Effects of increased functional residual capacity on finger-floor distance in healthy young adults.

[Purpose] To investigate the effect of increased functional residual capacity on the finger-floor distance and to assess spinal curvature in the sagittal plane using the Spinal Mouse in healthy young participants. [Participants and Methods] Thirty-nine healthy volunteers (age=21.2 ± 0.8 years) participated in this study. The finger-floor distance was used to measure trunk flexion and was recorded at the resting expiration level and at 2 different functional residual capacity levels: 1,000 and 2,000 ml air inhaled at the resting expiration level. Spinal curvature morphology was evaluated using the Spinal Mouse in the sagittal plane when flexion was completed under the 2 increased functional residual capacity and resting expiration level conditions during finger-floor distance measurement. Finger-floor distance and spinal curvature were assessed according to functional residual capacity using one-way repeated measures analysis of variance and post-hoc analysis. [Results] Significant effects and differences were found for the finger-floor distance under all conditions. No significant effect was found for spinal curvature. [Conclusion] An increase in functional residual capacity may decrease trunk flexion. This correlation might also be observed in patients with chronic obstructive pulmonary disease.

Effect of increased functional residual capacity on the active range of thoracic axial rotation in healthy young men.

[Purpose] To understand the effect of increased functional residual capacity (FRC) on the active range of thoracic axial rotation (AROTAR) in healthy young men. [Subjects and Methods] Thirty-nine right-handed healthy male volunteers (age=20.1 ± 1.6 years) participated in this study. A standard plastic goniometer was used to measure the AROTAR in the supine position with both glenohumeral joints fully flexed. AROTAR was recorded at the resting expiration level (REL) and for 4 different FRC levels: 500, 1,000, 1,500, and 2,000 ml air inhaled at REL. FRC volumes and laterality were analyzed using a two-way repeated measure of ANOVA and post-hoc analysis. Relationships between the relative value (AROTAR for each increased FRC level / REL AROTAR × 100) and AROTAR for each increased FRC level were analyzed using Pearson's correlation coefficient. [Results] A significant main effect was found for only FRC factor. AROTAR had a positive moderate correlation with relative value. The correlation coefficient was higher than 0.5 for in 1,500 and 2,000 ml. [Conclusion] An increase in FRC might decrease AROTAR and if the REL AROTAR is high, the decrease in AROTAR due to increased FRC is lesser. It is suggested that maintaining the thoracic mobility could minimize a COPD patient's AROTAR limitation and maintain physical ability.

Efficient Enantioselective Synthesis of Oxahelicenes Using Redox/Acid Cooperative Catalysts.

An efficient and enantioselective synthesis of oxa[9]helicenes has been established via vanadium(V)-catalyzed oxidative coupling/intramolecular cyclization of polycyclic phenols. A newly developed vanadium complex cooperatively functions as both a redox and Lewis acid catalyst to promote the present sequential reaction and afford oxa[9]helicenes in good yields with up to 94% ee.

Pd-catalyzed enantioselective intramolecular α-arylation of α-substituted cyclic ketones: facile synthesis of functionalized chiral spirobicycles.

Catalytic synthesis of chiral spirocyclic ketones was accomplished via the Pd-catalyzed intramolecular α-arylation of α-substituted cyclic ketones. The obtained spirocyclic ketone could be converted into a bifunctional organocatalyst.

Short-term ethanol exposure causes imbalanced neurotrophic factor allocation in the basal forebrain cholinergic system: a novel insight into understanding the initial processes of alcohol addiction.

