RESUMO
Alzheimer's disease (AD) is a serious health issue that has a significant social and economic impact worldwide. One of the key aetiological signs of the disease is a gradual reduction in cognitive function and irreversible neuronal death. According to a 2019 global report, more than 5.8 million people in the United States (USA) alone have received an AD diagnosis, with 45% of those people falling into the 75-84 years age range. According to the predictions, there will be 15 million affected people in the USA by 2050 due to the disease's steadily rising patient population. Cognitive function and memory formation steadily decline as a result of an irreversible neuron loss in AD, a chronic neurodegenerative illness. Amyloid-beta and phosphorylated Tau are produced and accumulate in large amounts, and glial cells are overactive. Additionally, weakened neurotrophin signalling and decreased synapse function are crucial aspects of AD. Memory loss, apathy, depression, and irritability are among the primary symptoms. The aetiology, pathophysiology, and causes of both cognitive decline and synaptic dysfunction are poorly understood despite extensive investigation. CRISPR/Cas9 is a promising gene-editing technique since it can fix certain gene sequences and has a lot of potential for treating AD and other human disorders. Regardless of hereditary considerations, an altered Aß metabolism is frequently seen in familial and sporadic AD. Therefore, since mutations in the PSEN-1, PSEN-2 and APP genes are a contributing factor to familial AD, CRISPR/Cas9 technology could address excessive Aß production or mutations in these genes. Overall, the potential of CRISPR-Cas9 technology outweighs it as currently the greatest gene-editing tool available for researching neurodegenerative diseases like AD.
RESUMO
A significant right-sided pleural effusion was seen on chest radiography in a 53-year-old adult male who complained of bilateral chest pain, shortness of breath, and other additional symptoms. The bloody pleural effusion was removed with a chest tube, and cytopathology analysis showed moderate cellularity. After performing a high-resolution computed tomography, it was discovered that the affected lung had a significant pleural effusion on the right side as well as collapsed and consolidated lung parenchyma. Upon further examination, the right lower lobe wedge biopsy cytology smear revealed mucinous adenocarcinoma. Adults rarely experience a severe malignant pleural effusion brought on by lung adenocarcinoma, particularly in the absence of risk factors.
RESUMO
Renal cell carcinoma (RCC) arises from the renal tubular epithelial cells and comprises a group of heterogenous renal tumors. Renal tumors can metastasize to involve almost any body organ, the common sites being the lung, liver, bone, brain, adrenal gland, head, neck, and rarely, inferior vena cava (IVC), leading to lethal outcomes. We present a case of RCC with IVC invasion in a patient who presented with right-sided flank pain and gross hematuria. His routine biochemical and hematological parameters were unremarkable, and an abdominal examination revealed a complex renal mass with mild hydronephrosis. The patient underwent contrast-enhanced magnetic resonance angiography with venography, which showed a right renal upper polar mass lesion extending into the right vein obliterating it up to its junction with the IVC. Integrating examination and imaging findings were suggestive of right renal RCC. Our case highlights the importance of standard preoperative MRI imaging to assess IVC invasion and its morphologic features including vessel breach or complete occlusion of the IVC.
