Correlation between tuberous sclerosis complex 2 and glycogen synthase kinase 3 beta levels, and outcomes of patients with hepatocellular carcinoma treated by hepatectomy.

AIM: Tuberous sclerosis complex 2 (TSC2), a tumor suppressor, may play an essential role in the regulation of cell growth and cell survival under energy stress conditions. In addition, TSC2 may act in concert with Wnt and energy signals by additional phosphorylation of glycogen synthase kinase 3ß (GSK3ß) to regulate cell growth. The expression levels and function of TSC2 and GSK3ß in hepatocellular carcinoma (HCC) remain unclear. METHODS: The protein levels of TSC2 and GSK3ß were measured by immunohistochemistry in normal liver (n = 20), HCC (n = 80) and pericancerous tissues (n = 80). The correlations between TSC2, and GSK3ß levels, clinicopathological features and patient survival were also analyzed. RESULTS: The protein levels of TSC2 and GSK3ß in HCC tissues were significantly lower than that in normal liver tissues and pericancerous tissues (P < 0.05). Decreased TSC2 and GSK3ß expression was found to be significantly correlated with advanced clinicopathological characteristics and poor prognosis. The results also showed that TSC2 protein levels were associated with GSK3ß expression in HCC specimens. CONCLUSION: This is the first demonstration that the decreases in TSC2 and GSK3ß levels may be associated with vascular invasion, histological grade and tumor-node-metastasis classification.

[Bacterial 16S rRNA genes and expression of IL-1ß, TNF-α and IgA in prostate tissues].

OBJECTIVE: To investigate the role of bacteria in the etiology of chronic prostatitis. METHODS: Complete prostate specimens were obtained at autopsy from 192 organ donors (aged 20 - 38 years old) during 2002 to 2008 who died of non-prostatic diseases. One tissue taken from the peripheral prostatic zone according to McNeal was divided into two pieces. One piece of tissue was taken for routine pathological examinations and immunohistochemical studies of interleukin (IL)-1ß, tumor necrosis factor-α (TNF-α) and IgA. Another one was taken for PCR assay to detect the bacterial 16S rRNA genes (16S rDNA). RESULTS: Of 192 prostate specimens, 64 (33.3%) had pathological changes of chronic prostatitis and 38 (19.8%) specimens was positive for bacterial 16S rDNA. Positive rates of 16S rDNA in chronic prostatitis and non-prostatitis specimens were 50.0% (32/64) and 4.6% (6/128) respectively (χ(2) = 55.185, P < 0.001). Expressions of IL-1ß, TNF-α and IgA in specimens of chronic prostatitis were significantly higher than those in non-prostatitis specimens (P < 0.001). A positive correlation could be found among three immunohistochemical indicators (P < 0.01). In 64 specimens with chronic prostatitis, a significant expression of IL-1ß, TNF-α and IgA was more often demonstrated in 16S rDNA positive group than in 16S rDNA negative group (P < 0.001). CONCLUSIONS: The up-regulations of bacterial 16S rDNA, cytokines and immunoglobulin A are involved in inflammatory response of chronic prostatitis. Bacterial infection may be an important cause of chronic prostatitis.

[Expressions of bacterial 16S rRNA, IL-1beta, TNF-alpha and NGF in prostate tissues].

OBJECTIVE: To investigate the role of bacteria in the etiology of chronic prostatitis. METHODS: A total of 162 complete prostate specimens were obtained at autopsy from organ donors (aged 20 -38 yr) who died of non-prostatic diseases. Each of the samples from the peripheral zone of the prostate was divided into two parts, one for routine pathological examination and immunohistochemical studies of interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha) and the nerve growth factor (NGF), and the other for PCR assay to detect the bacterial 16S rRNA gene (16S rDNA). RESULTS: Fifty-one (31.5%) of the total specimens presented pathological changes of chronic prostatitis, of which 44 had mild focal stromal, 5 mild focal stromal and periglandular and 2 mild focal periglandular inflammation. The positive rate of 16S rDNA was 19.1% (31/162), 51.0% (26/51) in the chronic prostatitis and 4.5% (5/111) in the non-prostatitis specimens (chi2 = 29.783, P < 0.01). In the specimens with chronic prostatitis, the expressions of IL-1beta, TNF-alpha and NGF were significantly higher in the 16S rDNA positive than in the 16S rDNA negative group (P < 0.01). CONCLUSION: Bacterial inflammation may play an important role in the etiology of chronic prostatitis.

[Detection of 16S ribosomal RNA gene of bacteria in prostate tissues of adults].

OBJECTIVE: To investigate the role of bacteria in chronic prostatitis. METHODS: Complete specimens of prostate were obtained from 140 organ donors, aged 20 - 35, at autopsy. A piece of tissue was collected from the peripheral zone of prostate from each specimen and was divided into 2 parts to undergo pathological examination and PCR so as to detect the 16S ribosomal RNA (16S rRNA) gene of bacteria. RESULTS: Focal mild inflammation was shown in 46 of the 104 specimens (32.9%), including interstitial inflammation in 42 specimens, inflammation in both interstitial and body of gland in 3 specimens, and perigladulitis in 1 specimen. Twenty-seven of the 140 specimens (19.3%) were positive in 16S rRNA gene. The positive rate of 16S rRNA gene of the specimens with prostatitis was 48.9%, significantly higher than that of the specimens without prostatitis (5.3%, P < 0.001). CONCLUSION: Bacteria may play an important role in the pathogenesis of chronic prostatitis.