Evaluation of stress changes in the maxilla with fixed functional appliances-A 3D FEM study.

Aim: To evaluate the stress changes in the maxilla during fixed functional appliance use using three-dimensional finite element method (FEM) stress analysis.

Settings And Sample Population: A three-dimensional finite element model of the maxilla was constructed using the images generated from the cone-beam computed tomography of a patient treated for Class II malocclusion with a fixed functional orthodontic appliance. The FEM was used to study the stress changes seen in the maxilla, which were evaluated in the form of highest von Mises stress and maximum principal stress before and after the application of fixed functional appliance.

Atraumatic fractures of the femur.

Atraumatic fractures of femur, although not as common as traumatic fractures, are frequently encountered in the clinical practice. They present with non-specific symptoms and can be occult on initial imaging making their diagnosis difficult, sometimes resulting in complications. Overlapping terminologies used to describe these fractures may hamper effective communication between the radiologist and the clinician.

The neuropeptides, VIP and NPY, that are present in the thyroid nerves are not released into the thyroid vein.

In the present study, we tested the hypothesis that the neuropeptides, vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), which are present in the thyroid nerves, act as physiological neurotransmitters involved in the regulation of thyroid hormone secretion and thyroid blood flow. Specifically, we examined whether these neuropeptides can be released into thyroid blood vessels by electrical stimulation of the major thyroid nerves or whether their expression is altered by changes in iodine intake. Sprague-Dawley rats were used in this study.

Immunization against vasoactive intestinal peptide does not affect thyroid hormone secretion or thyroid blood flow.

Vasoactive intestinal peptide (VIP) is present in thyroid parasympathetic nerves. To assess the involvement of endogenous VIP in the regulation of thyroid function, blood levels of thyroid hormones and thyroid blood flows (TBF) were measured after systemic immunization against VIP or after transection of the superior laryngeal nerves in male rats, which reduced the thyroid content of VIP but did not affect blood levels of thyroid hormones or TBF. Anti-VIP monoclonal antibody or anti-VIP serum was used for immunization against VIP in normal rats.

Sympathetic thyroidal vasoconstriction is not blocked by a neuropeptide Y antagonist or antiserum.

Sympathetic nerve fibers to thyroid blood vessels contain both norepinephrine (NE) and neuropeptide Y (NPY). To assess the involvement of endogenous NPY in the sympathetic neural control of thyroid blood flow, appropriate doses of a selective NPY antagonist, alpha-trinositol, and an NPY antiserum (NPY-AS) were used during cervical sympathetic trunk stimulation in anesthetized rats. During all experiments, thyroid blood flow was continuously monitored by laser Doppler blood flowmetry.

NPY is not a primary mediator of the acute thyroid blood flow response to sympathetic nerve stimulation.

It has been suggested that thyroid blood flow is regulated by both sympathetic and parasympathetic nerves. The purpose of our experiments was to study the role of neuropeptide Y (NPY) in the sympathetic neural control of thyroid blood flow. Sympathetic nerve fibers to the thyroid contain both norepinephrine (NE) and NPY.

Endogenous neuropeptide Y regulates thyroid blood flow.

Neuropeptide Y (NPY) is present in thyroid sympathetic nerve fibers. To assess the involvement of endogenous NPY in the regulation of thyroid function, a NPY antiserum was produced in a rabbit, characterized, and used for immunization of normal and hyperthyroid rats. Plasma thyroxine, thyroid-stimulating hormone (TSH), thyroidal, and other organ blood flows (BF) were measured in anesthetized (ketamine and pentobarbital sodium) male Sprague-Dawley rats at 1 h after intravenous administration of 1 ml of the antiserum, normal rabbit serum, or saline.

Thyroidal vascular responsiveness to parasympathetic stimulation is increased in hyperthyroidism.

It has been suggested that thyroid blood flow (TBF) is regulated by both parasympathetic and sympathetic nerves. Because thyroxine (T4) pretreatment increases the sensitivity of the thyroid to the effects of thyrotropin, the present study was conducted to determine whether T4 pretreatment can also sensitize the thyroid to the effect of parasympathetic stimulation on TBF. Untreated or T4-pretreated rats were anesthetized, and both superior laryngeal nerves (SLN) were transected.

