Effects of freezing storage on the stability of maternal cellular and humoral immune components in porcine colostrum.

The placental structure of sows is epitheliochorial and prevents maternal serum immunoglobulin transfer to the fetus; therefore, the piglet relies on the ingestion of colostrum to acquire passive immunity. Colostral antibody-mediated and cell-mediated immunity contribute to immunity in piglets. However, little is known about the effects of freezing at -20 °C on colostral immune components during short-term storage, whether this will somehow compromise the acquisition of passive immunity of newborn piglets fed with this colostrum and the humoral immunity in porcine colostrum, and to possible shifts in immunological levels in colostrum collections during the colostral period. Based on the average concentration of immunoglobulin, frozen and fresh colostrum did not differ significantly. Overall, there were no storage differences in total macrophages, granulocytes, and NK cells. However, the frozen colostrum presented T lymphocyte subsets and B lymphocytes significantly lower than the fresh colostrum (p ≤ 0.05). Therefore, to sustain higher piglet survival rates, B cells may be a selective strategy to ensure immune defense to neonatal piglets. According to our findings, colostrum can be stored by freezing at -20 °C for up to 30 days and surplus porcine colostrum can be collected from the sow up to eight hours after the start of farrowing.

The presence of maladaptive eating behaviors after bariatric surgery in a cross sectional study: importance of picking or nibbling on weight regain.

BACKGROUND: Maladaptive eating behaviors after bariatric surgery are thought to compromise weight outcomes, but little is known about their frequency over time. OBJECTIVE: This study investigates the presence of subjective binge eating (SBE), objective binge eating (OBE) and picking and nibbling (P&N) before surgery and at different time periods postoperative, and their association with weight outcomes. METHODS: This cross-sectional study assessed a group of patients before surgery (n=61), and three post-operative groups: 1) 90 patients (27 with laparoscopic adjustable gastric band (LAGB) and 63 with Laparoscopic Roux-en-Y Gastric Bypass (LRYGB)) assessed during their 6month follow-up medical appointment; 2) 96 patients (34 LAGB and 62 LRYGB) assessed during their one year follow-up medical appointment; and 3) 127 patients (62 LAGB and 55 LRYGB) assessed during their second year follow-up medical appointment. Assessment included the Eating Disorders Examination and a set of self-report measures. RESULTS: In the first ten months after surgery fewer participants reported maladaptive eating behaviors. No OBEs were reported at 6months. SBE episodes were present in all groups. P&N was the most frequently reported eating behavior. Eating behavior (P&N) was significantly associated with weight regain, and non-behavioral variables were associated with weight loss. CONCLUSIONS: This study is cross-sectional study which greatly limits the interpretation of outcomes and no causal association can be made. However, a subgroup of postoperative patients report eating behaviors that are associated with greater weight regain. The early detection of these eating behaviors might be important in the prevention of problematic outcomes after bariatric surgery.

Renal cyst growth is the main determinant for hypertension and concentrating deficit in Pkd1-deficient mice.

We have bred a Pkd1 floxed allele with a nestin-Cre expressing line to generate cystic mice with preserved glomerular filtration rate to address the pathogenesis of complex autosomal dominant polycystic kidney disease (ADPKD) phenotypes. Hypertension affects about 60% of these patients before loss of renal function, leading to significant morbimortality. Cystic mice were hypertensive at 5 and 13 weeks of age, a phenotype not seen in noncystic controls and Pkd1-haploinsufficient animals that do not develop renal cysts. Fractional sodium excretion was reduced in cystic mice at these ages. Angiotensinogen gene expression was higher in cystic than noncystic kidneys at 18 weeks, while ACE and the AT1 receptor were expressed in renal cyst epithelia. Cystic animals displayed increased renal cAMP, cell proliferation, and apoptosis. At 24 weeks, mean arterial pressure and fractional sodium excretion did not significantly differ between the cystic and noncystic groups, whereas cardiac mass increased in cystic mice. Renal concentrating deficit is also an early finding in ADPKD. Maximum urine osmolality and urine nitrite excretion were reduced in 10-13- and 24-week-old cystic mice, deficits not found in haploinsufficient and noncystic controls. A trend of higher plasma vasopressin was observed in cystic mice. Thus, cyst growth most probably plays a central role in early-stage ADPKD-associated hypertension, with activation of the intrarenal renin-angiotensin system as a key mechanism. Cyst expansion is also likely essential for the development of the concentrating deficit in this disease. Our findings are consistent with areas of reduced perfusion in the kidneys of patients with ADPKD.

Pkd1 haploinsufficiency increases renal damage and induces microcyst formation following ischemia/reperfusion.

Mutations in PKD1 cause the majority of cases of autosomal dominant polycystic kidney disease (ADPKD). Because polycystin 1 modulates cell proliferation, cell differentiation, and apoptosis, its lower biologic activity observed in ADPKD might influence the degree of injury after renal ischemia/reperfusion. We induced renal ischemia/reperfusion in 10- to 12-wk-old male noncystic Pkd1(+/-) and wild-type mice. Compared with wild-type mice, heterozygous mice had higher fractional excretions of sodium and potassium and higher serum creatinine after 48 h. In addition, in heterozygous mice, also cortical damage, rates of apoptosis, and inflammatory infiltration into the interstitium at time points out to 14 d after injury all increased, as well as cell proliferation at 48 h and 7 d. The mRNA and protein expression of p21 was lower in heterozygous mice than wild-type mice at 48 h. After 6 wk, we observed dilated tubules, microcysts, and increased renal fibrosis in heterozygotes. The early mortality of heterozygotes was significantly higher than that of wild-type mice when we extended the duration of ischemia from 32 to 35 min. In conclusion, ischemia/reperfusion induces a more severe injury in kidneys of Pkd1-haploinsufficient mice, a process that apparently depends on a relative deficiency of p21 activity, tubular dilation, and microcyst formation. These data suggest the possibility that humans with ADPKD from PKD1 mutations may be at greater risk for damage from renal ischemia/reperfusion injury.