Periodontitis and Subsequent Risk of Cataract: Results From Real-World Practice.

BACKGROUND: Periodontitis can lead to systemic inflammation and oxidative stress, contributing to the development of various diseases. Periodontitis could also be associated with several ocular diseases. METHODS: We conducted a retrospective population-based cohort study using the National Health Insurance Research Database of Taiwan to evaluate the risk of cataract in people with and without periodontitis. We established a periodontitis cohort and a non-periodontitis cohort, which included 359,254 individuals between 2000 and 2012. Age, gender, and enrolled year were matched. All participants were monitored until the end of 2013. Cox proportional hazard models were applied to estimate hazard ratios (HRs) and confidence intervals (CIs). RESULTS: Patients with periodontitis had a significantly higher risk to develop cataract than those without periodontitis [10.7 vs. 7.91 per 1,000 person-years, crude HR = 1.35 (95% CI = 1.32-1.39), and adjusted HR = 1.33 (95% CI = 1.30-1.36)]. The significant levels remained the same after stratifying by age, gender, presence of comorbidity, and use of corticosteroid. In addition, we found that diabetes mellitus and hyperlipidemia had a synergistic effect in the interaction of periodontitis and cataract development. CONCLUSION: Patients with periodontitis have a higher risk of cataract development than those without periodontitis. Such patients may request frequent ocular health check-up. Further studies should be performed to confirm the association and to understand the mechanisms.

GABA tea attenuates cardiac apoptosis in spontaneously hypertensive rats (SHR) by enhancing PI3K/Akt-mediated survival pathway and suppressing Bax/Bak dependent apoptotic pathway.

Cardiomyocyte apoptosis is the major risk factor for the development of heart failure (HF). The purpose of this study was to evaluate the effects of Gamma-aminobutyric acid (GABA) tea on hypertension-induced cardiac apoptotic pathways in spontaneously hypertensive rats (SHR). In order to reveal the mechanisms, 36 male SHR at eight weeks of age, 200 g were divided into six groups. One group was fed water as a control group. Other rats were administered one of the following treatments: GABA tea at dose 150 and 300 mg/kg/day as low GABA tea (LGT) and high GABA tea (HGT) groups, respectively, pure GABA at dose 150 and 300 mg/kg/day as LG and HG groups, respectively, green tea (GT) as control of LGT and HGT groups. After 12 weeks, cardiac tissues were analyzed by histological analysis, western blotting, and TUNEL assays. GABA tea, GT, and pure GABA decreased hypertension-induced cardiac abnormalities, including abnormal myocardial architecture. In addition, GABA tea, GT, and pure GABA dramatically increased anti-apoptotic protein, Bcl2. Furthermore, GABA tea, GT, and pure GABA also decreased activated-caspase 9 and activated-caspase 3. Additionally, the survival associated protein IGF-I and PI3K/Akt were enhanced in cardiac tissues upon treatment. Our results showed an optimistic anti-apoptotic and pro-survival effects of GABA tea treatment against hypertensive rat hearts.

Suppression of Ca(2+) influx in endotoxin-treated mouse cerebral cortex endothelial bEND.3 cells.

Release of nitric oxide (NO) is triggered by a rise in endothelial cell (EC) cytosolic Ca(2+) concentration ([Ca(2+)]i) and is of prime importance in vascular tone regulation as NO relaxes vascular smooth muscle. Agonists could stimulate EC [Ca(2+)]i elevation by triggering Ca(2+) influx via plasma membrane ion channels, one of which is the store-operated Ca(2+) channel; the latter opens as a result of agonist-triggered internal Ca(2+) release. Endotoxin (lipopolysaccharide, LPS) could cause sepsis, which is often the fatal cause in critically ill patients. One of the LPS-induced damages is EC dysfunction, eventually leading to perturbations in hemodynamics. We obtained data showing that LPS-challenged mouse cerebral cortex endothelial bEND.3 cells did not suffer from apoptotic death, and in fact had intact agonist-triggered intracellular Ca(2+) release; however, they had reduced store-operated Ca(2+) entry (SOCE) after LPS treatment for 3h or more. Using real-time PCR, we did not find a decrease in gene expression of stromal interaction molecule 1 (STIM1) and Orai1 (two SOCE protein components) in bEND.3 cells treated with LPS for 15h. LPS inhibitory effects could be largely prevented by sodium salicylate (an inhibitor of nuclear factor-κB; NF-κB) or SB203580 (an inhibitor of p38 mitogen-activated protein kinases; p38 MAPK), suggesting that the p38 MAPK-NF-κB pathway is involved in SOCE inhibition.

Difficult fiber-optic intubation in a patient with giant neck masses: The role of McCoy laryngoscope in elevating compressed laryngeal aperture.

Airway management in patients with giant neck masses is usually a challenge to anesthesiologists. A giant neck mass could compress the airway and thus impede endotracheal intubation. We encountered a situation where the giant neck masses of a patient pushed the epiglottis posteriorly toward the posterior pharyngeal wall and compressed the laryngeal aperture narrowing after anesthetic induction, causing direct laryngoscopic intubation and sequential fiber-optic intubation failed. The neck masses twisted the aryepiglottic fold tortuously and clogged the laryngeal aperture tightly, making a flexible fiber-optic bronchoscope unable to pass through the laryngeal aperture. Later, we utilized a McCoy laryngoscope alternately to lift the compressed larynx up and away from the posterior pharyngeal wall, creating a passage and completing endotracheal intubation successfully with the aid of a gum elastic bougie. Our case suggested that the tilting tip blade of the McCoy laryngoscope could lever the tongue base up against the tumor mass compression to improve laryngeal views and facilitate endotracheal intubation when a difficult fiber-optic intubation was encountered on a compressed laryngeal aperture.