[Form deprivation myopia in C57BL/6 mice].

OBJECTIVE: To investigate the changes of refraction and ocular biometric parameters in form deprived myopia, and try to find the effective duration to induce significant myopic shift in C57BL/6 mice. METHODS: It was an experimental study. Seventy-four C57BL/6 mice, approximately 23 days old, were divided into three groups randomly: FD (Form-deprivation), Recovery and Normal control groups. FD group was treated with diffuser worn on one eye for 2 weeks (n = 12), 3 weeks (n = 20) and 4 weeks (n = 18), respectively. In Recovery group, diffusers were removed after 4 weeks form deprivation, and vertical meridian refraction and other biometric parameters were performed immediately on 4(th) and 7(th) day. The same measurements were performed in the normal control group at the same time-points. Refraction was measured by photoretinoscopy and corneal radius of curvature (CRC) was measured by a modified keratometry. Corneal thickness (CT), anterior chamber depth (ACD), lens thickness (LT), vitreous chamber depth (VCD), and axial length (AL) were measured by optical coherence tomography (OCT) with focal plane advancement. RESULTS: The FD eyes were approximately -0.85 D more myopic compared to the fellow and the normal control eyes after 2 weeks form deprivation (P > 0.05). After 3 weeks form deprivation, treated eye had a obvious myopic shift (about -4.27 D) compared to fellow eye, with increased vitreous chamber depth and axial length, however, there was no statistic difference among FD eye, fellow eye and control eye. And after 4 weeks form deprivation, treated eyes were induced significant myopic shift (about -5.22 D) compared with the fellow eye. The difference in refraction of form-deprived and fellow eyes was significantly correlated with the difference in vitreous chamber depth and axial length, which indicate that the induced myopia was mainly axial. The relative myopia shifted rapidly diminished in 4 days after removing the diffuser, followed by a slower recovery. A complete refraction recovery occurred by 7 days after removal of the diffuser compared to the fellow and normal control eyes (P > 0.05). CONCLUSION: Form deprivation myopia can be induced in C57BL/6 mice, but it required longer period than other animals; A complete recovery occurred by 7 days after removal of the diffuser.Optical Coherence Tomography is a useful instrument to measure mouse eye dimension.

Propofol post-conditioning protects the blood brain barrier by decreasing matrix metalloproteinase-9 and aquaporin-4 expression and improves the neurobehavioral outcome in a rat model of focal cerebral ischemia-reperfusion injury.

Propofol, an intravenous anesthetic, inhibits neuronal apoptosis induced by ischemic stroke, protects the brain from ischemia/reperfusion injury and improves neuronal function. However, whether propofol is able to protect the blood brain barrier (BBB) and the underlying mechanisms have remained to be elucidated. In the present study, a rat model of cerebral ischemia/reperfusion was established, using a thread embolism to achieve middle cerebral artery occlusion. Rats were treated with propofol (propofol post-conditioning) or physiological saline (control) administered by intravenous injection 30 min following reperfusion. Twenty-four hours following reperfusion, neurobehavioral manifestations were assessed. The levels of cephaloedema, damage to the BBB and expression levels of matrix metalloproteinase-9 (MMP-9), aquaporin-4 (AQP-4) and phosphorylated c-Jun N-terminal kinase (pJNK) were determined in order to evaluate the effects of propofol on the BBB. In comparison to the cerebral ischemia/reperfusion group, the levels of brain water content and Evans blue content, as well as the expression levels of MMP-9, AQP-4 and pJNK were significantly reduced in the propofol post-conditioning group. These results indicated that propofol post-conditioning improved the neurobehavioral manifestations and attenuated the BBB damage and cephaloedema induced following cerebral ischemia/reperfusion. This effect may be due to the inhibition of MMP-9 and AQP-4 expression, and the concurrent decrease in JNK phosphorylation.

Curcumin exerts antinociceptive effects by inhibiting the activation of astrocytes in spinal dorsal horn and the intracellular extracellular signal-regulated kinase signaling pathway in rat model of chronic constriction injury.

BACKGROUND: Activation of glial cells and the extracellular signal-regulated kinase (ERK) signaling pathway play an important role in the development and maintenance of neuropathic pain. Curcumin can alleviate the symptom of inflammatory pain by inhibiting the production and release of interleukin and tumor necrosis factor. However, whether curcumin affects neuropathic pain induced by nerve injury and the possible mechanism involved are still unknown. This study investigated the effects of tolerable doses of curcumin on the activation of astrocytes and ERK signaling in the spinal dorsal horn in rat model of neuropathic pain. METHODS: Adult male Sprague-Dawley rats were randomly divided into three groups: a control (sham operated) group, and chronic constriction injury groups (to induce neuropathic pain) that were either untreated or treated with curcumin. Thermal and mechanical hyperalgesia thresholds were measured. The distribution and morphological changes of astrocytes were observed by immunofluorescence. Western blotting was used to detect changes in the expression of glial fibrillary acid protein (GFAP) and phosphorylated ERK. RESULTS: Injured rats showed obvious mechanical allodynia and thermal hyperalgesia. The number of GFAP-positive astrocytes, and the fluorescence intensity of GFAP were significantly increased in the spinal dorsal horn of injured compared with control rats. The soma of astrocytes also appeared hypertrophied in injured animals. Expression of GFAP and phosphorylated ERK was also significantly increased in the spinal dorsal horn of injured compared with control rats. Curcumin reduced the injury-induced thermal and mechanical hyperalgesia, the increase in the fluorescence intensity of GFAP and the hypertrophy of astrocytic soma, activation of GFAP and phosphorylation of ERK in the spinal dorsal horn. CONCLUSIONS: Curcumin can markedly alleviate nerve injury-induced neuropathic pain in rats. The analgesic effect of curcumin may be attributed to its inhibition of astrocyte hypertrophy in the spinal dorsal horn and phosphorylation of the ERK signaling pathway.

