Multi-phosphine-chelated iron-carbide clusters via redox-promoted ligand exchange on an inert hexa-iron-carbide carbonyl cluster, [Fe6(µ6-C)(µ2-CO)4(CO)12]2.

We report the reactivity, structures and spectroscopic characterization of reactions of phosphine-based ligands (mono-, di- and tri-dentate) with iron-carbide carbonyl clusters. Historically, the archetype of this cluster class, namely [Fe6(µ6-C)(µ2-CO)4(CO)12]2-, can be prepared on a gram-scale but is resistant to simple ligand substitution reactions. This limitation has precluded the relevance of iron-carbide clusters relating to organometallics, catalysis and the nitrogenase active site cluster. Herein, we aimed to derive a simple and reliable method to accomplish CO → L (where L = phosphine or other general ligands) substitution reactions without harsh reagents or multi-step synthetic strategies. Ultimately, our goal was ligand-based chelation of an Fe n (µ n -C) core to achieve more synthetic control over multi-iron-carbide motifs relevant to the nitrogenase active site. We report that the key intermediate is the PSEPT-non-conforming cluster [Fe6(µ6-C)(CO)16] (2: 84 electrons), which can be generated in situ by the outer-sphere oxidation of [Fe6(µ6-C)(CO)16]2- (1: closo, 86 electrons) with 2 equiv. of [Fc]PF6. The reaction of 2 with excess PPh3 generates a singly substituted neutral cluster [Fe5(µ5-C)(CO)14PPh3] (4), similar to the reported reactivity of the substitutionally active cluster [Fe5(µ5-C)(CO)15] with monodentate phosphines (Cooke & Mays, 1990). In contrast, the reaction of 2 with flexible, bidentate phosphines (DPPE and DPPP) generates a wide range of unisolable products. However, the rigid bidentate phosphine bis(diphenylphosphino)benzene (bdpb) disproportionates the cluster into non-ligated Fe3-carbide anions paired with a bdpb-supported Fe(ii) cation, which co-crystallize in [Fe3(µ3-CH)(µ3-CO)(CO)9]2[Fe(MeCN)2(bdpb)2] (6). A successful reaction of 2 with the tripodal ligand Triphos generates the first multi-iron-chelated, authentic carbide cluster of the formula [Fe4(µ4-C)(κ3-Triphos)(CO)10] (9). DFT analysis of the key (oxidized) intermediate 2 suggests that its (µ6-C)Fe6 framework remains fully intact but is distorted into an axially compressed, 'ruffled' octahedron distinct from the parent closo cluster 1. Oxidation of the cluster in non-coordinating solvent allows for the isolation and crystallization of the CO-saturated, intact closo-analogue [Fe6(µ6-C)(CO)17] (3), indicating that the intact (µ6-C)Fe6 motif is retained during initial oxidation with [Fc]PF6. Overall, we demonstrate that redox modulation beneficially 'bends' Wade-Mingo's rules via the generation of electron-starved (non-PSEPT) intermediates, which are the key intermediates in promoting facile CO → L substitution reactions in iron-carbide-carbonyl clusters.

Identification of potential crucial genes associated with vasculogenic mimicry in human osteosarcoma based on gene expression profile.

We previously reported the presence of vasculogenic mimicry (VM) in human osteosarcoma. However, the mechanistic basis of osteosarcoma VM remains unclear. Three hundred eighty-one upregulated differentially expressed genes (DEGs) and 526 downregulated DEGs between human osteosarcoma cell line 143B and HOS cell exposed to Matrigel were screened out by microarray. GO categories such as "cell adhesion", "angiogenesis" were enriched in 143B group. PATHWAY analysis showed enriched TGF-beta, Wnt and VEGF signaling pathway in 143B group. The hub gene ITGA2 in signal-network of DEGs exhibited pro-VM and pro-metastasis effect. Our study provides fundamental data for further studies regarding molecules involved in osteosarcoma VM.

