-
[show abstract]
[hide abstract]
ABSTRACT: A 46-year-old woman was admitted to our hospital because of behavioral changes. Her mentality was fluctuating vigorously and neurological examination revealed disorientation and word finding difficulty. MRI demonstrated bilateral frontal and right temporal lesions. Cerebrospinal fluid examination showed predominantly lymphocytic pleocytosis. Brain biopsy disclosed inflammation but not neoplasm. Repeated steroid therapy gave her a recovery in neurological manifestations and MRI findings. As we got a positive result of anti-Hu antibody after her complete recovery, we did screening for tumors and found small cell lung cancer. She got a chemotherapy and remains free of relapse of any symptoms. There have been few reports in that anti-Hu associated paraneolastic syndrome showed steroid responsive frontal lesions. We suggest that anti-Hu associated paraneoplastic encephalitis should be considered for steroid responsive encephalitis with brain lesions other than limbic system, because early detection of paraneoplastic encephalitis and timely antitumor treatment are important for patient's prognosis.
Rinshō shinkeigaku = Clinical neurology. 01/2013; 53(4):273-7.
-
Konstantinos Charizanis,
Kuang-Yung Lee,
Ranjan Batra,
Marianne Goodwin,
Chaolin Zhang,
Yuan Yuan,
Lily Shiue,
Melissa Cline,
Marina M Scotti,
Guangbin Xia, [......],
Kenji Jinnai, Hiroo Yoshikawa,
Mário Gomes-Pereira,
Geneviève Gourdon,
Noriaki Sakai,
Seiji Nishino,
Thomas C Foster,
Manuel Ares,
Robert B Darnell,
Maurice S Swanson
[show abstract]
[hide abstract]
ABSTRACT: The RNA-mediated disease model for myotonic dystrophy (DM) proposes that microsatellite C(C)TG expansions express toxic RNAs that disrupt splicing regulation by altering MBNL1 and CELF1 activities. While this model explains DM manifestations in muscle, less is known about the effects of C(C)UG expression on the brain. Here, we report that Mbnl2 knockout mice develop several DM-associated central nervous system (CNS) features including abnormal REM sleep propensity and deficits in spatial memory. Mbnl2 is prominently expressed in the hippocampus and Mbnl2 knockouts show a decrease in NMDA receptor (NMDAR) synaptic transmission and impaired hippocampal synaptic plasticity. While Mbnl2 loss did not significantly alter target transcript levels in the hippocampus, misregulated splicing of hundreds of exons was detected using splicing microarrays, RNA-seq, and HITS-CLIP. Importantly, the majority of the Mbnl2-regulated exons examined were similarly misregulated in DM. We propose that major pathological features of the DM brain result from disruption of the MBNL2-mediated developmental splicing program.
Neuron 08/2012; 75(3):437-50. · 14.74 Impact Factor
-
Koichi Suenaga,
Kuang-Yung Lee,
Masayuki Nakamori,
Yoshiki Tatsumi,
Masanori P Takahashi,
Harutoshi Fujimura,
Kenji Jinnai, Hiroo Yoshikawa,
Hongqing Du,
Manuel Ares,
Maurice S Swanson,
Takashi Kimura
[show abstract]
[hide abstract]
ABSTRACT: Myotonic dystrophy type 1 (DM1) is a multi-systemic disorder caused by a CTG trinucleotide repeat expansion (CTG(exp)) in the DMPK gene. In skeletal muscle, nuclear sequestration of the alternative splicing factor muscleblind-like 1 (MBNL1) explains the majority of the alternative splicing defects observed in the HSA(LR) transgenic mouse model which expresses a pathogenic range CTG(exp). In the present study, we addressed the possibility that MBNL1 sequestration by CUG(exp) RNA also contributes to splicing defects in the mammalian brain. We examined RNA from the brains of homozygous Mbnl1(ΔE3/ΔE3) knockout mice using splicing-sensitive microarrays. We used RT-PCR to validate a subset of alternative cassette exons identified by microarray analysis with brain tissues from Mbnl1(ΔE3/ΔE3) knockout mice and post-mortem DM1 patients. Surprisingly, splicing-sensitive microarray analysis of Mbnl1(ΔE3/ΔE3) brains yielded only 14 candidates for mis-spliced exons. While we confirmed that several of these splicing events are perturbed in both Mbnl1 knockout and DM1 brains, the extent of splicing mis-regulation in the mouse model was significantly less than observed in DM1. Additionally, several alternative exons, including Grin1 exon 4, App exon 7 and Mapt exons 3 and 9, which have previously been reported to be aberrantly spliced in human DM1 brain, were spliced normally in the Mbnl1 knockout brain. The sequestration of MBNL1 by CUG(exp) RNA results in some of the aberrant splicing events in the DM1 brain. However, we conclude that other factors, possibly other MBNL proteins, likely contribute to splicing mis-regulation in the DM1 brain.
