scholarly journals Focal Thalamic Degeneration from Ethanol and Thiamine Deficiency is Associated with Neuroimmune Gene Induction, Microglial Activation, and Lack of Monocarboxylic Acid Transporters

2013 ◽  
Vol 38 (3) ◽  
pp. 657-671 ◽  
Author(s):  
Liya Qin ◽  
Fulton T. Crews
Keyword(s):  
Thiamine Deficiency ◽  
Microglial Activation ◽  
Monocarboxylic Acid ◽  
Gene Induction ◽  
Thalamic Degeneration

Alteration of Mitochondria in Oxythiamine-Induced, Acute Thiamine Deficiency in the Mouse

1976 ◽  
Vol 34 ◽  
pp. 284-285
Author(s):  
Itaru Watanabe ◽  
Dante G. Scarpelli
Keyword(s):  
Electron Microscopy ◽  
Adult Male ◽  
Thiamine Deficiency ◽  
Light And Electron Microscopy ◽  
Fatty Change ◽  
Deficient Diet ◽  
Subcutaneous Injections ◽  
Swiss Mice ◽  
Time Period ◽  
Ad Libitum

Acute thiamine deficiency was produced in mice by the administration of oxythiamine, a thiamine analogue, superimposed upon a thiamine deficient diet. Adult male Swiss mice (30 gm. B.W.) were fed with a thiamine deficient diet ad libitumand were injected with oxythiamine (170 mg/Kg B.W.) subcutaneously on days 4 and 10. On day 11, severe lassitude and anorexia developed, followed by death within 48 hours. The animals treated daily with subcutaneous injections of thiamine (300 μg/Kg B.W.) from day 11 through 15 were kept alive. Similarly, feeding with a diet containing thiamine (600 μg/Kg B.W./day) from day 9 through 17 reversed the condition. During this time period, no fatal illness occurred in the controls which were pair-fed with a thiamine deficient diet.The oxythiamine-treated mice showed a significant enlargement of the liver, which weighed approximately 1.5 times as much as that of the pair-fed controls. By light and electron microscopy, the hepatocytes were markedly swollen due to severe fatty change and swelling of the mitochondria.

Paracrint regulation of decidual gene induction by trophoblast: Identification of tumor related genes

1998 ◽  
Vol 5 (1) ◽  
pp. 114A-114A
Author(s):  
R HINES ◽  
M BRACKIN ◽  
J ISAACSJR ◽  
W BENNETT ◽  
S CASE ◽  
...  
Keyword(s):  
Gene Induction

Serum Thiamine Values in End-Stage Renal Disease Patients under Maintenance Hemodialysis

2015 ◽  
Vol 85 (5-6) ◽  
pp. 348-355 ◽  
Author(s):  
Masamitsu Ubukata ◽  
Nobuyuki Amemiya ◽  
Kosaku Nitta ◽  
Takashi Takei
Keyword(s):  
Thiamine Deficiency ◽  
Risk Index ◽  
Nutritional Risk ◽  
Maintenance Hemodialysis ◽  
Dialysis Patients ◽  
Significant Difference ◽  
Nutritional Risk Index ◽  
Serum Aspartate Aminotransferase ◽  
Stage Renal Disease ◽  
End Stage

Abstract. Objective: Hemodialysis patients are prone to malnutrition because of diet or many uremic complications. The objective of this study is to determine whether thiamine deficiency is associated with regular dialysis patients. Methods: To determine whether thiamine deficiency is associated with regular dialysis patients, we measured thiamine in 100 patients undergoing consecutive dialysis. Results: Average thiamine levels were not low in both pre-hemodialysis (50.1 ± 75.9 ng/mL; normal range 24 - 66 ng/mL) and post-hemodialysis (56.4 ± 61.7 ng/mL). In 18 patients, post-hemodialysis levels of thiamine were lower than pre-hemodialysis levels. We divided the patients into two groups, the decrease (Δthiamine/pre thiamine < 0; - 0.13 ± 0.11) group (n = 18) and the increase (Δthiamine/pre thiamine> 0; 0.32 ± 0.21)) group (n = 82). However, there was no significance between the two groups in Kt/V or type of dialyzer. Patients were dichotomized according to median serum thiamine level in pre-hemodialysis into a high-thiamine group (≥ 35.5 ng/mL) and a low-thiamine group (< 35.4 ng/mL), and clinical characteristics were compared between the two groups. The low-thiamine value group (< 35.4 ng/ml; 26.8 ± 5.3 ng/ml) exhibited lower levels of serum aspartate aminotransferase and alanine aminotransferase than the high-thiamine value group (≥ 35.4 ng/ml; 73.5 ± 102.5 ng/ml) although there was no significance in nutritional marker, Alb, geriatric nutritional risk index , protein catabolic rate and creatinine generation rate. Conclusion: In our regular dialysis patients, excluding a few patients, we did not recognize thiamine deficiency and no significant difference in thiamine value between pre and post hemodialysis.

