Unilateral Pattern Research Articles

Axonal sprouting into the denervated spinal cord and synaptic and postsynaptic protein expression in the spinal cord after transplantation of bone marrow stromal cell in stroke rats

We investigated whether compensatory reinnervation in the corticospinal tract (CST) and the corticorubral tract (CRT) is enhanced by the administration of bone marrow stromal cells (BMSCs) after experimental stroke. Adult male Wistar rats were subjected to permanent right middle cerebral artery occlusion (MCAo). Phosphate-buffered saline (PBS, control, n = 7) or 3 × 10 6 BMSCs in PBS ( n = 8) were injected into a tail vein at 1 day postischemia. The CST of the left sensorimotor cortices was labeled with DiI 2 days prior to MCAo. Functional recovery was measured. Rats were sacrificed at 28 days after MCAo. The brain and spinal cord were removed and processed for vibratome sections for laser-scanning confocal analysis and paraffin sections for immunohistochemistry. Normal rats ( n = 4) exhibited a predominantly unilateral pattern of innervation of CST and CRT axons. After stroke, bilateral innervation occurred through axonal sprouting of the uninjured CRT and CST. Administration of BMSCs significantly increased the axonal restructuring on the de-afferented red nucleus and the denervated spinal motoneurons ( p < 0.05). BMSC treatment also significantly increased synaptic proteins in the denervated motoneurons. These results were highly correlated with improved functional outcome after stroke ( r > 0.81, p < 0.01). We conclude that the transplantation of BMSCs enhances axonal sprouting and rewiring into the denervated spinal cord which may facilitate functional recovery after focal cerebral ischemia.

Cerebrovascular accidents after cardiac surgery: An analysis of CT scans in relation to clinical symptoms

There is a link between aortic manipulation, particle embolization, and cerebrovascular accidents (CVA) in cardiac surgery. The present aim was to study hemispheric side differences of CVA. Cardiac-surgery patients with CVA and with computer tomography (CT) performed (n = 77) were analyzed within a total group of 2641 consecutive cases. CT data were reviewed for hemispheric and vascular distribution, and compared with CVA-symptom data of immediate and delayed type. Of the included patients, 66% had positive CT. In the group of ‘cardiac-type’ operations (e.g., routine clamping and cannulation) and having immediate CVA, right-hemispheric lesions were more frequent than of the contra-lateral side (p = 0.005). Patients with aortic dissections had strong dominance of bilateral findings, which was different from the unilateral pattern of ‘cardiac-type’ operations (p = 0.001). The middle-cerebral artery territory dominated, and when involved showed a significant (p = 0.022) right-sided distribution. Both CT and clinical symptoms confirmed that CVA after cardiac surgery has a right-hemispheric predominance. These observations may imply that aortic manipulation directs embolic material towards the brachiocephalic trunk.

207 高分子液晶を用いた片側パターン電極による選択的研磨制御の基礎実験(GS-13 加工(2))

207 高分子液晶を用いた片側パターン電極による選択的研磨制御の基礎実験(GS-13 加工(2))

208 高分子液晶を用いた片側パターン電極による研磨効果のAFMによる観察(GS-13 加工(2))

208 高分子液晶を用いた片側パターン電極による研磨効果のAFMによる観察(GS-13 加工(2))

1101 低分子液晶系ER流体の片側パターン電極におけるER効果の発現(GS-10 ダイナミクス計測)

Electrorheological(ER) fluids undergo a change in apparent viscosity upon application of electric field. In this paper, we report ER effect of low molecurar liquid crystal with unilateral(one-sided) pattern electrodes.

First Report of Fusarium Wilt of Exacum affine Caused by Fusarium oxysporum.

