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1.
PLoS One ; 9(5): e92784, 2014.
Article in English | MEDLINE | ID: mdl-24824520

ABSTRACT

BACKGROUND AND AIM: The optimal treatment for huge unresectable hepatocellular carcinoma (HCC) remains controversial. The outcome of transcatheter arterial chemoembolization (TACE) for patients huge unresectable HCC is generally poor and the survival benefit of TACE in these patients is unclear. The aim of the study is to compare the effect of hepatic arterial infusion chemotherapy (HAIC) versus symptomatic treatment in patients with huge unresectable HCC. METHODS: Since 2000 to 2005, patients with huge (size >8 cm) unresectable HCC were enrolled. Fifty-eight patients received HAIC and 44 patients received symptomatic treatment. In the HAIC group, each patient received 2.4+1.4 (range: 1-6) courses of HAIC. Baseline characteristics and survival were compared between the HAIC and symptomatic treatment groups. RESULTS: The HAIC group and the symptomatic treatment group were similar in baseline characteristics and tumor stages. The overall survival rates at one and two years were 29% and 14% in the HAIC group and 7% and 5% in the symptomatic treatment group, respectively. The patients in the HAIC group had significantly better overall survival than the symptomatic treatment group (P<0.001). Multivariate analysis revealed that HAIC was the significant factor associated with the overall survival (relative risk: 0.321, 95% confidence interval: 0.200-0.515, P<0.001). None of the patients died due to immediate complications of HAIC. CONCLUSIONS: HAIC is a safe procedure and provides better survival than symptomatic treatment in patients with huge unresectable HCC.


Subject(s)
Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Carcinoma, Hepatocellular/drug therapy , Liver Neoplasms/drug therapy , Aged , Aged, 80 and over , Antineoplastic Combined Chemotherapy Protocols/administration & dosage , Carcinoma, Hepatocellular/mortality , Carcinoma, Hepatocellular/pathology , Cisplatin/administration & dosage , Cisplatin/therapeutic use , Female , Fluorouracil/administration & dosage , Fluorouracil/therapeutic use , Hepatic Artery , Humans , Infusions, Intra-Arterial , Liver Neoplasms/mortality , Liver Neoplasms/pathology , Male , Middle Aged , Mitomycin/administration & dosage , Mitomycin/therapeutic use , Prognosis , Survival Rate , Treatment Outcome
2.
J Rehabil Med ; 41(1): 26-31, 2009 Jan.
Article in English | MEDLINE | ID: mdl-19197565

ABSTRACT

OBJECTIVE: To investigate the electrophysiological prevalence and associated risk factors of upper extremity entrapment neuropathies in a cohort of Taiwanese patients with prior paralytic poliomyelitis. DESIGN: Cross-sectional study involving a consecutive series of patients. SUBJECTS: Ninety-seven polio survivors. METHODS: Demographic factors, medical and work history were recorded. Symptoms and functional deficits of the hand, mobility impairment level, physical activity level and manual muscle testing were assessed, and nerve conduction studies were performed. RESULTS: The electrophysiological prevalence of nerve entrapment among the polio survivors was 80%. The most common electrodiagnostic dysfunction was median neuropathy at the wrist (62%), followed by ulnar neuropathy at the elbow (41%) and ulnar neuropathy at the wrist (38%). In multiple logistic regression, subjects who reported that their jobs involved repetitive hand movements, had a body mass index greater than 24 kg/m2, or used a cane/crutch were at increased risk of both median neuropathy at the wrist and ulnar neuropathy at the wrist. Subjects who used a wheelchair were also at increased risk of ulnar neuropathy at the wrist. CONCLUSION: These results indicate a high occurrence of upper extremity entrapment neuropathies in polio survivors. The documentation of risk factors in this study provides support for screening of at-risk subjects.


Subject(s)
Carpal Tunnel Syndrome/etiology , Postpoliomyelitis Syndrome/complications , Ulnar Nerve Compression Syndromes/etiology , Adult , Aged , Carpal Tunnel Syndrome/epidemiology , Carpal Tunnel Syndrome/physiopathology , Cohort Studies , Cross-Sectional Studies , Female , Humans , Male , Middle Aged , Mobility Limitation , Motor Activity/physiology , Postpoliomyelitis Syndrome/physiopathology , Postpoliomyelitis Syndrome/rehabilitation , Prevalence , Risk Factors , Taiwan/epidemiology , Ulnar Nerve Compression Syndromes/epidemiology , Ulnar Nerve Compression Syndromes/physiopathology
3.
Life Sci ; 81(4): 288-98, 2007 Jul 04.
Article in English | MEDLINE | ID: mdl-17612572

ABSTRACT

Traumatic brain injury (TBI) triggers a complex sequence of inflammatory responses that contribute to secondary injury. Statins have demonstrated neuroprotective effects against brain injury, but the underlying mechanisms remain unclear. This study evaluated the effects of lovastatin on a rat model of controlled cortical impact (CCI) injury. Our two hypotheses were that pre-administration of lovastatin would reduce functional deficits and extent of anatomical brain damage and that lovastatin would attenuate levels of pro-inflammatory cytokines. Rats were injected with lovastatin (4 mg/kg) or vehicle for 5 days and subjected to CCI. Neurological status was evaluated using rotarod and adhesive removal tests. Contusion volume and neuronal degeneration were examined using cresyl violet and FluoroJade B (FJB) histochemistry. Levels of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA and protein were assessed by real-time quantitative reverse transcriptase polymerase chain reaction, enzyme-linked immunosorbent assay, and immunohistochemistry. Lovastatin significantly improved performance on both the rotarod and adhesive removal tests before post-injury day 7. Lovastatin also significantly reduced contusion volume (20%) and number of FJB-positive degenerating neurons (35%) at 4 days. These changes were associated with a significant decrease in levels of TNF-alpha and IL-1beta mRNA and protein at the contusion site at 6 h and 4 days, respectively. Our results show that pre-administration of lovastatin improved functional outcomes and reduced extent of brain damage, with a concomitant decrease in tissue levels of TNF-alpha and IL-1beta mRNA and protein. These findings suggest that lovastatin's protective mechanisms may be partly attributed to a dampening of the inflammatory response.


Subject(s)
Brain Injuries/drug therapy , Cytokines/biosynthesis , Encephalitis/prevention & control , Gene Expression Regulation/drug effects , Inflammation/prevention & control , Lovastatin/pharmacology , Animals , Brain Injuries/complications , Brain Injuries/physiopathology , Cytokines/genetics , Disease Models, Animal , Encephalitis/etiology , Encephalitis/physiopathology , Gene Expression Regulation/genetics , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/pharmacology , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Immunohistochemistry , Inflammation/etiology , Inflammation/physiopathology , Interleukin-1beta/biosynthesis , Interleukin-1beta/genetics , Lovastatin/therapeutic use , Male , Neurons/metabolism , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , RNA, Messenger/isolation & purification , Rats , Rats, Sprague-Dawley , Reaction Time/drug effects , Reaction Time/genetics , Reverse Transcriptase Polymerase Chain Reaction , Rotarod Performance Test , Treatment Outcome , Tumor Necrosis Factor-alpha/biosynthesis , Tumor Necrosis Factor-alpha/genetics
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