined with an equal volume of saline on the other side. The effects of PRF were evaluated by comparing the remaining bilateral fat graft volumes through a digital three-dimensional reconstruction technique. Improvements in the appearance and recovery time of each temple were assessed by both a surgeon and patients who were blinded to the treatment assignment. Complications were also recorded. Results: Bilateral temple lipofilling showed no evidence of fat embolism, vascular/nerve injury, infection, massive edema, or prolonged bruising. Three-dimensional reconstruction data and the assessments from both the surgeon and patients revealed no significant differences in fat graft retention volume between the PRF-positive and PRF-negative lipofilling groups. However, recovery time in the PRF-positive lipofilling sites was significantly shortened compared with that of the PRF-negative lipofilling sites. Conclusion: Facial filling with autologous fat grafts is effective and safe. Our results show that PRF does not markedly improve fat graft volume retention in the temple but significantly reduces postoperative recovery time. Trial Registration Number: ChiCTR2100053663.

Photoaging of Baby Bottle-Derived Polyethersulfone and Polyphenylsulfone Microplastics and the Resulting Bisphenol S Release.

This study evaluated the release of bisphenol S (BPS) from polyethersulfone (PES) and polyphenylsulfone microplastics (MPs) derived from baby bottles under UV irradiation. Released BPS fluctuates over time because it undergoes photolysis under UV254 irradiation. Under UV365 irradiation, the highest released concentration at 50 °C was 1.7 and 3.2 times that at 35 and 25 °C, respectively, as the activation energy of the photochemical reactions responsible for MP decay was reduced at high temperatures. Low concentrations of humic acid (HA, ≤10 mg·L-1) promote BPS release because HA acts as a photosensitizer. A high concentration of HA (10∼50 mg·L-1) decreases the BPS release because HA shields MPs from light and scavenges reactive radicals that are produced via photochemical reactions. For example, under UV irradiation, hydroxyl radicals (•OH) attack results in the breakage of ether bonds and the formation of phenyl radicals (Ph•) and phenoxy radicals (Ph-O•).The•OH addition and hydrogen extractions further produce BPS from the decayed MPs. A leaching kinetics model was developed and calibrated by the experimental data. The calibrated model predicts the equilibrium level of BPS release from MPs that varies with the surface coverage density of BPS and leaching rate constants. This study provides groundwork that deepens our understanding of environmental aging and the chemical release of MPs.

[Effect of ZHU Lian's type â ¡ inhibition acupuncture on chronic migraine and serum 5-HT, VEGF, CGRP].

OBJECTIVE: To observe the clinical efficacy of ZHU Lian's type Ⅱ inhibition acupuncture for chronic migraine, and explore the possible mechanism. METHODS: A total of 120 patients with chronic migraine were randomized into an observation group (60 cases, 3 cases dropped off) and a control group (60 cases, 2 cases dropped off). In the control group, flunarizine hydrochloride capsule was taken orally, 5 mg each time, once a day. In the observation group, ZHU Lian's typeⅡ inhibition acupuncture was applied at Erheliao (TE 22), Shousanli (LI 10), Hegu (LI 4), Yangbai (GB 14), Tongziliao (GB 1), Zusanli (ST 36) ect., once every other day. The treatment was given 4 weeks in the two groups. Before and after treatment, the migraine clinical symptom score, cerebral hemodynamics indexes (blood flow velocity of arterior cerebral artery [ACA], posterior cerebral artery [PCA], bilateral middle cerebral artery [MCA] and basilar artery [BA]), serum related indexes (levels of 5-hydroxytryptamine [5-HT], vascular endothelial growth factor [VEGF] and calcitonin gene-related peptide [CGRP]) and migraine specific quality of life questionnaire (MSQ) score were observed in the two groups, and the clinical effect was evaluated. RESULTS: The total effective rate in the observation group was 93.0% (53/57), which was higher than 79.3% (46/58) in the control group (P<0.05). After treatment, the number of headache attack was reduced, duration time was shortened, and the scores of pain intensity and concomitant symptom, cerebral hemodynamics indexes (blood flow velocity of ACA, PCA, MCA and BA) and serum levels of VEGF and CGRP were lower than before treatment in the two groups (P<0.05, P<0.01), and those in the observation group were lower than the control group (P<0.05). After treatment, the serum levels of 5-HT and MSQ scores of functional limitation, dysfunction and emotion were higher than before treatment in the two groups (P<0.05), and those in the observation group were higher than the control group (P<0.05). CONCLUSION: ZHU Lian's type Ⅱ inhibition acupuncture could reduce frequency of migraine attack and duration time, improve pain intensity, cerebral blood flow velocity and quality of life for patients with chronic migraine, its mechanism may be related to regulating serum levels of 5-HT, CGRP and VEGF.

