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J H Su

Publications and source records attributed to J H Su.

49 records · Page 3Linked to original sources
PubMed1993

Neuritic involvement within bFGF immunopositive plaques of Alzheimer's disease.

As early as 1928, Cajal suggested that plaques contain a trophic substance which attracts neurites. Recently, basic fibroblast growth factor (bFGF) levels were shown to be elevated in Alzheimer's disease (AD) and localized to plaques and neurofibrillary tangles. We sought to clarify the subtype of plaques which contain bFGF and provide more detail on bFGFs neuronal and vascular localization in normal aged brain, AD brain, and Down's syndrome (DS) brain. We combined double-labeling immunocytochemistry for bFGF with heparan sulfate glycosaminoglycans, beta-amyloid, and thioflavine fluorescence. In addition, the neuritic markers tau-1 and PHF-1 were combined with bFGF staining. Eleven AD, five nondemented controls, and four DS cases were examined. Most bFGF immunopositive plaques contained numerous dystrophic fibers, indicating they were of the neuritic subtype. We also detected a variety of bFGF-positive cells, including hilar, dentate granule, pyramidal, and stellate neurons, as well as astrocytes. The basement membrane of large and small arterioles also contained bFGF. bFGF immunoreactivity within neurons, astrocytes and the vasculature was increased in AD cases relative to controls. Immunoreactivity within the DS cases was intermediate. These results suggest that bFGF is up-regulated in AD and support the hypothesis that bFGF may attract neurites into plaques. Alternatively, an injured neurite may induce bFGF production by responding glia, resulting in further neuritic attraction.

Aged↗
PubMed1992

Aggregation of the amyloid precursor protein within degenerating neurons and dystrophic neurites in Alzheimer's disease.

Using a monoclonal antibody raised against purified, native, human protease nexin-2/amyloid precursor protein, which recognizes an amino terminal epitope on the amyloid precursor protein and detects all major isoforms of amyloid precursor protein, we examined the localization of the amyloid precursor protein within Alzheimer's and aged control brains. Very light cytoplasmic neuronal amyloid precursor protein staining but no neuritic staining was visible in control brains. In the Alzheimer's brain, we detected numerous amyloid precursor protein-immunopositive neurons with moderate to strong staining in select regions. Many neurons also contained varying levels of discrete granular, intracellular accumulations of amyloid precursor protein, and a few pyramidal neurons in particular appeared completely filled with amyloid precursor protein granules. "Ghost"-like deposits of amyloid precursor protein granules arranged in pyramidal, plaque-like shapes were identified. We detected long, amyloid precursor protein-immunopositive neurites surrounding and entering plaques. Many contained swollen varicosities along their length or ended in bulbous tips. Amyloid precursor protein immunoreactivity in the Alzheimer's brain was primarily present as granular deposits (plaques). The amyloid precursor protein granules do not appear to co-localize within either astrocytes or microglia, as evidenced by double-labeling immunohistochemistry with anti-glial fibrillary acidic protein and anti-leukocyte common antigen antibodies or Rinucus cummunicus agglutin lectin. Amyloid precursor protein could occasionally be detected in blood vessels in Alzheimer's brains. The predominantly neuronal and neuritic localization of amyloid precursor protein immunoreactivity indicates a neuronal source for much of the amyloid precursor protein observed in Alzheimer's disease pathology, and suggests a time-course of plaque development beginning with neuronal amyloid precursor protein accumulation, then deposition into the extracellular space, subsequent processing by astrocytes or microglia, and resulting in beta-amyloid peptide accumulation in plaques.

Aged↗
PubMed1992

Localization of heparan sulfate glycosaminoglycan and proteoglycan core protein in aged brain and Alzheimer's disease.

