Neglected clubfoot is common, disabling, and contributes to poverty in developing nations. The Ponseti clubfoot treatment has high efficacy in correcting the clubfoot deformity in ideal conditions but is demanding on parents and on developing nations' healthcare systems.

Background: Ozone (O 3 ), a common air pollutant, induces exacerbation of asthma and chronic obstructive pulmonary disease. Pulmonary surfactant protein (SP)-D modulates immune and inflammatory responses in the lung. We have shown previously that SP-D plays a protective role in a mouse model of allergic airway inflammation. Here we studied the role and regulation of SP-D in O 3 -induced inflammatory changes in the lung.

Mesenteric lymphatic vessels actively transport lymph, immune cells, fat, and other macromolecules from the intestine via a rhythmical contraction-relaxation process called lymphatic pumping. We have previously demonstrated that mesenteric lymphatic pumping was compromised in the guinea pig model of 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced ileitis, corroborating clinical and experimental observations of a dilated and/or obstructed phenotype of these vessels in inflammatory bowel disease. Many mediators released during the inflammatory process have been shown to alter lymphatic contractile activity. Among them, nitric oxide (NO), an inflammatory mediator abundantly released during intestinal inflammation, decreases the frequency of lymphatic contractions through activation of ATP-sensitive potassium (K(ATP)) channels. The objective of this study was to investigate the role of NO and K(ATP) channels in the lymphatic dysfunction observed in the guinea pig model of TNBS-induced ileitis. Using quantitative real-time PCR, we demonstrated that expression of Kir6.1, SUR2B, and inducible NO synthase (iNOS) mRNAs was significantly upregulated in TNBS-treated animals. Pharmacological studies performed on isolated, luminally perfused mesenteric lymphatic vessels showed that the K(ATP) channels blocker glibenclamide, the selective iNOS inhibitor 1400W, and the guanylyl cyclase inhibitor ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one) significantly improved lymphatic pumping in quiescent lymphatic vessels from TNBS-treated animals. Membrane potential measurement with intracellular microelectrodes revealed that vessels from TNBS-treated animals were hyperpolarized compared with their sham counterpart and that the hyperpolarization was significantly attenuated in the presence of glibenclamide and ODQ. Our findings suggest that NO and K(ATP) play a major role in the lymphatic contractile dysfunction that occurred as a consequence of the intestinal inflammation caused by TNBS.

An outbreak of measles in 1985-86 in a community where measles vaccine trials had been carried out from 1974-76 allowed the assessment of the role of secondary vaccine failures in previously immunized children. A total of 188 children from the vaccine trial were followed. Of these, 175 seroconverted initially while 13 (6 per cent) required re-immunization (primary failure). A total of 13 cases of measles, eight of which were laboratory and/or physician-confirmed, were reported in this cohort. Of these, nine cases occurred in the 175 subjects who had hemagglutination inhibition test (HI) and neutralizing antibody responses following the

e73providers to be compared with infection incidence in the community.To date there are no reported clusters of respiratory-transmitted diseases, including severe acute respiratory syndrome coronavirus and SARS-CoV-2, in dental providers or patients in a dental setting.We declare no competing interests.