Osthole Protects Bone Marrow-Derived Neural Stem Cells from Oxidative Damage through PI3K/Akt-1 Pathway.

In recent years, neural stem cell (NSC) transplantation has been widely explored as a treatment for neurodegenerative diseases. NSCs are special cells that have some capacity for self-renewal and the potential to differentiate into multiple cell types. However, the inflammatory environment of diseased tissue is not conducive to the survival of transplanted cells. Osthole (Ost) is a principal bioactive component of Fructus Cnidii, Radix Angelicae Pubescentis and other traditional Chinese medicines. Ost has a wide range of pharmacological activities, such as anti-inflammation, immunomodulation, and neuroprotection. In the present study, we assessed the protective effects of Ost on bone marrow-derived-NSCs (BM-NSCs) against injury induced by hydrogen peroxide (H2O2). BM-NSCs were pre-treated with different doses of Ost and treated with H2O2. The cell counting kit-8 (CCK-8) method and lactate dehydrogenase (LDH) leakage assay were used to determine cell viability. Using the TUNEL assay and RT-PCR, we evaluated the effect of Ost on cell apoptosis. The results showed that Ost had protective effects against H2O2-induced cell damage, and the number of apoptotic cells was significantly decreased in the Ost pre-treated groups compared to the H2O2 group. The expression ratio of Bax/Bcl-2 mRNA was also decreased. Furthermore, western blotting was used to analyze levels of proteins related to PI3K/Akt-1 signaling pathway, and results indicated that ost can increase p-Akt and PI3K. Our findings suggested that Ost protects BM-NSCs against oxidative stress injury, and it can be used to improve the inflammatory environment of neurodegenerative diseases so and promote the survival rate of transplanted NSCs.

Neurotrophin-3 promotes proliferation and cholinergic neuronal differentiation of bone marrow- derived neural stem cells via notch signaling pathway.

AIMS: Recently, the potential for neural stem cells (NSCs) to be used in the treatment of Alzheimer's disease (AD) has been reported; however, the therapeutic effects are modest by virtue of the low neural differentiation rate. In our study, we transfected bone marrow-derived NSCs (BM-NSCs) with Neurotrophin-3 (NT-3), a superactive neurotrophic factor that promotes neuronal survival, differentiation, and migration of neuronal cells, to investigate the effects of NT-3 gene overexpression on the proliferation and differentiation into cholinergic neuron of BM-NSCs in vitro and its possible molecular mechanism. MAIN METHODS: BM-NSCs were generated from BM mesenchymal cells of adult C57BL/6 mice and cultured in vitro. After transfected with NT-3 gene, immunofluorescence and RT-PCR method were used to determine the ability of BM-NSCs on proliferation and differentiation into cholinergic neuron; Acetylcholine Assay Kit was used for acetylcholine (Ach). RT-PCR and WB analysis were used to characterize mRNA and protein level related to the Notch signaling pathway. KEY FINDINGS: We found that NT-3 can promote the proliferation and differentiation of BM-NSCs into cholinergic neurons and elevate the levels of acetylcholine (ACh) in the supernatant. Furthermore, NT-3 gene overexpression increase the expression of Hes1, decreased the expression of Mash1 and Ngn1 during proliferation of BM-NSCs. Whereas, the expression of Hes1 was down-regulated, and Mash1 and Ngn1 expression were up-regulated during differentiation of BM-NSCs. SIGNIFICANCE: Our findings support the prospect of using NT-3-transduced BM-NSCs in developing therapies for AD due to their equivalent therapeutic potential as subventricular zone-derived NSCs (SVZ-NSCs), greater accessibility, and autogenous attributes.

