Incidence and risk factors for bone metastases at presentation in solid tumors.

Introduction: Bone metastases are associated with increased morbidity and decreased quality of life in patients with solid tumors. Identifying patients at increased risk of bone metastases at diagnosis could lead to earlier interventions. We sought to retrospectively identify the incidence and predictive factors for bone metastases at initial diagnosis in a large population-based dataset.

The changing landscape of small cell lung cancer.

Background: Small-cell lung cancer (SCLC) is characterized by rapid proliferation and early dissemination. The objective of this study was to examine the demographic trends and outcomes in SCLC.

Methods: The authors queried the National Cancer Institute's Surveillance, Epidemiology, and End Results database to assess the trends in incidence, demographics, staging, and survival for SCLC from 1975 to 2019.

Distinct metabolic profile according to the shape of the oral glucose tolerance test curve is related to whole glucose excursion: a cross-sectional study.

Background: The shapes of the plasma glucose concentration curve during the oral glucose tolerance test are related to different metabolic risk profiles and future risk of type 2 DM. We sought to further analyze the relationship between the specific shapes and hyperglycemic states, the metabolic syndrome and hormones involved in carbohydrate and lipid metabolism, and to isolate the effect of the shape by adjusting for the area under the glucose curve.

Methods: One hundred twenty one adult participants underwent a 2-h oral glucose tolerance test and were assigned to either the monophasic (n = 97) or the biphasic (n = 24) group based upon the rise and fall of their plasma glucose concentration.

Effects of Veliparib on Microglial Activation and Functional Outcomes after Traumatic Brain Injury in the Rat and Pig.

The inflammation response induced by brain trauma can impair recovery. This response requires several hours to develop fully and thus provides a clinically relevant therapeutic window of opportunity. Poly(ADP-ribose) polymerase inhibitors suppress inflammatory responses, including brain microglial activation.

A Case Report of Mania and Psychosis Five Months after Traumatic Brain Injury Successfully Treated Using Olanzapine.

Background: There are few published pharmacologic trials for the treatment of acute mania following traumatic brain injury (TBI). To our knowledge, we present the first case report of an individual being treated and stabilized with olanzapine monotherapy for this condition.

Case Presentation: We describe the case of a 53-year-old African American male admitted to an inpatient psychiatric hospital with one month of behavioral changes including irritability, decreased need for sleep, hyperverbal speech, hypergraphia, and paranoia five months after TBI.

Neuronal Glutathione Content and Antioxidant Capacity can be Normalized In Situ by N-acetyl Cysteine Concentrations Attained in Human Cerebrospinal Fluid.

N-acetyl cysteine (NAC) supports the synthesis of glutathione (GSH), an essential substrate for fast, enzymatically catalyzed oxidant scavenging and protein repair processes. NAC is entering clinical trials for adrenoleukodystrophy, Parkinson's disease, schizophrenia, and other disorders in which oxidative stress may contribute to disease progression. However, these trials are hampered by uncertainty about the dose of NAC required to achieve biological effects in human brain.

Assessment at the single-cell level identifies neuronal glutathione depletion as both a cause and effect of ischemia-reperfusion oxidative stress.

Oxidative stress contributes to neuronal death in brain ischemia-reperfusion. Tissue levels of the endogenous antioxidant glutathione (GSH) are depleted during ischemia-reperfusion, but it is unknown whether this depletion is a cause or an effect of oxidative stress, and whether it occurs in neurons or other cell types. We used immunohistochemical methods to evaluate glutathione, superoxide, and oxidative stress in mouse hippocampal neurons after transient forebrain ischemia.