Ocular health screening among care-center residents with disabilities: a smartphone adaptive fundus camera cross-sectional study.

OBJECTIVE: The aim of this study was to evaluate the ocular health of care-center residents with disabilities who have difficulty accessing health care using a novel smartphone-adapted fundus camera device, and to compare the results to age- and gender-matched health subjects. PATIENTS AND METHODS: In this study, 47 care-center residents with disabilities were investigated between October 1, 2021, and December 31, 2021. A control group was made up of healthy volunteers. All participants underwent a comprehensive ocular exam, which included measuring visual acuity and assessing dry eye with Schirmer and tear break-up time tests. The posterior segment was examined using a smartphone-adapted fundus camera. The data gathered was compared with statistical significance between the two groups. RESULTS: The mean ages of disabled and healthy participants were 59.7±15.2 and 56.6±15.0 years, respectively (p=0.305). While 11.1% of the 36 visually impaired participants were legally blind, the percentage among healthy subjects was only 3.7% (p=0.168). In comparison to healthy participants, disabled people had statistically significantly higher rates of dry eye (27.7%), senile macular degeneration (23.4%), and cataracts (29.8%) (p<0.05). CONCLUSIONS: Screening for ocular health with a novel smartphone-adapted fundus camera revealed significantly higher rates of various ocular diseases in care center disabled residents. Given technological progress, remote control method-assisted ocular exams appear to be potentially feasible and clinically beneficial. This could allow trained allied health personnel to perform ocular health screenings without the need to transport a disabled person to the hospital. Thus, diagnosis and follow-up of various chronic ocular diseases may be properly organized.

Intravenous basic fibroblast growth factor (bFGF) decreases DNA fragmentation and prevents downregulation of Bcl-2 expression in the ischemic brain following middle cerebral artery occlusion in rats.

In previous studies, we showed that basic fibroblast growth factor (bFGF) reduced infarct volume when infused intravenously in animal models of focal cerebral ischemia. In the current study, we examined the potential mechanism of infarct reduction by bFGF, especially effects on apoptosis within the ischemic brain. We found that bFGF decreased DNA fragmentation in the ischemic hemisphere, as assessed by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) histochemical methods combined with morphological criteria. bFGF also prevented reduction of immunoreactivity of the anti-apoptotic protein Bcl-2 in the ischemic hemisphere, but did not alter immunoreactivity of the pro-apoptotic proteins Bax, Caspase-1, or Caspase-3. These changes in TUNEL histochemistry and Bcl-2 immunoreactivity were especially prominent in cortex at the borders ('penumbra') of infarcts, spared by bFGF treatment. We conclude that the infarct-reducing effects of bFGF may be due, in part, to prevention of downregulation of Bcl-2 expression and decreased apoptosis in the ischemic brain.

Hypertension increases the contractions to sumatriptan in the human internal mammary artery.

BACKGROUND: The internal mammary artery is the graft of choice for myocardial revascularization. The tendency to spasm increases toward the distal end of the internal mammary artery, which is the portion generally used for anastomosis. The distal internal mammary artery is more pharmacologically responsive to 5-hydroxytryptamine and several other vasoconstrictor agents than its midsection. METHODS: We examined the effects of 5-hydroxytryptamine and a 5-hydroxytryptamine1-like receptor agonist sumatriptan on internal mammary artery segments (length, 3-4 mm) obtained from patients undergoing coronary artery bypass grafting. To unmask a 5-hydroxytryptamine1-like receptor-mediated contractile response, threshold concentrations of potassium chloride were used. RESULTS: 5-Hydroxytryptamine induced concentration-dependent contractions in all, quiescent and potassium chloride precontracted, preparations. Sumatriptan induced marked contraction in some of the quiescent internal mammary artery rings, whereas it elicited marked and concentration-dependent contractions in all of the preparations given a moderate tone by a threshold concentration of potassium chloride. The sensitivity to sumatriptan was higher in potassium chloride-precontracted distal arteries than it was for the quiescent distal segments. Additionally, the sensitivity to and the efficacy of sumatriptan were much more markedly potentiated by precontraction in the preparations taken from hypertensive patients. CONCLUSIONS: The more marked potentiation of the responses in arteries from hypertensive patients may be one of the factors influencing the patency rates.

Vasodilatation induced by nicotine in the isolated perfused rat kidney.

1. In isolated perfused rat kidney, under a constant flow of 8-10 ml/min, mean basal perfusion pressure was found to be 82.57 +/- 8.96 mm Hg (n = 70). 2. After a bolus injection of 10 micrograms/0.1 ml phenylephrine (PE) which causes maximum vasopressor response, a 93.27 +/- 0.56 mm Hg increase in basal perfusion pressure was recorded (n = 70). In control experiments, a submaximum dose of PE (3 x 10(-6) M) caused a 68.37 +/- 0.47 mm Hg (n = 5) increase in perfusion pressure. 3. Nicotine, at a dose of 100 micrograms/0.1 ml, decreased the perfusion pressure raised by submaximum dose of PE. This nicotine-induced dilatation was 24.97 +/- 3.27% of maximum PE constriction (n = 5). 4. Nicotine-induced dilatation was not affected by atropine, guanethidine, hexamethonium, tetrodotoxin, capsaicin, indomethacin, quinacrine, NG-nitro-L-arginine, methylene blue, glibenclamide, tetraethylammonium, 4-aminopyridine and ouabain (n = 5).

Factors responsible for acetylcholine-induced dilatation in the isolated perfused rat kidney.