Arctigenin Confers Neuroprotection Against Mechanical Trauma Injury in Human Neuroblastoma SH-SY5Y Cells by Regulating miRNA-16 and miRNA-199a Expression to Alleviate Inflammation.

Mechanical trauma injury is a severe insult to neural cells. Subsequent secondary injury involves the release of inflammatory factors that have dramatic consequences for undamaged cells, leading to normal cell death after the initial injury. The present study investigated the capacity for arctigenin (ARC) to prevent secondary effects and evaluated the mechanism underlying the action of microRNA (miRNA)-199a and miRNA-16 in a mechanical trauma injury (MTI) model using SH-SY5Y cells in vitro. SH-SY5Y cells are often applied to in vitro models of neuronal function and differentiation. Recently, miRNAs have been demonstrated to play a crucial role in NF-κB and cholinergic signaling, which can regulate inflammation. The cell model was established by scratch-induced injury of human SH-SY5Y cells, which mimics the characteristics of MTI. A cell counting kit-8 (CCK-8), terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and immunocytochemistry were used to measure cell viability. Enzyme-linked immunosorbent assay (ELISA) was used to evaluate the inflammatory cytokine and cholinesterase (CHE) content. The lactate dehydrogenase (LDH) content was measured to assess the degree of cell injury. The mRNA levels were measured by RT-PCR to analyze ARC's mechanism of action. miRNA inhibitors and mimics were used to inhibit and strengthen the expression of miRNAs. Protein expression was detected by western blotting analysis. ARC treatment reduced the TNF-α and IL-6 levels as well as the number of TUNEL+ apoptotic SH-SY5Y cells surrounding the scratch and increased the IL-10 level compared to the controls. ARC attenuated the increase of the cell damage degree and LDH content induced by scratching, indicating increased cell survival. Mechanistic studies showed that ARC upregulated the miRNA-16 and miRNA-199a levels to reduce upstream protein (IKKα and IKKß) expression and inhibit NF-κB signaling pathway activity; moreover, the increased miRNA-199a suppresses cholinesterases to increase cholinergic signaling, resulting in decreased expression of proinflammatory cytokines. ARC treatment confers protection for SH-SY5Y cells through positive regulation of miRNA expression, thereby reducing the inflammatory response. In turn, these effects accelerate injury repair in the scratch-induced injury model. These results might provide insights into the pharmacological role of ARC in anti-inflammation and neuroprotection in neural cells.

Arctigenin Treatment Protects against Brain Damage through an Anti-Inflammatory and Anti-Apoptotic Mechanism after Needle Insertion.

UNLABELLED: Convection enhanced delivery (CED) infuses drugs directly into brain tissue. Needle insertion is required and results in a stab wound injury (SWI). Subsequent secondary injury involves the release of inflammatory and apoptotic cytokines, which have dramatic consequences on the integrity of damaged tissue, leading to the evolution of a pericontusional-damaged area minutes to days after in the initial injury. The present study investigated the capacity for arctigenin (ARC) to prevent secondary brain injury and the determination of the underlying mechanism of action in a mouse model of SWI that mimics the process of CED. After CED, mice received a gavage of ARC from 30 min to 14 days. Neurological severity scores (NSS) and wound closure degree were assessed after the injury. Histological analysis and immunocytochemistry were used to evaluated the extent of brain damage and neuroinflammation. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was used to detect universal apoptosis. Enzyme-linked immunosorbent assays (ELISA) was used to test the inflammatory cytokines (tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10) and lactate dehydrogenase (LDH) content. Gene levels of inflammation (TNF-α, IL-6, and IL-10) and apoptosis (Caspase-3, Bax and Bcl-2) were detected by reverse transcription-polymerase chain reaction (RT-PCR). Using these, we analyzed ARC's efficacy and mechanism of action. RESULTS: ARC treatment improved neurological function by reducing brain water content and hematoma and accelerating wound closure relative to untreated mice. ARC treatment reduced the levels of TNF-α and IL-6 and the number of allograft inflammatory factor (IBA)- and myeloperoxidase (MPO)-positive cells and increased the levels of IL-10. ARC-treated mice had fewer TUNEL+ apoptotic neurons and activated caspase-3-positive neurons surrounding the lesion than controls, indicating increased neuronal survival. CONCLUSIONS: ARC treatment confers neuroprotection of brain tissue through anti-inflammatory and anti-apoptotic effects in a mouse model of SWI. These results suggest a new strategy for promoting neuronal survival and function after CED to improve long-term patient outcome.

