Features of microcirculation in psoriatic arthritis

The literature review presents data on features of microcirculation in patients with psoriatic arthritis (PsA). The immune inflammation underlying PsA leads to increased permeability of the vascular wall, deposition of the immune complexes in it, a decreased capillary blood flow, and vascular sensitivity to sympathetic stimulation. In combination with impaired blood rheology during inflammation, these changes have a significant effect on the state of the microvasculature. Increased vascular permeability and a damaged connection between the endothelium and the extracellular matrix in PsA cause the formation of the capillaries with a pathological structure. Microscopic examination of the synovial membrane of patients with PsA shows vascular tortuosity, branching, and elongation. The duration, activity of articular inflammation, as well as severity of psoriasis are associated with the degree of microcirculatory disorders in PsA. The pathomorphological changes in the vessels of patients with PsA are detected not only in the articular tissues but also in the skin, which indicates dysregulation of angiogenesis in general. The mechanisms of the formation of new vessels with a pathological structure are not fully understood. However, most likely, an imbalance of the factors of angiogenesis and antiangiogenesis plays an important role. There is growing evidence that vascular endothelial growth factor (VEGF), transforming growth factor-beta (TGF-beta) and platelet growth factor (PDGF) are involved in the pathogenesis of PsA. At the moment, the issue of early diagnosis of PsA remains relevant, especially in cases with minor skin changes and rheumatoid-like joint lesions. Information on microcirculation obtained by capillaroscopy, video capillaroscopy, and fluorescence microscopy provides additional opportunities for a differential diagnosis of PsA, a determination of activity, and a prognosis of the disease.

To the technique of painting Nissl`evsky bodies

In view of the growing interest presented by Nissl's bodies for researchers studying the physiological and pathological structure of nerve cells, I consider it useful to publish the coloring method I have developed. In addition to the simplicity of the technique and the demonstrativeness of the preparations obtained, the proposed method has the advantage of great constancy: to this I can add that the studies of the fresh nervous cells (my studies have not yet been published) reveal the complete identity of the pictures obtained in the volume and in other cases.

Effect of Sulfur Dioxide Inhalation on Lung Microbiota in Rat Model

Purpose: To investigate the effect of sulfur dioxide on the lung microbiota of healthy rats. Methods Fifteen male rats were randomly divided into high dose and low dose exposure group and control group. After 7 days of SO2 exposure, the lung tissues were obtained and the lung microbiota was identified by Illumina high-throughput sequencing. Results The microbial community of lung microbiota was significantly alternated in the exposure group and the dominant phylum changed from Firmicutes to Proteobacteria. In addition, the SO2 exposure caused the bronchial wall thickening and a large number of inflammatory cell infiltration in the lungs of rats in exposure groups. Conclusions The results suggest that SO2 can significantly alter the lung microbiota and pathological structure of the lungs.

Electroacupuncture and Moxibustion Regulate Hippocampus Glia and Mitochondria Activation in DSS-Induced Colitis Mice

Objectives. To study the influence of electroacupuncture (EA) and moxibustion on the hippocampus astrocyte and microglia activation in the ulcerative colitis model and to evaluate the mitochondria activity. Methods. 2.5% dextran sodium sulfate-induced colitis mice were treated by EA or moxibustion. Intestinal pathological structure was observed by hematoxylin and eosin (H&E) staining; the expression of GFAP or S100b (markers for astrocyte), Iba-1 (a marker for microglia), and Mitofilin (a marker for mitochondria) in hippocampus was detected by immunofluorescence staining or western blot. Results. The results demonstrated that both EA and moxibustion could improve the morphology of distal colonic mucosal epithelia in DSS-induced colitis mice. Expression of GFAP in the hippocampus was significantly increased after EA or moxibustion treatment. The effects were further supported by WB results. Meanwhile, expression of mitofilin in the hippocampus CA1 and CA3 regions showed the same trend as that of GFAP. Expression of Iba-1 in the hippocampus showed no significant difference after EA or moxibustion treatment, while the state of microglia changed from resting in control mice to activated state in colitis mice. Conclusion. EA and moxibustion were able to modulate the activation of astrocyte, microglial, and mitochondria in the hippocampus area in the colitis model.