Overexpression of long non-coding RNA TUG1 alleviates TNF-α-induced inflammatory injury in interstitial cells of Cajal.

OBJECTIVE: Irritable bowel syndrome (IBS) is a common functional disorder in the gastrointestinal tract. Inflammatory response has been found to participate in the pathogenesis of IBS. This study aimed to explore the effects of long non-coding RNA taurine upregulated gene 1 (TUG1) on tumor necrosis factor alpha (TNF-α)-induced interstitial cells of Cajal (ICC) inflammatory injury, which was relevant to the pathogenesis of IBS. PATIENTS AND METHODS: The expression levels of TUG1 and microRNA-127 (miR-127) were analyzed by qRT-PCR. Viability, apoptosis and the expression of apoptosis-associated factors were analyzed by CCK-8 assay, flow cytometry and Western blot, respectively. The mRNA and protein levels of pro-inflammatory cytokines were detected by qRT-PCR and Western blot, respectively. Finally, activations of nuclear factor kappa-B (NF-κB) and Notch pathways were evaluated by Western blot. RESULTS: TNF-α treatment inhibited ICC viability, induced ICC apoptosis and promoted an inflammatory response in ICC. TUG1 was downregulated in TNF-α-treated ICC. TUG1 overexpression protected ICC from TNF-α-induced apoptosis and pro-inflammatory cytokines expression. TUG1 suppression showed opposite effects. MiR-127 was negatively regulated by TUG1 and implicated in the action of TUG1 in ICC. MiR-127 up-regulation largely reversed the effects of TUG1 on TNF-α-treated ICC. Mechanistically, TUG1 inhibited TNF-α-induced activation of NF-κB and Notch pathways in ICC by down-regulating miR-127. CONCLUSIONS: TUG1 attenuated TNF-α-caused apoptosis and inflammatory response in ICC by down-regulating miR-127 and then inactivating NF-κB and Notch pathways.

Long non-coding RNA UCA1 regulates the proliferation, migration and invasion of human lung cancer cells by modulating the expression of microRNA-143.

OBJECTIVE: Accounting for 25% of all the cancers and 20% of the cancer-related mortality, lung cancer is one of the devastating types of cancers. Due to an increase in the incidence of lung cancer and limited treatment options, there is a pressing need to look for novel drug options and to identify potential therapeutic targets. Long non-coding RNAs (LncRNAs) have been considered to be important therapeutic targets due to their plethora of cellular roles. Herein, we investigated the therapeutic potential of UCA1 in lung cancer and also attempted to examine the underlying mechanism through UCA1 exerts its growth inhibitory effects on cancer cells. MATERIALS AND METHODS: The quantitative Reverse-Transcriptase Polymerase Chain Reaction (qRT-PCR) was used to perform the expression analysis. The CCK-8 assay was used to monitor the growth of the cells. The AO/EB assay was used to check apoptosis and flow cytometry was used for cell cycle distribution. The wound heal and transwell assays were used to monitor the cell migration and invasion. RESULTS: It was found that the lncRNA UCA was significantly (p < 0.05) upregulated in the lung cancer cells and silencing of UCA1 could inhibit the proliferation of the SK-MES-1 lung cancer cells via induction of G2/M cell cycle arrest and apoptosis. Moreover, UCA1 silencing could also suppress the migration and invasion of the SK-MES-1 cells. The LncRNA UCA1 was also found to upregulate the expression of miR-143, and overexpression of miR-143 could also suppress the proliferation, migration, and invasion of the SK-MES-1 lung cancer cells. Both UCA1 silencing and miR-143 overexpression could cause a significant decrease in the expression of mitogen-activated protein kinase 1 (MAPK1). Therefore, it is concluded that UCA1 regulates the growth of the SK-MES-1 lung cancer by inhibition of MAPK1 via miR-143 upregulation. CONCLUSIONS: UCA1, as well as miR-143, may be essential therapeutic targets for the management of lung cancer and warrant further investigations.

