bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Artificial Organ Museum in Cleveland (1979–1999) Moved to Houston, Texas, and Named in 2002 as the ICMT Museum for Artificial Organs
Authors: Nosé Yukihiko 
Published: August 2003

Abstract: The artificial organ museum established in Cleveland, Ohio, in 1979 organized by the International Center for Artificial Organs and Transplantation (ICAOT), was moved to Houston, Texas, in 1999. The museum with expanded and renewed artificial organ exhibits was officially opened on the 8th and 9th of November, 2002, at the Cullen Pavilion of the original Memorial Hermann Hospital. This building is the oldest in the Texas Medical Center, which was built in 1922.The ICMT (International Center for Medical Technologies) Museum for Artificial Organs (Museum) was completed after phase I, II, and III expansions of the exhibit booths, which were made over the last two years. Approximately 250 historically important and currently widely used artificial organs are exhibited in the Museum. The official opening of the Museum was coordinated with the “Symposium on Artificial Organs: Past, Present, and Future” during two days in November. There were approximately 225 participants at these events, and approximately 40 pioneers and clinical experts in the development and practice of various types of artificial organs contributed. During these programs, a proposal to maintain human resources in addition to artificial organ hardware and software was made in addition to the Museum. This new organization would be called the International Academy of Artificial Organ Pioneers (Academy). All contributors to the symposium were invited to be members of the Academy. The attendants of the symposium accepted this proposal unanimously. An additional 40 individuals, who were recognized as contributors to artificial organ technologies, were later added to the original Academy members.Later, the effective utilization of the Museum and Academy was encompassed in the International Faculty for Health and Medical Technologies (Faculty), a new addition to the activities of the ICMT. Dr. Michael DeBakey was elected as Dean of the Faculty. This is considered a “university without walls,” a “university linked to the world,” and a “university providing simultaneous teaching at multiple sites”—a completely new concept in teaching tools for medical technologies.All of these subsidiary organizations of the ICMT were legally included as nonprofit, nontaxable charity organizations of the state of Texas.
Artificial Organs versus Regenerative Medicine: Is It True?
Authors: Nosé Yukihiko , Okubo Hisashi 
Published: August 2003

Abstract: Individuals engaged in the fields of artificial kidney and artificial heart have often mistakenly stated that “the era of artificial organs is over; regenerative medicine is the future.” Contrarily, we do not believe artificial organs and regenerative medicine are different medical technologies. As a matter of fact, artificial organs developed during the last 50 years have been used as a bridge to regeneration. The only difference between regenerative medicine and artificial organs is that artificial organs for the bridge to regeneration promote tissue regeneration in situ, instead of outside the body (for example, vascular prostheses, neuroprostheses, bladder substitutes, skin prostheses, bone prostheses, cartilage prostheses, ligament prostheses, etc.). All of these artificial organs are successful because tissue regeneration over a man‐made prosthesis is established inside the patient's body (artificial organs to support regeneration).Another usage of the group of artificial organs for the bridge to regeneration is to sustain the functions of the patient's diseased organs during the regeneration process of the body's healthy tissues and/or organs. This particular group includes artificial kidney, hepatic assist, respiratory assist, and circulatory assist. Proof of regeneration of these healthy tissues and/or organs is demonstrated in the short‐term recovery of end‐stage organ failure patients (artificial organs for bridge to regeneration).A third group of artificial organs for the bridge to regeneration accelerates the regenerating process of the patient's healthy tissues and organs. This group includes neurostimulators, artificial blood (red cells) blood oxygenators, and plasmapheresis devices, including hemodiafiltrators. So‐called “therapeutic artificial organs” fall into this category (artificial organs to accelerate regeneration).Thus, almost all of today's artificial organs are useful in the bridge to regeneration of healthy natural tissues and organs. It does not matter whether these tissues are cultivated inside or outside the patient's body. Thus, we strongly believe in the need for joint development programs between artificial organ technologies and regenerative medicine technologies. In particular, the importance of using both man‐made substitute organ technologies and natural tissue‐derived substitute organ technologies is stressed for improved medical care in the future.
Cultural variation in young children’s access to work or involvement in specialised child-focused activities
Authors: Morelli Gilda A. , Rogoff Barbara , Angelillo Cathy 
Published: August 2003

