[Diaphragmatic dysfunction post-COVID-19 infection: report of two cases].

Following the global outbreak of COVID-19, many patients have suffered from multi-system complications and long-term sequelae caused by the virus. Diaphragm dysfunction is an obscure post-COVID-19 symptom. Although a few cases of diaphragm dysfunction caused by COVID-19 infection have been reported abroad, there are no relevant reports in China. Herein, we present two cases of patients with respiratory distress after COVID-19 infection. On admission, dynamic chest radiographs revealed diaphragm dysfunction in these patients. Further investigations including diaphragm ultrasound, neurophysiological examinations, transdiaphragmatic pressure measurements cranial MRI, and antibody testing for autoimmune diseases, were conducted. The final diagnoses were severe myasthenia gravis induced by COVID-19 infection and diaphragmatic nerve and muscle involvement caused by COVID-19 infection. Both patients showed improvement in symptoms after treatment. Therefore, we summarized our case, with a review of the relevant literature to improve the understanding of the disease and to provide clinical evidence for future diagnosis and treatment.

Synergistically homogeneous-heterogeneous Fenton catalysis of trace copper ion and g-C3N4 for degradation of organic pollutants.

Using the bulk g-C3N4 as a precursor, four g-C3N4 nanosheets were further prepared by ultrasonic, thermal, acid, and alkali exfoliation. The structures of these materials were characterized by various techniques such as X-ray powder diffraction, Fourier transform infrared spectroscopy, scanning electron microscopy, energy dispersive X-ray spectroscopy, transmission electron microscopy, and X-ray photoelectron spectroscopy. The synergistical Fenton catalysis of these materials with Cu2+ was evaluated by using rhodamine B as a simulated organic pollutant. The results showed that there existed a significant synergistical Fenton catalysis between Cu2+ and g-C3N4. This synergistic effect can be observed even when the concentration of Cu2+ was as low as 0.064 mg L-1. The properties of g-C3N4 strongly influenced the catalytic activity of the Cu2+/g-C3N4 system. The coexistent of Cu2+ and the alkali exfoliated g-C3N4 showed the best catalytic activity. Hydroxyl radicals as oxidizing species were confirmed in the Cu2+/g-C3N4 system by electron paramagnetic resonance spectra. The synergistic catalysis may be attributed to the easier reduction of Cu2+ adsorbed on the g-C3N4. This study provided an excellent Fenton catalytic system, and partly solved the rapid deactivation of heterogeneous Fenton catalysts caused by the leaching of metal ions.

Graphitic carbon nitride (g-C3N4) as an efficient metal-free Fenton-like catalyst for degrading organic pollutants: the overlooked non-photocatalytic activity.

Graphitic carbon nitride (g-C3N4) has attracted a large amount of research, mainly being used as a photocatalyst, but its Fenton-like catalytic performance has been overlooked. In this paper, the dark Fenton-like catalytic performance of g-C3N4 was evaluated by degrading rhodamine B over a wide pH range. The results showed that the g-C3N4, which was synthesized by conventional urea pyrolysis without any modification, was an efficient metal-free heterogeneous Fenton-like catalyst. The highest activity occurred under a weakly alkaline condition of about pH 10. The experiment of catalyst recycling indicated that g-C3N4 had long-term stability. The reactive oxidizing species of HO·, generated by the g-C3N4 activating H2O2, was identified by EPR and further supported by a scavenging experiment of HO· using isopropanol as the scavenger. The HNO3 oxidation of g-C3N4 resulted in catalytic deactivation, implying the catalytic activity originated from the surface reduced groups of g-C3N4. The structure of synthesized g-C3N4 before and after the HNO3 oxidation was characterized by X-ray diffraction, Fourier transform infrared spectroscopy, and X-ray photoelectron spectroscopy, and a possible catalytic mechanism was proposed.

[FABP5 promotes cell growth, invasion and metastasis in cervical cancer].

