Herpes simplex virus esophagitis—clinical challenges in the elderly

A 77-year-old woman presented with a 2-week history of malaise, prostration, anorexia, abdominal pain, vomiting and diarrhoea. She had been taking systemic corticosteroids for the past year. During hospitalisation, renal insufficiency, ionic changes and liver function abnormalities were detected and corrected. However, the patient developed total dysphagia. UGE revealed multiple shallow ulcers below the cricopharyngeal level and in the distal oesophagus, with normal-appearing intervening mucosa. Histological examination allowed the diagnosis of herpes simplex virus esophagitis. Treatment with intravenous acyclovir was instituted for 14 days. In the elderly, herpetic esophagitis may present with non-specific complains, such as prostration or anorexia. In the reported case, dysphagia was only detected as a late symptom, addressing the importance of maintaining a high degree of suspicion for the diagnosis of herpes simplex virus esophagitis.

A Neurotoxic Ménage-à-trois: Glutamate, Calcium, and Zinc in the Excitotoxic Cascade

Fifty years ago, the seminal work by John Olney provided the first evidence of the neurotoxic properties of the excitatory neurotransmitter glutamate. A process hereafter termed excitotoxicity. Since then, glutamate-driven neuronal death has been linked to several acute and chronic neurological conditions, like stroke, traumatic brain injury, Alzheimer’s, Parkinson’s, and Huntington’s diseases, and Amyotrophic Lateral Sclerosis. Mechanisms linked to the overactivation of glutamatergic receptors involve an aberrant cation influx, which produces the failure of the ionic neuronal milieu. In this context, zinc, the second most abundant metal ion in the brain, is a key but still somehow underappreciated player of the excitotoxic cascade. Zinc is an essential element for neuronal functioning, but when dysregulated acts as a potent neurotoxin. In this review, we discuss the ionic changes and downstream effects involved in the glutamate-driven neuronal loss, with a focus on the role exerted by zinc. Finally, we summarize our work on the fascinating distinct properties of NADPH-diaphorase neurons. This neuronal subpopulation is spared from excitotoxic insults and represents a powerful tool to understand mechanisms of resilience against excitotoxic processes.

The Effect of Hypertension on Hearing Sense

Hypertension is an important health problem because it has a high prevalence and can cause damage to target organs. The relationship between hypertension and hearing loss is not difficult to understand, when blood pressure becomes high blood vessel damage occurs. Hearing loss cases caused by hypertension are considerable, in America 64 million people aged 18 to 75 years suffer from hypertension, 40% with hearing loss. This damage is not centered on one area of the body, but the whole body is also affected, including the ears. The incidence of hearing loss in hypertension is due to the occurrence of inner ear damage due to high pressure in the vascular system, changes in microcirculation and the occurrence of ionic changes.

Physiological and ionic changes in dwarf coconut seedlings irrigated with saline water

ABSTRACT Salt-tolerant plants are important to cope with salinity and/or sodicity problems in semiarid regions. The dwarf coconut palm (Cocos nucifera L.) has emerged as a salt-tolerant crop once established. However, little is known about the mechanisms that contribute to the survival of coconut seedlings under salinity stress. This study aimed to evaluate the effect of saline water on morpho-physiological and biochemical responses of dwarf coconut seedlings. Treatments were composed of five levels of water salinity, expressed by its electrical conductivity (ECw), as follows: 0.9 (control); 5.2; 10.1; 15.3 and 19.3 dS m-1 in a completely randomized design with four replications. The high levels of organic solutes (carbohydrates and soluble amino-N) and Na+ in roots, that contribute to the low values of Na+/K+ ratio in the leaves, suggest that roots play an important role in the mechanism of salt tolerance of coconut seedlings. The use of brackish water with ECw of 5.2 dS m-1 allows seedling production, with no loss of quality. Based on total dry matter accumulation, seedlings were classified as moderately tolerant to the salinity of 10.1 dS m-1.

