Corner Osteotomy as the more Advanced Approach to Deformity Correction in Adult Spinal Deformity: A Retrospective Comparative Study Between Two Osteotomy Techniques.

STUDY DESIGN: A retrospective study. OBJECTIVE: To investigate the usefulness of corner osteotomy (CO) in patients with adult spinal deformity (ASD) by comparing with pedicle subtraction osteotomy (PSO) for lordosis correction. SUMMARY OF BACKGROUND DATA: PSO remains a valuable procedure for patients with ASD, but it has a limit to obtaining correction angles exceeding 45° in patients with a large pelvic incidence or with previous spinal fusion surgeries. Theoretically, CO can exceed the limitation of PSO and can achieve a wide range of correction angles. However, no study has analyzed the clinical data and usefulness of CO. METHODS: This study included 115 patients (mean age 71.1 y, mean follow-up period 78.9 mo) with ASD who underwent deformity correction using PSO or CO. Comparative analysis was performed on spinopelvic parameters including segmental angle (SA) around the osteotomy site, and clinical and surgical assessment between the PSO and corner groups. RESULTS: In the corner group, the postoperative SA (35° vs. -39.3°, P=0.004) and the degree of SA correction (34.8° vs. 39.7°, P=0.004) were greater, and a broader range of SA correction was also possible (18-51° vs. 18-61°). Although the operative time was longer in the corner group (316.8 min vs. 342.3 min, P=0.014), the estimated blood loss (EBL) was lower (2841.3 mL vs. 2465.4 mL, P=0.032). There was no difference in major complication rates, but the frequency of rod fracture (RF) was lower in the corner group (36/27 vs. 1/51, P<0.05). CONCLUSION: CO showed a greater SA correction and achieved a broader range of SA correction angles than PSO with no difference in the incidence of major complications. In addition, the EBL and the frequency of RF were lower. Based on these results, we expect that CO can serve as a promising surgical alternative to PSO for spinal deformity correction among patients with ASD.

Rostral Agranular Insular Cortex Lesion with Motor Cortex Stimulation Enhances Pain Modulation Effect on Neuropathic Pain Model.

It is well known that the insular cortex is involved in the processing of painful input. The aim of this study was to evaluate the pain modulation role of the insular cortex during motor cortex stimulation (MCS). After inducing neuropathic pain (NP) rat models by the spared nerve injury method, we made a lesion on the rostral agranular insular cortex (RAIC) unilaterally and compared behaviorally determined pain threshold and latency in 2 groups: Group A (NP + MCS; n = 7) and Group B (NP + RAIC lesion + MCS; n = 7). Also, we simultaneously recorded neuronal activity (NP; n = 9) in the thalamus of the ventral posterolateral nucleus and RAIC to evaluate electrophysiological changes from MCS. The pain threshold and tolerance latency increased in Group A with "MCS on" and in Group B with or without "MCS on." Moreover, its increase in Group B with "MCS on" was more than that of Group B without MCS or of Group A, suggesting that MCS and RAIC lesioning are involved in pain modulation. Compared with the "MCS off" condition, the "MCS on" induced significant threshold changes in an electrophysiological study. Our data suggest that the RAIC has its own pain modulation effect, which is influenced by MCS.

Motor cortex stimulation and neuropathic pain: how does motor cortex stimulation affect pain-signaling pathways?

