Magnetic acupressure for management of postoperative nausea and vomiting: a preliminary study.

BACKGROUND: To assess the efficacy of magnetic acupressure in the prevention of postoperative nausea and vomiting (PONV). METHODS: Fifty-eight patients were included in this randomized, double blind, preliminary prospective study. Thirty-three underwent ear, nose, and throat (ENT) procedures and twenty-five underwent gynaecological procedures. A magnet patch (M) or a placebo patch (P) was applied to patients in each group randomly. The patch was applied 15 min before surgery to P6 a point situated above the wrist, on the medial aspect of the arm between the palmaris longus and flexor carpi radicis (REF point). Anaesthesia was standardized for all patients. Primary study endpoints included PONV scores and number of rescue antiemetic administrations. Secondary endpoints included pain scores, percentage of patients who required rescue analgesics and satisfaction scores. Study variables were measured on arrival in the PACU and 8, 16 and 24 h after surgery. RESULTS: The global incidence of PONV was 50%. We found no significant difference in the incidence of PONV between ENT patients (46%) and gynaecology patients (56%), and no difference between patients who received magnet treatment (47%) and those that did not (54%). Patients receiving the magnet had a similar satisfaction level (75% satisfied) to those receiving placebo (73% satisfied). In addition, magnet-treated patients had similar pain and PONV scores, and a similar percentage of patients in each groups received postoperative rescue analgesics. Finally, there was no difference in the number of rescue antiemetic administrations between the two groups. CONCLUSION: The use of magnetic acupressure as a prophylactic antiemetic treatment prior to ENT or gynaecology surgeries produced no benefit when compared to placebo.

ARP, a peptide derived from the stress-associated acetylcholinesterase variant, has hematopoietic growth promoting activities.

BACKGROUND: Psychological stress induces rapid and long-lasting changes in blood cell composition, implying the existence of stress-induced factors that modulate hematopoiesis. Here we report the involvement of the stress-associated "readthrough" acetylcholinesterase (AChE-R) variant, and its 26 amino acid C-terminal domain (ARP) in hematopoietic stress responses. MATERIALS AND METHODS: We studied the effects of stress, cortisol, antisense oligonucleotides to AChE, and synthetic ARP on peripheral blood cell composition and clonogenic progenitor status in mice under normal and stress conditions, and on purified CD34 cells of human origin. We employed in situ hybridization and immunocytochemical staining to monitor gene expression, and 5-bromo-2-deoxyuridine (BrdU), primary liquid cultures, and clonogenic progenitor assays to correlate AChE-R and ARP with proliferation and differentiation of hematopoietic progenitors. RESULTS: We identified two putative glucocorticoid response elements in the human ACHE gene encoding AChE. In human CD34+ hematopoietic progenitor cells, cortisol elevated AChE-R mRNA levels and promoted hematopoietic expansion. In mice, a small peptide crossreacting with anti-ARP antiserum appeared in serum following forced swim stress. Ex vivo, ARP was more effective than cortisol and equally as effective as stem cell factor in promoting expansion and differentiation of early hematopoietic progenitor cells into myeloid and megakaryocyte lineages. CONCLUSIONS: Our findings attribute a role to AChE-R and ARP in hematopoietic homeostasis following stress, and suggest the use of ARP in clinical settings where ex vivo expansion of progenitor cells is required.

Structural roles of acetylcholinesterase variants in biology and pathology.

Apart from its catalytic function in hydrolyzing acetylcholine, acetylcholinesterase (AChE) affects cell proliferation, differentiation and responses to various insults, including stress. These responses are at least in part specific to the three C-terminal variants of AChE which are produced by alternative splicing of the single ACHE gene. 'Synaptic' AChE-S constitutes the principal multimeric enzyme in brain and muscle; soluble, monomeric 'readthrough' AChE-R appears in embryonic and tumor cells and is induced under psychological, chemical and physical stress; and glypiated dimers of erythrocytic AChE-E associate with red blood cell membranes. We postulate that the homology of AChE to the cell adhesion proteins, gliotactin, glutactin and the neurexins, which have more established functions in nervous system development, is the basis of its morphogenic functions. Competition between AChE variants and their homologs on interactions with the corresponding protein partners would inevitably modify cellular signaling. This can explain why AChE-S exerts process extension from cultured amphibian, avian and mammalian glia and neurons in a manner that is C-terminus-dependent, refractory to several active site inhibitors and, in certain cases, redundant to the function of AChE-like proteins. Structural functions of AChE variants can explain their proliferative and developmental roles in blood, bone, retinal and neuronal cells. Moreover, the association of AChE excess with amyloid plaques in the degenerating human brain and with progressive cognitive and neuromotor deficiencies observed in AChE-transgenic animal models most likely reflects the combined contributions of catalytic and structural roles.

