The Effect of Oral Administration of PUFAs on the Matrix Metalloproteinase Expression in Gastric Adenocarcinoma Patients Undergoing Chemotherapy

Objective: Gastric cancer is the third-leading cause of cancer-related mortality and the fifth most common cancer globally. Polyunsaturated fatty acids (PUFAs) are considered as functional ingredients that improve the efficacy of chemotherapeutic drugs. The aim of this study is to investigate the effect of PUFAs administration on matrix metalloproteinases (MMPs).

Methods: This study was designed as a randomized, double-blind trial. Thirty-four newly diagnosed patients with gastric cancer were randomly divided into two groups: control group (n?=?17) and case group (n?=17). Both groups received the same dose (75?mg/m²) of cisplatin. Control group received cisplatin plus placebo and the case group received cisplatin plus PUFAs [3600?mg/day, for three courses (each course included 3 weeks)]. The mRNA and protein expression of MMPs determined by real-time polymerase chain reaction (qRT-PCR) and immunohistochemistry (IHC), respectively.

Results: The relative gene expression of MMP-1 and MMP-9 was significantly lower in case group than control. The protein expression of MMP-1 and MMP-9 was significantly lower in case group than control.

Conclusion: According to the results of this study, PUFAs reduced the expression of MMPs in gastric cancer cells. It seems that PUFAs may have an inhibitory effect on invasion and metastasis of gastric cancer cells.     

Attenuation Coefficient Estimation of Normal Placentas

Attenuation coefficient estimation has the potential to be a useful tool for placental tissue characterization. A current challenge is the presence of inhomogeneities in biological tissue that result in a large variance in the attenuation coefficient estimate (ACE), restricting its clinical utility. In this work, we propose a new Attenuation Estimation Region Of Interest (AEROI) selection method for computing the ACE based on the (i) envelope signal-to-noise ratio deviation and (ii) coefficient of variation of the transmit pulse bandwidth. The method was first validated on a tissue-mimicking phantom, for which an 18%–21% reduction in the standard deviation of ACE and a 14%–24% reduction in the ACE error, expressed as a percentage of reported ACE, were obtained. A study on 59 post-delivery clinically normal placentas was then performed. The proposed AEROI selection method reduced the intra-subject standard deviation of ACE from 0.72 to 0.39 dB/cm/MHz. The measured ACE of 59 placentas was 0.77 ± 0.37 dB/cm/MHz, which establishes a baseline for future studies on placental tissue characterization.     

Aortic Pulsatility Propagates Intracranially and Correlates with Dilated Perivascular Spaces and Small Vessel Compliance

Introduction: To test the hypotheses that changes in the aortic pulse-wave produced by arterial stiffening are (1) propagated into cerebral small vessels, (2) associated with reduced compliance of small cerebral arterial vessels, and (3) associated with the presence of dilated perivascular spaces (PVS). Methods: Fifteen volunteers and 19 patients with late-onset depression (LOD) were prospectively recruited, of which 6 fulfilled the criteria for treatment-resistant depression (TRD). Aortic pulse-wave velocity (PWV) was determined using Carotid-Femoral Doppler. Pulse-wave analysis (PWA) was performed using a SphygmoCor system. White-matter lesion load and PVS were scored on established MRI scales. Cerebral arterial and aqueductal cerebrospinal fluid (CSF) flow patterns were studied using quantitative phase-contrast angiography. Results: Depressed patients had more PVS (P < .05) and prolongation of the width of the arterial systolic pulse-wave in the carotid arteries (P < .01). There was no significant group difference for any PWV or PWA measurement. TRD patients showed more PVS than other LOD patients (P < .05). The fractional width of the arterial systolic peak correlated significantly with augmentation index (AIx) and heart rate-corrected augmentation index (AIx75; R²?=?0.302, P < .01and R²?=?0.363, P < .01 respectively). Arterial–aqueductal delay showed a negative correlation with estimated aortic systolic pressure (PWVsys; R²?=? 0.293; P < .01), AIx (R² = ?0.491; P < .01) and AIx75 (R² = ?0.310; P < .01). PVS scores correlated with AIx (R²?=?0.485; P < .01) and AIx75 (R²?=??0.292; P < .01). Conclusion: Our findings support the hypothesis that increased arterial pulsatility resulting from central arterial stiffness propagates directly into cerebral vessels and is associated with the development of microvascular angiopathy, characterized by dilated PVS and decreased compliance of small arterial vessels.