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Indoor air quality (IAQ) is increasingly recognised as one of the critical factors influencing human health, particularly given the amount of time people spend indoors. This study investigated the impact of real-life kitchen human activity (KHA) on IAQ. We used low-cost sensors to measure real-time concentrations of smoke, carbon monoxide (CO), and particulate matter (PM 10 and PM 2.5 ) in the kitchen of a household with three adults, analysing KHAs by dividing them into five categories. The fixed effect model was employed to analyse the data, explaining the impact of different KHAs on IAQ. The results showed that compared to other KHAs, using the gas stove had the greatest impact on IAQ, with average increases of 13% in smoke, 24.4% in CO, 9.8% in PM 10 , and 5.34% in PM 2.5 . The study also found that without windows and with insufficient ventilation, only using the range hood cannot effectively and obviously reduce PM levels. These findings highlight the need for comprehensive IAQ management strategies and further research. Despite its limitations, this study also validated the potential of low-cost sensors in IAQ monitoring., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Background: Clozapine has remarkable efficacy on both negative and cognitive symptoms of schizophrenia due to its slight activation of NMDA receptor. In fact, much evidence to the contrary. NMDAR is a complex containing specific binding sites, which are regulated to improve negative symptoms and cognitive deficits associated with individuals affected by schizophrenia. PQQ is a powerful neuroprotectant that specifically binds with NMDA receptors in the brain to produce beneficial physiological and cognitive outcomes. The aim of this study was to enhance NMDAR function and improve cognitive ability in schizophrenia by PQQ combined with clozapine., Methods: Rats were divided into four groups (n = 5) including control (saline), model (MK-801, 0.5 mg·kg - 1 ·d - 1 ), atypical antipsychotic (MK-801 (0.5 mg·kg - 1 ·d - 1 ) + Clozapine (1.0 mg·kg - 1 ·d - 1 ), and co-agonist NMDA receptor (MK-801 (0.5 mg·kg - 1 ·d - 1 ) + Clozapine (0.5 mg·kg - 1 ·d - 1 ) + PQQ (1.0 μg·kg - 1 ·d - 1 ) group. Each group of rats was injected subcutaneously every day for 6 weeks. Behavior test, including stereotyped behavior, locomotor hyperactivity, learning and memory, was performed. The Western blot assay was performed to analyze the expression of GSK-3β, Akt, NMDAR1, and MGLUR in rat hippocampus., Results: Results indicated that clozapine and PQQ combination therapy can improve MK801-induced schizophrenia behavior including stereotyped behavior, locomotor hyperactivity and cognitive impairment. Furthermore, we found that modulating NMDA receptors could ameliorate the memory impairments in Mk-801 induced schizophrenia rats by reducing the expression of NMDAR1 and MGLUR3, decreasing hippocampal tau hyperphosphorylation and inhibiting apoptosis through Akt /GSK-3β signaling pathway., Conclusions: These findings suggest that combination therapy for enhancing NMDA receptors may be able to rescue cognition deficit in schizophrenia. More studies are needed to better elucidate these mechanisms.

Objectives: The in vivo binding analysis of vesicular monoamine transporter type 2 (VMAT2) to radioligand has provided a means of investigating related disorders. Anesthesia is often inevitable when the investigations are performed in animals. In the present study, we tested effects of four commonly-used anesthetics: isoflurane, pentobarbital, chloral hydrate and ketamine, on in vivo VMAT2 binding to (18)F-FP-(+)-DTBZ, a specific VMAT2 radioligand, in rat brain., Methods: The transient equilibrium time window for in vivo binding of (18)F-FP-(+)-DTBZ after a bolus injection was firstly determined. The brain biodistribution studies under anesthetized and awake rats were then performed at the equilibrium time. Standard uptake values (SUVs) of the interest brain regions: the striatum (ST), hippocampus (HP), cortex (CX) and cerebellum (CB) were obtained; and ratios of tissue to cerebellum were calculated., Results: Isoflurane and pentobarbital did not alter distribution of (18)F-FP-(+)-DTBZ in the brain relative to the awake group; neither SUVs nor ratios of ST/CB and HP/CB were altered significantly. Chloral hydrate significantly increased SUVs of all the brain regions, but did not significantly alter ratios of ST/CB and HP/CB. Ketamine significantly increased SUVs of the striatum, hippocampus and cortex, and insignificantly increased the SUV of the cerebellum; consequently, ketamine significantly increased ratios of ST/CB and HP/CB., Conclusions: It is concluded that in vivo VMAT2 binding to (18)F-FP-(+)-DTBZ are not altered by isoflurane and pentobarbital, but altered by chloral hydrate and ketamine. Isoflurane and pentobarbital may be promising anesthetic compounds for investigating in vivo VMAT2 binding. Further studies are warranted to investigate the interactions of anesthetics with VMAT2 binding potential with in vivo PET studies., (Copyright © 2015 Elsevier Inc. All rights reserved.)