Ethnographic literature indicates that in many cultural communities around the world, children have extensive opportunities to learn through observing and participating in their community’s work and other mature activities. We argue that in communities in which children are often segregated from adult work (as in middle-class European American communities), young children instead are often involved in specialised child-focused activities such as lessons, adult–child play (and scholastic play), and conversation with adults on child-related topics. We examine this argument with systematic time-sampled observations of the extent of 2- to 3-year-old children’s access to adult work compared to their involvement in specialised child-focused activities. Observations focused on 12 children in each of four communities: two middle-class European American communities (West Newton, Massachusetts and Sugarhouse, Utah), Efe foragers of the Democratic Republic of Congo, and indigenous Maya of San Pedro, Guatemala. West Newton and Sugarhouse children had less frequent access to work and were involved more often in specialised child-focused activities than Efe and San Pedro children. The results support the idea that the middle-class European American children’s frequent involvement in specialised child-focused activities may relate to their more limited opportunities to learn through observing work activities of their communities. It may be less necessary for the Efe and San Pedro children to be involved in specialised child-focused activities to prepare them for involvement in mature community practices, because they are already a regular part of them.
Characterization of the growth‐inhibitory and apoptosis‐inducing activities of a triterpene saponin, securioside B against BAC1.2F5 macrophages
Authors: Yui Satoru , Kudo Tomoya , Hodono Kazumi , Mimaki Yoshihiro , Kuroda Minpei , Sashida Yutaka , Yamazaki Masatoshi 
Published: August 2003

Background: Since the growth state of macrophages in local pathological sites is considered a factor that regulates the processes of many disease, such as tumors, inflammation, and atherosclerosis, the substances that regulate macrophage growth or survival may be useful for disease control. We previously reported that securiosides A and B, novel triterpene saponins, exerted macrophage‐oriented cytotoxicity in the presence of a L‐cell‐conditioned medium containing macrophage colony‐stimulating factor (M‐CSF), while the compounds did not exhibit an effect on macrophages in the absence of the growth‐stimulating factors.Aim: This study was undertaken to characterize the growth‐inhibitory and the apoptosis‐inducing activities of securioside B, focusing on the effects of the macrophage‐growth factor(s), and to examine the implication of a mitochondria pathway in apoptosis induction.Methods: The effect of securioside B on a murine macrophage cell line (BAC1.2F5) was examined by MTT assay and lactose dehydrogenase release assay in the presence of L‐cell‐conditioned medium, M‐CSF, or granulocyte‐macrophage CSF (GM‐CSF).Results: Securioside B inhibited the growth of the cells stimulated by recombinant M‐CSF or GM‐CSF, but it scarcely induced cytolysis of the cells under the same conditions. Moreover, securioside B did not induce cell death when the compound only was added to the cells. On the other hand, the compound extensively induced apoptotic cell death in the presence of L‐cell‐conditioned medium, suggesting that apoptosis induction by securioside B requires the additional factor(s) present in L‐cell‐conditioned medium. Securioside B plus L‐cell‐conditioned medium induced the activation of caspase‐3 and caspase‐9, but not caspase‐8. In addition, cytochrome c release from the mitochondria into the cytosol, and disrupted mitochondria membrane potential, was also observed in the apoptotic BAC1.2F5 cells.Conclusion: These data suggest that securioside B has growth‐inhibitory activity against growth factor‐stimulated macrophages, and that it induces apoptotic macrophage death through the activation of a mitochondrial pathway in the presence of L‐cell‐conditioned medium.
Role of interleukin‐15 and interleukin‐18 in the secretion of sIL‐6R and sgp130 by human neutrophils
Authors: Jablonska E. , Marcinczyk M. 
Published: August 2003