Hypoxia-stimulated cardiac fibroblast production of IL-6 promotes myocardial fibrosis via the TGF-ß1 signaling pathway.

Interlukin-6 (IL-6) is a multifunctional cytokine produced by several cell types that has a role in fibrosis. Fibroblasts (FBs) maintain this underlying pathogenic change through regulation of IL-6 production; however, its potential functional role in regulating surrounding cellular structural changes during ischemic myocardial remodeling remains unexplored. Here, we generated FBs, cardiomyocytes (CMs), and blood vascular endothelial cells (ECs) from the ventricles of neonatal rats. IL-6 was then overexpressed in FBs and the cells were treated with IL-6 receptor inhibitor (IL6RI), TGF-ß1 receptor inhibitor (TßRI), or MMP2/MMP9 inhibitor (MMPI) using monoculture or coculture models under hypoxic conditions. The results indicate that overexpression of IL-6 is sufficient to induce myofibroblastic proliferation, differentiation, and fibrosis, probably via increased TGF-ß1-mediated MMP2/MMP3 signaling. The use of IL6RI, TßRI, or MMPI diminished these effects. In addition, IL-6 activated the apoptosis-associated factors Caspase3 and Smad3, and decreased the expression of anti-apoptotic factor Bcl2, resulting in apoptosis of CMs under hypoxic coculture: IL6RI or TßRI inhibited these effects. Unexpectedly, IL-6-overexpressing FBs significantly increased the angiogenesis of ECs, which involved significant increases in the expression of proangiogenic growth factors. Treatment of FBs with IL6RI or TßRI in coculture with ECs reduced the levels of secreted proangiogenic growth factors, and the angiogenesis of ECs was significantly downregulated. Thus, IL-6 functions in ischemic myocardial remodeling through multifunctional reprogramming of hypoxia-associated FBs towards fibrosis via upregulation of the TGF-ß1 signaling pathway.

[Expression of LRG-1 in clinical specimens and Tca8113 cell line of tongue carcinoma].

OBJECTIVE: To investigate the expression of LRG-1 in clinical specimens and Tca8113 cell line of tongue carcinoma and analyze the relationship between LRG-1 expression and the clinicopathological parameters. METHODS: LRG-1 expression was detected in 40 tongue squamous cell carcinoma (TSCC) tissues and paired normal adjacent tissues, 20 atypical hyperplasia tissues of the tongue, and 20 tissues of tongue cancer in situ using immunohistochemical method. The expression of LRG-1 in Tca8113 cell line was detected using flow cytometry. The expression of LRG-1 was also detected in human TSCC tissues and Tca8113 cells with Western blotting. The effect of LRG-1 on the proliferation of HUVECs was determined using MTT assay, and its effect on angiogenesis was evaluated with Matrigel tube formation assays. RESULTS: Human TSCC tissues had a significantly higher rate of positive expression for LRG-1 (85%, 34/40) than the adjacent tissues (10%, 4/40), invasive tongue cancer (30%, 6/20), and tongue cancer in situ (50%, 10/20) (P<0.05). LRG-1 expression was correlated with the degree of tumor differentiation, clinical stage and lymph node metastasis of the tumor (P<0.05) but not with the patients' age or gender. In the in vitro experiment, LRG-1 promoted HUVEC proliferation and angiogenesis. CONCLUSION: Abnormal LRG-1 expression is present in the human TSCC tissue and Tca8113 cells. LRG-1 can promote HUVEC proliferation and angiogenesis in vitro, suggesting its possible role in promoting tumor angiogenesis.

[Rare parotid gland tumors: enhanced computed tomography and pathological correlation].

