Activity

We consider how applying layer fMRI in association cortex may help inform computational models of brain function as well as shed light on consciousness and mental illness, and issue a call to arms to our fellow methodologists and neuroscientists to bring layer fMRI to this next frontier.Monkeys with selective bilateral lesions of area MT were trained on tasks designed to examine visuomotor function. They were required to 1- retrieve a small food pellet from a narrow slot; 2- locate and retrieve a loose peanut mounted on a background of fixed peanuts; and 3- retrieve an erratically moving food pellet from a spinning bowl. After the lesions, these monkeys were behaviorally impaired relative to their own preoperative performances and also relative to the postoperative performances of the control monkeys with lesions in optic radiation fibers (OR) under MT or lesions in the posterior parietal cortex (PP). Although their performance improved with practice and time, the MT-lesioned monkeys showed long-term impairments twenty weeks after surgery. Control monkeys performed no worse on the tasks after their lesions. Another task which required the monkeys to retrieve a food pellet without visual guidance revealed that all the animals performed equally poorly when visual cues were unavailable, but that only the control monkeys benefited when visual cues were available. None of the monkeys were impaired on a pattern discrimination learning task. Besides that, direct observations revealed that the MT-lesioned animals grasped peanuts in a manner different from the control animals.

Hair analysis is useful for monitoring exposure to drugs such as antiepileptics owing to long-term therapy and a high possibility of abuse of drugs, which could be fatal. An effective and rapid analytical method for the simultaneous determination of six barbiturates, as well as phenytoin and topiramate in hair samples was developed and validated by liquid-chromatography-tandem mass spectrometry (LC-MS/MS).

Three different extraction methods were investigated for the development of an appropriate analytical method. Hair was finely cut and then extracted with methanol, methanol containing 1% hydrochloric acid, and liquid-liquid extraction in acidic condition.

There was no significant difference in the matrix effects among these three methods. Recoveries clearly declined in the extraction involving both acidic methanol extraction and a LLE in acidic condition. Methanol incubation was chosen as the appropriate extraction method with acceptable matrix effects and recoveries. After validating the methanol inclogy fields.Alzheimer’s disease (AD) is regarded as one of the significant health burdens, as the prevalence is raising worldwide and gradually reaching to epidemic proportions. Consequently, a number of scientific investigations have been initiated to derive therapeutics to combat AD with a concurrent advancement in pharmacological methods and experimental models. Whilst, the available experimental pharmacological approaches both in vivo and in vitro led to the development of AD therapeutics, the precise manner by which experimental models mimic either one or more biomarkers of human pathology of AD is gaining scientific attentions. Caenorhabditis elegans (C. elegans) has been regarded as an emerging model for various reasons, including its high similarities with the biomarkers of human AD. Our review supports the versatile nature of C. elegans and collates that it is a well-suited model to elucidate various molecular mechanisms by which AD therapeutics elicit their pharmacological effects. It is apparent that C. elegans is capable of establishing the pathological processes that links the endoplasmic reticulum and mitochondria dysfunctions in AD, exploring novel molecular cascades of AD pathogenesis and underpinning causal and consequential changes in the associated proteins and genes. In summary, C. elegans is a unique and feasible model for the screening of anti-Alzheimer’s therapeutics and has the potential for further scientific exploration.The NLRP3 inflammasome plays a pro-tumorigenic role in various malignancies. However, its potential role in lymphomagenesis remains unclear. In this study, we identified an immunosuppressive state in patients with diffuse large B cell lymphoma (DLBCL), which was characterized by markedly elevated interleukin (IL)-18 levels in lymphoma tissues and positive correlation with programmed death ligand 1 (PD-L1) expression. Furthermore, NLRP3 inflammasome activation in DLBCL cell lines upregulated PD-L1 and reduced the proportion of cytotoxic T cells. NLRP3 inflammasome blockade in vivo suppressed lymphoma growth and ameliorated anti-tumor immunity by downregulating PD-L1 in the tumor microenvironment and decreasing the proportion of PD-1/TIM-3-expressing T cells, myeloid-derived suppressor cells, tumor-associated macrophages, and regulatory T cells. Further in vivo studies revealed IL-18 as the main effector cytokine involved in the negative regulation of anti-lymphoma immunity. Interestingly, NLRP3 blockers combined with anti-PD-L1 treatment exerted antagonistic effects during lymphoma therapy. Altogether, our findings indicate that NLRP3 inflammasome promotes immunosuppression by modulating PD-L1 and immune cells. Accordingly, this study highlights the prognostic and therapeutic values of the NLRP3 inflammasome in lymphoma.The wound healing process involves three continuous stages. Where, any imbalance can lead to the formation of unwanted keloids, hypertrophic scar, or tumors. Keloids are any unpleasant, non-compliant comorbidity affecting a major section of people around the globe who acquire it either genetically or by pathological means as a result of a skin injury. Angiogenesis is unavoidable in the healing process after an injury or disruption of skin to promote tissue regeneration. Uncontrolled angiogenesis during the healing process can initiate the unwanted response in the wound that facilitate keloid. Streptozotocin cell line Angiogenic therapy is adapted to accelerate healing after an injury. Else ways, there exists a risk of keloid formation due to excessive angiogenesis during the wound healing process. There are numerous strategies to treat keloid. Anti-angiogenic factors are provided to patients post-surgery to prevent the keloid formation; however, they come into the picture after the formation of keloid. The available strategies to treat keloids are steroidal injections, surgical excision of the keloid, radiotherapy, pressure therapy, the use of cryosurgery, and many more.