Diabetic cardiomyopathy is a growing challenge to global public health. The clinical characteristics are mainly fibrosis, hypertrophy, ventricular dysfunction, cardiac remodelling, and finally, heart failure. This alarming condition is often difficult to diagnose. Routine tests such as echocardiogram, electrocardiogram, and magnetic resonance imaging, along with specialized techniques such as transmitral Doppler, tissue Doppler imaging, and positron emission tomography, help diagnose and offer clearer insight into the condition. Current treatment strategies mainly address this medical condition as a condition secondary to diabetes. The main therapeutic practices involve glucose-lowering drugs such as glucagon-like peptide-1 modulators and sodium‒glucose cotransporter-2 inhibitors, along with other conventional lines of treatment to manage complications. Promising new potential therapeutic methods include gene therapy and noncoding RNA-mediated regulation of disarrayed signalling cascades. In this review, we address the benefits and limitations of the current system in the diagnosis and treatment of diabetic cardiomyopathy as well as the possibilities and advantages of novel techniques. In addition to discussing biomarkers for screening, diagnosis, and drug response for diabetic cardiomyopathy, we also discuss management and prevention strategies, adversities, and quality of life, and provide a brief outlook for research in this area. Graphical abstract

Alzheimer’s disease (AD) is an age-related progressive disorder characterized by neurodegeneration and accumulation of abnormal proteins. Artesunate, an anti-malarial drug has recently been shown to have anti-inflammatory, antiviral, angiogenic and other pleiotropic effects. It has also improved cognitive decline induced by hepatic coma which is suggestive of its role in learning and memory. In view of this, the current study was planned to assess the effect of the combination of artesunate with rivastigmine and memantine in aluminium chloride induced neurotoxicity. The study was conducted on 24 male adult albino wistar rats which were divided into four groups (n=6). Group - I to IV received saline, aluminium chloride (AlCl3), AlCl3 + artesunate +rivastigmine, AlCl3 + artesunate + memantine for 60 days respectively. After the 60th day of treatment, all animals were subjected to a passive avoidance task. All the animals were then sacrificed to study the histopathological changes in the hippocampus. Artesunate in combination with rivastigmine and memantine showed significant improvement in memory impairment and reduced neuronal death. Neuronal viability was more prominent in combination treatments as shown by histopathological results. Artesunate in combination with rivastigmine and memantine could be useful in AD. Artesunate can be used as an adjuvant therapy because artesunate combined with standard drugs produced significant neuroprotective effect.

Olanzapine, an atypical antipsychotic is considered superior to its conventional congeners. Here we report two cases of pedal edema secondary to olanzapine. In both cases the systemic causes of pedal edema were ruled out. On reducing the dose of olanzapine, pedal edema regressed and completely resolved after stopping the drug. So we attribute the edema to olanzapine therapy. As the definitive cause and further consequences of pedal edema are not known , hence stringent monitoring of adverse effects of this drug is required.

Lisinopril and fosinopril were compared on scopolamine-induced learning and memory deficits in rats. A total of eighty-four male Wistar rats were divided into seven groups. Group I received 2% gum acacia orally for 4 weeks, group II received normal saline, and group III received scopolamine (2 mg/kg/ip) as single dose. Groups IV and V received lisinopril ( 0.225 mg/kg and 0.45 mg/kg), while Groups VI and VII received fosinopril (0.90 mg/kg and 1.80 mg/kg), respectively, orally for four weeks, followed by scopolamine (2 mg/kg/ip) given 45 minutes prior to experimental procedure. Evaluation of learning and memory was assessed by using passive avoidance, Morris water maze, and elevated plus maze tests followed by analysis of hippocampal morphology and quantification of the number of surviving neurons. Scopolamine induced marked impairment of memory in behavioral tests which correlated with morphological changes in hippocampus. Pretreatment with fosinopril 1.80 mg/kg was found to significantly ameliorate the memory deficits and hippocampal degeneration induced by scopolamine. Fosinopril exhibits antiamnesic activity, indicating its possible role in preventing memory deficits seen in dementia though the precise mechanism underlying this effect needs to be further evaluated.