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PubMed1997

Coxsackievirus-induced chronic inflammatory myopathy: virus variants distinguish between acute cytopathic effects and pathogenesis of chronic disease.

Infection with the Tucson strain of coxsackievirus B1 (CVB1T) causes the development of chronic inflammatory myopathy (CIM) and hind limb weakness in susceptible strains of mice. In this study, a panel of six plaque-purified viruses exhibiting either small or large plaque phenotypes was derived from parental CVB1T and parental CVB1T that had been passaged through monkey kidney cells. All six variants caused similar acute histopathology in muscle, but three of four passaged viruses (AMP1, AMP2, and AMP3) did not induce CIM while the fourth (MP3) caused some hind limb weakness but without associated muscle inflammation. In contrast, both viruses (MP1 and MP2) isolated directly from the parental CVB1T stock were myopathic. Large plaque MP2 caused higher mortality and more rapid inhibition of host cell biosynthesis, but both MP1 and MP2 induced CIM that was comparable to that induced by parental CVB1T. Plaque size was a stable characteristic of the variants but did not correlate with their ability to induce CIM. Five of the six variants showed equivalent levels of replication in muscle, monkey kidney cells, and GB myoblasts while one, AMP3, was selectively impaired for replication. Receptor binding and virus-induced inhibition of host cell transcription and translation were not linked to myopathogenicity. Thus, most of the passaged variants are robust infectious viruses, suggesting that viral induction of CIM does not depend solely on cytopathogenicity during the acute infection.

Animals↗
PubMed2006

Difference of gene expression profiles between Barrett's esophagus and cardia intestinal metaplasia by gene chip.

The difference of gene expression profile changes in Barrett's esophagus (BE) and cardia intestinal metaplasia (CIM) epithelium was studied and the novel associated genes were screened in the early stage by cDNA microarray. The cDNA retro-transcribed from equal quantity mRNA from BE and CIM epithelial tissues were labeled with Cy3 and Cy5 fluorescence as probes. The mixed probe was hybridized with three pieces BiostarH-40s double dot human whole gene chip. The chips were scanned with a ScanArray 4000. The acquired images were analyzed using GenePix Pro 3.0 software. It was found a total of 141 genes were screened out that exhibited differentially expression more than 2 times in all three chips. It was identified that in gene expression profiles of BE, 74 genes were up-regulated and 67 down-regulated as compared with CIM. The comparison between the difference of gene expression profile changes in BE and CIM epithelia revealed that there existed the difference between BE and CIM at gene level. 141 genes with the expression more than two time were probably related to the occurrence and development of BE and the promotion or progress in adenocarcinoma.

Barrett Esophagus↗
PubMed2006

[Critical illness myopathy in intensive care patients. Pathogenetic concepts and clinical management].

Intensive care patients are at increased risk of developing sepsis with multi-organ failure during treatment (severe sepsis) possibly leading to complications of the central and peripheral nervous system. Among these, septic encephalopathy, critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) are the most important. Neuromuscular complications in particular are difficult to diagnose as they mostly become apparent only when sedation has ceased and the awakening patient experiences difficulties in weaning from the respirator and reduced voluntary strength. CIP and CIM are generally self-limiting, however, they greatly prolong ICU stay and rehabilitation, thus nowadays also imposing a real budget threat. The diagnostics, especially the differentiation between CIM and CIP is difficult and a multi-disciplinary approach involving ICU physicians, anesthetists and neurologists is needed. Our knowledge of the causes of the primary ICU myopathy, although rapidly evolving during recent years, is still in its infancy and specific treatment of CIM is not yet available. The present overview summarizes insights into clinical and new diagnostic strategies for early detection of neuromuscular dysfunction in ICU patients. This article focuses on current concepts and results revealing the pathomechanism(s) of CIM and some simple therapeutic or preventive measures have been deduced which are summarized and discussed.

Anti-Inflammatory Agents↗
PubMed1983

Effects of the chronic ingestion of therapeutic doses of chlorimipramine on the behavioral action of agonists and antagonists of serotonin in male rats.

