Does infant feeding method influence maternal postpartum weight loss?

We conducted a retrospective study of 411 women to determine whether a significant relationship existed between method of infant feeding (breast vs bottle) and postpartum weight loss at 6 weeks and 12 months. In addition to method of infant feeding, the variables parity, gravidity, mode of delivery, maternal age, maternal prepregnancy weight, infant sex, and payment status (whether receiving assistance from the Aid to Dependent Children [ADC] program) were studied in terms of their association with weight loss. In general, no consistent relationship was found between method of infant feeding and postpartum weight loss. However, in the ADC group at 6 weeks and in the non-ADC group at 12 months, nonlactating women had lost more weight than had their lactating counterparts, in spite of the theoretical energy deficiency of breast-feeding women. Women who gained more weight during pregnancy consistently lost more weight following delivery, regardless of their prepregnancy weight. These results indicate that infant feeding method was not related to differences in postpartum weight loss between lactating and nonlactating counterparts.     

INTRAUTERINE GROWTH RETARDATION

Intrauterine growth retardation (IUGR) occurs in 3% to 10% of all pregnancies. Although it is an uncommon occurrence in a low-risk nurse-midwifery practice, as many as 65% of the cases of IUGR are not identified until after the birth of the infant. Identification of IUGR is important because it carries a high risk of antepartum fetal death, anomalies, intrapartum asphyxia, and long-term morbidity. Additionally, identification of IUGR is essential for appropriate prenatal and intrapartum management. A review of etiologic factors, current assessment, and management of the pregnancy complicated by IUGR is presented, The use and interpretation of new technologies that the clinician may use in diagnosing and managing IUGR is reviewed.     

Identification and characterization of aquaporin-2 water channel mutations causing nephrogenic diabetes insipidus with partial vasopressin response

Congenital nephrogenic diabetes insipidus (NDI) is a rare disease caused most often by mutations in the vasopressin V2 receptor (AVPR2). We studied a family which included a female patient with NDI with symptoms dating from infancy. The patient responded to large doses of desmopressin (dDAVP) which decreased urine volume from 10 to 4 I/day. Neither the parents nor the three sisters were polyuric. The patient was found to be a compound heterozygote for two novel recessive point mutations in the aquaporin-2 (AQP2) gene: L22V in exon 1 and C181W in exon 3. Residue Cys181 in AQP2 is the site for inhibition of water permeation by mercurial compounds and is located near to the NPA motif conserved in all aquaporins. Osmotic water permeability (Pf) in Xenopus oocytes injected with cRNA encoding C181W-AQP2 was not increased over water control, while expression of L22V cRNA increased the Pf to approximately 60% of that for wild-type AQP2. Co-injection of the mutant cRNAs with the wild-type cRNA did not affect the function of the wild-type AQP2. Immunolocalization of AQP2-transfected CHO cells showed that the C181W mutant had an endoplasmic reticulum-like intracellular distribution, whereas L22V and wild-type AQP2 showed endosome and plasma membrane staining. Water permeability assays showed a high Pf in cells expressing wild-type and L22V AQP2. This study indicates that AQP2 mutations can confer partially responsive NDI.      

Successful transplantation of 50 single unit pediatric kidneys ages 11 to 48 months into adult recipients

There is currently an imbalance between the need for cadaveric kidneys for transplantation and the supply. The medical criteria for accepting cadaveric donors are changing and organs that were originally thought to be unacceptable have functioned well. Previous reports have discussed the problems with transplanting pediatric allografts less than 4 years old into adult recipients, and the results have not been encouraging. From 1986 to 1991 a total of 50 kidneys ages 11 to 48 months were transplanted as single units into adult recipients (Group A). Ninety-one adult donor cadaveric transplants were used as controls (Group B). The cadaveric transplants were 2nd or 3rd transplants in 7 of the Group A and 12 of the Group B patients. Renal preservation, storage times, and demographics were the same. Prednisone, cyclosporine, and either Minnesota ALG or OKT3 were used for immunosuppression in both groups. Imuran was added in immunologically high-risk patients. The 1-year actuarial patient and allograft survivals for Group A versus Group B were 89.5% versus 94.2% (p=0.49) and 71.3% versus 87.8% (p=0.01), respectively. There was no difference in allograft or patient survival in kidneys from donors 11-24 months of age or 25-48 months (p=0.56). Renal growth, as measured by sonography, occurred while on cyclosporine A. Excretory and hormonal function as measured by creatinine and hematocrit both improved. Seventy percent of the Group A patients and 76% of the Group B patients were free from rejection in the first 2 months post transplantation (p=0.45).(ABSTRACT TRUNCATED AT 250 WORDS)     

ATG16L1 and NOD2 polymorphisms enhance phagocytosis in monocytes of Crohn’s disease patients

AIM:To investigate if the presence of relevant genetic polymorphisms has effect on the effectual clearance of bacteria by monocytes and granulocytes in patients with Crohn’s disease(CD).METHODS:In this study,we assessed the differential responses in phagocytosis by measuring the phagocytic activity and the percentage of active phagocytic monocytes and granulocytes in inflammatory bowel disease patients as well as healthy controls.As both autophagy related like 1(ATG16L1)and immunityrelated guanosine triphosphatase gene are autophagy genes associated with CD and more recently nucleo-tide-binding ligomerization domain-containing protein2(NOD2)has been identified as a potent inducer of autophagy we genotyped the patients for these variants and correlated this to the phagocytic reaction.The genotyping was done with restriction fragment length polymorphisms analysis and the phagocytosis was determined with the pHrodo?Escherichia coli Bioparticles Phagocytosis kit for flowcytometry.RESULTS:In this study,we demonstrate that analysis of the monocyte and granulocyte populations of patients with CD and ulcerative colitis showed a comparable phagocytic activity(ratio of mean fluorescence intensity)between the patient groups and the healthy controls.CD patients show a significantly higher phagocytic capacity(ratio mean percentage of phagocytic cells)compared to healthy controls(51.91%±2.85%vs 37.67%±7.06%,P=0.05).The extend of disease was not of influence.However,variants of ATG16L1(WT:2.03±0.19 vs homozygoot variant:4.38±0.37,P<0.009)as well as NOD2(C-ins)(heterozygous variant:42.08±2.94 vs homozygous variant:75.58±4.34(P=0.05)are associated with the phagocytic activity in patients with CD.CONCLUSION:Monocytes of CD patients show enhanced phagocytosis associated with the presence of ATG16L1 and NOD2 variants.This could be part of the pathophysiological mechanism resulting in the disease.