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Biomedical subjects

T Shirai

Publications and source records attributed to T Shirai.

At least 397 records · Page 22Linked to original sources
PubMed1995

Prospective CT confirms differences between vascular and Alzheimer's dementia.

BACKGROUND AND PURPOSE: Cognitive test performances were correlated prospectively with changes in cerebral CT measurements of atrophy, infarct volume, ventricular enlargement, local tissue density, and local perfusion to contrast annual rates of changes among patients with ischemic vascular dementia (IVD) or dementia of the Alzheimer type (DAT). METHODS: The cerebral atrophic index (ATI; ratio of cerebrospinal fluid or infarcted brain to intracranial volume), infarct volume ratio, ventricular volume ratio (VVR; ventricular volume/intracranial volume), cortical and subcortical gray and white matter local perfusion (local cerebral blood flow [LCBF]), and local Hounsfield unit (HU) density were measured concurrently and compared longitudinally with Cognitive Capacity Screening Examinations (CCSE) scores among 24 treated IVD (age, 68.2 +/- 9.7 years; follow-up, 42 +/- 27 months) and 24 DAT patients (age, 74.2 +/- 6.2 years; follow-up, 30 +/- 19 months). RESULTS: IVD annual changes were as follows: CCSE, +1.2 +/- 5.9; ATI, +2.1%/y; VVR, +3.2%/y; and LCBF in the subcortical basal ganglia, -0.74 mL.100 g-1.min-1.y-1 (-1.8%/y). DAT annual changes were as follows: CCSE, -1.8/y; ATI, +8.1%/y; VVR, +9.6%/y; cortical LCBF, -2.0 mL.100 g-1.min-1.y-1 (-5.2%/y); LCBF in the basal ganglia, -3.0 mL.100 g-1.min-1.y-1 (-6.7%/y); white matter LCBF, -0.75 mL.100 g-1.min-1.y-1 (-4.1%/y); and all cortical tissue densities, -0.83 HU/y (-2.1%/y). In IVD, multiple regression analyses correlated cognitive changes directly with (1) recurrent silent infarctions and (2) bidirectional changes of perfusions within frontal white matter, thalamus, and internal capsules. In DAT, cognitive declines correlated with cerebral atrophy and cortical hypoperfusion related to frontotemporal and parietal cortical polioaraiosis (decreased gray matter tissue densities). CONCLUSIONS: In IVD, recurrent strokes were not observed clinically during risk factor control, and antiplatelet therapy and cognitive impairments improved or stabilized. In DAT, cognitive performance relentlessly declined. Ischemic pathogenesis for vascular dementia is supported by the following: (1) cognitive declines correlate directly with recurrent "silent" strokes, and (2) bidirectional cognitive changes correlate directly with frontal white matter, thalamic, and internal capsular perfusional changes.

Aged↗
PubMed1995

Polyethylene glycol-modified avidin: a novel agent for the selective extraction of biotinylated immune-complex in an aqueous two-phase system.

Chicken avidin was chemically modified with 2,4-bis[O-methoxypoly(ethylene glycol)]-6-chloro-s-triazine (activated PEG2) to form PEG-avidin. The PEG-avidin, in which 78% of the amino groups were modified, retained 49% of the active biotin-binding sites. The modified avidin was partitioned preferentially into the PEG-phase in an aqueous two-phase system (PEG/dextran). Using PEG-avidin, the immune-complex formed between biotinylated anti-mouse IgG and its antigen IgG (mouse) molecules, was successfully transferred into the PEG-phase in an aqueous two-phase system. This finding leads to the effective isolation of a specific antigen among various kinds of antigens by partitioning with a two-phase system using PEG-avidin.

Animals↗
PubMed1995

Causal association between major histocompatibility complex and myocardial infarction in NZW x BXSB F1 mice.

The NZW x BXSB F1 male mice that a model for systemic lupus erythematosus (SLE) develop myocardial infarction. To determine whether the gene(s) linked to the major histocompatibility complex (MHC) of NZW mice are involved in myocardial infarction, we developed an H-2-congenic NZW.H-2d strain and compared the incidence of myocardial infarction in NZW x BXSB F1 (H-2z/b) male mice to that in NZW. H-2d x BXSB F1 male mice (H-2d/b). H-2z/b heterozygous F1 male mice showed a higher incidence of myocardial infarction than H-2d/b F1 male mice. This observation suggests that the myocardial infarction seen in SLE may be related to MHC.

