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We developed equations to predict the asymptotic response due to two-stage selection, where first-stage selection was performed by using GEBVs based solely on genotypes and second-stage selection was performed with GEBVs that combined genotypes and phenotypes. The situation that we considered involved four-path selection executed as sires to breed sons, sires to breed daughters, dams to breed sons, and dams to breed daughters. We established two procedures to predict the response. The first incorporated correlated indices during the first and second-stage selections of two-stage selection. The other procedure used independent indices during two-stage selection. The response per generation in the initial generation was greater for the correlated indices than for the independent indices. However, the asymptotic response per generation was slightly greater for the independent indices than for the correlated indices. The asymptotic response per generation was lower during two-stage selection than during single-stage selection. However, the asymptotic response per year was greater for two-stage selection than for single-stage selection. In addition, that trend was more conspicuous when the economic weight was 1:3 for the first (h2 =0.3) to second (h2 =0.05) index trait compared with economic weights of 1:1 and 3:1. However, the magnitude of the response to the aggregate genotype-relative not to single-stage selection but to absolute magnitude was greater at an economic weight of 3:1 than at those of 1:1 and 1:3. The reduction in genetic variance from the initial to an asymptotic generation was greater for a scenario where young parents selected at the first-stage accounted for 30% of all parents in two-stage selection than where they accounted for 70%. The reduction in genetic variance of the aggregate genotype over generations was smaller for independent indices than correlated indices during two-stage selection. Our new formula for predicting genetic response applies to any combination of accuracies of GEBVs and intensities of selection. Therefore, the formula presented is a general equation for predicting genetic response over generations due to two-stage genomic index selection.

Introduction: Obturator hernia is an important cause of small bowel obstruction and is associated with difficult diagnosis and high mortality. Materials and Methods: We reviewed 22 cases of intestinal obstruction due to obturator hernia that necessitated surgical intervention over the last 17 years and evaluated the changes in the number of patients based on the census data. Results: All cases were elderly females. The Howship-Romberg sign was present in 15 patients (68%). Computed tomography (CT) correctly diagnosed 13/15 (87%) of cases in which it was performed prospectively. The median time to surgery was 7.5 ± 5.2 days for those patients with bowel resection, compared to 0.8 ± 1.3 days for those without (P

Endoscopic inspection of the porta hepatis was undertaken through external enterostomy in nine postoperative patients with biliary atresia. The endoscopic appearance of bile flow in the porta hepatis was classified into three types. 1) Ductal type (D-type), which revealed good bile flow from distinct bile duct orifices (4 cases); 2) Oozing type (O-type), which showed adequate bile flow, but no definite bile duct (3 cases); and 3) Covered type (C-type), in which the porta hepatis was covered with bile "clots" and fibrous tissue (2 cases). The clinical course of the D-type was excellent with immediate disappearance of jaundice and relatively good liver function. In the case of the O-type, jaundice disappeared in 2 but persisted in one. Two patients with C-type died of hepatic failure or sepsis in the early postoperative period. In the D-type intrahepatic bile ducts were well visualized by cholangiography; however, those of the O-type were not so clear. Endoscopic inspection of the porta hepatis is very useful for evaluation of the postoperative state of bilioenteric fistulae in patients with biliary atresia.

The influence of CPR on the blood-brain barrier (BBB) in dogs was studied by fluorescence microscopy using Evans blue as a BBB tracer. Three of 9 control dogs, whose blood pressure (BP) was increased by more than 130 mm Hg, showed dye extravasation (BBB impairment) into brain tissue, but no extravasation was seen in the other 6 controls whose BP increase was less than 110 mm Hg. In 11 experimental animals, extravasation of Evans blue occurred in 8 of 9 resuscitated dogs after several minutes of cardiac arrest and in 1 of 2 nonresuscitated dogs. In the resuscitated dogs, the maximum systolic BP (peak BP) after restoration of ventricular function ranged from -40 to +210 mm Hg compared to control values. They showed all grades of dye extravasation without significant correlation between the magnitude of BP increase and the severity of dye extravasation. The authors conclude that BBB disruption usually occurs during CPR and causes plasma protein extravasation into brain tissue. Arterial hypertension is a causative factor for BBB disruption, as was seen in the control dogs. In resuscitation, restoration of BP sufficient to overcome intracranial pressure and maintain cerebral blood flow may be high enough to induce BBB disruption because cerebral vessels are fully dilated and functionally impaired due to longstanding anoxia. The rapidity of BP increases after restoration of ventricular function could be another factor which might contribute to BBB impairment.

The participation of membrane inhibitors in C-mediated inflammation in vivo was analyzed in rats with the use of mAbs against membrane inhibitors of C. 512Ag inhibits C3 convertase of homologous rat C and rat CD59 prevents the formation of homologous membrane attack complexes. The histologic distributions of 512Ag and CD59 in rat skin were essentially the same. However, although intracutaneous administration of mAb against 512Ag (anti-512Ag) in the form of F(ab')2 induced a remarkable inflammatory response visualized by exudation of Evans blue that had been previously injected i.v., the mAb against CD59 caused no inflammatory exudate. Furthermore, anti-512Ag F(ab')2 caused deposition of C3 followed by intense polymorphonuclear leukocyte infiltration and hemorrhage at the injection sites within 24 h. This reaction was completely abrogated by depletion of C. Therefore, spontaneous C activation on self cell membranes requires amplification at the C3 convertase step, which is restricted by membrane inhibitors such as 512Ag, thus preventing inflammation. A type II allergic response might preferentially occur at sites that exhibit an impairment of membrane inhibitor(s) of C3 convertase. However, although depletion of leukocytes by preadministration of cyclophosphamide did not reduce C3 deposition by anti-512Ag. Evans blue exudation was appreciably reduced, indicating that infiltrated leukocytes play a role in enhancing and prolonging inflammation initiated by local C activation.

The role of the inducible L-selectin ligand was studied in complement-dependent acute dermatitis in rats. Although mAbs against typical sialyl Lewis(x) (CSLEX-1 and SNH-3) did not react with skin venules, a sialyl Lewis(x)-like epitope defined by mAb 2H5 (2H5-Ag) was de novo expressed on the endothelial cells of skin venules in the area of inflammation. Expression of 2H5-Ag increased concomitantly with the progression of inflammation. 2H5-Ag was identified at the 75-, 150-, and 180-kDa bands when inflammatory skin tissue was analyzed by Western blotting. In contrast, P- and E-selectins were not detectable. The role of 2H5-Ag in this model was studied in in vitro and in vivo methods. First, 2H5 was i.v. injected 15 min before induction of dermatitis. 2H5 bound to skin venules and significantly reduced the neutrophil infiltration and plasma protein leakage. In contrast, CSLEX-1, mAb ARP2-4 (P-selectin blocker), or mAb ARE-5 (E-selectin blocker) had no effects. Second, adhesion of isolated rat neutrophils to the inflammatory skin section was inhibited significantly when the sections, but not neutrophils, were preincubated with 2H5. Third, fluorescein-labeled normal rat neutrophils were injected into a rat 10 h after induction of dermatitis. The number of labeled neutrophils infiltrated into the inflammatory site was reduced significantly when they were preincubated with HRL-3 (blocking mAb against rat L-selectin), but not with 2H5 or HRL-4 (nonblocking mAb against rat L-selectin). These data show that de novo expressed 2H5-Ag/L-selectin adhesion pathway contributes to the development of acute complement-dependent inflammation in the skin.