OBJECTIVE: To investigate the correlation between enhanced computed tomography (CT) findings and pathological results of rare parotid gland tumors, and improve diagnosis accuracy. METHODS: The enhanced CT manifestations of 22 cases with pathologically documented rare parotid gland tumors, which included 6 cases of basal cell tumor, 5 cases of myoepithelioma, 4 cases of vascular invasion, 3 cases of lymphatic cyst, 3 cases of lipoma, and 1 case of chondrosarcoma, were retrospectively analyzed. The location, size, shape, density, and relationship with surrounding structure were evaluated on CT images. RESULTS: The enhanced CT showed that basal cell tumors occurred in the superficial lobe of the parotid gland, with clear boundary, within the cystic lesion. The lesions were moderate to obviously enhanced, which may be accompanied by enlarged lymph nodes. Myoepithelial tumors were located in the superficial lobe of the parotid gland, with a small cystic prone and microcalcification within a few cases. The lesions were moderate to obviously enhanced. Hemangiomas of soft tissue mass prominent in the parotid gland surface were mild to significantly enhanced. Larger lesions may occupy the entire parotid gland, with uneven density and visible vein stone. The CT density values of the lymphatic cyst were usually higher. Chondrosarcoma mainly manifested cystic mass at the calcification edge. Lipoma with fat density mass exhibited clear boundary without enhancement. Fiber separation could be observed in the lesion. CONCLUSION: CT can reflect the pathological features of rare parotid gland tumors by demonstrating their corresponding imaging features. Enhanced CT is the most effective means of imaging to identify the nature of rare tumor of the parotid gland lesions.

[Parotid adenolymphoma: the enhanced MSCT manifestations and clinical pathological analysis].

OBJECTIVE: To investigate the imaging manifestations of 16-slice enhanced CT of parotid adenolymphoma in the parotid gland and the corresponding pathology,in order to improve the understanding of the CT imaging manifestations of parotid adenolymphoma in the parotid gland. METHOD: The enhanced CT characteristics of 34 cases of parotid adenolymphoma in the parotid gland confirmed by histological pathology were retrospectively analyzed. RESULT: There were totally 86 lesions in 34 cases, of which 12 cases with lesions in bilateral sides and 22 cases with lesions in unilateral side. Sixty-six lesions located behind and below the superficial lobe of the parotid gland. The lesions showed moderate to obvious enhancement at arterial phase, and the cystic region within the lesions showed no enhancement. CONCLUSION: The relatively specific enhanced MSCT manifestations of parotid adenolymphoma in parotid gland include lesions located behind and below the superficial lobe of parotid gland unilaterally or bilaterally, sometimes exhibited as multiple masses, with clear edge, obvious enhancement and cystic degeneration inside.

CXCR6 deficiency attenuates pressure overload-induced monocytes migration and cardiac fibrosis through downregulating TNF-α-dependent MMP9 pathway.

An immerging role of TNF-α in collagen synthesis and cardiac fibrosis implies the significance of TNF-α production in the development of myocardial remodeling. Our previous study showed a reduction of TNF-α and attenuated cardiac remodeling in CXCR6 knockout (KO) mice after ischemia/reperfusion injury. However, the potential mechanism of TNF-α-mediated cardiac fibrosis with pressure overload has not been well elucidated. In the present study, we aim to investigate the role of CXCR6 in TNF-α release and myocardial remodeling in response to pressure overload. Pressure overload was performed by constriction of transverse aorta (TAC) surgery on CXCR6 KO mice and C57 wild-type (WT) counterparts. At 6 weeks after TAC, cardiac remodeling was assessed by echocardiography, cardiac TNF-α release and its type I receptor (TNFRI), were detected by ELISA and western blot, collagen genes Col1a1 (type I) and Col3a1 (type III) were examined by real-time PCR. Compared with CXCR6 WT mice, CXCR6 KO mice exhibited less cardiac dysfunction, reduced expression of TNFRI, Col1a1 and Col3a. In vitro, we confirmed that CXCR6 deficiency led to reduced homing and infiltration of CD11b(+) monocytes, which contributed to attenuated TNF-α release in myocardium. Furthermore, TNFRI antagonist pretreatment blocked AT1 receptor signaling and NOX4 expression, reduced collagen synthesis, and blunted the activity of MMP9 in CXCR6 WT mice after TAC, but these were not observed in CXCR6 KO mice. In the present work, we propose a mechanism that CXCR6 is essential for pressure overload-mediated myocardial recruitment of monocytes, which contributes to cardiac fibrosis through TNF-α-dependent MMP9 activation and collagen synthesis.