Objective: To investigate the functions of FABP5 in the carcinogenesis and development of cervical cancer. Methods: The expression of FABP5 was detected in several cervical cancer cell lines (C33A, Siha, Caski, HeLa and HCC94), 206 cases of cervical cancer tissues with stage Ⅰa2-Ⅱa2 and 40 cases of normal cervical tissues by real-time PCR and Western blotting. Then, the cells were infected with lentivirus-mediated siRNA-targeting FABP5. CCK-8 cell proliferation, colony formation, wound healing and transwell assays were used to investigate the effects of FABP5 on in vitro cell proliferation, migration and invasion. And in vivo xenograft model and lung metastasis model were used to observe the transplanted tumor growth and metastasis in female athymic nude mice. Furthermore, the total protein and RNA were extracted from the primary xenografts to determine the expression levels of FABP5, metalloproteinase-2 and metalloproteinase-9 using Enzyme linked immunosorbent assay (ELISA), real-time PCR and Western blotting. Results: FABP5 expression was found to be significantly unregulated in cervical cancer tissues than that in normal cervical tissues (P<0.05). Compared with the Siha-NC group and uninfected group, the expression of FABP5 mRNA and protein in Siha-FABP5-RNAi group was significantly inhibited along with the decrease of cell proliferation, colony formation, wound healing and invasion ability. The clone formation rates of Siha cells in uninfected group, Siha-NC group and Siha-FABP5-RNAi group were (84.6±4.5)%, (84.6±5.1)% and (21.2±2.6)%, respectively. Moreover, the transwell assay showed that invasive cells in three groups were (72.8±4.7)/HPF, (72.6±3.3)/HPF and (21.4±2.3)/HPF, respectively. All of the difference was statistically significant (P<0.05). Furthermore, FABP5 silencing significantly reduced tumor growth and lung metastases in nude mice in vivo (P<0.001). The subcutaneously xenografted volume in uninfected group, Siha-NC group and Siha-FABP5-RNAi group was (921.4±63.0) mm(3,) (1 021.4±56.0) mm(3) and (139.6±36.0) mm(3,) respectively. The real-time quantitative PCR results showed that the relative expression levels of MMP-2 and MMP-9 mRNA were 1.00±0.10 and 1.00±0.10, 1.00±0.10 and 1.00±0.10 as well as 0.34±0.13 and 0.38±0.17 in xenografted tumor tissues of uninfected group, Siha-NC group and Siha-FABP5-RNAi group, respectively. MMP-2 and MMP-9 was significantly downregulated after FABP5 inhibition(P<0.05). Additionally, the protein expression trend of MMP-2 and MMP-9 in three groups was consistent with the mRNA levels. Conclusion: FABP5 might promote the carcinogenesis and metastasis of cervical cancer via up-regulating MMP-2 and MMP-9.

[The indications for glucocorticoids in treating community-acquired pneumonia in adults: a meta-analysis].

OBJECTIVE: Community acquired pneumonia (CAP) is a common pulmonary infectious disease. Glucocorticoids (GCS) as one of the most powerful anti-inflammation drugs, are still the most controversial adjuvant therapy in treating CAP. Which sub-groups of CAP patients would benefit from GCS is a debating topic. Our aim of this study is to find the indications for GCS in treating adult CAP patients by using meta-analysis. METHOD: "Steroids, glucocorticoids, corticosteroids, hydrocortisone, prednisone, cortisol, methylprednisolone, dexamethasone"and"community-acquired pneumonia"were used as key words both in Chinese and English to search all published literature in Pubmed, EMBASE MEDLINE, Cochrane, CNKI and Wanfang Database until March 2015. RESULTS: All 840 articles were reviewed, and 11 high quality randomized clinical trials involving 1942 adult CAP patients were included in this meta-analysis. Using GCS did not significantly reduce mortality in all CAP patients (OR=0.68, 95%CI 0.46-0.99, P=0.04). But in the subgroup analysis, patients with severe CAP benefited from GCS treatment (OR=0.35, 95%CI 0.17-0.75, P=0.007). GCS also increased the risk of hyperglycemia (OR=1.99, 95%CI 1.50-2.65, P<0.000 01). CONCLUSION: RESULTS from this meta-analysis suggested that GCS should only be rigorously used in severe CAP patients.

Clinical features, STAT3 gene mutations and Th17 cell analysis in nine children with hyper-IgE syndrome in mainland China.