Animals↗
PubMed1995

Effect of 14-membered ring macrolide therapy on chronic respiratory tract infections and polymorphonuclear leukocyte activity.

We studied the efficacy of the long-term administration of 14-membered ring macrolides in treating patients with diffuse panbronchiolitis (DPB) (34 patients) and bronchiectasis (BE) (40 patients). Oral administration of erythromycin (400 or 600 mg), roxithromycin (150 or 300 mg) or clarithromycin (200 or 400 mg) given daily for at least 2 months, was evaluated. The efficacy of erythromycin, roxithromycin, and clarithromycin in DPB was 19/24 (79%), 6/7 (86%), and 2/3 (67%), respectively. Efficacy of these agents in BE exceeded 50%. We determined the effect of these macrolides on the activity of polymophonuclear leukocytes (PMNs) obtained from healthy volunteers. There were no significant differences between the effects of these 14-membered ring macrolides and josamycin, a 16-membered ring macrolide which was previously found to be ineffective in treating DPB. Thus, the effectiveness of the 14-membered ring macrolides in treating DPB appears to depend on mechanism(s) other than alterations in PMN activity.

Adult↗
PubMed1995

Maternal autoimmune response to recombinant Ro/SSA and La/SSB proteins in Japanese neonatal lupus erythem atosus.

BACKGROUND: Neonatal lupus erythematosus (NLE) is a syndrome characterized by dermatitis and congenital heart block (CHB). The disease is mostly associated with transplacental passage of maternal anti-Ro/SSA and/or La/SSB antibodies. OBJECTIVE: To examine maternal autoimmune response to recombinant Ro/SSA and La/SSB proteins in NLE with a single ethnic background. METHODS: This study examined 12 NLE infants and their mothers. Serum samples were tested by enzyme-linked immunosorbent assay for reactivity with full-length recombinant human 60-kd Ro/SSA, 52-kd Ro/SSA, and 48-kd La/SSB proteins. RESULTS: All 10 infants with skin lesions and/or CHB had maternal antibodies reactive to both the 60- and 52-kd Ro/SSA polypeptide components of the Ro/SSA particle. Anti-60-kd Ro/SSA without anti-52-kd Ro/SSA, or vice versa, was found in mothers of infants who had only hepatic manifestation of NLE. Nine of 12 NLE infants had anti-48-kd La/SSB. CONCLUSION: In the majority of Japanese infants with NLE, maternal anti-Ro/SSA autoimmune response was directed against both of 60-kd and 52-kd recombinant Ro/SSA proteins. There was no profile of anti-Ro/SSA and La/SSB response unique to mothers of children with CHB or cutaneous manifestations of NLE.

Adenosine Triphosphatases↗
PubMed1995

[A 49-year-old man with progressive dysarthria, dysphagia, and left hemiparesis].

We report a 49-year-old man who presented progressive dysarthria, dysphagia, and left hemiparesis. The patient was well until June 28th of 1993 when he noted 'weakness' in his both legs; despite his weakness, he could play golf on that day. In the beginning of July, he noted difficulty in swallowing solid foods. He was admitted to the neurosurgery service of our hospital on July 15th of 1993 and a neurologic consultation was asked on July 17th. Neurologic examination at that time revealed an alert but somewhat childish man who appeared to have some difficulty in paying attention to questions. He was disoriented to time and showed difficulty in recent memory and calculation. Higher cerebral functions were intact. The optic fundi were normal; pupils were isocoric and reacted to light promptly; ocular movements were intact, however, he showed difficulty in convergence. Facial sensation and facial muscles were intact. He had no deafness. He showed slurred speech and difficulty in swallowing solid foods. The remaining cranial nerves were intact. Motor-wise, he was able to walk normally and no weakness or atrophy was noted. Mild ataxia was noted in the finger-to-nose and the heel-to-knee test on the left. Muscle stretch reflexes were normal and symmetric, however, the plantar response was extensor bilaterally. Sensation was intact and no meningeal signs were noted. General routine laboratory findings were unremarkable. CSF was under a normal pressure containing 1 cell/microliter, 68 mg/dl of protein, and 54 mg/dl of glucose. Cranial CT scan showed low density areas involving the pons, midbrain, left thalamus, and the left parietal cortex. In MRI, these areas presented low signal intensity in T1-weighted images and high signal intensity in T2-weighted in images. The brain stem appeared swollen. Gadolinium enhancement was negative. He was given a course of steroid pulse with 1 g/day of DIV methylprednisolone for three days followed by oral steroid. He showed only temporary improvement in swallowing. In the subsequent course, he showed progressive deterioration in dysarthria and dysphagia. A biopsy was performed on the left parietal lobe lesion. After biopsy, he was treated with steroid and glycerol without improvement. A course of chemotherapy with procarbazine, MCNU, and vincristine was given; he did not respond to chemotherapy. His left hemiparesis deteriorated. He developed aspiration pneumonia from dysphagia and expired on October 22, 1993. The patient was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had astrocytoma grade III involving the pons, midbrain, thalamus, and the parietal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain Neoplasms↗
PubMed1995