Laparoscopic cholecystectomy under epidural anesthesia: a retrospective comparison of 100 patients.

There are limited data about laparoscopic cholecystectomy (LC) under epidural anesthesia. This retrospective comparative study aimed to evaluate on the feasibility and advantages of LC under epidural anesthesia. In this retrospective comparative study, 100 patients (46 men and 54 women) with symptomatic cholelithiasis undergoing laparoscopic cholecystectomy using epidural anesthesia (EA) were compared with 100 patients undergoing laparoscopic cholecystectomy using general anesthesia (GA). Both groups were evaluated with regard to intraoperative mean arterial pressure, heart rate, operation time, duration of stay in the recovery room, and hospital cost. Laparoscopic operation was performed for 200 patients. Mean age of patients was 46.4 ± 6.9 years and 45.3 ± 6.8 years in EA and GA, respectively. Forty-six and 50 per cent of subjects were male in EA and GA, respectively. The mean operation time was 24 minutes and 25.58 minutes for EA and GA, respectively (P = 0.652). The duration of stay in the recovery room was significantly shorter in EA than that in GA (19.56 ± 2.55 minutes vs 56.27 ± 6.85 minutes, respectively; P = 0.0001). In the EA group, 23 patients (23%) had severe shoulder pain during surgery. After receiving pethidine intravenously, all these patients could subsequently undergo surgery smoothly. There were no complications or mortality in either group. Most of the patients regarded EA as a comfortable procedure. The mean hospital cost for the EA group was only three-fourths that of the GA group. LC under EA is feasible and safe in selected patients.

Expression changes of parvalbumin and microtubule-associated protein 2 induced by chronic constriction injury in rat dorsal root ganglia.

BACKGROUND: Parvalbumin (PV), as a mobile endogenous calcium buffer, plays an important role in affecting temporospatial characteristics of calcium transients and in modulating calcium homeostasis. PV is expressed in neurons in the dorsal root ganglion (DRG) and spinal dorsal horn and may be involved in synaptic transmission through regulating cytoplasm calcium concentrations. But the exact role of PV in peripheral sensory neurons remains unknown. Microtubule-associated protein 2 (MAP-2), belonging to structural microtubule-associated protein family, is especially vulnerable to acute central nervous system (CNS) injury, and there will be rapid loss of MAP-2 at the injury site. The present study investigated the changes of PV expressing neurons and the MAP-2 neurons in the DRG after an operation for chronic constriction injury to the unilateral sciatic nerve (CCI-SN), in order to demonstrate the possible roles of PV and MAP-2 in transmission and modulation of peripheral nociceptive information. METHODS: Seventy-two adult male Sprague-Dawley (SD) rats, weighing 180 - 220 g, were randomly divided into two groups (36 rats in each group), the sham operation group and chronic constriction injury (CCI) group. Six rats in each group were randomly selected to receive mechanical and thermal sensitivity tests at one day before operation and 1, 3, 5, 7, and 14 days after surgery. After pain behavioral test, ipsilateral lumbar fifth DRGs were removed and double immunofluorescence staining was performed to assess the expression changes of PV and of MAP2 expressing neurons in the L5 DRG before or after surgery. RESULTS: The animals with CCI-SN showed obvious mechanical allodynia and thermal hyperalgesia (P < 0.05). Both the thermal and mechanical hyperalgesia decreased to their lowest degree at 7 days after surgery compared to the baseline before surgery (P < 0.01). In normal rats before surgery, a large number of neurons were MAP-2 single labeled cells, and just a small number of PV-expressed neurons were found. PV-positive neurons, PV-positive nerve fibers and PV-negative neurons, formed a direct or close contact for cross-talk. We used immunocytochemical staining to quantify the time course of changes to PV and MAP-2 expressing neurons in tissue, and found that the number of PV expressing neurons began to slightly decrease at 3 days after surgery, and had a significant reduction at CCI day 5, day 7 (P < 0.05). But MAP-2 neurons significantly decreased on just the 3rd day after CCI (P < 0.05). No changes in PV and MAP-2 expression were almost found in sham operated rats. The number of PV positive neurons, was positively correlated with the hyperalgesia threshold. CONCLUSIONS: A sharp decline in MAP-2 neurons may be the early response to surgical injury, and PV positive neurons were much more effective at affecting the changes of pain behaviors, indicating that the down-regulation of PV protein could participate in, at least in part, the modulation of nociceptive transmission.