Wilting Persian violets (Exacum affine) were observed in a Connecticut retail outlet. Diseased stems developed a dark coloration at the nodes, while the foliage turned papery, whitish tan. The vascular tissue in affected stems was reddish brown and extended from the base of the stem upward in a unilateral pattern. Fusarium grew from the discolored stem tissue when placed on Komada's medium (2). Single spores were cultured on carnation leaf agar and identified as F. oxysporum (2). Koch's postulates were completed by growing 12 2-month-old seedlings of E. affine 'Midget' in potting mix amended with ground dried millet seed (2.0 g/liter of soil) that had been colonized for 2 weeks by the fungus. Symptoms appeared slowly after 8 weeks, and F. oxysporum was re-isolated from the vascular tissue. Plants grown in soil mix with sterile millet remained healthy. Similar tests at different times of the year produced the same results. Other tests examined host specificity with two new isolates on seedlings of Persian violet, carnation, lisianthus, and basil. Both isolates caused symptoms only on Persian violets. Although Haematonectria haematococca (synonym Nectria haematococca, anamorph F. solani) causes Nectria canker of Persian violet (1), this is the first report of F. oxysporum causing Fusarium wilt of Persian violet. We propose the formae specialis be F. oxysporum f. sp. exaci. An isolate has been deposited at the Fusarium Research Center at The Pennsylvania State University, University Park, under Accession No. O-2282.

Magnetic resonance imaging follow-up of progressive hippocampal changes in a mouse model of mesial temporal lobe epilepsy.

Hippocampal sclerosis (HS) is the most frequent lesion found in mesial temporal lobe epilepsy (mTLE). MR imaging is considered to be the most sensitive and specific method to detect HS. Despite extensive studies performed on humans and except in a recent study, the morphologic pattern of HS is usually analyzed when the disease has already fully developed, thus not allowing any insight into the mapping of the progressive morphologic changes inducing the development of mTLE. We have recently characterized a model of mTLE that reproduces the unilateral pattern of HS, induced by intrahippocampal injection of low doses of kainate (KA) in mice. In this study, we monitored the temporal evolution of the development of HS in this model of mTLE by using T2-weighted sequence, T2-relaxation time measurements, and T1-weighted spin-echo technique after injection of gadolinium, from 1 h to 120 days after KA injection. HS induced by intrahippocampal KA injection occurred in two phases. First, we observed a transient hyperintense T2-weighted signal in the cortex above the injected hippocampus, most likely indicative of vasogenic edema partly due to the neurotoxic effect of KA. The concomitant increase in the T2 signal in the injected hippocampus and ipsilateral amygdala likely reflects the phase of cytotoxic edema occurring probably in relation to the excitotoxic consequences of both KA and seizure activity. Second, from 15 days on, a persistent unilateral increased T2 signal was detected in the hippocampus, which most probably reflects gliosis. Our findings indicate that longitudinal follow-up would permit a better understanding of the mechanisms underlying the constitution of HS in humans and eventually development of prevention strategies.

The refractive development of untreated eyes of rhesus monkeys varies according to the treatment received by their fellow eyes.

To determine the extent to which the visual experience of one eye may influence the refractive development of its fellow eye, we analyzed the data of untreated (UT) eyes of monkeys that received different types of unilateral pattern deprivation. Subjects were 15 juvenile rhesus monkeys, with five monkeys in each of three treatment groups: aphakic eyes with optical correction (AC), aphakic eyes with no correction (ANC), and eyes that were occluded with an opaque contact lens (OC). Under general anaesthesia, refractive error (D) was determined by cycloplegic retinoscopy and axial length (mm) was determined with A-scan ultrasonography. For measurements of refractive error of the UT eyes, there was a significant main effect of groups according to the treatment of the fellow eyes, F(2, 12) = 6.6. While UT eyes paired with AC fellow eyes (mean = +4.2 D) were significantly more hyperopic than the eyes of age-matched normal monkeys (mean = +2.4 D), t(25), = 2.5, UT eyes paired with OC fellow eyes (mean = -0.5 D) were significantly more myopic than the eyes of normal monkeys, t(25) = -9. UT eyes paired with ANC fellow eyes (mean = +1.9 D) were not significantly different from normal eyes. For measurements of axial length there was also a significant main effect of groups, F(2, 12) = 6.9. While UT eyes paired with AC fellow eyes (mean = 16.9 mm) were significantly shorter than the eyes of age-matched normal monkeys (mean = 17.5 mm), t(25) = 2.3, UT eyes paired with OC fellow eyes (mean = 18.1 mm) were significantly longer than the eyes of normal monkeys, t(25) = 2.3. UT eyes paired with ANC fellow eyes (mean = 17.5 mm) were not significantly different from the eyes of normal monkeys. The measurements of axial length and of refractive error of the UT eyes were also significantly correlated with one another, probably indicating that the differences in refractive error were due to differences in axial length, r = -0.8. The present data reveal that despite normal visual experience, UT eyes can have their refractive development altered, systematically, simply as a function of the type of pattern deprivation received by their fellow eyes. These data add to the growing evidence that there is an interocular mechanism that is active during emmetropization. As a consequence, future models of eye growth will need to consider both: (1) the direct influence of visual input on the growing eye; as well as (2) the indirect influence coming from the fellow eye.