Two monoclonal antibodies, one which recognizes a glycosaminoglycan epitope present in heparan sulfate glycosaminoglycan and another which recognizes the core protein of a basement membrane heparan sulfate proteoglycan, were used to study the distribution and localization of these components in Alzheimer's disease and control brain. The cytoplasm of neurons, and occasional neurofibrillary tangles, senile plaques and astrocytes were immunopositive for the heparan sulfate glycosaminoglycan antibody in control brains. In Alzheimer's tissue, however, the number and intensity of these elements was more extensive than in control brains. In addition, within the Alzheimer's brains studied, the nuclei of select neurons and a small number of microglia were also immunopositive for heparan sulfate glycosaminoglycan in contrast to controls, where nuclei and neuroglia were immuno-negative. Some senile plaques in Alzheimer's tissue also contained strong heparan sulfate glycosaminoglycan-positive neurites which were not seen in controls. In Alzheimer's tissue, double labeling for heparan sulfate glycosaminoglycans and the beta-amyloid protein in adjacent sections revealed that, in general, heparan sulfate glycosaminoglycan- and beta-amyloid protein-immunopositive plaques were co-localized. Occasionally, however, beta-amyloid-positive plaques were seen without heparan sulfate glycosaminoglycan immunoreactivity and vice versa. Heparan sulfate glycosaminoglycan immunoreactivity and Tau immunoreactivity co-localized in many neurofibrillary tangles; however a small number of heparan sulfate glycosaminoglycan-positive neurofibrillary tangles did not co-localize with Tau-positive neurofibrillary tangles. In contrast, the heparan sulfate proteoglycan antibody immunostained only the walls of blood vessels and a few senile plaques in Alzheimer's brains and primarily blood vessels in control brains. Heparan sulfate glycosaminoglycan immunostaining was present within neurons, glia, neurofibrillary tangles and senile plaques in Alzheimer's tissue. These results suggest that heparan sulfate-like molecules play an important role in the pathogenesis of the characteristic lesions of Alzheimer's disease and could serve as a marker reflecting early pathological changes.

Aged↗
PubMed1991

Ageing-associated 5 kb deletion in human liver mitochondrial DNA.

Using PCR technique and restriction mapping, we analyzed liver mitochondrial DNA (mtDNA) of 2 stillborn babies and 55 Chinese subjects from 27 to 86 years old and blood cell mtDNA from 20 subjects of various ages. An ageing-associated 4,977-bp deletion was detected between nucleotide position 8,469 and 13,447 (or between 8,482 and 13,460) in the liver mtDNA of older subjects. In the region containing the junction fragment, we observed a 13 bp repeat "ACCTCCCTCACCA". Moreover, the incidence of the deleted mtDNA of each of the study subjects was found to increase with age. The deletion was found in 5 out of 8 patients of the 31-40 age group and 9 out of 11 patients of the 41-50 age group, and in all the patients over 50 years old. The deletion was not observed in either the mtDNA of the liver of the stillbirth or the blood cells of subjects of all the age groups. These results support our previous contention that liver mitochondrial respiratory functions decline with age and the hypothesis that continuous accumulation of mitochondrial DNA mutation is an important contributor to ageing process.

Adult↗
PubMed1985

The time interval effect on two consecutive LHRH-TRH tests on adult female baboons.

To Clarify the relationship between the time interval and pituitary Luteinizing hormone (LH), Follicular stimulation hormone (FSH) and prolactin (PRL) secretion function under LHRH-TRH stimulation, 4 mature female baboons were used. Two consecutive LHRH (100 micrograms)-TRH (250 micrograms) stimulations with a 60 min interval between them was carried out in the early follicular phase, late follicular phase and mid luteal phase in the same baboon in the first menstrual cycle, then carried out with a 120 min interval between tests in the third menstrual cycle. The LH, FSH and PRL were measured by specific radioimmunoassay. The PRL maximum response to the first bolus of TRH was higher than maximum response to the second bolus of TRH. The PRL maximum response to the second TRH at a 120 min interval was higher than the maximum response to the second TRH at a 60 min interval. It seems that the TRH had the dominant effect on PRL releasing but not on PRL Priming. The maximum LH response to the second bolus of LHRH was higher than the maximum response to the first bolus of LHRH. The LH maximum response to the second bolus of LHRH at a 60 min interval was greater than the maximum response at a 120 min interval in the follicular phase but it was the reverse in the luteal phase. The FSH response to the second LHRH was different from the LH response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

[The influence of bromocriptine-induced pregnancy and delivery on infertile cases with pituitary microadenoma].

Two consecutive pregnancies were induced in three hyperprolactinemic primary infertile patients bearing intrasellar microadenoma without visual disturbance. Pretreatment prolactin levels, 224 -496ng/ml, were normalized by 10-22.5mg/day of bromocriptine and the initial conceptions occurred. No abnormal sign due to pituitary enlargement was detected throughout the period of gestation and they delivered single full-term babies. Since no significant change was observed in puerperium, it was decided to give the second bromocriptine therapy. The prolactin levels, 80-190ng/ml, measured before the second therapy were apparently lower than those seen prior to the first therapy and the minimum effective dose used to induce the second pregnancy (5-7.5mg/day) was identical to 1/3-1/2 of the first one. The course of the second pregnancy of each case was also uneventful and the babies were all normal and mature. The magnitude of the rise in the prolactin level during the second pregnancy was smaller than that observed during the first pregnancy. The present longitudinal study throughout two consecutive pregnancies in three cases indicates that resolution of prolactinoma was resulted in some extent after withdrawal of stimulative factors associated with pregnancy. Hence, hyperprolactinemic infertile cases with intrasellar microadenoma can be subjected to bromocriptine therapies inducing consecutive pregnancies under intensive follow-up.

