The association between breast feeding and acute lower respiratory infection (ALRI) was studied in a case-control study in southern Italy. Two groups of children were studied: the first group comprised 73 infants, aged 0-6 months, whose diagnosis was pneumonia or bronchiolitis; the second group included 88 infants less than 12 months of age with a diagnosis of pertussis-like illness. Control infants were two groups of infants admitted to the same ward. Compared with controls, infants in the first group were less likely to have been breast fed (odds ratio 0.42, 95% CI 0.19-0.90). The protection conferred by breast feeding was stronger among infants who were receiving human milk at the time of admission (odds ratio 0.22, 95% CI 0.09-0.55) and was absent among those infants who had stopped breast feeding for two or more weeks before admission. Among infants who were severely ill, breast feeding was less likely than among those with milder illnesses. There was evidence in the stratified analysis of effect modification by the presence of other children in the family. Among the infants with pertussis-like illness, the incidence and duration of breast feeding were not different compared with controls. The results suggest that breast feeding has a strong protective effect against ALRI in industrialized countries also. No protection seems to be conferred by human milk against pertussis-like illness.
The specificity of cellular effects of lysolipid phosphate (LLP) growth factors is determined by binding to endothelial differentiation gene‐encoded G protein‐coupled receptors (EDG Rs), which transduce diverse proliferative and effector signals. The primary determinants of cellular responses to LLPs are the generative and biodegradative events, which establish steady‐state concentrations of each LLP at cell surfaces, and the relative frequency of expression of each EDG R. There are major differences among types of cells in the net effective generation of the LLPs, lysophosphatidic acid (LPA) and sphingosine 1‐phosphate (S1P), and in their profile of expression of EDG Rs. The less well characterized secondary determinants of cellular specificity of LLPs are high‐affinity binding proteins with carrier and cell‐presentation functions, cell‐selective regulators of expression of EDG Rs, and cellular factors that govern coupling of EDG Rs to G protein transductional pathways. The roles of components of the LLP‐EDG R system in normal physiology and disease processes will be definitively elucidated only after development of animal models with biologically meaningful alterations in genes encoding EDG Rs and the discovery of potent and selective pharmacological probes.
Our results indicate that visualization of the gastroesophageal junction and measurement of the abdominal esophagus are readily achievable with real-time sonography in healthy children.
G protein-coupled receptors (GPCRs) for lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) transduce signals to many functions of normal cells. Most human cancer cells upregulate S1P and LPA GPCRs, in patterns distinctive for each type of tumor. The findings that 1-alpha, 25-dihydroxy-vitamin D(3) (VD3) and all-trans retinoic acid (RA) differentially alter expression of the predominant S1P(3) (Edg-3) R and S1P(2) (Edg-5) R in human breast cancer cells (BCCs) permitted analyses of their individual activities, despite a lack of selective pharmacological probes. S1P-evoked increases in [Ca(2+)](i) in S1P(3) R-predominant BCCs were suppressed by concentrations of VD3 and RA which decreased expression of S1P(3) Rs, despite RA-induced increases in S1P(2) Rs. S1P-elicited chemokinetic migration of S1P(3) R-predominant BCCs across a type IV collagen-coated micropore filter also was inhibited by concentrations of VD3 and RA which decreased expression of S1P(3) Rs. The RA-induced increase in expression of S1P(2) Rs did not prevent suppression by RA of S1P-elicited chemokinesis, which appears to be mediated by S1P(3) Rs, but instead exposed S1P(2) R-mediated inhibition of epidermal growth factor-stimulated chemotaxis of BCCs. In contrast, expression of the predominant LPA(2) Rs, LPA-evoked increase in [Ca(2+)](i) and LPA-stimulated chemokinetic migration were suppressed concomitantly by RA but not VD3. Thus two structurally-homologous S1P Rs of BCCs differ in coupling to [Ca(2+)](i) signaling and have opposite effects on protein growth factor-stimulated chemotaxis.
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