On Simultaneous Localization and Mapping inside the Human Body (Body-SLAM)

Wireless capsule endoscopy (WCE) offers a patient-friendly, non-invasive and painless investigation of the entire small intestine, where other conventional wired endoscopic instruments can barely reach. As a critical component of the capsule endoscopic examination, physicians need to know the precise position of the endoscopic capsule in order to identify the position of intestinal disease after it is detected by the video source. To define the position of the endoscopic capsule, we need to have a map of inside the human body. However, since the shape of the small intestine is extremely complex and the RF signal propagates differently in the non-homogeneous body tissues, accurate mapping and localization inside small intestine is very challenging. In this dissertation, we present an in-body simultaneous localization and mapping technique (Body-SLAM) to enhance the positioning accuracy of the WCE inside the small intestine and reconstruct the trajectory the capsule has traveled. In this way, the positions of the intestinal diseases can be accurately located on the map of inside human body, therefore, facilitates the following up therapeutic operations. The proposed approach takes advantage of data fusion from two sources that come with the WCE: image sequences captured by the WCE\u27s embedded camera and the RF signal emitted by the capsule. This approach estimates the speed and orientation of the endoscopic capsule by analyzing displacements of feature points between consecutive images. Then, it integrates this motion information with the RF measurements by employing a Kalman filter to smooth the localization results and generate the route that the WCE has traveled. The performance of the proposed motion tracking algorithm is validated using empirical data from the patients and this motion model is later imported into a virtual testbed to test the performance of the alternative Body-SLAM algorithms. Experimental results show that the proposed Body-SLAM technique is able to provide accurate tracking of the WCE with average error of less than 2.3cm

Design and validation of a virtual environment for experimentation inside the small intestine

ABSTRACT Designing a precise and reliable localization system for wireless capsule endoscopy (WCE) has always been a challenging problem due to the complicated in-body environment and uncontrollable movement of body tissue. Knowing the motion information of the capsule would greatly enhance the localization accuracy. However, design and validate any motion tracking algorithm inside small intestine faces a lot of difficulties since any experimentation on the human being is extremely costly and restricted by law. Having a virtual environment that looks and functions exactly like small intestine would facilitate the process of verifying the performance of existing algorithms without going into the real human body. In this paper, we established a virtual testbed that emulates the contraction of intestinal lumen and the transition of endoscopic capsule. Under this emulation environment, a velocity estimation algorithm based on a feature detection algorithm (ASIFT) and a velocity estimation algorithm (MDR) was implemented and its performances were evaluated. Experimental results showed that our proposed emulation environment is able to provide reliable platform for motion detection validation

Mesenchymal Stromal Cells Derived Extracellular Vesicles Ameliorate Acute Renal Ischemia Reperfusion Injury by Inhibition of Mitochondrial Fission through miR-30

Background. The immoderation of mitochondrial fission is one of the main contributors in ischemia reperfusion injury (IRI) and mesenchymal stromal cells (MSCs) derived extracellular vesicles have been regarded as a potential therapy method. Here, we hypothesized that extracellular vesicles (EVs) derived from human Wharton Jelly mesenchymal stromal cells (hWJMSCs) ameliorate acute renal IRI by inhibiting mitochondrial fission through miR-30b/c/d. Methods. EVs isolated from the condition medium of MCS were injected intravenously in rats immediately after monolateral nephrectomy and renal pedicle occlusion for 45 minutes. Animals were sacrificed at 24 h after reperfusion and samples were collected. MitoTracker Red staining was used to see the morphology of the mitochondria. The expression of DRP1 was measured by western blot. miR-30 in EVs and rat tubular epithelial cells was assessed by qRT-PCR. Apoptosis pathway was identified by immunostaining. Results. We found that the expression of miR-30 in injured kidney tissues was declined and mitochondrial dynamics turned to fission. But they were both restored in EVs group in parallel with reduced cell apoptosis. What is more, when the miR-30 antagomirs were used to reduce the miRNA levels, all the related effects of EVs reduced remarkably. Conclusion. A single administration of hWJMSC-EVs could protect the kidney from IRI by inhibition of mitochondrial fission via miR-30

Paeoniflorin Inhibits LPS-Induced Activation of Splenic CD4+ T Lymphocytes and Relieves Pathological Symptoms in MRL/lpr Mice by Suppressing IRAK1 Signaling

Interleukin-1receptor-associated kinase 1 (IRAK1) plays a critical role in systemic lupus erythematosus (SLE). It was reported that SLE was associated with an inflammatory response mediated by defective immune tolerance, including overproduction of autoantibodies, chronic inflammation, and organ damage. Previous reports stated paeoniflorin (PF) had an immunosuppressive effect. The purpose of this study was to determine the anti-inflammatory effect of PF in SLE and its underlying mechanisms. Followed by induced with lipopolysaccharide (LPS), the splenocytes and the isolated CD4+ T lymphocytes of MRL/lpr mice were divided into three groups: control group, LPS group, and LPS + PF group, respectively. MRL/MP mice were used as the control group (treated with distilled water). The MRL/lpr mice were randomly divided into three groups: the model group (treated with distilled water), the prednisone group, and the PF group. The MRL/lpr mice were treated with prednisone acetate (5 mg/kg) and PF (25, 50, and 75 mg/kg) for eight weeks. Subsequently, ELISA, qRT-PCR, western blotting, HE, and Masson staining were performed to detect various indicators. The results of Cell Counting Kit-8 (CCK-8) showed that 10 μg/mL of LPS had the optimum effect on cell viability, and 50 μmol/L of PF had no obvious cytotoxicity to LPS-treated cells. PF reduced the expression level of IRAK1-nuclearfactor-κB (NF-κB) and its downstream inflammatory cytokines in the splenocytes and CD4+ T lymphocytes of MRL/lpr mice stimulated by LPS, especially in the latter. The serum antibody contents in the PF group mice were reduced, and the kidney damage was also alleviated accordingly. Moreover, the IRAK1/inhibitor of the nuclear factor-κB kinase (IKK)/NF-κB inhibitor (IκB)/NF-κB pathways was found to be involved in the anti-inflammation effect of PF in the kidney and spleen. In conclusion, it is thought that PF may have the potential to be used as a therapeutic agent to reduce the inflammatory activity of SLE. Inhibition of the IRAK1-NF-κB pathway may help formulate novel therapeutic tactics for SLE