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OBJECTIVE: The purpose was to determine if intermittent pneumatic compression (IPC) affects muscle swelling, stiffness, and strength loss resulting from eccentric exercise-induced injury of the elbow flexors. We hypothesized that the compression would decrease swelling and stiffness. DESIGN: Repeated measures design with a before-after trial comparison within each day. SETTING: Conducted at a university Somatic Dysfunction Laboratory. SUBJECTS: Twenty-two college women students were studied. They had not been lifting weights or otherwise participating in regular arm exercise for the 6 months before the study. They had no history of upper extremity injury or cardiovascular disease. INTERVENTIONS: Subjects performed one bout of eccentric exercise at a high load to induce elbow flexor muscle injury. Uniform IPC was applied on the day of exercise and daily for 5 days at 60mmHg, 40 seconds inflation, 20 deflation for 20 minutes. MAIN OUTCOME MEASURES: Measurements of arm circumference, stiffness, and isometric strength were recorded before exercise, then before and after IPC for 5 days after exercise. Passive muscle stiffness was measured on a device that extends the elbow stepwise and records the torque required to hold the forearm at each elbow angle. RESULTS: Circumference and stiffness increased and strength decreased during the 5 days post-exercise (p < .05). IPC significantly decreased circumference and stiffness most notably on days 2 and 3 after exercise (p < .05). The strength loss was not affected by IPC. CONCLUSION: IPC is effective in temporarily decreasing the swelling and stiffness after exercise-induced muscle injury.

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In order to study the efficacy of an oral induction and consolidation regimen in the treatment of acute myeloid leukemia (AML) in elderly patients assessed not to tolerate full-scale intensive chemotherapy, 51 patients over 65 years of age with newly diagnosed AML were randomized to receive two cycles of either totally oral ETI (25 patients) or conventional 5-day TAD (26 patients). The median age of the patients was 73 years, range 65-87 years. Thirty-eight patients had de novo AML and the remaining patients AML subsequent to myelodysplastic syndrome ((n = 11) or treatment related AML (n = 2)). ETI consisted of etoposide 80 mg/m2 and thioguanine 100 mg/m2 twice a day on days 1-5, and idarubicin 15 mg/m2 on days 1-3, all given orally. TAD consisted of oral thioguanine and i.v. cytarabine, both in the dose of 100 mg/m2 twice a day on days 1-5, and daunorubicin 60 mg/m2 on day 5. The maintenance treatment was daily oral mercaptopurine 70 mg/m2 and weekly oral methotrexate 12 mg/m2. In the ETI group complete remission (CR) was achieved in six patients after the first cycle and in nine more patients after the second cycle. The CR rate was 15/25 = 60%. The corresponding figures for the TAD group were four and two remissions, CR rate 6/26 = 23% (p = 0.007). The survival was significantly longer in the ETI arm (p = 0.042). The median survival was 9.9 months in the ETI group and 3.7 months in the TAD group. There were no significant differences in the side effects between the two arms. In conclusion, the totally oral ETI regimen resulted in a significantly higher remission rate and longer survival than the 5-day TAD regimen in elderly patients with AML, with no more toxicity.

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Four patients with myelodysplastic syndrome (MDS), one with t(1;7) and three with trisomy 8, were studied by immunophenotyping and fluorescence in situ hybridization (FISH) to assess cell lineage involvement. The t(1;7) was detected using a biotin-labeled chromosome 1 centromere-specific DNA probe. This aberration was present in CD34-positive stem cells, the erythroid cell lineage (GPA+), and the granulocytic/monocytic (CD13+ and CD64+) cell lineages. We were not able to demonstrate the abnormality in the lymphoid cell lineages. In the patients with trisomy 8, the aberration was detected with chromosome 8 centromere-specific DNA probe or by chromosome in situ suppression hybridization (CISS) with a chromosome 8-specific library probe. The trisomy was detected in stem cells, erythroid precursor cells, megakaryocytes, and granulocytes/monocytes. In these MDS patients, the chromosome aberrations appear to occur only in cells of myeloid lineage.

