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Biomedical subjects

T Lin

Publications and source records attributed to T Lin.

At least 181 records · Page 10Linked to original sources

Germ cell tumors of the thalamus and the basal ganglia.

Two cases of germ cell tumors (GCTs) of the basal ganglia are presented and 40 previously reported cases are reviewed. The incidence of GCTs of the basal ganglia and thalamus was estimated as less than 14% of all intracranial GCTs. All patients except for two (95%) were male, aged 7-19 years. The clinical course was usually slow. The major symptoms were hemiparesis, mental deterioration such as dementia or character change, precocious puberty, diabetes insipidus, oculomotor palsy, speech disturbance, and hemianopsia. Signs of intracranial hypertension did not occur until the late stages of the disease. The plain CT finding was characterized by an irregularly defined, slightly high-density area frequently accompanied by central low-density areas without significant mass effect. The tumors showed mild to moderate and nonhomogeneous contrast enhancement. An ipsilateral cerebral hemiatrophy was often found. MR images demonstrated the corresponding findings. GCTs of the basal ganglia had a high possibility of containing components other than germinoma such as choriocarcinoma, endodermal sinus tumor, and embryonal carcinoma. Thus, tumor markers in the serum, CSF, or cyst fluid were frequently positive. With recent refinement of microsurgical techniques as well as immunohistochemical study and measurements of tumor markers of serum, CSF, and cyst fluid, major resections of tumor, accurate pretreatment histologic diagnosis, and early determination of the specific types of this tumor appear to be readily possible. This is essential for effective treatment of patients not only with radiosensitive germinoma, but also those with radioinsensitive nongerminoma variants and a combination of them located in this region.

Adolescent↗

Use of a new mixture for embolization of intracranial vascular malformations. Preliminary experimental experience.

The internal carotid artery system in swine has a special anatomic configuration similar to a brain "arterial-arterial malformation." The internal carotid artery breaks up into a multitude of fine channels (rete mirabile) situated at the base of the skull on the side of the hypophysis. This anatomic arterial model was used to analyze acute and chronic angiographic and histological changes after occlusion of the rete mirabile with I) avitene, II) avitene, and 50% ethanol, III) avitene, 30% ethanol and Polyvinyl alcohol, IV) avitene 50% ethanol and Polyvinyl alcohol, V) IBCA and VI) silk. Histopathological changes observed in the rete mirabile six weeks following occlusion demonstrated that a mixture of avitene, 30% ethanol and Polyvinyl alcohol and IBCA produced the best anatomic results. Embolization with avitene, PVA and ethanol induced a more bland histological reaction than the one observed with IBCA. Preliminary clinical experience with this mixture is reassuring in those cases in which the AVM was surgically resected. The partially thrombosed AVM was easily depressed and compressed by the neurosurgeon allowing for satisfactory hemostasis in and around the nidus of the AVM.

Animals↗

Inhibition of human cancer cell growth by periodate-oxidized 3-aminopyridine adenine dinucleotide phosphate.

1. Periodate-oxidized 3-aminopyridine-adenine dinucleotide phosphate inhibited the proliferation of oral epithelium cancer and breast cancer cell lines. 2. The fast growing less differentiated embryonic kidney cell was more affected by the reagent then the embryonic lung fibroblast cell. 3. Incorporation of [3H]leucine of the treated cancer cells was inhibited. Incorporation of [3H]uridine was increased. Incorporation of [3H]thymidine was first increased and then decreased. 4. Tumor malic enzyme activity was inhibited by the reagent; but the treated cells did not show any difference in malic enzyme or glucose-6-phosphate dehydrogenase levels.

Adenine Nucleotides↗

Interleukin-2 is a potent inhibitor of Leydig cell steroidogenesis.

