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Biomedical subjects

W H Yu

Publications and source records attributed to W H Yu.

At least 109 records · Page 6Linked to original sources
PubMed1982

A study of nutritional and bio-geochemical factors in the occurrence and development of Keshan disease.

Keshan disease is a chronic endemic cardiomyopathy, which was first discovered in the rural areas of China. The author proposes that Keshan disease is a nutritional bio-geochemical disease. The differences between the endemic and non-endemic areas consist of the water-soil factors (bio-geochemical elements) in the natural environment. The etiological factor of the natural environment in the endemic region acts on the human body by way of the food consumed. Those who lived on a "single type of food", which was produced from their own fields, were liable to suffer from Keshan disease. Young females of child-bearing age and children after lactation were the most frequent victims of the disease. The use of soy-beans to improve the diet and oral administration of sodium selenite will prevent Keshan disease. Experiments on animals fed on cereals and vegetables from the endemic areas areas have shown that there might be some myocardial necrotizing factor and/or growth inhibition factor in the water-soil elements.

Animals↗
PubMed1980

Uptake sites of horseradish peroxidase after injection into peritoneal structures: defining some pitfalls.

Following injection of horseradish peroxidase (HRP) either into the jejunal wall or the peritoneal cavity, neurons in the dorsal motor nucleus of the vagus nerve, celiac, nodose and spinal ganglia, and ventral and lateral horns of the spinal cord from the mid-thoracic to lumbar segments were labeled. When HRP was injected into the wall of the exteriorized gut, neurons of the spinal cord were not labeled. Furthermore, there was a significant decrease in the number of labeled neurons in the dorsal motor nucleus and ganglia examined. These results indicate that HRP injected into the intestinal wall could leak into the peritoneal cavity and be taken up and transported to neuronal cell bodies by nerve fibers not terminating in the injection area. The leakage of HRP to nearby abdominal structures and its subsequent uptake by nerve fibers is attributed to the lack of a diffusion barrier across the surfaces of the intestinal wall and the abdominal structures. It is suggested that in applying the HRP techniques for the study of neuronal connections in the peripheral nervous system, it is essential that carefully pla-ned control experiments be undertaken which can overcome the problem of mislabeling due to diffusion from the injection site.

Animals↗
PubMed1980

Origin of the preganglionic visceral efferent fibers to the glands in the rat tongue as demonstrated by the horseradish peroxidase method.

A study was made to identify the cells which give origin to the preganglionic visceral efferent fibers to the 'intralingual' glands in the tongue of the albino rat by the horseradish peroxidase (HRP) method. The medium-sized multipolar neurons whose cell bodies were filled with HRP were located in the lateral reticular formation at the level between the facial motor nucleus and the superior olivary nucleus. These HRP-labeled neurons were identified as belonging to the superior salivatory nuclear complex. There was no discernible topographical separation within the superior salivatory nucleus for the submandibular glands and 'intralingual' glands.

Animals↗
PubMed1976

The effect of 5-bromodeoxyuridine on the postnatal development of the rat cerebellum: a biochemical study.

The effect of a thymidine analog, 5-bromodeoxyuridine (BrdU), on the postnatal development of the cerebellum was studied. Rats were injected with 15 mg per 100 gram body weight of BrdU twice a day for 3 consecutive days from the second day after birth, and were killed at 5, 7, 15, 22 and 35 days of age. One hour prior to killing, the rats were given tritiated thymidine. The cerebellar DNA, RNA, protein and cerebroside, and the incorporation of thymidine were measured. BrdU administration caused a markedly retarded growth of the body and the cerebellum. At 35 days of age, the weights of the body and the cerebellum were 42 and 69% of the controls. Quantitative measurements of cerebellar nucleic acids and isotope uptake correlated well with previous morphological observation, and indicated that the analog caused a transient inhibition of cell formation and possibly destruction of stem cell population of the external granular layer. This inhibitory effect was compensated later by a more rapid DNA deposition and a prolongation of the period of cell proliferation. However, the restitution was incomplete and resulted in a permanent deficit in the final cell number, as reflected by the reduction in the size of the cerebellum of the BrdU-treated rats.

Age Factors↗
PubMed1971

Ultrastructural changes in chick cerebellum induced by polyinosinic polycytidylic acid.