Pyrroloquinoline quinone (PQQ), an essential nutrient, antioxidant, redox modulator and nerve growth factor found in a class of enzymes called quinoproteins, was labeled with 99m Tc by using stannous fluoride (SnF 2 ) method. Radiolabeling qualification, quality control and characterization of 99m Tc-PQQ and its biodistribution studies in mice were performed and discussed. Effects of pH values, temperature, time and reducing agents concentration on the radiolabeling yield were investigated. The quality control procedure of 99m Tc-PQQ was determined by thin layer chromatography (TLC), radio high-performance liquid chromatography (RHPLC) and paper electrophoresis methods. The average radiolabeling yield was 94 ± 1% under optimum conditions of 0.99 mg of PQQ, 30 μg of SnF 2 , 0.5 mg of ethylenediaminetetraacetic acid disodium salt (EDTA-2Na) and 18.5 MBq of Na 99m TcO 4 at pH 6 and 25 °C with a response volume of 1 ± 0.1 mL. 99m Tc-PQQ was stable and anionic. Lipid-water partition coefficient of 99m Tc-PQQ was -1.49 ± 0.16. The pharmacokinetics parameters of 99m Tc-PQQ were t 1/2α  = 18.16 min, t 1/2β  = 100.45 min, K 12  = 0.013 min -1 , K 21  = 0.017 min -1 , K e  = 0.016 min -1 , AUC (area under the curve) = 1040.78 ID% g -1  min and CL (plasma clearance) = 0.096 mL min -1 . The dual-exponential equation was Y  = 10.88e -0.038 t  + 5.21e -0.0069 t . The biodistribution of 99m Tc-PQQ was studied in ICR (Institute for Cancer Research 7701 Burhelme Are., Fox Chase, Philadelphia, PA 1911 USA) mice. In vitro autoradiographic studies clearly showed that the 99m Tc-PQQ radioactivity accumulated predominantly in the hippocampus and cortex, which had a high density of N -methyl-d-aspartate Receptor (NMDAR). The enrichment can be blocked by NMDAR redox modulatory site antagonists-ebselen (EB) and 99m Tc-PQQ is therefore a promising candidate for the molecular imaging of NMDAR. To date, however, there have been no studies characterizing 99m Tc-PQQ.

Dehydroepiandrosterone (DHEA), a steroid hormone that is secreted by the adrenal cortex in mammals, has an array of biological actions, including inhibition of fat synthesis, decreasing the number of adipocytes, and a reduction in mammalian metabolic efficiency. Recent studies showed that DHEA may decrease fat deposition in poultry, but the mechanism of action is unclear. In the present study, we demonstrate that DHEA stimulates intracellular cyclic adenosine 3',5'-monophosphate (cAMP) accumulation in chicken hepatocytes during a 30 min incubation period. Increases in intracellular cAMP are evoked by as low as 0.1 microm-DHEA. The cAMP induced by DHEA, while suppressing cAMP-specific phosphodiesterase activity, also activates cAMP-dependent protein kinase A (PKA) in chicken hepatocytes. In addition, the activation of PKA leads to down-regulation of sterol regulatory element-binding protein-1 (SREBP-1). These findings demonstrate that direct action by DHEA leads to activation of the cAMP/PKA signalling system in the modulation of lipid metabolism by repressing SREBP-1, thereby providing a novel explanation for some of the underlying effects proposed for DHEA in the prevention of fat deposition in poultry.