Silicon Resorption from Equisetum arvense Tea – A Randomized, Three-Armed Pilot Study

Planta Medica ◽  
2021 ◽  
Author(s):  
Moritz Winker ◽  
Amy Marisa Zimmermann-Klemd ◽  
Seema Devi ◽  
Aljoscha Waterstradt ◽  
Ann-Kathrin Lederer ◽  
...  

Abstract Equisetum arvense tea (TEA) contains high concentrations of silicon and has been used in folk medicine for the treatment of inflammatory ailments. We examined the resorption of silicon after TEA consumption. Safety and immunological effects were secondary outcomes. A monocentric, randomized, three-armed pilot study was conducted with 12 voluntary, healthy, male subjects. The study is registered in the German register for clinical trials (DRKS-ID: DRKS00016628). After a low silicon diet for 36 hours, 1000 mL TEA1 with approximately 200 000 µg silicon/L, TEA2 with approximately 750 000 µg silicon/L, or Si-low-Water (approximately 10 – 10 000 µg silicon/L as a control) were ingested on three consecutive days. Blood and urine samples were collected at baseline, day 1 examining silicon kinetics, day 3 examining silicon accumulation, and day 8 (safety, immunological parameters). Si-low-Water intake did not change silicon serum (Cmax 294 µg/L) or urine (19 000 µg/24 h) concentrations compared to baseline. Cmax was 2855 µg/L for TEA1 and 2498 µg/L for TEA2; tmax was 60 and 120 min, respectively. Silicon accumulation did not occur. Urine silica within 24 h (E24 h) was higher after TEA2 compared to TEA1 ingestion (142 000 vs. 109 000 µg/24 h). Serum silicon levels at t = 120 min differed significantly after intake of TEA2 or intake of Si-low-Water (p = 0.029). The immunological parameters did not show any significant changes indicating immunosuppressive effects in volunteers. TEA1 was well tolerated, while TEA2 caused diarrhoea in 4 subjects. Our investigations show that intake of TEA1 leads to significant rise in serum silicon concentration.

Author(s):  
D.T. Fefar ◽  
Ankita N. Brahmbhatt ◽  
B.P. Joshi ◽  
D.J. Ghodasara

A study was conducted on 5 weeks old 64 (32 male and 32 female) Swiss albino mice to assess the haemato-biochemical and immunological effects of acetamiprid. All the male and female mice were randomly divided into eight different groups. The groups I (male) and II (female) served as controls whereas remaining groups served as treatment groups and were administered acetamiprid at the daily dose rate of 20, 10, 5 mg/kg body weight in males(Group III, V, VII) and females (Group IV, VI,VIII),respectively for 28 days. After 28 days treatment, blood samples were collected for hematological, biochemical as well as immunological analysis. There was significant decrease in haematological parameters like Hb, TEC, TLC, neutrophils and lymphocytes count in high dose groups and revealed potential adversity of acetamiprid at rates of 20 mg/kg/day on haematopoetic system of mice. A dose dependent significant rise in mean values of AST and ALT was observed in treatment groups, whereas there was significant decrease in total protein and albumin and increase in BUN in high and mid dose treated groups, irrespective of sex of mice. Dinitroflurobenzene (DNFB) test conducted to assess the cell mediated immunity revealed the toxic effect of acetamiprid on cell mediated immunity of mice at dose level of 10 mg/kg/day. The mice of high dose group revealed a significant decrease in HA titer and indicated the immunotoxic potential of acetamiprid at dose level of 20 mg/kg/day.


1997 ◽  
Vol 15 (3) ◽  
pp. 204-211 ◽  
Author(s):  
Jonas C. S. Bergh ◽  
Thomas H. Tötterman ◽  
Birgitta C. Termander ◽  
Kerstin A.-M. P. Strandgarden ◽  
Per Olov G. Gunnarsson ◽  
...  

2002 ◽  
Vol 92 (4) ◽  
pp. 1619-1627 ◽  
Author(s):  
A. Choukèr ◽  
L. Smith ◽  
F. Christ ◽  
I. Larina ◽  
I. Nichiporuk ◽  
...  

The aim of the study was to evaluate the effects of long-term confinement on stress-permissive neuroendocrine and immune responses in humans. Two groups of four male subjects were confined 240 days ( group 240) or 110 days ( group 110) in two space modules of 100 or 200 m3, respectively. During confinement, none of the volunteers developed psychic stress as could be examined and verified by a current stress test. However, in g roup 240 but not in group 110, the diurnal rhythm of cortisol secretion was slightly depressed and the urine excretion of norepinephrine significantly increased. The innate part of the immune system became activated as seen by a rise in the number of circulating granulocytes and the enhanced expression of β2-integrins. In contrast, the ratio of T-helper to T-suppressor cells decreased. All these effects, observed during confinement, were even more pronounced in both groups when values of endocrinological and immunological parameters were compared between before and 1 wk after the end of the confinement period. Hence, return to normal life exerts pronounced effects to a much higher degree, irrespective of how long or under which conditions individuals were confined. Because the delayed-type hypersensitivity skin reaction against recall antigens remained unaffected, it is to be presumed that confinement appears to induce distinct sympathoadrenergic activation and immunological changes but no clinically relevant immunosuppression.


