Role of microRNAs in Vascular Remodeling.

Besides being involved in the gradual formation of blood vessels during embryonic development, vascular remodeling also contributes to the progression of various cardiovascular diseases, such as; myocardial infarction, heart failure, atherosclerosis, pulmonary artery hypertension, restenosis, aneurysm, etc. The integrated mechanisms; proliferation of medial smooth muscle cell, dysregulation of intimal endothelial cell, activation of adventitial fibroblast, inflammation of macrophage, and the participation of extracellular matrix proteins are important factors in vascular remodeling. In the recent studies, microRNAs (miRs) have been shown to be expressed in all of these cell-types and play important roles in the mechanisms of vascular remodeling. Therefore, some miRs may be involved in prevention and others in the aggravation of the vascular lesions. miRs are small, endogenous, conserved, single-stranded, non-coding RNAs; which degrade target RNAs or inhibit translation post-transcriptionally. In this paper, we reviewed the function and mechanisms of miRs, which are highly expressed in various cells types, especially endothelial and smooth muscle cells, which are closely involved in the process of vascular remodeling. We also assess the functions of these miRs in the hope that they may provide new possibilities of diagnosis and treatment choices for the related diseases.

The prognostic value of PD-L1 expression for non-small cell lung cancer patients: a meta-analysis.

BACKGROUND: A meta-analysis was conducted to investigate the much-debated relationship between the gene expression of programmed cell death-ligand 1 (PD-L1) and cancer patient prognosis. The prognostic value of measuring PD-L1 expression in non-small cell lung cancer (NSCLC) patients was analyzed. METHODS: We searched PubMed for studies about the relationship between PD-L1 expression and NSCLC patient prognosis. Only studies with patient survival data related to PD-L1 expression in NSCLC patients with different characteristics were included. The effect size (ES) for this analysis was the hazard ratio (HR) with 95% confidence intervals (CI) for overall survival (OS). RESULTS: Six studies with 1157 patients were included with the defined including and excluding criteria. There is no significant heterogeneity among the studies (I(2) = 0%, p = 0.683). PD-L1 expression was significantly associated with the differentiation of tumor (poor vs. well: OR = 1.91, 95% CI: 1.33-2.75, p = 0.001). High PD-L1 expression was also correlated with poor prognosis in terms of the OS of patients with NSCLC (pooled HR = 1.75, 95% CI: 140-2.20, p < 0.001; heterogeneity test: I(2) = 0%, p = 0.643). CONCLUSIONS: NSCLC patients with positive PD-L1 expression exhibited poor OS. The PD-L1 expression was higher in tumors with poor differentiation.

Mechanisms of resveratrol-induced changes in cytosolic free calcium ion concentrations and cell viability in OC2 human oral cancer cells.

Resveratrol is a natural compound that affects cellular calcium (Ca(2+)) homeostasis and viability in different cells. This study examined the effect of resveratrol on cytosolic free Ca(2+) concentrations ([Ca(2+)]i) and viability in OC2 human oral cancer cells. The Ca(2+)-sensitive fluorescent dye fura-2 was used to measure [Ca(2+)]i, and water-soluble tetrazolium-1 was used to measure viability. Resveratrol evoked concentration-dependent increase in [Ca(2+)]i. The response was reduced by removing extracellular Ca(2+). Resveratrol also caused manganese-induced fura-2 fluorescence quench. Resveratrol-evoked Ca(2+) entry was inhibited by nifedipine and the protein kinase C (PKC) inhibitor GF109203X but was not altered by econazole, SKF96365, and the PKC activator phorbol 12-myristate 13 acetate. In Ca(2+)-free medium, treatment with the endoplasmic reticulum Ca(2+) pump inhibitor 2,5-di-tert-butylhydroquinone (BHQ) abolished resveratrol-evoked [Ca(2+)]i rise. Conversely, treatment with resveratrol inhibited BHQ-evoked [Ca(2+)]i rise. Inhibition of phospholipase C (PLC) with U73122 abolished resveratrol-evoked [Ca(2+)]i rise. At 20-100 µM, resveratrol decreased cell viability, which was not affected by chelating cytosolic Ca(2+)with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester. Annexin V-fluorescein isothiocyanate staining data suggest that resveratrol at 20-40 µM induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, resveratrol induced [Ca(2+)]i rise by evoking PLC-dependent Ca(2+) release from the endoplasmic reticulum and by causing Ca(2+) entry via nifedipine-sensitive, PKC-regulated mechanisms. Resveratrol also caused Ca(2+)-independent apoptosis.