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In a randomised multicentre trial a combination of methylprednisolone, vincristine, lomustine, cyclophosphamide and melphalan (MOCCA) was compared with the same regimen omitting methylprednisolone after the first course (COLA) in previously untreated patients with multiple myeloma. The MOCCA arm showed a response rate of 72% among 79 patients and the COLA arm a response rate of 60% among 59 patients. This difference was not statistically significant. The median survival time was 56 months in the MOCCA arm and 61 months in the COLA arm. There was a slight increase of early deaths (within the first 6 months) in the MOCCA arm as compared with the COLA arm. We conclude that, in multidrug therapies, the continuation of corticosteroid at conventional dosage beyond the first course does not improve response rate or survival time in multiple myeloma.

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The presence, magnitude, and nature of the effect that low intensity laser irradiation has on nerve function, growth, and repair constitute a contentious area of research. We have addressed one aspect of this controversy by systematically examining the influence of 830 nm laser radiation on median nerve function. In particular, we investigated median nerve motor and sensory distal latencies, action potential amplitudes, action potential areas, and conduction velocities as well as dorsal hand skin temperatures in 33 normal subjects in a double-blinded, randomized controlled study. All subjects received identical treatment: 30 seconds of "irradiation" at 10 points over the course of the right median nerve (five sites on the forearm and five sites distal to the wrist crease) with either an active (1.2 J/point) or inactive (0 J/point) 40 mW 830 nm continuous wave IR laser diode. Latencies, conduction velocities, amplitudes, areas, and skin temperatures were collected bilaterally at a baseline immediately prior to irradiation and at intervals of 1, 5, 10, 15, 20, and 30 minutes following treatment. Analysis of the results reveals that motor and sensory distal latencies were decreased in the treated limbs of the laser-treated group relative to the control group by 3-4% (P < .016 and .046, respectively, rank sum test). No significant differences in these quantities were found between the limbs within either group. Similarly, no alterations of action potential amplitudes, action potential areas, forearm conduction velocities, or skin temperatures were detected within or between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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The purposes of this study were (1) to determine normal values for cervical active range of motion (AROM) obtained with a "cervical-range-of-motion" (CROM) instrument on healthy subjects whose ages spanned 9 decades, (2) to determine whether age and gender affect six cervical AROMs, and (3) to examine the intratester and intertester reliability of measurements obtained. Measurements were made on 337 subjects (171 females and 166 males) whose ages ranged from 11 to 97 years. Measurements were taken by five physical therapists with 7 to 30 years of clinical and teaching experience. Among male and female subjects of the same age, females had a greater AROM than did males for all AROMs except neck flexion. Among both males and females, each of the six cervical AROMs decreased significantly with age. From two pilot studies separate from the acquisition of the normal database, we determined our intratester and intertester reliabilities for making neck AROM measurements with the CROM instrument. We concluded that AROM measurements on the cervical spine with the CROM instrument demonstrated good intratester and intertester reliability, because the intraclass correlation coefficients were generally greater than .80.

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94 patients with refractory multiple myeloma were treated in a multicentre trial with combinations of cytotoxic drugs including anthracyclines. All were refractory to a 5-drug combination containing 3 alkylating agents, vincristine and methylprednisolone (MOCCA). With a combination of epirubicin and iphosphamide a 50% response was achieved in 9% of 22 patients. The response rate after schedule VAP (vincristine, doxorubicin and prednisolone) was 8% of 13 patients and that after schedule VAD (vincristine, doxorubicin and dexamethasone) 20% of 59 patients. The previous chemotherapy had lasted for less than 12 months in 13 cases from among all these patients, and 5 of these (38%) responded. In contrast, there were only 10 responders (12%) among the 81 patients with longer previous chemotherapy.

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The effect of 1 mW helium neon continuous-wave (0.633 microns) laser irradiation on superficial radical sensory and median sensory nerve function was examined in a double-blind, controlled study involving 40 volunteers. No differences in action potential amplitudes, distal latencies, or forearm skin temperatures were found between the treated and control groups either at the time of irradiation or at subsequent evaluations 15 and 30 minutes later. As a result, we are unable to confirm reports that low-energy lasers of this power and wavelength alter nerve function.