Locomotor activity and hole-board exploration (frequency and time spent head-dipping) were impaired in male rats by injecting IP the 5-HT agonists, fluoxetine and 5-HTP. This treatment produced also myoclonus and increased the time spent resting during trials. The chronic ingestion of chlorimipramine (CIM) or the injection of the 5-HT receptor blocker, methysergide (15 mg/kg) prevented the action of the 5-HT agonists on locomotion and resting and blocked the appearance of myoclonus. Both CIM and methysergide prevented to a minor degree the fluoxetine-5-HTP-induced decrease of exploration. The chronic ingestion of CIM clearly potentiated the effects of methysergide on hole-board exploration. Results suggest that the chronic treatment with therapeutic doses of CIM reduces the functional activity of some 5-HT systems in the brain of the rat, probably by blockade of post-synaptic 5-HT receptors. This does not preclude, however, that CIM may also alter some NA systems.

5-Hydroxytryptophan↗
PubMed1987

A cardioinhibitory area in the midbrain central tegmental field of cats.

A cardioinhibitory area in the central tegmental field of the midbrain (CIM) was studied in cats under chloralose-urethane anesthesia. Electrical and chemical (glutamate and DL-homocysteic acid) stimulations in this area produced marked bradycardia accompanied by mostly hypotension or minimal change in arterial pressure and by occasional hypertension particularly in the dorsal portion. CIM excitation potentiated the reflex bradycardia induced by IV phenylephrine, while bilateral electrolytic lesion of CIM neither changed the resting cardiovascular parameters nor the reflex bradycardia. The CIM bradycardia was not affected by supracollicular decerebration, but substantially reduced by unilateral vagotomy and completely eliminated by bilateral vagotomy. Destruction of the ambiguus nucleus (NA) and solitary and dorsal motor nuclei (NTS/DMV) abolished the bradycardia. Midline bisection at the midbrain-pontine level only slightly reduced the bradycardia while at the medullary level it was moderately attenuated. Electrolytic lesion of the cardioinhibitory area in gigantocellular reticular nucleus (GRN) abolished the bradycardia. These findings suggest that CIM is an independent mechanism which may send axons to GRN from which the axons may in turn synapse with the NTS/DMV complex and NA. Its final output may utilize both vagus nerves to modulate baroreceptor reflex in promoting bradycardia.

Animals↗
PubMed1999

Chronic but not acute clomipramine alters the effect of NMDA receptor regulation of dopamine release in rat frontal cortex.

The effect of acute or chronic treatment with the antidepressant clomipramine (CIM) on N-methyl-D-aspartate (NMDA) evoked release of dopamine (DA) in the frontal cortex of the rat has been studied using microdialysis. Acute injection of CIM (10 or 20 mg/kg) caused a decrease in dialysate DA in the frontal cortex. Infusion of 25-100 microM NMDA into the frontal cortex decreased DA release in this region. When NMDA infusion was preceded by a single injection of CIM no marked differences between NMDA and NMDA + CIM treated groups were observed. Chronic (15 day) treatment with CIM (10 or 20 mg/kg) caused a dose-dependent increase in basal extracellular DA. In these animals, however, the effects of infusion of NMDA on DA release in the cortex were greatly attenuated or abolished. This suggests that adaptive changes occur in NMDA receptor function during treatment with an antidepressant. The possible significance of this in the aetiology and treatment of depression is discussed.

Animals↗
PubMed2000

Conceptual and perceptual implicit memory in Huntington's disease.

The aims of this study were to examine and compare perceptual and conceptual implicit memory (CIM) in Huntington's disease (HD) and to characterize the relationship between tests of frontal lobe functioning and CIM. Sixteen HD patients and 16 normal controls completed structurally parallel tests of perceptual implicit memory and CIM (i.e., rhyme and category exemplar generation), tests of explicit memory, and verbal fluency. HD patients showed intact implicit memory for both rhyme and category exemplars, despite evidence of frontal dysfunction on other tests. An unexpected finding was that patients showed a deficit in cued rhyme generation that correlated with severity of neurological impairment. The authors replicated findings in controls of a correlation between letter fluency and CIM but found no relationship in patients. Frontal dysfunction in HD may lessen the influence of generative strategies on tests of CIM without compromising performance.