Alcohol ingestion affects both motor and cognitive functions. One brain system that is influenced by ethanol is the basal forebrain (BF) cholinergic projection system, which projects to diverse neocortical and limbic areas. The BF is associated with memory and cognitive function. Our primary interest is the examination of how regions that receive BF cholinergic projections are influenced by short-term ethanol exposure through alterations in the mRNA levels of neurotrophic factors [nerve growth factor/TrkA, brain-derived neurotrophic factor/TrkB, and glial-derived neurotrophic factor (GDNF)/GDNF family receptor α1]. Male BALB/C mice were fed a liquid diet containing 5 % (v/v) ethanol. Pair-fed control mice were maintained on an identical liquid diet, except that the ethanol was isocalorically substituted with sucrose. Mice exhibiting signs of ethanol intoxication (stages 1-2) were used for real-time reverse transcription-polymerase chain reaction analyses. Among the BF cholinergic projection regions, decreased levels of GDNF mRNA and increased levels of TrkB mRNA were observed in the basal nucleus, and increased levels of TrkB mRNA were observed in the cerebral cortex. There were no significant alterations in the levels of expression of relevant neurotrophic factors in the septal nucleus and hippocampus. Given that neurotrophic factors function in retrograde/anterograde or autocrine/paracrine mechanisms and that BF cholinergic projection regions are neuroanatomically connected, these findings suggested that an imbalanced allocation of neurotrophic factor ligands and receptors is an initial phenomenon in alcohol addiction. The exact mechanisms underlying this phenomenon in the BF cholinergic system are unknown. However, our results provide a novel notion for the understanding of the initial processes in alcohol addiction.

Early postnatal maternal separation causes alterations in the expression of ß3-adrenergic receptor in rat adipose tissue suggesting long-term influence on obesity.

The effects of early postnatal maternal deprivation on the biological characteristics of the adipose tissue later in life were investigated in the present study. Sprague-Dawley rats were classified as either maternal deprivation (MD) or mother-reared control (MRC) groups. MD was achieved by separating the rat pups from their mothers for 3h each day during the 10-15 postnatal days. mRNA levels of mitochondrial uncoupling protein 1 (UCP-1), ß3-adrenergic receptor (ß3-AR), and prohibitin (PHB) in the brown and white adipose tissue were determined using real-time RT-PCR analysis. UCP-1, which is mediated through ß3-AR, is closely involved in the energy metabolism and expenditure. PHB is highly expressed in the proliferating tissues/cells. At 10 weeks of age, the body weight of the MRC and MD rats was similar. However, the levels of the key molecules in the adipose tissue were substantially altered. There was a significant increase in the expression of PHB mRNA in the white adipose tissue, while the ß3-AR mRNA expression decreased significantly, and the UCP-1 mRNA expression remained unchanged in the brown adipose tissue. Given that these molecules influence the mitochondrial metabolism, our study indicates that early postnatal maternal deprivation can influence the fate of adipose tissue proliferation, presumably leading to obesity later in life.

BDNF-dependent accumulation of palmitoleic acid in CNS neurons.

Although it is known that brain-derived neurotrophic factor (BDNF) plays a critical role in neuronal survival and differentiation, its effect on lipid homeostasis is poorly understood. To understand them, we here investigated the effect of BDNF on the fatty acid composition of primary neurons. A detailed analysis of the fatty acid composition of BDNF-stimulated primary neurons revealed that BDNF treatment led to a significant and selective increase in intracellular palmitoleic acid (PLO) levels. Correspondingly, BDNF induced the expression of the enzyme responsible for PLO synthesis [stearoyl-CoA desaturase-1]. In addition, this increase was suppressed by K252a, an inhibitor for tropomyosin-related kinase (Trk) receptors, indicating that BDNF-dependent increase in the PLO was mediated through the activation of TrkB. Further, PLO in culture media was reduced by BDNF treatment. This result suggested that BDNF suppressed extracellular release of PLO. Taken together, these data indicate that BDNF increases intracellular PLO both by activating its biosynthesis and by suppressing its extracellular release.

Morphological evidence of an altered process of synaptic transcytosis in adult rats exposed to ethanol.