Background: Available data indicate that neutrophils (PMN) produce a wide range of cytokines with the potential to modulate immune response. Recent investigation have shown that interleukin (IL)‐15 and IL‐18 potentiated several functions of normal neutrophils. It has been reported that IL‐18‐induced cytokine production may be significantly enhanced by coincident addition of IL‐15.Aims: In the present study we compared the effect of recombinant human (rh)IL‐15 and rhIL‐18 as well as effect of a rhIL‐15 and rhIL‐18 combination on the induction secretion of sIL‐6Rα and sgp130 by human neutrophils. Methods: PMN were isolated from heparinized whole blood of healthy persons. The PMN were cultured for 18 h at 37°C in a humidified incubator with 5% CO2. rhIL‐15 and/or rhIL‐18 and lipopolysaccharide were tested to PMN stimulation. The culture supernatants of PMN were removed and examined for the presence of sIL‐6R and sgp130 by human enzyme‐linked immunosorbent assay kits. Cytoplasmic protein fractions of PMN were analysed for the presence of sIL‐6R and sgp130 by western blotting using monoclonal antibodies capable of detecting these proteins. Cells were lysed and cytoplasmic proteins were electrophoresed on sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. The resolved proteins were transferred onto nitrocellulose and incubated with the primary monoclonal antibodies anti‐sIL‐6R and anti‐sgp130. The membranes were incubated at room temperature with alkaline phosphatase anti‐mouse immunoglobulin G. Immunoreactive protein bans were visualized by an AP Conjugate Substrate Kit.Results and conclusion:The results of our investigation revealed that IL‐15 alone, similarly to IL‐18, has no significant ability for the regulation of both soluble IL‐6 receptors, sIL‐6R and sgp130, released by human neutrophils. It is interesting to note that the secretion of sgp130 was changed after PMN stimulation with rhIL‐15 in the presence of rhIL‐18. The combination of rhIL‐15 and rhIL‐18 was shown to induce PMN to secretion relatively higher amounts of sgp130 compared with the stimulation of PMN with rhIL‐15 alone and rhIL‐18 alone. The results obtained suggest that IL‐15 and IL‐18, belonging to the inflammatory cytokines, through the regulation of sgp130 secretion must be also considered as anti‐inflammatory mediators that may influence the balance reactions mediated by the IL‐6 cytokine family.
Cytokine soluble receptors in perinatal and early neonatal life
Authors: Protonotariou Efthimia , Rizos Demetrios , Malamitsi-puchner Ariadne , Moira Evangelia , Sarandakou Angeliki , Salamalekis Emmanuil 
Published: August 2003

Background: In contrast to cellular receptors, soluble receptors do not enhance the cellular activation because they do not have transmembranic and cytoplasmic parts, acting thereby as endogenous regulatory mechanisms against systemic functions of cytokines.Aim: To measure serum concentrations of the soluble interleukin‐2 receptor (sIL2R), soluble interleukin‐4 receptor (sIL4R), soluble interleukin‐6 receptor (sIL6R), and soluble tumor necrosis factor‐α receptor I and soluble tumor necrosis factor‐α receptor II, during the perinatal and early neonatal period, in order to evaluate their role in activation of immune response in labor and the first days postpartum.Methods: Soluble receptor serum concentrations were determined by enzyme‐linked immunosorbent assay, in 45 healthy, full‐termed neonates during the first and fifth days after birth, in 25 of their mothers (MS), in 25 samples of umbilical cords (UC) and in 25 healthy adult donors age‐matched with the mothers (controls).Results: Soluble receptor serum concentrations showed considerable changes during labor and early neonatal life, being significantly higher both in MS (except sIL6R) and in neonatal sample UC, first and fifth days after birth, compared with controls (P < 0.0001). Neonatal serum sIL2R and sIL6R increased significantly from birth to the fifth day, while the remaining receptors showed a rapid increase in the first day (P < 0.0001), declining significantly thereafter (P < 0.0001).Conclusion: Our findings suggest that the elevated concentrations of all studied soluble cytokine receptors reflect the activation of immune response, and represent also regulatory protective mechanisms for mother and fetus‐neonate against the systemic function of cytokines during labor and early neonatal life.
Altered Affinity Maturation in Primary Response to (4‐hydroxy‐3‐nitrophenyl) Acetyl (NP) after Autologous Reconstitution of Irradiated C57BL/6 Mice
Authors: De Trez Carl , Van Acker Annette , Vansanten Georgette , Urbain Jacques , Brait Maryse 
Published: August 2003