Adult↗
PubMed2000

Microsatellite alterations in differentiated-type adenocarcinomas and precancerous lesions of the stomach with special reference to cellular phenotype.

To elucidate the relationship between genetic alterations and cellular phenotype of differentiated-type adenocarcinomas and precancerous lesions of the stomach, we phenotyped 61 gastric tumors consisting of 33 noninvasive lesions and 28 submucosal invasive carcinomas by histochemical and immunohistochemical techniques, including analysis of mucin expression. We then analyzed loss of heterozygosity (LOH) at tumor suppressor loci, examined microsatellite instability (MSI), and compared the results according to cellular phenotype. Of the 61 gastric tumors studied, 7% (4 of 61) were classified as tumors with a gastric foveolar epithelial phenotype (foveolar-type), 8% (5 of 61) as tumors with a complete-type intestinal metaplastic phenotype (CIM-type), and the remaining 85% (52 of 61) as tumors with an ordinary phenotype (ordinary-type). Forty-two percent (26 of 61) of the tumors showed LOH on at least 1 chromosomal arm. Although LOH was rare in foveolar-type tumors, it was present at variable frequencies at each tumor suppressor loci in tumors with other cellular phenotypes. p53 overexpression was observed in 0% (0 of 4) of foveolar-type, 48% (25 of 52) of ordinary-type, and 80% (4 of 5) of CIM-type tumors. With regard to MSI, all (4 of 4) of the foveolar-type tumors were classified as having high-rate MSI (MSI-H), whereas all (5 of 5) of the CIM-type tumors were microsatellite stable (MSS). Of 52 ordinary-type tumors, 19% (10 of 52) were classified as MSI-H, 12% (6 of 52) as low-rate MSI (MSI-L), and 69% (36 of 52) as MSS. The incidence of MSI-H was found to be significantly higher in foveolar-type tumors (100%; 4 of 4) than in ordinary-type (19%; 10 of 52) or CIM-type tumors (0%; 0 of 5) (P < .01). An inverse correlation between MSI-H and p53 overexpression was also noticed (P < .01). Results suggested that each cellular phenotype followed a different genetic pathway; foveolar-type tumors followed the "mutator" pathway, characterized by MSI, CIM-type tumors followed the "suppressor" pathway, characterized by LOH of tumor suppressor loci and p53 overexpression, and ordinary-type tumors appeared to show mixed genetic alterations of both types.

Adenocarcinoma↗
PubMed1993

Peptide translocation by variants of the transporter associated with antigen processing.

Major histocompatibility complex (MHC) class I molecules associate with peptides that are delivered from the cytosol to the lumen of the endoplasmic reticulum by the transporter associated with antigen processing (TAP). Liver microsomes of SHR and Lewis rats, which express different alleles of TAP (cim(b) and cim(a), respectively), accumulate different sets of peptides. Use of MHC congenic rats assigned this difference to the MHC, independent of the class I products expressed. Both the cim(a) and cim(b) TAP complexes translocate peptides with a hydrophobic carboxyl terminus, but translocation of peptides with a carboxyl-terminal His, Lys, or Arg residue is unique to cim(a). Thus, the specificity of the TAP peptide translocator restricts the peptides available for antigen presentation.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1988

Histaminergic mediation of the stress-induced release of prolactin in male rats.

