[Digital Pathology: Current Status and Prospects of Clinical Application].

In recent years, with the progress of image processing and network transmission technology, digital pathology (DP) is being more and more extensive applied in clinical practice, and new artificial-intelligence-assisted diagnosis technology based on digital imaging is emerging. Being a widely-used mature field, telepathology is changing the temporal and spatial scope of pathological diagnosis through remote electronic transmission of digital images. Fully digitized pathology departments are realizing the transformation of diagnostic modes and workflow from microscopic diagnosis to digital image computer review, and there have already been successful examples of large-scale fully digitized pathology departments. However, there are still many problems in the implementation of DP, for example, the quality stability and cost of the scanner, the validation of the system, the reengineering of the workflow, the training of pathologists and the change of their perception of DP, which all await further improvement. Although artificial intelligence diagnostic technology is showing great potential, its application in pathological work is still limited to the field of auxiliary diagnostics, and there is still a long way to go to the realization of comprehensive intelligent pathology. The rise of DP will bring about a profound change in the way of how pathological work is done and become a solid foundation for intelligent pathology.

lncRNA PITPNA-AS1 promotes cell proliferation and metastasis in hepatocellular carcinoma by upregulating PDGFD.

Hepatocellular carcinoma (HCC) ranks high in morbidity and mortality among notorious malignancies because of the lack of effective biomarkers and treatments. LncRNA PITPNA antisense RNA 1 (PITPNA-AS1) plays an oncogenic role in HCC, yet the mechanistic basis remains unprobed. Here using Bioinformatics and PCR analyses, we validated that PITPNA-AS1 expression was significantly increased in HCC. The levels of PITPNA-AS1 in tumors were reversely correlated with the prognosis in HCC patients. Downregulation of PITPNA-AS1 inhibited malignant activities of HCC cells. Next, we elucidated that PITPNA-AS1 acts as a competing endogenous RNA (ceRNA) to sponge miR-363-5p, thereby regulating the expression of platelet-derived growth factor-D (PDGFD). Moreover, the suppression of HCC cell activities by PITPNA-AS1 downregulation can be removed by PDGFD overexpression or miR-363-5p inhibition. Collectively, our work reveals the involvement of the PITPNA-AS1/miR-363-5p/PDGFD regulatory axis in HCC progression.

Rice Plant Counting, Locating, and Sizing Method Based on High-Throughput UAV RGB Images.

Rice plant counting is crucial for many applications in rice production, such as yield estimation, growth diagnosis, disaster loss assessment, etc. Currently, rice counting still heavily relies on tedious and time-consuming manual operation. To alleviate the workload of rice counting, we employed an UAV (unmanned aerial vehicle) to collect the RGB images of the paddy field. Then, we proposed a new rice plant counting, locating, and sizing method (RiceNet), which consists of one feature extractor frontend and 3 feature decoder modules, namely, density map estimator, plant location detector, and plant size estimator. In RiceNet, rice plant attention mechanism and positive-negative loss are designed to improve the ability to distinguish plants from background and the quality of the estimated density maps. To verify the validity of our method, we propose a new UAV-based rice counting dataset, which contains 355 images and 257,793 manual labeled points. Experiment results show that the mean absolute error and root mean square error of the proposed RiceNet are 8.6 and 11.2, respectively. Moreover, we validated the performance of our method with two other popular crop datasets. On these three datasets, our method significantly outperforms state-of-the-art methods. Results suggest that RiceNet can accurately and efficiently estimate the number of rice plants and replace the traditional manual method.

Effects of Cranioplasty on Contralateral Subdural Effusion After Decompressive Craniectomy: A Literature Review.

BACKGROUND: Contralateral subdural effusion (CSE) after decompressive craniectomy (CSEDC) is occasionally observed. Cranioplasty is routinely performed for reconstruction and has recently been associated with improving contralateral subdural effusion. We sought to systematically review all available literature and evaluate the effectiveness of cranioplasty for CSE. METHODS: A PubMed, Web of Science, and Google Scholar search was conducted for preferred reporting items following the guidelines of systematic review and meta-analysis, including studies reporting patients who underwent cranioplasty because of CSEDC. RESULTS: The search yielded 8 articles. A total of 56 patients ranging in age from 21 to 71 years developed CSEDC. Of them, 32 patients underwent cranioplasty. Eighteen cases with symptomatic CSE underwent cranioplasty alone, 2 cases received Ommaya drainage later because of a recurrence of CDC, and 1 case underwent a ventriculoperitoneal shunt because the CSE did not resolve completely and the ventricle was dilated again. The symptoms of 14 cases lessened without recurrence after simultaneous cranioplasty and drainage or a shunt. The total success rate (CSE disappeared without recurrence) was 90.6% for patients who underwent cranioplasty; however, the total incidence of hydrocephalus was 40.1%. CONCLUSIONS: This review suggests that cranioplasty is effective for the treatment of CSEDC, particularly intractable cases, but early cranioplasty may be more effective. In addition, hydrocephalus is fairly common after cranioplasty and requires further treatment.