Suppression of long non-coding RNA UCA1 inhibits proliferation and invasion and induces apoptosis in human lung cancer cells.

OBJECTIVE: Lung cancer is one of the deadliest cancers responsible for significant mortality and morbidity across the globe. The unavailability of efficient treatments, lack of reliable biomarkers and potent therapeutic targets, limit the treatment of lung cancer. In this study, we explored the potential of long non-coding RNA (lncRNA) urothelial carcinoma-associated 1 (UCA1) as the therapeutic target for lung cancer. MATERIALS AND METHODS: The expression analysis was carried out by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell viability was monitored by cell counting kit 8 (CCK-8) assay. The 4',6-diamidino-2-phenylindole (DAPI), annexin-V/Propidium iodide staining and comet assays were used to detect apoptosis. Boyden chamber and wound heal assays were used for cell to asses cell invasion and migration respectively. Protein expression was determined by immunoblotting. RESULTS: The expression of lncRNA UCA1 was determined by qRT-PCR in six different types of lung cancer cell lines. It was observed that lncRNA UCA1 was significantly (p < 0.05) upregulated in all the lung cancer cell lines. To investigate the role of lncRNA UCA1 in lung cancer, its expression was suppressed by transfection of the lung cancer NCI-H23 cells by si-UCA1. The results showed that suppression of lncRNA UCA1 significantly (p < 0.05) reduced the viability of NCI-H23 cancer cells via induction of the apoptosis. Furthermore, the lncRNA UCA1 suppression (p < 0.05) significantly inhibited the migration and invasion of the NCI-H23 lung cancer at least in part via inhibition of mitogen-activated protein kinase 1 (MAPK1). Additionally, the suppression of MAPK1 exhibited similar effects on the proliferation, migration, and invasion of the NCI-H23 cells as that of UCA1 silencing. Finally, the co-suppression of lncRNA UCA1 and MAPK1 exhibited synergistic effects on cell proliferation, migration, and invasion. CONCLUSIONS: We demonstrated that lncRNA UCA1 could be an important therapeutic target for curbing lung cancer.

Effects of ulinastatin on inflammatory response and cognitive function after hip arthroplasty for the elderly patients with femoral neck fracture.

OBJECTIVE: To investigate the effects of ulinastatin on inflammatory response and cognitive function after hip arthroplasty for the elderly patients with femoral neck fracture. PATIENTS AND METHODS: A total of 80 patients with femoral neck fracture receiving hip arthroplasty in our hospital from August 2016 to February 2017 were selected and divided into observation group (n=40) and control group (n=40) using a random number table. The control group was treated with hip arthroplasty and symptomatic and supportive treatment after operation, while the observation group was treated with ulinastatin based on the treatment means of control group. The changes in antioxidant capacities, plasma noradrenaline (NA) and adrenaline (A) levels between the two groups before and after intervention were compared. The changes in neuron-specific enolase (NSE) and plasma S-100B protein levels before intervention and at 48 h after intervention were also compared. Moreover, the changes in mini-mental state examination (MMSE) scores during intervention and the Harris hip scores before intervention and at discharge between the two groups were compared. Finally, the off-bed walking time and postoperative discharge time of the two groups were recorded. RESULTS: After intervention, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) and the total antioxidant capacity in observation group were significantly superior to those in observation group before intervention and control group after intervention (p<0.05). After intervention, the levels of NA and A in observation group were lower than those in control group (p<0.05), and the levels of interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α) and high-sensitivity C-reactive protein (hs-CRP) in observation group were also lower than those in control group (p<0.05). At 48 h after intervention, the levels of NSE and plasma S-100B protein in observation group were significantly lower than those in observation group before intervention and control group at 48 h after intervention (p<0.05). At 12 h, 24 h and 48 h after intervention, the MMSE scores of observation group were superior to those of control group in the same period (p<0.05). After intervention, the Harris hip score of observation group was superior to that of control group before and after intervention (p<0.05). The postoperative discharge time of observation group was earlier than that of control group (p<0.05), and the off-bed walking time was also earlier than that of control group (p<0.05). CONCLUSIONS: The combined application of ulinastatin could effectively reduce the oxidative stress and inflammatory response, improve the neurological functions, and promote the postoperative recovery in the elderly patients with femoral neck fracture after hip arthroplasty.