OBJECTIVE: Neuropathic pain is often severe. Motor cortex stimulation (MCS) is used for alleviating neuropathic pain, but the mechanism of action is still unclear. This study aimed to understand the mechanism of action of MCS by investigating pain-signaling pathways, with the expectation that MCS would regulate both descending and ascending pathways. METHODS: Neuropathic pain was induced in Sprague-Dawley rats. Surface electrodes for MCS were implanted in the rats. Tactile allodynia was measured by behavioral testing to determine the effect of MCS. For the pathway study, immunohistochemistry was performed to investigate changes in c-fos and serotonin expression; micro-positron emission tomography (mPET) scanning was performed to investigate changes of glucose uptake; and extracellular electrophysiological recordings were performed to demonstrate brain activity. RESULTS: MCS was found to modulate c-fos and serotonin expression. In the mPET study, altered brain activity was observed in the striatum, thalamic area, and cerebellum. In the electrophysiological study, neuronal activity was increased by mechanical stimulation and suppressed by MCS. After elimination of artifacts, neuronal activity was demonstrated in the ventral posterolateral nucleus (VPL) during electrical stimulation. This neuronal activity was effectively suppressed by MCS. CONCLUSIONS: This study demonstrated that MCS effectively attenuated neuropathic pain. MCS modulated ascending and descending pain pathways. It regulated neuropathic pain by affecting the striatum, periaqueductal gray, cerebellum, and thalamic area, which are thought to regulate the descending pathway. MCS also appeared to suppress activation of the VPL, which is part of the ascending pathway.

The role of chronic inflammation in the development of gastrointestinal cancers: reviewing cancer prevention with natural anti-inflammatory intervention.

Inflammatory mediators alter the local environment of tumors, known as the tumor microenvironment. Mechanistically, chronic inflammation induces DNA damage, but understanding this hazard may help in the search for new chemopreventive agents for gastrointestinal (GI) cancer which attenuate inflammation. In the clinic, GI cancer still remains a major cause of cancer-associated mortality, chemoprevention with anti-inflammatory agents is thought to be a realistic approach to reduce GI cancer. Proton pump inhibitors, monoclonal antibodies targeting tumor necrosis factor-alpha, anti-sense targeted smad7 and non-steroidal anti-inflammatory agents have been investigated for their potential to prevent inflammation-based GI cancer. Besides these, a wide variety of natural products have also shown potential for the prevention of GI cancer. In this review, the authors will provide insights to explain the mechanistic connection between inflammation and GI cancer, as well as describe a feasible cancer prevention strategy based on anti-inflammatory treatments.

Longitudinal FDG microPET imaging of neuropathic pain: does cerebellar activity correlate with neuropathic pain development in a rat model?

BACKGROUND: We used [F-18] FDG microPET imaging as part of a longitudinal study to investigate changes in the brain. METHODS: Glucose metabolism during the development of neuropathic pain after tibial and sural nerve transection (TST) model rats. MicroPET images were obtained 1 week before operation and then weekly for 8 weeks post-operation. RESULTS: The behavioral test was performed immediately after the every FDG administration. After TST modeling, neuropathic pain rats showed increased mechanical sensitivity of the injured hind paw. The withdrawal response to mechanical pain stimulation by von Frey filaments was observed within the first week (3.8 ± 0.73), and it rapidly increased in the third week (7.13 ± 0.82). This response reached a peak in the fourth week after surgery (9.0 ± 0.53), which persisted until the eighth week. In microPET scan imaging, cerebellum, which initially started from the ansiform lobule, was activated gradually to all part from the third week in all image acquisitions through the eighth week. CONCLUSIONS: The longitudinal microPET scan study of brains from neuropathic pain rat models showed sequential cerebellar activity that was in accordance with results from behavioral test responses, thus supporting a role for the cerebellum in the development of neuropathic pain.

Protective effect of Bojungbangdocktang on cisplatin-induced cytotoxicity and apoptosis in MCF-10A breast endothelial cells.

Although cisplatin has been extensively used as a cancer chemotherapeutic agent for the treatment of various human cancers, it causes significant side effects such as nephrotoxicity and hepatotoxicity due to lethal bystander damage to normal cells. Thus, in the current study, we investigated the Oriental herbal medicine Bojungbangdocktang (BJBDT), as we reported previously its anti-angiogenic activity at nontoxic concentrations that could prevent cisplatin-induced toxicity and apoptosis in human normal breast epithelial cell MCF-10A, but not in MCF-7 and MDA MB-231 breast cancer cells. BJBDT protected cisplatin-induced cytotoxicity in MCF-10A cells and potentiated cytotoxicity and MMP loss in MCF-7 cells. Also, 4',6-diamidino-2-phenylindole (DAPI) staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay revealed that BJBDT reduced cisplatin-induced apoptotic bodies in MCF-10A cells compared with cisplatin-treated control. Consistently, BJBDT attenuated the apoptotic portion sub-G1 DNA contents as well as blocked the activation of caspase-3 and -9 and poly(ADP-ribose)polymerase (PARP) cleavage in cisplatin-treated MCF-10A cells. Taken together, our findings suggest that BJBDT can protect cisplatin-induced cytotoxicity and apoptosis in normal MCF-10A breast cells as a cancer chemopreventive agent.

