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Object detection in high-definition video is required in video artificial intelligence (AI) applications for edge/terminals to detect a wide range of objects with one camera at one time. Although various AI inference schemes for object detection (e.g., You Only Look Once (YOLO)) have been proposed, they have a limitation regarding the input image size, thus need to shrink the input high-definition image into that limited size. This collapses small objects, making them undetectable. This article introduces highdefinition AI inference technology we previously proposed for solving this problem, with which multiple object detectors cooperate to detect small and large objects in high-definition video. [ABSTRACT FROM AUTHOR]

The article discusses the case of a 67-year-old man with Alzheimer's disease presented with a history of abdominal fullness and profound chronic constipation. He was admitted to the surgical hospital immediately for emergency surgical procedure to decompress the abdomen and his dilated sigmoid colon was surgically removed and an artificial anus was made. He needed treatment with antibiotics as he developed bacterial translocation due to increased permeability of the intestinal mucosal barrier.

The article reports on a case study of an 82-year old woman diagnosed with anticonvulsant valproate-associated-hypoglycemic attack. Topics discussed include the medical background of the patient, the clinical tests she underwent, her medical conditions, the treatment options given to her, and an overview of her illness.

The article discusses the case of a 78-old woman with a 50-year history of bipolar disorder who was diagnosed to have suffered the Adam-Stokes syndrome three months after the initiation of lithium therapy. Topics covered are the gastrointestinal, neurologic and cardiologic manifestations of lithium toxicity, the cardiac complications of conduction block or bradyarrythmias, the increase in deaths among psychiatric patients due to psychotropic medications.

Respiratory chain dysfunction can decrease ATP and increase reactive oxygen species (ROS) levels. Despite the importance of these metabolic parameters to a wide range of cellular functions and disease, we lack an integrated understanding of how they are differentially regulated. To address this question, we adapted a CRISPRi-and FACS-based platform to compare the effects of respiratory gene knockdown on ROS to their effects on ATP. Focusing on genes whose knockdown is known to decrease mitochondria-derived ATP, we showed that knockdown of genes in specific respiratory chain complexes (I, III, and CoQ10 biosynthesis) increased ROS, whereas knockdown of other low ATP hits either had no impact (mitochondrial ribosomal proteins) or actually decreased ROS (complex IV). Moreover, although shifting metabolic conditions profoundly altered mitochondria-derived ATP levels, it had little impact on mitochondrial or cytosolic ROS. In addition, knockdown of a subset of complex I subunits--including NDUFA8, NDUFB4, and NDUFS8--decreased complex I activity, mitochondria-derived ATP, and supercomplex level, but knockdown of these genes had differential effects on ROS. Conversely, we found an essential role for ether lipids in the dynamic regulation of mitochondrial ROS levels independent of ATP. Thus, our results identify specific metabolic regulators of cellular ATP and ROS balance that may help dissect the roles of these processes in disease and identify therapeutic strategies to independently target energy failure and oxidative stress. [ABSTRACT FROM AUTHOR]

The author discusses a cross-sectional study which assessed the relationship of fasting insulin levels with cognitive function of non-diabetic individuals with Alzheimer's Disease (AD). The authors observed that higher levels of insulin were associated with less cognitive decline in the non-diabetic AD cohort which suggests that improvement of an insulin signal by the insulin supplement might control the decline of cognitive function in non-diabetic AD.

The article describes the case of an 80-year old woman with schizophrenia and demonstrated changes of pituitary computed tomography (CT) level due to mineralocorticoid responsive hyponatremia of the elderly (MRHE). Laboratory results presented indicate the patient's serum sodium, potassium and serum creatinine levels. It discusses the response of the patient to hydrocortisone and suggests the potential compensatory secretion of antidiuretic hormone caused by adrenal insufficiency.

Mitochondria are important sources of energy, but they are also the target of cellular stress, toxin exposure, and aging-related injury. Persistent accumulation of damaged mitochondria has been implicated in many neurodegenerative diseases. One highly conserved mechanism to clear damaged mitochondria involves the E3 ubiquitin ligase Parkin and PTEN-induced kinase 1 (PINK1), which cooperatively initiate the process called mitophagy that identifies and eliminates damaged mitochondria through the autophagosome and lysosome pathways. Parkin is a mostly cytosolic protein, but is rapidly recruited to damaged mitochondria and target them for mitophagy. Moreover, Parkin interactomes also involve signaling pathways and transcriptional machinery critical for survival and cell death. However, the mechanism that regulates Parkin protein level remains poorly understood. Here, we show that the loss of homeodomain interacting protein kinase 2 (HIPK2) in neurons and mouse embryonic fibroblasts (MEFs) has a broad protective effect from cell death induced by mitochondrial toxins. The mechanism by which Hipk2 -/- neurons and MEFs are more resistant to mitochondrial toxins is in part due to the role of HIPK2 and its kinase activity in promoting Parkin degradation via the proteasome-mediated mechanism. The loss of HIPK2 leads to higher cytosolic Parkin protein levels at basal conditions and upon exposure to mitochondrial toxins, which protects mitochondria from toxin-induced damage. In addition, Hipk2 -/- neurons and MEFs show increased expression of PGC-la (peroxisome proliferator-activated receptor-y coactivator 1), a Parkin downstream target that can provide additional benefits via transcriptional activation of mitochondrial genes. Together, these results reveal a previously unrecognized avenue to target HIPK2 in neuroprotection via the Parkin-mediated pathway. [ABSTRACT FROM AUTHOR]