Valsalva-Like Retinopathy Spontaneously Occurred after Ocular Massage

Purpose

The aim of this study is to describe a case of Valsalva-like retinopathy that occurred after ocular massage.

Case Presentation

A healthy 44-year-old Japanese female had massaged her eye with strong pressure several times. Subsequently, she noticed a loss in the left central vision. A left-eye fundus examination showed a dense preretinal hemorrhage located under the internal limiting membrane at the posterior pole and a mild vitreous hemorrhage. We performed a neodymium-doped yttrium-aluminium-garnet laser membranotomy to perforate the internal limiting membrane. Her best-corrected visual acuity improved from 0.01 to 1.0. No retinal vascular abnormalities in the macular area were found.

Conclusion

Ocular massage can cause Valsalva-like retinopathy.Key Words: Neodymium-doped yttrium-aluminium-garnet laser membranotomy, Ocular massage, Valsalva-like retinopathy     

Withdrawal of repeated morphine enhances histamine-induced scratching responses in mice

An itch is experientially well known that the scratching response of conditions such as atopic dermatitis is enhanced under psychological stress. Morphine is typical narcotic drug that induces a scratching response upon local application as an adverse drug reaction. Although long-term treatment with morphine will cause tolerance and dependence, morphine withdrawal can cause psychologically and physiologically stressful changes in humans. In this study, we evaluated the effects of morphine withdrawal on histamine-induced scratching behavior in mice. Administration of morphine with progressively increasing doses (10–50?mg/kg, i.p.) was performed for 5 consecutive days. At 3, 24, 48, and 72?hr after spontaneous withdrawal from the final morphine dose, histamine was intradermally injected into the rostral part of the back and then the number of bouts of scratching in 60?min was recorded and summed. We found that at 24?hr after morphine withdrawal there was a significant increase in histamine-induced scratching behavior. The spinal c-Fos positive cells were also significantly increased. The relative adrenal weight increased and the relative thymus weight decreased, both significantly. Moreover, the plasma corticosterone levels changed in parallel with the number of scratching bouts. These results suggest that morphine withdrawal induces a stressed state and enhances in histamine-induced scratching behavior. Increased reaction against histamine in the cervical vertebrae will participate in this stress-induced itch enhancement.     

Expression of DDX27 contributes to colony-forming ability of gastric cancer cells and correlates with poor prognosis in gastric cancer

Previously, we have reported that gain at chromosome 20q13 is the most common genomic copy number aberration in gastric cancer (GC) (29/30 cases), and that among the genes located in this region, we have identified DDX27, whose expression level shows the highest correlation with genomic copy number, as a candidate therapeutic target for GC. Here, we analyzed the clinicopathological significance of DDX27 using immunohistochemistry and studied its functions using knockdown assays. We found that DDX27 was frequently upregulated in GC tissues (98 of 140 cases, 70%), and significantly associated with venous invasion and liver metastasis. Furthermore, multivariate analysis of GC patients showed that high expression of DDX27 was independently associated with poorer prognosis. In functional assays, knockdown of DDX27 reduced the ability of GC cells to form colonies both on conventional plates and soft agar, but had little effect on their invasiveness. We also found that knockdown of DDX27 reduced the viability of GC cells through inhibition of cell cycle progression independently of apoptosis. Interestingly, DDX27 depletion induced accumulation of TP53 in a TP53 wild-type cell line, AGS, but not in a TP53-deleted cell line, 44As3, although DDX27 knockdown commonly reduced the viability of both, indicating the TP53-dependent and independent cell cycle control of DDX27. Thus, our results suggest that expression of DDX27 contributes to colony formation by GC cells through cell cycle control and may be a potential therapeutic target for GC patients with chromosome gain at 20q13.     

Renal effects of prostaglandin E1 in hypertensive patients.