Expression of preproNPY and precursor VIP mRNAs in rats under hypo- or hyperthyroid conditions.

Both neuropeptide Y (NPY) and vasoactive intestinal peptide (VIP) are present in thyroid nerves and have been shown to alter thyroid activity. The present study was conducted to determine whether hypo- or hyperthyroidism is associated with changes in the expression of the mRNAs for these neuropeptides in the major ganglia which supply nerves to the thyroid or within the thyroid gland itself. Hypo- or hyperthyroid conditions were induced by the administration of propylthiouracil (PTU) or thyroxine (T(4)), respectively, for 6 days.

Vasoactive intestinal peptide enhances thyroidal iodide uptake during dietary iodine deficiency.

The presence of vasoactive intestinal peptide and neuropeptide Y in thyroid nerves and their effects on thyroid blood flow are well known. However, the effects of these two neuropeptides on the various processes involved in thyroid hormone biosynthesis and release have not been fully explored. We have now tested these two peptides for effects on an early step in thyroid hormone biosynthesis, namely iodide uptake, a process which is comprised of trapping and organification.

Lack of effect of vasoactive intestinal peptide antagonists on blood flow in the rat thyroid.

We used three putative vasoactive intestinal peptide (VIP) antagonists: 1) [4C1-D-Phe6,Leu17]VIP, 2) [N-Ac-Tyr1,D-Phe2] GRF(1-29)-NH2, and 3) VIP(10-28) to assess the involvement of endogenous VIP in the regulation of thyroid hormone secretion and thyroid blood flow (BF). We measured thyroid BF in ketamine-pentobarbital-anesthetized rats using the microsphere technique. Increases in thyroid BF induced by VIP administration (30 pmol-1.

Peripheral vascular resistance and regional blood flows in hypertensive Dahl rats.

The aim of this study was to determine whether different organs undergo similar increases in vascular resistance with hypertension in the Dahl salt-sensitive rat. Cardiac output and organ blood flows were measured with microspheres in anesthetized salt-sensitive and salt-resistant rats fed a high- (7%) or normal- (0.45%) salt diet for 4 wk.

Thyroid vascular conductance: differential effects of elevated plasma thyrotropin (TSH) induced by treatment with thioamides or TSH-releasing hormone.

We have reported previously that thyroid gland blood flow, expressed as vascular conductance (C) per mass, is decreased at very low and increased at very high chronic plasma TSH concentrations, but is apparently unchanged over a broad range of plasma TSH concentrations encompassing normal levels. The aim of the present study was to examine the apparently very steep dose-response relationship between elevated plasma TSH and thyroid vascular C/mass. In the first series of experiments, endogenous plasma TSH concentrations were manipulated by treating male Sprague-Dawley rats (250-280 g) for 6 days as follows: 1) controls (0.

Compensatory changes in thyroid blood flow are only partially mediated by thyrotropin.

It has been shown that the compensatory growth of the thyroid gland and the compensatory increase in hormone secretion that occur after hemithyroidectomy are preceded by a dramatic increase in thyroid blood flow (BF). These alterations in the thyroid remnant may be due to the concomitant increase in plasma thyrotropin (TSH) concentrations. It has been suggested, however, that the compensatory thyroid growth may also involve a neural reflex.

Muscarinic modulation of the vasodilatory effects of vasoactive intestinal peptide at the rat thyroid gland.

In the thyroid gland, vasoactive intestinal peptide (VIP) and acetylcholine (ACh) are found in nerve fibers associated with secretory cells and blood vessels. We have, therefore, initiated studies to explore the actions of and interactions between cholinergic agents and VIP in the regulation of thyroid vascular conductance (VC). Thyroid and other organ blood flows were measured using radiolabelled (141Ce) microspheres injected directly into the left cardiac ventricle of anesthetized male rats.

Helodermin, but not cholecystokinin, somatostatin, or thyrotropin releasing hormone, acutely increases thyroid blood flow in the rat.

In the present study, we investigated whether peptides located within the thyroid gland, but not directly found in nerve fibers associated with blood vessels, might influence thyroid blood flow. Specifically, we evaluated the effects of helodermin, cholecystokinin (CCK), somatostatin (SRIF) and thyrotropin releasing hormone (TRH) given systemically on thyroid blood flow and circulating thyroid hormone levels. Blood flows in the thyroid and six other organs were measured in male rats using 141Ce-labeled microspheres.

