Recent trends in stem cell-based therapies and applications of artificial intelligence in regenerative medicine

Stem cells are undifferentiated cells that can self-renew and differentiate into diverse types of mature and functional cells while maintaining their original identity. This profound potential of stem cells has been thoroughly investigated for its significance in regenerative medicine and has laid the foundation for cell-based therapies. Regenerative medicine is rapidly progressing in healthcare with the prospect of repair and restoration of specific organs or tissue injuries or chronic disease conditions where the body’s regenerative process is not sufficient to heal. In this review, the recent advances in stem cell-based therapies in regenerative medicine are discussed, emphasizing mesenchymal stem cell-based therapies as these cells have been extensively studied for clinical use. Recent applications of artificial intelligence algorithms in stem cell-based therapies, their limitation, and future prospects are highlighted.     

An unlinked mutation affecting control of purine metabolism in a revertant of an ad-7 auxotroph of Neurospora crassa lacking the phosphoribosylpyrophosphate amidotransferase

Summary Prototrophic revertants of an ad-7 mutant recover phosphoribosylpyrophosphate amidotransferase activity, indicating ad-7 is the structural gene for the first enzyme in the de novo biosynthesis of purine nucleotides. Some revertants excrete purines and cross-feed ad-3A conidia which have a lesion in the de novo pathway. A mutant apu, not linked to ad-7 or ad-8, is responsible for the ability to excrete purines. This mutation is not allelic to a mutant in the aza-1 locus which is also known to excrete purines.     

Pyruvate Dehydrogenase Kinase-mediated Glycolytic Metabolic Shift in the Dorsal Root Ganglion Drives Painful Diabetic Neuropathy

The dorsal root ganglion (DRG) is a highly vulnerable site in diabetic neuropathy. Under diabetic conditions, the DRG is subjected to tissue ischemia or lower ambient oxygen tension that leads to aberrant metabolic functions. Metabolic dysfunctions have been documented to play a crucial role in the pathogenesis of diverse pain hypersensitivities. However, the contribution of diabetes-induced metabolic dysfunctions in the DRG to the pathogenesis of painful diabetic neuropathy remains ill-explored. In this study, we report that pyruvate dehydrogenase kinases (PDK2 and PDK4), key regulatory enzymes in glucose metabolism, mediate glycolytic metabolic shift in the DRG leading to painful diabetic neuropathy. Streptozotocin-induced diabetes substantially enhanced the expression and activity of the PDKs in the DRG, and the genetic ablation of Pdk2 and Pdk4 attenuated the hyperglycemia-induced pain hypersensitivity. Mechanistically, Pdk2/4 deficiency inhibited the diabetes-induced lactate surge, expression of pain-related ion channels, activation of satellite glial cells, and infiltration of macrophages in the DRG, in addition to reducing central sensitization and neuroinflammation hallmarks in the spinal cord, which probably accounts for the attenuated pain hypersensitivity. Pdk2/4-deficient mice were partly resistant to the diabetes-induced loss of peripheral nerve structure and function. Furthermore, in the experiments using DRG neuron cultures, lactic acid treatment enhanced the expression of the ion channels and compromised cell viability. Finally, the pharmacological inhibition of DRG PDKs or lactic acid production substantially attenuated diabetes-induced pain hypersensitivity. Taken together, PDK2/4 induction and the subsequent lactate surge induce the metabolic shift in the diabetic DRG, thereby contributing to the pathogenesis of painful diabetic neuropathy.     

Priestia flexa KS1: A new bacterial strain isolated from human faeces implicated in mucin degradation

International Microbiology - The human gut acts as a habitat for diverse microbial communities, including mucin utilizers that play a significant role in host health and diseases. In this study, a...     

Photosystem I P700 chlorophyll a apoprotein A1 as PCR marker to identify diatoms and their associated lineage

The morphological characteristics of diatoms are useful for studying their taxonomy. However, the distinction between closely related diatom taxa can be very difficult, especially when the morphological characters are modified by environmental constraints. In the present study, 13 fresh water diatoms were identified morphologically and cultured under axenic conditions. To check this, PCR primers specific for multilocus genes were designed to amplify and screen 13 fresh water diatom monocultures. Multilocus PCR primers (DRR3, scfcpA, Lhcf11, SIT1, SIT3, SIT4, LOC101218388, COI-5P, rbcL, rbcL-3P, LSU D2/D3, UPA, psaA, and 18S rRNA) were tested. It was found that psaA gene, a plant pigment chlorophyll-based PCR marker, amplified in all the diatoms. Out of 13 diatom amplicons, only two fresh water diatoms DNA were sequenced. This included Cyclotella meneghiniana and Sellaphora pupula. The Sanger sequencing results thus established that morphologically identified diatom, Sellaphora pupula, exhibited close phylogeny to Sellaphora whereas fresh water Cyclotella meneghiniana has close lineage to marine diatom Thallosiosira.