AIMS: The effects of ethanol exposure on synaptic structure were investigated in the nucleus of solitary tract (NST) in rats, using the horse-radish peroxidase (HRP) method. METHODS: Eight-week-old experimental rats were allowed free access to a liquid diet containing ethanol for 3 weeks, while controls were given an isocaloric diet. Some of the control and experimental animals were given an injection of wheat germ agglutinin conjugated with HRP (WGA-HRP) into the vagus nerve toward the end of the treatment period. After the treatment, the neuropil region of the NST was examined under an electron microscope. RESULTS: We observed that a few terminals were characterized by deep indentation of axodendritic membranes into the post-synaptic neurons. This appeared to be similar to that commonly seen in exocrine glands. Interestingly, the indented portion often contained various sizes of vacuoles and flattened cisternae. HRP-reaction product (RP) transported to terminals was recognized easily as an electron-dense lysosomal substance when lead citrate staining was omitted. Terminals containing HRP-RP also revealed quite a similar structure with indentation of axodendritic membranes as described earlier. The results are considered to confirm that terminals forming 'apocrine-like structures' observed in the ethanol-fed animals with no injection of WGA-HRP originate from afferent fibers of the vagus nerve. CONCLUSION: The present study suggests the possibility that the alteration of the synaptic structure induced by ethanol exposure can lead to the neuronal transcytosis of materials including proteins which is different from the normal vesicular exocytosis involved in chemical synaptic transmission.

Agreement in rotator cuff muscles measurement between ultrasonography and magnetic resonance imaging.

Background/objective: It is important to assess the atrophy of the rotator cuff to better understand shoulder function and pain. Previously, magnetic resonance imaging has been used for the evaluation of atrophy of rotator cuff muscles, which is time consuming. Therefore, a measurement tool requiring little time and easy accessibility is clinically desirable to be used frequently in rehabilitation. Recently, rotator cuff muscles have been evaluated using ultrasonography. However, little is known about the agreement of evaluation in rotator cuff muscles between magnetic resonance imaging and ultrasonography. The purpose of this study was to demonstrate the agreement between the muscle thickness measurements of supraspinatus, infraspinatus, and teres minor muscles by ultrasonography and the cross-sectional area measured by magnetic resonance imaging in the patient with rotator cuff tears. Methods: A total of 47 patients with rotator cuff tears were enrolled. There were the 37 small tears, four medium tears, and six large tears, and the involved rotator cuff muscles were the supraspinatus in 37 shoulders, and the supraspinatus and infraspinatus in 10 shoulders. The measuring variables were muscle thickness and cross-sectional area of supraspinatus, infraspinatus, and teres minor muscles by using magnetic resonance imaging. Further, the muscle thickness of the rotator cuff were assessed using ultrasonography. A single regression model was used for demonstrating the agreement between the cross-sectional area measurement by magnetic resonance imaging and the muscle thickness measured using ultrasonography and magnetic resonance imaging of rotator cuff muscles. Additionally, the Bland-Altman plots between magnetic resonance imaging and ultrasonography was analyzed. Results: The cross-sectional area were correlated with the muscle thickness measurement of rotator cuff muscles by magnetic resonance imaging, significantly (supraspinatus: r = 0.84, infraspinatus: ρ = 0.63, teres minor: ρ = 0.61, all p < 0.001). There were significant agreements between the cross-sectional area measured by magnetic resonance imaging and muscle thickness measured by ultrasonography (supraspinatus: r = 0.80, infraspinatus: ρ = 0.78, teres minor: ρ = 0.74, all p < 0.001). Bland-Altman plots revealed significant correlations between the average and the difference of the two measurements in supraspinatus (r = 0.36, p = 0.012), infraspinatus (r = 0.38, p < 0.001), and teres minor (r = 0.42, p < 0.001). These results clarified the proportional bias between MRI and US. Conclusion: This study showed that, similar to magnetic resonance imaging, ultrasonography is a useful tool for assessing muscle atrophy of supraspinatus, infraspinatus, and teres minor muscles.

A high cholesterol diet given to apolipoprotein E-knockout mice has a differential effect on the various neurotrophin systems in the hippocampus.

