The objective of this study was to define the patterns of myoelectric activity that occur throughout the gastrointestinal tract during normal recovery from laparotomy. Electrodes were placed on the stomach, jejunum, and transverse colon of 44 patients undergoing laparotomy. Basal electric rhythms in all areas showed no changes in frequency after operation (up to 1 month). Gastric spike wave activity showed a gradient of increasing activity from fundus to antrum. Antral spike activity was unchanged during the study. Jejunal spike activity was present in the earliest recordings and occurred in 45.9% +/- 3.5% to 59.9% +/- 5.5% of slow waves. Recovery of normal colon discrete and continuous electric response activity occurred on postoperative day 5.9 +/- 1.5. Bowel sounds returned on day 2.4 +/- 0.5 and passage of flatus and stool occurred on day 5.1 +/- 0.2. The myoelectric parameters measured are not absolutely predictive of uneventful recovery from postoperative ileus but they are, as a group, more informative than any currently available clinical criteria.

Infrarenal circumaortic occlusion devices were operatively placed in 74 New Zealand white rabbits. Two days after operation the animals were randomly assigned to one of seven treatment groups: I, control, n = 23; II, halothane, n = 8; III, thiopental, n = 12; IV, ketamine (30 mg/kg intravenously), n = 6; V, halothane+hypothermia, n = 8; VI, thiopental+hypothermia, n = 12; VII, ketamine+hypothermia, n = 5. In each group, the infrarenal aorta was occluded for 21 minutes. Final neurologic recovery after restitution of blood flow was graded as acute paraplegia, delayed paraplegia (neurologic deficit developing after initial recovery), or normal. Halothane alone was of no benefit. Hypothermia with any anesthetic was completely protective and reduced neurologic deficits to 0% compared with 91% in controls (p less than 0.05). Thiopental and ketamine treatment each reduced acute paraplegia to 17% (as compared with 61% in controls) and increased delayed paraplegia from 30% in controls to 75% and 50%, respectively (p less than 0.05 for thiopental, p = 0.10 for ketamine). The authors interpret the increase in delayed deficits and decrease in acute deficits as being the result of partial spinal cord protection. These findings document that this model of spinal cord ischemia is sufficiently sensitive to identify interventional treatments that protect the ischemic spinal cord.

Aim: Sentinel node biopsy is a prognostic indicator of melanoma recurrence. We hypothesized that adding the primary melanoma molecular signature from the 31-gene expression profile (31-GEP) test could refine the risk of recurrence prognosis for patients with stage I–III melanoma. Materials & methods: Four hundred thirty-eight patients with stage I–III melanoma consecutively tested with the 31-GEP were retrospectively analyzed. The 31-GEP stratified patients as low-risk (Class 1A), intermediate-risk (Class 1B/2A) or high risk (Class 2B) of recurrence or metastasis. Results: The 31-GEP significantly stratified patient risk for recurrence-free survival (p < 0.001), distant metastasis-free survival (p < 0.001) and melanoma-specific survival (p < 0.001) and was a significant, independent predictor of metastatic recurrence (hazard ratio: 5.38; p = 0.014). Conclusion: The 31-GEP improves prognostic accuracy in stage I–III melanoma.

In an effort to lower healthcare costs, this study was undertaken to evaluate the utility of routine postoperative (PO) laboratory studies and determine whether abnormalities alter patient (PT) care. This was a retrospective review of 105 PTs undergoing elective curative resection for colorectal cancer. A serum electrolyte and liver panel and a hematologic panel were drawn in all PTs. OF 8749 total laboratory values obtained, 5894 (67%) were normal. Two of these (0.03%) elicited a therapeutic intervention. Of the 2004 values that were low (23%), 103 (5.1%) elicited a therapeutic response. Of the 851 that were high (10%), 21 (2.5%) elicited a therapeutic response. Of 2089 preoperative laboratory values, 252 (12%) were abnormal, but in only 15 incidences in 9 PTs was any action taken. Three PTs required potassium supplementation and 6 PTs were transfused packed red blood cells before surgery. In the PO period 2603 laboratory values of 6660 obtained (39%) were abnormal. Of these, 735 (28%) were high and 1868 (72%) were low. Twenty of 735 (27%) high values triggered a therapeutic response that most commonly required administration of insulin for elevated serum glucose in 17 of 197 occasions in five diabetic PTs. On three occasions potassium was removed from intravenous fluids. Five of 275 (1.8%) low calcium values were treated in five patients. Potassium was replaced in 17 of 32 occasions in 14 patients where it was low. In this group of PTs, PO serum potassium, hemoglobin levels, and serum glucose in diabetics were the only values important in making therapeutic decisions. If laboratory studies can be streamlined into only those necessary, substantial savings in health care will be seen without sacrificing quality medical care.

The newly synthesized calcium channel blocker, Ro44-5912, significantly potentiates doxorubicin (Dox)-induced cytotoxicity at non-cytotoxic concentrations in Dox-resistant human ovarian cell line, A2780/DX5, overexpressing P170-glycoprotein (Pgp). Induction of DNA single- and double-strand breaks (ssbs and dsbs) was measured using alkaline elution and constant-field gel electrophoresis (CFGE) assays. The results indicate that potentiation of the cytotoxicity of Dox by Ro44-5912 was accompanied by significant increases in both, Dox-induced DNA ssbs and dsbs in the resistant cells. Pulsed-field gel electrophoresis (PFGE) analysis showed that Dox induced DNA fragments in the 50-800 kilobase (kb) and 0.8-5.7 megabase (Mb) ranges. The majority of the newly synthesized DNA fragments were in the 50-800 kb range. Ro44-5912 treatment resulted in significant potentiation of DNA fragmentation in the 50-800 kb range with a minor increase in 0.8-5.7 Mb DNA fragments, suggesting that the modulator functions by potentiating nascent DNA fragmentation in the resistant cells. Exposure to Dox with Ro44-5912 was associated with a prolonged blockage of cells in the S-phase. In contrast, exposure to Dox alone resulted in temporary blockage of cells in G2/M phase (approximately 24 h) followed by restoration of cell proliferation and normal DNA histograms at 48 h after 2 h drug exposure. Incorporation of BrdUrd by flow cytometric analysis was inhibited by Dox in the presence of Ro44-5912, showing that there is a block of DNA replication. An increased damage in newly synthesized DNA could concur with a blocked DNA replication. Moreover, slowing progression through the S-phase in cells exposed to Dox in combination with Ro44-5912 is accompanied by increased sensitivity of Dox poisons, indicating a correlation of specific S-phase perturbation with the reversal of Dox resistance by Ro44-5912 in cells expressing Pgp. The results suggest that drug-induced augmentation of nascent DNA fragmentation and specific cell-cycle perturbation are potentially important molecular determinants for reversal of multidrug resistance in addition to restoration of intracellular drug retention.