To characterize the course of therapy in a large cohort of Chinese patients with thyrotoxic periodic paralysis (TPP), a reversible electrolyte emergency fraught with therapeutic challenges.In this prospective interventional study, 78 patients with TPP (75 males and three females with an age range of 16-48 years) were consecutively enrolled over a 6-year period. Intravenous KCl at a rate of 10 mmol/h was administered until muscle strength recovered. Serum potassium (K(+)) and phosphorus concentrations were measured hourly during the paralytic attack and for 6 h after recovery.The serum potassium (K(+)) on attack was 2.1+/-0.2 mmol/l. The dose of KCl administered to restore muscle strength was 63+/-32 mmol, and peak serum K(+) concentration after recovery was 5.3+/-0.5 mmol/l. A paradoxical fall in serum K(+) concentration >0.1 mmol/l difference between presentation and treatment nadir was observed in approximately one-fourth of TPP patients (n=20). These patients had significantly higher serum-free thyroxine concentration, systolic blood pressure, and heart rate on presentation, as well as serum phosphate concentration on recovery. They not only needed much more KCl supplementation (104+/-34 vs 48+/-19 mmol, P<0.001), but also had significantly more severe rebound hyperkalemia (5.8+/-0.5 vs 5.1+/-0.4 mmol/l, P<0.001) on recovery than those who did not have paradoxical hypokalemia. There was a positive correlation between the dose of KCl administered and the difference between peak and nadir serum K(+) (Delta K(+)) (r=0.68, P<0.001).TPP patients who do not develop paradoxical hypokalemia need a smaller KCl dose to achieve recovery, whereas those who develop paradoxical hypokalemia have more severe hyperthyroidism and hyperadrenergic activity and may require blockage of intracellular K(+) shift to prevent rebound hyperkalemia.
Interleukin (IL)-25 is a cytokine released by airway epithelial cells responding to pathogens. Excessive production of reactive oxygen species (ROS) leads to airway inflammation and remodeling in asthma. Mitochondria are the major source of ROS. After stress, defective mitochondria often undergo selective degradation, known as mitophagy. In this study, we examined the effects of IL-25 on ROS production and mitophagy and investigated the underlying mechanisms. The human monocyte cell line was pretreated with IL-25 at different time points. ROS production was measured by flow cytometry. The involvement of mitochondrial activity in the effects of IL-25 on ROS production and subsequent mitophagy was evaluated by enzyme-linked immunosorbent assay, Western blotting, and confocal microscopy. IL-25 stimulation alone induced ROS production and was suppressed by N-acetylcysteine, vitamin C, antimycin A, and MitoTEMPO. The activity of mitochondrial complex I and complex II/III and the levels of p-AMPK and the mitophagy-related proteins were increased by IL-25 stimulation. The CCL-22 secretion was increased by IL-25 stimulation and suppressed by mitophagy inhibitor treatment and PINK1 knockdown. The Th2-like cytokine IL-25 can induce ROS production, increase mitochondrial respiratory chain complex activity, subsequently activate AMPK, and induce mitophagy to stimulate M2 macrophage polarization in monocytes.
In this research, nanoporous silver foams are fabricated through dealloying Ag35Al65 (as atomic percentage, at%) thin films in supercritical (SC) carbon dioxide. The supercritical CO2 is mixed with either HCl, water or H2C2O4 aqueous solution as the solute in the reaction chamber. Due to the low tension of the supercritical fluid, under the best operating conditions, the surface area of the as-dealloyed Ag35Al65 can reach 4.6 m2 g-1, and the porosity volume fraction value can reach 74%, with a smallest average pore size of around 75 nm. In an optimum supercritical CO2 environment, a lower chemical concentration can be applied and it can take less time to form a uniform nanoporous structure.
The CMOS nonthreshold logic (NTL) is derived from its bipolar counterpart, which is the fastest bipolar logic, and takes the NOR gate as its basic building gate. It is shown that by applying the nonthreshold principle to CMOS circuits speed performance can be highly improved, but with an increase of DC power consumption. From transient analyses the speed of CMOS NTL is found quite comparable to that of I/sup 2/L (integrated injection logic) or even ECL (emitter-coupled logic) and is about 20-60% better than that of conventional CMOS. Meanwhile, the power-delay product of CMOS NTL is smaller than those of I/sup 2/L and ECL and is nearly the same as that of conventional CMOS operated at high frequency. The nonthreshold principle is applied to the CMOS cascode structure to form the CMOS cascode nonthreshold logic (CNTL), in which there is a tradeoff between speed performance and power dissipation. It is shown from the design of full adders that the CMOS NTL is the fastest of all the static CMOS logic circuits. The speed of the CNTL circuit, although slower than that of the NTL circuit, is still higher than that of the DSL circuit, which is the fastest static circuit proposed so far. The CNTL circuit also has a smaller power-delay product than the DSL circuit.< >
Haemolytic-uremic syndrome (HUS) is a severe, life-threatening disease with symptoms such as haemolytic anaemia, renal failure, and a low platelet count. Possible aetiology includes bacterial infections, medication, post-hematopoietic cell transplantation, pregnancy, autoimmune disease, and acquired immunodeficiency syndrome.We report the case of a 21-year-old healthy man who developed acute renal failure caused by HUS. Typical symptoms of HUS combined with severe uraemia developed following a large local reaction after suspected Solenopsis invicta (fire ant) bites. He was successfully treated with plasma exchange and achieved complete recovery of renal function.This is the first case illustrating a serious systemic reaction of HUS to fire ant bites, and highlights this severe complication in patients who sustain fire ant bites.