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The actual use of hospital beds for patients with multiple myeloma was calculated from a randomised trial of primary treatment with either melphalan and prednisone (MP, 66 patients) or intensive combination chemotherapy with vincristine, cyclophosphamide, lomustine, melphalan and methylprednisolone (MOCCA, 64 patients). The survival of the patients was similar in both arms, and the samples, 20 and 32 patients, respectively, were well representative for the whole arms. The average numbers of hospital days were similar fur both arms. For the first year MP 33.2 (SD 27.6) vs. MOCCA 32.1 (SD 19.0), and during the first to 4th years 78.5 (SD 45.9) vs. 67.8 (SD 34.1). For the year of death it was 50.4 (SD 33.1) vii. 36.3 (SD 27.0), respectivelly. Thus the choice of primary chemotherapy whether conventional or more aggressive had no influence on the actual number of in-patient hospital days concerned. When the combination chemotherapy schedule is well tolerated it can be administered just as well on an ambulatory basis or by using it with very short admissions. It seems that the need for inpatient care for patients with multiple myeloma is mostly related to the complications of the disease itself and to intercurrent disorders including infections.

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The distribution of specific binding sites for the peptide galanin was studied in the monkey brain by using 125I-galanin and the method of quantitative in vitro autoradiography. The binding to tissue sections was found to be rapid, reversible and saturable with a calculated Bmax of around 13 fmol mg-1 tissue in cortical regions and a KD ranging between 0.39 and 0.22 nM in different brain regions. Specifically bound 125I-galanin was detected in a number of brain regions throughout the rostrocaudal axis of the monkey brain. More specifically, the majority of the 125I-galanin binding sites were present in the basal forebrain (e.g. olfactory tubercle, lateral septal nuclei, nucleus accumbens, substantia innominata and the basal nucleus of Meynert), the amygdala (e.g. the lateral, medial accessory and central nuclei), the amygdala-hippocampal area, hypothalamus (e.g. the anterior hypothalamic area, the ventro-medial hypothalamus and the zona incerta), as well as in certain brain stem cell groups such as the substantia nigra (pars compacta), locus coeruleus, central grey substance, parabrachial nucleus, sensory and motor nuclei of the trigeminal nerve and the dorsal vagal complex. In the neocortex, highest binding density occurred in layer 4 of all neocortical fields, except in the visual cortex where the highest densities occurred in layers 4cb, 5a and 6. Major fibre tracts such as the fimbria and the stria terminalis also contained high densities of 125I-galanin binding sites. Areas poor in, or lacking, specific 125I-galanin binding sites included the basal ganglia, the thalamus, the mammillary bodies, the cerebellum, and the reticular formation of the brain stem. The pattern of galanin receptor distribution in the monkey brain reported here closely resembles that observed for galanin receptors and galanin-immunoreactive preterminal processes described previously in the rat brain. An exception, however, was neocortex, where in the rat neither 125I-galanin binding nor galanin-positive fibres have been observed. The present findings may indicate a close association between galanin receptors and nerve terminals containing galanin immunoreactivity in the monkey brain and implies important role(s) for galanin in neurotransmission in the monkey central nervous system.

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Nine patients with, and 11 without, venous thromboses (DVT) from two families were studied. In family 1, four members with, and one without, DVT had t-PA activity below the lower limit of the controls (21.3 IU/ml, n = 19) after 20 min venous occlusion (VO). After VO t-PA antigen (t-PA:Ag) was below the lowest value of the controls (22.8 ng/ml) in all five cases with low t-PA activity. All the family members, both with and without thrombosis, had normal t-PA inhibitor activities (PAI). In family 2 t-PA activity after VO was low in three symptomatic and four asymptomatic family members. t-PA:Ag was also low in four of these. PAI level was normal in all but one family member. Mild type I von Willebrand's disease was discovered in four members of family 2. Deficient t-PA:Ag response was found in two of these. Antithrombin III, protein C and protein S were normal in both families. It is concluded that low fibrinolytic capacity, independent of PAI, is associated with familial DVT. Our data suggests autosomal dominant inheritance.

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The relative proportion, ultrastructure and DNA-content of the binucleate cells in the celiac superior mesenteric ganglion of the guinea pig was studied using light and electron microscopy as well as computerized image analysis of Feulgen stained cells. The number of mono - versus binucleate cells was found to vary with stage of development with about 40% of the cells being binucleate in adult animals and 50% in late prenatal stage. No difference in ultrastructure was observed between the nuclei of the two cell types. The binucleate cells contain twice the amount of DNA found in the mononucleate cells.