The ultrastructural changes in cerebellar encephalopathy induced by intravenous injection of poly I:C in young chickens were studied. The neuroglia and the small blood vessels showed the most severe injury. In the astroglia, initial alterations consisted of a mild cytoplasmic swelling whereas terminally, evagination of the outer nuclear membrane, formation of large vacuoles, and mitochondrial swelling occurred. In the cortex, oligodendroglial alterations consisted of dilatation of the nuclear membranes and of the endoplasmic reticulum, whereas in the white matter, the interfascicular oligodendroglia exhibited clumping and coagulation of the chromatin material. Some small blood vessels appeared normal, while others showed massive erosion of the endothelium resulting in aneurysm-like ballooning of the vascular wall. The granule cells displayed marked edema. The myelin of nerve fibers showed an accumulation of fluid initially, with splitting occurring in the terminal stages. These studies indicated a severe cytotoxic effect of poly I:C on the cerebella of young chickens.

Animals↗
PubMedDate not supplied

Effects of the gonadotropin-releasing hormone associated peptides (GAP) on the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in vivo.

Six peptide sequences residing between basic amino acid residues in GAP were tested for effects on the release of FSH, LH and PRL in vivo in ovariectomized, estrogen-progesterone-primed (OEP) rats. Synthetic GAP peptides (1-13, 1-23, 15-23, 25-36, 38-53 and 41-53) were injected intravenously (IV) into conscious OEP rats and plasma levels of FSH, LH and PRL were measured by RIA. The activity of GAP peptides in the control of PRL was further examined in ether-stressed male rats which were injected IV with GAP peptides just prior to a 1-min etherization. GAP(1-13) significantly stimulated FSH release at doses of 1, 10 and 100 micrograms, whereas it stimulated LH release only at the highest dose of 100 micrograms. GAP(1-23) elevated plasma levels of FSH and LH only at a dose of 100 micrograms. The other 4 peptides had no effect on the release of gonadotropins. Of these 6 peptides, only GAP(1-13) partially lowered the plasma levels of PRL at the high dose of 100 micrograms in OEP rats, but it had no effect on the ether-induced PRL surge at doses of 10 and 100 micrograms. In conclusion, both GAP(1-13) and GAP(1-23) stimulate FSH and LH release in vivo; these 2 peptides are much less potent in stimulating gonadotropin release than is LHRH. GAP(1-13) exerts a preferential FSH-releasing activity, but its PRL-inhibiting activity is minimal.

Animals↗
PubMedDate not supplied

Effect of sympathectomy on isoproterenol-induced expression of the cysteine proteinase inhibitor gene, cystatin S, in rat submandibular glands.

The autonomic nervous system regulates the secretory function of salivary glands. The volume, rate of secretion and composition of saliva are regulated by both sympathetic (alpha 1-, alpha 2 and beta 1-adrenergic) and parasympathetic (muscarinic and cholinergic) receptor systems. The rat cystatin S gene, a member of family 2 of the cysteine proteinase inhibitor superfamily, has a very defined pattern of expression during the postnatal development of the rat submandibular gland. Its expression is not detected in the fetus or in rats up to three weeks of age. After this time, the amount of cystatin S mRNA increases, reaching a conspicuously high concentration at 28 days, and then it declines to a barely detectable level at 32 days of age; cystatin S mRNA is not detectable in the glands of adult animals. However, the beta-adrenoreceptor agonist isoproterenol (IPR) induces high concentrations of cystatin S mRNA in the submandibular gland in vivo. This paper reports experiments analysing the participation of the sympathetic nervous system in the IPR-induced expression of the cystatin S gene. Sympathetic denervation (unilateral and bilateral) by removing the superior cervical ganglion 14 days before a single injection of IPR reduced the expression of the cystatin S gene. Chemical denervation by reserpine (a drug that depletes neurotransmitters in sympathetic nerve terminals) also reduced IPR-induced expression of the gene. Morphological analyses of sympathectomized and reserpine-treated glands showed that the structure of the gland was similar to that of glands of intact animals and to those not treated with reserpine. The hypertrophic response to IPR was less obvious in the sympathectomized glands, but was similar in reserpine treated animals. Collectively, these data suggest that even in the presence of a functional beta 1-adrenergic receptor pathway, factor(s) from the sympathetic nervous system may be required for IPR-induced expression of the cystatin S gene.

Adrenergic beta-Agonists↗
PubMedDate not supplied

Control of gonadotropin secretion by follicle-stimulating hormone-releasing factor, luteinizing hormone-releasing hormone, and leptin.