Immune responses developing in irradiated environment are profoundly altered. The memory anti‐arsonate response of A/J mice is dominated by a major clonotype encoded by a single gene segment combination called CRIA. In irradiated and autoreconstituted A/J mice, the level of anti‐ARS antibodies upon secondary immunization is normal but devoid of CRIA antibodies. The affinity maturation process and the somatic mutation frequency are reduced. Isotype switching and development of germinal centers (GC) are delayed.The primary antibody response of C57BL/6 mice to the hapten (4‐hydroxy‐3‐nitrophenyl) acetyl
(NP)‐Keyhole Limpet Hemocyanin (KLH) is dominated by antibodies encoded by a family of closely
related VH genes associated with the expression of the λ1 light chain.We investigated the anti‐NP
primary response in irradiated and autoreconstituted C57BL/6 mice. We observed some splenic
alterations as previously described in the irradiated A/J model. Germinal center reaction is delayed
although the extrafollicular foci appearance is unchanged. Irradiated C57BL/6 mice are able to mount
a primary anti‐NP response dominated by λ1 positive antibodies but fail to produce high affinity
NP‐binding IgGl antibodies. Following a second antigenic challenge, irradiated mice develop enlarged
GC and foci. Furthermore, higher affinity NP‐binding IgG1 antibodies are detected.
Alcohol misuse and renal damage
Authors: CECCHIN EMANUELA , DE MARCHI SERGIO 
Published: August 2003

AbstractRecent clinical and experimental studies have demonstrated that the habitual consumption of large amounts of ethanol has deleterious effects on the kidney. A variety of tubular defects have been described in patients with chronic alcoholism. Evidence is emerging that tubular dysfunction has an important pathophysiological role in a wide range of electrolyte and acid‐base disturbances commonly observed in these patients, and possibly in alcohol‐induced bone disease. These renal abnormalities are often reversible, disappearing with abstinence. However, since 1990 a few cases of a syndrome of acute tubular necrosis due to binge drinking of ethanol in the absence of other evident nephrotoxic mechanisms, or in association with the use of nonsteroidal anti‐inflammatory drugs, have been reported. A link between glomerulonephritis and alcoholism has become evident. IgA nephropathy has been demonstrated at autopsy in 64% of chronic alcoholics and, more recently, the association between alcoholism and postinfectious glomerulonephritis has been described. Structural and functional abnormalities of the kidney are reported with increasing frequency in the fetal alcohol syndrome seen in children who have been prenatally exposed to ethanol. In addition, over the last few years experimental studies in vitro or in animal models have provided information about the biochemical and molecular basis of alcohol‐induced injury to kidney. It is hoped that future experimental and clinical research will provide us with a more comprehensive knowledge of the mechanisms of renal damage in alcohol misuse.
The μ opioid receptor: from molecular cloning to functional studies
Authors: YU LEI 
Published: August 2003

AbstractOpioids have been used and abused by humans for centuries. The μ opioid receptor represents the high affinity binding site for opioid narcotics with high abuse liability such as morphine, codeine and fentanyl. Heroin (diacetylmorphine), a semi‐synthetic derivative of morphine, crosses the blood‐brain barrier more readily than morphine due to its increased hydrophobicity. Once in the brain heroin is hydrolyzed to morphine, which acts at the μ opioid receptor and results in euphoria, thus conferring the reinforcing properties of heroin. Using molecular biology techniques, the μ opioid receptors from several species have been cloned. This article reviews recent progress in this area, with respect to the two major cellular functions of the μ opioid receptor: reduction of intracellular cAMP concentration by inhibiting adenylyl cyclase activity, and inhibition of neuronal firing by modulating membrane ion channels.
Cocaine and cardiovascular toxicity
Authors: SCHINDLER CHARLES 
Published: August 2003