Interstitial tissue of the testis consists of Leydig cells, macrophages, lymphocytes, plasma cells, mast cells and fibroblasts. Previously we have reported that interleukin-1 (IL-1) inhibits Leydig cell androgen production. In the present study, the effect of IL-2 was investigated. Leydig cells (10(5) cells/ml) from adult Sprague-Dawley rats were cultured with or without IL-2 for 24 h. After medium changes, human CG (hCG), 8-bromo-cAMP, or forskolin was added with or without IL-2. Cultures were continued for an additional 24 h, and testosterone and cAMP levels were measured. IL-2 up to 100 U/ml had no effect on basal testosterone production. hCG-stimulated testosterone formation was inhibited in a dose-dependent manner by the addition of IL-2. IL-2 in a concentration of 100 U/ml decreased hCG-induced testosterone formation from 49.6 +/- 3.6 ng/ml (mean +/- SE) to 8.5 +/- 4.2 ng/ml. The hCG dose-response curve was shifted to the right by the addition of IL-2. Maximal testosterone production in response to hCG was reduced 40% in the presence of IL-2 (50 U/ml) without alteration of median effective dose (ED50). IL-2 also inhibited hCG-induced cAMP formation and 8-bromo cAMP- and forskolin-stimulated testosterone production. However, IL-2 did not alter the binding of [125I]hCG to purified Leydig cells. Furthermore, IL-2 significantly inhibited the conversion of 20-OH-cholesterol, 22-OH-cholesterol, pregnenolone, progesterone, 17 alpha-hydroxypregnenolone, and 17 alpha-hydroxyprogesterone to testosterone but did not alter the conversion of dehydroepiandrosterone and androstenedione to testosterone. Our results suggest that a T cell growth factor, IL-2, is a potent inhibitor of steroidogenesis. IL-2 may play a paracrine role in modulating Leydig cell function.

8-Bromo Cyclic Adenosine Monophosphate↗

Zygosity in two cases of triplet.

A total of 11 techniques including 57 items for zygosity diagnosis was employed in two sets of triplet. Namely, placenta-fetal membrane, LDH isoenzymes, etc. The authors made an investigation in detail on the pedigree history of polyembryony and systematic analysis of two sets of male triplets. The conclusion was that the first triplet came from a single ovum, whereas the second triplet developed from double ova. Different methods for the zygosity diagnosis were discussed. It was considered that there was hereditary influence in the occurrence of triplets developing either from a single ovum or from multiple ova.

Adult↗

Neurovascular lesions and endovascular therapy: the role of MR.

Magnetic resonance imaging (MRI) studies were performed on 27 patients with vascular lesions of the central nervous system before and after embolization with either IBCA, polyvinyl alcohol foam particles, Avitene (microfibrillar collagen) or balloons. Thirteen pial brain arteriovenous malformations (AVMs), 3 brain AV fistulas, 2 giant aneurysms, 5 dural AVMs, 1 vertebro-vertebral fistula and 3 meningiomas were studied. The pre-embolization MR demonstrated the nidus and venous drainage of all pial AVMs. MR failed to detect 3 out of 5 dural AVMs using only spin echo sequences. A draining vein alone was seen in the remaining two cases. MR was superior to CT in detecting contiguous parenchymal changes such as atrophy, reversible ischemia, and mass effect in the pre-embolization studies. Following embolization, MR demonstrated partial or complete obliteration of the vascular nidus in all 13 pial AVMs. The embolized area was seen as an area of increased signal consistent with thrombus where previously there had been signal void. Ischemic or edematous changes in the brain parenchyma following embolization were seen on MR more easily than on CT scans. MR was accurate in the assessment of aneurysm patency, degree of thrombosis and balloon position in both giant aneurysms, and AV fistulae. These MR findings had an impact on patient management. MR will be an increasingly useful tool in the diagnosis and management of a number of neurovascular diseases requiring endovascular intervention.

Arteriovenous Malformations↗

Retinal dopamine and form-deprivation myopia.

Investigation of retinal neurochemistry in a well-defined chick model of form-deprivation myopia indicated that dopamine and its metabolite 3,4-dihydroxyphenylacetic acid are reduced in myopic as compared to control eyes. The reduction in retinal dopamine is evident only during light adaptation and is accompanied by a decreased rate of dopamine biosynthesis. To test whether the alteration in dopamine metabolism is related to eye growth, agents known to interact with dopamine receptors were administered locally to deprived eyes. Remarkably, the expected growth in the axial dimension was reduced, while that in the equatorial dimension was not. Therefore retinal dopamine may participate in the pathway linking visual experience and the postnatal regulation of the eye's growth in the axial dimension. The mechanism for control of chick eye growth in the equatorial dimension remains unknown.

Animals↗

Hypercalcemia of immobilization in an adult patient with peripheral neuropathy.