Effect of aniline on cadmium adsorption by sulfanilic acid-grafted magnetic graphene oxide sheets.

Cd(II) has posed severe health risks worldwide. To remove this contaminant from aqueous solution, the sulfanilic acid-grafted magnetic graphene oxide sheets (MGOs/SA) were prepared and characterized. The mutual effects of Cd(II) and aniline adsorption on MGOs/SA were studied. The effects of operating parameters such as pH, ionic strength, contact time and temperature on the Cd(II) enrichment, as well as the adsorption kinetics and isotherm were also investigated. The results demonstrated that MGOs/SA could effectively remove Cd(II) and aniline from the aqueous solution and the two adsorption processes were strongly dependent on solution pH. The Cd(II) adsorption was reduced by the presence of aniline at pH<5.4 but was improved at pH>5.4. The presence of Cd(II) diminished the adsorption capacity for aniline at pH<7.8 but enhanced the aniline adsorption at pH>7.8. The decontamination of Cd(II) by MGOs/SA was influenced by ionic strength. Besides, the adsorption process could be well described by pseudo-second-order kinetic model. The intraparticle diffusion study revealed that the intraparticle diffusion was not the only rate-limiting step for the adsorption process. Moreover, the experimental data of isotherm followed the Freundlich isotherm model.

[MDCT features and anatomic-pathological basis of thyroid diseases involving the upper mediastinum].

To determine the multidetector computed tomography (MDCT) features as well as the anatomic-pathological basis in thyroid diseases involving the upper mediastinum, we performed a retrospective analysis of 49 patients who had thyroid diseases involving the upper mediastinum. In the study, 22 cases were nodular goiter, 13 cases were thyroid adenoma, and 14 cases were thyroid cancer. The relevance between MDCT appearances and their diffusing route of common thyroid diseases as well as the anatomic-pathological features in this region were evaluated. It was found that the lesions located in the upper anterior mediastinum, the upper posterior mediastinum, and both sides were 67.3% (33/49), 14.3% (7/49), 18.4% (9/49), respectively. Different diseases had their distinct MDCT features nodular goiter mainly showed localized and multiple nodules or tumor bulk (77.3%), thyroid adenoma mainly showed solitary tumor bulk (92.3%), and thyroid cancer mainly demonstrated solitary tumor bulk (57.1%), respectively. Among the 49 cases, 9 cases had cervical and/or mediastinal metastases in lymph nodes. The thyroid diseases involving the upper mediastinum most commonly occurred in the upper anterior mediastinum. The MDCT features and distribution of diffusing thyroid lesions in cervico-thoracic junctional region closely correlated with the anatomic-pathological characteristics in this region.

A new choice for the treatment of segmental tibial bone defects: intramedullary nail internal fixation combined adipose-derived stem cells technique.

The repair of various segmental tibial bone defects continues to be a challenging part of many reconstructive procedures. Many methods have been tried to repair the defects, followed by many complications and the results may be unsatisfied. Since 2001 Zuk et al. established human adipose-derived stem cells (hASCs) as a multipotent stem cell population with the ability to assume osteogenic phenotypes through chemically induced differentiation, hASCs represent a valuable tool for pharmacological and biological studies of osteoblast differentiation in vitro and bone development in vivo, and have been proved to be a useful source of stem cells in bone repair. Recently, hASCs have been found to repair both animals and human calvarial defects. In this paper, we hypothesize that hASCs cultured on custom scaffolds can be used to repair of tibial segmental bone defects with intramedullary nail internal fixed. Unlike current treatment modalities, it would promote the regeneration of tibial defects, provide structural support and allow for weight bearing and bony substitution over time.

Clinical application of endoscopic inguinal lymph node resection after lipolysis and liposuction for vulvar cancer.