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Expression and regulation of the catecholamine-synthesizing enzymes phenylethanolamine N-methyltransferase (PNMTase; S-adenosyl-L-methionine:phenylethanolamine N-methyltransferase, EC 2.1.1.28) and tyrosine hydroxylase [TyrOHase; tyrosine 3-monooxygenase, L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] and the coexisting neuropeptide tyrosine (NPY) were studied in rat and bovine adrenal medulla. By using both immunohistochemistry and in situ hybridization, PNMTase- and NPY-positive cells exhibited a close overlap in bovine medulla and were preferentially localized in the outer two-thirds of the medulla. Although TyrOHase and its mRNA were observed in virtually all medullary gland cells, TyrOHase mRNA levels were much higher in the PNMTase- and NPY-positive cells. After administration of the catecholamine-depleting drug reserpine to rats, a brief increase, followed by a dramatic decrease, in the level of PNMTase mRNA was observed in the adrenal medulla. In contrast, mRNA for both TyrOHase and NPY only exhibited an increase, whereby the TyrOHase mRNA peak preceded that of NPY mRNA. Different regulatory mechanisms may thus operate for these three compounds coexisting in the adrenal medulla.

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Cultured human fibroblasts were treated in a controlled, randomized manner to assess the effect of low-energy (0.9 mW) helium-neon (HeNe) laser irradiation on cellular proliferation. Two trials were performed: one with fibroblasts in the third to fourth passage and the other with fibroblasts in the 13th to 14th passage. In each trial, separate plastic petri dishes were inoculated with the cells, maintained in a 5% CO2-95% air atmosphere, and nourished with HB 102 media. Treatment began 48 h after inoculation with daily 60-s irradiations of the "treated" cultures over a 5-d period. Control cultures underwent the same handling but were not irradiated. A significant stimulative, or inhibitive, effect on replication was not found in either trial.

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The adrenal gland of the rat was analysed with immunohistochemistry and antisera to neuropeptide tyrosine, to the catecholamine-synthesizing enzymes tyrosine hydroxylase, phenyl-ethanolamine-N-methyltransferase, and to acetylcholinesterase and with in situ hybridization using a nick-translated 280 base pair deoxyribonucleic acid probe coding for exon 2 of the rat neuropeptide tyrosine gene. Neuropeptide tyrosine-like immunoreactivity was observed in three structures: chromaffin cells, medullary ganglion cells and nerve fibers. The chromaffin cells were of both the noradrenaline- and adrenaline-type. The ganglion cells did not seem to contain any catecholamine-synthesizing enzymes but exhibited a strong immunoreaction for acetylcholinesterase. They were thus in all probability cholinergic neurons. In situ hybridization using the nick-translated deoxyribonucleic acid probe to rat neuropeptide tyrosine messenger ribonucleic acid revealed a very high-grain density over the ganglion cells, a moderate density over the chromaffin cells and a low background over cortex, in agreement with the immuno-histochemical demonstration of neuropeptide tyrosine-like immunoreactivity both in chromaffin and ganglion cells. The intense neuropeptide tyrosine-like immunoreactivity and low content of neuropeptide tyrosine messenger ribonucleic acid suggest that the chromaffin cells have fairly large peptide stores but that the peptide turnover is low. In contrast, the ganglion cell bodies seem to contain low amounts of neuropeptide tyrosine-like immunoreactivity but exhibit a high neuropeptide tyrosine synthesis rate. Preliminary studies with the amine-depleting drug reserpine revealed an increase in messenger ribonucleic acid both in ganglion cells and medullary cells. In the chromaffin cells the highest activity was seen 3 and 4 days after injection, and the levels were down to normal after 8 days. The present findings demonstrate neuropeptide tyrosine synthesis and storage in two cell populations in the adrenal medulla. In situ hybridization with its cellular resolution can provide information on possible differential effects of drugs and experimental procedures on these two neuropeptide tyrosine stores.

