SIRT1 expression is associated with poor prognosis of diffuse large B-cell lymphoma

Sirtuin1 (SIRT1) is a nicotinamide adenine dinucleotide-dependent deacetylase. Recently, it is suggested that SIRT1 may be involved in the development of malignant tumors including mouse lymphoma. Therefore, we investigated the prevalence and the prognostic impact of SIRT1 expression in diffuse large B-cell lymphoma (DLBCL). Immunohistochemical expression of SIRT1, p53, bcl2, CD10, bcl6, and multiple myeloma-1 (MUM1) were evaluated by using a 2 mm core from 104 DLBCL patients for tissue microarray. Positive expression of SIRT1 was seen in 74% (77/104) of patients. In total DLBCL patients, SIRT1 and p53 expression were significantly associated with shorter overall survival (OS) by univariate analysis (P=0.001 and P=0.011, respectively). SIRT1 was also an independent prognostic factor by multivariate analysis (P=0.01). According to the expression patterns of CD10, bcl6, and MUM1, germinal center B cell (GCB) types were represented in 38 cases (37%) and non-GCB types were represented in 66 cases (63%). In the GCB type, only p53 expression was associated with a significantly shorter OS (P=0.032). In the non-GCB type, expression of SIRT1 correlated with shorter OS by univariate analyses (P=0.005) and multivariate analyses (P=0.049). In conclusion, we showed that SIRT1 expression is a clinically significant prognostic indicator for DLBCL patients.     

Arthroscopic physeal sparing all inside repair of the tibial avulsion fracture in the anterior cruciate ligament: technical note

We describe a new and effective arthroscopic physeal sparing repair of the tibial eminence avulsion fracture using all an inside repair technique. The treatment of ACL avulsion is controversial, especially in skeletally immature patients, with concerns about physeal damage, and a more reliable way of fixation is still being pursued for small or comminuted fragments. Screw fixation and suture cerclage has some limitations, especially in the small fragment or skeletally immature patients. We fixed avulsion fragment using all inside repair between the distal portion of the ACL and transverse ligament and periosteum. A crescent suture hook loaded with NO. 0 PDS is introduced and the suture hook pierces the transverse intermeniscal ligament and periosteum. The half length of the PDS is now advanced out through the hook and the end is brought out to the anterolateral portal. With the suture hook located intra-articularly and loaded with half the length of the original PDS, the suture hook repierces the transverse intermeniscal ligament at 5 mm on the side and the remaining half length of PDS is now advanced out through the hook and the end is brought out to the anterolateral portal. After that procedure, the suture hook loaded with NO. 0 absorbable Maxon is introduced through the anteromedial portal for the role of shuttle relay. The suture hook pierces the ACL just above the superior border of the avulsion fragment, the Maxon is now advanced out through the hook and the end is brought out to the anterolateral portal. Subsequently, the suture hook is removed and a suture retriever is introduced through the anterolateral portal. PDS and Maxon are held together and retrieved out of the anterolateral portal by the suture retriever at the same time. Our technique has advantages in small comminuted fractures and skeletally immature patients.     

Dysfunction in configural face processing in patients with schizophrenia

BACKGROUND: Face recognition has important implications for patients with schizophrenia, who exhibit poor interpersonal and social skills. Previous reports have suggested that patients with schizophrenia have deficits in their ability to recognize faces, and because face recognition relies heavily on information about the configuration of faces, we hypothesized that patients with schizophrenia would have specific problems in processing configural information. METHODS: We measured the performance of 20 patients with schizophrenia and 20 normal subjects in a face-discrimination task, using upright and inverted pairs of face photographs that differed in featural or configural information. RESULTS: The patients with schizophrenia showed disproportionately poorer performance in discriminating configural compared with featural face sets. CONCLUSION: The result suggests that the face-recognition deficit in schizophrenic patients is due to specific impairments in configural processing of faces.     

STN DBS of Advanced Parkinson's Disease Experienced in a Specialized Monitoring Unit with a Prospective Protocol

Objective

In the evaluation of patients with Parkinson''s disease (PD), most neurologists only see their patients during a limited period of their fluctuating 24-hour-a-day lives. This study aimed to assess the short-term outcome of STN stimulation for patients with advanced PD evaluated in a 24-hour monitoring unit for movement disorder (MUMD) using a prospective protocol.

Methods

Forty-two patients with advanced PD consecutively treated with bilateral STN stimulation using multi-channel microelectrode recording were included in this study. All patients were evaluated using a 24-hour MUMD with a video recording/editing system and were evaluated with a prospective protocol of the Unified Parkinson''s Disease Rating Scale, Hoehn and Yahr Staging, Schwab and England Activities of Daily Living, levodopa equivalent daily dose (LEDD), Short Form-36 Health Survey, and neuropsychological tests. Magnetic resonance (MR) images of the brain were performed prior to and six months after surgery.

Results

All patients were evaluated at three and six months after surgery. There was a rapid and significant improvement of the motor symptoms, especially in tremor and rigidity, after STN stimulation with low morbidity. Dyskinesia was markedly decreased with much lowered LEDD values by 50% after STN stimulation. 1.5T MR images were safely taken according to the manufacturer''s guidelines at six months after surgery without any adverse effects in 41 patients treated with STN stimulations.