Apolipoprotein E (apoE) is one of the major transporters of cholesterol in the body and is essential for maintaining various neural functions in the brain. Given that hypercholesterolemia is a risk factor in Alzheimer's disease (AD), it has been suggested that altered cholesterol metabolism may be involved in the development of the pathogenesis, including neural degeneration, commonly observed in AD patients. Neurotrophic factors and their receptors, which are known to regulate various neural functions, are also known to be altered in various neurodegenerative diseases. We therefore hypothesized that cholesterol metabolism may itself influence the neurotrophin system within the brain. We decided to investigate this possibility by modulating the amount of dietary cholesterol given to apoE-knockout (apoE-KO) and wild-type (WT) mice, and examining the mRNA expression of various neurotrophin ligands and receptors in their hippocampal formations. Groups of eight-week-old apoE-KO and WT mice were fed a diet containing either "high" (HCD) or "normal" (ND) levels of cholesterol for a period of 12 weeks. We found that high dietary cholesterol intake elevated BDNF mRNA expression in both apoE-KO and WT mice and TrkB mRNA expression in apoE-KO animals. On the other hand, NGF and TrkA mRNA levels remained unchanged irrespective of both diet and mouse type. These findings indicate that altered cholesterol metabolism induced by HCD ingestion combined with apoE deficiency can elicit a differential response in the various neurotrophin ligand/receptor systems in the mouse hippocampus. Whether such changes can lead to neural degeneration, and the mechanisms that may be involved in this, awaits further research.

Pyrene-labeled deoxyguanosine as a fluorescence sensor to discriminate single and double stranded DNA structures: design of ends free molecular beacons.

A novel fluorescent DNA probe containing pyrene-labeled C8 alkylamino-substituted 2'-deoxyguanosine was designed in order to discriminate single stranded and double stranded regions in DNA. This fluorescent sensor was used for the design of practically useful 3'- and 5'-ends free self-quenched molecular beacon (MB). Unique MB detectable by pyrene excimer fluorescence was also demonstrated.

Ethanol neurotoxicity and dentate gyrus development.

Maternal alcohol ingestion during pregnancy adversely affects the developing fetus, often leading to fetal alcohol syndrome (FAS). One of the most severe consequences of FAS is brain damage that is manifested as cognitive, learning, and behavioral deficits. The hippocampus plays a crucial role in such abilities; it is also known as one of the brain regions most vulnerable to ethanol-induced neurotoxicity. Our recent studies using morphometric techniques have further shown that ethanol neurotoxicity appears to affect the development of the dentate gyrus in a region-specific manner; it was found that early postnatal ethanol exposure causes a transitory deficit in the hilus volume of the dentate gyrus. It is strongly speculated that such structural modifications, even transitory ones, appear to result in developmental abnormalities in the brain circuitry and lead to the learning disabilities observed in FAS children. Based on reports on possible factors deciding ethanol neurotoxicity to the brain, we review developmental neurotoxicity to the dentate gyrus of the hippocampal formation.

Early postnatal ethanol exposure induces fluctuation in the expression of BDNF mRNA in the developing rat hippocampus.

Effects of early postnatal ethanol exposure on brain-derived neurotrophic factor (BDNF) mRNA expression in the rat hippocampus were investigated. Wistar rats were assigned to either ethanol treatment (ET) separation control (SC) or mother-reared control (MRC) groups. Ethanol exposure was achieved by a vapor inhalation method for 3 hours a day between postnatal days (PND) 1015. On PND 16, 20, 30, and 60, the expression of BDNF mRNA in the hippocampus was determined using real-time RT-PCR analysis. There was a significant age-related increase in the BDNF mRNA expression between PND 3060 in MRC animals. The BDNF mRNA expression in ET rats was increased at both PND 16 and 20 and thereafter decreased at PND 60 compared to SC animals. Such age-related fluctuation in the expression of BDNF mRNA differed from that of MRC animals. The exact functional implications, if any, of these ethanol-induced changes in BDNF mRNA expression remain unknown although it can be speculated that they may have an effect on the behaviors known to be influenced by the hippocampal formation.

