Sarcoptic mange is an emerging threat to biodiversity in the Qinling Mountains in China.

Sarcoptic mange, a disease caused by the burrowing mite Sarcoptes scabiei, is globally endemic and an emerging threat to wildlife. Although many studies have shown that wildlife diseases play key roles in biodiversity conservation, knowledge about sarcoptic mange is still insufficient. In this study, we aim to improve the understanding of the impacts of sarcoptic mange on wildlife populations, the mechanisms involved in its eco-epidemiology and the associated risks to public and ecosystem health by investigating mass death events in gorals and serows in the Qinling Mountains. We conducted interviews with practitioners and local people in the central Qinling Mountains. From the same locations, we collected 24 cutaneous samples from various animals and surveillance data from infrared cameras. Pathological, parasitological and microbiological examinations of the samples were performed. Mite-induced cutaneous lesions, mites and eggs were observed in samples from dead gorals and one dead serow but not in other species. Molecular analysis confirmed the mites to be S. scabiei and shared the same cox 1 genotype. The data obtained from the interviews and infrared cameras indicated that the death of wildlife was related to sarcoptic mange infection and that there had been a decrease in the goral population since the outbreak of the disease. We confirmed that sarcoptic mange was the major cause of the mass death events and may have spread from the western to eastern Qinling Mountains. Based on our findings, we propose several protection strategies to help preserve biodiversity in the Qinling Mountains.

From luminescence quenching to high-efficiency phosphorescence: a theoretical study on the monomeric and dimeric forms of platinum(II) complexes with both 2-pyridylimidazol-2-ylidene and bipyrazolate chelates.

To develop solid-state light-emitting materials with high luminescence efficiency, determining the potential photophysics and luminescence mechanisms of the aggregation state remains a challenge and a priority. Here, we apply density functional theory to study the photophysical properties of a series of square planar Pt(ii) complexes in both monomeric and dimeric forms. We reveal that four monomeric Pt(ii) complexes are dominated by triplet ligand-to-ligand charge-transfer, and the lack of the triplet metal-to-ligand charge-transfer feature results in weak spin-orbit coupling (SOC), which leads to limited radiative rates; moreover, calculated nonradiative transition rates are one or two orders of magnitude higher than those radiative rates because a large amount of reorganization energy caused by the vibration of the bipyrazolate (bipz) ligand cannot be readily suppressed in the monomeric form. Therefore, four monomers exhibit photoluminescence quenching in CH2Cl2 solution in both theoretical calculations and experiments. However, in the solid state, the intense luminescence phenomenon indicates obviously distinct properties between the monomer and aggregation. We carried out a dimer model to interpret that the interaction of PtPt induces a metal-metal-to-ligand charge-transfer excimeric state, which leads more metal components to participate in the charge transfer and enhance the SOC effect. At the same time, the ligand vibration can be significantly reduced by the shortened distance, and there is a strong π-π packing interaction in the dimer; thus, an excellent quantum yield can be achieved in aggregation. In addition, we disclose that introducing bulky substituents bearing electron-donating groups at R' and R'' positions have little effect on the properties of the monomers; however, there is a benefit of restricting the internal reorganization energy through the intermolecular interaction when packing in the solid state. Therefore, substitutions can be tuned to improve the properties of monomers (such as emission energy and reorganization energy). We hope that our work will shine some light on Pt(ii) emitters in the fabrication of efficient OLEDs.

Diffuse telangiectasia of the colon: A case report.

RATIONALE: Colonic telangiectasia, also known as colonic angiodysplasia, refers to arteriovenous malformations that occur in the colon, which are common vascular lesions in the GI tract. PATIENT CONCERNS: We report a patient, who was admitted to our hospital for colonoscopy. DIAGNOSES: Under a microscope, all the segments of the whole colon and the varicose veins showed multiple flaky spider-like telangiectasia changes. The blood vessels were radially distributed and converged in the center. The largest blood vessel was about 10 mm in diameter and had a smooth surface with no ulcers, erosion, or bleeding. INTERVENTIONS: It was recommended that the patient undergo a capsule endoscopy to examine small intestine. OUTCOMES: The patient did not agree to endoscopy for personal reasons. During the follow-up half a year later, the patient had no melena with normal range of hemoglobin and red blood cell counts. The fecal occult blood test came out negative. LESSONS: While the etiology of colonic telangiectasia remains unclear, it is common in the elderly, and is more associated with geriatric conditions and diseases, especially atherosclerotic diseases. Patients who are diagnosed with colonic telangiectasia but are asymptomatic, do not need further treatment. It is usually recommended to monitor the color of stool and check the hemoglobin and fecal occult blood regularly. Colonoscopy is the main method of diagnosis of colonic telangiectasia, and the positive rate is greater than 90%. This procedure should be performed when there is no bleeding or a small amount of bleeding.

Cyclin A2 regulates symmetrical mitotic spindle formation and centrosome amplification in human colon cancer cells.

Colon cancer is one of the most fatal cancers in the United States, and is characterized by the presence of chromosomal instability (CIN), causes of which are largely unclear. Emerging evidence indicates that abnormal spindle geometry and supernumerary centrosomes lead to CIN in cells. However, if and how spindle geometry defects and centrosomes amplification occur in colon cancer remains unknown. Here we show that decrease in the cell cycle regulatory protein, cyclin A2, induces spindle geometry defects in colon cancer cells. In mechanistic studies, we found that cyclin A2 is located at the centrosomes, and its depletion reduces phosphorylation of EG5, which is important for centrosome localization and movement of duplicated centrosomes to opposite poles. We also found that cyclin A2 silencing leads to centrosome amplification in the cells. Collectively, these findings demonstrate previously unrecognized role for cyclin A2 in preventing centrosomal defects in colon cancer cells and provide insights into mechanisms that may potentially cause CIN in these tumors.

miR-223-RhoB signaling pathway regulates the proliferation and apoptosis of colon adenocarcinoma.

