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Background: Medical radiation is considered a factor responsible for cataractogenesis. However, the incidence of this ophthalmologic complication resulting from gamma knife radiosurgery (GKRS) has not yet been reported. The present study aimed to determine the risk of cataractogenesis associated with radiation exposure from GKRS.Methods: This study used information from a random sample of one million persons enrolled in the nationally representative Taiwan National Health Insurance Research Database. The GK group consisted of patients who underwent GKRS between 2000 and 2009. The non-GK group was composed of subjects who had never undergone GKRS, but who were matched with the case group for time of enrollment, age, sex, history of coronary artery disease, hypertension, and diabetes.Results: There were 277 patients in the GK group and 2770 matched subjects in the non-GK group. The GK group had a higher overall incidence of cataracts (10.11% vs. 7.26%; crude hazard ratio [cHR], 1.59; 95% CI, 1.07-2.36; adjusted hazard ratio [aHR], 1.25; 95% CI, 0.82-1.90) than the non-GK group. Patients who had undergone computed tomography and/or cerebral angiography (CT/angio) studies had a higher risk of developing cataracts than those who did not (10.82% vs. 6.64%; cHR, 1.74; 95% CI, 1.31-2.30; aHR, 1.65; 95% CI, 1.22-2.23). The age group between 30 and 50 years had the highest risk of cataractogenesis in both the GK and CT/angio groups (cHR, 3.50; 95% CI, 1.58-7.72; aHR, 2.43; 95% CI, 1.02-5.81; cHR, 2.96; 95% CI, 1.47-5.99; aHR, 2.27; 95% CI, 1.05-4.93, respectively).Conclusions: Radiation exposure due to GKRS and CT/angio study may be independently associated with increased risk of cataractogenesis. We suggest routine dosimetry measurement of eye lens and proper protection for patients with benign lesions during GKRS. Regular follow-up imaging studies should avoid the use of CT/angio, and particular care should be taken in the 30-50-year-old age group, due to their significantly increased risk of cataract formation. [ABSTRACT FROM AUTHOR]

In this study, the effects of carbachol (CCh) on twitch tension, intracellular Na[sup +] activity (a[sup i] [sub Na] ), and action potential were simultaneously measured in canine cardiac Purkinje fibers in order to examine the regulation of inotropy through muscarinic receptors and its relation to a[sup i] [sub Na] . In fibers driven at 1 Hz, CCh (10 μM) initially and transiently decreased and then increased the twitch tension by 36 ± 8%. The action potential showed a significant elevation of the plateau and a significant shortening of the duration at 90% repolarization (APD[sub 90] ), from 403 ± 7 to 389 ± 7 ms. The a[sup i] [sub Na] decreased from 7.4 ± 0.4 to 6.7 ± 0.3 mM (n = 23, p < 0.05). Atropine (1 μM) decreased the twitch tension by 21 ± 6% (n = 7, p < 0.05) without significant effects on the action potential and a[sup i] [sub Na] , and inhibited the effects of CCh. Cs[sup +] (20 mM) increased the plateau height and APD[sub 90] , enhanced the twitch tension by 66 ± 24%, but decreased a[sup i] [sub Na] from 7.3 ± 0.3 to 6.3 ± 0.4 mM (n = 6, p < 0.05). In the presence of 20 mM Cs[sup +] , some fibers generated slow responses. The addition of 10 μM CCh further increased the twitch tension and APD[sub 90] , and decreased a[sup i] [sub Na] from 6.3 ± 0.4 to 5.3 ± 0.3 mM. Ouabain (0.3 μM) increased the twitch tension and a[sup i] [sub Na] , and inhibited the CCh-induced decrease of a[sup i] [sub Na] . In the presence of ouabain, 20 mM Cs[sup +] depolarized the fiber and generated slow responses with a decreased a[sup i] [sub Na] . The addition of 10 μM CCh enhanced the slow action potential, and increased a[sup i] [sub Na] although there was a transient decrease during early exposure. These results suggest that activation of muscarinic receptors in canine Purkinje fibers results in an enhancement of the Na[sup +] -K[sup +] pump activity and a biphasic inotropic response, probably via different receptor subtypes. The inhibitory effect, most likely through M[sub 2] receptors, is associated with the activation of K[sup +] channels. The stimulatory effect, on the other hand, is probably due to the action on the M[sub 1] receptors, resulting in increases in Ca[sup 2+] currents. [ABSTRACT FROM AUTHOR]

Background: Medical radiation is considered a factor responsible for cataractogenesis. However, the incidence of this ophthalmologic complication resulting from gamma knife radiosurgery (GKRS) has not yet been reported. The present study aimed to determine the risk of cataractogenesis associated with radiation exposure from GKRS., Methods: This study used information from a random sample of one million persons enrolled in the nationally representative Taiwan National Health Insurance Research Database. The GK group consisted of patients who underwent GKRS between 2000 and 2009. The non-GK group was composed of subjects who had never undergone GKRS, but who were matched with the case group for time of enrollment, age, sex, history of coronary artery disease, hypertension, and diabetes., Results: There were 277 patients in the GK group and 2770 matched subjects in the non-GK group. The GK group had a higher overall incidence of cataracts (10.11% vs. 7.26%; crude hazard ratio [cHR], 1.59; 95% CI, 1.07-2.36; adjusted hazard ratio [aHR], 1.25; 95% CI, 0.82-1.90) than the non-GK group. Patients who had undergone computed tomography and/or cerebral angiography (CT/angio) studies had a higher risk of developing cataracts than those who did not (10.82% vs. 6.64%; cHR, 1.74; 95% CI, 1.31-2.30; aHR, 1.65; 95% CI, 1.22-2.23). The age group between 30 and 50 years had the highest risk of cataractogenesis in both the GK and CT/angio groups (cHR, 3.50; 95% CI, 1.58-7.72; aHR, 2.43; 95% CI, 1.02-5.81; cHR, 2.96; 95% CI, 1.47-5.99; aHR, 2.27; 95% CI, 1.05-4.93, respectively)., Conclusions: Radiation exposure due to GKRS and CT/angio study may be independently associated with increased risk of cataractogenesis. We suggest routine dosimetry measurement of eye lens and proper protection for patients with benign lesions during GKRS. Regular follow-up imaging studies should avoid the use of CT/angio, and particular care should be taken in the 30-50-year-old age group, due to their significantly increased risk of cataract formation.

Background: Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain., Results: We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury., Conclusions: These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.