Alterations in thyroid blood flow induced by varying levels of iodine intake in the rat.

Thyroid hormone biosynthesis depends upon the presence of adequate amounts of thyroidal iodine, and during fluctuations in dietary iodine intake, relatively constant thyroid hormone levels are maintained by various homeostatic mechanisms. These mechanisms include an enhancement of iodide pump efficiency and organification when iodine intake is limited, and significant decreases in iodide uptake and hormone synthesis when excess iodine intake occurs. The present study was designed to determine whether acclimation to different dietary iodine regimens is associated with changes in thyroid blood flow and to assess the time course of any such alterations in relation to pituitary-thyroid axis hormone levels.

Increases in thyroid gland blood flow after hemithyroidectomy in the rat.

After subtotal thyroidectomy, the thyroid gland remnant undergoes compensatory alterations in function and morphology. Under the trophic stimulation of elevated plasma TSH concentrations, the thyroid remnant responds with an increase in hormone synthesis and secretion and, in addition, increases in mass. We have examined the alterations in thyroid blood flow which accompany increased secretion and growth after hemithyroidectomy (HTX) in male Sprague-Dawley rats (200-220 g).

Effects of vasoactive intestinal peptide on vascular conductance are unaffected by anesthesia.

In rats anesthetized with ketamine and pentobarbital (KET/PB), vasoactive intestinal peptide (VIP) increases vascular conductance (VC) in the salivary gland, pancreas, and thyroid gland, whereas no changes in VC are observed in a number of other organs. Because anesthesia may alter the responsiveness of physiological systems, we compared the effects of VIP on organ VC in conscious or anesthetized rats. Chronically catheterized rats were studied in the conscious state or 30 min after induction of anesthesia with KET/PB, isoflurane, or Inactin.

Vasoactive intestinal peptide treatment that increases thyroid blood flow fails to alter plasma T3 or T4 levels in the rat.

Vasoactive-intestinal-peptide (VIP)-containing nerve fibers impinge upon both follicle cells and blood vessels in the thyroid gland. We have previously shown that VIP induces a specific, dose-related increase in thyroid blood flow in the rat. However, our VIP treatments had no effect on circulating thyroid hormone levels.

VIP and its homologues increase vascular conductance in certain endocrine and exocrine glands.

The effects of vasoactive intestinal peptide (VIP) and related structural homologues on tissue vascular conductances were investigated in anesthetized male rats. VIP, peptide histidine isoleucine (PHI), secretin, growth hormone-releasing factor (GHRF), gastric inhibitory peptide (GIP), or saline was infused intravenously over 4 min. Tissue blood flows were measured during this time by use of 141Ce-labeled microspheres.

Effects of thyrotropin on the vascular conductance of the thyroid gland.

It is well established that TSH from the anterior pituitary is the principal stimulatory agent in the physiological regulation of the thyroid gland. Chronic elevations of plasma TSH induce hyperplasia and hypertrophy of thyroid follicular cells and enlargement of blood capillaries. At low plasma TSH levels the thyroid gland atrophies.

Early development of the thyroid axis in the Brattleboro rat.

Plasma concentrations of thyrotrophin (TSH), thyroxine (T4), and triiodothyronine (T3), and pituitary TSH concentrations were determined at weekly intervals during the first 42 days following birth in Brattleboro homozygous (DI), Brattleboro heterozygous (HZ), and Long-Evans (LE) rats. Offspring from matings of Brattleboro rats were divided into DI and HZ animal subgroups on the basis of hypothalamic vasopressin content. In control LE rats, circulating levels of TSH, T4, and T3, and pituitary TSH concentrations increased during the early postnatal period to reach relatively stable levels between 28 and 42 days of age.

Immunoreactive prolactin in the rat hypothalamus: in vitro release and subcellular localization.

Immunocytochemical studies have identified immunoreactive prolactin (IR-PRL) in the hypothalamus and other areas of the rat brain. However, neither the release of IR-PRL from the hypothalamus nor its subcellular localization have been demonstrated. In this study, the release of IR-PRL from hypothalami obtained from female rats was examined using hypothalamic units incubated in vitro in Krebs-Ringer bicarbonate-glucose buffer.