Hemolytic Uremic Syndrome Caused by Enteroviral Infection

A 4-year-old boy presented with enteroviral infection complicated with atypical hemolytic uremic syndrome (aHUS). Enterovirus RNA was detected by reverse transcription polymerase chain reaction (RT-PCR) of both blood and kidney biopsy specimens. A survey of the complement system did not reveal a specific complement defect. Supportive therapy with blood components transfusion, plasma therapy, and immunosuppressants was administered, however, renal function did not recover. The results of this report demonstrate that the enterovirus is the cause of aHUS

Mechanism of Evolution Shared by Gene and Language

We propose a general mechanism for evolution to explain the diversity of gene and language. To quantify their common features and reveal the hidden structures, several statistical properties and patterns are examined based on a new method called the rank-rank analysis. We find that the classical correspondence, "domain plays the role of word in gene language", is not rigorous, and propose to replace domain by protein. In addition, we devise a new evolution unit, syllgram, to include the characteristics of spoken and written language. Based on the correspondence between (protein, domain) and (word, syllgram), we discover that both gene and language shared a common scaling structure and scale-free network. Like the Rosetta stone, this work may help decipher the secret behind non-coding DNA and unknown languages.Comment: 15 pages, 13 figures, 3 tabl

Generalist Versus Specialist Nurses\u27 Knowledge, Attitudes, and Behavioral Intentions Toward Promoting Pulmonary Rehabilitation for Patients with Chronic Obstructive Pulmonary Disease: A Cross-Sectional Correlational Study

Pulmonary rehabilitation (PR) is an effective strategy to manage chronic obstructive pulmonary disease (COPD), though its utilization rate is low. One reason for this low utilization rate is that nurses do not provide COPD patients with enough health education to increase the patient\u27s motivation for PR participation. This study examined knowledge, attitudes, and behavioral intention toward PR promotion. The study also investigated the correlates of behavioral intentions to promote PR among pulmonary nurses. A cross-sectional correlational design was used. Overall, 284 nurses (all women) from chest medicine and general internal medicine wards in 3 hospitals within Midwest Taiwan were recruited. Data were collected by anonymous, self-administered questionnaires. We aimed to understand if there would be differences in the Chest Medicine and Generalist nurses on these outcomes, given the specialty versus generalist nature of their practice. Results were analyzed using multiple linear regressions. Although the 2 groups of nurses (ie, Chest Medicine, General Medicine) showed no differences in PR knowledge, attitudes, or behavioral intentions, they lacked sufficient PR knowledge and skills. The accuracy rate of PR knowledge was approximately 12% and self-evaluated PR skills were less than 50%. Self-efficacy in promoting PR was above average (ie, 57%–60%), and the strength of attitudes and behavioral intentions was over 70%. A multiple linear regression revealed that behavioral intentions of nurses working in the chest medicine ward were influenced by behavioral attitudes, and also PR skills and self-efficacy (explanatory power 33.3%). Attitudes, skills, and self-efficacy heavily affected pulmonary nurses’ ability to promote PR; however, PR knowledge and skills remain low. Therefore, future implementation of practical PR training courses is needed to strengthen nurses’ behavioral intentions toward PR promotion. Improved pulmonary rehabilitation-related skill, attitudes, clinical experience of PR programs, and/or practical PR training are needed among both generalist and specialist nurses. Education courses and clinical practice training should be increased in the future to promote pulmonary rehabilitation of COPD patients

Panax notoginseng Attenuates Bleomycin-Induced Pulmonary Fibrosis in Mice

Panax notoginseng (PN) is a traditional Chinese herb experimentally proven to have anti-inflammatory effects, and it is used clinically for the treatment of atherosclerosis, cerebral infarction, and cerebral ischemia. This study aimed to determine the anti-inflammatory effects of PN against bleomycin-induced pulmonary fibrosis in mice. First, in an in vitro study, culture media containing lipopolysaccharide (LPS) was used to stimulate macrophage cells (RAW 264.7 cell line). TNF-α and IL-6 levels were then determined before and after treatment with PN extract. In an animal model (C57BL/6 mice), a single dose of PN (0.5 mg/kg) was administered orally on Day 2 or Day 7 postbleomycin treatment. The results showed that TNF-α and IL-6 levels increased in the culture media of LPS-stimulated macrophage cells, and this effect was significantly inhibited in a concentration-dependent manner by PN extract. Histopathologic examination revealed that PN administered on Day 7 postbleomycin treatment significantly decreased inflammatory cell infiltrates, fibrosis scores, and TNF-α, TGF-β, IL-1β, and IL-6 levels in bronchoalveolar lavage fluid when compared with PN given on Day 2 postbleomycin treatment. These results suggest that PN administered in the early fibrotic stage can attenuate pulmonary fibrosis in an animal model of idiopathic pulmonary fibrosis

The nucleolar protein NIFK promotes cancer progression via CK1α/β-catenin in metastasis and Ki-67-dependent cell proliferation.

Nucleolar protein interacting with the FHA domain of pKi-67 (NIFK) is a Ki-67-interacting protein. However, its precise function in cancer remains largely uninvestigated. Here we show the clinical significance and metastatic mechanism of NIFK in lung cancer. NIFK expression is clinically associated with poor prognosis and metastasis. Furthermore, NIFK enhances Ki-67-dependent proliferation, and promotes migration, invasion in vitro and metastasis in vivo via downregulation of casein kinase 1α (CK1α), a suppressor of pro-metastatic TCF4/β-catenin signaling. Inversely, CK1α is upregulated upon NIFK knockdown. The silencing of CK1α expression in NIFK-silenced cells restores TCF4/β-catenin transcriptional activity, cell migration, and metastasis. Furthermore, RUNX1 is identified as a transcription factor of CSNK1A1 (CK1α) that is negatively regulated by NIFK. Our results demonstrate the prognostic value of NIFK, and suggest that NIFK is required for lung cancer progression via the RUNX1-dependent CK1α repression, which activates TCF4/β-catenin signaling in metastasis and the Ki-67-dependent regulation in cell proliferation