A 48-year-old man developed a marked and persistent hypercalcemia 3 months after admission for paraplegia resulting from severe peripheral neuropathy most likely of alcoholic etiology. Serum ionized calcium was elevated, and parathyroid hormone levels were low normal by the two separate radioimmunoassays. Urinary calcium excretion was markedly elevated, and serum 1,25-dihydroxyvitamin D level was decreased. An extensive clinical evaluation for possible occult malignancy, myeloma, and sarcoidosis as a cause of hypercalcemia produced no positive findings. Treatment with calcitonin caused prompt normalization of serum calcium, and its discontinuation resulted in recurrence of hypercalcemia. With improvement of neuropathy, the patient started active physical therapy. We gradually discontinued calcitonin, and the patient's serum calcium remained normal during the following 11 months. We discuss difficulties in both clinical and laboratory diagnosis of hypercalcemia of immobilization in the adult patient because no specific laboratory test is available.

Alcoholism↗

Regulation of Leydig cell function in primary culture by inhibin and activin.

Inhibin and activin are gonadal glycoproteins that selectively inhibit and stimulate FSH release, respectively. Previously we have reported that transforming growth factor-beta inhibited hCG-stimulated testosterone formation in mature Leydig cells. In the present study we evaluated the effects of other members of the transforming growth factor-beta family, inhibin and activin, on Leydig cell function. We found that activin (0.1-10 ng/ml) had no effect on basal testosterone formation, but inhibited hCG-stimulated testosterone formation in a dose-dependent manner. Activin (10 ng/ml) inhibited hCG-stimulated testosterone formation by 42%. Activin also inhibited hCG-stimulated cAMP formation. In the presence of activin (5 ng/ml), forskolin (10 microM)- and 8-bromo-cAMP (0.1 mM)-induced testosterone formation were reduced about one third. Conversions of pregnenolone and progesterone to testosterone were also blocked by activin. Interestingly, [125I]hCG binding to Leydig cells and forskolin-induced cAMP formation were not affected by the addition of activin. In contrast to activin, inhibin (0.1-10 ng/ml) had no effect on hCG-induced testosterone formation at any concentration used. However, the inhibitory effects of activin on Leydig cell function were reversed by the concomitant addition of inhibin. Our results suggest that activin inhibits testosterone formation by the Leydig cells derived from normal mature rats. Multiple steps of the steroidogenic pathway are affected by testosterone. Inhibin alone has no effect, but reverses the inhibitory action of activin.

8-Bromo Cyclic Adenosine Monophosphate↗

Regrowth of aneurysm sacs from residual neck following aneurysm clipping.

It is recognized that incomplete treatment of an aneurysm may result in recurrent hemorrhage with serious or fatal consequences. For this reason, patients treated at the authors' institution in whom a large portion of the aneurysm neck or sac remained after application of a clip or ligature have been subjected to reoperation. However, 1- to 2-mm residual necks seen in postoperative angiography have been thought to pose little risk. Some cases of aneurysms recurring from a narrow residual neck after clipping have been reported, and a few instances of recurrent aneurysm have been described after apparently complete occlusion of the neck (as observed angiographically or in the surgeon's judgment). In recent years, a surprising number of cases have been presented in which this seemingly unimportant remnant of the neck dilated over a long period to become a dangerous aneurysm. This finding stresses the importance of complete aneurysm occlusion and of postoperative angiography for the recognition of a residual aneurysm neck. This should be important not only in aneurysm clipping but also in the endovascular treatment of intracranial aneurysms with detachable balloons.

Adolescent↗

2(3)-tert-butyl-4-hydroxyanisole inhibits oxidative metabolism of aflatoxin B1 in isolated rat hepatocytes.