Inhibition of Brain Swelling after Ischemia-Reperfusion byβ-Adrenergic Antagonists: Correlation with Increased K+and Decreased Ca2+Concentrations in Extracellular Fluid

Infarct size and brain edema following ischemia/reperfusion are reduced by inhibitors of the Na+, K+, 2Cl−, and water cotransporter NKCC1 and byβ1-adrenoceptor antagonists. NKCC1 is a secondary active transporter, mainly localized in astrocytes, driven by transmembrane Na+/K+gradients generated by the Na+,K+-ATPase. The astrocytic Na+,K+-ATPase is stimulated by small increases in extracellular K+concentration and by theβ-adrenergic agonist isoproterenol. Larger K+increases, as occurring during ischemia, also stimulate NKCC1, creating cell swelling. This study showed no edema after 3 hr medial cerebral artery occlusion but pronounced edema after 8 hr reperfusion. The edema was abolished by inhibitors of specificallyβ1-adrenergic pathways, indicating failure of K+-mediated, but notβ1-adrenoceptor-mediated, stimulation of Na+,K+-ATPase/NKCC1 transport during reoxygenation. Ninety percent reduction of extracellular Ca2+concentration occurs in ischemia. Ca2+omission abolished K+uptake in normoxic cultures of astrocytes after addition of 5 mM KCl. A large decrease in ouabain potency on K+uptake in cultured astrocytes was also demonstrated in Ca2+-depleted media, and endogenous ouabains are needed for astrocytic K+uptake. Thus, among the ionic changes induced by ischemia, the decrease in extracellular Ca2+causes failure of the high-K+-stimulated Na+,K+-ATPase/NKCC1 ion/water uptake, makingβ1-adrenergic activation the only stimulus and its inhibition effective against edema.

Development of K+ and Na+ conductances in rodent postnatal semicircular canal type I hair cells

The rodent vestibular system is immature at birth. During the first postnatal week, vestibular type I and type II hair cells start to acquire their characteristic morphology and afferent innervation. We have studied postnatal changes in the membrane properties of type I hair cells acutely isolated from the semicircular canals (SCC) of gerbils and rats using whole cell patch clamp and report for the first time developmental changes in ionic conductances in these cells. At postnatal day (P) 5 immature hair cells expressed a delayed rectifier K+ conductance ( GDR) which activated at potentials above approximately −50 mV in both species. Hair cells also expressed a transient Na+ conductance ( GNa) with a mean half-inactivation of approximately −90 mV. At P6 in rat and P7 in gerbil, a low-voltage activated K+ conductance ( GK,L) was first observed and conferred a low-input resistance, typical of adult type I hair cells, on SCC type I hair cells. GK,L expression in hair cells increased markedly during the second postnatal week and was present in all rat type I hair cells by P14. In gerbil hair cells, GK,L appeared later and was present in all type I hair cells by P19. During the third postnatal week, GNa expression declined and was absent by the fourth postnatal week in rat and the sixth postnatal week in gerbils. Understanding the ionic changes associated with hair cell maturation could help elucidate development and regeneration mechanisms in the inner ear.

Evolution of blood magnesium and phosphorus ion levels following thyroidectomy and correlation with total calcium values

CONTEXT AND OBJECTIVE: Magnesium ion concentration is directly related and phosphorus ion concentration is inversely related to calcemia. The aim of this study was to evaluate the evolution of magnesium and phosphorus ion levels in patients undergoing thyroidectomy and correlate these with changes to calcium concentration. DESIGN AND SETTING: Prospective study at the Alpha Institute of Gastroenterology, Hospital das Clínicas, Universidade Federal de Minas Gerais. METHODS: The study included 333 patients, of both genders and mean age 45 ± 15 years, who underwent thyroidectomy between 2000 and 2005. Total calcium, phosphorus and magnesium were measured in the blood preoperatively and 24 and 48 hours postoperatively. Ionic changes were evaluated according to the presence or absence of postoperative hypocalcemia. RESULTS: There were statistically significant drops in blood phosphorus levels 24 and 48 hours after thyroidectomy, compared with preoperative values, in the patients without hypocalcemia. In the patients who developed hypocalcemia, there was a significant drop in plasma phosphorus on the first postoperative day and an increase (also statistically significant) on the second day, in relation to preoperative phosphorus levels. A significant drop in postoperative magnesium was also observed on the first and second days after thyroidectomy in the patients with hypocalcemia, in relation to preoperative levels. In the patients without hypocalcemia, the drop in magnesium was significant on the first day, but there was no difference on the second day. CONCLUSION: Despite the postoperative changes, neither magnesium nor phosphorus ion levels had any role in post-thyroidectomy calcemia.