[Effect of oxymatrine on Cryptosporidium parvum infection in mice based on the HMGB1-TLR2/TLR4-NF-κB pathway].

OBJECTIVE: To investigate the involvement of the high mobility group box protein B1 (HMGB1)-Toll-like receptor 2 (TLR2)/TLR4-nuclear factor κB (NF-κB) pathway in the intestinal mucosal injury induced by Cryptosporidium parvum infection, and to examine the effect of oxymatrine (OMT) on C. parvum infection in mice. METHODS: Forty SPF 4-week-old BALB/c mice were randomly divided into four groups, including the control group, infection group, glycyrrhizin (GA) group and OMT group. Each mouse was orally administered with 1 × 105 C. parvum oocysts one week in the infection, GA and OMT groups following dexamethasone-induced immunosuppression to model C. parvum intestinal infections in mice. Upon successful modeling, mice in the GA group were intraperitoneally injected with GA at a daily dose of 25.9 mL/kg for successive two weeks, and animals in the OMT group were orally administered OMT at a daily dose of 50 mg/kg for successive two weeks, while mice in the control group were given normal food and water. All mice were sacrificed two weeks post-treatment, and proximal jejunal tissues were sampled. The pathological changes of mouse intestinal mucosal specimens were observed using hematoxylin-eosin (HE) staining, and the mouse intestinal villous height, intestinal crypt depth and the ratio of intestinal villous height to intestinal crypt depth were measured. The occludin and zonula occludens protein 1 (ZO1) expression was determined in mouse intestinal epithelial cells using immunohistochemistry, and the relative expression of HMGB1, TLR2, TLR4, myeloid differentiation primary response gene 88 (MyD88) and NF-κB p65 mRNA was quantified in mouse jejunal tissues using quantitative real-time PCR (qPCR) assay. RESULTS: HE staining showed that the mouse intestinal villi were obviously atrophic, shortened, and detached, and the submucosal layer of the mouse intestine was edematous in the infection group as compared with the control group, while the mouse intestinal villi tended to be structurally intact and neatly arranged in the GA and OMT groups. There were significant differences among the four groups in terms of the mouse intestinal villous height (F = 6.207, P = 0.000 5), intestinal crypt depth (F = 6.903, P = 0.000 3) and the ratio of intestinal villous height to intestinal crypt depth (F = 37.190, P < 0.000 1). The mouse intestinal villous height was lower in the infection group than in the control group [(321.9 ± 41.1) µm vs. (399.5 ± 30.9) µm; t = 4.178, P < 0.01] and the GA group [(321.9 ± 41.1) µm vs. (383.7 ± 42.7) µm; t = 3.130, P < 0.01], and the mouse intestinal crypt depth was greater in the infection group [(185.0 ± 35.9) µm] than in the control group [(128.4 ± 23.6) µm] (t = 3.877, P < 0.01) and GA group [(143.3 ± 24.7) µm] (t = 2.710, P < 0.05). The mouse intestinal villous height was greater in the OMT group [(375.3 ± 22.9) µm] than in the infection group (t = 3.888, P < 0.01), and there was no significant difference in mouse intestinal villous height between the OMT group and the control group (t = 1.989, P > 0.05). The mouse intestinal crypt depth was significantly lower in the OMT group [(121.5 ± 27.3) µm] than in the infection group (t = 4.133, P < 0.01), and there was no significant difference in mouse intestinal crypt depth between the OMT group and the control group (t = 0.575, P > 0.05). The ratio of the mouse intestinal villous height to intestinal crypt depth was significantly lower in the infection group (1.8 ± 0.2) than in the control group (3.1 ± 0.3) (t = 10.540, P < 0.01) and the GA group (2.7 ± 0.3) (t = 7.370, P < 0.01), and the ratio of the mouse intestinal villous height to intestinal crypt depth was significantly higher in the OMT group (3.1 ± 0.2) than in the infection group (t = 15.020, P < 0.01); however, there was no significant