Application value of transcranial contrast-enhanced ultrasonography in evaluating middle cerebral artery stenosis.

OBJECTIVE: To detect the display rate and flow velocity of intracranial circle of Willis (anterior, middle, and posterior cerebral arteries) with transcranial contrast-enhanced transcranial color-coded sonography (CE-TCCS), using digital subtraction angiography (DSA) as the golden diagnostic standard. PATIENTS AND METHODS: We collected data from 104 patients with suspected stroke treated in our hospital between December 2019 and October 2021. The detection rate of the intracranial circle of Willis, anterior cerebral artery (ACA), middle cerebral artery (MCA), and posterior cerebral artery (PCA) were analyzed based on routine TCCS and CE-TCCS data. Based on digital subtraction angiography (DSA) data, the degree of MCA stenosis was divided into mild stenosis (<50%), moderate stenosis (50-69%), severe stenosis (70-99%), and bilateral middle cerebral artery CE-TCCS examinations were performed. We evaluated MCA color blood flow on CE-TCCS, and recorded the peak systolic velocity (PSV), end-diastolic velocity (EDV), and mean flow velocity (MFV). RESULTS: The display rates of ACA, MCA, and PCA were significantly improved on the CE-TCCS, and the PSV, EDV and MFV of the MCA stenosis group were higher than those of the normal group. The flow velocity of each stenosis subgroup was increased compared to the normal group. The optimal cutoff values of normal and stenosis under the receiver operating characteristic (ROC) curve were PSV = 168.5 cm/s, EDV = 61.5 cm/s, and MFV = 110.5 cm/s. The optimal cutoff values for mild and moderate stenosis and for moderate and severe stenosis were PSV = 201.5 cm/s and 249.5 m/s, EDV = 95.2 cm/s and 141.5 cm/s, and MFV = 137.6 cm/s and 160.5 cm/s, respectively. PSV and MFV had the most significant sensitivity, specificity, and accuracy. CONCLUSIONS: Transcranial contrast-enhanced ultrasonography can improve the display rate of intracranial blood vessels and can accurately diagnose MCA stenosis.

LINC00961 suppresses cell proliferation and induces cell apoptosis in oral squamous cell carcinoma.

OBJECTIVE: Oral squamous cell carcinoma (OSCC) is still one of the most frequent neck and head malignancies and is one of the most common cancers in the world. The main purpose of this research was to illustrate the functional role of LINC00961 in OSCC and provide novel insight of biomarkers and therapeutic strategies in OSCC. PATIENTS AND METHODS: The relative expression level of LINC00961 was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell counting kit-8 (CCK-8) assay was involved for determining the ability of cell proliferation. Flow cytometric analysis was performed to detect the cell cycle and cell apoptosis. Expressions of AKT, p-AKT, BCL2, Bax protein levels were detected in Western blotting. Transfected cells were used to perform tumor xenograft formation assay. RESULTS: Low-expression of LINC00961 was detected in both OSCC tissues and cell lines. Through CCK-8 assay and flow cytometric analysis, we validated that up-regulated LINC00961 suppressed cell proliferation and promoted cell apoptosis in OSCC. Besides, over-expressed LINC00961 suppressed PI3K/AKT signaling pathways. In tumor xenograft formation assay, over-expressed LINC00961 inhibited tumor formation. CONCLUSIONS: Our research verified that LINC00961 functioned as a tumor suppressor in OSCC. Regulation of PI3K/AKT might be the underlying mechanism of the tumor suppressor role of LINC00961. The current study might bring a novel insight of biomarkers and therapeutic strategies in OSCC.

MiR-223-3p inhibits proliferation and metastasis of oral squamous cell carcinoma by targeting SHOX2.

