First report of Ctenocephalides felis felis on the Asiatic Golden Cat, Catopuma temminckii in Thailand

The cat flea, Ctenocephalidesfelisfelis (Siphonaptera: Pulicidae) has been reported to parasitize many species of wild and domestic animals and could serve as a vector of zoonotic pathogens. This is the first report of the presence of cat fleas on the Asiatic Golden Cat, Catopuma temminckii (Carnivora: Felidae), quarantined in Khao Pratabchang Wildlife and Breeding Center, Ratchaburi Province, Thailand. The findings of this report may be helpful in evaluating the potential risks associated with increased contact between wild and domestic animals and humans in this region.     

Donepezil Protects Against Doxorubicin-Induced Chemobrain in Rats via Attenuation of Inflammation and Oxidative Stress Without Interfering With Doxorubicin Efficacy

Although doxorubicin (Dox) is an effective chemotherapy medication used extensively in the treatment of breast cancer, it frequently causes debilitating neurological deficits known as chemobrain. Donepezil (DPZ), an acetylcholinesterase inhibitor, provides therapeutic benefits in various neuropathological conditions. However, comprehensive mechanistic insights regarding the neuroprotection of DPZ on cognition and brain pathologies in a Dox-induced chemobrain model remain obscure. Here, we demonstrated that Dox-treated rats manifested conspicuous cognitive deficits and developed chemobrain pathologies as indicated by brain inflammatory and oxidative insults, glial activation, defective mitochondrial homeostasis, increased potential lesions associated with Alzheimer’s disease, disrupted neurogenesis, loss of dendritic spines, and ultimately neuronal death through both apoptosis and necroptosis. Intervention with DPZ co-treatment completely restored cognitive function by attenuating these pathological conditions induced by DOX. We also confirmed that DPZ treatment does not affect the anti-cancer efficacy of Dox in breast cancer cells. Together, our findings suggest that DPZ treatment confers potential neuroprotection against Dox-induced chemobrain.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13311-021-01092-9.     

Pulpal blood flow recorded from human premolar teeth with a laser Doppler flow meter using either red or infrared light

Objective

To compare red (635 nm) and infrared (780 nm) light for recording pulpal blood flow from human premolar teeth.

Design

Recordings were made from 11 healthy teeth in 9 subjects (aged 16–30 years) using a laser Doppler flow meter (Periflux 4001) equipped with both red and infrared lasers. Average blood flow signals were obtained with both light sources alternately from each tooth under five conditions: intact tooth without opaque rubber dam, intact tooth with dam, after injecting local anaesthetic (3% Mepivacaine) (LA) over the apex of the tooth and cavity preparation to almost expose the pulp, after removal and replacement of the pulp, and with the root canal empty.

Results

With infrared light, the dam significantly decreased the mean blood flow by 80%. Injecting LA and cavity preparation had no significant effect. Removal and replacement of the pulp reduced the mean blood flow by 58%. There was no further change when the pulp was removed. With red light, the dam reduced the signal from intact teeth by 60%. Injecting LA and cavity preparation had no significant effect. The signal fell by 67% after pulp removal and replacement and did not change significantly when the pulp was removed.

Conclusions

Opaque rubber dam minimises the contribution of non-pulpal tissues to the laser Doppler signal recorded from premolars. Using dam, the pulp contributed about 60% to the blood flow signal with both red and infrared light. The difference between them in this respect was not significant.     

PPARγ activator,rosiglitazone: Is it beneficial or harmful to the cardiovascular system?