difference in the ratio of the mouse intestinal villous height to intestinal crypt depth between the OMT group and the control group (t = 0.404, P > 0.05). Immunohistochemical staining showed significant differences among the four groups in terms of occludin (F = 28.031, P < 0.000 1) and ZO1 expression (F = 14.122, P < 0.000 1) in mouse intestinal epithelial cells. The proportion of positive occluding expression was significantly lower in mouse intestinal epithelial cells in the infection group than in the control group [(14.3 ± 4.5)% vs. (28.3 ± 0.5)%; t = 3.810, P < 0.01], and the proportions of positive occluding expression were significantly higher in mouse intestinal epithelial cells in the GA group [(30.3 ± 1.3)%] and OMT group [(25.8 ± 1.5)%] than in the infection group (t = 7.620 and 5.391, both P values < 0.01); however, there was no significant differences in the proportion of positive occluding expression in mouse intestinal epithelial cells between the GA or OMT groups and the control group (t = 1.791 and 2.033, both P values > 0.05). The proportion of positive ZO1 expression was significantly lower in mouse intestinal epithelial cells in the infection group than in the control group [(14.4 ± 1.8)% vs. (24.2 ± 2.8)%; t = 4.485, P < 0.01], and the proportions of positive ZO1 expression were significantly higher in mouse intestinal epithelial cells in the GA group [(24.1 ± 2.3)%] (t = 5.159, P < 0.01) and OMT group than in the infection group [(22.5 ± 1.9)%] (t = 4.441, P < 0.05); however, there were no significant differences in the proportion of positive ZO1 expression in mouse intestinal epithelial cells between the GA or OMT groups and the control group (t = 0.037 and 0.742, both P values > 0.05). qPCR assay showed significant differences among the four groups in terms of HMGB1 (F = 21.980, P < 0.000 1), TLR2 (F = 20.630, P < 0.000 1), TLR4 (F = 17.000, P = 0.000 6), MyD88 (F = 8.907, P = 0.000 5) and NF-κB p65 mRNA expression in mouse jejunal tissues (F = 8.889, P = 0.000 7). The relative expression of HMGB1 [(5.97 ± 1.07) vs. (1.05 ± 0.07); t = 6.482, P < 0.05] 、TLR2 [(5.92 ± 1.29) vs. (1.10 ± 0.14); t = 5.272, P < 0.05] 、TLR4 [(5.96 ± 1.50) vs. (1.02 ± 0.03); t = 4.644, P < 0.05] 、MyD88 [(3.00 ± 1.26) vs. (1.02 ± 0.05); t = 2.734, P < 0.05] and NF-κB p65 mRNA [(2.33 ± 0.72) vs. (1.04 ± 0.06); t = 2.665, P < 0.05] was all significantly higher in mouse jejunal tissues in the infection group than in the control group. A significant reduction was detected in the relative expression of HMGB1 (0.63 ± 0.01), TLR2 (0.42 ± 0.10), TLR4 (0.35 ± 0.07), MyD88 (0.70 ± 0.11) and NF-κB p65 mRNA (0.75 ± 0.01) in mouse jejunal tissues in the GA group relative to the control group (t = 8.629, 5.830, 11.500, 4.729 and 6.898, all P values < 0.05), and the relative expression of HMGB1, TLR2, TLR4, MyD88 and NF-κB p65 mRNA significantly reduced in mouse jejunal tissues in the GA group as compared to the infection group (t = 7.052, 6.035, 4.084, 3.165 and 3.274, all P values < 0.05). In addition, the relative expression of HMGB1 (1.14 ± 0.60), TLR2 (1.00 ± 0.24), TLR4 (1.14 ± 0.07), MyD88 (0.96 ± 0.25) and NF-κ B p65 mRNA (1.12 ± 0.17) was significantly lower in mouse jejunal tissues in the OMT group than in the infection group (t = 7.059, 5.320, 3.510, 3.466 and 3.273, all P values < 0.05); however, there were no significant differences between the OMT and control groups in terms of relative expression of HMGB1, TLR2, TLR4, MyD88 or NF-κB p65 mRNA in mouse jejunal tissues (t = 0.239, 0.518, 1.887, 0.427 and 0.641, all P values > 0.05). CONCLUSIONS: C. parvum infection causes intestinal inflammatory responses and destruction of intestinal mucosal barrier through up-regulating of the HMGB1-TLR2/TLR4-NF-κB pathway. OMT may suppress the intestinal inflammation and repair the intestinal mucosal barrier through inhibiting the activity of the HMGB1-TLR2/TLR4-NF-κB pathway.

