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Biomedical subjects

C Reichert

Publications and source records attributed to C Reichert.

16 recordsLinked to original sources

Bending-related faulting and mantle serpentinization at the Middle America trench.

The dehydration of subducting oceanic crust and upper mantle has been inferred both to promote the partial melting leading to arc magmatism and to induce intraslab intermediate-depth earthquakes, at depths of 50-300 km. Yet there is still no consensus about how slab hydration occurs or where and how much chemically bound water is stored within the crust and mantle of the incoming plate. Here we document that bending-related faulting of the incoming plate at the Middle America trench creates a pervasive tectonic fabric that cuts across the crust, penetrating deep into the mantle. Faulting is active across the entire ocean trench slope, promoting hydration of the cold crust and upper mantle surrounding these deep active faults. The along-strike length and depth of penetration of these faults are also similar to the dimensions of the rupture area of intermediate-depth earthquakes.

Journal Article↗

Activation of myocardial angiogenesis and upregulation of fibroblast growth factor-2 in transmyocardial-revascularization-treated mice.

OBJECTIVE: To evaluate the growth factor responses associated with myocardial angiogenesis. DESIGN: Mice were treated with transmyocardial revascularization (TMR) and evaluated for angiogenic and growth factor responses. METHODS: TMR was performed via thoractomy with a 27 g needle. At 2, 5, and 7 days post-treatment, hearts were removed from the TMR treated and control groups, then assayed for angiogenesis, fibroblast growth factor (FGF)-2 expression and vascular endothelial cell growth factor (VEGF) expression. RESULTS: TMR caused an angiogenic reaction in the myocardial blood vessels at 7 days post-TMR treatment. Elevated FGF-2 corresponded with increased TMR related angiogenesis. VEGF levels only increased in hearts that were prewounded then TMR treated. CONCLUSIONS: The data show that TMR stimulates myocardial angiogenesis. The angiogenic reaction is mediated by FGF-2 which increased in most experimental treatment groups. The VEGF response was more specific, requiring prewounding then TMR treatment for a VEGF increase.

Animals↗

Failure to transmit disease from gray tremor mutant mice.

Mice homozygous for mutant alleles at the gray tremor (gt) locus develop a marked non-intention tremor beginning at 8 days of age. Most homozygous mice die by 3 months. Homozygotes exhibit intense vacuolation of the central nervous system gray matter and vacuolation and hypomyelination of some white matter tracts. Based on neuropathological similarities with scrapie, other investigators inoculated wild-type mice with gray tremor brain homogenates to test the hypothesis of transmissibility. Published reports indicated that spongiform encephalopathy (R. L. Sidman, H. C. Kinney, and H. O. Sweet, Proc. Natl. Acad. Sci. USA 82:253-257, 1985) and disease, including hind limb paralysis in NFS mice (P. M. Hoffman, R. G. Rohwer, C. MacAuley, J. A. Bilello, J. W. Hartley, and H. C. Morse III, Proc. Natl. Acad. Sci. USA 84:3866-3870, 1987), were transmitted by inoculation of gt/gt brain homogenates. In our hands, however, no NFS/NCr animals inoculated intracerebrally with gt/gt or +/+ brain preparations showed any signs of disease or pathological changes in the brain. Positive transmission by other investigators may reflect the microbiological status of their donor or recipient mice.

Animals↗

The effect of preoperative tranexamic acid on blood loss after cardiac operations in children.

Children undergoing cardiac operations in which cardiopulmonary bypass is used are at risk of significant postoperative blood loss. The acquired coagulopathy is complex but is thought to be due, in part, to excessive fibrinolysis. We examined the possibility of reducing postoperative blood loss in children by using the antifibrinolytic drug tranexamic acid. Using a prospective, randomized, double-blind study design, we administered a single dose of tranexamic acid (50 mg/kg intravenously) or saline placebo, before skin incision, in 88 children undergoing cardiac operations. Post-operative blood loss and fluid replacement were recorded for the next 24 hours. In addition, hemoglobin, platelet counts, and coagulation measures were recorded every 6 hours. When all patients were examined, there was no significant difference in postoperative blood loss between the treated and placebo groups (21.2 +/- 12 ml/kg per 24 hours, tranexamic acid, vs 27.2 +/- 20.3 mls/kg per 24 hours, placebo). However, when the children with cyanosis were analyzed separately, there was a highly significant difference in blood loss between the groups during the first 6 hours (11.2 +/- 3.7 ml/kg per 6 hours, tranexamic acid, vs 27.2 +/- 11.4 mls/kg per 6 hours, placebo; p < 0.002), as well as the overall 24 hour study period (23.7 +/- 7.5 mls/kg per 24 hours, tranexamic acid, vs 48.9 +/- 27.6 mls/kg per 24 hours, placebo; p < 0.02). Also significantly less blood and blood products were administered to the treated cyanosed group. Tranexamic acid produced a significant reduction in postoperative blood loss and blood product requirements in children with cyanosis undergoing heart operations. The drug had no effect in children without cyanosis or those requiring a second thoracotomy.