Effect of diindolylmethane on Ca(2+) homeostasis and viability in MDCK renal tubular cells.

The effect of the natural product diindolylmethane (DIM) on cytosolic Ca(2+) concentrations ([Ca(2+)]i) and viability in MDCK renal tubular cells was explored. The Ca(2+)-sensitive fluorescent dye fura-2 was applied to measure [Ca(2+)]i. DIM at concentrations 1-50 µM induced a [Ca(2+)]i rise in a concentration-dependent manner. The response was reduced partly by removing Ca(2+). DIM induced Mn(2+) influx leading to quenching of fura-2 fluorescence. DIM-evoked Ca(2+) entry was suppressed by nifedipine, econazole, SK&F96365 and protein kinase C modulators. In the absence of extracellular Ca(2+), incubation with the endoplasmic reticulum Ca(2+) pump inhibitor thapsigargin (TG) or 2,5-di-tert-butylhydroquinone (BHQ) greatly inhibited DIM-induced [Ca(2+)]i rise. Incubation with DIM abolished TG or BHQ-induced [Ca(2+)]i rise. Inhibition of phospholipase C with U73122 reduced DIM-induced [Ca(2+)]i rise by 50%. At 1, 10, 40 and 50 µM, DIM slightly enhanced cell proliferation. The effect of 50 µM DIM was reversed by chelating cytosolic Ca(2+) with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid. In sum, in MDCK cells, DIM induced a [Ca(2+)]i rise by evoking phospholipase C-dependent Ca(2+) release from the endoplasmic reticulum and Ca(2+) entry via protein kinase C-sensitive store-operated Ca(2+) channels. DIM did not induce cell death.

Effect of thimerosal on Ca(2+) movement and viability in human oral cancer cells.

The effect of thimerosal on cytosolic free Ca(2+) concentrations ([Ca(2+)](i) ) in human oral cancer cells (OC2) is unclear. This study explored whether thimerosal changed basal [Ca(2+)](i) levels in suspended OC2 cells using fura-2. Thimerosal at concentrations between 1and 50 microM increased [Ca(2+)](i) in a concentration-dependent manner. The Ca(2+) signal was reduced partly by removing extracellular Ca( 2+). Thimerosal-induced Ca(2+) influx was not blocked by L-type Ca(2+) entry inhibitors and protein kinase C modulators (phorbol 12-myristate 13-acetate [PMA] and GF109203X). In Ca(2+)-free medium, 50 microM thimerosal failed to induce a [Ca(2+)](i) rise after pretreatment with thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor). Inhibition of phospholipase C with U73122 did not change thimerosal-induced [Ca(2+)](i) rises. At concentrations between 5 and 10 microM, thimerosal killed cells in a concentration-dependent manner. The cytotoxic effect of 8 muM thimerosal was potentiated by prechelating cytosolic Ca(2+) with the Ca(2+) chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetate/acetomethyl (BAPTA/ AM). Flow cytometry data suggested that 1-7 microM thimerosal-induced apoptosis in a concentration-dependent manner. Collectively, in OC2 cells, thimerosal-induced [Ca(2+)](i) rises by causing phospholipase C-independent Ca(2+) release from the endoplasmic reticulum and Ca(2+) influx through non-L-type Ca(2+) channels. Thimerosal killed cells in a concentration-dependent manner through apoptosis.

Inflammatory pseudotumour associated with chronic persistent Eikenella corrodens infection: a case report and brief review.