Environmental drivers of increased ecosystem respiration in a warming tundra.

Arctic and alpine tundra ecosystems are large reservoirs of organic carbon1,2. Climate warming may stimulate ecosystem respiration and release carbon into the atmosphere3,4. The magnitude and persistency of this stimulation and the environmental mechanisms that drive its variation remain uncertain5-7. This hampers the accuracy of global land carbon-climate feedback projections7,8. Here we synthesize 136 datasets from 56 open-top chamber in situ warming experiments located at 28 arctic and alpine tundra sites which have been running for less than 1 year up to 25 years. We show that a mean rise of 1.4 °C [confidence interval (CI) 0.9-2.0 °C] in air and 0.4 °C [CI 0.2-0.7 °C] in soil temperature results in an increase in growing season ecosystem respiration by 30% [CI 22-38%] (n = 136). Our findings indicate that the stimulation of ecosystem respiration was due to increases in both plant-related and microbial respiration (n = 9) and continued for at least 25 years (n = 136). The magnitude of the warming effects on respiration was driven by variation in warming-induced changes in local soil conditions, that is, changes in total nitrogen concentration and pH and by context-dependent spatial variation in these conditions, in particular total nitrogen concentration and the carbon:nitrogen ratio. Tundra sites with stronger nitrogen limitations and sites in which warming had stimulated plant and microbial nutrient turnover seemed particularly sensitive in their respiration response to warming. The results highlight the importance of local soil conditions and warming-induced changes therein for future climatic impacts on respiration.

Finite element modelling of thermal and moisture mapping of layered cricket helmets.

This paper presents the development of numerical modelling to simulate thermal and moisture mapping of layered cricket helmets. The 3D laser scanning methodology was used to obtain geometrical data of a dummy human head with non-ventilated (NVL) and ventilated (VL) helmets to generate the meshes. Here, heat transfer and mass diffusion were applied in the finite element simulations to model the temperature and relative humidity (RH) distributions inside NVL and VL helmets, which were processed as the temperature-time and RH-time charts. The simulated results were validated against the corresponding experimental measurements with reasonably good correlation, in terms of the general trend on reginal temperature and RH against time, although parameters such as helmet movement and local sweating were not considered in the modelling to simplify the simulation. The discrepancies between the FE simulation results and the measurements are generally within 7% for in-helmet temperature and 5% for RH, for both types of helmets in the low ambient conditions (20 °C and 50% RH), although such the discrepancy is about 10% for the VL helmet subjected to the high ambient conditions (35 °C and 30% RH). The models developed are ready to be used for parametric studies on non-ventilated helmet to optimize the ventilation openings for improving the thermal comfort.

[Transcriptomic analysis of the ΔPaLoc mutant of Clostridioides difficile and verification of its toxicity].

Objective: Comparative analyses of wild-type Clostridioides difficile 630 (Cd630) strain and pathogenicity locus (PaLoc) knockout mutant (ΔPaLoc) by using RNA-seq technology. Analysis of differential expression of Cd630 wild-type strain and ΔPaLoc mutant strain and measurement of its cellular virulence changes. Lay the foundation for the construction of an toxin-attenuated vaccine strain against Clostridioides difficile. Methods: Analysis of Cd630 and ΔPaLoc mutant strains using high-throughput sequencing (RNA-seq). Clustering differentially expressed genes and screening differentially expressed genes by DESeq software. Further analysis of differential genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Finally, cytotoxicity assays of ΔPaLoc and Cd630 strains were performed in the African monkey kidney epithelial cell (Vero) and the human colonic cell (Caco-2) lines. Results: The transcriptome data showed that the ΔPaLoc mutant toxin genes tcdA and tcdB were not transcribed. Compared to the wild-type strain, CD630_36010, CD630_020910,CD630_02080 and cel genes upregulated 17.92,11.40,8.93 and 7.55 fold, respectively. Whereas the hom2 (high serine dehydrogenase), the CD630_15810 (spore-forming protein), CD630_23230 (zinc-binding dehydrogenase) and CD630_23240 (galactitol 1-phosphate 5-dehydrogenase) genes were down-regulated by 0.06, 0.075, 0.133 and 0.183 fold, respectively. The GO and KEGG enrichment analyses showed that the differentially transcribed genes in ΔPaLoc were enriched in the density-sensing system, ABC transport system, two-component system, phosphotransferase (PTS) system, and sugar metabolism pathway, as well as vancomycin resistance-related pathways. Cytotoxicity assays showed that the ΔPaLoc mutant strain lost its virulence to Vero and Caco-2 cells compared to the wild-type Cd630 strain. Conclusion: Transcriptional sequencing analysis of the Cd630 and ΔPaLoc mutant strains showed that the toxin genes were not transcribed. Those other differential genes could provide a reference for further studies on the physiological and biochemical properties of the ΔPaLoc mutant strain. Cytotoxicity assays confirmed that the ΔPaLoc mutant lost virulence to Vero and Caco-2 cells, thus laying the foundation for constructing an toxin-attenuated vaccine strain against C. difficile.