Previous studies indicate that dietary administration of phenolic antioxidants, 2(3)-tert-butyl-4-hydroxyanisole (BHA) and 3,5-di-tert-butyl-4-hydroxytoluene, inhibits the carcinogenic effect of a number of chemical carcinogens including aflatoxin B1 (AFB1). Induction of hepatic enzymes, such as glutathione S-transferase, UDP-glucuronyltransferase, and epoxide hydrolase, has been shown to be responsible for the reduction of AFB1 cytotoxic and carcinogenic effects. The effect of BHA on AFB1 activation was examined in vitro utilizing isolated rat hepatocytes and liver microsomes. In hepatocytes, the total AFB1 content and bound form of AFB1 were 3.4 and 1.4 pmol/10(6) cells, respectively. In the cell-free microsomal activating system, 2.2 pmol were activated per mg of microsomal protein during 60 min of incubation. BHA (0.1-0.5 mM) inhibited AFB1 activation and binding in both systems in a dose-dependent manner; in hepatocytes, 90% inhibition was observed at 0.5 mM. Analyzing various AFB1 adducts, BHA (0.25 mM)-treated hepatocytes contained a significantly reduced amount of AFB1 macromolecular adducts. The antioxidant neither stimulated nor inhibited the cytosolic glutathione S-transferase and microsomal UDP-glucuronyltransferase activities. Analysis of various hydroxylated (aflatoxins M1 and Q1 (AFM1 and AFQ1] and demethylated (aflatoxin P1 (AFP1] metabolites of AFB1 in both the conjugated and unconjugated form indicated that there was a 30-50% reduction of unconjugated AFP1, AFQ1, and AFM1, whereas AFB1 was increased 3-fold. There was no significant change of conjugated metabolites. The effect of BHA on AFB1 activation in hepatocytes was compared with that of other cytochrome P-450 inhibitors; the ED50 values of SKF 525A, BHA, and metyrapone were 9 microM, 40 microM, and 280 microM, respectively. In the cell-free microsomal system, biotransformation of AFB1 to AFP1, AFM1, and AFQ1 was also inhibited. Kinetic analysis of p-nitroanisole O-demethylase activity of rat liver microsomes demonstrated that BHA inhibited noncompetitively with an apparent Ki of 90 microM. In the absence of enzyme induction, the phenolic antioxidant, BHA, blocks the oxidative biotransformation of AFB1 in isolated hepatocytes.

Aflatoxin B1↗

Transient activation of c-myc protooncogene expression in Leydig cells by human chorionic gonadotropin.

This study evaluated the effects of in vivo administration of human chorionic gonadotropin (hCG) on c-myc oncogene expression in Leydig cells. Sprague-Dawley rats (46-50 days old) were treated with hCG (10 units, i.p.), and purified Leydig cells were isolated 1-24 h later. HCG caused a transient elevation of c-myc mRNA in 4 h and returned to normal or lower than normal levels at 24 h. There was no change in c-fos or beta-actin mRNA levels. Our results suggest that the growth promoting effects of hCG on Leydig cells may be mediated by the transient expression of c-myc protooncogene.

Actins↗

Nerve pathways between the pterygopalatine ganglion and eye in cats.

By dissection of thiocholine-stained orbital preparations, it has been determined that three different nerve pathways link the pterygopalatine ganglion and the eye in cats. 1) Nerves from the proximal half of the ganglion join a plexus of nerves and ganglion cells in the rete mirabile of the maxillary artery. Branches of the internal carotid nerve also supply this plexus. Fine nerves from the plexus travel to the optic nerve and then to the eye, accompanying both the nasociliary nerve that passes through the rete and the ciliary arteries that arise from the rete. 2) One or more nerves from the nerve of the pterygoid canal and from a prominent accessory ganglion near the orbital apex course to the inferior optic nerve surface at the optic foramen; these then run distally along the optic nerve to fuse with ciliary nerves or to accompany ciliary arteries entering the eye. 3) Other nerves from the pterygopalatine ganglion travel medially around the extraocular muscle cone to join the ethmoidal and infratrochlear branches of the nasociliary nerve; some nerves from the ganglion then take a retrograde course to the optic nerve, where they join ciliary nerves or arteries to the eye. All three pathways may transmit sympathetic, parasympathetic and somatic sensory nerve fibers.

Animals↗

Correlation of ultrasonic attenuation with pathologic fat and fibrosis in liver disease.

The attenuation coefficient in two groups (n1 = 70; n2 = 59) of pathologically graded in vitro human liver specimens was measured over a frequency range from 1.25-8.0 MHz and fitted to a power law model. The slopes of the power law curves at 5 MHz were correlated with pathological scores for fat in Group I, which consisted of normal and fatty livers (no fibrosis); they were also correlated with the pathological score for fibrosis in Group II, which consisted of normal and fibrotic livers (no intracellular fat). Significant (p less than 0.002) differences were found between the two groups. The fatty liver group exhibited approximately a 0.23 +/- 0.06 dB cm-1 MHz-1 (fat grade)-1 behavior (mean +/- s.d.), while the fibrotic liver group exhibited approximately a 0.11 +/- 0.01 dB cm-1 MHz-1 (fibrosis grade)-1 behavior. These results may explain some of the conflicting literature in this area, and suggest that attenuation may in principle be used for screening for liver disease, but not for differentiation between fatty and fibrotic conditions.

Fatty Liver↗

Hormonal regulation of type I insulin-like growth factor receptors of Leydig cells in hypophysectomized rats.