AbstractOver the past 10 years a great deal has been learned about the cardiovascular effects of cocaine. In particular, the acute effects of cocaine have been studied extensively. Upon acute administration cocaine increases blood pressure and heart rate, primarily through an action on the sympathetic nervous system. Cocaine also suppresses the baroreflex response and vagal tone, further contributing to its effects on heart rate. At the same time cocaine is increasing the work‐load on the heart it induces coronary artery vasoconstriction, potentially leading to cardiac ischemia. At higher doses cocaine can depress ventricular function and slow electrical conduction in the heart. Both these effects appear to be mediated by cocaine's local anesthetic action. The effects of cocaine mediated by the sympathetic nervous system are greatly reduced in anesthetized animals. Further, when cocaine is administered repeatedly over a short period of time, acute tolerance can develop to the sympathomimetic effects of cocaine. In contrast, the effects of cocaine mediated by its local anesthetic action do not appear blunted by anesthesia or susceptible to acute tolerance. With chronic administration, higher doses appear to induce tolerance while lower doses may induce sensitization to cocaine's sympathomimetic effects. Cocaine also induces a variety of pathological changes in the heart, including myocardial contraction band necrosis and ventricular hypertrophy. These effects of cocaine on the heart can all contribute to potentially lethal cardiovascular events. In addition to the effects of cocaine alone, the metabolites of cocaine may also contribute to cocaine's cardiovascular toxicity, and both licit and illicit drugs used in combination with cocaine might potentially alter its cardiovascular effects.
Functional coupling of a μ opioid receptor to G proteins and adenylyl cyclase: modulation by chronic morphine treatment
Authors: CHEN YAN , LIU JIAN , YU LEI 
Published: August 2003

AbstractA cloned μ opioid receptor was used to study its coupling to signal transduction pathways and its involvement in morphine‐induced opioid dependence in stably transfected Chinese hamster ovary (CHO) cells. Membrane binding assays with a μ‐selective agonist [3 H]DAMGO showed that one cell line expresses a high level of μ opioid receptors with a B max of ∼ 630 fmol/mg membrane protein and a K d of 0.47 nM for DAMGO. Stimulation of the transfected cells with DAMGO led to an increase in the low K m GTPase activity, indicative of activation of guanine nucleotide regulatory proteins (G proteins), and this effect was blocked by the opioid antagonist naloxone. In addition, binding of the μ opioid receptor to DAMGO was affected by GTP and nonhydrolizable GTP analogs, Gp(NH)pp and GTP‐γ‐S. These results suggest a functional coupling between the μ opioid receptor and G proteins. Furthermore, DAMGO treatment of the cells produced a dose‐dependent inhibition of the intracellular cyclic adenosine monophosphate (cAMP) level, with an EC 50 value of approximately 30 nM. Chronic treatment of the cells with morphine not only elevated the basal and forskolin‐stimulated cAMP levels after morphine withdrawal, but also increased the extent of the DAMGO‐induced reduction of intracellular cAMP levels. The whole cell binding assay with [3 H]DAMGO, on the other hand, did not detect receptor down‐regulation after chronic morphine treatment. These results suggest that chronic morphine treatment may trigger a compensatory mechanism in cellular signaling pathways to offset the inhibitory input from the μ receptor without down‐regulation of the surface receptor number, and that withdrawal of chronic inhibition leads to elevated activities of adenylyl cyclase to provide a basis for system sensitization.
Alcohol and glucose metabolism in skeletal muscles in the rat
Authors: XU DAN , DHILLON AMARDEEP , DAVEY CHRISTOPHER , FOURNIER PAUL , PALMER T. NORMAN 
Published: August 2003

AbstractEthanol is known to cause an acute and profound insulin resistance in man and the rat primarily via effects on glucose utilization. This paper examines the nature of these inhibitory effects on whole‐body glucose utilization using the euglycaemic hyperinsulinaemic clamp in the conscious unrestrained rat. We confirm that ethanol infusion causes an acute insulin resistance, the rate of glucose infusion required to maintain euglycaemia (GIR) being decreased markedly by ethanol. To ensure that the GIR is a measure of whole‐body glucose disposal, glucose turnover and hepatic glycogen levels were measured. These studies showed that ethanol totally suppressed hepatic glucose production. The reduction in GIR is associated with marked decreases in glucose uptake and glycogen synthesis in most skeletal muscles. In oxidative but not in non‐oxidative muscles, the activation of glycogen synthase in response to insulin was decreased by ethanol, suggesting that a defect in glycogen synthase activation may be responsible for the decrease in glycogen synthesis. The basis of the inhibitory effects of ethanol on insulin‐stimulated glucose metabolism in muscle is unknown, but may involve membrane‐associated impairments in insulin signalling and/or the glucose transport system.