Bioassembly lines: a general mechanism for maintaining the specific architecture of a cell, with an implication for the function of a small RNA

We show numerical evidence of continuous and discontinuous transitions between entrainment (frequency-locking) and beating regimes in a driven non-linear oscillator.     

Degradation of thyroxine by microsomal particles from rat liver II. Purification of Fe3+-dependent particles and some of their properties

Particles, which catalyze the deiodination of thyroid hormones in the presence of Fe²⁺, have been purified about 25-fold with respect to the rat liver microsomes. This purification involves deoxycholate treatment, trypsin treatment and density gradient centrifugutions.The purified particles range from 1.019 to 1.063 in density and consist of 21% protein, 60% phospholipid and 19% neutral fat. No hemoprotein moiety is associated with the purified particles. The purified particles degrade not only l-thyroxine but also other iodinated thyronines and their derivatives, such as d-thyroxine, l-3′,3,5- triiodothyronine and tetraiodothyropropionic acid. They are inactive towards monoiodotyrosine and diiodotyrosine.Thyroxine is not metabolized in the drug hydroxylation system which involves cytochrome P-450.     

Interleukin-6 Deficiency Does Not Affect Motor Neuron Disease Caused by Superoxide Dismutase 1 Mutation

MethodsMice with mutant SOD1 (G93A) transgene, a model for familial ALS, were used in this study. The expression of the major inflammatory cytokines, IL-6, IL-1β and TNF-α, in spinal cords of these SOD1 transgenic (TG) mice were assessed by real time PCR. Mice were then crossed with IL-6(-/-) mice to generate SOD1TG/IL-6(-/-) mice. SOD1 TG/IL-6(-/-) mice (n = 17) were compared with SOD1 TG/IL-6(+/-) mice (n = 18), SOD1 TG/IL-6(+/+) mice (n = 11), WT mice (n = 15), IL-6(+/-) mice (n = 5) and IL-6(-/-) mice (n = 8), with respect to neurological disease severity score, body weight and the survival. We also histologically compared the motor neuron loss in lumber spinal cords and the atrophy of hamstring muscles between these mouse groups.ResultsLevels of IL-6, IL-1β and TNF-α in spinal cords of SOD1 TG mice was increased compared to WT mice. However, SOD1 TG/IL-6(-/-) mice exhibited weight loss, deterioration in motor function and shortened lifespan (167.55 ± 11.52 days), similarly to SOD1 TG /IL-6(+/+) mice (164.31±12.16 days). Motor neuron numbers and IL-1β and TNF-α levels in spinal cords were not significantly different in SOD1 TG /IL-6(-/-) mice and SOD1 TG /IL-6 (+/+) mice.ConclusionThese results provide compelling preclinical evidence indicating that IL-6 does not directly contribute to motor neuron disease caused by SOD1 mutations.     

SERUM DOPAMINE-β-HYDROXYLASE IN SCHIZOPHRENIC PATIENTS

Abstract— Dopamine-β-hydroxylase (DBH) activity in serum was decreased significantly in schizophrenic patients (16.17 ± 12.60 μmol/min/1 of serum, mean ± S.D., n = 149) when compared with that of normal controls (42.53 ± 30.94 μmol/min/1 of serum, mean ± S.D., n= 153) and neurotic patients. Long duration of disease did not cause any significant changes in serum DBH activity except a tendency for increase in patients of lodger than 18 years duration. We also examined the possibility that the serum DBH deficiency in the schizophrenic group was an artifact of treatment with antipsychotic drugs, especially phenothiazines. No significant difference was observed between the patients treated with the drugs and the patients not receiving the drugs.     

Impaired autophagy by soluble endoglin,under physiological hypoxia in early pregnant period,is involved in poor placentation in preeclampsia

In early pregnancy, trophoblasts and the fetus experience hypoxic and low-nutrient conditions; nevertheless, trophoblasts invade the uterine myometrium up to one third of its depth and migrate along the lumina of spiral arterioles, replacing the maternal endothelial lining. Here, we showed that autophagy, an intracellular bulk degradation system, occurred in extravillous trophoblast (EVT) cells under hypoxia in vitro and in vivo. An enhancement of autophagy was observed in EVTs in early placental tissues, which suffer from physiological hypoxia. The invasion and vascular remodeling under hypoxia were significantly reduced in autophagy-deficient EVT cells compared with wild-type EVT cells. Interestingly, soluble endoglin (sENG), which increased in sera in preeclamptic cases, suppressed EVT invasion by inhibiting autophagy. The sENG-inhibited EVT invasion was recovered by TGFB1 treatment in a dose-dependent manner. A high dose of sENG inhibited the vascular construction by EVT cells and human umbilical vein endothelial cells (HUVECs), meanwhile a low dose of sENG inhibited the replacement of HUVECs by EVT cells. A protein selectively degraded by autophagy, SQSTM1, accumulated in EVT cells in preeclamptic placental biopsy samples showing impaired autophagy. This is the first report showing that impaired autophagy in EVT contributes to the pathophysiology of preeclampsia.     

Presence of rhodopsin-like proteins in the planarian head

The presence of rhodopsin-like protein was detected in the head of the freshwater planarian Dugesia japonica japonica Ichikawa et Kawakatsu by use of anti-frog-rhodopsin rabbit IgG. Two membrane proteins of molecular weights 65000 and 62000 were separated by sodium-dodecyl-sulfate polyacrylamide gel electrophoresis and found to react with the anti-rhodopsin IgG. The antibody may be useful for monitoring regeneration of the planarian eye.     

Fructose 2,6-bisphosphate-dependent regulation of phosphofructokinase in rat submandibular gland

1. Regulation of phosphofructokinase in rat submandibular gland was non-Michaelis-Menten type at physiological pH. 2. At pH 7.3, ATP played a dual role on phosphofructokinase acting as a substrate and inhibitor at high concentration of ATP. 3. The activator of phosphofructokinase was present in cytosol fraction, and its properties were resemble to those of fructose 2,6-bisphosphate. 4. Both the activator and authentic fructose 2,6-bisphosphate relieved the inhibition of phosphofructokinase by ATP, and increased the affinity for fructose 6-phosphate. 5. Concentration of fructose 2,6-bisphosphate in rat submandibular gland was 8.22 nmol/g tissue, and which was about the half of that in liver. 6. Phosphofructokinase in rat submandibular gland was found to be regulated synergistically by ATP, fructose 6-phosphate and fructose 2,6-bisphosphate.