Comparison of posterior capsule opacification in rabbits receiving either mitomycin-C or distilled water for sealed-capsule irrigation during cataract surgery.

PURPOSE: To compare posterior capsule opacification (PCO) in rabbits who undergo cataract surgery and receive either mitomycin-C (MMC) or distilled water (DW) during sealed-capsule irrigation (SCI). In addition, we examined the toxicity of DW and MMC. METHODS: Twenty-four eyes from 12 rabbits were divided into three groups. Balanced salt solution (BSS), DW, MMC 0.4 mg/mL was injected into the capsular bag for 2 min after endocapsular phacoemulsification and insertion of a SCI device. The degree of PCO was assessed by POCOman software at 3 months post surgery. Central corneal thickness, anterior chamber inflammation were assessed 1 day, 1 week, 2 weeks, 3 weeks, 1 month and 3 months postoperatively. RESULTS: A statistically significant difference in PCO scores was noted between the control and study groups (P < 0.05). The PCO scores of the MMC group were significantly lower than those of the DW group (P < 0.05). The MMC and DW groups did not show significant toxicity compared with the BSS group. CONCLUSIONS: MMC is more effective in reducing PCO than DW; the SCI device can protect the surrounding ocular tissue from MMC toxicity in rabbit eyes.

Caspase activation and extracellular signal-regulated kinase/Akt inhibition were involved in luteolin-induced apoptosis in Lewis lung carcinoma cells.

Luteolin was isolated from Scutellaria barbata D. Don (S. barbata). In the present study, we examined the underlying molecular mechanism of luteolin and its effect on in vivo tumor growth of Lewis lung carcinoma (LLC) cells. Luteolin exhibited antiproliferative activity against LLC cells with IC50 of 12 microM. Luteolin effectively increased Annexin-V-positive cells as well as sub G1 DNA portion as seen on flow cytometric analysis. Western blotting has revealed that luteolin effectively activates caspase 9 and 3, cleaves poly (ADP-ribose) polymerase (PARP), and increases the ratio of Bax/Bcl-2. Furthermore, mitochondrial membrane potential was reduced by luteolin as seen on fluorescence microscopy. Luteolin downregulated the expression of extracellular signal-regulated kinase (ERK) and Akt in a concentration-dependent manner. In addition, luteolin significantly inhibited the growth of LLC cells implanted on the flank of mice to 40% and 60% of untreated control group values at 2 mg/kg and 10 mg/kg, respectively. Similarly, luteolin significantly reduced the expression of proliferating cell nuclear antigen (PCNA) as well as increased the expression of terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) in tumor section of LLC-bearing mice as determined by immunohistochemistry. Taken together, these results suggest that luteolin exerts antitumor activity by caspase activation and ERK/Akt inhibition.

Nasal augmentation using injectable alginate and mesenchymal stem cells in the rabbit.

BACKGROUND: The goal of this study was to evaluate the use of the autogenous mesenchymal stem cells (MSCs) impregnated in an injectable alginate gel containing platelet-rich plasma (PRP) for nasal augmentation in rabbit model. METHODS: Bone marrow-derived MSCs were isolated and expanded from New Zealand white rabbits. At confluence, the cells were mixed with sodium alginate solution. PRP was prepared from the rabbits and it was immediately mixed into the alginate-cell mixture. The cell-PRP-alginate mix was injected into a subcutaneous nasal area. Eight weeks after injection changes in facial contour, newly formed nasal hump was analyzed and the amount of chondroitin sulfate in tissue was measured. RESULTS: Augmented nasal dorsa maintained their original shape until harvest. Immunohistochemical staining revealed that the deposited matrix was composed of type II collagen and that it was distributed abundantly and widely in the connective tissue of the tissue generated. The amount of chondroitin sulfate (main component of the proteoglycan in cartilage) produced was significantly higher when MSCs and PRP-alginate were used. CONCLUSION: Injectable PRP-alginate gel containing autologous mesenchymal stem cells may offer a useful means of facial soft tissue augmentation.