Adolescent↗

Continuous quality improvement: a perioperative nursing approach.

This article describes in detail the steps taken in the Operating Room at the Toronto Hospital in implementing a Continuous Quality Management framework. Focusing on active participation, all levels of the O.R. staff worked through a process of identifying, developing, measuring and evaluating standards of practice. A step by step framework was followed in order to monitor current standards and develop new ones, thereby complying with the institution's mandate of supporting Continuous Quality Improvement.

Humans↗

[Comparison of a long-acting and short-acting GnRH analog in combination with gonadotropins in in vitro fertilization under various indications].

The occurrence of a premature luteinizing hormone (LH)-surge during gonadotropin stimulation for in-vitro fertilization leads to cancellation of the cycle. Moreover, insufficient follicular maturation is often caused by elevated basal gonadotropin levels. Therefore the gonadotropin releasing hormone (GnRH) agonist, D-TRP6-LHRH, was applied to patients exhibiting premature LH-surges, hyperandrogenemia or incipient premature menopause. 119 cycles were treated, using a long-acting versus a short-acting GnRH agonistic analogue. In protocol 1, patients received daily subcutaneous injections of 100-500 micrograms of a short-acting compound. In protocol 2, a long-acting bolus of 3.2 mg was given intramuscularly. Concomitant human gonadotropin (HMG) stimulation started in protocol 1 after clinical and biochemical evidence of pituitary suppression and in protocol 2 after a fixed suppression interval of 14 days. In protocol 1 higher estrogen levels were reached with more oocytes harvested. The pregnancy rate per transfer was increased from 3.5% to 18%, with most pregnancies occurring with protocol 2. The cancellation rate of 13.4% was mainly due to insufficient follicular development in patients, in whom premature menopause was suspected. Hyper-androgenemic patients with an elevated LH/FSH-ratio exhibited the best follicular recruitment with the highest pregnancy rate of 25% per transfer. Thus combined GnRH-agonist/gonadotropin stimulation offers a causal treatment for patients susceptible to premature LH-surges and for hyperandrogenemic patients.

Adult↗

Monoclonal antibodies against glycophorin A.

Two mouse IgM monoclonal antibodies, 177.1 and 179.3, are directed against glycophorin A, the major sialoglycoprotein of human erythrocytes. Both antibodies agglutinate blood group M and N erythrocytes equally well, both before and after treatment with neuraminidase or trypsin, but fail to agglutinate erythrocytes treated with papain. Antibody 179.3 agglutinates MiVII(K.T.) cells, whose glycophorin A probably contains some alterations in amino acid sequence between residues 46-56, but antibody 177.1 does not agglutinate these cells. Neither antibody agglutinates En(a-)G.W. cells, which lack glycophorin A completely. The hemagglutinating activity of antibody 177.1 is inhibited by purified glycophorin A and its chymotryptic glycopeptides CH1 (amino acid residues 1-64) and CH3 (amino acid residues 35-64), whereas the hemagglutinating activity of 179.3 is inhibited weakly by glycophorin A but not by chymotryptic peptides. These antibodies both are classified as anti-En(a-)FS but apparently bind different epitopes.

Antibodies, Monoclonal↗

Combined GnRH-agonist/gonadotrophin stimulation for in-vitro fertilization.

