Disc related and non-disc related disorders of the thoracic spine.

Different anatomical structures and pathophysiological functions can be responsible for lumbar pain, each producing a distinctive clinical profile. Pain can arise from the intervertebral disc, either acutely as a primary disc related disorder, or as result of the degradation associated with chronic internal disc disruption. In either case, greatest pain provocation will be associated with movements and functions in the sagittal plane. Lumbar pain can also arise from afflictions within the zygapophyseal joint mechanism, as a result of synovitis or chondropathy. Either of these conditions will produce the greatest pain provocation during three-dimensional movements, due to maximal stress to either the synovium or joint cartilage. Finally, patients can experience different symptoms associated with irritation to the dural sleeve, dorsal root ganglion, or chemically irritated lumbar nerve root. Differential diagnosis of these conditions requires a thorough examination and provides information that can assist the clinician in selecting appropriate management strategies.

Pain generators of the lumbar spine.

Different anatomical structures and pathophysiological functions can be responsible for lumbar pain, each producing a distinctive clinical profile. Pain can arise from the intervertebral disc, either acutely as a primary disc related disorder, or as result of the degradation associated with chronic internal disc disruption. In either case, greatest pain provocation will be associated with movements and functions in the sagittal plane. Lumbar pain can also arise from afflictions within the zygapophyseal joint mechanism, as result of synovitis or chondropathy. Either of these conditions will produce the greatest pain provocation during three-dimensional movements, due to maximal stress to either the synovium or joint cartilage. Finally, patients can experience different symptoms associated with irritation to the dural sleeve, dorsal root ganglion, or chemically irritated lumbar nerve root. Differential diagnosis of these conditions requires a thorough examination and provides information that can assist the clinician in selecting appropriate management strategies.

Influence of age on the development of pathology.

Patients of different ages present with different lumbar spine afflictions. These afflications are linked to age-related changes in the intervertebral disc, zygapophyseal joints, and capsuloligamentous structures. Disc degeneration precedes all other changes, resulting in nonspecific low back pain that can potentially advance into specific low back pain conditions.

Autologous bone marrow transplantation for acute myeloid leukemia in remission or first relapse using monoclonal antibody-purged marrow: results of phase II studies with long-term follow-up.

One hundred and thirty-eight patients with AML underwent ABMT with monoclonal antibody plus complement-purged marrow between August 1984 and March 1997. One hundred and ten patients were in CR (CR1: 23; CR2/3: 87) and 28 were in first relapse (R1) at ABMT. Preparative regimens included busulfan (16 mg/kg) and CY (120 mg/kg) (n = 93), CY (120 mg/kg over 2 days) with TBI (1200 cGy) (n = 35), and busulfan (16 mg/kg) plus etoposide (60 mg/kg) (n = 10). CR1 patients treated with CY/TBI (n = 7) had 3- and 5-year disease-free survival (DFS) rates of 71% and 57%. CR1 patients treated with BU/CY (n = 12), had 3- and 5-year DFS rates of 45%. Three and 5-year DFS for CR2/3 patients treated with CY/TBI (n = 26) was 23%. Three- and 5-year DFS for patients in CR2/3 treated with BU/CY (n = 55) was 31 and 28%. Three- and 5-year DFS for patients in R1 treated with BU/CY (n = 26) was 37%. In multivariate analysis, increased age was associated with greater risk of death and relapse. For CR2/3 patients, the length of CR1 was a significant predictor of DFS. ABMT performed in CR or R1 results in excellent 5-year DFS and OS. The contribution of purging may require a randomized trial comparing purged vs unpurged stem cell infusions.

Thy-1 expression on blast cells from adult patients with acute myeloid leukemia.

Bone marrow and peripheral blood from 28 adult patients with acute myeloid leukemia (AML) were analyzed for the surface expression of the Thy-1 antigen by dual-colour flow cytometry. The Thy-1 antigen was expressed on greater than 5% of cells from seven patients with the proportions of Thy-1 positive cells ranging from 8.1% to 85.0%. The CD34+ Thy-1+ phenotype was present in all seven cases. The expression of Thy-1 on leukemia cells from patients with AML may need to be considered in the development of methods of normal stem cell isolation from these patients.

The buffering ability of commonly employed cardiopulmonary bypass solutions and alkalizing agents.

This experiment evaluated the hydrogen ion (H+) buffering capacity (BC) of solutions and alkalizing agents employed during cardiopulmonary bypass (CPB). A solution's BC can be determined when a known quantity of H+ is titrated into the solution and the change () in pH (-log of the hydrogen ion activity ([H+]a)) is measured ([H+]a/mmole H+). Eleven solutions were studied:Lactated Ringers (LR), 0.9% NaCl (NS), Plasma-Lyte A, Hespan (6% hetastarch), banked donor blood with citrate phosphate dextrose adenine (CPDA-1), fresh donor blood, THAM, sodium bicarbonate (NaHCO3; 1 mEq/ml), high potassium crystalloid cardioplegic solution (HKCCPS), oxygenated crystalloid cardioplegic solution (OCCPS), and adult crystalloid priming solution (AP) per institutional protocol. The solutions were studied at three temperatures: 37 degrees C, 28 degrees C, and 18 degrees C. The null hypothesis stated there was no difference in the BC of the solutions studied. The solutions were first titrated to the same starting pH of 8.0. The solutions were then titrated with a predetermined concentration of hydrochloric acid (HCl) to a pH of 7.0. A higher quantity of H+ added to a solution indicated a greater ability of that solution to buffer H+ within pH limits of 8.0 to 7.0. The data was analyzed with a two way ANOVA and Bonferonni method. A p value < 0.05 was considered to be statistically significant. The significant results of our study indicated that THAM demonstrated the best BC, followed in decreasing order by NaHCO3, banked blood, fresh blood, HKCCPS, AP, OCCPS, Plasmalyte, LR, Hespan, and NS.

Serum high-density lipoprotein particles of alcohol-fed rats are deficient in apolipoprotein E.

Effects of chronic ethanol consumption on serum lipoproteins have been studied in the rat. The serum levels of triglycerides, cholesterol, phospholipids and apolipoproteins AI and AIV increased significantly after 1 week of ethanol feeding, and they remained elevated up to 7 weeks of alcohol drinking. By contrast, serum total apolipoprotein E decreased or, sometimes, did not change. Very-low-density lipoprotein cholesterol, triglycerides and very-low-density lipoprotein apolipoprotein E of the alcohol-fed rats increased in parallel and were about 2- to 2.5-fold over the controls. Whereas high-density lipoprotein cholesterol, phospholipids, apolipoprotein AI and AIV increased 1.2-fold by chronic alcohol feeding, the level of high-density lipoprotein apolipoprotein E decreased to 70% of that of the control rats. The rates of secretion of apolipoprotein AI, E and AIV into the culture medium by hepatocytes isolated from ethanol-fed rats were 1.8-, 1.3- and 1.1-fold higher than those from control rats. These data indicate that (i) chronic ethanol feeding increases very-low-density lipoprotein and high-density lipoprotein in the rat; (ii) serum high-density lipoprotein particles of the ethanol-fed rats are deficient in apolipoprotein E, and (iii) chronic ethanol feeding increases hepatic secretion of apolipoprotein AI, E and AIV. Since the steady-state serum level of apolipoprotein E decreases or remains unchanged in the presence of increased hepatic apolipoprotein E secretion, this imbalance suggests that alcohol feeding either accelerates the rate of degradation of serum apolipoprotein E or suppresses apolipoprotein E synthesis by nonhepatic tissues.