1965 ◽  
Vol 20 (6) ◽  
pp. 1136-1140 ◽  
Author(s):  
Leo C. Senay ◽  
Margaret L. Christensen

Progressive dehydration of resting male subjects was accomplished by exposure to 43.3 C dry bulb, 29 C wet bulb for 12 hr. For control experiments, evaporative weight loss was replaced with 0.1% saline. For dehydrating subjects, the following relationships with evaporative weight losses were obtained: %Delta osmotic pressure = 1.14 (% evap wt loss) — 0.43; %Delta [Na+] = 1.37 (% evap wt loss) — 0.45; %Delta [K+] — 2.19 (% evap wt loss) — 1.29; %Delta hematocrit = 1.4 (%Delta evap wt loss) — 2.65. Comparison of dehydration with rehydration results indicated augmentation of plasma volume with fluids containing high concentrations of potassium. An average decrease in plasma volume of 13.6% (T-1824) from 2.5 to 11 hr after initial heat exposure in dehydrating subjects was accompanied by a 15.7% increase in total protein. Albumin increased 11.6% while globulin increase averaged 22.5%. Plasma protein fractions are not static during dehydration, probably due to augmentation of each protein fraction, particularly globulin. Measurement of plasma volume by T-1824 more likely indicates changes in protein concentration rather than plasma volume changes. A relationship between hematocrit changes and plasma albumin concentrations is suggested. plasma sodium; plasma potassium; plasma osmolarity; hematocrits; plasma albumin; plasma globulins Submitted on February 23, 1965


Author(s):  
Marieke Heiden ◽  
Anna Nopp ◽  
Josef Brandström ◽  
Claudia Carvalho‐Queiroz ◽  
Caroline Nilsson ◽  
...  

1981 ◽  
Vol 51 (3) ◽  
pp. 686-692 ◽  
Author(s):  
S. S. Khosla ◽  
A. B. DuBois

The aim of the present study was to determine the magnitude and direction of the shift of body fluids during water immersion of humans to the neck. Five healthy male subjects were studied lying in air for 1.5 h, sitting in 34 degrees C water to the neck for 1 h, and again lying in air for 1.5 h in two sets of experiments. For the first set, vasopressin (0.75 IU, sc) was injected before immersion. Blood and urine samples were drawn every 30 min in air and every 20 min in water. Urinary sodium, potassium, and osmolal clearances were significantly increased during immersion. When the mean maximum change during immersion was calculated for five subjects hematocrit fell by 1.1 U, plasma concentrations of sodium by 3.9 meq/l, chloride by 3.5 meq/l, potassium by 0.2 meq/l, osmolality by 7.9 mosmol/kg H2O, and proteins by 0.25 g/100 ml, whereas total plasma CO2 content increased by 1.33 mmol/l, threonine by 11.6%, proline by 9.0%, methionine by 14.0%, and alanine by 29%. Plasma volume increased 6.1%, and red blood cell volume calculated from hematocrit and hemoglobin increased 3.5%. In the second set of immersion experiments, without vasopressin injection, interstitial fluid pressures were measured with a cotton wick in PE-50 tubing inserted subcutaneously. A mean interstitial fluid pressure of -0.5 cmH2O was observed when the subjects were lying in air. Interstitial fluid pressure had started to decrease by 20 min of immersion, with a maximum decrease during immersion averaging 2.10 cmH2O. We conclude that hyposmotic fluid is mobilized into the blood from interstitial and other extravascular spaces during immersion.