OBJECTIVE: The aim of this study was to explore the role of microRNA-233-3p (miR-233-3p) in the development of oral squamous cell carcinoma (OSCC), and to elucidate the underlying mechanism. PATIENTS AND METHODS: The expression of miR-233-3p in OSCC tissues and cell lines was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The target of miR-233-3p was detected and evaluated by L-test and Western blot assays, respectively. Furthermore, the effects of miR-233-3p on cell proliferation, migration and apoptosis were discussed by cell counting kit-8 (CCK-8), scratch-wound and flow cytometry test. RESULTS: MiR-233-3p was lowly expressed in OSCC tissues and cells. Short stature homeobox 2 (SHOX2) was predicted and verified as the downstream target gene of miR-233-3p. Inhibiting the expression of SHOX2 could significantly reduce the malignant behaviors of OSCC cells. The proliferation, migration and anti-apoptotic abilities of miR-233-3p overexpressed cells were obviously limited. However, the recovery of SHOX2 counteracted the beneficial effect of miR-233-3p. CONCLUSIONS: MiR-223-3p acted as a tumor suppressor gene in OSCC by targeting SHOX2. Our findings revealed that miR-223-3p/SHOX2 axis could be a potential therapeutic target for OSCC.

Ad-PUMA sensitizes ovarian cancer cells to chemotherapeutic agents.

OBJECTIVE: Ovarian cancer accounted for the first cause of death in female reproductive system tumor even with the operation and chemotherapy. We sought to evaluate the therapeutic potential of p53 up-regulated modulator of apoptosis (PUMA) in ovarian cancer. MATERIALS AND METHODS: An adenovirus expressing PUMA (Ad-PUMA), alone or in combination with chemotherapeutic agents, was used to treat two different ovarian cancer cell lines. The mechanism of PUMA-mediated growth suppression and apoptosis was investigated by analysis of caspase-9 activation and the change of mitochondrial membrane potential (Δψm). RESULTS: The exogenous PUMA was expressed 6 h after Ad-PUMA infection, which increased the chemosensitivity of the cancer cells and decreased the IC50 of chemotherapeutic agents compared with uninfected cells. The apoptotic percentage of OVCAR-3 and SKOV3 increased greatly compared with Taxol or Cisplatin alone. There was shear zone in caspase-9 and Δψm decrease after Ad-PUMA infection which suggested apoptosis started in mitochondrial mediated pathway. CONCLUSIONS: PUMA plays a role in suppressing tumor growth and sensitizing ovarian cancer cells to anticancer drugs and may be a promising tool for cancer biotherapy.

Analysis of 85Kr: a comparison at the 10 -14 level using micro-liter samples.

The isotopic abundance of (85)Kr in the atmosphere, currently at the level of 10(-11), has increased by orders of magnitude since the dawn of nuclear age. With a half-life of 10.76 years, (85)Kr is of great interest as tracers for environmental samples such as air, groundwater and ice. Atom Trap Trace Analysis (ATTA) is an emerging method for the analysis of rare krypton isotopes at isotopic abundance levels as low as 10(-14) using krypton gas samples of a few micro-liters. Both the reliability and reproducibility of the method are examined in the present study by an inter-comparison among different instruments. The (85)Kr/Kr ratios of 12 samples, in the range of 10(-13) to 10(-10), are measured independently in three laboratories: a low-level counting laboratory in Bern, Switzerland, and two ATTA laboratories, one in Hefei, China, and another in Argonne, USA. The results are in agreement at the precision level of 5%.

An efficient magneto-optical trap of metastable krypton atoms.

We report a magneto-optical trap of metastable krypton atoms with a trap loading rate of 3×10(11) atoms/s and a trap capture efficiency of 3×10(-5). The system starts with an atomic beam of metastable krypton produced in a liquid-nitrogen cooled, radio-frequency driven discharge. The metastable beam flux emerging from the discharge is 1.5×10(14) atoms/s/sr. The flux in the forward direction is enhanced by a factor of 156 with transverse laser cooling. The atoms are then slowed inside a Zeeman slower before captured by a magneto-optic trap. The trap efficiency can be further improved, possibly to the 10(-2) level, by gas recirculation. Such an atom trap is useful in trace analysis applications where available sample size is limited.