PLoS ONE 01/2012; 7(3):e33218. · 4.09 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: The subthalamic nucleus (STN) is a frequent target of deep brain stimulation (DBS), which is used to treat patients with advanced Parkinson's disease (PD). However, few studies have assessed the relationship between the STN and the clinical characteristics of PD patients. We identified the STN of 17 PD patients and 7 control subjects using coronal Short TI Inversion Recovery (STIR) magnetic resonance imaging (MRI) and estimated the T2 relaxation time (T2) of the STN on the subsequent coronal images that were acquired from T2-weighted MRI. The relationships between the STN T2 measurements and the PD patients' age, disease duration, laterality, and clinical scores were examined. STN T2 measurements tended to be lower in PD patients than in controls, although the difference was not significant. STN T2 measurements were significantly and inversely correlated (p=0.03) with scores on the Unified Parkinson's Disease Rating Scale (UPDRS) part 1, which was applied to evaluate the mentation, behavior, and mood of PD patients. However, no significant correlations were found between the STN T2 measurements and the patients' age, disease duration, laterality, or motor clinical scores. These results suggest that degeneration of the STN in PD patients may contribute to their neuropsychological symptoms.
Journal of the neurological sciences 11/2011; 315(1-2):96-9. · 2.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Increasing evidence shows that neural stem/progenitor cells (NSPCs) can be activated in the nonconventional neurogenic zones such as the cortex following ischemic stroke. However, the precise origin, identity, and subtypes of the ischemia-induced NSPCs (iNSPCs), which can contribute to cortical neurogenesis, is currently still unclear. In our present study, using an adult mouse cortical infarction model, we found that the leptomeninges (pia mater), which is widely distributed within and closely associated with blood vessels as microvascular pericytes/perivascular cells throughout central nervous system (CNS), have NSPC activity in response to ischemia and can generate neurons. These observations indicate that microvascular pericytes residing near blood vessels that are distributed from the leptomeninges to the cortex are potential sources of iNSPCs for neurogenesis following cortical infarction. In addition, our results propose a novel concept that the leptomeninges, which cover the entire brain, have an important role in CNS restoration following brain injury such as stroke.
Stem cells and development 08/2011; 20(12):2037-51. · 4.15 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: We report on a Japanese 13-year-old male without a family history of muscle disease admitted to our hospital due to an elevated serum creatine kinase. From the age of 3 he was complaining of muscle stiffness during and after exercise. At the age of 7 he experienced muscle stiffness and weakness during long-distance running, which would continue till the next day, disappearing only after resting for a day. Upon examination, we noted that repeated eyelid contractions induced myotonia that increased in the cold. Electromyography revealed myotonic discharge in the tongue muscle. Genetic analysis revealed a mutation of Nav1.4, M1592V. Although this mutation had originally been reported in families with Hyperkalemic periodic paralysis (Hyper PP), we diagnosed as paramyotonia congenita due to the symptoms of exercise and cold-induced myotonia without an attack of generalized weakness. This case suggest that sodium channelopathy is very rare, but should be considered in the differential diagnosis of an elevation of serum creatine kinase even if coexisting myotonia is only mild.
Rinsho shinkeigaku = Clinical neurology 02/2011; 51(2):120-4.
-
Masashi Munemoto,
Yoshinaga Otaki,
Shuhei Kasama,
Masayoshi Nanami,
Masanori Tokuyama,
Mana Yahiro,
Yukiko Hasuike,
Takahiro Kuragano, Hiroo Yoshikawa,
Hiroshi Nonoguchi,
Takeshi Nakanishi
[show abstract]
[hide abstract]
ABSTRACT: Multiple sclerosis (MS) in Asian countries, including Japan, is classified into two types: conventional MS (C-MS), characterized mainly by cerebral lesions, and opticospinal MS (OS-MS) or neuromyelitis optica (NMO), characterized by selective involvement of the optic nerve and spinal cord. Recently, a serum immunoglobulin-G-antibody was discovered in patients with NMO that targets aquaporin-4 (AQP4). The existence of the anti-AQP4 antibody shows the pathogenetic role of humoral immune factors in OS-MS/NMO. We treated eight patients with anti-AQP4 antibody-positive MS with double filtration plasmapheresis (DFPP) to remove the antibody. Improvement of vision was observed in two patients. Motion improvement was seen in seven patients. Sensory improvement was observed in four patients. In total, six out of eight patients (75%) showed therapeutic improvement after DFPP treatment. We propose that DFPP might be an effective therapeutic option for patients with anti-AQP4 antibody-positive MS.