Adenoma↗
PubMed1983

[Visual and neurological disturbances accompanying with pregnancies of hyperprolactinemic patients].

Twenty-three hyperprolactinemic infertile cases become pregnant after surgical treatment and/or bromocriptine administration, and 18 of them accomplished normal full-term deliveries. Serial ophthalmological examination which had been performed monthly throughout pregnancy revealed that four cases bearing pituitary adenomas developed visual disturbances which manifested themselves in the latter part of gestational period. The objective signs detected in these cases were bitemporal hemianopsia, temporal and nasal visual defects and the disappearance of central isopter. Another patient with microadenoma complained of headache at 16 weeks of gestation and it became more severe as gestation progressed. Bromocriptine (1.25 mg/day) was effective in diminishing this symptom. Although all these cases recovered from visual disturbances and headache after delivery, two of them were operated on transsphenoidally when radiological evidence of pituitary enlargement was found in the postpartum period. It is generally accepted that nearly 20% of hyperprolactinemic patients have pituitary adenomas. In view of the limited accuracy of techniques used in diagnosing pituitary tumor, it is legitimate to postulate that most hyperprolactinemic infertile patients have microadenoma to some extent. For this reason, a detailed follow up of visual field and neurological signs throughout pregnancy of hyperprolactinemic patients is important in early detection of changes in pituitary size.

Adenoma↗
PubMed1981

[The change of hypothalamic-pituitary-ovarian function during peripubertal period in female baboons (author's transl)].

To clarify the relationship between the change in plasma levels of pituitary and ovarian hormones and the development of hypothalamic-pituitary-ovarian function in the course of sexual maturation, longitudinal studies were performed using seven peripubertal female baboons (Papio cynocephalus). Serial blood samples were collected every two weeks from 12 months before menarche to 8 months after menarche. Plasma levels of prolactin, LH, FSH and estradiol were determined by specific radioimmunoassay methods. Periodic injections of synthetic LHRH (100 microgram) + TRH (500 microgram) and conjugated estrogen (Premarin 20mg) at one month interval were also conducted throughout the period studied. Furthermore, daily blood samples were drawn from two baboons from the first day of menarche up to the subsequent onset of vaginal bleeding, and the fluctuations of the same kinds of plasma hormonal levels were analysed. The basal plasma levels of FSH showed the earliest significant increase seven months prior to menarche, while those of LH, prolactin and estradiol exhibited no apparent change. Statistically significant elevations of basal plasma LH, prolactin and estradiol levels were observed one month before menarche. Intravenous injections of LHRH which were given earlier than two months before menarche induced marked responses in FSH with limited changes in LH patterns. After this stage of puberty, the response of LH stimulated by LHRH administrations were augmented progressively, whereas those of FSH became impaired. The peak values of prolactin after TRH injections increased, obviously around the same period of sexual development. The LH positive feedback induced by Premarin was observed one month before menarche in four baboons whose LH responses were exaggerated significantly by LHRH, and the sex skin reached turgidity to a certain extent. The evaluation of the hormonal changes during the first menstrual cycles after menarche indicated that the follicular phases were prolonged due to delayed elevation of FSH during the early follicular phase, and the length of the luteal phases were shorter in comparison to those seen in the normal ovulatory cycles of adult baboons. The results from the present longitudinal studies on baboons revealed characteristic changes accompanied by the maturation of the hypothalamic-pituitary-ovarian function during the peripubertal period. The initial change was the increase of basal FSH levels, which was caused by the alteration of hypothalamic sensitivity to endogenous estrogen, and that FSH stimulated the ovary to secrete estrogen. The increased basal estradiol secretion influenced both hypothalamic and pituitary functions, namely, the dominant gonadotropin secretion by the pituitary shifted from FSH to LH, a positive feedback mechanism was established, and prolactin level secretions with enhanced response after TRH stimulations were increased. This sequence of events indicates that hypothalamic-pituitary-ovarian interaction occurs during maturation in the peripubertal period.

Animals↗
PubMed1980

Radioimmunoassay method for baboon plasma gonadotropins.