[A 56-year-old woman with parkinsonism and dementia with the age of onset at 41 years].

We report a 56-year-old woman with parkinsonism and dementia who died of respiratory failure. The patient was well until the age of 41 when she noted insidious onset of difficulty in moving around. Soon after, she noted tremor in both her hands and gait disturbance. She received stereotaxic right thalamotomy when she was 46-year-old; after thalamotomy, improvement was noted in her tremor, rigidity, and in gait. However, a few months later, she started to experience motor fluctuations with worsening of her symptoms in the afternoon. This worsening was temporarily relieved by increasing her levodopa/benserazide dose. She started to show visual hallucination and agitation when she was 54-year-old. Her symptoms had progressively become worse with marked motor fluctuations and she was admitted to our hospital when she was 56-year-old. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed that she was disoriented to time and place; memory was markedly disturbed and calculation was poor. Hasegawa dementia scale was 7/30. Higher cerebral functions appeared intact. She showed masked face, small voice, and some dysphagia. Other cranial nerves were intact including ocular movements. She was unable to walk by herself; when supported she walked in small steps with marked disturbance in the righting reflex. Mixed rigidity and Gegenhalten was noted in her four limbs and in the neck. Tremor was absent. She showed marked akinesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Age of Onset↗
PubMed1995

[A 51-year-old man with early onset parkinsonism].

We report of 51-year-old man with early onset parkinsonism. The patient was well until 38 years of age, when he noted a difficulty in the use of his right leg; this difficulty improved after he received a medicine from his physician. He did not take medicine regularly, and he noted difficulty in standing up from a chair and in rolling over at age 40. Tremor was not a feature, but he noted slowness in his movements at age 42; at age 49, he noted diurnal fluctuation in his symptoms and at times he experienced hallucination. He was admitted to our hospital in September of 1992 for the first time when he was 50-year-old. At that time, neurologic examination revealed an alert and somewhat bradyphrenic man; Hasegawa dementia rating scale was 20/30. Cranial nerves were intact except for masked face and small voice. He showed stooped posture and small step gait cogwheel rigidity was noted in the four limbs more on the left; tremor was absent. Deep reflexes were within normal range and the sensation was intact. As he showed diurnal fluctuation in his symptoms, his medication was switched to levodopa 3,000 mg/day without a peripheral decarboxylase inhibitor. He was discharged for out patient follow up. But he did not take drugs regularly, and his neurologic condition deteriorated; he was admitted to another hospital. Neurologic examination at that time was essentially similar to that of his first admission to our hospital, except that he showed more severe rigidity and akinesia; again tremor was not detected. His cranial CT scan showed a mild ventricular dilatation without cortical or brain stem atrophy. During his hospital stay, he developed episodes of oculogyric crisis during peak dose of levodopa, and orthostatic hypotension. He developed pneumonia and expired on October 28, 1993. He was discussed in a neurological CPC, and the chief discussion arrived at the conclusion that the patient had early onset Parkinson's disease of Lewy body type. As differential diagnoses, early onset parkinsonism without Lewy body, pure form of diffuse Lewy body disease, pallidoluysian atrophy, and other conditions were considered; however, all of those possibilities were excluded. Early onset parkinsonism without Lewy body would have much earlier onset than this patient, and diffuse Lewy body disease would show more profound dementia 13 years after the onset. Pallidoluysian atrophy would be complicated with some dystonic features. Post-mortem examination showed marked discoloration and degeneration of the substantia nigra. The degeneration was most prominent in the ventrolateral tier of the substantia nigra.(ABSTRACT TRUNCATED AT 400 WORDS)

Brain↗
PubMed1995

[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies].