Overexpression of alternative human acetylcholinesterase forms modulates process extensions in cultured glioma cells.

In addition to its well-known synaptic function, acetylcholinesterase was recently shown to stimulate neurite outgrowth from cultured chick neurons in a manner unrelated to its catalytic activity. It remained unclear, however, whether each of the variant acetylcholinesterase enzyme forms can promote such process extension and whether this effect of acetylcholinesterase was limited to neurite outgrowth. Using DNA microinjections and stable transfections of cultured glioma cells, we explored the possibility that specific acetylcholinesterase isoforms affect cellular development and morphology of CNS astrocytes. Cells microinjected with human ACHEDNA constructs that differ in their exon-intron composition displayed rapid yet stable induction of cell body enlargement and process extensions. Cells transfected with ACHEDNA carrying the neuronal-characteristic 3'-E6 domain also displayed stable process extensions. However, stable transfections with ACHEDNAs including the 3'-alternative 14/E5 region induced the appearance of small, round cells in a dominant manner. This was associated with expression of 14/E5-ACHEmRNA transcripts and the production of soluble acetylcholinesterase monomers that were catalytically indistinguishable from the 3'-E6 enzyme but displayed higher electrophoretic mobility than that of the 3'-E6 form. Thus, variable expression levels and alternative splicing modes of the ACHE gene correlated in these experiments with glial development in a manner that was apparently unrelated to catalysis.

[Benefits of perioperative hemodynamic monitoring in coronary patients].

During 1987-1991, 78 coronary patients were admitted to the intensive care unit (ICU) for noncardiac surgery. 40 were under invasive hemodynamic monitoring and treatment before operation (group A) and 38 were only admitted to the ICU postoperatively, since ICU beds were not available before surgery (group B). The overall incidence of the perioperative complications, ischemic heart, myocardial infarction and cardiac arrhythmias was significantly higher in group B than in group A (p < 0.01). 5% of group A and 11% of group B died in the ICU postoperatively. These data indicate the importance of preoperative hemodynamic and cardiac monitoring and treatment in coronary patients.

Expression of three alternative acetylcholinesterase messenger RNAs in human tumor cell lines of different tissue origins.

To study the molecular mechanisms underlying the intensive expression of acetylcholinesterase (AChE) in different tumor types, we characterized levels and composition of its messenger RNA (mRNA) sequences in heterologous tumor cell lines, primary tumor biopsies, and normal fetal and adult tissues and determined their exon-intron origin within the corresponding ACHE gene. Reverse transcription followed by polymerase chain reaction (RT-PCR) revealed three alternatively spliced ACHE mRNAs in NT2/D1 teratocarcinoma, NCI-N-592 small cell lung carcinoma, TE671 medulloblastoma, K-562 erythroleukemia, and 293 transformed embryonal kidney cells. The three ACHE mRNAs include the principal species expressed in brain and muscle and two additional transcripts containing insertions of 751 or 829 residues downstream from the exon 4 domain. The inserted region, which represents an intron in brain and muscle, is expressed in the tumor cell lines either as a "readthrough" form or with 78 residues deleted from its 5' end. A major band of 2.5 kb was labeled with ACHE cDNA in poly(A)+ RNA blots from medulloblastoma cells or brain tissue, whereas a PCR-amplified probe from the inserted domain labeled a 3.4-kb band but not the 2.5-kb band in poly(A)+ RNA from small cell lung carcinoma. The ACHE mRNAs including the alternative insertions were found only in cell lines with levels of the principal ACHE mRNA species equal to or higher than those in brain (1-10 molecules/cell), determined by following the kinetics of mRNA PCR amplification. Genomic DNA sequencing revealed that the inserted domains in the ACHE mRNAs expressed in the tumor cell lines encode C-terminal peptides of 40 and 14 residues. These include a free cysteine, terminate with the consensus HG element, and continue by a 29-residue-long C-terminal hydrophobic cleavable peptide, properties characteristic of precursors to phosphoinositide (PI)-linked proteins. In extension of the reported expression of PI-linked AChE in hemopoietic cells including K-562, our findings demonstrate the existence of ACHE mRNAs with the potential to encode one hydrophilic and two PI-linked forms of AChE in tumor cells from both hemopoietic and nonhemopoietic origins.

