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Human gut microbiota contains a large, complex, dynamic microbial community of approximately 1014 microbes from more than 1,000 microbial species, i.e., equivalent to 4 × 106 genes. Numerous evidence links gut microbiota with human health and diseases. Importantly, gut microbiota is involved in the development and function of the brain through a bidirectional pathway termed as the gut-brain axis. Interaction between gut microbiota and immune responses can modulate the development of neuroinflammation and cancer diseases in the brain. With respect of brain cancer, gut microbiota could modify the levels of antioxidants, amyloid protein and lipopolysaccharides, arginase 1, arginine, cytochrome C, granulocyte–macrophage colony-stimulating factor signaling (GM-CSF), IL-4, IL-6, IL-13, IL-17A, interferon gamma (IFN-γ), reactive oxygen species (ROS), reactive nitrogen species (e.g., nitric oxide and peroxynitrite), short-chain fatty acids (SCFAs), tryptophan, and tumor necrosis factor-β (TGF-β). Through these modifications, gut microbiota can modulate apoptosis, the aryl hydrocarbon receptor (AhR), autophagy, caspases activation, DNA integrity, microglia dysbiosis, mitochondria permeability, T-cell proliferation and functions, the signal transducer and activator of transcription (STAT) pathways, and tumor cell proliferation and metastasis. The outcome of such interventions could be either oncolytic or oncogenic. This review scrutinizes the oncogenic and oncolytic effects of gut microbiota by classifying the modification mechanisms into (i) amino acid deprivation (arginine and tryptophan); (ii) kynurenine pathway; (iii) microglia dysbiosis; and (iv) myeloid-derived suppressor cells (MDSCs). By delineating the complexity of the gut-microbiota-brain-cancer axis, this review aims to help the research on the development of novel therapeutic strategies that may aid the efficient eradication of brain cancers.

There are 17 human-biting ticks known in Australia. The bites of Ixodes holocyclus, Ornithodoros capensis, and Ornithodoros gurneyi can cause paralysis, inflammation, and severe local and systemic reactions in humans, respectively. Six ticks, including Amblyomma triguttatum, Bothriocroton hydrosauri, Haemaphysalis novaeguineae, Ixodes cornuatus, Ixodes holocyclus, and Ixodes tasmani may transmit Coxiella burnetii, Rickettsia australis, Rickettsia honei, or Rickettsia honei subsp. marmionii. These bacterial pathogens cause Q fever, Queensland tick typhus (QTT), Flinders Island spotted fever (FISF), and Australian spotted fever (ASF). It is also believed that babesiosis can be transmitted by ticks to humans in Australia. In addition, Argas robertsi, Haemaphysalis bancrofti, Haemaphysalis longicornis, Ixodes hirsti, Rhipicephalus australis, and Rhipicephalus sanguineus ticks may play active roles in transmission of other pathogens that already exist or could potentially be introduced into Australia. These pathogens include Anaplasma spp., Bartonella spp., Burkholderia spp., Francisella spp., Dera Ghazi Khan virus (DGKV), tick-borne encephalitis virus (TBEV), Lake Clarendon virus (LCV), Saumarez Reef virus (SREV), Upolu virus (UPOV), or Vinegar Hill virus (VINHV). It is important to regularly update clinicians' knowledge about tick-borne infections because these bacteria and arboviruses are pathogens of humans that may cause fatal illness. An increase in the incidence of tick-borne infections of human may be observed in the future due to changes in demography, climate change, and increase in travel and shipments and even migratory patterns of birds or other animals. Moreover, the geographical conditions of Australia are favorable for many exotic ticks, which may become endemic to Australia given an opportunity. There are some human pathogens, such as Rickettsia conorii and Rickettsia rickettsii that are not currently present in Australia, but can be transmitted by some human-biting ticks found in Australia, such as Rhipicephalus sanguineus, if they enter and establish in this country. Despite these threats, our knowledge of Australian ticks and tick-borne diseases is in its infancy.

Application of acid-activated bentonite and SO3H-functionlized multiwall carbon nanotubes (SO3H-MWCNTs) for lowering free fatty acids (FFAs) content of low-quality residual olive oil, prior to alkali-catalyzed transesterification was investigated. The used bentonite was first characterized by Scanning Electron Microscopy (SEM), Inductively Coupled Plasma mass spectrometry (ICP-MS), and X-ray fluorescence (XRF), and was subsequently activated by different concentrations of H2SO4 (3, 5, and 10 N). Specific surface area of the original bentonite was measured by Brunauer, Emmett, and Teller (BET) method at 45 m2/g and was best improved after 5 N-acid activation (95–98°C, 2 h) reaching 68 m2/g. MWCNTs was synthesized through methane decomposition (Co-Mo/MgO catalyst, 900°C) during the chemical vapor deposition (CVD) process. After two acid-purification (HCl, HNO3) and two deionized-water-neutralization steps, SO3H was grafted on MWCNTs (concentrated H2SO4, 110°C for 3 h) and again neutralized with deionized water and then dried. The synthesized SO3H-MWCNTs were analyzed using Fourier-Transform Infrared Spectroscopy (FTIR) and Transmission Electron Microscopy (TEM). The activated bentonite and SO3H-MWCNTs were utilized (5 wt.% and 3 wt.%, respectively), as solid catalysts in esterification reaction (62°C, 450 rpm; 15:1 and 12:1 methanol-to-oil molar ratio, 27 h and 8 h, respectively), to convert FFAs to their corresponding methyl esters. The results obtained revealed an FFA to methyl ester conversion of about 67% for the activated bentonite and 65% for the SO3H-MWCNTs. More specifically, the acid value of the residual olive oil was decreased significantly from 2.5 to 0.85 and 0.89 mg KOH/g using activated bentonite and SO3H-MWCNTs, respectively. The total FFAs in the residual olive oil after esterification was below 0.5%, which was appropriate for efficient alkaline-transesterification reaction. Both catalysts can effectively pretreat low-quality oil feedstock for sustainable biodiesel production under a biorefinery scheme. Overall, the acid-activate bentonite was found more convenient, cost-effective, and environment-friendly than the SO3H-MWCNTs.

Advancement of science has gifted the human a longer life; however, as neuron cells do not regenerate, the number of people with neurodegeneration disorders rises with population aging. Neurodegeneration diseases occur as a result of neuronal cells loss caused by environmental factors, genetic mutations, proteopathies and other cellular dysfunctions. The negative direct or indirect contributions of various microorganisms in onset or severity of some neurodegeneration disorders and interaction between human immune system and pathogenic microorganisms has been portrayed in this review article. This association may explain the early onset of neurodegeneration disorders in some individuals, which can be traced through detailed study of health background of these individuals for infection with any microbial disease with neuropathogenic microorganisms (bacteria, fungi, viruses). A better understanding and recognition of the relation between microorganisms and neurodegeneration disorders may help researchers in development of novel remedies to avoid, postpone, or make neurodegeneration disorders less severe.