Comparison of super resolution methods in magnetic resonance images for small animals

Super resolution (SR) is an array of methods that utilize different approaches to enhance the quality and resolution of an image. This is particularly useful for images that are very small and have low quality. Small images are usually obtained due to the limitation of imaging capture systems or the subject captured is small. For small animals such as rats, imaging can be difficult and expensive to produce high-resolution images. Therefore, SR is a very relevant field of study for small animals. The study of small animals involve many impactful fields such as testing of harmful chemicals on the biological processes. The objective of this study is to compare 11 SR methods for rat magnetic resonance images (MRI). This study is a pilot study and the beginning of the research to see the effect of kratom that is a hallucinogen misused in south east Asia. This study used chosen images from six rats. These MRI images were captured at UM MRI Research Centre. This study compared the quality of SR methods using several measures including Peak Sound to Noise Ratio (PSNR), Sound to Noise Ratio (SNR), Mean Square Error (MSE), Structural Similarity Index (SSI). This study compared these methods on two different size factors of resolution which were two and four. The results show promising results for the next stage of research

Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stressmediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ

Neuroprotective Potentials of Natural Vitamin E for Cerebral Small Vessel Disease

Cerebral small vessel disease (CSVD) refers to a spectrum of clinical and neuroimaging findings resulting from pathological processes of various etiologies affecting cerebral arterioles, perforating arteries, capillaries, and venules. It is the commonest neurological problem that results in significant disability, but awareness of it remains poor. It affects over half of people over 65 years old and inflicts up to third of acute strokes, over 40% of dementia, and a significant decline in physical ability in otherwise asymptomatic, aging individuals. Moreover, the unifying theory for the pathomechanism of the disease remains elusive and hence the apparent ineffective therapeutic approaches. Given the growing literature for natural vitamin E (tocopherols and tocotrienols) as a potent antioxidant, this chapter attempts to consolidate the contemporary evidence to shed plausible insights on the neuroprotective potentials of natural vitamin E in addressing the heterogenous CSVD spectrum, in health and in disease

TUALANG HONEY ATTENUATES KAINIC ACID-INDUCED OXIDATIVE STRESS IN RAT CEREBELLUM AND BRAINSTEM

Objective: The present study examined the protective effect of tualang honey (TH) against kainic acid (KA)-induced oxidative stress in the cerebellum and brainstem of rats.Methods: Male Sprague-Dawley rats were randomly divided into four groups: Control, KA-treated, TH+KA-treated, and topiramate (TPM, an antiepileptic agent)+KA-treated groups. Rats were pretreated orally with drinking water, TH (1.0 g/kg body weight), or TPM (40 mg/kg body weight), respectively, five times at 12 h intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment. Rats were sacrificed at 2 h, 24 h, and 48 h after KA administration. Oxidative stress markers were analyzed in different brain regions (cerebellum and brainstem) 2 h, 24 h, and 48 h after KA administration.Results: KA caused significant (p<0.05) elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production, impairment of glutathione system, and a significant reduction in the total antioxidant status in the rat cerebellum and brainstem at multiple time-points, as compared to control groups. Pretreatment with TH significantly (p<0.05) reduced the elevation in the thiobarbituric acid reactive substances level, protein carbonyl contents, and nitric oxide production and increasing a reduction in the total antioxidant status in the rat cerebellum and brainstem induced by KA at multiple time-points, as compared to KA only-treated group.Conclusion: Taken together, this study suggests that TH has therapeutic potential in reducing oxidative stress in the cerebellum and brainstem of KA-induced rats via its antioxidant property

Investigating white matter changes in auditory cortex and association fibres related to speech processing in noise-induced hearing loss : A diffusion tensor imaging study

This study explores the impact of noise-induced hearing loss (NIHL) on the microstructural integrity of white matter tracts in the brain, focusing on areas involved in speech processing. While the primary impact of hearing loss occurs in the inner ear, these changes can extend to the central auditory pathways and have broader effects on brain function. Our research aimed to uncover the neural mechanisms underlying hearing loss-related deficits in speech perception and cognition among NIHL patients. Methods: The study included two groups: nine bilateral NIHL patients and nine individuals with normal hearing. Advanced diffusion tensor imaging techniques were employed to assess changes in the white matter tracts. Regions of interest (ROIs), including the auditory cortex, cingulum, arcuate fasciculus, and longitudinal fasciculus, were examined. Fractional anisotropy (FA) values from these ROIs were extracted for analysis. Results: Our findings indicated significant reductions in FA values in NIHL patients, particularly in the left cingulum, right cingulum, and left inferior longitudinal fasciculus. Notably, no significant changes were observed in the auditory cortex, arcuate fasciculus, superior longitudinal fasciculus, middle longitudinal fasciculus, and right inferior longitudinal fasciculus, suggesting differential impacts of NIHL on various white matter tracts. Conclusions: The study's findings highlight the importance of considering association fibres related to speech processing in treating NIHL, as the broader neural network beyond primary auditory structures is significantly impacted. This research contributes to understanding the neurological impact of NIHL and underscores the need for comprehensive approaches in addressing this condition

Preliminary study on the effect of Tualang Honey and its silver nanoparticles on Kainic Acid-Induced memory deficits and oxidative damage in rat hippocampus