Fluoride induced down-regulation of IKBKG Gene expression inhibits hepatocytes senescence.

BACKGROUND: Accumulating evidences have confirmed that liver is one of the more severely damaged organs during chronic fluorosis. However, the detail mechanism is unclear to data. At present, the objective of this study was to investigate the relationship between down-regulation of IKBKG gene expression and hepatocyte senescence induced by sodium fluoride (NaF). METHODS: Chronic fluorosis rats and NaF-exposure human liver L02 cells were reproduced the model of hepatocyte senescence in vivo and in vitro. The mRNA and protein levels of p16, p21 and IKBKG, the IL-8 level were determined. The role of IKBKG in fluoride-induced senescence of hepatocytes was explored by knock down in hepatocytes in vivo and in vitro. RESULTS: The number of senescence-positive cells in rat liver tissues was increased as well as the level of IL-8 and the expression levels of p16, p21 and IKBKG in fluoride exposure to rat depending on the fluoride concentration. The similar results were obtained in NaF treated liver L02 cells, and the number of cells that stagnated in the G2 phase increased significantly. Further, our results confirmed that decreasing the expression of IKBKG in hepatocytes could reduce fluoride-induced hepatocyte senescence and the changes of senescence-related indicators both in vivo and in vitro. CONCLUSION: These results indicated that the elevated expression of IKBKG was positive relation with the fluoride-induced senescence in hepatocytes, suggesting the hepatocyte senescence might have a special relationship with fluoride-caused liver damage. Because of the present results limitation, the mechanism of fluoride induced senescence in hepatocytes should be concentrated in the future in detail, especially the novel targets for fluoride induced liver injury.

[The prediction of disease progression by 18Fluorodeoxyglucose-positron emission computed tomography/CT in patients with dermatomyositis and interstitial lung disease].

To investigate the predictive value of [18F]fluorodeoxyglucose-positron emission computed tomography(PET)/CT for disease progression in patients with dermatomyositis (DM) and interstitial lung diseases (ILD). Sixty-seven DM patients who underwent [18F] FDG-PET/CT imaging were retrospectively analyzed from January 2012 to September 2017 at PLA General Hospital. Their clinical manifestations and imaging characteristics were recorded. Compared with those chronically progressed (C-ILD), patients with rapid progression (RP-ILD) had significantly higher erythrocyte sedimentation rate (ESR) and standardized uptake value (SUV) in lungs (P<0.05). In patients with RP-ILD, SUV in lungs was positively correlated with age, disease course, and ESR. Receiver operating characteristic curve analysis suggested that when lung SUV cut off value was 2.25, the sensitivity and specificity to predict disease progression was 77.8% and 72.8%, respectively. Old age, longer disease course, low creatine kinase level, higher ESR, and high SUV are prognostic factors for DM-associated ILD.

[Impact of health literacy on patient experience of outpatients in China and its mechanism].

