The impact of a repeated bout of eccentric exercise on muscular strength, muscle soreness and creatine kinase.

The purpose of this study was to determine if there were any beneficial or detrimental effects regarding delayed onset muscle soreness (DOMS), serum creatine kinase (CK), and maximum concentric strength at 80% of 1-RMconc, if a bout of eccentric exercise was repeated at 48 h after an initial bout. A secondary purpose was to determine whether unaccustomed eccentrics might affect plasma cholesterol (TC). Twenty-six men were randomly assigned to a control (Group 1) or experimental group (Group 2). Both groups performed three sets (12 repetitions per set) of the eccentric phase of a chest press, at 80% of one repetition maximum (1-RMconc); Group 2 repeated this exercise 48 h later. DOMS and CK were measured before, and every 24 h for 8 days after; TC was measured before, and every 24 h for 4 days. Maximum strength during the concentric phase of a chest press (1-RMconc) was measured before and at 48-h intervals after. A repeated measures analysis of variance revealed a significant time effect (P < 0.05) for DOMS, CK and strength, but no significant difference between groups (P < 0.05). An interesting finding was the significant (P < 0.05) reduction in TC at 24, 48 and 72 h, after exercise in both groups, which we hypothesized was associated with cellular repair. From these results we concluded that when a bout of eccentrics is repeated 48 h after an initial bout, there is no change in the characteristic time-course and/or intensity of DOMS, CK or 1-RMconc.

Formation, absorption, and biotransformation of delta 6-lithocholenic acid in humans.

delta 6-Lithocholenic acid was identified in small amounts in fecal samples in vitro after incubation with ursodeoxycholic acid and in vivo in controls and after chenodeoxycholic and ursodeoxycholic acid ingestion. Fourteen to 45.0% of delta 6-[24-14C]lithocholenic acid was biotransformed in vitro in feces within 30 s. After colonic instillation of delta 6-[24-14C]lithocholenic acid, 50% of the radioactivity appeared in bile acids, most of it in lithocholic acid, within 3 h. Jejunal perfusions with delta 6-[24-14C]lithocholenic acid showed 33-92% absorption. One hour after jejunal instillation of 1 mmol, 4.4-27.5% of the biliary radioactivity was found in ursodeoxycholic, chenodeoxycholic, lithocholic, and 7-ketolithocholic acids. A sulfated glycine conjugate of delta 6-lithocholenic acid was identified in bile. One hour after intravenous injection of delta 6-[24-14C]lithocholenic acid, 40.1-42.6% of biliary radioactivity appeared in 7-ketolithocholic, chenodeoxycholic, lithocholic/isolithocholic, and ursodeoxycholic acids. The studies show that delta 6-lithocholenic acid is 1) formed in colonic lumen from chenodeoxycholic and ursodeoxycholic acids, 2) well absorbed in small intestine, and 3) biotransformed in both the colonic lumen and liver. The studies also identified delta 6-lithocholenic acid as a new intermediate in formation of lithocholic acid. Finally, the studies showed that a small portion of delta 6-lithocholenic acid is excreted as a sulfated glycine conjugate in bile.

Marked hyperlipasemia in diabetic ketoacidosis. A report of three cases.

We report three patients with diabetic ketoacidosis (DKA) who presented with striking elevations of serum lipase levels and less striking elevations of amylase and trypsinogen. All three had nausea and vomiting, but none had objective evidence of abdominal pain, and computed tomography scans of the pancreas were unremarkable. These cases suggest the association of asymptomatic enzyme elevations with DKA. We review the literature on this subject.

Single-parameter DNA flow cytometric analysis of normal-appearing colonic mucosa does not predict the presence of colonic neoplasia.

We wished to determine whether DNA flow cytometric analysis could detect DNA abnormalities in normal-appearing mucosa of patients with colonic neoplasia. Eighty-five patients were studied either at colonoscopy or at surgical resection. Forty-five had macroscopically normal colonoscopy; 13 had adenomatous polyps, and 27 had colorectal carcinoma. Biopsies were obtained from the cancer and from normal-appearing mucosa 5 cm from the lesion. The patients who had normal colonoscopy had rectal biopsies. The samples were prepared for analysis on a Coulter EPICS C flow cytometer. Cells were analyzed for presence of aneuploidy (%AN), percent in DNA synthetic phase (%S), and percent growth fraction (%GF = %S + %G2M). Aneuploidy was present in 12 of 27 carcinomas (44%), but in none of the samples from polyps or normal-appearing colorectal mucosa adjacent to cancers. The %S from cancers was greater than those from polyps (9.6 +/- 6.3 vs. 5.1 +/- 1.8, p less than 0.005). However, %S from specimens arising from normal-appearing mucosa 5 cm distant from cancer could not be differentiated from the rectal mucosa of macroscopically normal colons (5.9 +/- 2.5 vs. 5.2 +/- 2.7). The %GF of cancer specimens was greater than those from adenomas (26.0 +/- 11.0 vs. 10.8 +/- 3.7, p less than 0.005). However, the %GF of normal-appearing mucosa 5 cm distant from the cancer was similar to the findings from mucosa arising from macroscopically normal colons (10.5 +/- 3.3 vs. 11.0 +/- 3.4). In conclusion, DNA flow cytometric analysis of normal-appearing colonic mucosa from patients with colonic carcinoma does not demonstrate abnormalities of DNA content or cell cycle kinetics, and therefore, cannot predict the presence of colonic neoplasia.