A high body mass index tilts the pelvis caudally in the lateral decubitus position for total hip arthroplasty.

Background: Accurate cup placement is essential for obtaining excellent outcomes in total hip arthroplasty (THA). We evaluated the pelvic lateral tilt of the patient (which affects the incline of the acetabular cup in THA) and investigated the factors affecting it.

Methods: We reviewed the medical records of THA procedures performed at our hospital between October 2015 and January 2021 for which an anteroposterior pelvic radiograph was always taken preoperatively once the patient was placed in the lateral decubitus position.

No effect of anti-leprosy drugs in the prevention of Alzheimer's disease and beta-amyloid neurotoxicity.

There is continuing controversy as to whether or not anti-leprosy drugs prevent Alzheimer's disease (AD). Therefore, we examined the effect of anti-leprosy drugs on the prevalence of AD in leprosy patients, and also investigated the effect of anti-leprosy drugs on amyloid beta-protein (Abeta)-induced neurotoxicity in vitro. The present study suggests that anti-leprosy treatments do not prevent the onset of AD.

Both N-terminal and C-terminal fragments of presenilin 1 colocalize with neurofibrillary tangles in neurons and dystrophic neurites of senile plaques in Alzheimer's disease.

Presenilin 1 (PS1) is a causative gene for chromosome 14-linked familial Alzheimer's disease. The gene product is known to be cleaved into N-terminal fragments (PS1-N) and C-terminal fragments (PS1-C). To understand the pathophysiological role of PS1, we conducted immunohistochemical studies using antibodies specific for PS1-N and PS1-C in sporadic Alzheimer's disease (AD).

Determination of a cleavage site of presenilin 2 protein in stably transfected SH-SY5Y human neuroblastoma cell lines.

Mutations in the presenilin 1 (PS1) and presenilin 2 (PS2) genes are associated with early-onset autosomal dominant familial Alzheimer's disease, and the gene products are endoproteolytically processed to yield N-terminal fragments (NTF) and C-terminal fragments (CTF). We have studied the cleavage site of the PS2 protein in stably transfected human neuroblastoma cells. The 23 kD PS2-CTF was isolated by a combination of anion exchange chromatography and affinity chromatography and directly sequenced.

Identifying monoaminergic, GABAergic, and cholinergic characteristics in immortalized neuronal cell lines.

We measured the concentration of neurotransmitters in immortalized neural cell lines of hippocampal, septal, brainstem and cerebellar origin. While in most of the cell lines, concentrations of monoamines, gamma-aminobutyric acid (GABA) and acetylcholine were low, in some they were markedly higher. This made it quite easy to identify possible monoaminergic, GABAergic or cholinergic cell lines.

Analysis of lymphoproliferative cytokines produced by thymic myoid cells.

Lymphoproliferative activities produced by cloned thymic myoid cell 871207B were analysed by immunological and biochemical methods. The lymphoproliferative activities were separated into two fractions by DEAE-Sepharose CL-6B chromatography: one is in the fraction passed through the column and the other in the fraction eluated from the column with a low concentration of NaCl. The eluated fraction induced the proliferation of interleukin-1 (IL-1)-dependent D10N4 M cells.

Neurotransmitter synthesis by SN6 cell lines, a family of hybrid cell lines of embryonic septal origin.

Previously, we reported the presence of multiple neurotransmitters in subclones of SN6, a septal cholinergic hybrid cell line. To obtain information concerning the functionality of these transmitters, we measured transmitter contents, activities of transmitter-producing enzymes, and the effect of serum-free culture medium in two different batches (SN6.1.

Analysis of proteolipid protein (PLP)-specific T cells in multiple sclerosis: identification of PLP 95-116 as an HLA-DR2,w15-associated determinant.

Multiple sclerosis (MS) is a putative autoimmune disease that is linked with HLA-DR2,w15. Proteolipid protein (PLP) is a candidate autoantigen in MS, but the disease-associated epitopes have not been determined. Using overlapping and non-overlapping PLP peptides, we have studied the T cell response to the major hydrophilic domain PLP 85-159 in the peripheral blood of MS and healthy subjects (HS).

Secretion kinetics of Alzheimer's amyloid beta-protein differs from secreted beta-amyloid precursor protein.