Rosiglitazone is a synthetic agonist of peroxisome proliferator-activated receptor γ which is used to improve insulin resistance in patients with typeⅡdiabetes.Rosiglitazone exerts its glucose-lowering effects by improving insulin sensitivity.Data from various studies in the past decade suggest that the therapeutic effects of rosiglitazone reach far beyond its use as an insulin sensitizer since it also has other benefits on the cardiovascular system such as improvement of contractile dysfunction,inhibition of the inflammatory response by reducing neutrophil and macrophage accumulation,and the protection of myocardial injury during ischemic/reperfusion in different animal models.Previous clinical studies in typeⅡdiabetes patients demonstrated that rosiglitazone played an important role in protectingagainst arteriosclerosis by normalizing the metabolic disorders and reducing chronic inflammation of the vascular system.Despite these benefits,inconsistent findings have been reported,and growing evidence has demonstrated adverse effects of rosiglitazone on the cardiovascular system,including increased risk of acute myocardial infarction,heart failure and chronic heart failure.As a result,rosiglitazone has been recently withdrawn from EU countries.Nevertheless,the effect of rosiglitazone on ischemic heart disease has not yet been firmly established.Future prospective clinical trials designed for the specific purpose of establishing the cardiovascular benefit or risk of rosiglitazone would be the best way to resolve the uncertainties regarding the safety of rosiglitazone in patients with heart disease.     

Roles of mitochondrial benzodiazepine receptor in the heart

Mitochondrial benzodiazepine receptor (mBzR) is a type of peripheral benzodiazepine receptor that is located in the outer membrane of mitochondria. It is an 18-kDa protein that can form a multimeric complex with voltage-dependent anion channel (32 kDa) and adenine nucleotide translocator (30 kDa). mBzR is found in various species and abundantly distributed in peripheral tissues, including the cardiovascular system. The mitochondria are well known as the site of energy production, and the heart is the organ that highly requires this energy supply. In the past decades, it has been shown that mBzR plays a critical role in regulating mitochondrial and heart functions. A growing body of evidence demonstrates that mBzR is associated with regulation of mitochondrial respiration, mitochondrial membrane potential, apoptosis, and reactive oxygen species production. Moreover, mBzR has been suggested to play a role in alteration of physiological effects in the heart such as contractility and heart rate. mBzR is involved in the pathologic condition such as ischemia/reperfusion injury, responses to stress, and changes in electrophysiological properties and arrhythmogenesis. In this review, evidence of the roles of mBzR in the heart under both physiological and pathologic conditions is presented. Clinical studies regarding the use of pharmacologic intervention involving mBzR in the heart are also discussed as a possible target for the treatment of electrical and mechanical dysfunction in the heart.     

T-type calcium channel as a portal of iron uptake into cardiomyocytes of beta-thalassemic mice

Objectives: Iron‐overload condition can be found in β‐thalassemic patients with regular blood transfusion, leading to iron deposition in various organs including the heart. Elevated cardiac iron causes iron‐overload cardiomyopathy, a condition that provokes mortality because of heart failure in patients with thalassemia. Previous studies demonstrated that myocardial iron uptake may occur via L‐type calcium channels (LTCCs). However, direct evidence regarding the claimed pathway in thalassemic cardiomyocytes has never been investigated. Methods: Hearts from genetic‐altered β‐thalassemic mice and adult wild‐type mice were used for cultured ventricular cardiomyocytes. Blockers for LTCC, T‐type calcium channel (TTCC), transferrin receptor1 (TfR1), and divalent metal transporter1 (DMT1) were used, and quantification of cellular iron uptake under various iron loading conditions was performed by Calcein‐AM fluorescence assay. Microarray analysis was performed to investigate gene expressions in the hearts of these mice. Results: This study demonstrated that iron uptake under iron‐overload conditions in the cultured ventricular myocytes of thalassemic mice was greater than that of wild‐type cells (P < 0.01). TTCC blocker, efonidipine, and an iron chelator, deferoxamine, could prevent iron uptake into cultured cardiomyocytes, whereas blockers of TfR1, DMT1, and LTCC could not. Microarray analysis from thalassemic hearts demonstrated highly up‐regulated genes of TTCC, zinc transporter, and transferrin receptor2. Conclusions: Our findings indicated that iron uptake mechanisms in cultured thalassemic cardiomyocytes are mainly mediated by TTCC, suggesting that TTCC is the important pathway for iron uptake in this cultured thalassemic cardiomyocyte model.