Epidemiology and prognosis of peripheral obliterative arteriopathy

Peripheral arterial disease has received less attention from epidemiologists than coronary and cerebrovascular disease. Prevalence and incidence data typically show that peripheral arterial disease increases with age, is more common in men than women, and that symptomatic disease is only the tip of the iceberg. Studies concerning the prevalence of peripheral arterial disease rely mainly on the Rose questionnaire, which is used to screen for intermittent claudication, and on the ankle/brachial index, used to detect asymptomatic disease. Although there is a certain parallel between the 2 sets of data, the figures for asymptomatic disease consistently surpass those for clinical disease, and there is a wide variation between frequencies obtained in individual studies. In general, the prevalence of peripheral arterial disease is estimated to be under 2% for men aged less than 50 years, increasing to over 5% in those aged more than 70 years. Women reach these rates almost 10 years after men, although this gender difference decreases with increasing age. Figures for incidence follow a similar trend. The incidence of chronic critical ischaemia is estimated to be between 0.05% and 0.1% of the population. Asymptomatic disease detected with noninvasive tests is 3 to 4 times more frequent than intermittent claudication: its prevalence increases from under 5% for individuals aged less than 50 years to over 20% for individuals aged more than 70 years. The classical risk factors for atherosclerosis also apply to peripheral arterial disease, although their order of importance may be different from that for coronary and carotid disease. Several studies have shown that peripheral arterial disease correlates most strongly with cigarette smoking. Smoking is also the single greatest predictor of the progression of peripheral arterial disease. Other risk factors include hypertension, raised lipid levels (cholesterol and triglycerides for severe disease), diabetes, increased plasma viscosity, fibrinogen and homocysteine levels. Divergent views have been expressed in individual epidemiological studies with regard to the respective contribution of these risk factors to the development and progression of peripheral arterial disease. The natural history of peripheral arterial disease is characterised by a relatively benign local evolution. It can be estimated that, in general, 3 of 4 men presenting with intermittent claudication will never have a serious problem necessitating vascular intervention, and that no more than 5% are ever likely to require a major amputation. However, the underlying atherosclerotic pathology progresses with time: nondiseased arteries become obliterated and disease with an initially unilateral pattern frequently progresses to become bilateral. In addition, the few patients who do progress to critical ischaemia are at a significantly higher risk of amputation. The general prognosis for patients with peripheral arterial disease is particularly negative. There is a high prevalence of coronary heart disease and cerebrovascular disease in such patients, although the exact percentages depend on the patient population selected and on the method used for their evaluation. Coronary heart disease is detected in 40 to 60% of patients through a medical history combined with electrocardiography, while systematic coronary angiography detects coronary heart disease in 90% of those undergoing surgery. Although few patients with peripheral arterial disease have a history of stroke, in studies of surgical patients almost 30% appear to have significant extracranial disease. Patients with peripheral arterial disease have a poor life expectancy: the mortality rate is 3 to 5% per year in those with intermittent claudication and 20% per year in those with critical ischaemia. Coronary heart disease accounts for half of the total mortality, while vascular disease in general accounts for almost two-thirds.

The aetiology of mandibular fractures at an urban centre.

The objectives of this study were to determine the common aetiological factors leading to the fracture of the lower jaw (mandible) at an urban centre in England. A total of 96 patients presented to the Manchester Royal Infirmary with mandibular fractures during the calendar years 1991 and 1992. It was determined that the main aetiological factor leading to the disturbance of the mandibular contours was assault or interpersonal violence (74%) followed by falls, road traffic accidents and sporting injuries. The majority of the subjects were males and most of the patients were in the age group of 20-29 years. In most of the patients there was a unilateral pattern of injury and the angle was the most vulnerable area of the lower jaw to be traumatised.