The occurrence of a premature luteinizing hormone (LH) surge during gonadotrophin stimulation for in-vitro fertilization leads to cancellation of the cycle. Moreover, insufficient follicular maturation is often caused by elevated basal gonadotrophin levels. Therefore, the gonadotrophin-releasing hormone (GnRH) agonist, D-Trp-6-LHRH, was applied to patients exhibiting premature LH surges, hyperandrogenaemia or incipient premature menopause. A total of 119 cycles were treated using a long-acting versus a short-acting GnRH agonistic analogue. In protocol 1, patients received daily s.c. injections of 100-500 micrograms of a short-acting compound. In protocol 2, a long-acting bolus of 3.2 mg was given i.m. Concomitant human gonadotrophin stimulation was started in protocol 1 after clinical and biochemical evidence of pituitary suppression and in protocol 2 after a fixed suppression interval of 14 days. In protocol 1, higher oestrogen levels were reached with more oocytes harvested. The pregnancy rate per transfer was increased from 3.5 to 18%, with most pregnancies occurring with protocol 1. The cancellation rate of 13.4% was mainly due to insufficient follicular development in patients in whom premature menopause was suspected. Hyperandrogenaemic patients with an elevated LH/FSH ratio exhibited the best follicular recruitment with the highest pregnancy rate of 25% per transfer. Thus, combined GnRH-agonist/gonadotrophin stimulation offers a causal treatment for patients susceptible to premature LH surges and for hyperandrogenaemic patients.

Adult↗

Thoracic manifestations of the acquired immune deficiency syndrome.

The acquired immune deficiency syndrome is characterized by the development of multiple recurrent opportunistic infections or unusual neoplasms in individuals with no prior history of immune suppression. This report summarizes the thoracic diseases encountered in such patients before after death and the role of diagnostic techniques currently used in the evaluation of thoracic disease in 15 patients with this syndrome. Efficacy of treatment was determined by correlation with postmortem findings in all patients. Pulmonary disease was present in all 15 patients and necessitated 23 transbronchial biopsies in 11 patients. Pneumocystis carinii pneumonia and cytomegalovirus pneumonia were the most common findings. Nine open lung biopsies in eight patients disclosed either Pneumocystis carinii pneumonia or Kaposi's sarcoma. Esophageal disease was present in four patients, and endoscopic evaluation demonstrated Candida esophagitis (two), esophageal Kaposi's sarcoma (one), and cytomegalovirus esophagitis and Kaposi's sarcoma (one). Mean time to death from diagnosis of acquired immune deficiency syndrome was 7.7 months, with respiratory insufficiency being the most common cause of death (9/15, 60%). Pneumocystis carinii pneumonia was successfully eradicated in 70% of the patients. Candida esophagitis was ameliorated in both patients with the disease. Unsuspected pulmonary Kaposi's sarcoma, cytomegalovirus pneumonitis, and other infectious pathogens were documented at autopsy. These data reveal that Pneumocystis carinii pneumonia and Candida esophagitis can be managed successfully in patients with acquired immune deficiency syndrome if appropriately diagnosed. The major cause of death in this series was pulmonary insufficiency, often the result of severe cytomegalovirus infection. Thoracic surgeons must continue to play an aggressive and important role in the early diagnosis and management of potentially treatable pulmonary and esophageal disease in these patients.

Acquired Immunodeficiency Syndrome↗

Melatonin inhibition and pinealectomy enhancement of 7,12-dimethylbenz(a)anthracene-induced mammary tumors in the rat.

The effects of the pineal hormone, melatonin, and of pinealectomy on the incidence of mammary adenocarcinoma in Sprague-Dawley rats treated with 7,12-dimethylbenz(alpha)-anthracene (DMBA) were investigated. Melatonin (2.5 mg/kg), begun on the same day as DMBA (5 mg) treatment and given daily in the afternoon for 90 days, significantly reduced the incidence of mammary tumors from 79% (control) to 20% (treated) (p less than 0.002). Rats pinealectomized at 20 days of age and treated with 7 mg of DMBA at 50 days of age had a higher incidence of tumors (88%) compared to control animals (22%). Fifteen mg of DMBA, which resulted in a higher incidence of tumors, reduced the difference between pinealectomized and control animals. Melatonin only partially reversed the effects of pinealectomy, reducing the incidence from 87% (pinealectomy alone) to 63% (pinealectomy plus melatonin); however, the tumor incidence was still lower (27%) in nonpinealectomized, melatonin-treated animals. Assessment of plasma prolactin, luteinizing hormone, follicle-stimulating hormone, estradiol, and cortisol in DMBA-treated tumor-free and tumor-bearing animals revealed a significantly lower plasma prolactin concentration [27 +/- 5 (S.E.) ng/ml] in melatonin-treated animals as compared to vehicle-treated animals [65 +/- 8 ng/ml]. The concentration of plasma prolactin was less in melatonin-treated, pinealectomized rats (55 +/- 10 ng/ml) as compared to vehicle-treated, pinealectomized animals (101 +/- 13 ng/ml). Other hormones were not affected by melatonin treatment. These data support the hypothesis that melatonin inhibits the development of DMBA-induced mammary tumors in the rat while removal of the pineal gland stimulates development of such tumors. Additionally, these experiments provide evidence that these effects may be mediated by a suppression of plasma prolactin levels.