Histamine (HA) is likely to participate in the neuroendocrine regulation of prolactin (PRL) secretion. We, therefore, studied the possible involvement of HA in the stress-induced release of PRL in conscious male rats. HA (30 micrograms) infused intracerebroventricularly 15 min before decapitation elevated PRL plasma levels from 5 +/- 1 to 54 +/- 6 ng/ml (p less than 0.01). Intracerebroventricular infusion of the H2 receptor antagonists cimetidine (CIM: 100 micrograms) or ranitidine (RAN: 125 micrograms) abolished the PRL response to HA (p less than 0.01), while intracerebroventricular infusion of the H1 receptor antagonist mepyramine (MEP; 100 micrograms) inhibited the response only 40% (p less than 0.05). Intra-arterial infusion of CIM (2,000 micrograms) or RAN (2,500 micrograms) inhibited the HA-stimulated PRL secretion 52% (p less than 0.01) or 63% (p less than 0.01), respectively. The H1 receptor antagonists MEP (1,000 micrograms) and SKF-93944 (1,500 micrograms) had no effect following intra-arterial administration. Restraint stress increased the PRL level to 84 +/- 6 ng/ml (p less than 0.01 vs. control). This effect was prevented by intracerebroventricular infusion of CIM or RAN (p less than 0.01) and inhibited 75% by MEP (p less than 0.01). Intra-arterial infusion of CIM, MEP, and SKF-93944 inhibited the stress response about 50% (p less than 0.01), while RAN decreased the response only 25% (p less than 0.05). Ether stress elevated the plasma PRL concentration to 46 +/- 5 ng/ml (p less than 0.01 vs. control). When infused intracerebroventricularly CIM or RAN prevented the response (p less than 0.01), while MEP had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Left ventricular diastolic chamber stiffness and intramyocardial coronary capacitance in isolated dog hearts.

BACKGROUND: Because the myocardium is perfused primarily during diastole, changes in diastolic properties of the left ventricle (LV) should influence the intramyocardial circulation. METHODS AND RESULTS: We examined the influence of LV diastolic properties on the magnitude and localization of intramyocardial coronary capacitance by analyzing the coronary pressure-venous flow relation in isolated, isovolumic dog heart preparations. After sudden occlusion of the left coronary artery during a long diastole, we measured precapacitance and postcapacitance resistances (RPRE and RPOST) and calculated intramyocardial coronary capacitance (CIM) from RPOST and the time constant of the coronary venous flow decay. Using this method, we characterized the effects of coronary vasodilation, LV diastolic volume, and LV diastolic chamber stiffness on the coronary circulation. The magnitude of CIM increased from 0.09 +/- 0.01 to 0.24 +/- 0.20 mL.mm Hg-1 x 100 g-1 (P < .01) after adenosine-induced vasodilation, whereas both RPOST and RPRE decreased significantly. The ratio of RPOST to RPRE+RPOST decreased from 0.35 +/- 0.02 to 0.23 +/- 0.02 (P < .01), suggesting redistribution of CIM to the distal portion of the coronary vascular tree. An increase in LV volume and wall stress was imposed to increase LV diastolic pressure from 2 +/- 0.1 to 25 +/- 1 mm Hg: this increased RPOST significantly but not RPRE and decreased the magnitude of CIM. The resistance ratio did not change significantly. Increased LV diastolic chamber stiffness induced by hypoxic perfusion (isovolumic LV diastolic pressure increased from 11 +/- 1 to 28 +/- 1 mm Hg) raised RPOST and decreased the magnitude of CIM from 0.32 +/- 0.12 to 0.17 +/- 0.04 mL.mm Hg-1 x 100 g-1 (P < .05). The resistance ratio increased significantly from 0.21 +/- 0.05 to 0.33 +/- 0.05 with increased LV diastolic chamber stiffness. Adjustment of LV diastolic volume to lower diastolic pressure to 10 +/- 1 mm Hg did not alter these changes significantly, suggesting that an intrinsic increase in myocardial stiffness played a major role in these changes. CONCLUSIONS: Extravascular compression by raised LV diastolic volume and/or increased LV diastolic chamber stiffness acted mainly on coronary vessels that determine intramyocardial capacitance and postcapacitance resistance.

Animals↗
PubMed1989

[The effects of the intracerebroventricular administration of cimetidine on hemodynamics in conscious rats: relation to the sympathetic nervous system].