Mechanism of acetylcholine (ACh)-induced dilatation was investigated in isolated perfused rat kidney. Under a constant flow of 8-10 ml/min, ACh (0.001-3 microg/0.1 ml) caused a dose-dependent decrease in perfusion pressure raised by submaximum concentration of phenylephrine (PE). ACh-induced dilatations were inhibited by atropine (10(-6) mol/l), hexamethonium (10(-4) mol/l), indomethacin (10(-5) mol/l), methylene blue (10(-5) mol/l), N(G)-nitro-L-arginine (L-NOARG, 10(-4) mol/l), tetrodotoxin (TTX, 10(-6) mol/l), capsaicin (10(-6) mol/l), and glibenclamide (10(-5) mol/l). These results suggest that in the isolated perfused rat kidney, endothelium-derived hyperpolarizing factor (EDHF), nitric oxide (NO), and tachykinin neuromediators may play a role in ACh-induced dilatation via stimulation of guanylate cyclase and opening of ATP-sensitive potassium channels.

The relaxation induced by nicotine in the rat isolated renal artery.

The mechanism of nicotine-induced relaxation was investigated in the rat isolated renal artery. Nicotine (10(-3) M) produced a relaxation when preparations were precontracted by phenylephrine (3 x 10(-6) M). Nicotine-induced relaxation was 27.3 +/- 2.5% of phenylephrine contraction and was not affected by atropine (10(-5) M), guanethidine (10(-5) M), hexamethonium (10(-4) M), indomethacin (10(-5) M), N(G)-nitro-L-arginine (10(-4) M), methylene blue (10(-5) M), glibenclamide (10(-5) M), quinacrine (3 x 10(-6) M), tetrodotoxin (10(-6) M), capsaicin (10(-6) M), tetraethylammonium (10(-3) M), 4-aminopyridine (10(-3) M), and ouabain (10(-6) M) (n = 6, Mann-Whitney U-test). A calcium antagonizing effect of nicotine was not observed. Therefore, it appears that nicotine relaxes rat isolated renal artery by a nonspecific action on the vascular smooth muscle.

Effects of Androctonus crassicauda scorpion venom on endothelium-dependent and -independent vascular responses of rabbit aorta.

The effects of Androctonus crassicauda scorpion venom on acetycholine (ACh)-induced relaxations and contractions of rabbit thoracic aorta were studied. Endothelium-dependent relaxations induced by ACh in phenylephrine-precontracted arteries were enhanced by the scorpion venom. ACh-induced contractions in endothelium-intact open aortic rings were less than those obtained in denuded preparations (n = 6, P < 0.05, ANOVA). Venom (5, 10 and 30 micrograms/ml) potentiated ACh-induced contractions in intact and denuded segments. In the denuded segments, this potentiation was inhibited by indomethacin (10 microM). Thromboxane synthase inhibitor, BW 149H (100 microM) and thromboxane A2 (TXA2) receptor antagonist, R 68070 (10 microM) partly inhibited venom-induced potentiation. NG-nitro-L-arginine (100 microM) increased venom-potentiated ACh responses in intact arterial segments. Venom increased the basal tone by 25-35% at 30 micrograms/ml. These results suggest that A. crassicauda venom may release a relaxing factor from endothelium and contracting factor from the smooth muscle of rabbit isolated thoracic aorta. The contracting factor may be a cyclooxygenase-like product, most likely TXA2. The increase in basal tone by 30 micrograms/ml venom was inhibited by phentolamine (10 microM) and guanethidine (10 microM), indicating a venom-induced release of a neurotransmitter from adrenergic nerve endings.

Potential usefulness of basic fibroblast growth factor as a treatment for stroke.

Within the past few years, a growing body of evidence has accumulated indicating that exogenously administered neurotrophic growth factors may limit the extent of acute ischemic neural injury and enhance functional neurorecovery following stroke. One of the most widely studied growth factor in this regard is basic fibroblast growth factor (bFGF). In preclinical studies, bFGF administered intravenously within hours after the onset of ischemia reduces infarct size, presumably due to direct protection of cells at the borders (penumbra) of cerebral infarction. On the other hand, if bFGF is administered intracisternally starting at one day after ischemia, infarct size is not reduced, but recovery of sensorimotor function of the impaired limbs is increased, presumably due to enhancement of new neuronal sprouting and synapse formation in the intact uninjured brain. Clinical trials of the intravenous administration of bFGF as a cytoprotective agent in acute stroke are in progress. Trials of the delayed administration of bFGF as a recovery-promoting agent in subacute stroke are anticipated.

5-HT1-like receptor-mediated contraction in the human internal mammary artery.

We wished to characterize the 5-hydroxytryptamine (5-HT) receptors mediating vasoconstriction in the human internal mammary artery (IMA). Segments of the IMA obtained from patients undergoing coronary by-pass surgery were suspended in an organ bath and exposed to 5-HT and sumatriptan (SUM), a 5-HT1-like receptor agonist, in the presence and absence of potassium chloride (KCl) and angiotensin II. 5-HT induced concentration-dependent contractions in all quiescent and pre-contracted preparations. SUM induced small contractions in 70% of quiescent IMA rings, whereas it elicited marked and concentration-dependent contractions in all of the preparations given a moderate tone by a threshold concentration of KCl and angiotensin II. The efficacy of SUM was higher in precontracted arteries. Concentration-effect curves (CEC) of 5-HT and SUM were not affected by the 5-HT3-receptor antagonist tropisetron (1 microM). The nonselective antagonist, methiothepin (30 nM), shifted the CEC of SUM to the right. 5-HT2A-receptor antagonist, ketanserin (1 microM) inhibited responses to 5-HT, whereas it affected only the responses to the smaller concentrations of SUM. When methiothepin (30 nM) was applied in the presence of ketanserin (1 microM), a further inhibition in the responses to 5-HT was observed. These results suggest that 5-HT1-like receptors mediate the contractile action of SUM and contribute to that of 5-HT in IMA.