Driving effect of BDNF in the spinal dorsal horn on neuropathic pain.

Neuropathic pain (NP) is caused by direct or indirect damage to the nervous system and is a common symptom of many diseases. The mechanisms underlying the onset and persistence of NP are unclear. Therefore, research concerning these mechanisms has become an important focus in the medical field. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic factor family of signaling molecules. BDNF is an important regulator of neuronal development, synaptic transmission, and cellular and synaptic plasticity, which are essential for nerve maintenance and repair. However, BDNF is upregulated in the spinal dorsal horn and can promote NP by activating glial cells, reducing inhibitory functions and enhancing excitement after nociceptive stimulation. This review considers the relationship between NP and BDNF signaling in the spinal dorsal horn and discusses potentially related pathological mechanisms.

Curcumin attenuates doxorubicin-induced cardiotoxicity via suppressing oxidative stress and preventing mitochondrial dysfunction mediated by 14-3-3γ.

Doxorubicin (Dox) induces cardiotoxicity, thereby limiting its clinical application for chemotherapy of cancer. The mechanism of cardiotoxicity includes the production of excess intracellular ROS. 14-3-3s have been found to protect the myocardium against various types of injury. Curcumin (Cur) is a polyphenolic compound that is derived from turmeric and has multiple bioactivities, including anti-oxidative and radical-scavenging activities that exert cytoprotection. We hypothesize that the cardioprotective effects of Cur are exerted by regulating 14-3-3γ. To test the hypothesis, Dox-induced cardiotoxicity was used to establish an in vivo myocardial injury model in mice (in vivo) and primary cardiomyocytes (in intro). The effects of Cur were assessed by determining the heart rate and ECG's ST segments, as well as lactate dehydrogenase (LDH) and creatine kinase (CK) activities in the serum, caspase-3 activity, apoptosis rate, and histopathological changes of the myocardium (in vivo). In addition, cell viability, LDH, SOD, CAT, GPx, and caspase-3 activities, levels of ROS, MDA, and MMP, mPTP opening, and the apoptosis rate (in vitro) were evaluated. The expression of 14-3-3γ and Bcl-2 as well as the phosphorylation levels of Bad (S112) were determined by western blot analysis. Our results showed that Dox-induced injury to the myocardium was decreased by Cur treatment via upregulating the protein expression of 14-3-3γ in total protein and Bcl-2 expression on mitochondria, activating Bad (S112) phosphorylation, reducing the heart rate and ST segment, and reducing LDH and CK activities in the serum, thereby causing a reduction in caspase-3 activity, the apoptosis rate, and histopathological changes of the myocardium (in vivo). Furthermore, Dox treatment increased cell viability and MMP levels, decreased LDH and caspase-3 activity, ROS levels, mPTP opening, and the apoptosis rate (in vitro). However, the cardioprotective effects of Cur were attenuated by pAD/14-3-3γ-shRNA, an adenovirus that caused a knock-down of intracellular 14-3-3γ expression. In conclusion, this is the first study to demonstrate that Cur protected the myocardium against Dox-induced injury via upregulating 14-3-3γ expression, thereby promoting the translocation of Bcl-2 to mitochondria, suppressing oxidative stress, and improving mitochondrial function.

Automated on-line liquid chromatography-photodiode array-mass spectrometry method with dilution line for the determination of bisphenol A and 4-octylphenol in serum.