Journal of Clinical Neuroscience 02/2011; 18(4):478-80. · 1.25 Impact Factor
-
Orie Saino,
Akihiko Taguchi,
Takayuki Nakagomi,
Akiko Nakano-Doi,
Shin-Ichiro Kashiwamura,
Nobutaka Doe,
Nami Nakagomi,
Toshihiro Soma, Hiroo Yoshikawa,
David M Stern,
Haruki Okamura,
Tomohiro Matsuyama
[show abstract]
[hide abstract]
ABSTRACT: Acute inflammation in the poststroke period exacerbates neuronal damage and stimulates reparative mechanisms, including neurogenesis. However, only a small fraction of neural stem/progenitor cells survives. In this report, by using a highly reproducible model of cortical infarction in SCID mice, we examined the effects of immunodeficiency on reduction of brain injury, survival of neural stem/progenitor cells, and functional recovery. Subsequently, the contribution of T lymphocytes to neurogenesis was evaluated in mice depleted for each subset of T lymphocyte. SCID mice revealed the reduced apoptosis and enhanced proliferation of neural stem/progenitor cells induced by cerebral cortex after stroke compared with the immunocompetent wild-type mice. Removal of T lymphocytes, especially the CD4(+) T-cell population, enhanced generation of neural stem/progenitor cells, followed by accelerated functional recovery. In contrast, removal of CD25(+) T cells, a cell population including regulatory T lymphocytes, impaired functional recovery through, at least in part, suppression of neurogenesis. Our findings demonstrate a key role of T lymphocytes in regulation of poststroke neurogenesis and indicate a potential novel strategy for cell therapy in repair of the central nervous system.
Journal of Neuroscience Research 08/2010; 88(11):2385-97. · 2.74 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Increasing evidence shows that administration of bone marrow mononuclear cells (BMMCs) is a potential treatment for various ischemic diseases, such as ischemic stroke. Although angiogenesis has been considered primarily responsible for the effect of BMMCs, their direct contribution to endothelial cells (ECs) by being a functional elements of vascular niches for neural stem/progenitor cells (NSPCs) has not been considered. Herein, we examine whether BMMCs affected the properties of ECs and NSPCs, and whether they promoted neurogenesis and functional recovery after stroke. We compared i.v. transplantations 1 x 10(6) BMMCs and phosphate-buffered saline in mice 2 days after cortical infarction. Systemically administered BMMCs preferentially accumulated at the postischemic cortex and peri-infarct area in brains; cell proliferation of ECs (angiogenesis) at these regions was significantly increased in BMMCs-treated mice compared with controls. We also found that endogenous NSPCs developed in close proximity to ECs in and around the poststroke cortex and that ECs were essential for proliferation of these ischemia-induced NSPCs. Furthermore, BMMCs enhanced proliferation of NSPCs as well as ECs. Proliferation of NSPCs was suppressed by additional treatment with endostatin (known to inhibit proliferation of ECs) following BMMCs transplantation. Subsequently, neurogenesis and functional recovery were also promoted in BMMCs-treated mice compared with controls. These results suggest that BMMCs can contribute to the proliferation of endogenous ischemia-induced NSPCs through vascular niche regulation, which includes regulation of endothelial proliferation. In addition, these results suggest that BMMCs transplantation has potential as a novel therapeutic option in stroke treatment.
Stem Cells 07/2010; 28(7):1292-302. · 7.78 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Neuromyelitis optica (NMO) is an inflammatory demyelinating disease of the central nervous system (CNS). Anti-aquaporin-4 antibody (AQP4-Ab) is a highly specific serum autoantibody that is detected in patients with NMO. Several lines of evidence indicate that AQP4-Ab not only serves as a disease marker but also plays a pivotal role in the pathogenesis of NMO. Although the pathogenicity of AQP4-Ab in vivo has recently been demonstrated, the presence of CNS antigen-specific T cells is recognized as a prerequisite for the antibody to exert pathogenic effects. Thus, it remains unclear whether AQP4-Ab is the primary cause of the disease or a disease-modifying factor in NMO. Here we report that pre-treatment with complete Freund's adjuvant (CFA) alone is sufficient for AQP4-Ab to induce astrocytic damage in vivo. Our results show the primary pathogenic role of AQP4-Ab in the absence of CNS antigen-specific T cells, and suggest that danger signals provided by nonspecific inflammation can be a trigger for those who harbor the autoantibody to develop NMO.