Simultaneous bilateral spontaneous pneumothorax: case report.

A 22-year-old previously healthy male was admitted to the emergency department for chest pain and dyspnea of 1-day's duration. He had a history of heavy smoking. The patient was cyanotic, agitated, and severely dyspneic. Lung auscultation revealed severe diffuse bronchospasm and equally diminished breath sounds on both sides. Nasotracheal intubation and mechanical ventilation were performed shortly after admission due to acute respiratory failure. Simultaneous bilateral spontaneous pneumothorax was diagnosed from the chest x-ray, and chest tube drainage was immediately performed bilaterally. Computerized tomography of the chest 1 month later showed diffuse emphysematous bullae of the lungs. The case presented here should increase physicians' awareness of this rare form of spontaneous pneumothorax and its diverse manifestations.

Synoviocytes synthesize, bind, and respond to basic fibroblast growth factor.

Rheumatoid arthritis (RA) is a systemic disease characterized by the destructive proliferation of synovial tissue. It has been suggested that this proliferative lesion resembles a malignancy. Although polypeptide growth factors have been implicated in malignant cell growth, their role in the pathogenesis of proliferative but non-neoplastic diseases such as RA has not been extensively studied. We tested the hypothesis that the synoviocyte itself may be a source of growth factor activity. We demonstrated that culture supernatants from synoviocytes obtained from patients with RA, osteoarthritis, and traumatic joint disease contain mitogenic activity. This activity has biologic properties identical to those of basic fibroblast growth factor (bFGF). Specifically, the mitogenic activity is synergistic with insulin and binds to heparin-agarose, but elutes with 2.0M NaCl. In addition, synoviocyte extracts contain a peptide with a molecular weight of approximately 16,000, which reacts with antibody specific for bFGF. Cultured synoviocytes express the bFGF gene, express receptors for bFGF, and proliferate in response to bFGF. We conclude that bFGF derived from the synoviocytes themselves may play a role in stimulating their proliferation in an autocrine manner in disease states such as RA.

Cell membrane activities and regeneration mechanisms as therapy mediators in moxibustion and acupuncture treatments: theoretical considerations.

Needling by acupuncture or heating by moxibustion, the major Chinese medicine modalities, include tissue destruction or increased permeability of cell membrane. Both action potential activities and the release of cellular metabolites responsible for regeneration occurs. These phenomena are eventually abolished by local and systemic inhibitory elements being metabolites or neurogenic. The inhibitory effect induced by the acupuncture and moxibustion and directed to the manipulation site of these modalities may affect other anatomical sites and reduce or prevent neoplastic growth and neuromuscular or cardiac membrane activity disturbances.

[Decreased bone marrow cellularity and hemosiderin in normal and overtrained runners].

The frequency and significance of decreased bone marrow cellularity (BMC) and bone marrow hemosiderin (BMH), and their possible relations to hemoglobin, iron, iron saturation and serum ferritin levels, were studied in 18 normally trained and 18 overtrained competitive distance runners. Decreased BMC was more pronounced in the overtrained runners: mild to moderate hypocellular marrow was found in 25% of them, and severe hypocellularity in another 25%, as compared to 18% and 3.5%, respectively, in the healthy runners. Increased erythrocyte mean corpuscular volume (greater than 95 mu 3) was found in 24% of the runners, but in only 3.5% of the controls. Decreased BMH was found in both the overtrained (1.3 +/- 2.0 hemosiderin granules per 100 normoblasts) and the controls (1.5 +/- 1.9 granules). There were no significant differences in levels of hemoglobin, mean corpuscular volume and serum iron, iron saturation and ferritin. The decreased BMH in the face of normal hemoglobin and serum iron and ferritin suggests that as a group, competitive distance runners do not suffer from overt iron deficiency but that iron might be stored differently, with a lesser proportion in the bone marrow. The more pronounced decrease in BMH of overtrained distance runners may indicate a possible relationship, and decreased BMC may identify runners who may be becoming overtrained.

Splenic Rupture in Chronic Lymphoid Disorders: Possible Role of Opportunistic Infections.

Two patients with lymphoproliferative disorders, one with chronic lymphocytic leukemia and the other hairy cell leukemia, developed spontaneous rupture of the spleen during the course of their disease. In both cases, this rare complication occurred during systemic atypical infections with Salmonella Dublin and Candida tropicalis respectively. We suggest that severe infection may sometimes play a decisive role in the development of the splenic rupture in some patients who have splenomegaly due to these disorders.