Caspase activation and extracellular signal-regulated kinase/Akt inhibition were involved in luteolin-induced apoptosis in Lewis lung carcinoma cells.

Luteolin was isolated from Scutellaria barbata D. Don (S. barbata). In the present study, we examined the underlying molecular mechanism of luteolin and its effect on in vivo tumor growth of Lewis lung carcinoma (LLC) cells. Luteolin exhibited antiproliferative activity against LLC cells with IC50 of 12 microM. Luteolin effectively increased Annexin-V-positive cells as well as sub G1 DNA portion as seen on flow cytometric analysis. Western blotting has revealed that luteolin effectively activates caspase 9 and 3, cleaves poly (ADP-ribose) polymerase (PARP), and increases the ratio of Bax/Bcl-2. Furthermore, mitochondrial membrane potential was reduced by luteolin as seen on fluorescence microscopy. Luteolin downregulated the expression of extracellular signal-regulated kinase (ERK) and Akt in a concentration-dependent manner. In addition, luteolin significantly inhibited the growth of LLC cells implanted on the flank of mice to 40% and 60% of untreated control group values at 2 mg/kg and 10 mg/kg, respectively. Similarly, luteolin significantly reduced the expression of proliferating cell nuclear antigen (PCNA) as well as increased the expression of terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) in tumor section of LLC-bearing mice as determined by immunohistochemistry. Taken together, these results suggest that luteolin exerts antitumor activity by caspase activation and ERK/Akt inhibition.

The effect of capsular tension ring on posterior capsular opacity in cataract surgery.

This study was performed to evaluate the efficacy and safety of the capsular tension ring on posterior capsular opacity in comparison with cases undergoing intraocular lens (IOL) implantation alone. We analyzed 127 eyes which had undergone cataract surgery, including capsular tension ring insertion, along with 127 eyes which had undergone IOL implantation alone by the same surgeon from September 1998 to March 2003. In the insertion group, 41 eyes (group A) had been followed up for more than one year after silicone IOL implantation, as had 40 eyes (group B) in the control group. We compared the incidence, type, and degree of capsular opacity between A and B groups and also endothelial cell loss after surgery between the two groups. For insertion group A, the frequency of posterior capsular opacity was lower(7.3%), the duration to development was longer, and the energy required for Nd-Yag capsulotomy of PCO was less than for control group B (25%) (p=0.037). The endothelial cell count loss rate was not significantly different between the two groups (p=0.522). The capsular tension ring is associated with a significantly reduced incidence of posterior capsular opacity and is a safe procedure.

Methylene chloride fraction of Spatholobi Caulis induces apoptosis via caspase dependent pathway in U937 cells.

Spatholobi Caulis has been used in Oriental medicine to treat cancer and blood stasis. In this study, the methylene chloride fraction of Spatholobi Caulis (MCSC) was examined to determine if it possesses anti-cancer activity via its apoptosis-inducing activity. MCSC exhibited a strong cytotoxic effect against human monocyte leukemia U937 cells (IC(50)=15.1 microg/ml). A TUNEL assay showed that the MCSC caused a characteristic ladder pattern of discontinuous DNA fragments and apoptotic bodies. Flow cytometric analysis confirmed that MCSC significantly increases the number of apoptotic cells stained by annexin V(+)/PI(-) cells. Western blotting revealed that MCSC activated caspase-3 expression and cleaved poly (ADP-ribose) polymerase (PARP) in a concentration-dependent manner. An enzyme-linked immunosorbent assay (ELISA) demonstrated that MCSC significantly activated the caspase-3 activity compared with the untreated control by. Taken together, these results suggest that MCSC can induce apoptosis in U937cells via the caspase dependent pathway.