The effect of prenatal X-irradiation on the developing cerebral cortex of rats. II: A quantitative assessment of glial cells in the somatosensory cortex.

The developing central nervous system is known to be highly vulnerable to X-irradiation. Although glial cells are involved in various brain functions, knowledge on the effects of X-irradiation on glial cells is limited. Therefore, the purpose of the present study was to evaluate the effects of prenatal X-irradiation on glial cells. Pregnant Wistar rats were exposed to X-irradiation at a dose of 1.0 Gy on day 15 of gestation. Their offspring were examined at 7 weeks of age. The forebrain weight of X-irradiated rats was significantly lower than that of the age-matched controls. Histological quantification with stereology of the somatosensory cortex (SC) revealed no significant difference in the numerical density of glial cells between the X-irradiated and control rats. However, the glial cells in the X-irradiated animals had significantly larger nuclear size. We had previously reported that a similar X-irradiation paradigm resulted in no significant change in the numerical density of neurons in the SC. According to the results of the present study, there were no significant differences in the glial cell-to-neuron ratios between the X-irradiated and control animals. Taken together, it is speculated that prenatal X-irradiation has an equal effects on the numerical densities of glial cells and neurons.

c-Fos expression in the periaqueductal gray is induced by electroacupuncture in the rat, with possible reference to GABAergic neurons.

Electroacupuncture (EA) delivered to the acupoint (AP) called Zusanli (ST36) was administered on the bilateral hindlimb. This experiment resulted in strong expression of c-Fos immunoreactivity in the ventrolateral to lateral subdivision throughout the periaqueductal gray (PAG) compared to the non-AP and sham cases. On the other hand, it was of particular interest in the experiment of the AP that strong expression of gamma aminobutylic acid (GABA) frequently showed similar pattern of distribution to that of c-Fos in the PAG. This overlapped pattern of distribution, demonstrated in the present study, suggests that the PAG neurons activated by EA at the AP might play an important role in the descending pain control system involving the GABA since the PAG has special reference to the dorsal horn of the spinal cord and function of pain control.

Changes of parvalbumin immunoreactive neurons and GFAP immunoreactive astrocytes in the rat lateral geniculate nucleus following monocular enucleation.

The expression of calcium binding proteins (CaBPs) has been linked to protection of neurons. The present study investigated the effects of monocular enucleation on the distribution of parvalbumin immunoreactive (PV-IR) neurons and glial fibrillary acidic protein immunoreactive (GFAP-IR) astrocytes in both the dorsal (dLGN) and ventral (vLGN) regions of the lateral geniculate nucleus (LGN). Our results demonstrated an increase in PV-IR neuronal density on the contralateral vLGN at 1-week post-enucleation (PE), which was maintained without significant change for 12 weeks. By contrast, PV-IR neurons in dLGN decreased significantly at all time point examined. The number of GFAP-IR astrocytes showed an initial increase from 1 to 4 weeks PE and then gradually decreased until 48 weeks in both regions of the LGN with contralateral side predominance. The present results suggest that monocular enucleation results in variable expression of PV-IR neurons and GFAP-IR astrocytes in the LGN complex, which may play an important role in neuronal degeneration and neuroplasticity of the rat visual system.

Regional differences in vulnerability of the cerebellar foliations of rats exposed to neonatal X-irradiation.

The purpose of the present study was to elucidate regional differences in the vulnerability of cerebellar foliations of rats exposed to X-irradiation. Effects of X-irradiation on foliations were examined with respect to histological changes in Purkinje cells and Bergmann glial fibers by calbindin-D28k (CB) and glial fibrillary acidic protein (GFAP) immunohistochemistry, respectively. Wistar rats were exposed to X-irradiation (1.5 Gy) on postnatal day (PND) 1. At 3 weeks of age, the cerebellum was examined. The cerebella of rats exposed to X-irradiation showed smaller and abnormal foliations compared with controls. Fewer cerebellar foliations due to fusion with neighboring folia were observed in folia I-III and VIa-VII. Moreover, the extent of such abnormalities was more severe in the latter folia. CB-immunoreactive (IR) Purkinje cells exhibited thin, short, disoriented dendrites that had invaded the granular layer or white matter. On the other hand, GFAP-IR Bergmann glial fibers had not extended their processes into the molecular layer perpendicular to the pial surface, and they appeared thin and disoriented. Accordingly, the above cerebellar abnormalities were more severe in folia I-III, VIa-VII and X than in other regions. In contrast to the histological alterations in these folia, there were no apparent qualitative differences in folia IV-V between X-irradiated and controls. These findings indicate regional difference in the vulnerability of cerebellar folia to X-irradiation. Such differences might be attributed to the cerebellar neurogenetic gradient.