Hyper-IgE syndrome (HIES) is a rare primary immunodeficiency disease characterized by eczema, recurrent staphylococcal aureus skin abscesses, pneumonia with pneumatocele formation, remarkably high serum IgE levels, eosinophilia and involvement of skeleton and connective tissues. Heterozygous signal transducer and activator of transcription 3 (STAT3) mutations were shown to be the cause of autosomal dominant HIES (AD-HIES). In this study, we diagnosed nine patients with HIES from 9 unrelated families on the basis of a National Institutes of Health (NIH) score of ≥40 points, sequenced the STAT3 gene of all nine patients, and quantified Th17 cells in peripheral blood of seven patients by flow cytometry in mainland China. All nine patients had characteristic manifestation of HIES with the range of NIH scores 45-77 points. STAT3 hot mutations V637M or R382W/Q were identified in five patients. We identified two novel heterozygous missense mutations (T620S and R609G) located in Src homology 2 (SH2) domain in two patients, respectively. In two other patients, no STAT3 mutations were found. Quantified Th17 cell numbers were markedly decreased or absent (0-0.28% of CD4(+) T cells) in six patients with STAT3 mutations and almost normal (0.53% of CD4(+) T cells) in one wild-type STAT3 patient compared with healthy controls (0.40-2.25% of CD4(+) T cells). These results suggest that not all patients with HIES who had NIH scores over 40 points carry STAT3 mutations, those whose Th17 cell numbers strikingly decreased probably had AD-HIES with STAT3 mutations.

Abundances and host relationships of chigger mites in Yunnan Province, China.

This paper reports on ectoparasitic chigger mites found on small mammals in Yunnan Province, southwest China. Data were accumulated from 19 investigation sites (counties) between 2001 and 2009. A total of 10 222 small mammal hosts were captured and identified; these represented 62 species, 34 genera and 11 families in five orders. From the body surfaces of these 10 222 hosts, a total of 92 990 chigger mites were collected and identified microscopically. These represented 224 species, 22 genera and three subfamilies in the family Trombiculidae (Trombidiformes). Small mammals were commonly found to be infested by chigger mites and most host species harboured several species of mite. The species diversity of chigger mites in Yunnan was much higher than diversities reported previously in other provinces of China and in other countries. A single species of rodent, Eothenomys miletus (Rodentia: Cricetidae), carried 111 species of chigger mite, thus demonstrating the highest species diversity and heaviest mite infestation of all recorded hosts. This diversity is exceptional compared with that of other ectoparasites. Of the total 224 mite species, 21 species accounted for 82.2% of all mites counted. Two species acting as major vectors for scrub typhus (tsutsugamushi disease), Leptotrombidium scutellare and Leptotrombidium deliense, were identified as the dominant mite species in this sample. In addition to these two major vectors, 12 potential or suspected vector species were found. Most species of chigger mite had a wide range of hosts and low host specificity. For example, L. scutellare parasitized 30 species of host. The low host specificity of chigger mites may increase their probability of encountering humans, as well as their transmission of scrub typhus among different hosts. Hierarchical clustering analysis showed that similarities between different chigger mite communities on the 18 main species of small mammal host did not accord with the taxonomic affinity of the hosts. This suggests that the distribution of chigger mites may be strongly influenced by the environment in which hosts live.

A novel angiogenesis inhibitor impairs lovo cell survival via targeting against human VEGFR and its signaling pathway of phosphorylation.

Colorectal cancer represents the fourth commonest malignancy, and constitutes a major cause of significant morbidity and mortality among other diseases. However, the chemical therapy is still under development. Angiogenesis plays an important role in colon cancer development. We developed HMQ18-22 (a novel analog of taspine) with the aim to target angiogenesis. We found that HMQ18-22 significantly reduced angiogenesis of chicken chorioallantoic membrane (CAM) and mouse colon tissue, and inhibited cell migration and tube formation as well. Then, we verified the interaction between HMQ18-22 and VEGFR2 by AlphaScreen P-VEGFR assay, screened the targets on angiogenesis by VEGF Phospho Antibody Array, validated the target by western blot and RNAi in lovo cells. We found HMQ18-22 could decrease phosphorylation of VEGFR2(Tyr(1214)), VEGFR1(Tyr(1333)), Akt(Tyr(326)), protein kinase Cα (PKCα) (Tyr(657)) and phospholipase-Cγ-1 (PLCγ-1) (Tyr(771)). Most importantly, HMQ18-22 inhibited proliferation of lovo cell and tumor growth in a human colon tumor xenografted model of athymic mice. Compared with normal lovo cells proliferation, the inhibition on proliferation of knockdown cells (VEGFR2, VEGFR1, Akt, PKCα and PLCγ-1) by HMQ18-22 decreased. These results suggested that HMQ18-22 is a novel angiogenesis inhibitor and can be a useful therapeutic candidate for colon cancer intervention.