[Clinical significance of NS1-BP expression in esophageal squamous cell carcinoma].

Objective: To investigate the clinical significance of NS1-BP expression in patients with esophageal squamous cell carcinoma (ESCC), and to study the roles of NS1-BP in proliferation and apoptosis of ESCC cells. Methods: A total of 98 tumor tissues and 30 adjacent normal tissues from 98 ESCC patients were used as study group and control group, and these samples were collected in Sun Yat-Sen University Cancer Center between 2002 and 2008. In addition, 46 ESCC tissues which were collected in Cancer Institute and Hospital of Tianjin Medical University were used as validation group. Expression of mucosal NS1-BP was detected by immunohistochemistry. Kaplan-Meier curve and log-rank test were used to analyze the survival rate. Multivariate Cox proportional hazard model was used to analyze the prognostic factors. Furthermore, NS1-BP was over expressed or knocked down in ESCC cells by transient transfection. Protein levels of c-Myc were detected by western blot. Cell viability and apoptosis was analyzed by MTT assay and flow cytometry. Results: Among all of tested samples, NS1-BP were down-regulated in 9 out of 30 non-tumorous normal esophageal tissues (30.0%) and 85 out of 144 ESCC tissues (59.0%), respectively, showing a statistically significant difference (P=0.012). In the study group, three-year disease-free survival rate of NS1-BP high expression group (53.2%) was significantly higher than that of NS1-BP low expression group (27.6%; P=0.009). In the validation group, the three-year disease-free survival rates were 57.8% and 25.5% in NS1-BP high and low levels groups, respectively, showing a similar results (P=0.016). Importantly, multivariate analyses showed that low expression of NS1-BP was an independent predictor for chemoradiotherapy sensitivity and shorter disease-free survival time in ESCC patients(P<0.05 for all). Furthermore, overexpressed NS1-BP in TE-1 cells repressed c-Myc expression, inhibited cell proliferation and promoted apoptosis. In contrast, knockdown NS1-BP in KYSE510 cells induced c-Myc expression, increased cell proliferation and repressed apoptosis. Conclusions: NS1-BP is an independent favorable prognostic factor in ESCC. It inhibits cell proliferation and enhances cell apoptosis via repressing c-Myc. Targeting NS1-BP may be a new therapeutic strategy for ESCC patients.

Electroacupuncture alleviates chemotherapy-induced pain through inhibiting phosphorylation of spinal CaMKII in rats.