[Mammary tuberculosis mimicking breast cancer].

Breast masses in the 7th decade of life should be considered cancerous and immediate diagnosis and treatment are indicated. Mammary tuberculosis is rare, especially in developed countries. It usually results from reactivation of dormant pulmonary and pleural tuberculous foci. We present a 66-year-old woman who was hospitalized for biopsy of a breast mass. 4 years previously there had been trauma to the chest, and several pleurocenteses were required to remove sterile exudate. The past history, recent immigration from an endemic area, physical examination and chest X-ray, suggested tuberculosis. Needle aspiration of the affected breast yielded M. tuberculosis. Specific therapy and corticosteroids resulted in complete cure.

[Endobronchial tuberculosis].

Endobronchial tuberculosis (EBTB) is not rare. It usually affects the upper lobe bronchi. Bronchoscopic examination may reveal white gelatinous material in the bronchial lumen, mucosal ulcerations, polypoid inflammation, scattered green-blue pigmented areas and narrowed bronchi with post-stenotic dilatation, some of which resemble colored dolomite caves. 2 women, aged 70 and 84, are presented, 1 of whom had been suffering for a year from persistent dry cough and the other from diffuse pneumonia resistant to several antibiotics. Fibreoptic bronchoscopy showed the characteristic picture of EBTB, later confirmed by positive cultures. Recognition of the clinical, radiological and bronchoscopic spectrum of EBTB makes it possible to start treatment before bacteriological diagnosis of tuberculosis from endoscopically recovered material.

Differential expression of mRNA coding for heparin-binding growth factor type 2 in human cells.

The proliferation of normal human fibroblasts, keratinocytes, and melanocytes in vitro can be controlled by purified polypeptide growth factors and serum. We have studied the cellular expression of the heparin-binding growth factor type 2/basic fibroblast growth factor (HBGF-2/bFGF) gene to determine whether these cell types synthesize mRNA for this mitogen. Our results indicate that normal human fibroblasts synthesize four distinct mRNAs of 7.0, 3.7, 2.2, and 1.5 kilobases, which hybridize to a specific HBGF-2/bFGF cDNA probe. In fibroblasts, the level of all four of these transcripts increases dramatically (more than tenfold) within 4 hours of treatment of quiescent cells with fresh fetal bovine serum. Of the purified growth factors tested, transforming growth factor type-beta also increased HBGF-2/bFGF mRNA abundance, but not to the levels attained by serum treatment. Treatment of fibroblasts with cycloheximide before and during serum treatment blocked the ability of serum to induce the expression of the HBGF-2/bFGF gene. The gene is expressed at low levels in human fibroblasts rapidly growing in serum-free medium and at higher levels in cells rapidly growing in serum-containing medium. In contrast to fibroblasts, mRNA coding for HBGF-2/bFGF is undetectable in proliferating normal human keratinocytes, melanocytes, or mammary epithelial cells. Because keratinocytes and melanocytes proliferate in response to purified HBGF-2/bFGF, our results suggest that HBGF-2/bFGF may mediate the proliferation of epidermal cells through paracrine mechanisms involving stromal fibroblasts. Moreover, we have shown that a human squamous cell carcinoma cell line (SCC-25) expresses mRNA coding for HBGF-2/bFGF, suggesting that the gene may become activated in some carcinomas.

Immunocytochemistry of the estrogen receptor in spontaneous endometriosis in rhesus macaques.

Immunocytochemical, biochemical, and histologic analysis of endometriotic lesions and endometria from rhesus macaques with endometriosis revealed several distinctions between ectopic and eutopic endometrium. In lesions, unlike endometrium, neither the mean percentages of estrogen receptor positive (ER+) cells nor the total ER content changed significantly during the menstrual cycle. In eutopic endometria, ER staining in both stromal and epithelial cells increased and decreased synchronously during the cycle, but in endometriotic lesions, such synchrony was lacking. Moreover, in lesions, unlike endometria, the percentage of ER+ cells was low in the stroma and highly variable in epithelium throughout the cycle. These data, taken together, indicate a defect in the hormonal regulation of ER in endometriotic lesions of monkeys.

Serratia marcescens infected silk suture rejected by combined acupuncture, moxibustion and low-power laser therapy from the abdominal fascia.