A novel on-line liquid chromatography-photodiode array detection-mass spectrometry (LC-DAD-MS) system was established with restricted-access media (RAM) pre-column and dilution line combined with a column-switching valve. The serum samples were injected directly onto pre-column under diluted condition by dilution line. After elution of proteins in the serum, the analytes were backflushed onto an ODS analytical column using a six-port column-switching device. The influence of the composition of the mobile phase, for instance, organic modifer, ionic strength, pH, dilution times and the rotation time of the switching valve have been investigated using bisphenol A (BPA) and 4-octyphenol (4-OP) as analytes. The evaluations for peak responses and sensitivity were conducted by MS, and proteins were removed by RAM-column with DAD monitoring at 280 nm. The peak shape was improved by adding a dilution line, especially in the case of large volume injection (LVI), which increased the sensitivity of the analysis. The selective and sensitive quantification of BPA and 4-OP in serum sample could be finished within 25 min. The method had linearity in the range 0.1-500 ng/mL with a limit of quantification for BPA and 4-OP of 0.1 and 0.5 ng/mL, respectively. The recoveries were in the range of 80-101% with less than 9.0% RSDs. This on-line LC-MS method demonstrates potential application to evaluating the exposure and risk of BPA and 4-OP in human.

Long-term oral resveratrol intake provides nutritional preconditioning against myocardial ischemia/reperfusion injury: involvement of VDAC1 downregulation.

SCOPE: This study elucidates the effects of long-term nutritional preconditioning by resveratrol on ischemia/reperfusion (I/R) injury and its underlying mechanisms. METHODS AND RESULTS: Mice were treated with resveratrol at 2.0 mg/kg/day by gastric gavages for 6 wk. Then hearts were isolated and subjected to I/R injury in a Langendorff apparatus. Resveratrol significantly improved left ventricular pressure, ±dp/dtmax, and coronary flow; decreased the lactate dehydrogenase and creatine phosphokinase activities; and reduced the infarction size. Additionally, long-term oral resveratrol intake prevented mitochondrial permeability transition pore opening and subsequently inhibited mitochondria-mediated apoptosis, as demonstrated by decrease of cytochrome c release, inactivation of caspase-3, and reduction of terminal deoxynucleotidyl transferase mediated nick end labeling positive cells. Furthermore, resveratrol inhibited the upregulation of voltage-dependent anion channel 1 (VDAC1) expression induced by I/R injury. Local left-ventricle overexpression of VDAC1 by adenovirus diminished the protective effect of resveratrol against I/R injury, indicating that VDAC1 plays an important role in resveratrol-mediated cardioprotection. CONCLUSION: Our data revealed that long-term oral intake of resveratrol sets nutritional preconditioning to cope with myocardial I/R injury. Strikingly, we found that resveratrol downregulates VDAC1, leading to prevention of mitochondrial permeability transition pore opening and cardiomyocyte apoptosis.

14-3-3γ protein attenuates lipopolysaccharide-induced cardiomyocytes injury through the Bcl-2 family/mitochondria pathway.

Previous studies have indicated that 14-3-3γ is upregulated by stress in LPS-induced cardiovascular injury. In this study, we investigated the interaction of 14-3-3γ and Bcl-2 family members in the control of the mitochondrial permeability transition (MPT) to test the hypothesis that abundant levels of 14-3-3γ can protect against LPS-induced injury via a Bcl-2 family/mitochondria pathway. The cardiomyocytes were treated with LPS (1mg l(-1)) for 6h; the interaction between 14-3-3γ and phospho-Bad(S112) was detected by co-immunoprecipitation (co-IP); the levels of Bcl-2 family members in the cytosolic and mitochondrial fractions were examined by Western blot; the apoptosis and mitochondrial membrane potential (ΔΨm) were detected by flow cytometry; and the mitochondrial permeability transition pore (mPTP) opening was tested by mitochondrial swelling. Our results revealed that LPS treatment results in cardiomyocyte injury, and these effects were significantly attenuated by pFLAG-14-3-3γ. Moreover, LPS treatment induced Bax translocation to the mitochondria, ΔΨm loss, mitochondrial swelling, and cytochrome c release, and pFLAG-14-3-3γ reversed these effects induced by LPS. Moreover, overexpressed 14-3-3γ protein could assist Bad(S112) phosphorylation and interact with it to form a complex, which might result in the disassociation of Bcl-2 from the Bad/Bcl-2 complex and its translocation from the cytosol to the mitochondria. Our data firstly confirmed that a high level of 14-3-3γ protects against LPS-induced cardiomyocyte injury likely through a pathway associated with the regulation of the subcellular localizations of Bcl-2 and Bad that results in the prevention of mPTP opening, the maintenance of ΔΨm, and ultimately the inhibition of apoptosis.