Filtyp
Professor Kontaktinformation E-post: henrik [dot] tehler [at] risk [dot] lth [dot] seOrganisation Avdelningen för Riskhantering och Samhällssäkerhet Hämtställe: 3 WebbplatsHenrik Tehlers profil i Lunds universitets forskningsportalAndra roller Profilområdesmedlem LTH profilområde: Livsmedel och bioteknikProfessor Henrik Tehler är biträdande föreståndare för CenCIP och anställd vid Avdelningen för
https://www.cencip.lu.se/henrik-tehler - 2026-06-29
1 Överenskommelse om Bestämmelser för arbetstagare i arbetsmarknadspolitiska insatser – BEA Parter Sveriges Kommuner och Regioner och Sobona – Kommunala företagens arbetsgivarorganisation å ena sidan, samt Svenska Kommunalarbetareförbundet å den andra. § 1 Innehåll m.m. Parterna träffar detta kollektivavtal Bestämmelser för arbetstagare i arbetsmarknadspolitiska insatser, BEA 25. Till avtalet hör
Professor emeritus Kontaktinformation E-post: neelambar [dot] hatti [at] ekh [dot] lu [dot] se Telefon: +46 46 222 74 88 Mobil: +46 70 148 00 01Organisation Ekonomisk-historiska institutionen Besöksadress: Scheelevägen 15 B, Lund Rumsnummer: Alfa 1:2111 Hämtställe: 10 WebbplatsNeelambar Hattis profil i Lunds universitets forskningsportalAndra roller Professor emeritus Ekonomisk utveckling i det gl
https://www.ehl.lu.se/neelambar-hatti - 2026-06-29
LITERATURE LISTS: 1 Collection Łakociński, Z. PIZ’s Collections in Lund Printed and stencilled material Content: Literature in English 71 volumes p. 1-14 Literature in French 9 volumes p. 14-17 Literature in other Roman languages 1 volume p. 17 Literature in Norwegian, Danish, and Icelandic 15 volumes p. 17-21 Literature in Polish 70 volumes p. 21-42 Literature in other Slavonic languages 1 volume
https://www.ub.lu.se/en/sites/ub.lu.se.en/files/piz_printed_material_eng.pdf - 2026-06-30
Experimental stroke and excitotoxic brain lesion to the striatum or cortex increase the proliferation of cells residing within the ventricular wall and cause subsequent migration of newborn neuroblasts into the lesioned brain parenchyma. In this study, we clarify the different events of neurogenesis following striatal or cortical excitotoxic brain lesions in adult rats. Newborn cells were labeled
At advanced stages of Alzheimer's disease, cognitive dysfunction is accompanied by severe alterations of hippocampal circuits that may largely underlie memory impairments. However, it is likely that anatomical remodeling in the hippocampus may start long before any cognitive alteration is detected. Using the well-described Tg2576 mouse model of Alzheimer's disease that develops progressive age-dep
Cerebellar dysfunction is commonly observed following traumatic brain injury (TBI). While direct impact to the cerebellum by TBI is rare, cerebellar pathology may be caused by indirect injury via cortico-cerebellar pathways. To address the hypothesis that degeneration of Purkinje cells (PCs), which constitute the sole output from the cerebellum, is linked to long-range axonal injury and demyelinat
The effect of the immunosuppressant FK506 on ischaemic neuronal damage was studied in a rat model of transient cerebral ischemia induced by occlusion of both common carotid arteries in combination with hypotension for 10 min. Neuronal damage was assessed morphologically after 4 days of recovery. Treatment with FK506, given at a dose of 2 mg kg-1 by intraperitoneal injections 30 min prior to ischem
CEREBRAL ISCHEMIA ASSOCIATED with subarachnoid hemorrhage may have severe consequences for neuronal functioning. The excitatory amino acid neurotransmitters glutamate and aspartate have been shown to he of particular importance for ischemia and ischemic neuronal damage. For seven patients who underwent early surgery for ruptured intracranial aneurysms, intracerebral microdialysis of glutamate and
Abstract: The influence of brain ischemia on the subcellular distribution and activity of Ca2+/calmodulin‐dependent protein kinase II (CaM kinase II) was studied in various cortical rat brain regions during and after cerebral ischemia. Total CaM kinase II immunoreactivity (IR) and calmodulin binding in the crude synaptosomal fraction of all regions studied increase but decrease in the microsomal a
Abstract: Casein kinase II (CKII) is a protein kinase acting in the intracellular cascade of reactions activated by growth factor receptors, and that has a profound influence on cell proliferation and survival. In this investigation, we studied the changes in the activity and levels of CKII in the rat brain exposed to 10. 15 and 20 min of transient forebrain ischemia followed by variable periods
A brief period of sublethal cerebral ischemia, followed by several days of recovery, renders the brain resistant to a subsequent lethal ischemic insult, a phenomenon termed ischemic preconditioning or tolerance. Ischemic tolerance was established in the rat two-vessel occlusion model of ischemia, induced by occlusion of both carotid arteries in combination with hypotension. Ischemic preconditionin
A short period of sublethal preconditioning ischemia (3 min) followed by two days of reperfusion provides almost complete protection against ischemic cell death induced by a second (9 min) lethal ischemic episode. Here, we have investigated the extracellular signal-regulated protein kinase kinase and extracellular signal-regulated protein kinase, two kinases known to activate gene transcription an
A brief, 3 min period of global forebrain ischemia in the rat, induced by bilateral common carotid occlusion combined with hypotension, confers resistance to hippocampal pyramidal neurons against a subsequent 10 min ischemia, which is normally lethal to these cells. The molecular mechanisms underlying this ischemic preconditioning, or tolerance, are poorly understood. The tumor suppressor p53 is a
The changes in extracellular Ca2+ (Cae) and K+ (Ke) activities were studied in the rat brain during insulin-induced hypoglycemia. At about the time of onset of isoelectric EEG in severe insulin-induced hypoglycemia (300-g male Wistar rats under 70% N2O anaesthesia), there was an increase in Ke which, at ∼13 mM, was associated with a fall in Cae. Ke peaked at 48 ± 12 mM, and Cae at 0.18 ± 0.28 mM.