The effects of prostaglandin E1 on fluid and sodium excretion, creatinine clearance and renin release were examined in 26 hypertensive patients including 9 cases of essential hypertension, 10 of renovascular hypertension and 7 of primary aldosteronism. When prostaglandin was infused intravenously in a total dose of 120 mug in 60 min, urine volume was increased in 70% of cases, and sodium excretion in 61%, but little changes were observed in creatinine clearance. The most prominent diuresis and natriuresis were obtained in primary aldosteronism (mean increase was 319% in urinary volume, and 222% in sodium output). The average increases in urinary volume were 61% in patients with essential hypertension and 97% in renovascular hypertension. And urinary output of sodium was increased by 63% in the former and 56% in the latter. The remarkable renal effects of prostaglandin E1 in primary aldosteronism were completely abolished after the administration of spironolactone. Significant elevation of plasma renin activity resulted from prostaglandin E1 infusion in essential hypertension, while no constant effect was obtained in renovascular hypertension and primary aldosteronism. The present experiments indicate that prostaglandin E1 has different effects on the kidney according to the types of hypertension and the effects correlate closely with patient's status of extracellular fluid volume or sodium balance.     

Simultaneous measurements of cytosolic free calcium level and prostaglandin synthesis reveal a correlation between them in perfused monolayer of cultured rat vascular smooth muscle cells: effects of bradykinin and angiotensin II.

The level of cytosolic free calcium ([Ca2+]i) and the production rate of prostacyclin were simultaneously measured in perfused monolayers of cultured vascular smooth muscle (VSM) cells. After loading of fura-2 (a fluorescent calcium indicator), the monolayer of VSM cells (cultured on a cover glass) was fixed in the perfusion cuvette and the cuvette was placed in a fluorometer to monitor the change in [Ca2+]i. The monolayer was perfused and the fractionated perfusion solution was collected to determine 6-keto-PGF1 alpha (a metabolite of prostacyclin) production found in the solution. Afterwards, the time-dependent changes in [Ca2+]i and 6-keto-PGF1 alpha synthesis were compared. Bradykinin (BK, 10(-6) M), angiotensin (Ang) II (10(-7) M) as well as ionomycin (10(-6) M) induced simultaneous increases in [Ca2+]i and 6-keto-PGF1 alpha production. An inhibitor against prostaglandin synthesis, acetylsalicylic acid (ASA, 10(-6) M) abolished BK-induced 6-keto-PGF1 alpha synthesis, whereas ASA did not affect the increase in [Ca2+]i. BK-induced increases in [Ca2+]i and 6-keto-PGF1 alpha production occurred in a dose-dependent manner and the half-maximal response was observed at the same concentration of BK (10(-7) M). These results indicate that an increase in [Ca2+]i is closely associated with BK as well as AngII-induced prostacyclin synthesis. It is suggested that an increase in [Ca2+]i plays a prior role in prostacyclin synthesis. Thus, an interaction between phospholipase A2 (prostaglandin synthesis) and phospholipase C (inositol trisphosphate-Ca2+ mobilization) is suggested.     

Higher activity of oxidative drug demethylation in the liver microsomes from dystrophic mouse.

The activities of NADPH-dependent oxidative demethylation of aminopyrine and other methyl compounds in the liver microsomes from dystrophic mice were found to be about 30% higher than those of the normal mice. Consumption of reduced pyridine nucleotides during the demethylation reactions was also significantly larger in the dystrophic mouse system than in the normal mouse system. The synergistic effect of further addition of NADH on the oxidative demethylation in the reaction system with NADPH, however, was not significant in either the normal or the dystrophic mouse system. The activities of NADPH-cytochrome c reductase and lipid peroxidation were also higher by about 30% in the dystrophic mouse than in the normal mouse, but the contents of cytochrome P-450 and phospholipids in the liver microsomes from normal and dystrophic mice were not appreciably different. The results suggest the possibility that the progressive muscular dystrophy may involve abnormal features in not only muscle but also liver and other tissues.