Author(s):  
Subhash T. Kumbhar ◽  
Hemant D. Une ◽  
Anagha M. Joshi ◽  
Pralhad B. Wangikar

<p><strong>Objective: </strong>This study evaluated the toxic effect of simultaneously injected normal doses of caffeine and nicotine in diabetic lab animals.</p><p><strong>Methods: </strong>A study was conducted for three weeks in seven rat groups (n=6); viz. first non-diabetic group treated with caffeine (20 mg/kg, ip) twice daily, second with nicotine (0.4 mg/kg, ip) twice daily and third with both treatments simultaneously; whereas other three groups treated in the same way but inducing diabetes; and employing the seventh group as diabetic control. Type 2 diabetes was induced by high fatty diet prior for two weeks and a single streptozotocin injection on 1<sup>th</sup> day of study in all diabetic groups. Blood and urine samples were collected weekly to estimate blood parameters. Animals were sacrificed, and organs were collected for histopathology analysis.</p><p><strong>Results: </strong>Most blood parameters showed a rapid increase in diabetes in co-addiction group compared with their single addiction or non-addiction control groups. Caffeine-nicotine co-addiction group showed about 60-80 mg/dl (p&lt;0.05) rise in serum glucose, 15-20 U/l in AST (p&lt;0.01), 80-100 U/l in ALT (p&lt;0.01), 20-30 mg/dl in Urea (p&lt;0.01), 02 mg/dl in creatinine (p&lt;0.05), 12-15 mg/dl (p&lt;0.01) in LDL-C, 6-9 mg/dl in VLDL-C (p&lt;0.01) and 60-90 mg/dl in TC levels (p&lt;0.01) when compared with non-addicted diabetic control. There was a significant reduction in HDL-C (p&lt;0.01) while the less significant rise in triglycerides in the case of co-addiction as compared to non-addiction diabetic control group. Histopathology results exhibited moderate to severe tissue damage in agreement with clinical biochemistry results.</p><p><strong>Conclusion: </strong>Nicotine-caffeine co-addiction harms exceptionally more in type 2 diabetes greater than their single addiction or non-addiction.</p>


1987 ◽  
Author(s):  
J Kienast ◽  
J Arnout ◽  
G Pfliegler ◽  
H Deckmyn ◽  
B Hoet ◽  
...  

Elevated cytosolic free Ca2+ concentrations ([Ca2+]i) are thought to be required for phosphol ipase A2 activity to liberate arachidonic acid (AA) from membrane phospholipids in platelets. The major AA metabolite formed during agonist-induced platelet activation is thromboxane A2 (TxA2). We have investigated the effect of sodium fluoride (NaF) on platelet TxAz formation in correlation to platelet functional changes (aggregation and release of ATP) and intracellular events specific for either agonist- or antagonist-induced platelet responses. A first peak in platelet TxAffi formation reaching 30 × control values was observed at 20 - 30 mM of NaF which also induced platelet aggregation and release of ATP in association with a rise in [Ca2+]i . Increasing the concentration of NaF resulted in a decrease in TxA2 release to a minimum of 12 × control values at 50 mM. A second, concentration-dependent rise in TxA2 formation was observed at higher concentrations of NaF with a maximum of 40 × control values at 100 mM. These concentrations, however, did induce neither aggregation nor a significant rise in [Ca2+]i but a rapid, transient increase in platelet cAMP levels. Activation of phospholipase C and protein kinase C was observed at all concentrations of NaF tested whereby the rate rather than the extent of activation of these enzymes was concentration-dependent. Our results demonstrate that fluoride at high concentrations can induce platelet TxA2 formation in the absence of elevated [Ca2+]i suggesting an additional, Ca2+-independent mechanism of phospholipase A2 activation possibly mediated by fluoride sensitive GTP-binding regulatory proteins.


Author(s):  
Navraj S. Heran ◽  
Stephen J. Hentschel ◽  
Brian D. Toyota

Background:Cerebral vasospasm adversely impacts the outcome of those suffering aneurysmal subarachnoid hemorrhage (SAH). Prediction of vasospasm could improve outcomes. We hypothesized that preclinical vasospasm would be heralded by an increase in cerebral oxygen extractions (AVDO2) which could be detected by jugular bulb oximetry. A pilot study was conducted to address this hypothesis.Methods:Fourteen consenting patients with aneurysmal SAH, undergoing early surgery, were entered into the study. Four patients were withdrawn from the study secondary to failure of catheters or religious belief. At the time of craniotomy, a jugular bulb catheter was placed. Post-operatively, arterial and jugular bulb blood samples were taken every 12 hours to calculate AVDO2. As this was an observational study, no change in management occurred based on measurements.Results:Four of 10 patients had clinical vasospasm. These patients had a significant rise in AVDO2 approximately one day prior to the onset of neurologic deficits (P<0.001). Symptoms resolved along with a significant improvement in AVDO2 on instituting hypertensive, hemo-dilutional, and hypervolemic therapy in these patients. The six patients who did not exhibit clinical vasospasm did not demonstrate significant rise in AVDO2.Conclusion:Jugular bulb oximetry is simple and cost effective. Increases in AVDO2 using this technique were predictive of clinically evident vasospasm in the subsequent hours to days. This investigation supports a larger study to assess the utility of jugular bulb oximetry in predicting vasospasm in aneurysmal SAH.


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