Inflammatory pseudotumour is an uncommon mass forming lesion, representing the histological expression of an infective or reactive/reparative process (pseudotumour) in most cases, and a bona fide neoplasm (for example, inflammatory myofibroblastic tumour) in a minority of cases. This report describes the case of an inflammatory pseudotumour with a pathology that unveiled proliferative CD68 positive and actin negative spindle shaped cells, with a mild mixed inflammatory infiltrate, and a culture that yielded an uncommon fastidious bacillus, Eikenella corrodens. The clinical course was indolent but protracted, with insidious progression to multifocal non-contiguous lesions, involving the lungs, liver, spleen, left kidney, and deep neck tissue, all of which responded to medical treatment with appropriate antibiotics. It is of paramount importance that clinicians search for an infective cause of an inflammatory pseudotumour, to ensure appropriate treatment.

Destruction efficiencies and dynamics of reaction fronts associated with the permanganate oxidation of trichloroethylene.

Although potassium permanganate (KMnO4) flushing is commonly used to destroy chlorinated solvents in groundwater, many of the problems associated with this treatment scheme have not been examined in detail. We conducted a KMnO4 flushing experiment in a large sand-filled flow tank (L x W x D = 180 cm x 60 cm x 90 cm) to remove TCE emplaced as a DNAPL in a source zone. The study was specifically designed to investigate cleanup progress and problems of pore plugging associated with the dynamics of the solid-phase reaction front (i.e., MnO2) using chemical and optical monitoring techniques. Ambient flow through the source zone formed a plume of dissolved TCE across the flow tank. The volume and concentration of TCE plume diminished with time because of the in situ oxidation of the DNAPL source. The migration velocity of the MnO2 reaction front decreased with time, suggesting that the kinetics of the DNAPL oxidation process became diffusion-controlled because of the pore plugging. A mass balance calculation indicated that only approximately 18% of the total applied KMnO4 (MnO4- = 1250 mg/ L) participated in the oxidation reaction to destroy approximately 41% of emplaced TCE. Evidently, the efficiency of KMnO4 flushing scheme diminished with time due to pore plugging by MnO2 and likely CO2, particularly in the TCE source zone. In addition, the excess KMnO4 used for flushing may cause secondary aquifer contamination. One needs to be concerned about the efficacy of KMnO4 flushing in the field applications. Development of a new approach that can provide both contaminant destruction and plugging/ MnO4- control is required.

Complications of renal transplantation: MR findings.

Because of its direct multiplanar capability, superb soft tissue contrast and ability to obtain dynamic three-dimensional angiograms using contrast agents without nephrotoxicity, magnetic resonance (MR) imaging and magnetic resonance angiography are ideal techniques for evaluating renal transplants. The following pictorial essay reviews the normal MR appearance of the transplant kidney as well as parenchymal, vascular, and peritransplant complications.

Staging of bladder cancer by transabdominal real-time ultrasound.

In the past six years, there were 726 cases of proved bladder cancer in our hospital. Among these, 376 cases received transabdominal ultrasonographic examination of the urinary bladder for evaluation of the bladder tumor. Two hundred and fourteen cases of them were newly diagnosed as bladder cancer and had adequate pathological specimens for staging of the tumor. The retrospective comparison between preoperative local staging of the bladder tumor by ultrasound and final pathological report showed 78.5% of total accuracy, 9.8% of overstaging, and 11.7% of understaging. The accuracy is 87% for stage A tumor; 60.5% for stage B; 41.2% for stage C; 83.3% for stage D. Strong echogenic foci on the surface or in the tumor were detected in 39.3% (84/214) of cases, which may indicate encrusted stones on the surface of the tumor or intratumoral dystrophic calcification. There was no strong correlation between tumor grading and staging, except that most of the grade I lesions were at stage A (30/31, 97%). The preoperative local staging of urinary bladder cancer by real-time ultrasound might be of great value to determine the management planning and prognosis of the patients.

A case of acute renal artery thrombosis caused by blunt trauma: computed tomographic and Doppler ultrasonic findings.

A 16-year-old girl who was involved in a traffic accident subsequently received emergency surgery for facial lacerations and an exploratory laparotomy. She had gross hematuria which was ignored initially. A left renal infarction, detected by computed tomography on the 12th post-operative day, showed no enhancement of the left renal artery with the cortical rim sign. Further study by color and pulsed Doppler ultrasound revealed the absence of normal renal arterial flow with only venous flow detected, confirming the diagnosis of acute renal artery thrombosis.