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenocarcinoma↗
PubMed1995

[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance].

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1995

[Usefulness of percutaneous instillation of antifungal agents for pulmonary aspergilloma].

We studied the usefulness of percutaneous instillation of antifungal agents for treatment of pulmonary aspergilloma. The subjects were six patients, four males and two females, with a mean age of 69 years (range, 45 to 90 years). In all cases, radiography revealed a fungus ball or thickened cavity wall in residual tuberculous cavities. The patients had clinical symptoms including hemoptysis, fever, cough and sputum, and most of them showed severe emaciation, anemia, hypoalbuminemia and hypoxia. Miconazole or fluconazole was instilled through an indwelling catheter inserted percutaneously into the cavity from the anterior chest wall or parascapular region under fluoroscopic observation. After treatment with a total dose of 610 to 2070 mg over a period of 6 to 18 weeks, clinical symptoms were diminished in all patients and radiographic findings were improved in five. Furthermore, Aspergillus fumigatus, which had been isolated from sputum samples of three patients, was eradicated. According to evaluation of the overall therapeutic effects, this therapy was considered to be effective in five patients, giving an efficacy rate of 83%. No recurrence has been detected in six patients during a mean follow-up of 13 months after treatment. Since percutaneous instillation involves less pain and stress than other kinds of

Aged↗
PubMed1995

[A 75-year-old man with parkinsonism and sudden death].

We report a 75-year-old man with parkinsonism who died suddenly. The patient was well until 64 years of the age when he had an onset of tremor in his left hand. He was treated with a medicine in another hospital, and his tremor subsided. Five years after the onset, he started to note difficulty in fine finger movements and gait disturbance. He tended to lean backward with frequent falls. He was treated with bromocriptine, trihexyphenydil, and L-dops without apparent improvement. He visited our out patient clinic on November 11, 1993 when he was 75 years of the age. Neurologic examination at that time revealed an alert and well oriented man in no acute distress. Higher cerebral functions were intact. In the cranial nerves, he showed restriction in the upward as well as down ward gaze (40% of normal). He showed masking of the face and spoke in small voice. He walked in a stooped posture with small steps; retropulsion was present. Muscle rigidity was moderately positive in the neck, however, no rigidity was noted in the limbs. No abnormal involuntary movements were seen. He showed moderate bradykinesia and difficulty in finger tapping. Muscle stretch reflexes were normally elicited and the plantar response was flexor bilaterally. Sensation was intact. The autonomic nervous system appeared intact. He was treated with 300 mg/day of Sinemet with marginal improvement in his balance. In February 4, 1994, he had a common cold. On the next day, his parkinsonism worsened and he became unable to walk by himself. He was found unconscious in the bathroom on the same day. He was brought to our hospital by an ambulance. Upon arrival, he was unresponsive and was not breathing. Blood pressure could not be measured. Pupils were dilated without reaction to light. Cardiac resuscitation was attempted, however, ventricular fibrillation appeared on an EEG monitor, and he was pronounced dead at eleven o'clock in the morning. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had progressive supranuclear palsy because of vertical gaze palsy, axial rigidity, and poor response to levodopa. Regarding the cause of his sudden death, the chief discussant thought that he developed pulmonary embolism. Postmortem examination revealed non-bacterial thrombotic endocarditis in the heart, but this did not appeared to be related to his sudden death. Multiple disseminated small emboli were found occluding small arteries of the left lung; this was consistent with acute pulmonary embolism, and this was thought to be the cause of his sudden death. In the central nervous system, marked atrophy of the globus pallidus was noted; both internal as well as external segments showed marked atrophy; no myelinated fibers were seen in the globus pallidus. Neuronal cell loss was marked in the globus pallidus, the subthalamic nucleus, and the substantia nigra. No Lewy bodies or tangles were seen. The histologic diagnosis was consistent with pallido-nigro-luysian atrophy. Brownish pigments such as seen in Hallervorden-Spatz disease were seen in the globus pallidus. In addition, formy spheroids were seen in the substantia nigra. However, iron deposits were not so strong as to suggest Hallervorden-Spatz disease. Pallido-nigro-luysian atrophy is a rare neurodegenerative disorder. It is interesting to note that this condition may mimic progressive supranuclear palsy or pure akinesia clinically.