BACKGROUND: Current medical treatments for chemotherapy-induced pain (CIP) are either ineffective or have adverse side effects. Acupuncture may alleviate CIP, but its effectiveness against this condition has not been studied. Paclitaxel causes neuropathic pain in cancer patients. METHODS: We evaluated the effects of electroacupuncture (EA) on paclitaxel-induced CIP in a rat model. Paclitaxel (2 mg/kg) or vehicle was injected (i.p.) on alternate days of 0-6. The resulting pain was treated with 10 Hz/2 mA/0.4 ms pulse EA for 30 min at the equivalent of human acupoint GB30 (Huantiao) once every other day between days 14 and 26. For sham control, EA needles were inserted into GB30 without stimulation. Von Frey filaments with bending forces of 2-8 g and 15 g were used to assess mechanical allodynia and hyperalgesia, respectively, on day 13 and once every other day between 14-26 days and then for 2-3 weeks after EA treatment. RESULTS: Compared to sham control, EA significantly alleviated paclitaxel-induced mechanical allodynia and hyperalgesia, as shown by less frequent withdrawal responses to the filaments. The alleviation of allodynia/hyperalgesia lasted up to 3 weeks after the EA treatment. EA significantly inhibited phosphorylation of Ca2+ /calmodulin-dependent protein kinase II (CaMKII) in the spinal cord. KN-93, a selective inhibitor of p-CaMKII, inhibited mechanical allodynia/hyperalgesia and p-CaMKII. 5-HT1A receptor antagonist blocked EA inhibition of allodynia/hyperalgesia and p-CaMKII. CONCLUSIONS: Electroacupuncture activates 5-HT 1A receptors in the spinal cord and inhibits p-CaMKII to alleviate both allodynia and hyperalgesia. The data support acupuncture/EA as a complementary therapy for CIP. SIGNIFICANCE: Electroacupuncture (EA) activates spinal 5-HT1A receptors to inhibit p-CaMKII to alleviate paclitaxel-induced pain. Acupuncture/EA may be used as a complementary therapy for CIP.

MiR-144 functions as tumor suppressor by targeting PIM1 in gastric cancer.

OBJECTIVE: Gastric cancer (GC) is one of the most prevalent types of malignant disease Worldwide. Mounting evidence has demonstrated the involvement of miRNAs in the development of GC. One of these miRNAs, miR-144 has been found aberrantly expressed in a variety of human malignancies. PATIENTS AND METHODS: GC tissues were collected from patients, and the level of miR-144 was determined by qRT-PCR. GC cell lines SGC7901 and AGS were used as model cell lines and the anti-tumor effect of miR-144 in both cells were examined. The level of miR-144 was restored in GC cells using miR-144 mimic. Moreover, the target gene of miR-144 wad identified. RESULTS: In this study, our results showed that low miR-144 level significantly correlated with lymph node metastasis stage, TNM stage and differentiation degree. In addition, we found that miR-144 acted as a tumor suppressor in GC. Moreover, our findings showed that miR-144 exerted an anti-tumor effect by directly targeting RLIP76. CONCLUSIONS:   miR-144 acts as a tumor suppressor in GC and it is a potential therapeutic target for GC treatment.

WITHDRAWN: Expression and clinicopathological significance of Mel-18 and Bmi-1 in oesophageal squamous cell carcinoma.

This article has been withdrawn at the request authors.

Thoracic stomach-right main bronchus fistula treated with dual Y-shaped covered airway stents.

AIM: To determine the efficacy of dual Y-shaped covered airway stents to treat thoracic stomach-right main bronchus fistulae. MATERIAL AND METHODS: Fifteen patients who developed thoracic stomach-right main bronchus fistula after oesophageal cancer resection and postoperative irradiation were retrospectively analysed. All fistulae were close to the right upper lobe bronchus. Two Y-shaped covered airway stents were designed for each patient. Under radiographic guidance, one stent was placed from the right main bronchus into the bifurcation of upper lobe and intermediate bronchus, the other was placed from the trachea into both main bronchi. RESULTS: All fistulae were closed immediately after stenting. All patients could eat a semi-solid diet. The symptom of coughing while lying down resolved in all patients, and no complications, such as airway bleeding or pneumothorax, occurred. The average survival time was 26.65 months (range 2-40 months, 11 patients were still alive at the study end). Two patients died of tumour recurrence. Another two patients died of pulmonary infections. In one of these patients, there was a long delay between symptom onset and stenting. In the other patient, a small rupture occurred in the silicone membrane covering the stent, which allowed the leakage of gastric contents into the lung. CONCLUSION: Dual Y-shaped covered airway stent placement is feasible and safe to treat thoracic stomach-right main bronchus fistulae. Improvements to the material covering the stents is required.

Liver Transplant Recipient With Tumefactive Demyelinating Lesions: A Case Report and Literature Review.

