Objective Lung cancer is the leading cause of cancer death in both men and women. Non-small cell lung cancer (NSCLC) has an overall 5-year survival rate of 15%. While aberrant STAT3 activation has previously been observed in NSCLC, the scope of its contribution is uncertain and agents that target STAT3 for treatment are not available clinically. Methods We determined levels of activated STAT3 (STAT3 phosphorylated on Y705, pSTAT3) and the two major isoforms of STAT3 (α and β) in protein extracts of 8 NSCLC cell lines, as well as the effects of targeting STAT3 in vitro and in vivo in NSCLC cells using short hairpin (sh) RNA and two novel small-molecule STAT3 inhibitors, C188-9 and piperlongumine (PL). Results Levels of pSTAT3, STAT3α, and STATβ were increased in 7 of 8 NSCLC cell lines. Of note, levels of pSTAT3 were tightly correlated with levels of STAT3β, but not STAT3α. Targeting of STAT3 in A549 cells using shRNA decreased tSTAT3 by 75%; this was accompanied by a 47–78% reduction in anchorage-dependent and anchorage-independent growth and a 28–45% reduction in mRNA levels for anti-apoptotic STAT3 gene targets. C188-9 and PL (@30μM) each reduced pSTAT3 levels in all NSCLC cell lines tested by ≥50%, reduced anti-apoptotic protein mRNA levels by 25–60%, and reduced both anchorage-dependent and anchorage-independent growth of NSCLC cell lines with IC50 values ranging from 3.06–52.44μM and 0.86–11.66μM, respectively. Treatment of nude mice bearing A549 tumor xenografts with C188-9 or PL blocked tumor growth and reduced levels of pSTAT3 and mRNA encoding anti-apoptotic proteins. Conclusion STAT3 is essential for growth of NSCLC cell lines and tumors and its targeting using C188-9 or PL may be a useful strategy for treatment.

Candida pericarditis is a rare condition which has previously been described after cardiothoracic surgery and immunosuppressive states (Geisler et al., 1981; Eng et al., 1981; Kraus et al., 1988; Kaufman et al., 1988; Tang et al., 2009; Glower et al., 1990; Carrel et al., 1991; Rabinovici et al., 1997; Canver et al., 1998; Farjah et al., 2005; Gronemeyer et al., 1982 [1-11]). We describe the case of a 19-year-old male blunt trauma patient, who survived a damage control thoracotomy and laparotomy with splenectomy, who later developed a loculated Candida pericardial effusion, complicated with cardiac tamponade and multiple organ failure, and required antifungals and surgical reintervention with thoracotomy for drainage. A literature search of the reported cases demonstrates that Candida pericarditis is indeed a rare but fatal condition if not identified and treated appropriately. This article discusses the difficulties we encountered while recognizing the disorder in our patient and proposes a guideline to adequately treat the condition in an effective and timely manner. Candida pericarditis poses a special challenge for the physician since its correct diagnosis and management requires a multidisciplinary approach.

Cysticercosis is an infection of tissues with the larval cysts of the cestode, Taenia   solium. While live parasites elicit little or no inflammation, dying parasites initiate a granulomatous reaction presenting as painful muscle nodules or seizures when cysts are located in the brain. We previously showed in the T. crassiceps murine model of cysticercosis that substance P (SP), a neuropeptide, was detected in early granulomas and was responsible for promoting granuloma formation, while somatostatin (SOM), another neuropeptide and immunomodulatory hormone, was detected in late granulomas; SOM's contribution to granuloma formation was not examined. In the current studies, we used somatostatin knockout (SOM−/−) mice to examine the hypothesis that SOM downmodulates granulomatous inflammation in cysticercosis, thereby promoting parasite growth. Our results demonstrated that parasite burden was reduced 5.9-fold in SOM−/− mice compared to WT mice (P < 0.05). This reduction in parasite burden in SOM−/− mice was accompanied by a 95% increase in size of their granulomas (P < 0.05), which contained a 1.5-fold increase in levels of IFN-γ and a 26-fold decrease in levels of IL-1β (P < 0.05 for both) compared to granulomas from WT mice. Thus, SOM regulates both parasite burden and granulomatous inflammation perhaps through modulating granuloma production of IFN-γ and IL-1β.

In the paper titled "Somatostatin Negatively Regulates Parasite Burden and Granulomatous Responses in Cysticercosis" there was an error in the Discussion and Bibliography section. The changes made to the references section are as follows.