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The distribution of binding sites for the neuropeptide cholecystokinin octapeptide in the rat hippocampal region was studied by using quantitative in vitro receptor autoradiography. Biochemical analysis of [3H]cholecystokinin octapeptide binding to tissue sections of the hippocampal region showed it to be of high affinity, to be saturable and approximately 50% specific at saturating concentrations. The binding of [3H]cholecystokinin octapeptide to hippocampal sections was dose-dependently blocked by cholecystokinin octapeptide, cholecystokinin and by pentagastrin. The autoradiographic analysis showed high densities of [3H]cholecystokinin octapeptide binding sites in the hilus of the area dentata, the outer three layers of the retrosplenial area and the presubiculum, layer 3 of the medial, but not the lateral, entorhinal area and the deep and superficial parts of layer 1 and 2, respectively of both the medial and the lateral entorhinal area. Medium binding densities were found in the parasubiculum and remaining layers of the entorhinal area and low densities occurred in the subiculum and in all subfields of Ammon's horn. The angular bundle and fornix-fimbria lacked specific [3H] cholecystokinin octapeptide binding sites. A very similar pattern of binding densities was found for [3H]pentagastrin. Comparisons of the cholecystokinin octapeptide receptor distribution with the cholecystokinin octapeptide innervation of the hippocampal region suggest that there exists a relatively good concordance in some hippocampal subfields such as the presubiculum and the entorhinal area between binding sites for [3H]cholecystokinin octapeptide and cholecystokinin-immunoreactive afferent input.

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The brain and spinal cord of untreated and cysteamine-treated rats were analyzed with immunohistochemistry using antisera raised against somatostatin (SOM)-28(1-14) and SOM-28(15-28). Sections incubated with increasing dilutions of antiserum were evaluated subjectively on coded slides and with computer-assisted image analysis. For control experiments, antisera raised against methionine-enkephalin, neuropeptide Y (NPY) and dynorphin (DYN)(1-13) were used. The latter antiserum does not visualize the conventional DYN systems in the brain, but reacts with an unknown epitope, which here could be shown to be present in SOM neurons. In cysteamine-treated rats a marked decrease in SOM-28(15-28)-like immunoreactivity (1.1) could be recorded subjectively at all antibody concentrations in fibers in several brain areas, including nucleus accumbens, tuberculum olfactorium and the hypothalamic ventromedial and arcuate nuclei. In these areas SOM-LI is fairly weak in untreated rats. In SOM-rich regions such as the median eminence and the dorsal horn of the spinal cord, the depleting effect of cysteamine could be recorded subjectively only when diluted antisera were used. Image analysis confirmed the subjective analysis, and, in addition, differences between controls and cysteamine-treated rats could be shown also at high antiserum concentrations. SOM-28(15-28)-immunoreactive cell bodies could be seen in the brains of either control or drug-treated rats. No effect of cysteamine could be observed when antiserum raised to SOM-28(1-14) was used. Cysteamine did not seem to affect enkephalin-LI, NPY-LI or an epitope in SOM neurons reacting with DYN(1-13) antiserum. After preabsorption of SOM-28(15-28) antiserum with SOM-28(15-28) peptide, the staining patterns described above disappeared completely. However, if the SOM-28(15-28) peptide was pretreated with a high concentration (1 M) of cysteamine before being used for absorption with SOM antiserum, no blocking effect could be observed. The present results demonstrate with immunohistochemistry that cysteamine causes depletion of SOM-28(15-28) in fibers but apparently not in cell bodies. No effects on SOM-28(1-14)-LI were observed. This supports earlier evidence that cysteamine interacts with the disulphide bond in the SOM-28(15-28) molecule. The present results also emphasize that when analyzing drug effects on peptide neurons with immunohistochemical techniques, it is important to use dilution series of antibodies and preferably to carry out the analysis with objective image analysis methods.

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In a randomised multicentre trial a combination of methylprednisolone, vincristine, CCNU, cyclophosphamide and melphalan (MOCCA) was compared with intermittent melphalan and prednisone (MP) as primary treatment in multiple myeloma. In the MP arm the refractory or relapsed patients were treated with regimen MOCCA. The MOCCA arm produced a response rate of 75% among 64 patients and the MP arm a response rate of 54% among 66 patients. The median survival was 41 months in the MOCCA arm and 45 months in the patients primarily randomised to the MP arm. The initial response to MOCCA improved the survival, while this effect was not statistically significant in the MP arm. The results show that the median survival does not increase if aggressive chemotherapy is employed as the first line treatment in multiple myeloma.

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