Tumefactive demyelinating lesions (TDLs) that may resemble brain neoplasms or abscesses are uncommon but noteworthy. A solid knowledge of how to distinguish TDLs from malignancy or infection is a key step to avoid unnecessary medical or surgical interventions. Almost all the intracranial demyelination diseases after liver transplantation (LT) refer to central pontine myelinolysis or extrapontine myelinolysis; TDLs after LT have never been reported. In 2005, a 45-year-old Chinese male underwent orthotopic LT due to "acute on chronic liver failure" in our hospital. He took triple anti-rejection drugs including tacrolimus, mycophenolate mofetil, and corticosteroids after LT. In 2010, he was admitted for right limb weakness, and the head magnetic resonance imaging and magnetic resonance spectroscopy revealed the lesions were more likely to be TDLs. His symptoms disappeared after he was administered corticosteroid therapy which proved the diagnosis. Five years later, he was admitted again to hospital with dizziness and double version. The magnetic resonance image and magnetic resonance spectroscopy showed that the new solitary lesion in the cerebellum may in fact be the new TDL. He received corticosteroid therapy and was discharged after symptoms improved. Herein, to our knowledge, we reported the first case of TDL after LT. We reported this case to provide helpful information to clinicians about intracranial demyelination diseases after LT which maybe are not always central pontine myelinolysis or extrapontine myelinolysis.

Long intergenic non-coding RNA APOC1P1-3 inhibits apoptosis by decreasing α-tubulin acetylation in breast cancer.

Increasing evidence indicates that long non-coding RNAs (lncRNAs) act as important regulatory factors in tumor progression. However, their roles in breast cancer remain largely unknown. In present studies, we identified aberrantly expressed long intergenic non-coding RNA APOC1P1-3 (lincRNA-APOC1P1-3) in breast cancer by microarray, verified it by quantitative real-time PCR, and assessed methylation status in the promoter region by pyrosequencing. We also investigated the biological functions with plasmid transfection and siRNA silencing experiments, and further explored their mechanisms by RNA pull-down and RNA immunoprecipitation to identify binding proteins. We found that 224 lncRNAs were upregulated in breast cancer, whereas 324 were downregulated. The lincRNA-APOC1P1-3 was overexpressed in breast cancer, which was related to tumor size and hypomethylation in its promoter region. We also found that APOC1P1-3 could directly bind to tubulin to decrease α-tubulin acetylation, to inactivate caspase-3, and to inhibit apoptosis. This study demonstrates that overexpression of APOC1P1-3 can inhibit breast cancer apoptosis.

Celecoxib inhibits cell growth and modulates the expression of matrix metalloproteinases in human osteosarcoma MG-63 cell line.

OBJECTIVE: The goal of this study was to determine the effect of celecoxib, a selective COX-2 inhibitor, on the growth inhibition of osteosarcoma and its potential anticancer mechanisms. MATERIALS AND METHODS: Human osteosarcoma cell line MG-63 was used as a model. The inhibitory effect of celecoxib on cell proliferation was assessed by MTT assay. Flow cytometric analysis was used to detect the effects of celecoxib on cell cycle and apoptosis. Western blot analysis was used to detect the protein expression of RECK, matrix metalloproteinase (MMP)-2 and MMP-9 in celecoxib-treated MG-63 cells. RESULTS: MTT assays showed that at a range of concentrations (0-80 µg/ml), celecoxib significantly inhibited the MG-63 cell proliferation in a time- and concentration-dependent manner. The half maximal inhibitory concentration (IC50) of celecoxib was 47.5 µg/ml for 24 h-treatment and 19.2 µg/ml for 48 h-treatment. Flow cytometric analysis demonstrated that treatment with 20 µg/ml celecoxib led to a significant cell cycle arrest at S-phase and an enhancement of apoptosis induction in MG-63 cells at 24 or 48h. Moreover, compared with 24 h-treatment, 48 h-treatment induced more S-phase arrest and apoptosis in MG-63 cells. Western blot analyses revealed that the expression of MMP-2 and MMP-9 was markedly down-regulated but RECK, an inhibitor of MMPs, was markedly up-regulated in MG-63 cells exposed to 20 µg/ml celecoxib for 24 or 48h. Furthermore, the effects of celecoxib on the expression of these molecules were more evident with the increase of treatment time. CONCLUSIONS: Celecoxib inhibits the MG-63 cells proliferation through S-phase arrest and apoptosis induction. Celecoxib-induced down-regulation of MMP-2 and MMP-9 and up-regulation of RECK may contribute to the apoptosis induction and an alteration in local tumor microenvironment. These findings suggest that celecoxib may exert at least in part of its anticancer effects via up-regulation of RECK to inhibit the expression of MMP-2 and MMP-9.