A new CMOS inverter-based wideband transresistance (R/sub m/) amplifier is proposed and analyzed. Using the R/sub m/ amplifier, tunable VHF/UHF R/sub m/-C bandpass biquadratic filters can be designed. In these filters, the center frequency f/sub 0/ can be post-tuned by adjusting the control voltages of the R/sub m/ amplifier. Experimental results have shown that the single-ended-output R/sub m/-C bandpass biquad has the center frequency f/sub 0/=368 MHz and the quality factor Q=1.95 whereas the fully-differential-output configuration has Q=360 and f/sub 0/=222.7 MHz.< >
Asthma is a chronic inflammatory airway disease induced by many environmental factors. The inhalation of allergens and pollutants promotes the production of reactive oxygen species (ROS) leading to airway inflammation, hyper-responsiveness, and remodeling in allergic asthma. The effects of asthma medications on ROS production are unclear. The present study investigated the anti-ROS effects of current asthma medications including inhaled corticosteroid (ICS; budesonide and fluticasone), leukotriene receptor antagonist (LTRA; montelukast), long-acting β2 agonists (LABAs; salmeterol and formoterol), and a new extra-LABA (indacaterol).The human monocyte cell line THP-1 cells were pre-treated with different concentrations of the asthma medications at different time points after hydrogen peroxide (H2O2) stimulation. H2O2 production was measured with DCFH-DA by flow cytometry.Montelukast, fluticasone, and salmeterol suppressed H2O2-induced ROS production. Indacaterol enhanced H2O2-induced ROS production. Budesonide and formoterol alone had no anti-ROS effects, but the combination of these two drugs significantly suppressed H2O2-induced ROS production.Different asthma medications have different anti-ROS effects on monocytes. The combination therapy with LABA and ICS seemed not to be the only choice for asthma control. Montelukast may also be a good supplemental treatment for the poorly controlled asthma because of its powerful anti-ROS effects. Our findings provide a novel therapeutic view in asthma.
Angiotensin-converting enzyme inhibitors (ACEIs) are used to control hypertension and are superior to other antihypertensive agents in protecting the progressive deterioration of autoimmune-related nephritis. An imbalance of T helper 1 (Th1)/Th2 is thought to contribute to the pathogenesis of autoimmune diseases and their related glomerulonephritis. I-309 is a Th2-related chemokine involved in the recruitment of Th2 cells toward Th2-related inflammation. Tumor necrosis factor α (TNF-α) and Th1-related chemokines, interferon-inducible protein 10 (IP-10)/CXCL10 are also involved in autoimmune glomerulonephritis. However, the modulatory effects and the mechanisms of ACEIs on TNF-α and Th1- and Th2-related chemokines in monocytes remain poorly defined.We investigated the effects of imidapril and perindopril, 2 ACEIs, on the expression of IP-10, I-309, and TNF-α in human monocytes and also the associated intracellular mechanism.Imidapril and perindopril significantly downregulated lipopolysaccharide (LPS)-induced TNF-α, I-309, and IP-10 in THP-1 cells and human primary monocytes. All 3 mitogen-activated protein kinase inhibitors suppressed LPS-induced TNF-α and I-309 expression in human primary monocytes. Only extracellular signal-regulated kinases and c-Jun N-terminal kinases (JNK) mitogen-activated protein kinase inhibitors suppressed LPS-induced IP-10 expression. Lipopolysaccharide-induced mitogen-activated protein kinase kinase 4 (MKK4), p-JNK, and c-Jun expression in human primary monocytes was suppressed by imidapril.These data demonstrate that ACEI is effective in downregulating LPS-induced TNF-α, I-309, and IP-10, which play important roles in the pathogenesis of inflammation. Its suppressive effect on TNF-α, I-309, and IP-10 may, at least in part, involve the down-regulation of LPS-induced MKK4-JNK-c-Jun expression.
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