9,10-Dimethyl-1,2-benzanthracene↗

Direct cloning of human neuroblastoma cells in soft agar culture.

An in vitro soft agar technique was used in an attempt to culture neuroblastoma cells from 71 bone marrow, 3 lymph node, and 2 solid tumor specimens from 18 patients with neuroblastoma. One-half of each specimen was sent for routine pathology studies and one-half was cultured in the soft agar system. Colonies appeared within 10 days in histologically positive bone marrows. Light microscopy, electron microscopy, catecholamine secretion, and karyology provided evidence that the colonies were composed of neuroblastoma cells. There were 38 instances in which histological study of the specimen demonstrated neuroblastoma cells. The soft agar system showed colony growth in 30 of these samples (79%). There were a total of 38 specimens that were histologically negative for neuroblastoma. Thirty of these 38 specimens showed no growth in the stem cell assay. Eight histologically negative specimens from 6 patients formed colonies in the soft agar system. Five of these 6 patients showed tumor histologically on prior or subsequent marrow examinations. In addition to a significant correlation between histological and soft agar culture results (p < 0.001), there exists a highly significant positive correlation between the number of colonies per plate and the histological status of the specimen (p < 0.005). Serial marrow samples were cultured on 7 patients. There appears to be an association between the number of colonies that develop in the plate and the clinical course and prognosis of the patient. Decreasing plating efficiencies (number of colonies per number of cells plated) correlated with tumor response. Increasing plating efficiencies indicated tumor relapse. A plating efficiency of greater than or equal to 0.1% portended a particularly poor prognosis. Neuroblastoma grows well in this soft agar culture system. This excellent growth provides a good model for both clinical and basic science studies of neuroblastoma.

Abdominal Neoplasms↗

Staurosporine, a protein kinase inhibitor, stimulates cartilage differentiation by embryonic facial mesenchyme.

We have examined the effects of staurosporine, a potent inhibitor of protein kinase C, on cartilage differentiation in cultured mesenchyme of embryonic facial primordia. Mesenchymal cells from the frontonasal, maxillary, and mandibular processes and hyoid arches of stage 24/25 chicken embryos were maintained in high density micromass cell cultures in the presence or absence of 5 nM staurosporine. In cultures of frontonasal and mandibular process mesenchyme, which spontaneously developed numerous chondrogenic cell aggregates, staurosporine treatment enhanced Alcian blue-positive matrix accumulation, increased pericellular sulfated glycosaminoglycan (GAG) deposition by 5.8- and 2.7-fold, respectively, and elevated cytoplasmic levels of cartilage-specific proteoglycan mRNA. In maxillary process mesenchyme, which formed little cartilage matrix under control culture conditions, staurosporine treatment stimulated extensive cartilage nodule formation, promoted a 5.4-fold rise in matrix GAG accumulation, and increased expression of both type II collagen and cartilage proteoglycan mRNA. Moreover, staurosporine treatment initiated chondrocyte differentiation and induced the expression of type II collagen and cartilage proteoglycan gene transcripts in hyoid arch mesenchyme, which exhibited no spontaneous chondrogenesis in control cultures. The results demonstrate that staurosporine promotes cartilage formation in embryonic facial mesenchyme, and suggest the possibility that protein kinase C might function as an inhibitory modulator of chondrocyte differentiation in the neural crest-derived progenitor cells of the embryonic facial skeleton.

Alkaloids↗