Focal adhesion kinase is involved in the migration of human osteosarcoma cells.

The aim of the present study was to analyze the expression of focal adhesion kinase (FAK) in osteosarcoma (OS) cell lines with different migration abilities in order to determine the role of FAK in migration. A number of different 143B subclone cell lines (A1, A2, A3, A4 and A5) were obtained by a limiting dilution method, and the expression of FAK was detected using western blot analysis. The role of FAK in the migration of OS cells was investigated using small interfering RNA (siRNA), and the ratio of the number of lamellipodia was compared by immunofluorescence staining. The A2 and A3 OS 143B subclone cell lines demonstrated a stronger migration ability and exhibited higher FAK expression compared with the A1 cell line (P<0.05). Following transfection with FAK-siRNA, the migration ability of the A3 cells was significantly decreased (P<0.05), and the ratio of the number of lamellipodia formed was reduced from 35 to 11% (P<0.05). In conclusion, the level of FAK expression was higher in the cell lines with a stronger migration ability. FAK affects the migration ability of OS cells by suppressing the formation of lamellipodia.

Treatment of vertebral body compression fractures using percutaneous kyphoplasty guided by a combination of computed tomography and C-arm fluoroscopy with finger-touch guidance to determine the needle entry point.

This study aimed to evaluate the results and complications of image-guided percutaneous kyphoplasty (PKP) using computed tomography (CT) and C-arm fluoroscopy, with finger-touch guidance to determine the needle entry point. Of the 86 patients (106 PKP) examined, 56 were treated for osteoporotic vertebral compression fractures and 30 for vertebral tumors. All patients underwent image-guided treatment using CT and conventional fluoroscopy, with finger-touch identification of a puncture point within a small incision (1.5 to 2 cm). Partial or complete pain relief was achieved in 98% of patients within 24 h of treatment. Moreover, a significant improvement in functional mobility and reduction in analgesic use was observed. CT allowed the detection of cement leakage in 20.7% of the interventions. No bone cement leakages with neurologic symptoms were noted. All work channels were made only once, and bone cement was distributed near the center of the vertebral body. Our study confirms the efficacy of PKP treatment in osteoporotic and oncological patients. The combination of CT and C-arm fluoroscopy with finger-touch guidance reduces the risk of complications compared with conventional fluoroscopy alone, facilitates the detection of minor cement leakage, improves the operative procedure, and results in a favorable bone cement distribution.

Effect of salt intake and potassium supplementation on brachial-ankle pulse wave velocity in Chinese subjects: an interventional study

