Bioscience hypotheses最新文献

Human endogenous retroviruses (HERVs) represent the footprints of previous retroviral infections. They are integrated within the human germ line and constitute approximately 7% of our genome. They have the potential to harm, given their capacity to alter the cellular metabolism, and could be involved in various pathological processes such as systemic lupus erythematosus or multiple sclerosis. In this respect it has been found that the stimulation of HERVs genome expression was observed after a steroid hormone treatment, stating the first evidence that an enhanced expression of the HERVs genome by hormones may be involved in the etiology of breast cancer. There is now increasing evidence that HERVs may in fact be involved in the etiology of schizophrenia, a disorder characterized by heterogeneous presence of positive, negative and cognitive symptoms that affect all aspects of mental activity, with a first peak incidence for males and females in the decade 15–24 and a second peak at age 55–64 for females, both periods characterized by two moments of significant hormonal changes. In connection with genetic aspects, several studies suggest a linkage between chromosome 22 (22q) and schizophrenia, being different genes of this chromosomal region reported as candidate genes for association with the disorder. Likewise, in a closely region of these genes, on 22q13, is located a gene named APOBEC3G, a potent intrinsic inhibitor of retroviral replication that also includes some HERVs. We propose that hormonal changes that coincide with two peak incidences in schizophrenia produce an enhancement in the expression of some HERV families implicated in the etiopathology of the disorder. The expression of HERVs is followed by a defective action of APOBEC3G that avoids carry out its function, that is, the inhibition of retroviral replication. This altered process might play a critical role in the etiopathogenesis of schizophrenia.

Does the primary visual cortex mediate consciousness for higher-level stages of information processing by providing an outlet for mental imagery? Evidence based on neural electrical activity is inconclusive as reflected in the “imagery debate” in cognitive science. Neural information and activity, however, also depend on regulated biophoton (optical) signaling. During encoding and retrieval of visual information, regulated electrical (redox) signals of neurons are converted into synchronized biophoton signals by bioluminescent radical processes. That is, visual information may be represented by regulated biophotons of mitochondrial networks in retinotopically organized cytochrome oxidase-rich neural networks within early visual areas. Therefore, we hypothesize that regulated biophotons can generate intrinsic optical representations in the primary visual cortex and then propagate variably degraded versions along cytochrome oxidase pathways during both perception and imagery. Testing this hypothesis requires to establish a methodology for measurement of in vivo and/or in vitro increases of biophoton emission in humans' brain during phosphene inductions by transcranial magnetic stimulation and to compare the decrease in phosphene thresholds during transcranial magnetic stimulation and imagery. Our hypothesis provides a molecular mechanism for the visual buffer and for imagery as the prevalent communication mode (through optical signaling) within the brain. If confirmed empirically, this hypothesis could resolve the imagery debate and the underlying issue of continuity between perception and abstract thought.

If endorphins participate in mental processes and these also activate sperm functions, then it is reasonable to deduce that thoughts biochemically modify sperm and egg genes throughout life, and that this is inherited.

Rosiglitazone is widely used to improve diabetes mellitus, but its adverse cardiovascular effect is recently recognized. The exact mechanism is still unknown. In this paper, we predict that rosiglitazone probably regulates the insulin gene expression, which cause complications in the long term use.

Severe acute pancreatitis (SAP) is a serious systemic disease. It exacerbates when complicated with multiple organ dysfunction syndrome or failure (MODS or MOF). However, the aggravating mechanism of SAP is still unknown up to now. Study showed that maintaining integrity of intestinal mucosal barrier function by given effective antibiotics, selective digestive decontamination (SDD) and enteral nutrition therapy to the patients with SAP could significantly reduce infection of pancreatic necrotic tissue and improve the patient's outcome. Combining the findings of gut-derived bacteria in animals' pancreas, liver, spleen, mesenteric lymph nodes with increasing concentration of inflammatory cytokines and endotoxin in plasma with SAP, we hypothesize that gut-derived endotoxin translocation is the main aggravating mechanism of SAP. The hypothesis holds potential as a target for therapeutic intervention.

Immune reconstitution inflammatory syndrome (IRIS) is an inflammatory manifestation that occurs subsequent to initiation of highly active antiretroviral therapy in terminal (HAART) HIV infection, mainly due to the restoration of robust immune responses directed against latent microbial antigens. IRIS is believed to be multifactorial and less studied. Herein, we postulate that hypothalamo–pituitary–adrenal (HPA) dysregulation, a well-documented manifestation in HIV/AIDS, could possibly disturb the balance between pro-inflammatory and anti-inflammatory cytokines leading to clinical IRIS. Drugs, opportunistic infections, stress and numerous intrinsic and extrinsic factors have been described to be the possible causes of IRIS in HIV illness.

In patients with severe traumatic brain injury (TBI), healing of a fracture of long or large bone has been observed to be accelerated with excessive callus formation and united at a faster rate. It seems that the enhanced osteogenesis in patients strongly promotes the growth of osteoblast cells. The existing hypothesis is not convincing in explaining the mechanisms of this problem. Craniocerebral trauma patients present a state of hypercoagulability at early stage and thrombin content was very high level at the site of injury. Thrombin is an important link between coagulation and inflammation, and exerts multiple effects upon osteoblasts including stimulating proliferation and inhibiting osteoblast differentiation and apoptosis. Whether this rapidly forming new bone is caused by thrombin has not yet been identified. We hypothesize that in the case of an individual with a head injury, thrombin might be a potential regulator of early fracture healing, which result in accelerated bone healing and hypertrophic callus. If this hypothesis is verified, it will be helpful for the understanding of the basic mechanisms involved in control of bone repair and potential for the development of new novel therapeutic agents.

The need to publish ideas so that they can be explored, debated and extended by others before they are fully tested in the lab or the clinic is in conflict with the need to patent those ideas to provide a commercial incentive to apply them. I discuss why this conflict occurs, why it is important, and suggest three ways to get round it: root-and-branch reform of patent law (which seems impossible), extension of the US system's ‘grace period’ between publishing and filing a patent to longer times in the US and implementing the same system in other countries (which seems unlikely to happen), and binding readers of journals with a network of optional confidentiality agreements that allow publication but not citation without the authors’ permission. This latter appears too complex and conflicting an idea to work either, but while many conflicts with common scientific practice exist, the complexity of the system need not deter us, as at root the idea is simple and so it could be managed by software instead of patent lawyers.