Muscle activity in autotomized tails of a lizard (Gekko gecko): a naturally occurring spinal preparation.

We quantified muscle activity in tails of lizards (Gekko gecko) during running and after autotomy of the tail. We chose different animals and varied where we broke the tails in order to obtain three experimental preparations having: no regenerated tissue or prior tail loss (non-regenerated), a large regenerated portion and a few original caudal vertebrae (partially regenerated), and only regenerated tissue (fully regenerated). All observed axial motor patterns were rhythmic. During running of intact animals, muscles in non-regenerated tails were activated in an alternating, unilateral pattern that was propagated posteriorly. After autotomy, non-regenerated tails had unilateral muscle activity that alternated between the left and right sides and propagated anteriorly. Autotomized, partially regenerated tails had unilateral, alternating muscle activity that lacked any longitudinal propagation. Autotomized, fully regenerated tails had periodic muscle activity that occurred simultaneously for both left and right sides and all longitudinal positions. Neither tactile stimulation nor removal of the tail tip prior to autotomizing the tail affected the motor pattern. Several features of the motor pattern of autotomized tails changed significantly with increased time after autotomy. Autotomized tails with one or more spinal segments moved longer and more vigorously than autotomized tails consisting entirely of regenerated (unsegmented) tissue.

Fetal pelvi-ureteric junction obstruction: predictors of outcome.

To examine the relationship between pre-natal ultrasonographic findings typical of pelvi-ureteric junction (PUJ) obstruction and post-natal renal function in the affected kidney. This retrospective study comprised 35 infants in whom pre-natal ultrasonography had identified a unilateral pattern of dilatation of the renal pelvis and calices typical of PUJ obstruction. In each case, the presence of unilateral hydronephrosis had been confirmed post-natally by ultrasonography, and differential function and drainage evaluated by isotope renography. The results of isotope renography were compared with the severity and timing of onset of the fetal hydronephrosis. Eleven kidneys (31%) appeared normal in the second trimester and dilatation only became apparent during the third trimester. Mean differential function in these kidneys was 48%. However, mean differential function was reduced (mean 38%) in those kidneys noted to be dilated between 16 and 24 weeks gestation. Differential function was loosely correlated with the severity of dilatation in early onset cases, i.e. the mean differential function was 42% for mild, 37% for moderate and 27% for severe dilatation. A considerable variation in differential function values was present in each group except for those with severe dilatation, which was a significant predictor of poor functional outcome when compared with mild and moderate dilatation combined (P < 0.01). Fetal PUJ obstruction is a heterogeneous condition permitting only broad predictions of functional outcome. Severe dilatation detected on second trimester imaging predicted significant loss of function. Mild and moderate degrees of dilatation were associated with a one in three risk of functional impairment in the obstructed kidney.

C- fos immunoreactivity in the brain following electrical or chemical stimulation of the medial hypothalamus of freely moving rats

c- fos immunoreactivity was used to map brain areas in which neurons reacted either to electrical stimulation or to microinjection of the excitatory amino acid kainate and of the GABA A antagonist, SR-95531, applied to the medial hypothalamus of freely moving rats. All these stimulations induced flight behavior of moderate intensity. Immunoreactive cells were found within a radius of 0.5 mm around the stimulated area. Distally, clusters of labeled cells were found ipsilaterally in the piriform and entorhinal cortices, in several amygdaloid nuclei, in the bed nucleus of the stria terminalis, in the septo-hypothalamic nucleus, in the paraventricular, anterior and dorsomedial hypothalamic nuclei, in the paraventricular thalamic nucleus, in the dorsal periaqueductal gray extending to the cuneiform nucleus, and bilaterally in the supramamillary decussation and the locus coeruleus. The specificity of the brain areas thus labeled was indicated by the unilateral pattern of activation as well as by the different pattern obtained after control microinjection of saline. Therefore, these results are likely to provide sound information about the brain structures involved in defensive/aversive behavior evoked from the medial hypothalamus.