MicroRNAs (miRNAs) can function as tumor suppressor or oncogenic genes. The putative targets of miR-223 include tumor suppressor gene, RhoB. Here we sought to investigate the role of miR-223-RhoB signaling pathway in proliferation of colon cancer. We used Western blot, immunofluorescence staining, or RT-PCR to detect expression levels of miR-223 and RhoB in colon adenocarcinoma and adjacent non-cancerous tissue samples, or in human colon adenocarcinoma cell lines. MTT assay was used to determine proliferation and apoptosis in cell lines. We further used Western blot to determine levels of cell cycle regulators CDK1 and Cyclin B1 with anti-miR-223 or apoptosis with overexpression of RhoB. The expression level of miR-223 was significantly upregulated in clinical samples and cell lines of colon adenocarcinoma, in contrast to down-regulation of RhoB. In addition, we showed that inhibition of miR-223 led to upregulation of RhoB and in turn suppression of proliferation of colon adenocarcinoma. Moreover, inhibition of miR-223 or overexpression of RhoB induced cell arrest or apoptosis in colon adenocarcinoma. These results suggest that miR-223-RhoB signaling pathway plays an important role in modulation of proliferation, cell arrest, and apoptosis in colon cancer.

[Effects of danshen injection on the proliferation of rheumatoid arthritis fibroblast-like synoviocytes cultured with human serum].

OBJECTIVE: To investigate the effects of Danshen Injection (DSI) on the proliferation of rheumatoid arthritis fibroblast-like synoviocytes (RA FLSs) cultured in RA patients' serum. METHODS: The RA FLSs harvested from RA patients' synovial fluid were primarily cultured by routines. The cells were cultured with 10% inactivated human serum (the healthy human serum and the RA patients' serum) for 24 h. Then DSI at the final concentration of 0. 4 mg/mL was added in the cells for further 24 h culture. By taking 10% fetal calf serum as the control, the morphological changes were observed under optical microscope. The proliferation was analyzed by MTT. The apoptosis was detected by flow cytometry. The total RNA was extracted and reverse transcription was performed. The Bax mRNA expression was detected by fluorescent quantitative PCR. RESULTS: (1) After human serum was added in the healthy human serum and RA patients' serum, cells could grow adhering to the wall. Compared with the fetal calf serum group (FCS), the cell density was higher in the healthy human serum group than in the fetal calf serum group, with no obvious morphological changes. (2) MTT results showed that, compared with the fetal calf serum group, the absorbance value (OD) obviously increased in the healthy human serum group and the RA patients' serum group, showing statistical difference (P <0.01). After adding DSI at the final concentration of 0.4 mg/mL, cells from different serums were inhibited to various degrees (with OD significantly decreased, P <0.05). The OD value significantly increased more in the healthy human serum group and the RA patients' serum group than in the fetal calf serum group, showing statistical difference (P <0.01). There was statistical difference between the healthy human serum group and the RA patients' serum group (P <0.01). (3) The apoptosis rate in the RA patients' serum group obviously decreased with statistical difference, when compared with the Salvia miltiorrhiza free fetal calf serum group (P >0. 01). The apoptosis rate in the fetal calf serum group and the RA patients' serum group significantly increased after adding 0.4 mg/mL Salvia miltiorrhiza, showing statistical difference when compared with the Salvia miltiorrhiza free fetal calf serum group and the Salvia miltiorrhiza free RA patients' serum group (P <0.05). The FLSs were effected by 0.4 mg/mL Salvia miltiorrhiza, the apoptosis rate significantly decreased in the healthy human serum group and the RA patients' serum group, showing statistical difference when compared with the fetal calf serum group (P <0. 05, P <0.01). (4) The expression of Bax gene significantly increased in the RA patients' serum group and the fetal calf serum group after action of 0.4 mg/mL Salvia miltiorrhiza, showing statistical difference (P <0. 01). When 0.4 mg/mL Salvia miltiorrhiza was added, the expression of Bax mRNA obviously increased in the healthy human serum group and the RA patients' serum group, showing statistical difference when compared with the fetal calf serum group (P <0.01). CONCLUSIONS: (1) Although healthy human serum can be favorable to the growth of RA FLSs, the fetal calf serum could reflect the actual results better in the cyto biological research on specific diseases (if there is no serum from patients with corresponding disease). (2) DSI could inhibit the proliferation of RA FLSs through promoting their apoptosis.

Med19 promotes gastric cancer progression and cellular growth.

Med19 was a member of the Mediator complex which forms the bridge between transcriptional activators and RNA polymerase II. We aim to investigate the functional role of Med19 in the progression of human gastric carcinoma. The correlation between Med19 expression and clinicopathologic features in 60 gastric carcinoma specimens was analyzed by using immunohistochemistry. Recombinant lentivirus expressing Med19 short hairpin RNA (shRNA) was constructed and infected into human gastric carcinoma SGC7901 and MGC803 cells. MTT, colony formation and cell cycle analysis were used to study the effect of Med19 shRNA on gastric cancer cell proliferation. Expression of Med19 was associated with tumor size, cancer cell differentiation, and TNM stages (P<0.05). Downregulation of Med19 significantly inhibited cell proliferation and colony-formation capacity, and induced G1 phase cell-cycle arrest. Collectively, Med19 functions in promoting cellular growth and may be a useful therapeutic target in malignant gastric carcinoma.