Extracting Retinal Anatomy and Pathological Structure Using Multiscale Segmentation

Fundus image segmentation technology has always been an important tool in the medical imaging field. Recent studies have validated that deep learning techniques can effectively segment retinal anatomy and determine pathological structure in retinal fundus photographs. However, several groups of image segmentation methods used in medical imaging only provide a single retinopathic feature (e.g., roth spots and exudates). In this paper, we propose a more accurate and clinically oriented framework for the segmentation of fundus images from end-to-end input. We design a four-path multiscale input network structure that learns network features and finds overall characteristics via our network. Our network’s structure is not limited by segmentation of single retinopathic features. Our method is suitable for exudates, roth spots, blood vessels, and optic discs segmentation. The structure has general applicability to many fundus models; therefore, we use our own dataset for training. In cooperation with hospitals and board-certified ophthalmologists, the proposed framework is validated on retinal images from large databases and can improve diagnostic performance compared to state-of-the-art methods that use smaller databases for training. The proposed framework detects blood vessels with an accuracy of 0.927, which is comparable to exudate accuracy (0.939) and roth spot accuracy (0.904), providing ophthalmologists with a practical diagnostic and a robust analytical tool.

Ca2+/Calmodulin-Dependent Protein Kinase II Regulation by Inhibitor 1 of Protein Phosphatase 1 Protects Against Myocardial Ischemia–Reperfusion Injury

Ca2+/calmodulin-dependent protein kinase IIδ (CaMKIIδ) plays a vital role in cardiovascular system. However, the potential protective role of inhibitor 1 of protein phosphatase 1 (I1PP1), which can regulate CaMKII, on myocardial ischemia–reperfusion (I/R) injury remains unknown. In the present study, expression of CaMKIIδ variants was detected by quantitative real-time polymerase chain reaction. I1PP1 was overexpressed by pericardial injection of recombinant adenovirus. Two weeks later, rats were subjected to left anterior descending ligation for 30 minutes followed by reperfusion. Myocardial infarct size was assessed by Evans blue/triphenyl tetrazolium chloride staining. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activity as well as myocardial pathological structure were detected. CaMKII activity was evaluated by phosphorylation of phospholamban (PLB) and oxidation of CaMKII. Expression of dynamin-related protein 1 (DRP1) and optic atrophy 1 (OPA1) in the mitochondria was measured by Western blot. We found that CaMKIIδA and CaMKIIδB expression decreased, while the expression of CaMKIIδC increased after myocardial I/R. Moreover, after 30-minute ischemia followed by 6 hours of reperfusion, I1PP1 overexpression reduced myocardial infarct size, decreased serum CK and LDH activity, ameliorated myocardial pathological structure, inhibited PLB phosphorylation at Thr17, suppressed CaMKII oxidation, elevated CaMKIIδA and CaMKIIδB variants but reduced CaMKIIδC variants, attenuated myocardial oxidative stress, improved myocardial mitochondrial ultrastructure, increased mitochondrial number and mitochondrial DNA copy number, and decreased DRP1 but increased OPA1 protein expression from the mitochondria in rats. Thus, I1PP1 regulated CaMKII, protected mitochondrial function, reduced oxidative stress, and attenuated myocardial I/R injury.

Overexpression of Salusin-α Inhibits Vascular Intimal Hyperplasia in an Atherosclerotic Rabbit Model

Inhibiting vascular endothelial foam is the focus of clinical attention. Using SonoVue (an ultrasound contrast agent), the salusin-α gene was transfected into the arterial intima of an atherosclerotic rabbit model induced by a high-fat diet in this study. Subsequently the model of blood lipid indexes, the pathological structure of the intima, and changes in molecules regulating atherosclerosis were investigated. The high-density lipoprotein C and apolipoprotein A values in the salusin-α gene overexpression (P) group were higher than those in the salusin-α gene interference (RP) group (P < 0.05), whereas the total cholesterol, low-density lipoprotein C, and apolipoprotein B values were reversed. Rabbits in the P group showed significantly thinner vascular intimal thickness than that of other experimental groups (P < 0.05). The expression of positive regulators of atherosclerosis (ABCA1, ABCG1) was higher in the P group than that in the RP group (P < 0.05), and the opposite effect was observed for negative regulators (ACAT1, CD36). Thus, our results showed that the overexpression of salusin-α gene inhibited the proliferation of the vascular intima, thereby throwing some light on understanding the mechanism how salusin-α gene expression interfered with the foaming of vascular intimal cells.