Histamine H2-receptor antagonists administered into the central nervous system have been shown to increase arterial pressure (AP) in anaesthetized animals (Paakkari et al., 1982). Few studies have been reported on the effects of centrally administered cimetidine (CIM), one of the histamine H2-receptor antagonists, in conscious animals. However, the mechanism of the pressor action of histamine H2-receptor antagonists remains unclear. The present study was designed to investigate the hemodynamic effects of intracerebroventricular (i.c.v.) CIM and the interaction between the sympathetic nervous system and histamine receptor system in conscious rats. Male Wistar rats weighing 200 gr were prepared for the experiment under a conscious and minimally restricted state. Five micrograms of i.c.v. saline (SAL-ICV group, n = 5) did not produce significant changes in mean arterial pressure (MAP) or heart rate (HR) (MAP from 85.6 +/- 3.4 to 86.0 +/- 4.3 mmHg and HR from 395.0 +/- 13.9 to 395.2 +/- 8.2 bpm, respectively). Twenty micrograms of i.c.v. phenoxybenzamine (POB-ICV group, n = 6) decreased MAP from 95.8 +/- 4.1 to 85.2 +/- 3.1 mmHg, -10.7 +/- 2.2 mmHg as delta MAP, and increased HR from 392.5 +/- 8.5 to 435.3 +/- 13.9 bpm, +42.8 +/- 6.8 bpm as delta HR. Two-hundred micrograms of intravenous (i.v.) POB (POB-IV group, n = 5) also decreased MAP from 96.0 +/- 4.3 to 71.0 +/- 5.1 mmHg, -25.0 +/- 2.7 mmHg as delta MAP, and increased HR from 395.8 +/- 10.5 to 473.0 +/- 12.4 bpm, +77.2 +/- 7.6 bpm as delta HR. The changes in MAP and HR were much greater in the POB-IV group than those in the other two groups. The subsequent i.c.v. administration of 250 micrograms of CIM induced an increase in MAP (+19.4 +/- 1.7 mmHg as delta MAP) and a decrease in HR (-36.4 +/- 3.1 bpm as delta HR) in the SAL-ICV group, which continued for at least 30 minutes producing peak effects 2 minutes after i.c.v. administration of CIM. However, an elevation of MAP caused by i.c.v. CIM was much more inhibited in the POB-ICV group than in the POB-IV group (+2.5 +/- 0.7 mmHg as delta MAP in the POB-ICV group and +5.0 +/- 1.3 mmHg as delta MAP in the POB-IV group, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1998

The beta-agonist cimaterol directly enhances chronic protein accretion in skeletal muscle.

Our objective was to determine whether the chronic anabolic effects of beta-adrenergic agonists on skeletal muscle are direct and how long they are maintained. We studied acute (6 h) and chronic (1 to 20 d) effects of cimaterol (CIM) on skeletal muscle metabolism and protein accretion by use of close arterial infusion in the hindlimbs of six young steers. Surgical catheterizations were conducted to allow continuous infusion of CIM (.5 microg/min) or saline into the external iliac artery of contralateral hindlimbs and simultaneous sampling for arteriovenous difference measurements. Hindlimb blood flow and net flux of amino acids, glucose, lactate, and NEFA were determined during a basal period before infusion, at 6 h, and at 1, 3, 7, 14, and 20 d of infusion. Cimaterol infusion acutely stimulated blood flow and caused acute mobilization of nitrogen (alanine), NEFA, and lactate from the treated hindlimb. Cimaterol infusion increased net uptake of amino acids (P < .05) in treated and control hindlimbs after 1 d of CIM infusion, but a progressive increase between 1 and 14 d of infusion was observed only in the treated hindlimbs. Net uptake of total amino acids in the treated hindlimb was increased 50 and 80% (P < .05) at 7 and 14 d, respectively, when compared to the control hindlimb and was increased 260% at d 14 when compared with the basal period. Net amino acid uptake was not different between treated and control hindlimbs by d 20 of CIM infusion. Integration of net tyrosine and phenylalanine uptake over the entire infusion period predicted a 10% difference in skeletal muscle protein mass between treated and control hindlimbs. Semitendinosus and semimembranosus muscles in the treated hindlimb contained 9 and 11% greater protein content, respectively (P < .05), at the end of the infusion period. Results provide a quantitative description of the temporal pattern of transient effects of CIM on skeletal muscle metabolism and protein accretion and provide evidence that these are direct effects.