Double antibody radioimmunoassay methods were developed for the determination of baboon luteinizing hormone (bLH) and follicle stimulating hormone (bFSH). The bLH radioimmunoassay employs a unique anti-ovine LH serum (GDN-15) and ovine LH (LER-1056-C2) for radioiodination, while the bFSH radioimmunoassay employs an heterologous system, i.e., an anti-ovine FSH serum (H-31) and purified human FSH for radioiodination. The reference standard used in both assays is a crude rhesus pituitary extract (LER-1909-2). Elevated endogeneous baboon plasma TSH and prolactin induced by the intravenous administration of 500 microgram of TRH had no influence on the levels of LH and FSH, whereas simultaneous intravenous administration of 100 microgram LHRH and 500 microgram TRH raised the levels of LH and FSH in plasma. hPRL, hCG, hTSH and hGH did not cross react with either the bLH or the bFSH assay system. The determination of plasma LH and FSH concentrations in daily samples from 6 mature female baboons throughout ovulatory menstrual cycles revealed patterns qualitatively similar to those of the rhesus monkey and human females.

Animals↗
PubMedDate not supplied

MRI demonstration of peritoneal implants.

The magnetic resonance imaging (MRI) findings of 12 proven cases of peritoneal implants, mainly carcinomatosis, were reviewed for evidence of peritoneal seedings. The seeded sites include the pouch of Douglas, the ileocecal and retrocecal regions, the right and left paracolic gutters, Morison's pouch, the right subdiaphragmatic parietal peritoneum, the greater and lesser omentum, the gastrocolic, gastrosplenic, and phrenicocolic ligaments, the small bowel mesentery, the sigmoid and transverse mesocolons, and the small and large bowel walls. Sizes varied from less than 1 cm to omental cake and bulky tumors. The findings include linear or tiny nodular infiltrations of the omentum and subperitoneal fat (ligamentous, mesenteric, and mesocolic), focal or segmental wall thickenings, loss of unilateral colonic haustration with sacculation on the contralateral side, and nodular soft tissue masses along different locations of the peritoneal surfaces. Air was introduced via an antegrade or retrograde method to act as a gastrointestinal contrast agent and was found to be useful for delineating the seedings. As is true with computed tomography scan, miliary implants are also not detectable with MRI. The sensitivity and specificity of MRI in detecting peritoneal implants remain to be determined.

Abdominal Neoplasms↗
PubMedDate not supplied

Beta-amyloid accumulation in aged canine brain: a model of early plaque formation in Alzheimer's disease.

We characterized eight aged beagles (maintained from birth in a laboratory colony) and one black Labrador using Bielschowsky's, thioflavine S, and Congo red staining, and antibodies to the beta-amyloid peptide, dystrophic neurites, and other plaque components. All plaques within these canine brains were of the diffuse subtype and were neither thioflavine S- nor Congo red-positive. The majority of plaques in the entorhinal cortex contained numerous neurons within them while plaques in the dentate gyrus did not. beta-Amyloid immunoreactivity was also present within select neurons and neuronal processes and was detected as a diffuse linear zone corresponding to the terminal fields of the perforant path. There was no significant correlation between extent of beta-amyloid accumulation and neuron number in entorhinal cortex. Neither tau-1, PHF-1, nor SMI-31-immunostaining revealed dystrophic fibers, confirming the classification of these plaques as diffuse. Canine plaques did not appear to contain bFGF- or HS-positive immunostaining. This may explain why neuritic involvement was not detected within these canine plaques. It is possible that the beta-amyloid within the canine brain has a unique primary structure or may not be in an assembly state that adversely affects neurons.

Adolescent↗
PubMedDate not supplied

Astrocytes degenerate in frontotemporal dementia: possible relation to hypoperfusion.

To understand the extent and specificity of astrocyte pathology in sporadic frontotemporal dementia (FTD), we examined several FTD cases for molecular and morphologic characteristics of astrocyte degeneration. We quantified reactive and degenerating astrocytes in sections of frontal, temporal, parietal, and occipital cortex identified using glial fibrillary acidic protein (GFAP) immunoreactivity, terminal deoxynucleotidyl transferase (TdT) labeling, and morphological characteristics and compared them with nondemented, age-matched control brains. Conventional and confocal microscopy revealed that a subpopulation of GFAP(+) astrocytes exhibited positive TdT labeling and beading of their processes in the frontal, temporal, and parietal cortices in 5 of 7 FTD cases that also exhibited gliosis. This morphology was reproduced in cultured astrocytes using ischemic insults. Degenerating astrocytes in FTD correlated inversely with cerebral blood flow as measured by single photon emission computed tomography (SPECT) analysis of (133)Xe inhalation (r = 0.55, p < 0.05). Furthermore, areas of significant astrogliosis corresponded to areas of SPECT hypoperfusion, suggesting that astrocytes may be affected by or perhaps have a causal role in the disturbances of cerebral perfusion in FTD.

Aged↗