63 research outputs found
Thyroid hormone uptake in cultured rat anterior pituitary cells: effects of energy status and bilirubin
Transport of thyroxine (T(4)) into the liver is inhibited in fasting and
by bilirubin, a compound often accumulating in the serum of critically ill
patients. We tested the effects of chronic and acute energy deprivation,
bilirubin and its precursor biliverdin on the 15-min uptake of
[(125)I]tri-iodothyronine ([(125)I]T(3)) and [(125)I]T(4) and on TSH
release in rat anterior pituitary cells maintained in primary culture for
3 days. When cells were cultured and incubated in medium without glucose
and glutamine to induce chronic energy deprivation, the ATP content was
reduced by 45% (P<0. 05) and [(125)I]T(3) uptake by 13% (NS), but TSH
release was unaltered. Preincubation (30 min) and incubation (15 min) with
10 microM oligomycin reduced ATP content by 51% (P<0.05) and 53% (P<0. 05)
under energy-rich and energy-poor culture conditions respectively;
[(125)I]T(3) uptake was reduced by 66% (P<0.05) and 64% (P<0.05). Neither
bilirubin nor biliverdin (both 1-200 microM) affected uptake of
[(125)I]T(3) or [(125)I]T(4). Bilirubin (1-50 microM) did not alter basal
or TRH-induced TSH release. In conclusion, the absence of inhibitory
effects of chronic energy deprivation and bilirubin on thyroid hormone
uptake by pituitary cells supports the view that the transport is
regulated differently than that in the liver
Grex: A Decentralized Hive Mind
Swarm Robotics (SR) faces a series of challenges impeding widespread adoption for real-world applications. Distributed Ledger Technology (DLT) has shown it can solve a number of these challenges. An experiment was conducted to showcase the resolution of these challenges. A search and rescue mission was simulated using drones coupled with single board computers and several simulated agents. Inter-agent communications were facilitated through DLT in a completely decentralized network. A frontend interface was built to demonstrate the ease with which information can be extracted from the system. This paper shows the feasibility of the application of DLT to SR-related challenges in a practical experiment. For future work, it is proposed to focus on more complex tasks through federated learning or inter-swarm communications, possibly through Cosmos
Reduced activation and increased inactivation of thyroid hormone in tissues of critically ill patients
Critical illness is often associated with reduced TSH and thyroid hormone
secretion as well as marked changes in peripheral thyroid hormone
metabolism, resulting in low serum T(3) and high rT(3) levels. To study
the mechanism(s) of the latter changes, we determined serum thyroid
hormone levels and the expression of the type 1, 2, and 3 iodothyronine
deiodinases (D1, D2, and D3) in liver and skeletal muscle from deceased
intensive care patients. To study mechanisms underlying these changes, 65
blood samples, 65 liver, and 66 skeletal muscle biopsies were obtained
within minutes after death from 80 intensive care unit patients randomized
for intensive or conventional insulin treatment. Serum thyroid parameters
and the expression of tissue D1-D3 were determined. Serum TSH, T(4), T(3),
and the T(3)/rT(3) ratio were lower, whereas serum rT(3) was higher than
in normal subjects (P < 0.0001). Liver D1 activity was down-regulated and
D3 activity was induced in liver and skeletal muscle. Serum T(3)/rT(3)
ratio correlated positively with liver D1 activity (P < 0.001) and
negatively with liver D3 activity (ns). These parameters were independent
of the type of insulin treatment. Liver D1 and serum T(3)/rT(3) were
highest in patients who died from severe brain damage, intermediate in
those who died from sepsis or excessive inflammation
Changes in renal tri-iodothyronine and thyroxine handling during fasting
OBJECTIVE: Liver handling of thyroid hormones (TH) has been known to alter
significantly during fasting. This study investigates whether renal
handling of TH is also changed during fasting. METHODS: We measured
urinary excretion rates and clearances of free tri-iodothyronine (T(3))
and free thyroxine (T(4)) in healthy subjects prior to and on the third
day of fasting. RESULTS: During fasting, both mean T(3) and T(4) urinary
excretion decreased significantly to a mean value of 42% of control. Also,
total and free (F) serum T(3) concentrations declined significantly, but
serum T(4) did not change. Both FT(3) and FT(4) clearance decreased
significantly during fasting (62% and 42% of control). The fasting-induced
decrease in uric acid clearance correlated well with the decrease in FT(3)
clearance (r=0.94; P<0.001). Serum concentrations of non-esterified fatty
acids (NEFA) were significantly elevated during fasting. CONCLUSIONS: The
findings cannot be fully explained by the fasting-induced decrease in
serum T(3), a
Effects of interleukin-1 beta on thyrotropin secretion and thyroid hormone uptake in cultured rat anterior pituitary cells
The effects of interleukin-1 beta (IL-1 beta) and tumor necrosis
factor-alpha (TNF alpha) on basal and TRH-induced TSH release, and the
effects of IL-1 beta on the uptake of [125I]T3 and [125I]T4 and on nuclear
binding of [125I]T3 were examined. Furthermore, the release of other
anterior pituitary hormones in the presence of IL-1 beta was measured.