Adrenergic beta-Agonists↗
PubMed1989

Effects of cimaterol on nitrogen retention and energy utilization in lambs.

Fifty-two weaned lambs were used in a comparative slaughter feeding trial and six lambs in a concurrent digestibility trial to investigate the effects of cimaterol on nitrogen retention and energy utilization. Cimaterol (CIM) was administered in the feed at 10 ppm for 90 and 14 d, respectively, in a comparative slaughter feeding trial and in a digestibility trial. No difference was found in dry matter digestibility. Nitrogen retention in the CIM group (739 mg/Wkg.75/d) was greater (P less than .01) than that of the control group (321 mg/Wkg.75/d). This difference was accounted for primarily by reduced nitrogen loss in urine of the CIM group. Cimaterol improved growth rate and feed/gain ratio, although these improvements were only evident during the first 42 d of the 90-d feeding trial. The improvement in growth performance of the CIM group was associated with increased protein gain in the empty body (40.2 g/d, P less than .01) as well as in carcass (26.9 g/d, P less than .01), compared with 30.1 and 14.5 g/d of the control group. Cimaterol decreased (P less than .01) fat gain (91.4 vs 109.9 g/d), total daily energy gain (1.08 vs 1.22 Mcal) and energy gain/kg gain (4.17 vs 5.11 Mcal) compared with the control. Feeding CIM increased (P less than .01) estimated fasting heat production (73 vs 64 Kcal/Wkg.75) and metabolizable energy requirement for maintenance (110.2 vs 92.7 Kcal/Wkg.75) over the control.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Agonists↗
PubMed2003

Involvement of H2-receptors in the mechanism of analgesic action of Tyr-MIF-1.

The antinociceptive effects of H2-agents cimetidine (CIM) and dimaprit (DMP) as well as their effects on the Tyr-MIF-1-evoked analgesia have been studied after intraperitoneal (i.p.) administration in rats. In the paw-pressure (PP) test Tyr-MIF-1 (1 mg/kg), CIM (50 and 100mg/kg) and DMP (5 and 10mg/kg) induced analgesia. Injected before DMP, naloxone (NAL) and CIM diminished or completely prevented the pain-relieving effect of H2-agonist DMP. The antinociceptive effect of Tyr-MIF-1 has been potentiated by DMP dose-dependently. CIM (50mg/kg) decreased the antinociceptive action of the combination Tyr-MIF-1 + DMP, while CIM (100mg/kg) expressed a weaker inhibitory effect on it. The data obtained clearly show that H2-receptor activation is involved in the mechanism of the Tyr-MIF-1 antinociceptive action.

Analgesics↗
PubMed2002

Interval and composite interval mapping of somatic cell score, yield, and components of milk in dairy cattle.

Single-marker, interval-mapping (IM) and composite interval mapping (CIM) were used to detect quantitative trait loci (QTL) controlling milk, fat and protein yields, and somatic cell score (SCS). A granddaughter design was used to combine molecular genetic information with predicted transmitting abilities (PTA) and estimated daughter yield deviations (DYD) from eight Dairy Bull DNA Repository Holstein families. Models that included and excluded weights accounting for the uncertainty of the response variable were evaluated in each trait, family and phenotype (DYD and PTA) combination. The genotypic information consisted of 174 microsatellite markers along 29 Bos taurus autosomes. The average number of informative markers per autosome was three and the number of informative sons per family and marker varied between 21 and 173. Within-family results from the least squares single-marker analyses were used in expectation-maximization likelihood IM and CIM implemented with QTL Cartographer. Different CIM model specifications, offering complementary control on the background QTL outside the interval under study, were evaluated. Permutation techniques were used to calculate the genome-wide threshold test statistic values based on 1,000 samples. Results from the DYD and PTA analyses were highly consistent across traits and families. The minor differences in the estimates from the models that accounted for or ignored the uncertainty of the DYD (variance) and PTA (inverse of reliability) may be associated to the elevated and consistent precision of the DYD and PTA among sons. The CIM model best supported by the data had 10 markers controlling for background effects. On autosome (BTA) three, a QTL at 32 cM influencing protein yield was located in family five and a QTL at 74 cM for fat yield was located in family eight. Two map positions associated with SCS were detected on BTA 21, one at 33 cM in family one and the other at 84 cM in family three. A QTL for protein yield was detected between 26 and 36 cM on BTA six, family six, and a QTL for milk yield was detected at 116 cM on BTA seven in family three. The IM and CIM approaches detected a QTL at 3 cM on BTA 14 influencing fat yield in family four. Two map positions on BTA 29 were associated with significant variation of milk (0 cM) and fat yield (14 cM) in family seven. These results suggest the presence of one QTL with pleiotropic effects on multiple traits or multiple QTL within the marker interval. Findings from this study could be used in subsequent fine-mapping work and applied to marker-assisted selection of dairy production and health traits.

