Dry eye disease (DED) is a complex and multifactorial ocular surface disease affecting a large proportion of the population. There is emerging evidence of the impact of the microbiomes of the ocular surface and gut on the symptoms of DED, with many parallels being drawn to inflammatory diseases of other organ systems. A key factor involved in the promotion of healthy microbiomes, and which has been associated with ocular surface disease, is micro- and macronutrient deficiency. A comprehensive review of how these deficiencies can contribute to DED is absent from the literature. This review reports the composition of healthy ocular and gut microbiomes, and how nutrient deficiencies may impact these floral populations, with linkage to the subsequent impact on ocular health. The review highlights that vitamin B1 and iron are linked to reduced levels of butyrate, a fatty acid implicated in inflammatory conditions such as ulcerative colitis which itself is a condition known to be associated with ocular surface diseases. Vitamin B12 has been shown to have a role in maintaining gut microbial eubiosis and has been linked to the severity of dry eye symptoms. Similar beneficial effects of gut microbial eubiosis were noted with vitamin A and omega-3 polyunsaturated fatty acids. Selenium and calcium have complex interactions with the gut microbiome and have both been implicated in the development of thyroid orbitopathy. Further, diabetes mellitus is associated with ocular surface diseases and changes in the ocular microbiome. A better understanding of how changes in both the gut and eye microbiome impact DED could allow for an improved understanding of DED pathophysiology and the development of new, effective treatment strategies.

Nerve cell death is the central aspect of human neurodegenerative disorders. Neuronal death in results leads to the onset of various human neurological disorders such as Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, amyotrophic lateral sclerosis, and stroke. In developing neurons, apoptosis is assumed to provide a counterbalance to overexuberant cell replication. Numerous signals may induce apoptosis in neurons, such as the absence of neurotrophic factor support, increased levels of metabolic and oxidative stress, and overstimulation of glutamate receptors (leading to the calcium influx). Cell death and neurological disorders have been related to oxidative stress, which creates an imbalance between antioxidant defenses and free radical production. In this paper, a summary of the engrossment of oxidative stress, neuronal apoptosis, and mitochondrial dysfunction in neurodegenerative disorders has been discussed. Antioxidant therapy’s potential assistance for neurodegenerative illnesses in human beings is still up for dispute, despite encouraging pre-clinical research findings. One elucidation for this disparity could be the non-existence of an accurate way to assess oxidative stress in the brain. The explosion in research on apoptosis in neurodegeneration has stemmed from the conception that persuading neuronal apoptotic death may be crucial to the progression of a disease and that anti-apoptotic approaches may be useful in the prevention of neurodegenerative processes. A deeper understanding of the role that apoptosis plays in neurodegenerative processes will serve as the foundation for future research into the development of focused, effective treatment modalities.

Acquired or hereditary epilepsy affects millions of people. Today, the disease is pharmacoresistant in about 30 percent of cases, meaning that the seizures do not come under acceptable control in response to medication. Therefore, there is a great need for the development of novel methods for epilepsy research and treatment. Although in vivo animal models best mimic the clinical features of epilepsy, in vitro models have clear advantages in elucidating the fine details and cellular mechanisms of neurological disorders. In contrast to short-lived experiments in acute brain slices, cell cultures are often chosen as chronic models for antiseizure medication screening and epilepsy research under reduced, well-controlled in vitro conditions that still include all major cell types susceptible to epileptic seizures. Organotypic brain slices or dissociated cells produce spontaneous synchronized epileptiform discharges classified as interictal and ictal-like. In addition, pharmacologically or electrically induced seizures and status epilepticus can be obtained for electrophysiological and imaging experiments. Relatively simple cell cultures of primary rodent neurons provide entry-level models for the initial screening of antiseizure medications and basic epilepsy research. However, more sophisticated human cultures of stem cell-derived neurons offer the possibility of medical studies using the human genotype without the need to obtain brain tissue from patients. As an evolution of this method, programmed differentiation of brain cells is now being used in stem cell therapy for neurological disorders. Overall, cell culture greatly expands the repertoire of methods available to study epileptic disorders and potential cures.

Atypical ductal hyperplasia (ADH) is a benign lesion of the breast that is associated with an increased risk of invasive breast cancer. This review explores the pathophysiology, risk factors for progression to breast cancer, and lifetime management for patients diagnosed with ADH on core needle biopsy (CNB). The management plan for patients diagnosed with ADH includes regular clinical surveillance, diagnostic mammography, along with risk-reduction strategies such as lifestyle modifications or the use of adjuvant endocrine therapies. This review aims to delve into the complexities of ADH from diagnosis to management to aid clinicians in finding the best way to approach this high-risk breast lesion.

Schizophrenia is a serious mental disorder affecting about 1% of the population. It is characterised by multiple symptoms which are mostly responsive to treatment with antipsychotic medications. Cognitive impairment is regarded as a core feature of illness which is mostly poorly responsive to treatment with the current antipsychotic medications. Improving cognitive function is an important treatment goal as it is associated with better outcomes in employment and quality of life. Adjunctive pharmacological treatments have been examined to improve measures of cognition but with limited success. Cannabidiol (CBD), has shown promise in preclinical models of cognitive deficits of schizophrenia. On the other hand, limited studies in small groups of patients with schizophrenia have shown no significant clinical benefits for cognitive function as an adjunct to ongoing treatment with antipsychotics. A single trial, in which CBD as a standalone treatment was compared to the antipsychotic medication amisulpride, showed significant changes in cognitive measures for both agents, with no statistically significant difference between them. It might therefore be concluded that the preclinical findings have failed to translate to the clinic. However, the preclinical findings themselves are based on a circumscribed set of studies in multiple cognitive models and have used varying doses and routes of drug administration. The same general methodological issues are present in the suite of clinical studies. Issues such as patient heterogeneity in terms of illness duration, formulation and dose of CBD employed, and length of cannabinoid treatment might militate positive findings. The limited clinical database available makes the benefits (or lack thereof) of CBD for the cognitive effects of schizophrenia uncertain. Continued research in much larger patient populations than have so far been investigated as well as a consideration of dose ranging studies are required to fully assess the potential risks against the benefits of CBD treatment for cognitive deficits in schizophrenia.

Three-dimensional (3D) and four-dimensional (4D) printing have emerged as the next-generation fabrication technologies, covering a broad spectrum of areas, including construction, medicine, transportation, and textiles. 3D printing, also known as additive manufacturing (AM), allows the fabrication of complex structures with high precision via a layer-by-layer addition of various materials. On the other hand, 4D printing technology enables printing smart materials that can alter their shape, properties, and functions upon a stimulus, such as solvent, radiation, heat, pH, magnetism, current, pressure, and relative humidity (RH). Myriad of biomedical materials (BMMs) currently serve in many biomedical engineering fields aiding patients’ needs and expanding their life-span. 3D printing of BMMs provides geometries that are impossible via conventional processing techniques, while 4D printing yields dynamic BMMs, which are intended to be in long-term contact with biological systems owing to their time-dependent stimuli responsiveness. This review comprehensively covers the most recent technological advances in 3D and 4D printing towards fabricating BMMs for tissue engineering, drug delivery, surgical and diagnostic tools, and implants and prosthetics. In addition, the challenges and gaps of 3D and 4D printed BMMs, along with their future outlook, are also extensively discussed. The current review also addresses the scarcity in the literature on the composition, properties, and performances of 3D and 4D printed BMMs in medical applications and their pros and cons. Moreover, the content presented would be immensely beneficial for material scientists, chemists, and engineers engaged in AM manufacturing and clinicians in the biomedical field.