HIF1-α-Mediated Gene Expression Induced by Vitamin B1 Deficiency

2013 ◽  
Vol 83 (3) ◽  
pp. 188-197 ◽  
Author(s):  
Rebecca L. Sweet ◽  
Jason A. Zastre
Keyword(s):  
Gene Expression ◽  
Thiamine Deficiency ◽  
Glucose Transporter ◽  
Neuroblastoma Cell ◽  
Hypoxia Inducible Factor ◽  
Clinical Manifestations ◽  
Vitamin B1 ◽  
Low Oxygen ◽  
Glucose Transporter 1 ◽  
Metabolic Intermediates

It is well established that thiamine deficiency results in an excess of metabolic intermediates such as lactate and pyruvate, which is likely due to insufficient levels of cofactor for the function of thiamine-dependent enzymes. When in excess, both pyruvate and lactate can increase the stabilization of the hypoxia-inducible factor 1-alpha (HIF-1α) transcription factor, resulting in the trans-activation of HIF-1α regulated genes independent of low oxygen, termed pseudo-hypoxia. Therefore, the resulting dysfunction in cellular metabolism and accumulation of pyruvate and lactate during thiamine deficiency may facilitate a pseudo-hypoxic state. In order to investigate the possibility of a transcriptional relationship between hypoxia and thiamine deficiency, we measured alterations in metabolic intermediates, HIF-1α stabilization, and gene expression. We found an increase in intracellular pyruvate and extracellular lactate levels after thiamine deficiency exposure to the neuroblastoma cell line SK-N-BE. Similar to cells exposed to hypoxia, there was a corresponding increase in HIF-1α stabilization and activation of target gene expression during thiamine deficiency, including glucose transporter-1 (GLUT1), vascular endothelial growth factor (VEGF), and aldolase A. Both hypoxia and thiamine deficiency exposure resulted in an increase in the expression of the thiamine transporter SLC19A3. These results indicate thiamine deficiency induces HIF-1α-mediated gene expression similar to that observed in hypoxic stress, and may provide evidence for a central transcriptional response associated with the clinical manifestations of thiamine deficiency.

Inflammational Animal Models for Schizophrenia

2015 ◽  
Vol 223 (3) ◽  
pp. 157-164 ◽  
Author(s):  
Georg Juckel
Keyword(s):  
Animal Model ◽  
Animal Models ◽  
Immune Activation ◽  
Microglial Activation ◽  
Treatment Options ◽  
Early Adulthood ◽  
Brain Regions ◽  
Synaptic Connections ◽  
Preventive Interventions ◽  
Immunological System

Abstract. Inflammational-immunological processes within the pathophysiology of schizophrenia seem to play an important role. Early signals of neurobiological changes in the embryonal phase of brain in later patients with schizophrenia might lead to activation of the immunological system, for example, of cytokines and microglial cells. Microglia then induces – via the neurotoxic activities of these cells as an overreaction – a rarification of synaptic connections in frontal and temporal brain regions, that is, reduction of the neuropil. Promising inflammational animal models for schizophrenia with high validity can be used today to mimic behavioral as well as neurobiological findings in patients, for example, the well-known neurochemical alterations of dopaminergic, glutamatergic, serotonergic, and other neurotransmitter systems. Also the microglial activation can be modeled well within one of this models, that is, the inflammational PolyI:C animal model of schizophrenia, showing a time peak in late adolescence/early adulthood. The exact mechanism, by which activated microglia cells then triggers further neurodegeneration, must now be investigated in broader detail. Thus, these animal models can be used to understand the pathophysiology of schizophrenia better especially concerning the interaction of immune activation, inflammation, and neurodegeneration. This could also lead to the development of anti-inflammational treatment options and of preventive interventions.

The Impact of Timing of Microglial Activation by Inflammation and Hypoxia Regarding Additive Neurotoxic Effects

2014 ◽  
Vol 45 (S 01) ◽  
Author(s):  
S. Jung ◽  
D. Frey ◽  
F. Brackmann ◽  
M. Richter-Kraus ◽  
R. Trollmann
Keyword(s):  
Microglial Activation ◽  
Neurotoxic Effects ◽  
The Impact
Sign in / Sign up

Export Citation Format

Share Document