Animals↗
PubMed2004

Plastic changes of motor network after constraint-induced movement therapy.

The effects of short-term constraint-induced movement (CIM) therapy on the activation of the motor network were investigated with functional magnetic resonance imaging (fMRI). Movement of the less-affected arms of five patients was restricted and intensive training of the affected upper limb was performed. Functional MRI was acquired before and after two-weeks of CIM therapy. All patients showed significant improvement of motor function in their paretic limbs after CIM therapy. For three patients, new activation in the contralateral motor/premotor cortices was observed after CIM therapy. Increased activation of the ipsilateral motor cortex and SMA was observed in the other patient. Our results demonstrated that plastic changes of the motor network occurred as a neural basis of the improvement subsequent to CIM therapy following brain injury.

Adult↗
PubMed2004

Perioperative cimetidine administration promotes peripheral blood lymphocytes and tumor infiltrating lymphocytes in patients with gastrointestinal cancer: Results of a randomized controlled clinical trial.

AIM: To study the effects of perioperative administration of cimetidine (CIM) on peripheral blood lymphocytes, natural killer (NK) cells and tumor infiltrating lymphocytes (TIL) in patients with gastrointestinal (GI) cancer. METHODS: Forty-nine GI cancer patients were randomized into treatment group, who took CIM in perioperative period, and control group, who did not take the drug. The treatment was initiated 7 days before operation and continued for 10 days after surgery. At baseline examination before operation, on the 2nd and 10th postoperative days, total T lymphocytes, T helper cells, T suppressor cells, and NK cells in peripheral blood were measured respectively by immunocytochemical method using mouse-anti human CD(3), CD(4), CD(8) and CD(57) monoclonal antibodies. Blood samples from 20 healthy volunteers were treated in the same way as normal controls. Surgical specimens were examined during routine histopathological evaluation for the presence of TIL in tumor margin. Immunohistochemical study was performed to measure the proportion of T and B lymphocytes in TIL population. T and B lymphocytes were detected respectively using mouse-anti-human CD(3) and CD(20) monoclonal antibodies. RESULTS: In comparison with normal controls, both the treatment and control groups had decreased T cells, T helper cells and NK cells at baseline. In control group, total T cells, T helper cells and NK cells declined continuously with the disease progression and the decrease became more obvious after operation. From baseline to the 2nd postoperative day, the proportion of total T cells, T helper cells, and NK cells went down from 60.5+/-4.6% to 56.2+/-3.8%, 33.4+/-3.7% to 28.1+/-3.4%, and 15.0+/-2.8% to 14.2+/-2.2%, respectively. On the other hand, there were significant improvements in these parameters after CIM treatment. On the 10th postoperative day, the treatment group had significantly higher percentages of total T cells, T helper cells and NK cells than control group. Moreover, CIM treatment also boosted TIL response, as was reflected by findings that 68% (17/25) of the patients in treatment group had significant TIL responses and only 25% (6/24) of the cases had discernible TIL responses (P<0.01). CONCLUSION: Perioperative application of CIM to GI cancer patients could help restore the diminished cellular immunity induced by tumor burden and surgical maneuver. The drug could also boost TIL responses to tumor. These effects suggest that the drug be used as an immunomodulator for GI cancer patients.

Adjuvants, Immunologic↗