Interactions during a critical period inhibit bilateral projections in embryonic neurons

The anterior pagoda (AP) neurons in the CNS of the medicinal leech are found as homologous pairs in 20 of the 21 midbody ganglia. Each AP is the mirror image of its mate, extending its main axon across the midline of the CNS and eventually into the contralateral body wall, thereby attaining a unilateral pattern of innervation. Certain features of the adult AP morphology are known to arise through interactions among homologs early in development (Gao and Macagno, 1987b), but it is not known whether the contralateral nature of the projection pattern is due to intrinsic "one-sidedness" or rather to cell-cell interactions that inhibit the formation of a second, ipsilateral projection. In the experiments described in this report, we tested the possibility that an AP's contralateral homolog itself inhibits the formation of bilateral projections. One AP was photoablated in the intact embryo early in development and then the response of the remaining AP was examined. We found that an AP can extend bilaterally symmetrical projections when its homolog is missing, but only during a critical period that, interestingly, begins when an AP's interactions with other specific neurons come to an end. To determine whether synaptic communication between AP homologs could be responsible for the timing of this critical period, we recorded electrophysiologically from pairs of embryonic AP neurons. Although no detectable chemical signaling was observed, AP cells were electrically coupled throughout the entire critical period. Further, the junctions between these neurons were permeated by 5-HT, whereas larger molecules such as carboxyfluorescein were impermeant. This dye coupling decreased with age even while electrical coupling persisted, suggesting but not proving that the properties of the gap junctions between AP neurons may also change with time. We conclude that unilateral AP cells possess the intrinsic ability to project bilaterally, but are inhibited from doing so by age-dependent interactions with homologous neurons, possibly mediated by gap-junctional communication.

Clonal haematopoiesis in children with acquired aplastic anaemia

The methylation pattern of three X-linked genes, phosphoglycerate kinase (PGK), hypoxanthine phosphoribosyl transferase (HPRT) and DXS255 detected by hypervariable M27 beta probe, was analysed to determine the proportion of aplastic anaemia (AA) with clonal haematopoiesis in Japanese children. Methylation analysis was performed on DNA from separated granulocytes and compared to that of bone marrow derived fibroblasts to exclude selective lyonization in all somatic cells. Of 20 female patients examined, the methylation pattern of at least one gene was informative in granulocyte DNA from 18 patients (90%). Of these, 8/20 patients (40%) were heterozygous for PGK, 8/18 (44%) were heterozygous for HPRT and 17/18 (94%) were heterozygous for DXS255. In 14/18 patients both alleles were equally methylated. Four patients exhibited a unilateral methylation pattern in their granulocytes. The same unilateral pattern was again demonstrated in fibroblasts from two of the four patients suggesting that in the latter one X chromosome was selectively inactivated in all of the somatic cells. The remaining two patients showed a unilateral methylation pattern that was restricted to their granulocytes, suggesting the existence of true clonal haematopoiesis. They responded well to antilymphocyte globulin (ALG) and presently have no evidence of a clonal disorder such as myelodysplastic syndrome (MDS) or paroxysmal nocturnal haemoglobinuria (PNH). Although these results indicate that some children with AA exhibit clonal haematopoiesis, analysis of a greater number of subjects will be required to establish the clinical value of clonal haematopoiesis in patients with AA.

Clonal Involvement of Granulocytes and Monocytes, But Not of T and B Lymphocytes and Natural Killer Cells in Patients With Myelodysplasia: Analysis by X-Linked Restriction Fragment Length Polymorphisms and Polymerase Chain Reaction of the Phosphoglycerate Kinase Gene