Biochemical and Biophysical Research Communications 02/2010; 394(1):205-10. · 2.48 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A 26-year-old woman with primary amenorrhea in association with hypergonadotropinism, and lacking a vagina and uterus, suffered from a gradually progressive gait disturbance in her adolescence. The patient has no family history of ataxia and a chromosome study showed a normal karyotype (46,XX). Using the revised Hasegawa Dementia Scale, her cognitive function was measured as that of a normal adult, however, neurological examination revealed symptoms of scanning speech, horizontal gaze-evoked nystagmus, and ataxia. Bulging eyes, high-arched palate, scoliosis and ventricular septal defect were also observed. A brain MRI showed atrophy of the cerebellum. A 123I-IMP brain SPECT study showed hypoperfusion in the cerebellum. Previous studies show that among patients with cerebellar ataxia and hypergonadotropic hypogonadism, some show an autosomal recessive inheritance, while others have no family history. As a cause, a chromosomal abnormality is unlikely because all reported karyotypes were normal. This case is different from other reported cases in that she is not mentally impaired or deaf. The present case indicates that there is a close relationship between cerebellar ataxia and hypogonadism, and that other symptoms such as deafness and mental impairment could be an additional variable in patients with cerebellar ataxia arid hypergonadotropic hypogonadism.
Rinsho shinkeigaku = Clinical neurology 01/2010; 50(1):20-3.
-
[show abstract]
[hide abstract]
ABSTRACT: Recent studies have suggested that the elevation of intracellular chloride contributes to excitotoxic cell death in motor neuron and can be related to the pathogenesis of amyotrophic lateral sclerosis (ALS). We investigated whether chloride levels in cerebrospinal fluid (CSF) and serum were lower in ALS patients than in control patients with other neurological diseases (OND). We also examined the relationship between chloride levels and clinical ALS phenotypes. We measured chloride levels (CSF and serum) in 27 ALS patients and 33 age- and gender-matched OND controls admitted to our hospital for diagnosis. The CSF chloride levels were lower in ALS patients (117 [range 102-130] mmol/L) than in OND controls (126 [range 114-134] mmol/L) (P<0.0001). However, no significant difference was found in their serum chloride levels (P>0.05). There was no significant difference in CSF chloride levels among the sub-groups of ALS patients classified according to their age, gender, duration of illness, clinical state and type of onset (P>0.05). CSF chloride levels already significantly decreased in ALS patients at the time of diagnosis. We conclude that the elevation of intracellular chloride would cause the reduction of chloride in CSF and be related to the pathogenesis of ALS.
Journal of the neurological sciences 07/2009; 285(1-2):146-8. · 2.32 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Transplantation of neural stem cells (NSCs) has been proposed as a therapy for a range of neurological disorders. To realize the potential of this approach, it is essential to control survival, proliferation, migration, and differentiation of NSCs after transplantation. NSCs are regulated in vivo, at least in part, by their specialized microenvironment or "niche." In the adult central nervous system, neurogenic regions, such as the subventricular and subgranular zones, include NSCs residing in a vascular niche with endothelial cells. Although there is accumulating evidence that endothelial cells promote proliferation of NSCs in vitro, there is no description of their impact on transplanted NSCs. In this study, we grafted cortex-derived stroke-induced neural stem/progenitor cells, obtained from adult mice, onto poststroke cortex in the presence or absence of endothelial cells, and compared survival, proliferation, and neuronal differentiation of the neural precursors in vivo. Cotransplantation of endothelial cells and neural stem/progenitor cells increased survival and proliferation of ischemia-induced neural stem/progenitor cells and also accelerated neuronal differentiation compared with transplantation of neural precursors alone. These data indicate that reconstitution of elements in the vascular niche enhances transplantation of adult neural progenitor cells.