Accumulating evidence has suggested that high salt and potassium might be associated with vascular function. The aim of this study was to investigate the effect of salt intake and potassium supplementation on brachial-ankle pulse wave velocity (PWV) in Chinese subjects. Forty-nine subjects (28-65 years of age) were selected from a rural community of northern China. All subjects were sequentially maintained on a low-salt diet for 7 days (3.0 g/day NaCl), a high-salt diet for an additional 7 days (18.0 g/day NaCl), and a high-salt diet with potassium supplementation for a final 7 days (18.0 g/day NaCl+4.5 g/day KCl). Brachial-ankle PWV was measured at baseline and on the last day of each intervention. Blood pressure levels were significantly increased from the low-salt to high-salt diet, and decreased from the high-salt diet to high-salt plus potassium supplementation. Baseline brachial-ankle PWV in salt-sensitive subjects was significantly higher than in salt-resistant subjects. There was no significant change in brachial-ankle PWV among the 3 intervention periods in salt-sensitive, salt-resistant, or total subjects. No significant correlations were found between brachial-ankle PWV and 24-h sodium and potassium excretions. Our study indicates that dietary salt intake and potassium supplementation, at least in the short term, had no significant effect on brachial-ankle PWV in Chinese subjects.

Salt-induced epithelial-to-mesenchymal transition in Dahl salt-sensitive rats is dependent on elevated blood pressure

Dietary salt intake has been linked to hypertension and cardiovascular disease. Accumulating evidence has indicated that salt-sensitive individuals on high salt intake are more likely to develop renal fibrosis. Epithelial-to-mesenchymal transition (EMT) participates in the development and progression of renal fibrosis in humans and animals. The objective of this study was to investigate the impact of a high-salt diet on EMT in Dahl salt-sensitive (SS) rats. Twenty-four male SS and consomic SS-13BN rats were randomized to a normal diet or a high-salt diet. After 4 weeks, systolic blood pressure (SBP) and albuminuria were analyzed, and renal fibrosis was histopathologically evaluated. Tubular EMT was evaluated using immunohistochemistry and real-time PCR with E-cadherin and alpha smooth muscle actin (α-SMA). After 4 weeks, SBP and albuminuria were significantly increased in the SS high-salt group compared with the normal diet group. Dietary salt intake induced renal fibrosis and tubular EMT as identified by reduced expression of E-cadherin and enhanced expression of α-SMA in SS rats. Both blood pressure and renal interstitial fibrosis were negatively correlated with E-cadherin but positively correlated with α-SMA. Salt intake induced tubular EMT and renal injury in SS rats, and this relationship might depend on the increase in blood pressure.

Percutaneous transhepatic cholangiobiopsy to determine the pathological cause of anastomotic stenosis after cholangiojejunostomy for malignant obstructive jaundice.

AIM: To investigate the feasibility and advantages of cholangiobiopsy during percutaneous transhepatic cholangiography in the histopathological diagnosis of anastomotic stenosis after cholangiojejunostomy for malignant obstructive jaundice. MATERIALS AND METHODS: Using biopsy forceps, specimens were collected from the site of stenosis in patients with recurrent jaundice (n = 24) who had previously undergone cholangiojejunostomy for malignant obstructive jaundice. RESULTS: Stenosis occurred in all patients at the biliary-enteric anastomosis based on percutaneous transhepatic cholangiography, and was the location of the biopsy. Satisfactory specimens were obtained from 22 out of 24 patients. The sensitivity was 91.7% (22/24). Tumour tissue was obtained in 18 cases, confirming disease recurrence. Histopathological changes in four patients were diagnosed as fibroplasia and/or inflammation. These were considered cicatricial stenoses based on histopathological, imaging, and laboratory findings. The remaining two histopathology-negative patients were proven to have recurrent tumour based on imaging, laboratory, and follow-up data. No complications occurred during biopsy, including gastrointestinal haemorrhage or perforation. Either cholangial drainage and/or an inner stent was used following biopsy, which resulted in a noticeable decrease in jaundice postoperatively (p < 0.05). CONCLUSION: Percutaneous transhepatic cholangiobiopsy using biopsy forceps for the diagnosis of anastomotic stenosis after cholangiojejunostomy for malignant biliary obstructive jaundice is easy to perform and safe, with a high level of sensitivity. Interventional therapies, such as percutaneous transhepatic cholangial drainage and stent placement, can be performed concurrently, markedly improving the symptoms of patients with obstructive jaundice.