AIM: To examine lymph nodes obtained after lipolysis and liposuction of subcutaneous fat of the inguinal region of female vulvar cancer patients to explore the feasibility of clinical application. METHODS: The field of operation was on the basis of the range of the conventional resection of inguinal lymph nodes. We injected lipolysis liquid fanwise, started liposuction after 15-20 minutes; then the subcutaneous fatty tissue was sucked out clearly by suction tube. We selected the first puncture holes located on 2-3 cm part below anterior superior spine, the others respectively being located 3cm and 6cm below the first for puncturing into the skin, imbedding a trocar to intorduce CO2 gas and the specular body, and excise the lymph nodes by ultrasonic scalpel. The surgical field chamber was set with negative pressure drainage and was pressured with a soft saline bag after surgery. RESULTS: A lacuna emerged from subcutaneous of the inguinal region after lipolysis and liposuction, with a wide fascia easily exposed at the bottom where lymph nodes could be readily excised. The number of lymph nodes of ten patients excised within the inguinal region on each side was 4-18. The excised average number of lymph nodes was 11 when we had mature technology. CONCLUSION: Most of adipose tissue was removed after lipolysis and liposuction of subcutaneous tissue of inguinal region, so that the included lymph nodes were exposed and easy to excise by endoscope. This surgery avoided the large incision of regular surgery of inguinal region, the results indicating that this approach is feasible and safe for used as an alternative technology.

[Evaluation of regnant anatomic distribution and metastatic type in skeletal thorax metastasis of breast cancer with multi-detector CT].

To determine the characteristics and regularity of multi-detector CT (MDCT) in breast cancer with skeletal thorax metastasis, we retrospectively analyzed the imaging findings of MDCT in 72 cases of breast cancer with bone metastasis before treatment. There were totally 455 metastasis involved sites. The most common metastatic site was thoracic vertebra. And the fourth left rib was most common lesion in rib metastasis. Right breast cancer was more likely to take place at the bilateral ribs (65%) and pectoral girdle (54.5%) metastasis. The lesions in 28 cases demonstrated osteolytic destruction (38.9%), while 30 cases showed osteogenic appearance (41.7%). In conclusion, the development of breast cancer with skeletal thorax metastasis has certain characteristics and regularity.

[MDCT features and anatomic-pathological basis of lymphoid neoplasm in cervico-thoracic junctional region].

To determine the relevance between MDCT features and anatomic-pathological basis of lymphoid neoplasm in cervico-thoracic junctional region, we performed a retrospective analysis of 69 patients with lymphoid neoplasm (lymphoma: 41 patients; metastatic tumor: 28 patients) involving the cervico-thoracic junctional region for MDCT features and distribution of lesions. The relevance between MDCT features and the anatomic-pathological basis in this region were evaluated. Among all the 41 patients with lymphoma, 29 with NHL (70.7%), 12 with HD (29.3%). The lymphomatous lymphadenopathy mainly located in superficial lateral cervix (51.2%, 21/41) ,deep jugular chain (65.9%, 27/41), supraclavicular fossa (75.6%, 31/41), paratrachea space in anterior mediastinum (46.3%, 19/41), around aortic arch (56.1%, 23/41), aortopulmonary window (53.7%, 22/41), upper anterior mediastinum (41.5%, 17/41), subcarinal space (26.8%, 11/41) and paraesophageal space (17.1%, 7/41). 28 patients had metastatic lymphoid tumor. The primary tumor were nasopharynx tumor (5 patients), thyroid cancer (7 patients), lung cancer (10 patients), and esophageal cancer (6 patients). Most metastasis took stage by stage in the way of lymphatic return, but a minority of cases migrated jumpily. The main metastatic sites were: beside jugular chain (82.1%), supraclavicular fossa (75%), paratracheal in anterior mediastinum (60.7%), upper anterior mediastinum (64.3%), beside aortic arch (35.7%), aortopulmonary window (39.2%), and paraesophageal space (28.6%). So lymphoid neoplasms in cervico-thoracic junctional region were involving both lower cervix and upper thorax simultaneously. The MDCT features and main distribution of lesions correlated with the anatomic-pathological characteristics in this region.