OBJECTIVE: To understand the relationship between health literacy and patient experience of outpatients in China, and to explore its mechanism. METHODS: The conceptual framework was developed based on Andersen's behavioral model of health services use and health literacy skills framework. An online cross-sectional survey was conducted with snowball sampling method, while the health literacy was measured by self-designed patient health literacy scale, and the patient experience was measured by the Chinese patient experience questionnaire for ambulatory care developed by Peking Union Medical College. And a structural equation model was built to explore the relationship between them and test the mechanism of health literacy influencing patient experience. RESULTS: A total of 2 773 subjects were investigated. The average score of health literacy was (90.72±12.90) points, accounting for 78.89% of the full score, and the dimension of seeking social support had the lowest score. The average score of overall rating of patient experience was (3.71±0.74) points, and the scores of each dimension of patient experience were between 3.56 and 3.80. The model fit indices of structural equation model for overall rating of patient experience among the outpatients were χ2/df=9.29 (χ2=4 107.27, df=442), root mean square error of approximation (RMSEA)=0.055 (< 0.06), comparative fit index (CFI)=0.926 (>0.90), Tucker-Lewis index (TLI)=0.918 (>0.90), standardized root mean square residual (SRMR)=0.061 (< 0.08), the model was acceptable. The variance in patient experience explained by the model was 0.108. The structural equation model analysis results showed that the overall rating of outpatient experience was directly affected by health literacy (ß=0.263, P < 0.001), also indirectly affected by health literacy (ß=0.012, P < 0.001). In other words, the overall rating increased by 0.275 units for each standard deviation increase of health literacy. Self-evaluated health status mediated the relationship between health literacy and the overall rating of outpatient experience. In terms of diffe-rent dimensions of patient experience, the standardized path coefficient of the total effect of health literacy on patient experience was as follows: Information guidance 0.337, humanistic care 0.319, communication with doctors 0.294, service efficiency 0.240, and hospital environment 0.173. CONCLUSION: The patients with higher level of health literacy were more likely to have a better outpatient experience in China, and the information guidance experience and humanistic care experience were most affected by health literacy. And the communication and information utilization ability had the greatest influence on patient experience.

[Prevention and treatment of bearing dislocation of mobile-bearing unicompartmental knee arthroplasty].

Bearing dislocation is a special complication of mobile-bearing unicompartmental arthroplasty, caused by many factors, such as imbalance of the flexion and extension gap, malposition of components, impingement by the remaining osteophytes and cement, damage or delayed chronic laxity of medial collateral ligament, traumatic accident and habitual high knee flexion. It can be reduced by strictly controlling the operation indications before operation, osteotomy and implanting the prosthesis accurately while protecting the medial collateral ligament during operation, actively guiding the appropriate rehabilitation actions and activity intensity of patients after operation. Treatment should be individualized according to the causes and individual conditions of patients.

[Comparison of the early efficacy of unicompartmental and total knee arthroplasty in patients with medial compartmental osteoarthritis of the knee: a propensity score matching study].

Objective: To compare the short-term efficacy of unicompartmental knee arthroplasty (UKA) and total knee arthroplasty(TKA) in the treatment of medial compartmental knee osteoarthritis. Methods: A retrospective analysis was performed on 197 patients with medial compartment osteoarthritis of the knee treated by the same group of doctors from January 2015 to December 2018.There were 86 males and 111 females, aged (67.7±10.5) years (range: 46 to 92 years), among which 101 cases received UKA and 96 cases received TKA.The UKA and TKA patients were matched by the propensity score matching method, and a total of 41 pairs of patients were successfully matched.The difference of short-term outcomes between the two groups were compared by t test, χ(2) test or Fisher exact probability methods. Results: Compared with TKA group, the postoperative reduction of hemogloblin in the UKA group was lower ((15.3±6.4) g/L vs. (20.1±7.5) g/L, t=-3.117, P<0.01), opioid dosage was lower ((160.5±29.3) mg vs. (186.1±46.8) mg, t=-2.969, P<0.01), and the length of hospital stay was shorter ((7.0±2.0)d vs. (10.0±2.5)d, t=-6.000, P<0.01). Forgotten joint score of UKA group was higher ( (65.1±7.6) vs. (58.3±13.9) , t=2.732, P<0.01), the incidence of knee clunk or crepitus was lower (P=0.03) . There was no significant difference in the time of surgical tourniquet, range of motion, American knee society clinical score and incidence of deep vein thrombosis in lower extremities between the two groups.No complications such as surgical site infection, prosthesis loosening and dislocation occurred in the two groups. Conclusion: The early effect of UKA is similar to that of TKA, and it is better than TKA in the aspects of knee clunk or crepitus, forgotten joint score, blood loss, opioid dosage and postoperative hospital stay.