Aged↗
PubMed1995

Carcinogenicity of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) in rats: dose-response studies.

The carcinogenic potential of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), identified as the most abundant mutagenic heterocyclic amine in cooked meat and fish, was investigated in dose-response studies. Six-week-old F344 rats of both sexes were administered PhIP in the diet at concentrations of 0, 25, 100, or 400 ppm for up to 104 weeks. Animals receiving the highest dose were killed at week 52 due to marked retardation in body weight gain. PhIP was demonstrably carcinogenic for the colon in males and for the mammary glands in females, in a clear dose-dependent manner for both cases. Mammary carcinogenicity of PhIP was also confirmed in female SD rats with a clear dose-response relationship. In rat two-stage carcinogenicity models, PhIP exerted tumor-promoting activity in the small intestine as well as in the large intestine, but no promoting effects were apparent in the liver, although DNA adducts were formed dose dependently. The virtually safe dose (VSD) at the 10(-6) risk level calculated from the long-term carcinogenicity test was 0.023-0.52 ppm in the diet. This range of values is very close to or lower than human intake in daily life. Since PhIP is a most abundant heterocyclic amine and its carcinogenic organotropism overlaps with the types of neoplasias most commonly observed in western countries, the compound is likely to be extremely important with respect to human cancer development.

Adenocarcinoma↗
PubMed1994

Initiation-stage enhancement by uracil of N-ethyl-N-hydroxyethylnitrosamine-induction of kidney carcinogenesis in rats.

The present study was conducted to clarify the effects of N-ethyl-N-hydroxyethylnitrosamine (EHEN) and uracil in combination on renal carcinogenesis in female F344 rats. Group 1 animals (n = 30) received a 3-week simultaneous administration of 0.05% EHEN and 3% uracil, and group 2 (n = 26) 0.05% EHEN with a lower 1.5% dose of uracil. Group 3 (n = 30) was treated with 0.05% EHEN alone and group 4 (n = 28) received only 3% uracil for 3 weeks. In all the above four groups, the rats were given basal diet and water without chemical addition for a 48-week period after the 3-week treatment period. Group 5 (n = 33) received no chemicals for the entire 52 weeks. At the end of week 52, renal adenocarcinomas were found in 53%, 31% and 13% of the rats in groups 1, 2, and 3, respectively. The present study thus demonstrated that simultaneous administration of uracil enhances the occurrence of EHEN-induced renal adenocarcinomas in rats.

Adenocarcinoma↗
PubMed1994

Biochemical characterization and immunolocalization of SC2 protein: SC2 protein is indistinguishable from the cell adhesion molecule axonin-1.

SC2 is a monoclonal antibody that was previously shown to recognize a subset of neurons in the developing nervous system of the chick. We have now used the SC2 monoclonal antibody to purify from chick embryo brain membranes a glycoprotein that migrates at approximately 125 kDa on SDS/PAGE. The size of this protein and its distribution pattern in the spinal cord are similar to that observed for axonin-1. A polyclonal anti-axonin-1 antibody R26 specifically reacted with the SC2 protein from brain. This antibody, as well as polyclonal antibody (369) against purified SC2 protein, reacted with 115-130 kDa proteins in vitreous humor, a rich source of axonin-1, and with similar sized proteins precipitated from vitreous humor by the 369, and SC2 antibodies. Treatment of SC2 protein isolated from chick brain membranes with PI-PLC indicated that it contains a glycophosphatidylinositol (GPI) moiety. Co-aggregation experiments using Covaspheres with covalently bound proteins indicated that SC2 protein binds heterophilically to Ng-CAM. Immunohistochemical analysis of chick embryos showed that SC2 protein is abundant in the sensory nerve bundles of both the central and peripheral nervous systems during development. Its expression was restricted and it was specifically localized in the dorsal funiculus of the spinal cord, as well as in olfactory, retinal, trigeminal, vestibulocochlear, glossopharyngeal and vagal nerve fibers. The biochemical and immunohistochemical data show that SC2 protein is axonin-1, and the immunolocalization studies support the hypothesis that SC2 protein may play a role during development of particular fiber systems by interacting with other cell adhesion molecules such as Ng-CAM.

Animals↗