1-12). Intrathoracic disease was present in 294 (75%) children

and extrathoracic disease in 98 (25%). The Beijing genotype was the most prevalent (32.9%), followed by the Latin American Mediterranean (LAM, 28.8%), and S genotypes (6.4%). Age was significantly associated with genotype. Children with the Beijing (OR = 2.36, 95%CI 1.21-4.60) and S genotypes (OR = 3.47, 95%CI 1.26-9.56) were more likely to have extrathoracic disease compared to children infected with the LAM genotype, in analyses adjusted for age and drug resistance.

CONCLUSIONS: TB genotype and disease phenotype in children were associated. Beijing and S genotypes were more frequently cultured from extrathoracic cultures, indicating potential improved ability to disseminate. Strain-related phenotypes could explain different disease spectra in geographic settings where certain strains are selleckchem successful. Studies

of mycobacterial human interaction should consider host immune responses, clinical and epidemiological factors.”
“Dermatologic toxicities associated with anticancer-targeted therapy include hand-foot skin reactions, vasculitis, cutaneous epithelial proliferations, such as keratosis, keratoacanthoma, and invasive squamous cell carcinoma. In this case report, we describe alterations of tumor morphology and patterns of cyclin-dependent kinase inhibitor (CDKI) expression in a patient who received GSK2118436, a second-generation RAF inhibitor, for stage see more IV (M1c) metastatic melanoma. To explore the effects

of GSK2118436 on the expression patterns of CDKI (p16(INK4a), p21(CIP1), p27(KIP1), p57(KIP2)), we immunohistochemically evaluated in vivo melanoma cells pre- and posttreated with GSK2118436. After GSK2118436 treatment, the melanoma cells decreased in size and demonstrated hyperchromatic nuclei and indistinct nucleoli. p16(INK4a) AZD6094 chemical structure was strongly expressed in the cytoplasm of pretreated melanoma cells and in the nucleus and cytoplasm in posttreated melanoma cells. Expression of both p27(KIP1) (nucleus) and p57(KIP2) (cytoplasm) was increased in posttreated melanoma cells and no significant difference in p21(CIP1) expression was noted in either pre- or posttreated tumor cells. These findings may help explain the molecular mechanisms by which tumor cells retain the ability to proliferate. The persistent activation of pro-oncogenic activities of CDKI (eg, p27(KIP1) and p57(KIP2)) and/or compartmentalization of p16(INK4a) in cytoplasm or nucleus may allow tumor cells to bypass BRAF-induced senescence mechanisms. Furthermore, awareness of changes in tumor morphology after treatment with RAF inhibitors may be helpful in histologic evaluation of the spectrum of dermatologic toxicity, which may occur on targeted therapy.”
“SETTING: National Tuberculosis Reference Laboratory, Addis Ababa, Ethiopia.

OBJECTIVES: To determine the drug susceptibility pattern of Mycobacterium tuberculosis isolates and to genetically characterise multidrug-resistant tuberculosis (MDR-TB) isolates.