Amyloid beta-protein (A beta) and secreted beta-amyloid precursor protein (sAPP), derived from beta-amyloid precursor protein (APP), are normally released by cultured mammalian cells. We investigated by pulse-chase analysis the secretion kinetics of these two APP derivatives using mouse cholinergic SN49 cell lines stably transfected with mouse APP695 cDNA. After both A beta and sAPP peaked at about the second hour, sAPP decreased with a half-life of approximately 5 hours, but A beta remained almost unchanged for at least 14 hours.

Demonstration of interleukin-3 receptor-associated antigen in the central nervous system.

We previously reported that interleukin-3 (IL-3) acts as a neurotrophic factor for cholinergic neurons. However, it has not yet been determined whether the action is derived from the interaction of IL-3 with IL-3 receptors. As the first step to study IL-3 receptors in the central nervous system, we examined the presence and localization of IL-3 receptor-associated antigen (IL-3RAA) in mouse and rat brain.

Production of interleukin-3 by murine central nervous system neurons.

We examined expression and production of interleukin-3 (IL-3) mRNA and IL-3 protein in mouse primary cultured neurons and glia by the reverse transcription and polymerase chain reaction and a bioassay using an IL-3-dependent cell line. IL-3 mRNA was demonstrated mainly in hippocampal neurons but not in glia, while a small but definite production of bioactive IL-3 was detected in septal and hippocampal neuronal cultures. Thus, endogenous IL-3 might be produced by certain neurons in situ.

The decrement of muscarinic receptor-mediated calcium influx by overexpression of APP in a mouse cholinergic cell line.

The effects of beta-amyloid precursor protein (APP) overexpressing on cell metabolisms of cholinergic neuronal hybridoma cell line (SN49) were examined. The cells stably overexpressing APP contained higher amount of GTP binding protein Go and cytosolic inactive protein kinase C epsilon, and showed less Ca2+ influx through muscarinic acetylcholine receptor ml compared to original and mock cells which had been transfected with a vector alone. The contents of sn-1, 2-diacylglycerol and cyclic AMP were also reduced in the APP transfectants, although the similar changes were observed in the mock cells.

High expression on Kunitz-type protease inhibitor-containing substances in the cerebral vessels of patients with Down syndrome.

Down syndrome (DS) brains, from 19 gestational weeks to 50 years of age were studied by immunohistochemical methods with a polyclonal antibody against synthetic peptide comprising part of the Kunitz-type protease inhibitor (KPI) domain of Alzheimer disease amyloid precursor protein (APP), residues 301 to 323 of APP 770. In DS, positive KPI immunoreactivity was observed in early infancy and from child to adulthood on the tunica media of the arteries in the leptomeninges, cerebral cortex and white matter, but negative or little in controls. In DS with Alzheimer type dementia, KPI immunoreactivity in the arteries was reduced, but a gross granular reactivity was noted in neurons and glial cells.

Demonstration of amyloid beta-protein secretion in a mouse neuronal cell line.

We investigated the secretion of amyloid beta-protein (beta AP) in a mouse neuronal cell line SN49. SN49 cells stably transfected with mouse beta-amyloid precursor protein (APP) 695 cDNA released approximately three times greater amounts of a 4 kDa protein immunoreactive with anti-beta AP antibodies than untransfected and mock-transfected cells. This 4 kDa protein was further identified as mouse beta AP by direct amino acid sequence analysis.

T lymphocyte lines and clones selected against synthetic myelin basic protein 82-102 peptide from Japanese multiple sclerosis patients.

As has been indicated in experimental autoimmune encephalomyelitis (EAE), the application of synthetic peptides for the selection of T cell lines may provide new insights into the pathogenesis of multiple sclerosis (MS). We report here on T cell lines/clones generated from peripheral blood of MS patients against an immunodominant myelin basic protein (MBP) peptide 82-102. This study demonstrates that the selection of T cell lines against the MBP peptide is much more efficient than against whole MBP in generating a large panel of T cell lines/clones, and therefore provides a powerful strategy for studying autoimmune T cell repertoire in individual subjects.

Characterization of a macrophage lineage cell colony-stimulating factor produced by thymic myoid cells.

Thymic myoid cells produced macrophage lineage cell stimulatory factors. Activities were separated into two factors on DEAE-Sepharose CL-6B chromatography: one eluted at lower concentrations of NaCl and the other at higher concentrations of NaCl. The latter fraction was purified to homogeneity with an apparent molecular weight of 100,000.

Thioredoxin from activated macrophages as a trophic factor for central cholinergic neurons in vitro.