First-principles investigation of nonmetal doped single-layer BiOBr as a potential photocatalyst with a low recombination rate.

Nonmetal doping is an effective approach to modify the electronic band structure and enhance the photocatalytic performance of bismuth oxyhalides. Using density functional theory, we systematically examine the fundamental properties of single-layer BiOBr doped with boron (B) and phosphorus (P) atoms. The stability of the doped models is investigated based on the formation energies, where the substitutional doping is found to be energetically more stable under O-rich conditions than under Bi-rich ones. The results showed that substitutional doping of P atoms reduced the bandgap of pristine BiOBr to a greater extent than that of boron substitution. The calculation of the effective masses reveals that B doping can render the electrons and holes of pristine BiOBr lighter and heavier, respectively, resulting in a slower recombination rate of photoexcited electron-hole pairs. Based on the results of HOMO-LUMO calculations, the introduction of B atoms tends to increase the number of photocatalytically active sites. The top of the valence band and the conduction band bottom of the B doped BiOBr monolayer match well with the water redox potentials in an acidic environment. The absorption spectra propose that B(P) doping causes a red-shift. Overall, the results predict that nonmetal-doped BiOBr monolayers have a reduced bandgap, a slow recombination rate, more catalytically active sites, enhanced optical absorption edges, and reduced work functions, which will contribute to superior photocatalytic performance.

Follicle Stimulating Hormone Inhibits the Expression of p53 Up-Regulated Modulator of Apoptosis Induced by Reactive Oxygen Species Through PI3K/Akt in Mouse Granulosa Cells.

In mammalian ovaries, follicular atresia occurs periodically and destroys almost all the follicles in the ovary. Follicle-stimulating hormone (FSH) acts as the primary survival factor during follicular atresia by preventing apoptosis in granulosa cells (GCs). Many studies have demonstrated that oxidative stress-induced apoptosis is a main cause of follicular atresia. Reactive oxygen species (ROS)-induced GCs apoptosis is regulated by a variety of signaling pathways involving numerous genes and transcription factors. Therefore, we examined whether FSH inhibits the expression of p53 up-regulated modulator of apoptosis (PUMA) induced by reactive oxygen species (ROS) through phosphoinositide 3-kinase (PI3K) / protein kinase B (AKT) in mouse GCs. In vivo study: thirty-two-mice were randomly assigned to four groups and given FSH. We found that FSH can inhibit the 3-nitropropionic acid (3-NP) induced apoptosis and PUMA expression in mRNA level. Moreover, In vitro experiment, we found that FSH can inhibit the H(2)O(2)-induced apoptosis and PUMA expression in mRNA level. Additionally, we also found that PI3K/AKT inhibitor LY294002 abolished the downregulation of PUMA mRNA by FSH in vitro, In conclusion, FSH inhibit the expression of PUMA induced by ROS through PI3K/AKT pathway in vivo and vitro.

Purinoceptors, renal microvascular function and hypertension.

Proper renal blood flow (RBF) and glomerular filtration rate (GFR) are critical for maintaining normal blood pressure, kidney function and water and electrolyte homeostasis. The renal microvasculature expresses a multitude of receptors mediating vasodilation and vasoconstriction, which can influence glomerular blood flow and capillary pressure. Despite this, RBF and GFR remain quite stable when arterial pressure fluctuates because of the autoregulatory mechanism. ATP and adenosine participate in autoregulatory control of RBF and GFR via activation of two different purinoceptor families (P1 and P2). Purinoceptors are widely expressed in renal microvasculature and tubules. Emerging data show altered purinoceptor signaling in hypertension-associated kidney injury, diabetic nephropathy, sepsis, ischemia-reperfusion induced acute kidney injury and polycystic kidney disease. In this brief review, we highlight recent studies and new insights on purinoceptors regulating renal microvascular function and renal hemodynamics. We also address the mechanisms underlying renal microvascular injury and impaired renal autoregulation, focusing on purinoceptor signaling and hypertension-induced renal microvascular dysfunction. Interested readers are directed to several excellent and comprehensive reviews that recently covered the topics of renal autoregulation, and nucleotides in kidney function under physiological and pathophysiological conditions (Inscho 2009, Navar et al. 2008, Carlstrom et al. 2015, Vallon et al. 2020).