Upper abdominal pains lasting 12 years after cholecystectomy, were improved in an 82-year-old woman following the rejection of indigestable silk surgical sutures induced by combined therapy of acupuncture, moxibustion and low-power laser beam irradiation directed to an old post-cholecystectomy scar. An inflammatory reaction followed by granulation tissue mass was developed. Embedded in the granulation tissue were the above mentioned silk sutures which finally were expelled through the skin at the operation scar. A surgical procedure suggested to the patient, in case of acupuncture therapy failure, was obviously avoided. Serratia-marcescens infection of the expelled material was bacteriologically defined.

Sheep bronchoalveolar carcinoma: tissue associated protein complex (TAPC) in normal lung tissue and in the tumor differed quantitatively.

Sheep lungs experimentally and naturally affected by bronchoalveolar carcinoma were washed out exhaustively of soluble components by phosphate-buffered saline, pH 7.4 (PBS), followed by glycine buffer, pH 2.8 (GB), and then again by 1M KCl followed by PBS. The tissue matrix (TM) of the tumor-free region and the tumor-affected tissue were analysed separately by sodium dodecyl sulfate (SDS) polyacrylamide electrophoresis. Normal lung tissues obtained from normal sheep served as controls. Several protein fractions and fragments, identified in both the normal and the tumorous lung, have the molecular weight (MW) of 130,000-228,000, as compared with the major soluble tissue associated protein having MW of 70,000. Coomassie blue staining used in the SDS polyacrylamide system and alkaline phosphatase immunoreaction used in the Enzyme Linked Immunosorbant Assay (ELISA) showed tenfold increased concentration of the TAPC in the TM of the tumor tissue and in the blood of tumor-affected animals, respectively. Total concentration of the TAPC in the serum of tumor-affected animals was higher than in the normal. Immunofluorescent antibody test (IAT) detected the TAPC in the cytoplasm of tumor as well as in normal lung cells, and the study suggested that the TAPC reaches the peripheral blood during tissue destruction occurring at the tumor site, as observed by light and electron microscopy (LM and EM). The concentration of each of the TAPC fractions was higher in the tumor-affected sheep lung as compared with normal sheep lung. Antibodies prepared against the TAPC fractions were toxic to sheep lung cells in tissue culture. Tumor cells were more susceptible.

Immunocytochemistry versus binding assays of the estrogen receptor in the reproductive tract of spayed and hormone-treated macaques.

We used immunocytochemistry (ICC) with monoclonal antibodies to the estrogen receptor (ER) to localize ER in the oviducts, uteri, and cervix of untreated, estrogen-treated, and estrogen-progestin-treated spayed macaques. We also used binding assays with labeled estrogens to quantify nuclear and cytosolic ER levels in parallel samples of the same tissues. In untreated spayed animals, cytosolic ER levels were much higher than nuclear ER levels, but all specific staining was nuclear. After treatment for 14 days with estradiol (E2), the degree of staining for ER in cell nuclei in the oviduct, cervix, and endometrium had increased, and there were significant increases in both nuclear and cytosolic ER levels. In the myometrium, ER levels and ICC staining of nuclei increased minimally with E2 treatment. In animals treated for 2 weeks with E2 followed by 2 weeks with E2 and progesterone (P; sequential P treatment) the degree of nuclear ER staining in the oviduct, endometrium, and cervix greatly decreased, and cytosolic and nuclear levels of ER declined significantly. In the myometrium of such animals there was a minimal decrease in the degree of staining and a nonsignificant decline in cytosolic and nuclear ER levels. Sequential P treatment reduced the degree of nuclear staining in the oviduct and endometrium below that found in spayed animals; however, such treatment only lowered the amount of cytosolic, not nuclear, ER significantly below spayed levels in those same tissues. Some animals were treated sequentially with P and sampled 1, 3, 12, and 24 h after the onset of P treatment. By 1 h, nuclear ER levels in the endometrium were significantly suppressed, but cytosolic levels were not lowered until 3 h of treatment; ICC staining was also not substantially reduced until 3 h of P treatment. In the oviduct, nuclear ER levels were significantly reduced by 1 h of P treatment, but cytosolic levels were not lowered until after 12-24 h of P treatment; the degree of nuclear staining in the oviduct was also not substantially reduced until 12-24 h of P treatment. In myometrium, there was no significant decline in ER in nuclear or cytosolic fractions or any substantial decrease in the degree of nuclear staining at any time during this treatment. These observations suggest that the ER detected by ICC in the nuclei of target cells in frozen sections represents the total ER detectable by binding assays in cytosolic and nuclear fractions.(ABSTRACT TRUNCATED AT 400 WORDS)