The conditioned medium from gamma-interferon-stimulated macrophages elevated the choline acetyltransferase activity in mouse septal neurons as well as in cholinergic hybrid cell lines SN6.10.2.

Trophic effect of erythropoietin and other hematopoietic factors on central cholinergic neurons in vitro and in vivo.

In vitro granulocyte colony-stimulating factor (G-CSF), macrophage colony-stimulating factor (M-CSF), erythropoietin (EPO), and erythroid differentiation factor (EDF) augmented choline acetyltransferase (ChAT) activity in mouse embryonic primary septal neurons and in cholinergic hybridoma cell line, SN6.10.2.

Establishment of mouse-immortalized hybrid clones expressing characteristics of differentiated neurons derived from the cerebellar and brain stem regions.

Two clonal immortalized neurons designated CL8c4.7 and CL8a5.2 were established by somatic cell fusion between a hypoxanthine phosphoribosyltransferase-(HPRT-) deficient neuroblastoma N18TG2 and newborn mouse cerebellar/brain stem neurons.

Coexistence of cholinergic, catecholaminergic, serotonergic, and glutamatergic neurotransmitter markers in mouse clonal hybrid neurons derived from the septal region.

Two clonal immortalized neurons designated SN6.1b and SN6.2a were isolated by limiting dilution from a mouse embryonic septal cholinergic neuronal hybrid cell line SN6 (Hammond et al.

Stress induces neuronal death in the hippocampus of castrated rats.

Whereas loss of CA3 neurons in the hippocampus of monkeys which died of stress ulcers suggests that some structural changes may occur, there is no direct evidence that shows stress-induced irreversible changes of neurons. When rats were orchidectomized (castrated) and stressed by restraint and immersion in water for 15 min/day for 30 days, significant loss of hippocampal CA3 and CA4 neurons was observed. Furthermore, primary cultured hippocampal neurons survived shorter when treated with corticosterone.

Heterogeneous induction of 72-kDa heat shock protein (HSP72) in cultured mouse oligodendrocytes and astrocytes.

The expression of 72-kDa heat shock protein (HSP72) in cultured mouse oligodendrocytes and astrocytes exposed to heat shock was investigated by double immunolabelling with anti-HSP72 monoclonal antibody (C92F3B-1) and antibodies against galactocerebroside (GalC) or glial fibrillary acidic protein (GFAP). After 3 h recovery from heat shock, an intermediate level of HSP72 immunolabelling was localized in the nucleolus and cytoplasm of astrocytes (less than 25%) and to a lesser extent in oligodendrocytes (less than 2%). After 8-48 h, HSP72 was expressed intensely in the cytoplasm and nuclear matrix of oligodendrocytes (20-40%), while weak/intermediate immunostaining was detectable in astrocytes (5-15%).

Potentially amyloidogenic, carboxyl-terminal derivatives of the amyloid protein precursor.

The 39- to 43-amino acid amyloid beta protein (beta AP), which is deposited as amyloid in Alzheimer's disease, is encoded as an internal peptide that begins 99 residues from the carboxyl terminus of a 695- to 770-amino acid glycoprotein referred to as the amyloid beta protein precursor (beta APP). To clarify the processing that produces amyloid, carboxyl-terminal derivatives of the beta APP were analyzed. This analysis showed that the beta APP is normally processed into a complex set of 8- to 12-kilodalton carboxyl-terminal derivatives.

Alzheimer's disease amyloid beta-clipping enzyme (APP secretase): identification, purification, and characterization of the enzyme.

Alzheimer's disease (AD) is the most frequent cause of dementia, although no genetic abnormality has been identified. Recent studies have elucidated the molecular defect in AD, including the abnormal deposition of amyloid beta peptide (beta/A4) in senile plaques of affected individuals. Normal brain contains the enzyme, APP secretase, which cleaves inside the beta/A4 portion of the precursor protein (APP); abnormal processing of APP occurs in AD brain.

Interleukin 3 as a trophic factor for central cholinergic neurons in vitro and in vivo.

We have found that interleukin 3 (IL-3), a growth factor for hematopoietic cells, is a novel trophic factor for mouse and rat central cholinergic neurons. It enhanced neurite outgrowth and elevated choline acetyltransferase activity. The effect seems to be specific for cholinergic neurons, since somatostatin release and glutamic acid decarboxylase and 2',3'-cyclic nucleotide 3'-phosphodiesterase activities were not significantly influenced by IL-3.