To determine the clonal nature of hematopoiesis and to assess lineage involvement in patients with myelodysplastic syndromes (MDS), we used restriction fragment length polymorphisms of the X-linked genes phosphoglycerate kinase (PGK1) and hypoxanthine phosphoribosyltransferase (HPRT) and the X-linked probe M27 beta. Eleven female MDS patients heterozygous for at least one of these probes were studied: 3 with refractory anemia (RA), 2 with RA with ringed sideroblasts (RARS), 2 with chronic myelomonocytic leukemia (CMML), and 4 with RA with excess of blasts in transformation (RAEB-t). All exhibited clonal hematopoiesis as determined by Southern analysis of DNA prepared from peripheral blood (PB) and/or bone marrow (BM) cells. In three of the six patients heterozygous for the PGK1 gene, purified cell suspensions of polymorphonuclear cells (PMN), monocytes, lymphocytes, and/or T cells prepared from PB were tested. In addition, five of these patients were analyzed by a polymerase chain reaction (PCR)-based procedure as described recently. This method was slightly adapted to facilitate the analysis of cell lysates of fluorescence-activated cell sorted (FACS) monocytes, T and B lymphocytes, and natural killer (NK) cells. The outcome of Southern and PCR analysis was concordant, showing that PMN and monocytes were clonally derived, whereas circulating T and B lymphocytes and NK cells exhibited random X-chromosome inactivation compatible with a polyclonal pattern. To address the question of whether T cells are derived from unaffected progenitor cells or that their origin had antedated the onset of MDS, naive and memory T cells were analyzed separately. Both subsets showed a polyclonal pattern. However, in one patient analysis of constitutive DNA suggested a skewed methylation, and the presence of clonal lymphocytes against a background of polyclonal lymphoid cells cannot be ruled out in this patient. PCR analysis of PB and BM cells showed a nonrandom, unilateral pattern of X-inactivation, compatible with a mixture of clonally (myeloid) and polyclonally (lymphoid) derived cells. In conclusion, in some patients, MDS represents a disorder with clonal hematopoiesis restricted to cells of myeloid origin, whereas a random X-inactivation pattern is found in lymphoid cells.

Clonal involvement of granulocytes and monocytes, but not of T and B lymphocytes and natural killer cells in patients with myelodysplasia: analysis by X-linked restriction fragment length polymorphisms and polymerase chain reaction of the phosphoglycerate kinase gene

To determine the clonal nature of hematopoiesis and to assess lineage involvement in patients with myelodysplastic syndromes (MDS), we used restriction fragment length polymorphisms of the X-linked genes phosphoglycerate kinase (PGK1) and hypoxanthine phosphoribosyltransferase (HPRT) and the X-linked probe M27 beta. Eleven female MDS patients heterozygous for at least one of these probes were studied: 3 with refractory anemia (RA), 2 with RA with ringed sideroblasts (RARS), 2 with chronic myelomonocytic leukemia (CMML), and 4 with RA with excess of blasts in transformation (RAEB-t). All exhibited clonal hematopoiesis as determined by Southern analysis of DNA prepared from peripheral blood (PB) and/or bone marrow (BM) cells. In three of the six patients heterozygous for the PGK1 gene, purified cell suspensions of polymorphonuclear cells (PMN), monocytes, lymphocytes, and/or T cells prepared from PB were tested. In addition, five of these patients were analyzed by a polymerase chain reaction (PCR)-based procedure as described recently. This method was slightly adapted to facilitate the analysis of cell lysates of fluorescence- activated cell sorted (FACS) monocytes, T and B lymphocytes, and natural killer (NK) cells. The outcome of Southern and PCR analysis was concordant, showing that PMN and monocytes were clonally derived, whereas circulating T and B lymphocytes and NK cells exhibited random X- chromosome inactivation compatible with a polyclonal pattern. To address the question of whether T cells are derived from unaffected progenitor cells or that their origin had antedated the onset of MDS, naive and memory T cells were analyzed separately. Both subsets showed a polyclonal pattern. However, in one patient analysis of constitutive DNA suggested a skewed methylation, and the presence of clonal lymphocytes against a background of polyclonal lymphoid cells cannot be ruled out in this patient. PCR analysis of PB and BM cells showed a nonrandom, unilateral pattern of X-inactivation, compatible with a mixture of clonally (myeloid) and polyclonally (lymphoid) derived cells. In conclusion, in some patients, MDS represents a disorder with clonal hematopoiesis restricted to cells of myeloid origin, whereas a random X-inactivation pattern is found in lymphoid cells.

Inhibition of 5'-nucleotidase by concanavalin A: evidence for localization on the outer surface of the plasma membrane.

5'-Nucleotidase activity of rat liver plasma membrane is markedly inhibited by concanavalin A. Taken together with a unilateral pattern of labelling of concanavalin A binding sites with hemocyanin, the results indicate that an allosteric site of the enzyme is at the outer surface of the membrane.