Stem Cells 07/2009; 27(9):2185-95. · 7.78 Impact Factor
-
Takayuki Nakagomi,
Akihiko Taguchi,
Yoshihiro Fujimori,
Orie Saino,
Akiko Nakano-Doi,
Shuji Kubo,
Akinobu Gotoh,
Toshihiro Soma, Hiroo Yoshikawa,
Tomoyuki Nishizaki,
Nami Nakagomi,
David M Stern,
Tomohiro Matsuyama
[show abstract]
[hide abstract]
ABSTRACT: The CNS has the potential to marshal strong reparative mechanisms, including activation of endogenous neurogenesis, after a brain injury such as stroke. However, the response of neural stem/progenitor cells to stroke is poorly understood. Recently, neural stem/progenitor cells have been identified in the cerebral cortex, as well as previously recognized regions such as the subventricular or subgranular zones of the hippocampus, suggesting that a contribution of cortex-derived neural stem/progenitor cells may repair ischemic lesions of the cerebral cortex. In the present study, using a highly reproducible murine model of cortical infarction, we have found nestin-positive cells in the post-stroke cerebral cortex, but not in the non-ischemic cortex. Cells obtained from the ischemic core of the post-stroke cerebral cortex formed neurosphere-like cell clusters expressing nestin; such cells had the capacity for self-renewal and differentiated into electrophysiologically functional neurons, astrocytes and myelin-producing oligodendrocytes. Nestin-positive cells from the stroke-affected cortex migrated into the peri-infarct area and differentiated into glial cells in vivo. Although we could not detect differentiation of nestin-positive cells into neurons in vivo, our current observations indicate that endogenous neural stem/progenitors with the potential to become neurons can develop within post-stroke cerebral cortex.
European Journal of Neuroscience 06/2009; 29(9):1842-52. · 3.63 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: In our previous study, we found that CD36-deficient mice showed significant delays in peripheral nerve remyelination after sciatic nerve crush injury and suggested that CD36 played an important role in the restoration of injured peripheral nerves. The aim of this study was to investigate whether CD36 upregulation can promote peripheral nerve remyelination. We made crush injury that caused demyelination and mild axonal degeneration to sciatic nerves and investigated the effect of pioglitazone (PIO) on the remyelination post-injury in C57Bl/6 wild-type and CD36-deficient mice. The immunohistochemistry with anti-CD36 antibody showed that CD36 was upregulated in macrophages infiltrating peripheral nerves from the wild-type mice by PIO administration at 1 week post-injury. The lectin histochemistry represented that infiltrating macrophages lessened in the wild-type mice at 3 weeks post-injury by PIO administration. General histopathology and morphometry indicated that thinly myelinated fibers and naked axons diminished in PIO-treated wild-type mice compared with non-treated wild-type mice at 3 weeks post-injury. No significant differences were observed in remyelination and number of infiltrating macrophages between PIO-treated and non-treated CD36-deficient mice. These results indicate that PIO promotes peripheral nerve remyelination possibly through CD36. It may be possible to apply PIO to the remedy against demyelinating neuropathies.
Journal of the Peripheral Nervous System 10/2008; 13(3):242-8. · 2.80 Impact Factor
-
Akihiko Taguchi,
Nami Nakagomi,
Tomohiro Matsuyama,
Akie Kikuchi-Taura, Hiroo Yoshikawa,
Yukiko Kasahara,
Haruka Hirose,
Hiroshi Moriwaki,
Takayuki Nakagomi,
Toshihiro Soma,
David M Stern,
Hiroaki Naritomi
[show abstract]
[hide abstract]
ABSTRACT: Increasing evidence points to a role for circulating endothelial progenitors, including populations of CD34-positive (CD34(+)) cells present in peripheral blood, in vascular homeostasis and neovascularization. In this report, circulating CD34(+) cells in individuals with a history of cerebral infarction were correlated with changes in neurologic function over a period of 1 year. Patients with decreased levels of CD34(+) cells displayed significant worsening in neurologic function, evaluated by the Barthel Index and Clinical Dementia Rating. These results support the hypothesis that levels of circulating CD34(+) cells have prognostic value for neural function, consistent with their potential role in maintaining cerebral circulation.
Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 08/2008; 29(1):34-8. · 5.46 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: A 54-year-old woman, who was treated with chemotherapy for acute lymphoblastic leukemia, developed dysesthesia in her hands and feet at the age of 50 in 2003. The following year she underwent hematopoietic stem cell transplantation. In 2005, she was diagnosed with chronic graft versus host disease (cGVHD). In December 2006, she developed dysesthesia in her face and tongue (onset). 50 days after the onset, she had a respiratory infection. 10 days later, she was hospitalized for muscle weakness of four extremities and progression of dysesthesia. Nerve conduction studies and superficial peroneal nerve biopsy revealed demyelination. After high-dose immunoglobulin therapy, her muscle strength recovered. Hyponatremia was resolved by restriction of fluid intake and administration of NaCl. We suggest immunological mechanisms such as cGVHD may cause chronic inflammatory demyelinating polyradiculoneuropathy and hyponatremia.
Rinsho shinkeigaku = Clinical neurology 07/2008; 48(6):426-9.
-
Tomoyuki Yoshihara,
Akihiko Taguchi,
Tomohiro Matsuyama,
Yoko Shimizu,
Akie Kikuchi-Taura,
Toshihiro Soma,
David M Stern, Hiroo Yoshikawa,
Yukiko Kasahara,
Hiroshi Moriwaki,
Kazuyuki Nagatsuka,
Hiroaki Naritomi
[show abstract]
[hide abstract]
ABSTRACT: Increasing evidence points to a role for circulating endothelial progenitor cells, including populations of CD34-positive (CD34(+)) cells, in maintenance of cerebral blood flow. In this study, we investigated the link between the level of circulating CD34(+) cells and neovascularization at ischemic brain. Compared with control subjects, a remarkable increase of circulating CD34(+) cells was observed in patients with angiographic moyamoya vessels, although no significant change was observed in patients with major cerebral artery occlusion (or severe stenosis) but without moyamoya vessels. Our results suggest that the increased level of CD34(+) cells associated with ischemic stress is correlated with neovascularization at human ischemic brain.
Journal of Cerebral Blood Flow & Metabolism 07/2008; 28(6):1086-9. · 5.01 Impact Factor
-
Akihiko Taguchi,
Tomohiro Matsuyama,
Takayuki Nakagomi,
Yoko Shimizu,
Ryuzo Fukunaga,
Yoshiaki Tatsumi, Hiroo Yoshikawa,
Akie Kikuchi-Taura,
Toshihiro Soma,
Hiroshi Moriwaki,
Kazuyuki Nagatsuka,
David M Stern,
Hiroaki Naritomi
[show abstract]
[hide abstract]
ABSTRACT: Maintenance of uninterrupted cerebral circulation is critical for neural homeostasis. The level of circulating CD34-positive (CD34(+)) cells has been suggested as an index of cerebrovascular health, although its relationship with cognitive function has not yet been defined. In a group of individuals with cognitive impairment, the level of circulating CD34(+) cells was quantified and correlated with clinical diagnoses. Compared with normal subjects, a significant decrease in circulating CD34(+) cells was observed in patients with vascular-type cognitive impairment, although no significant change was observed in patients with Alzheimer's-type cognitive impairment who had no evidence of cerebral ischemia. The level of cognitive impairment was inversely correlated with numbers of circulating CD34(+) cells in patients with vascular-type cognitive impairment, but not Alzheimer's type. We propose that the level of circulating CD34(+) cells provides a marker of vascular risk associated with cognitive impairment, and that differences in the pathobiology of Alzheimer's- and vascular-type cognitive impairment may be mirrored in levels of circulating CD34(+) cells in these patient populations.
Journal of Cerebral Blood Flow & Metabolism 04/2008; 28(3):445-9. · 5.01 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Upper gastrointestinal tract surgery and diuretic use are 2 unrecognized causes of thiamine (vitamin B1) deficiency. Upper gastrointestinal tract surgery decreases the thiamine absorption, and diuretic use increases urinary excretion of thiamine. We present a case of a patient with a history of pancreaticoduodenectomy who had development of beriberi by diuretic use. A 68-year-old man was referred to our hospital because of pretibial pitting edema, foot numbness, and gait disturbance. He had a history of pancreaticoduodenectomy 8 years before and had been taking loop diuretics for 2 months. He had signs of polyneuropathy and hyperkinetic heart. Beriberi was suspected, and thiamine supplementation was started immediately. Edema disappeared within several days, and signs of polyneuropathy gradually subsided. Because diuretics enhance urinary thiamine excretion, practitioners should use caution for thiamine deficiency when they prescribe diuretics for patients who have a history of upper gastrointestinal surgery and potentially have latent thiamine deficiency.
The American Journal of the Medical Sciences 12/2007; 334(5):407-9. · 1.39 Impact Factor