Conclusion

Evaluations in a 24-hour monitoring unit could reduce the dose of medication efficiently to an optimal level with patients''comfort and improve the clinical symptoms in harmony with STN stimulation.     

A peroxisome proliferator-activated receptor gamma antagonist induces vimentin cleavage and inhibits invasion in high-grade hepatocellular carcinoma

Increased expression of vimentin in carcinomas correlates with parameters of malignant potential such as tumor grade and tumor metastasis. Peroxisome proliferator-activated receptor gamma (PPARgamma) has been intensively evaluated as a potential target for the inhibition of cell growth and metastasis in cancer cells. In the present study, we examined whether PPARgamma is a possible target molecule for the prevention of cell growth and invasion by treatment with agonists (troglitazone, rosiglitazone) and antagonists (T0070907, GW9662) in four different hepatocellular carcinoma (HCC) cell lines. We also evaluated the effects of the PPARgamma agonists and antagonists on tumor cell migration and invasion. The expression level of PPARgamma protein was higher in the sarcomatoid SH-J1 and poorly differentiated HLE cell lines than that in the well-differentiated HCC cell lines (HepG2 and Huh-7). Expression of vimentin was high in the SH-J1 HCC cell line and minimally detected in the HLE cell line. Treatment with low doses of the PPARgamma antagonists inhibited cell growth and colony formation of all four of the HCC cell lines. Vimentin in the high-grade HCC cells was cleaved by the treatment with the PPARgamma antagonists. Furthermore, treatment with the PPARgamma antagonists also strongly inhibited migration and invasion of the SH-J1 and HLE cells. However, treatment with low doses of the agonists had no effect on vimentin expression, migration, and invasion of the high-grade HCC cells but cell growth was inhibited by treatment with high concentrations of the agonists. Our results indicate that treatment with a PPARgamma antagonist may prevent cell growth and invasion of high-grade HCC cells. Our findings also suggest that PPARgamma antagonists inhibit cell growth and invasion through vimentin disarrangement in high-grade HCC.     

Small-sized liver graft does not increase the risk of hepatocellular carcinoma recurrence after living donor liver transplantation

PURPOSE: Following implantation into adult recipients, living donor liver grafts usually undergo liver regeneration. This regeneration process may provoke the growth of occult hepatocellular carcinoma (HCC) cells in the recipient body. To assess the risk of HCC recurrence, we analyzed the influence of graft-recipient weight ratio (GRWR). METHODS: The 181 recipients with HCC within the University of California at San Francisco (UCSF) criteria were divided into four groups according to GRWR: low GRWR (<0.8; n = 30), mid GRWR (0.8-1.0; n = 65), high GRWR (>1.0; n = 64), and whole liver graft group (>1.5; n = 22). RESULTS: There were no differences in overall patient survival (P = .105) and recurrence-free survival (P = .406) among these four groups. GRWR <0.8 was not a significant risk factor for HCC recurrence. Similar outcomes were obtained in HCC patients who met the Milan criteria (n = 170). CONCLUSIONS: We think that small living donor liver graft and subsequent liver regeneration do not increase the risk of posttransplant HCC recurrence when HCC is within the Milan or UCSF criteria.     

Blood group Lewis alloantibodies cause antibody-mediated rejection in renal transplant recipients

Three patients with negative Lewis phenotypes who displayed anti-Lewis antibodies suffered severe kidney allograft dysfunction. One woman and two men (22-44 years) received ABO compatible kidney transplants with negative donor-recipient cross-match tests. Two patients had the phenotype Le(a-b-) with anti-Le(a) and anti-Le(b) complement binding antibodies. The third patient of phenotype Le(a+b-) developed anti-Lewis(b) antibody a few months after transplantation. One patient presented recurrence of worsened graft function from the day 6 to 4 months after transplantation; despite treatment there was not full recovery. The second patient had recurrences of acute graft dysfunction at 4 and 6 months after transplantation with nephrotic range proteinuria. The third patient showed progressive graft dysfunction at 7 months after transplantation. Biopsy specimens showed histological changes of antibody-mediated rejection. In the third patient, we observed fibrinoid necrosis and thrombosis of arterioles and glomerular capillaries. Immunofluorescence studies showed immunoglobulin IgG and IgM in glomerular capillaries and C4d and C3 on endothelial cells of peritubular capillaries. Posttransplantation cross-match tests with donor lymphocytes were negative. Anti-Lewis antibodies were observed during follow-up. All patients were treated with methylprednisolone boluses. In addition, one subject received antithymocyte globulin (ATG) and 1 received plasmapheresis. Two patients had moderate renal dysfunction (creatinine levels 1.8 and 1.9 mg/dL) after 8-17 months follow-up. The third patient lost her graft at 11 months after transplantation. Lewis antibodies may injure a renal allograft. C4d deposition and failure to show donor-specific anti-HLA antibodies suggested the participation of other antibodies.