74 resultados para Nerves, Peripheral
Resumo:
Neuropeptide F (Moniezia expansa) immunoreactivity (NPF-IR) has been detected in the nervous system of plerocercoid and adult stages of the gull-tapeworm Diphyllobothrium dendriticum, using immunocytochemical methodology. The application of the antiserum for this authentic flatworm neuropeptide to whole-mounts and frozen sections of the worm has resulted in new information about its neuroanatomy. Thus, at regular intervals, transverse nerves extend from the main nerve cords laterally, joining the longitudinal lateral minor cords in the cortical parenchyma. In the adult worm, the transverse nerves are located at the posterior border of each proglottis. The medullary parenchyma lacks NPF-IR. The NPF-immunoreactive cell bodies are bi- to multipolar and preferentially located in the peripheral nervous system, in close association with the holdfast musculature of the scolex and the extensive body musculature. NPF-IR was observed in the innervation to the muscular ducts of the reproductive system. The pattern of NPF-IR was compared with that recorded for RFamide- and 5-HT-IR and double-immunostaining has revealed separate populations of serotoninergic and peptidergic neurones.
Resumo:
The localization and distribution of cholinergic, serotoninergic and peptidergic nerve elements in the proteocephalidean tapeworm, Proteocephalus pollanicola, have been investigated by enzyme histochemistry, and by an indirect immunofluorescence technique interfaced with confocal scanning laser microscopy. Cholinesterase (ChE) activity was localized in the major components of the central nervous system (CNS) and the peripheral nervous system (PNS), including the innervation of the reproductive structures of the worm. Serotoninergic (5-HT) nerves were found in the paired cerebral ganglia, transverse commissure and in the 10 longitudinal nerve cords. Antisera to 17 mammalian regulatory peptides and the invertebrate peptide FMRFamide have been used to explore the peptidergic nervous system of the worm. The most extensive immunostaining occurred with antisera raised to members of the neuropeptide Y superfamily, namely neuropeptide Y (NPY), peptide YY (PYY) and pancreatic polypeptide (PP). In all cases, intense immunoreactivity was found in numerous cell bodies and fibres of both the CNS and PNS, including the innervation of the reproductive apparatus. FMRFamide antisera stained the same structures to a comparable degree as those raised to the NPY superfamily. Cholinergic and peptidergic elements were much more prevalent within the CNS, while the serotoninergic nerve fibres tended to dominate in the PNS. The overlap obtained in staining patterns for the peptidergic and cholinergic components suggests that there may be a certain amount of co-localization of peptides with small-molecule transmitter substances in the same neurone. Weak staining for the tachykinin, substance P and for calcitonin gene-related peptide(CGRP) was confined to the major longitudinal nerve cords.
Resumo:
1. The effects of equipotent doses of frusemide (10 mg and 100 mg) and bumetanide (250 micrograms and 2.5 mg) upon renal and peripheral vascular responses, urinary prostaglandin excretion, plasma renin activity, angiotensin II and noradrenaline were compared in nine healthy volunteers. 2. Frusemide (10 mg and 100 mg) and bumetanide (2.5 mg) increased renal blood flow acutely compared with placebo but bumetanide (250 micrograms) had no effect. The changes in peripheral vascular responses were not significantly different from placebo. 3. Urinary prostaglandin metabolite excretion was acutely increased by all treatments, with no inter-treatment difference. Plasma renin activity was increased acutely by both doses of frusemide and by bumetanide (2.5 mg) compared with placebo and to bumetanide (250 micrograms). There were no differences between the latter two treatments. Angiotensin II was increased significantly 30 min after frusemide 100 mg and bumetanide 2.5 mg, and by all four treatments at 50 min when compared with placebo. There were no significant differences between either of the low doses or the higher doses. Plasma noradrenaline was unchanged by all treatments. 4. Frusemide 100 mg and bumetanide 2.5 mg have the same effects on the renal vasculature and the renin-angiotensin-prostaglandin system. Under the conditions of this study, frusemide 10 mg had different effects on plasma renin activity than bumetanide 250 micrograms.
Resumo:
Purpose: A peripheral iridotomy (PI) is the treatment of choice for pupillary block. In this study we investigated the effect of enlarging the size of a small PI on the anterior chamber angle in patients with angle closure using ultrasound biomicroscopy (UBM). Patients and Methods: Patients who had been treated with laser peripheral iridotomy for angle closure and were identified to have a small patent PI (<100 µm) with still appositionally closed anterior chamber angle were selected prospectively. The anterior chamber angle was assessed using UBM. The angle opening distance 500 µm from the scleral spur (AOD500) as well as the anterior and posterior chamber depth (ACD and PCD) 1000 µm from the scleral spur was measured. In addition, the ACD/PCD ratio was calculated. Afterwards, the PI was enlarged using an Nd: YAG laser and the UBM measurements were repeated as described above. Results: Six eyes of six patients were examined. After the enlargement of the PI the average AOD500 increased from 109 µm (±36) to 147 µm (±40) (p
Resumo:
BACKGROUND: Angle-closure glaucoma is a leading cause of irreversible blindness in the world. Treatment is aimed at opening the anterior chamber angle and lowering the IOP with medical and/or surgical treatment (e.g. trabeculectomy, lens extraction). Laser iridotomy works by eliminating pupillary block and widens the anterior chamber angle in the majority of patients. When laser iridotomy fails to open the anterior chamber angle, laser iridoplasty may be recommended as one of the options in current standard treatment for angle-closure. Laser peripheral iridoplasty works by shrinking and pulling the peripheral iris tissue away from the trabecular meshwork. Laser peripheral iridoplasty can be used for crisis of acute angle-closure and also in non-acute situations.
