Type 2 diabetes mellitus (T2DM) is a severe disease caused by metabolic disorders, particularly carbohydrate metabolism disorders. The disease is a fatal global trouble characterised by high prevalence rates, causing death, blindness, kidney failure, myocardial infarction, amputation of lower limps, and stroke. Biochemical metabolic pathways like glycolysis, gluconeogenesis, glycogenesis, and glycogenolysis are critical pathways that regulate blood glucose levels with the glucokinase (GK) enzyme playing a central role in glucose homeostasis. Any factor that perturbs the aforementioned biochemical pathways is detrimental. Endocrinological, neurophysiological, and molecular biological pathways that are linked to carbohydrate metabolism should be studied, grasped, and manipulated in order to alleviate T2DM global chaos. The challenge, howbeit, is that, since the body is an integration of systems that complement one another, studying one “isolated” system is not very useful. This paper serves to discuss endocrinology, neurophysiology, and molecular biology pathways that are involved in carbohydrate metabolism in relation to T2DM.

Cellular microbiology, which is the interaction between harmful microbes and infected cells, is important in the determination of the bacterial infection processes and in the progression of data of different cellular mechanisms. The therapeutic role of bacteria has gained attention since the known methods such as radiation, chemotherapy, and immunotherapy have got drawbacks. Bacteria have demonstrated a favorable impact in treating cancer through eradication of tumors. Bacteria, in cancer treatment, have proven to be promising and have been shown in some of the previous work that it can successfully suppress the growth of tumors. In this paper, we analyzed the difficulties and settlement for using bacteria in cancer therapy as well the mechanisms in which bacteria works in order to achieve tumor eradication. Future works may focus on the use of bacteria along with other treatments in order to achieve effective tumor therapy.

Prostate cancer is a global fatal type of cancer. It is a type of cancer that affect men. Signs and symptoms of the disease include blood in the urine, pain when one micturates, and difficulties in penis erection. Cisplatin chemotherapy is a principal treatment normally given to the prostate cancer patients. Nonetheless, on its own, cisplatin loses efficacy once administered due to liver pass effects and other biochemical attacks. In this paper, we looked at preparation of PCL nanoparticles loaded with cisplatin and their potential for the treatment of prostate cancer. PCL nanoparticles protect cisplatin from biochemical attack, thus increasing drug efficacy. Incorporation of P-glycoprotein inhibitors in PCL nanoparticles (NPs) loaded with cisplatin could improve prostate cancer treatment even more.

The medical field is looking for drugs and/or ways of delivering drugs without harming patients. A number of severe drug side effects are reported, such as acute kidney injury (AKI), hepatotoxicity, skin rash, and so on. Nanomedicine has come to the rescue. Liposomal nanoparticles have shown great potential in loading drugs, and delivering drugs to specific targeted sites, hence achieving a needed bioavailability and steady state concentration, which is achieved by a controlled drug release ability by the nanoparticles. The liposomal nanoparticles can be conjugated to cancer receptor tags that give the anticancer-loaded nanoparticles specificity to deliver anticancer agents only at cancerous sites, hence circumventing destruction of normal cells. Also, the particles are biocompatible. The drugs are shielded by attack from the liver and other cytochrome P450 enzymes before reaching the desired sites. The challenge, however, is that the drug release is slow by these nanoparticles on their own. Scientists then came up with several ways to enhance drug release. Magnetic fields, UV light, infrared light, and so on are amongst the enhancers used by scientists to potentiate drug release from nanoparticles. In this paper, synthesis of liposomal nanoparticle formulations (liposomal-quantum dots (L-QDs), liposomal-quantum dots loaded with topotecan (L-QD-TPT)) and their analysis (cytotoxicity, drug internalization, loading efficiency, drug release rate, and the uptake of the drug and nanoparticles by the HeLa cells) are discussed.

One of the most burning issues in health system is the concern of handling patients that requires emergency surgery. Emergency general surgery is done on both traumatic and nontraumatic acute disorders. Severe traumatic injury and bleeding is one of the causing agents for high mortality rate globally. Another group of patients that are in need of emergency surgery are those with heart failure, and in this particular paper, we analyzed emergency medicine with advanced surgery protocols focusing on gastric cancer, cardiac surgery, and bleeding as well as coagulopathy following traumatic injury.

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Chronic obstructive pulmonary diseases (COPD) and asthma are fatal. The respiratory tract may be blocked, robbed of the adequate amounts of oxygen; hence, death ensues if a quick medical attention is not provided. The treatment available for the duo are inhaled corticosteroids (ICS). The ICS can work synergically with LABAS (long-acting β2-antagonists) and so many other medicines like bronchodilators. The drugs used for the treatment of asthma and COPD are metabolised once in the body system and at the same time exerting the therapeutic effect provided the concentration of the drug is within the therapeutic window. The CYP3A isoforms metabolise the ICS, in this case, salmeterol and fluticasone propionate (FP). Methods of administration are not limited to inhalation. Specific doses are prescribed accurately paying attention to factors like age, gender, race, and genetic makeup since these affect drug metabolisms. Generally, the ICS work by translocating glucocorticoid receptors to the nucleus from the cytosol. The mechanism is potentiated by the β-antagonists and this brings about an anti-inflammatory effect which is greater than either of the two drugs alone. Once this happens, it is not necessary to increase ICS dose. The ICS, in addition, cause more production of β-receptors by activating the β-receptor genes. This mode of action begets the LABAs’ bronchodilator-effects. The challenge is that ICS are not limited only to “double” therapy. Analysing such therapies is daunting since coadministration interferes with pharmacology and pharmacokinetics of drugs. This work focuses on salmeterol/fluticasone propionate combination and aspects which has to do with administration, monitoring, metabolism, toxicity, and adverse effects.