Fractionation of hypothalamic extracts on a Sephadex G-25 column separates follicle-stimulating hormone-releasing factor (FSHRF) from luteinizing hormone-releasing hormone (LHRH). The FSH-releasing peak contained immunoreactive lamprey gonadotropin-releasing hormone (lGnRH) by radioimmunoassay, and its activity was inactivated by an antiserum specific to lGnRH. The identity of lGnRH-III with FSHRF is supported by studies with over 40 GnRH analogs that revealed that this is the sole analog with preferential FSH-releasing activity. Selective activity appears to require amino acids 5-8 of lGnRH-III. Chicken GnRH-II has slight selective FSH-releasing activity. Using a specific lGnRH-III antiserum, a population of lGnRH-III neurons was visualized in the dorsal and ventral preoptic area with axons projecting to the median eminence in areas shown previously to control FSH secretion based on lesion and stimulation studies. Some lGnRH-III neurons contained only this peptide, others also contained LHRH, and still others contained only LHRH. The differential pulsatile release of FSH and LH and their differential secretion at different times of the estrous cycle may be caused by differential secretion of FSHRF and LHRH. Both FSH and LHRH act by nitric oxide (NO) that generates cyclic guanosine monophosphate. lGnRH-III has very low affinity to the LHRH receptor. Biotinylated lGnRH-III (10(-9) M) labels 80% of FSH gonadotropes and is not displaced by LHRH, providing evidence for the existence of an FSHRF receptor. Leptin has equal potency as LHRH to release gonadotropins by NO. lGnRH-III specifically releases FSH, not only in rats but also in cows.

Animals↗
PubMedDate not supplied

The nitric oxide hypothesis of aging.

Nitric oxide (NO), generated by endothelial (e) NO synthase (NOS) and neuronal (n) NOS, plays a ubiquitous role in the body in controlling the function of almost every, if not every, organ system. Bacterial and viral products, such as bacterial lipopolysaccharide (LPS), induce inducible (i) NOS synthesis that produces massive amounts of NO toxic to the invading viruses and bacteria, but also host cells by inactivation of enzymes leading to cell death. The actions of all forms of NOS are mediated not only by the free radical oxidant properties of this soluble gas, but also by its activation of guanylate cyclase (GC), leading to the production of cyclic guanosine monophosphate (cGMP) that mediates many of its physiological actions. In addition, NO activates cyclooxygenase and lipoxygenase, leading to the production of physiologically relevant quantities of prostaglandin E2 (PGE2) and leukotrienes. In the case of iNOS, the massive release of NO, PGE2, and leukotrienes produces toxic effects. Systemic injection of LPS causes induction of interleukin (IL)-1 beta mRNA followed by IL-beta synthesis that induces iNOS mRNA with a latency of two and four hours, respectively, in the anterior pituitary and pineal glands, meninges, and choroid plexus, regions outside the blood-brain barrier, and shortly thereafter, in hypothalamic regions, such as the temperature-regulating centers, paraventricular nucleus containing releasing and inhibiting hormone neurons, and the arcuate nucleus, a region containing these neurons and axons bound for the median eminence. We are currently determining if LPS similarly activates cytokine and iNOS production in the cardiovascular system and the gonads. Our hypothesis is that recurrent infections over the life span play a significant role in producing aging changes in all systems outside the blood-brain barrier via release of toxic quantities of NO. NO may be a major factor in the development of coronary heart disease (CHD). Considerable evidence has accrued indicating a role for infections in the induction of CHD and, indeed, patients treated with a tetracycline derivative had 10 times less complications of CHD than their controls. Stress, inflammation, and infection have all been shown to cause induction of iNOS in rats, and it is likely that this triad of events is very important in progression of coronary arteriosclerosis leading to coronary occlusion. Aging of the anterior pituitary and pineal with resultant decreased secretion of pituitary hormones and the pineal hormone, melatonin, respectively, may be caused by NO. The induction of iNOS in the temperature-regulating centers by infections may cause the decreased febrile response in the aged by loss of thermosensitive neurons. iNOS induction in the paraventricular nucleus may cause the decreased nocturnal secretion of growth hormone (GH) and prolactin that occurs with age, and its induction in the arcuate nucleus may destroy luteinizing hormone-releasing hormone (LHRH) neurons, thereby leading to decreased release of gonadotropins. Recurrent infections may play a role in aging of other parts of the brain, because there are increased numbers of astrocytes expressing IL-1 beta throughout the brain in aged patients. IL-1 and products of NO activity accumulate around the plaques of Alzheimer's, and may play a role in the progression of the disease. Early onset Parkinsonism following flu encephalitis during World War I was possibly due to induction of iNOS in cells adjacent to substantia nigra dopaminergic neurons leading to death of these cells, which, coupled with ordinary aging fall out, led to Parkinsonism. The central nervous system (CNS) pathology in AIDS patients bears striking resemblance to aging changes, and may also be largely caused by the action of iNOS. Antioxidants, such as melatonin, vitamin C, and vitamin E, probably play an important acute and chronic role in reducing or eliminating the oxidant damage produced by NO.

Aging↗
PubMedDate not supplied

Restitution of bromodeoxyuridine-induced changes in cerebellar development.