OBJECTIVES: To assess the effectiveness of laser peripheral iridoplasty in the treatment of narrow angles (i.e. primary angle-closure suspect), primary angle-closure (PAC) or primary angle-closure glaucoma (PACG) in non-acute situations when compared with any other intervention. In this review, angle-closure will refer to patients with narrow angles (PACs), PAC and PACG.
SEARCH METHODS: We searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2011, Issue 12), MEDLINE (January 1950 to January 2012), EMBASE (January 1980 to January 2012), Latin American and Caribbean Literature on Health Sciences (LILACS) (January 1982 to January 2012), the metaRegister of Controlled Trials (mRCT) (www.controlled-trials.com), ClinicalTrials.gov (www.clinicaltrials.gov) and the WHO International Clinical Trials Registry Platform (ICTRP) (www.who.int/ictrp/search/en). There were no date or language restrictions in the electronic searches for trials. The electronic databases were last searched on 5 January 2012.
SELECTION CRITERIA: We included only randomised controlled trials (RCTs) in this review. Patients with narrow angles, PAC or PACG were eligible. We excluded studies that included only patients with acute presentations, using laser peripheral iridoplasty to break acute crisis.
DATA COLLECTION AND ANALYSIS: No analysis was carried out as only one trial was included in the review.
MAIN RESULTS: We included one RCT with 158 participants. The trial reported laser peripheral iridoplasty as an adjunct to laser peripheral iridotomy compared to iridotomy alone. The authors report no superiority in using iridoplasty as an adjunct to iridotomy for IOP, number of medications or need for surgery.
AUTHORS' CONCLUSIONS: There is currently no strong evidence for laser peripheral iridoplasty's use in treating angle-closure.
Resumo:
BACKGROUND: Angle-closure glaucoma is a leading cause of irreversible blindness in the world. Treatment is aimed at opening the anterior chamber angle and lowering the IOP with medical and/or surgical treatment (e.g. trabeculectomy, lens extraction). Laser iridotomy works by eliminating pupillary block and widens the anterior chamber angle in the majority of patients. When laser iridotomy fails to open the anterior chamber angle, laser iridoplasty may be recommended as one of the options in current standard treatment for angle-closure. Laser peripheral iridoplasty works by shrinking and pulling the peripheral iris tissue away from the trabecular meshwork. Laser peripheral iridoplasty can be used for crisis of acute angle-closure and also in non-acute situations. OBJECTIVES: To assess the effectiveness of laser peripheral iridoplasty in the treatment of narrow angles (i.e. primary angle-closure suspect), primary angle-closure (PAC) or primary angle-closure glaucoma (PACG) in non-acute situations when compared with any other intervention. In this review, angle-closure will refer to patients with narrow angles, PAC and PACG. SEARCH STRATEGY: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library), MEDLINE, EMBASE and LILACS (Latin American and Caribbean Literature on Health Sciences). The databases were last searched on 11 February 2008. SELECTION CRITERIA: Only randomised controlled trials (RCTs) were eligible for inclusion in this review. Patients with narrow angles, PAC or PACG were eligible. Studies that included only patients with acute presentations, using laser peripheral iridoplasty to break acute crisis were excluded. DATA COLLECTION AND ANALYSIS: No analysis was carried out due to lack of trials. MAIN RESULTS: There were no RCTs assessing laser peripheral iridoplasty in the non-acute setting of angle-closure. AUTHORS' CONCLUSIONS: There is currently no strong evidence for laser peripheral iridoplasty's use in treating angle-closure.
Resumo:
When a subject is heated, the stimulation of temperature-sensitive nerve endings in the skin, and the raising of the central body temperature, results in the reflex release of sympathetic vasoconstrictor tone in the skin of the extremities, causing a measurable temperature increase at the site of release. In the sympathetic release test, the subject is gently heated by placing the feet and calves in a commercially available foot warming pouch or immersing the feet and calves in warm water and wrapping the subject in blankets. Skin blood flow is estimated from measurements of skin temperature in the fingers. Normally skin temperature of the fingers is 65-75 degrees F in cool conditions (environmental temperature: 59-68 degrees F) and rises to 85-95 degrees F during body heating. Deviations in this pattern may mean that there is abnormal sympathetic vasoconstrictor control of skin blood flow. Abnormal skin blood flow can substantially impair an individual's ability to thermoregulate and has important clinical implications. During whole body heating, the skin temperature from three different skin sites is monitored and oral temperature is monitored as an index of core temperature. Students determine the fingertip temperature at which the reflex release of sympathetic activity occurs and its maximal attainment, which reflects the vasodilating capacity of this cutaneous vascular bed. Students should interpret typical sample data for certain clinical conditions (Raynaud's disease, peripheral vascular disease, and postsympathectomy) and explain why there may be altered skin blood flow in these disorders.
Resumo:
Human B cell colonies were grown from peripheral blood of 12 patients with systemic lupus erythematosus (SLE) and from 12 healthy control subjects. The SLE group showed a large increase (p less than 0.001) in the number of colony forming cells (CFC) present in peripheral blood as compared with controls. The CFC were of the pre-B cell type. There was also a loss of OKT8+ cell inhibition of B cell colony growth in the SLE group compared with control subjects.