No abstract

Glucocorticoids are steroid hormones that regulate a host of cellular and physiological functions. However, they are arguably best known for their potent anti-inflammatory properties. Chronic inflammation is well-known to promote the development and progression of numerous types of cancer, and emerging evidence suggests that glucocorticoid regulation of inflammation affects cancer development. However, the timing, intensity, and duration of glucocorticoid signaling have important but often contradictory effects on cancer development. Moreover, glucocorticoids are widely used in parallel with radiation and chemotherapy to control pain, dyspnea, and swelling, but their use may compromise anti-tumor immunity. This review will explore the effects of glucocorticoids on cancer development and progression with particular focus on pro and anti-tumor immunity.

Aberrant gastric inflammation damages the stomach and induces gastric metaplasia (spasmolytic polypeptideexpressing metaplasia). Increased expression of the RNA binding protein tristetraprolin suppresses adrenalectomyinduced gastric inflammation and spasmolytic polypeptideexpressing metaplasia development. BACKGROUND & AIMS:Aberrant immune activation is associated with numerous inflammatory and autoimmune diseases and contributes to cancer development and progression. Within the stomach, inflammation drives a wellestablished sequence from gastritis to metaplasia, eventually resulting in adenocarcinoma. Unfortunately, the processes that regulate gastric inflammation and prevent carcinogenesis remain unknown. Tristetraprolin (TTP) is an RNAbinding protein that promotes the turnover of numerous proinflammatory and oncogenic messenger RNAs. Here, we assess the role of TTP in regulating gastric inflammation and spasmolytic polypeptide-expressing metaplasia (SPEM) development. METHODS:We used a TTP-overexpressing model, the TTPDadenylate-uridylate rich element mouse, to examine whether TTP can protect the stomach from adrenalectomy (ADX)-induced gastric inflammation and SPEM. RESULTS:We found that TTPDadenylate-uridylate rich element mice were completely protected from ADX-induced gastric inflammation and SPEM. RNA sequencing 5 days after ADX showed that TTP overexpression suppressed the expression of genes associated with the innate immune response. Importantly, TTP overexpression did not protect from highdose-tamoxifen-induced SPEM development, suggesting that protection in the ADX model is achieved primarily by suppressing inflammation. Finally, we show that protection from gastric inflammation was only partially due to the suppression of Tnf, a well-known TTP target. CONCLUSIONS:Our results show that TTP exerts broad antiinflammatory effects in the stomach and suggest that therapies that increase TTP expression may be effective treatments of proneoplastic gastric inflammation. Transcript profiling:

Respiratory Syncytial Virus (RSV) is the most common causative agent for lower respiratory tract infections in children particularly in infants. At least 50% of children are infected with RSV by the age of 2 to 3 years of age. However, the diagnosis of the RSV infection and its association with risk factors for asthma in asthmatic children is not studied in Nepal. The objectives of this study were to determine the prevalence of RSV in asthmatic children. This work was a hospital based cross-sectional prospective study and conducted from September 2017 to February 2018. Ethical approval was obtained from the Institutional Review Committee (IRC) of Kanti Children’s Hospital, Maharajgunj. Suspected asthmatic children visiting the Special Asthma OPD of Kanti Children’s Hospital, Maharajgunj were selected with the help of asthma specialist using a set of inclusion criteria for asthma. A total of 32 nasal swab samples were obtained from suspected asthmatic children. Initially, samples were processed for RNA extraction. The extracted RNA was then used for cDNA synthesis followed by PCR using primers for the Nucleocapsid (N) gene of RSV. Out of total 32 samples, 9 (28%) samples were positive for the N gene of RSV. There was no significant association of different variables including age (P=0.187), sex (P=0.264), family history of asthma (P=0.115), passive smoking (P=0.88), birth weight (P=0.954), seasonality (P=0.298) and history of pneumonia (P=0.457) with the RSV infection in this study.

No abstract