Kainic acid (KA) mediated excitotoxicity has been shown to cause memory impairment and oxidative stress in rats brain. The aim of this study was to investigate the effect of Tualang honey (TH) and its silver nanoparticles (THSN) on the KA-induced memory deficits and oxidative damage in rats’ hippocampus.Twenty-four adult male Sprague-Dawley rats were randomized into eight groups: (i) control, (ii) THSN (10mg/kg), (iii) THSN (50mg/kg), (iv) KA only, (v) KA+TH, (vi) KA+THSN (10mg/kg), (vii) KA+THSN (50mg/kg), and (viii) KA+Topiramate. Based on their respective groups, rats were pretreated orally with either distilled water, THSN (10 or 50 mg/kg body weight), Tualang honey (1.0 g/kg body weight), or Topiramate (40 mg/kg body weight), five times at 12 hours intervals. Saline or KA (15 mg/kg body weight) were injected subcutaneously 30 min after last oral treatment.Novel object recognition test (NORT) was performedfor memory assessment. The rats were sacrificed 24 hours post KA induction and hippocampus was harvested. Malondialdehyde (MDA) and superoxide dismutase (SOD) were measured using commercially available ELISA kits. The results showed that there was a trend of decreased in MDA level in both TH and THSN groups, however there were no significance difference. There wassignificantly increased level in SOD following pretreatment with TH and THSN groups compared to KA only group. Interestingly, these pretreatmentgroups also demonstrated enhanced memory as evidenced by significant increase in recognition index in NORT when compared to KA only group. In conclusion, this preliminary finding suggests that the pretreatment with TH and THSN might have potential role toimprove the memory and ameliorate oxidative stress in the KA-induced exitotoxicity rats. However, further study needs to be carried out to understand the precise mechanism

Reduced cerebral vascular fractal dimension among asymptomatic individuals as a potential biomarker for cerebral small vessel disease

Cerebral small vessel disease is a neurological disease frequently found in the elderly and detected on neuroimaging, often as an incidental finding. White matter hyperintensity is one of the most commonly reported neuroimaging markers of CSVD and is linked with an increased risk of future stroke and vascular dementia. Recent attention has focused on the search of CSVD biomarkers. The objective of this study is to explore the potential of fractal dimension as a vascular neuroimaging marker in asymptomatic CSVD with low WMH burden. Df is an index that measures the complexity of a self-similar and irregular structure such as circle of Willis and its tributaries. This exploratory cross-sectional study involved 22 neurologically asymptomatic adult subjects (42 ± 12 years old; 68% female) with low to moderate 10-year cardiovascular disease risk prediction score (QRISK2 score) who underwent magnetic resonance imaging/angiography (MRI/MRA) brain scan. Based on the MRI findings, subjects were divided into two groups: subjects with low WMH burden and no WMH burden, (WMH+; n = 8) and (WMH−; n = 14) respectively. Maximum intensity projection image was constructed from the 3D time-of-flight (TOF) MRA. The complexity of the CoW and its tributaries observed in the MIP image was characterised using Df. The Df of the CoW and its tributaries, i.e., Df (w) was significantly lower in the WMH+ group (1.5172 ± 0.0248) as compared to WMH− (1.5653 ± 0.0304, p = 0.001). There was a significant inverse relationship between the QRISK2 risk score and Df (w), (rs = −.656, p = 0.001). Df (w) is a promising, non-invasive vascular neuroimaging marker for asymptomatic CSVD with WMH. Further study with multi-centre and long-term follow-up is warranted to explore its potential as a biomarker in CSVD and correlation with clinical sequalae of CSVD

Role of purinergic signalling in endothelial dysfunction and thrombo-inflammation in ischaemic stroke and cerebral small vessel disease

The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier between the blood and the brain, the endothelium also actively regulates metabolic homeostasis, vascular tone and permeability, coagulation, and movement of immune cells. Being part of the blood–brain barrier, endothelial cells of the brain have specialized morphology, physiology, and phenotypes due to their unique microenvironment. Known cardiovascular risk factors facilitate cerebral endothelial dysfunction, leading to impaired vasodilation, an aggravated inflammatory response, as well as increased oxidative stress and vascular proliferation. This culminates in the thrombo-inflammatory response, an underlying cause of ischemic stroke and cerebral small vessel disease (CSVD). These events are further exacerbated when blood flow is returned to the brain after a period of ischemia, a phenomenon termed ischemia-reperfusion injury. Purinergic signaling is an endogenous molecular pathway in which the enzymes CD39 and CD73 catabolize extracellular adenosine triphosphate (eATP) to adenosine. After ischemia and CSVD, eATP is released from dying neurons as a damage molecule, triggering thrombosis and inflammation. In contrast, adenosine is anti-thrombotic, protects against oxidative stress, and suppresses the immune response. Evidently, therapies that promote adenosine generation or boost CD39 activity at the site of endothelial injury have promising benefits in the context of atherothrombotic stroke and can be extended to current CSVD known pathomechanisms. Here, we have reviewed the rationale and benefits of CD39 and CD39 therapies to treat endothelial dysfunction in the brain