Previously, it was shown that bromodeoxyuridine (BrdU) in 2-day-old rats caused hypoplasia of the external cerebellar granular layer. Significant restitution was achieved after removal of BrdU by an increase in the rate and duration of proliferative activity of the EGL cells, but abnormal cerebellar cytoarchitecture remained detectable at 35 days of age due mainly to polarity changes in the regenerated cells. The present report concerns repair of the EGL after giving BrdU to 7-day-old rats i.p. (15 mg/100 g body weight) twice daily for 3 days and killed at 15 days-of-age. Now, the regenerative capacity of the EGL was severely curtailed. The proliferative activity of the EGL of the treated animals was similar to normal controls and there was no change in the orientation of either the EGL cells or the parallel fibers. The only noticeable differences were a decrease in the width of the molecular layer and the presence of unusually elongated primary dendrites in many Purkinje cells of the BrdU treated rats. It was concluded that lengthening of the cell cycle time had slowed down the removal of BrdU and thus reduced the regenerative potential of the EGL at this age.

Animals↗
PubMedDate not supplied

Hypothalamic control of FSH and LH by FSH-RF, LHRH, cytokines, leptin and nitric oxide.

Gonadotropin secretion by the pituitary gland is under the control of luteinizing hormone-releasing hormone (LHRH) and the putative follicle-stimulating hormone-releasing factor (FSHRF). Lamprey III LHRH is a potent FSHRF in the rat and appears to be resident in the FSH controlling area of the rat hypothalamus. It is an analog of mammalian LHRH and may be the long-sought FSHRF. Gonadal steroids feedback at hypothalamic and pituitary levels to either inhibit or stimulate the release of LH and FSH, which is also affected by inhibin and activin secreted by the gonads. Important control is exercised by acetylcholine, norepinephrine (NE), dopamine, serotonin, melatonin and glutamic acid (GA). Furthermore, LH and FSH also act at the hypothalamic level to alter secretion of gonadotropins. More recently, growth factors have been shown to have an important role. Many peptides act to inhibit or increase release of LH, and the sign of their action is often reversed by estrogen. A number of cytokines act at the hypothalamic level to suppress acutely the release of LH but not FSH. NE, GA and oxytocin stimulate LHRH release by activation of neural nitric oxide synthase (nNOS). The pathway is as follows: oxytocin and/or GA activate NE neurons in the medial basal hypothalamus (MBH) that activate NOergic neurons by alpha1 receptors. The NO released diffuses into LHRH terminals and induces LHRH release by activation of guanylate cyclase (GC) and cyclooxygenase. NO not only controls release of LHRH bound for the pituitary, but also that which induces mating by actions in the brain stem. An exciting recent development has been the discovery of the adipocyte hormone, leptin, a cytokine related to tumor necrosis factor-alpha (TNF-alpha). In the male rat, leptin exhibits a high potency to stimulate FSH and LH release from hemipituitaries incubated in vitro, and increases the release of LHRH from MBH explants by stimulating the release of NO. LHRH and leptin release LH by activation of NOS in the gonadotropes. The NO released activates GC that releases cyclic GMP which induces LH release. Leptin induces LH release in conscious, ovariectomized estrogen-primed female rats, presumably by stimulating LHRH release. At the effective dose of estrogen to activate LH release, FSH release is inhibited. Leptin may play an important role in induction of puberty and control of LHRH release in the adult as well.

Animals↗
PubMedDate not supplied

Role of nitric oxide in control of growth hormone release in the rat.

Previous experiments in this and other laboratories have revealed that nitric oxids (NO) plays a role in controlling the release of corticotropin-releasing hormone (CRH) and luteinizing-hormone-releasing hormone (LHRH). Therefore, we have investigated its role in control of growth hormone (GH) release in conscious rats by microinjecting NG-monomethyl-L-arginine (NMMA), an inhibitor of NO synthase (NOS), into the third ventricle (3V) of conscious, freely moving castrate male rats. An initial blood sample (0.3 ml) was drawn from an indwelling intra-atrial catheter just prior to injection of NMMA [1 mg in 5 microliters of 0.9% NaCl (saline)] into the 3V. To maintain the inhibitory action on NOS, a second injection of NMMA was administered into the 3V 60 min after the first. Additional blood samples (0.3 ml) were removed at 10 min intervals for 120 min. Other animals received injections of the diluent at the same times and volumes as NMMA. Interleukin (IL)-1 alpha (0.06 pmol in 2 microliters saline) was injected into the 3V immediately after the first injection of NMMA, whereas other animals received the NMMA diluent followed by IL-1 alpha. The effects of IL-1 alpha were almost identical to those of NMMA in that there was a dramatic lowering of plasma GH achieved primarily by a reduction in height of the GH pulses without a significant reduction in their number.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