Oligodendrocyte myelin glycoprotein (OMgp) in rat hippocampus is depleted by chronic ethanol consumption.

The hippocampal formation has been shown to be particularly vulnerable to the neurotoxic effects of chronic ethanol consumption. It was hypothesized that this damage was due to the disruption of the expression of neurotrophic factors and certain other proteins within the hippocampus. By using real-time reverse transcription-polymerase chain reaction (RT-PCR) techniques, this study aimed to determine whether chronic ethanol consumption could alter the mRNA expression level of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF), and oligodendrocyte myelin glycoprotein (OMgp) in the hippocampus. Wistar male rats received an unrestricted access to a liquid diet containing 5% (v/v) ethanol as the sole source of fluid from 10 to 29 weeks of age. Control rats had unlimited access to a liquid diet containing an isocaloric amount of sucrose. We found that chronic ethanol consumption did not cause significant changes in the levels of mRNA for BDNF and GDNF. However, OMgp mRNA showed a significant deficit in ethanol-treated animals. It is suggested that this deficit may be related to the demyelination that is commonly observed in human alcoholics and that this may contribute to the functional and cognitive deficits.

Autopsy study of anatomical features of the posterior gastric artery for surgical contribution.

AIM: To investigate features of the posterior gastric artery (PGA) with respect to incidence, location and size by using autopsy subjects. METHODS: Autopsies were performed on 72 cadavers of adults with no history of abdominal operations. The localization of the PGA, the distance between the root of the splenic artery and the origin of the PGA, and the external diameter of the PGA were examined. RESULTS: The PGA was recognized in all patients. In 70 (97.2%) cadavers, the PGA branched from the splenic artery, and one female in this group had two PGAs. In 1 (1.4%) patient, the PGA originated from the root of the celiac trunk and in another (1.4%) patient, the PGA branched from the superior polar artery. Overall, the PGA extended for a length of 5.8-12.2 (mean, 8.4) cm from the root of the splenic artery, and the external diameter of the PGA was 1.2-3.2 (mean, 2) mm. CONCLUSION: The anatomical features of the PGA can be readily observed and characterized by autopsy. This study has provided valuable information on the features of the PGA useful in the planning of surgical treatment.

Age-related changes in growth hormone-immunoreactive cells in the anterior pituitary gland of Jcl: Wistar-TgN (ARGHGEN) 1Nts rats (Mini rats).

Rats of the Jcl: Wistar-TgN (ARGHGEN) 1Nts strain (Mini rats) are transgenic animals carrying an antisense RNA transgene for rat growth hormone (GH); they show poor somatic growth and a low blood GH level compared to age-matched wild-type Wistar (non-Mini) rats. The purpose of the present study was to investigate age-related changes in growth hormone-immunoreactive (GH-IR) cells in the anterior pituitary gland (AP) of Mini rats at four, six, and eight weeks of age. The body weight and size of the GH-IR cells of Mini rats was significantly lower than that of non-Mini rats at six and eight weeks of age; however, this difference was not observed at four weeks of age. The AP volume and the number of GH-IR cells in Mini rats were significantly smaller than those of the age-matched non-Mini rats at the three ages. These results suggest that the abnormal development of GH-IR cells in the AP induced by the GH antisense RNA transgene is responsible for the poor somatic growth and the low blood GH levels in Mini rats.