Zeitschriften

Ohne Zusammenfassung     

Zeitschriften

Ohne Zusammenfassung     

Zeitschriften

Ohne Zusammenfassung     

Paratyphus-B-Meningitis bei Einem Säugling

Ohne Zusammenfassung     

Cue exposure to food plus response prevention of binges for bulimia: A pilot study

In a single-case multiple-baseline design, 4 chronic bulimics had 12 sessions (3 per week) of therapist-aided cue exposure to food while resisting the temptation to binge that ensued. Two patients improved markedly during treatment. A third patient improved mainly after, not during, treatment. The fourth patient had a strong within-session response decrement, and showed some improvement by session 9, but then dropped out. These preliminary results warrant a larger controlled trial of cue exposure and response prevention of binging as an adjuvant in the management of bulimia.     

Return to Play After Distal Biceps Tendon Repair

Purpose of ReviewDistal biceps tendon ruptures (DBTR) are uncommon injuries in 40- to 50-year-old men but occur at a younger age in the athlete population. The distal biceps tendon is an important supinator of the forearm and flexor of the elbow. A complete injury results in limiting function in the upper extremity. The current review evaluates the different options in management and the current literature on return to play in athletes.Recent FindingsThe distal biceps tendon inserts on the posterior aspect of the radial tuberosity as two independent heads. The long head footprint is more proximal and posterior giving it a better lever arm for supination. The short head footprint is more distal and anterior giving it a better lever arm for flexion. Surgical anatomic repair is highly recommended among the athlete population, to restore proper function of the upper extremity. There is scarce literature on return to play among athletes. The most recent studies on high-performance athletes are on National Football League (NFL) players. These studies showed that 84–94% of NFL players returned to play at least one game after distal biceps repair. Compared to matched control groups, there was no difference in the player’s performance after surgery.SummaryAnatomic repair of DBTR results in excellent outcomes, high return to work, and high rate of return to play among athletes. When compared to matched control groups, NFL players have the performance score and play the same number of games after surgery.Supplementary InformationThe online version contains supplementary material available at 10.1007/s12178-022-09742-x.     

Phagocytic function of polymorphonuclear leukocytes and the RES in endotoxemia

The reticuloendothelial system (RES) and the polymorphonuclear leukocytes (PMNs) are thought to play a major role in defense against sepsis. Disturbances in the function of these two phagocytic systems during a septic event is associated with the development of lung capillary injury. Endotoxemia is said to lead to similar changes. Our study examined the function of the RES and PMNs after bolus injection of endotoxin (2 micrograms/kg BW) in a standardized sheep model. For up to 24 hr after endotoxin, blood samples were drawn and PMN function was followed by chemiluminescence, chemotaxis, and adherence as well as the phagocytosis and killing of bacteria. RES function was determined by the blood clearance of a labeled Tc99 colloid. We found an increase of RES clearance directly after endotoxin. Chemotaxis, phagocytosis, and killing were reduced. Adherence was increased. Chemiluminescence peak maximum (CLPM), representing the metabolic activity of the PMNs, was initially increased but shortly thereafter showed a significant decline (at 1 hr: 0.52 +/- 0.13 X 10(6) cpm with P less than 0.05 compared to baseline). The chemiluminescence peak time (CLPT), a measure of membrane receptor function, was significantly reduced (10.0 +/- 2.2 min with P less than 0.001 compared to baseline). Endotoxin led to a reduction of intracellular PMN functions (phagocytosis, killing, CLPM) within 1 hr. Membrane localized functions (adherence, CLPT) were increased. The changes in PMN function might be the reason for the development of lung capillary injury, in spite of undisturbed RES clearance.     

Inhibition of the phosphatidylinositol 3’-kinase signaling pathway increases the responsiveness of pancreatic carcinoma cells to sulindac

Nonsteroidal anti-inflammatory drugs (NSAIDs) may be effective treatment for pancreatic cancer. We have previously demonstrated that NSAIDs suppress pancreatic cell growth in vitro by inhibiting cell cycle progression but have little effect on apoptosis. In fact, we have shown that NSAIDs, in some instances, increase Akt phosphorylation in human pancreatic carcinoma cells suggesting activation of the phosphatidy linositol 3’-kinase (PI3K)-Akt survival (antiapoptotic) pathway. We subsequently examined the effects of treating the human pancreatic cancer cell lines BxPC-3 and PaCa-2 with a specific inhibitor of the PI3K/Akt pathway, LY294002, in the presence or absence of the NSAID sulindac. The growth effects of sulindac (250 to 500 ώmol/L) and/or LY2 94002 (1 to 100 ώmol/L) were determined by a colorimetric proliferation assay and cell counts. The combination of low-dose LY294002 (10 ώmol/L) and sulindac enhanced the growth inhibitory effects of sulindac in BxPC-3 and PaCa-2 cells. Treatment of both cell lines with the LY294002/sulindac combination altered the cell cycle distribution as determined by flow cytometry and also lowered the apoptotic threshold as measured with an enzyme-linked immunosorbent asssay to detect DNA fragmentation. These effects were associated with changes in the expression and/or phosphorylation level of proteins and kinases that regulate cell cycle progression and apoptosis. Taken together, our results suggest that inhibition of the PI3K/Akt signaling pathway may sensitize pancreatic tumor cells to therapy with NSAIDs such as sulindac. Presented at the Forty-Third Annual Meeting of The Society for Surgery of the Alimentary Tract, San Francisco, California, May 19–22, 2002 (poster presentation). Supported by institutional research grant IRG-84-002-18 from the American Cancer Society.