Anterior pituitary cells from male Wistar rats were cultured for 3 days in
medium containing 10% FCS. Incubation were performed at 37 C in medium
with 0.5% BSA for measurement of [125I]T3 uptake and with 0.1% BSA for
measurement of [125I]T4 uptake. Exposure to IL-1 beta (1 pM-1 nM) or TNF
alpha (100 pM) for 2-4 h resulted in a significant decline in TSH release,
which was almost 50% (P < 0.05) for 1 nM IL-1 beta and 24% (P < 0.05) for
100 pM TNF alpha. Measurement of other anterior pituitary hormones (FSH,
LH, PRL, and ACTH) in the same incubation medium showed that IL-1 beta did
not alter their release. When the effects of IL-1 beta (1 pM-1 nM) and TNF
alpha (100 pM) on TRH-induced TSH release were measured in short term
experiments, the inhibitory effects had disappeared. The addition of 1-100
nM octreotide, a somatostatin analog, resulted in a decrease in
TRH-induced TSH release up to 33% of the control value (P < 0.05).
Exposure to dexamethasone (1 nM to 1 microM) affected basal and
TRH-induced TSH release similar to the effect of IL-1 beta. The 15-min
uptake of [125I]T3 and [125I]T4, expressed as femtomoles per pM free
hormone, was not affected by the presence of IL-1 beta (1-100 pM). When
IL-1 beta (100 pM) was present during 3 days of culture, TSH release was
reduced to 88 +/- 2% of the control value (P < 0.05). This effect was not
associated with an altered [125I]T3 uptake (15 min to 4 h) or with any
change in nuclear T3 binding. We conclude that 1) IL-1 beta decreases TSH
release by a direct action on the pituitary; 2) this effect is not due to
elevated thyroid hormone uptake or increase T3 nuclear occupancy; 3) IL-1
beta does not affect TRH-induced TSH release or the release of other
anterior pituitary hormones; and 4) TNF alpha affects basal and
TRH-induced TSH release in the same way as IL-1 beta
Different effects of continuous infusion of interleukin-1 and interleukin-6 on the hypothalamic-hypophysial-thyroid axis
The cytokines interleukin-1 (IL-1) and IL-6 are thought to be important
mediators in the suppression of thyroid function during nonthyroidal
illness. In this study we compared the effects of IL-1 and IL-6 infusion
on the hypothalamus-pituitary-thyroid axis in rats. Cytokines were
administered by continuous ip infusion of 4 micrograms IL-1 alpha/day for
1, 2, or 7 days or of 15 micrograms IL-6/day for 7 days. Body weight and
temperature, food and water intake, and plasma TSH, T4, free T4 (FT4), T3,
and corticosterone levels were measured daily, and hypothalamic pro-TRH
messenger RNA (mRNA) and hypophysial TSH beta mRNA were determined after
termination of the experiments. Compared with saline-treated controls,
infusion of IL-1, but not of IL-6, produced a transient decrease in food
and water intake, a transient increase in body temperature, and a
prolonged decrease in body weight. Both cytokines caused transient
decreases in plasma TSH and T4, which were greater and more prolonged with
IL-1 than with IL-6, whereas they effected similar transient increases in
the plasma FT4 fraction. Infusion with IL-1, but not IL-6, also induced
transient decreases in plasma FT4 and T3 and a transient increase in
plasma corticosterone. Hypothalamic pro-TRH mRNA was significantly
decreased (-73%) after 7 days, but not after 1 or 2 days, of IL-1 infusion
and was unaffected by IL-6 infusion. Hypophysial TSH beta mRNA was
significantly decreased after 2 (-62%) and 7 (-62%) days, but not after 1
day, of IL-1 infusion and was unaffected by IL-6 infusion. These results
are in agreement with previous findings that IL-1, more so than IL-6,
directly inhibits thyroid hormone production. They also indicate that IL-1
and IL-6 both decrease plasma T4 binding. Furthermore, both cytokines
induce an acute and dramatic decrease in plasma TSH before (IL-1) or even
without (IL-6) a decrease in hypothalamic pro-TRH mRNA or hypophysial TSH
beta mRNA, suggesting that the acute decrease in TSH secretion is not
caused by decreased pro-TRH and TSH beta gene expression. The
TSH-suppressive effect of IL-6, either administered as such or induced by
IL-1 infusion, may be due to a direct effect on the thyrotroph, whereas
additional effects of IL-1 may involve changes in the hypothalamic release
of somatostatin or TRH.(ABSTRACT TRUNCATED AT 400 WORDS
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