Friction properties of in vivo human skin from visualized friction testing.

Investigations on mechanical behaviors of intravital human skin are of significance in various fields. However, due to the great complexity and the individual variation of human skin, traditional experimental mechanics often fails to work in such research objects. In this study, the friction property considering the skin-uplift effect of human skin was in vivo studied experimentally and theoretically. An in situ and noninvasive friction experiment was performed in vivo on human skin, where the projected contact morphology was captured through a novel specially developed optical system. According to the contact morphology, a model taking uplift resistance into account is proposed based on Greenwood model, in which the contact area was depicted as a combination of two ellipses to better characterize the skin deformation. Moreover, since the model degrades into Greenwood model in small deformation, it can be considered as an extension from the perspective of small deformation to large deformation. Based on the model, the adhesion friction and deformation friction have been separated according to the ratio of indentation depth to probe radius. The results show that the friction property of skin varies with the indentation depth changing, and the deformation friction is positively correlated with the ratio of indentation depth to probe radius.

The importance of proper and prompt treatment of ocular syphilis: a lesson from permanent vision loss in 52 eyes.

BACKGROUND: Ocular involvement can occur at any stage of syphilis. Prompt diagnosis and proper treatment of ocular syphilis are vital to avoid long-term consequences. OBJECTIVES: To describe the risk factors for ocular syphilis and clinical features of blindness caused by syphilis. METHODS: We report risk factors for ocular syphilis amongst patients seen at the Shanghai Skin Disease Hospital between October 2009 and October 2017. We identify patients with ocular syphilis resulting in blindness and report the clinical characteristics, laboratory findings and treatment outcomes of these patients. RESULTS: A total of 8310 new cases of syphilis were seen, of which 213 patients had ocular disease and 50 patients had blindness due to syphilis. Increasing age and higher RPR titres were associated with ocular involvement but there was no association with HIV status. Blindness in syphilis was restricted predominantly to patients with optic nerve involvement and not patients with isolated uveitis. Fifty patients (and a total of 67 eyes) met the WHO definition of blindness prior to treatment for syphilis. At the end of follow-up, vision had improved in 24 of 67 eyes (35.8%) after treatment. Successful treatment of uveitis was associated with the best improvement in visual acuity, whilst patient with underlying optic atrophy prior to treatment had the worst visual outcome. CONCLUSIONS: Ocular involvement is an important manifestation of syphilis which may result in blindness. Our data demonstrate outcomes for ocular syphilis are poor if detected late; early recognition and diagnosis is therefore vital to avoid permanent visual loss.

[Epidemiological characteristics of malaria in Henan Province from 1950 to 2019].

OBJECTIVE: To analyze the epidemiological characteristics of malaria in Henan Province from 1950 to 2019, so as to provide the scientific evidence for consolidating malaria elimination achievements in the province. METHODS: The epidemiological situation of malaria and demographic data in Henan Province from 1950 to 2019 were collected, and the statistical analyses were performed using a descriptive epidemiological method. The spatial temporal distribution of malaria cases was identified using the software ArcGIS version 10.3. RESULTS: During the period from 1950 through 2019, the progress of malaria elimination was divided into 4 stages in Henan Province, including the baseline-survey and key-control stage, morbidity-control and incidence-reduction stage, basic-eradication and achievement-consolidation stage and elimination stage. The spatial distribution of malaria cases shifted from south of the Huai River and the plain regions between the Yellow River and Taihang Mountain to the Huang-Huai-Hai Plain and Nanyang Basin, then was concentrated in eastern part of southern Huai River where Anopheles anthropophagus was distributed, and finally was gradually under control following malaria outbreak in Eastern Henan Plain. In addition, the species of Plasmodium changed from P. vivax, P. falciparum and P. malariae co-endemics to a single P. vivax infection, and the current co-endemics of 5 invasive malaria parasites, and the malaria vectors shifted from co-existence of Anopheles sinensis and An. anthropophagus to An. sinensis alone. CONCLUSIONS: There has been a large change in the epidemiological characteristics of malaria in Henan Province from 1950 to 2019. Although malaria has been eliminated in Henan Province, the consolidation of the malaria elimination achievements remain a great challenge due to overseas imported malaria.