The effects of hCG and various pituitary hormones on type I insulin-like growth factor (IGF) receptors of purified Leydig cells of hypophysectomized rats were studied. The number of type I IGF receptors of Leydig cells obtained from hypophysectomized rats (18.0 +/- 1.5 fmol/10(6) cells) was lower than that in normal rats (54.6 +/- 5.3 fmol/10(6) cells; P less than 0.05). After a single administration of hCG (10 U, ip), specific binding of [125I]IGF-I to purified Leydig cells increased 3-fold. Scatchard analyses of the binding data suggested that increased binding was the result of an increase in receptor number, whereas binding affinity remained unaltered. Type I IGF receptor increased within 12 h and remained persistently elevated 96 h after hCG treatment. Administration of hCG (10 U, ip) daily for 5 days increased type I IGF receptor levels to 73.2 +/- 8 fmol/10(6) cells (P less than 0.001). FSH caused a small but significant increase in type I IGF receptors. Concomitant administration of FSH and hCG further enhanced IGF-I-binding capacity. IGF-I-binding affinity of Leydig cells treated with FSH or FSH plus LH was not significantly different from that in the control hypophysectomized rats. Daily administration of GH for 5 days also upregulated type I IGF receptors, whereas PRL had no effect. FSH, GH, and PRL administration had no effect on serum testosterone levels. Serum testosterone levels increased to 3.99 +/- 0.35 ng/ml after 5 days of treatment with hCG. Concomitant administration of FSH and hCG caused a further increased in serum testosterone levels (6.13 +/- 0.46 ng/ml; P less than 0.01). The present study suggests that type I IGF receptors of Leydig cells can be up-regulated by LH, FSH, and GH. However, hCG/LH seems to be the most important factor in maintaining and regulating type I IGF receptors of Leydig cells. Steroidogenic and growth-promoting effects of hCG and pituitary hormones on Leydig cells may be mediated by increased type I IGF receptors.

Animals↗

Interleukin-1 inhibits Leydig cell steroidogenesis in primary culture.

Inflammation and infection induce an acute phase response. The response is characterized by fever and production of interleukin-1 (IL-1). In the present study we evaluated the effects of interleukin-1 on Leydig cell function in primary culture. hCG-stimulated testosterone formation was markedly reduced by IL-1, with an ED50 of 1 U/ml. Basal testosterone production was slightly enhanced in the presence of low concentrations of IL-1, while high concentrations of IL-1 inhibited testosterone formation. Significant inhibition of hCG-stimulated testosterone formation was noted as early as 8 h after the addition of IL-1. IL-1 also inhibited hCG-stimulated cAMP formation, as well as 8-bromo-cAMP- and forskolin-stimulated testosterone synthesis. Furthermore, LH binding to Leydig cells was reduced by human IL-1. The inhibitory effects of IL-1 were reversed only partially by the addition of a cyclooxygenase inhibitor, indomethacin (0.1 mM), even though prostaglandin E2 formation was completely blocked. This indicates that the observed effects of IL-1 are not completely mediated by increased PGE2 formation. The present study suggests that IL-1 is a potent modulator of Leydig cell steroidogenesis. Decreased testosterone formation may modulate the immune response and contribute to the catabolic changes occurring during infection.

8-Bromo Cyclic Adenosine Monophosphate↗

Study of prostaglandins and intraocular pressure in rabbits after Nd:YAG laser anterior segment procedures.

Radioimmunoassay of rabbit aqueous humor one hour after Nd:YAG laser anterior capsulotomies revealed increased concentrations of 6-keto-prostaglandin F1 alpha (PGF1 alpha), and thromboxane B2 (TBB2). Coincidental rises in intraocular pressure (IOP) and aqueous humor protein were observed. These changes correlated with the laser power used. Pretreatment with topical 1% prednisolone acetate or 1% indomethacin prior to anterior capsulotomies inhibited the post laser rise in PGF1 alpha and TBB2, but did not eliminate the post laser rise in IOP. Small rises in IOP and the concentrations of aqueous PGF1 alpha, TBB2, and protein were observed after Nd:YAG laser iridectomies. These changes were not affected by prior treatment with 1% topical prednisolone acetate. Although PGF1 alpha and TBB2 are elevated after Nd:YAG laser anterior segment procedures, a causal relationship between post treatment IOP rise and PGF1 alpha or TBB2 release could not be determined.

Animals↗