Although California was relatively unaffected by the destruction of the Civil War, California's new statehood and Gold Rush brought thousands of migrants from the war-torn areas. These migrants brought with them their ideologies--and sometimes their slaves. In Northern California's Sonoma County, the battle of civil war ideologies was fought over land rights. Southern Squatters settled in Sonoma County, voted for the pro-slavery Democratic Party, sang Dixie, and after the start of the Civil War, fought off sheriffs and residents trying to remove them and their politics. In Northern California, the rhetoric of the Civil War was played out in the "Healdsburg Squatter War." Opportunistic landowners used the Civil War as a political, moral, and ideological weapon to eject Southern squatters from profitable Sonoma County lands

Membranes of endolysosomal compartments in macrophages are often damaged by physical or chemical effects of particles ingested through phagocytosis or by toxins secreted by intracellular pathogens. This study identified a novel inducible activity in macrophages that increases resistance of phagosomes, late endosomes, and lysosomes to membrane damage. Pretreatment of murine macrophages with LPS, peptidoglycan, TNF-α, or IFN-γ conferred protection against subsequent damage to intracellular membranes caused by photooxidative chemistries or by phagocytosis of ground silica or silica microspheres. Phagolysosome damage was partially dependent on reactive oxygen species but was independent of the phagocyte oxidase. IFN-γ-stimulated macrophages from mice lacking the phagocyte oxidase inhibited escape from vacuoles by the intracellular pathogen Listeria monocytogenes, which suggested a role for this inducible renitence (resistance to pressure) in macrophage resistance to infection by pathogens that damage intracellular membranes. Renitence and inhibition of L. monocytogenes escape were partially attributable to heat shock protein-70. Thus, renitence is a novel, inducible activity of macrophages that maintains or restores the integrity of endolysosomal membranes.

As the list of anti-tumor immunotherapy agents and the list of cancers treated by these novel agents grow, a subset of patients are experiencing immune-related adverse events as a result of prolonged stimulation of the immune system. Many different immune related adverse events including colitis, hepatitis, pneumonitis, thyroiditis, hypophysitis, and cutaneous reactions can result from blocking these inhibitory pathways. The full spectrum of cutaneous immune related adverse events secondary to checkpoint inhibitor therapy is still being defined. The reported varied presentations include lichenoid reactions and bullous pemphigoid, amongst others. We present a severe cutaneous reaction, a case of debilitating erosive lichenoid dermatitis. This case emphasizes both the wide range of possible cutaneous reactions and the potential severity of these reactions.

Catecholamines play an important regulatory role in cutaneous wound healing. The exact role of dopamine in human epidermis has yet to be fully elucidated. Current published evidence describes its differential effects on two separate families of G protein coupled receptors: D1-like and D2-like dopamine receptors. Dopamine may enhance angiogenesis and wound healing through its action on dopamine D1 receptors, while impairing wound healing when activating D2 receptors. This review summarizes the evidence for the role of dopamine in wound healing and describes potential mechanisms behind its action on D1 versus D2-like receptors in the skin.

We have systematically investigated how vascular smooth muscle α₁ -adrenoceptor activation impacts endothelium-mediated vasodilation in isolated, myogenically active, rat cremaster muscle 1A arteries. Cannulated cremaster arteries were pressurized intraluminally to 70 mmHg to induce myogenic tone, and exposed to vasoactive agents via bath superfusion at 34°C. Smooth muscle membrane potential was measured via sharp microelectrode recordings in pressurized, myogenic arteries. The α₁ -adrenergic agonist phenylephrine (25-100 nmol/L) produced further constriction of myogenic arteries, but did not alter the vasorelaxant responses to acetylcholine (0.3 μmol/L), SKA-31 (an activator of endothelial Ca²⁺ -dependent K⁺ channels) (3 μmol/L) or sodium nitroprusside (10 μmol/L). Exposure to 0.25-1 μmol/L phenylephrine or 1 μmol/L norepinephrine generated more robust constrictions, and also enhanced the vasodilations evoked by acetylcholine and SKA-31, but not by sodium nitroprusside. In contrast, the thromboxane receptor agonist U46619 (250 nmol/L) dampened responses to all three vasodilators. Phenylephrine exposure depolarized myogenic arteries, and mimicking this effect with 4-aminopyridine (1 mmol/L) was sufficient to augment the SKA-31-evoked vasodilation. Inhibition of L-type Ca²⁺ channels by 1 μmol/L nifedipine decreased myogenic tone, phenylephrine-induced constriction and prevented α₁ -adrenergic enhancement of endothelium-evoked vasodilation; these latter deficits were overcome by exposure to 3 and 10 μmol/L phenylephrine. Mechanistically, augmentation of ACh-evoked dilation by phenylephrine was dampened by eNOS inhibition and abolished by blockade of endothelial KCa channels. Collectively, these data suggest that increasing α₁ -adrenoceptor activation beyond a threshold level augments endothelium-evoked vasodilation, likely by triggering transcellular signaling between smooth muscle and the endothelium. Physiologically, this negative feedback process may serve as a "brake" to limit the extent of vasoconstriction in the skeletal microcirculation evoked by the elevated sympathetic tone.

Adult acquired flatfoot deformity (AAFD) is a common disorder that typically affects middle-aged and elderly women, resulting in foot pain, malalignment, and loss of function. The disorder is initiated most commonly by degeneration of the posterior tibialis tendon (PTT), which normally functions to maintain the talonavicular joint at the apex of the three arches of the foot. PTT degeneration encompasses tenosynovitis, tendinosis, tendon elongation, and tendon tearing. The malaligned foot is initially flexible but becomes rigid and constant as the disorder progresses. Tendon dysfunction commonly leads to secondary damage of the spring ligament and talocalcaneal ligaments and may be associated with injury to the deltoid ligament, plantar fascia, and other soft-tissue structures. Failure of multiple stabilizers appears to be necessary for development of the characteristic planovalgus deformity of AAFD, with a depressed plantar-flexed talus bone, hindfoot and/or midfoot valgus, and an everted flattened forefoot. AAFD also leads to gait dysfunction as the foot is unable to change shape and function adequately to accommodate the various phases of gait, which require multiple rapid transitions in foot position and tone for effective ambulation. The four-tier staging system for AAFD emphasizes physical examination findings and metrics of foot malalignment. Mild disease is managed conservatively, but surgical procedures directed at the soft tissues and/or bones become necessary and progressively more invasive as the disease progresses. Although much has been written about the imaging findings of AAFD, this article emphasizes the anatomy and function of the foot's stabilizing structures to help the radiologist better understand this disabling disorder. Online supplemental material is available for this article. ©RSNA, 2019.