Transcorneal electrical stimulation promotes survival of retinal ganglion cells after optic nerve transection in rats accompanied by reduced microglial activation and TNF-α expression.

Microglial activation plays a crucial role in the pathological processes of various retinal and optic nerve diseases. TNF-α is a pro-inflammatory cytokine that is rapidly upregulated and promotes retinal ganglion cells (RGCs) death after optic nerve injury. However, the cellular source of TNF-α after optic nerve injury remains unclear. Thus, we aimed to determine the changes of retinal microglial activation in a rat model of optic nerve transection (ONT) after transcorneal electrical stimulation (TES). Furthermore, we assessed TNF-α expression after ONT and evaluated the effects of TES on TNF-α production. Rats were divided into 2 control groups receiving a sham surgery procedure, 2 ONT+Sham TES groups, and 2 ONT+TES groups. The rats were sacrificed on day 7 or 14 after ONT. RGCs were retrogradely labelled by Fluorogold (FG) 7 days before ONT, one TES group and corresponding controls were stimulated on day 0, 4, and the second were stimulated on day 0, 4, 7, 10. Whole-mount immunohistofluorescence, quantification of RGCs and microglia, and western blot analysis were performed on day 7 and 14 after ONT. TES significantly increased RGCs survival on day 7 and 14 after ONT, which was accompanied by reduced microglia on day 7, but not 14. TNF-α was co-localized with ameboid microglia and significantly increased on day 7 and 14 after ONT. TES significantly reduced TNF-α production on day 7 and 14 after ONT. Our study demonstrated that TES promotes RGCs survival after ONT accompanied by reduced microglial activation and microglia-derived TNF-α production.

Clinical manifestations and management of acute thallium poisoning.

Clinical information regarding 3 patients diagnosed with acute thallium poisoning was collected and retrospectively analyzed. All 3 patients presented with severe burning pain in the lower limbs and the abdomen. Diffuse alopecia, hepatic dysfunction and Mees' lines in the digits of each limb were observed between 2 and 3 weeks after onset. A physical examination demonstrated paresthesia of all 4 limbs, but normal deep tendon reflexes. Blood and urine thallium concentrations were significantly elevated. Treatment was initiated using hemoperfusion, hemodialysis, potassium supplementation, oral laxatives and B complex supplementation. Clinical symptoms improved as blood and urine thallium concentrations decreased, although a residual sensory neuropathy remained. This study demonstrated that the primary clinical manifestations of acute thallium poisoning include gastrointestinal symptoms, polyneuropathy and dermatological changes. Hemoperfusion and hemodialysis may be effective treatments for acute thallium poisoning.