Rare case of brucellosis misdiagnosed as prostate carcinoma with lumbar vertebra metastasis: A case report.

BACKGROUND: Prostatitis caused by Brucella infection is rare and usually lacks typical lower urinary tract symptoms. However, Brucella infection can cause serum prostate-specific antigen levels to become abnormally elevated. When concurrent with lumbar vertebra infection and erosion, brucellosis can easily be misdiagnosed as prostate cancer with bone metastasis. CASE SUMMARY: A 45-year-old man complained of recurrent low back pain and fever for 2 wk. Magnetic resonance imaging of the lumbar vertebrae showed abnormal signs at the rear of the L4-5 vertebral body. Serum prostate-specific antigen level was 17.64 ng/mL, and positron emission tomography/computed tomography suggested the possibility of prostate cancer with liver and lumbar metastases. The patient was transferred to our department for further treatment. He experienced repeated bouts of fever and low back pain during hospitalization. Biopsy results indicated prostatitis. There was no significant increase in white blood cell count or procalcitonin levels. The Mycobacterium tuberculosis smear and antibody detection results were negative. Cefoperazone sulbactam was not effective. Blood culture test results were positive for brucellosis, confirming the diagnosis of brucellosis. After oral anti-infection treatment with doxycycline and rifampicin, the body temperature gradually returned to normal, and lumbago improved. After continuous treatment for 6 mo, the patient recovered. CONCLUSION: In patients with low back pain and fever accompanied by elevated prostate-specific antigen levels and lesions of the prostate and lumbar spine, a detailed medical history and blood and urine cultures should be obtained, and attention should be given to the local epidemic infectious disease situation.

The platelet-derived growth factor receptor/STAT3 signaling pathway regulates the phenotypic transition of corpus cavernosum smooth muscle in rats.

Erectile dysfunction (ED) is a common clinical disease that is difficult to treat. We previously found that hypoxia modulates the phenotype of primary corpus cavernosum smooth muscle cells (CCSMCs) in rats, but the underlying molecular mechanism is still unknown. Platelet-derived growth factor receptor (PDGFR)-related signaling pathways are correlated with cell phenotypic transition, but research has been focused more on vascular smooth muscle and tracheal smooth muscle and less on CCSMCs. Here, we investigated the role of PDGFR-related signaling pathways in penile CCSMCs, which were successfully isolated from rats and cultured in vitro. PDGF-BB at 5, 10, or 20 ng/ml altered CCSMC morphology from the original elongated, spindle shape to a broader shape and promoted the synthetic phenotype and expression of the related proteins vimentin and collagen-I, while inhibiting the contractile phenotype and expression of the related proteins smooth muscle (SM) α-actin (α-SMA) and desmin. Inhibition of PDGFR activity via siRNA or the PDGFR inhibitor crenolanib inhibited vimentin and collagen-I expression, increased α-SMA and desmin expression, and considerably inhibited serine-threonine protein kinase (AKT) and signal transducer and activator of transcription 3 (STAT3) phosphorylation. STAT3 knockdown promoted the contractile phenotype, inhibited vimentin and collagen-I expression, and increased α-SMA and desmin expression, whereas AKT knockdown did not affect phenotype-associated proteins. STAT3 overexpression in CCSMC cells weakened the suppressive effect of PDGFR inhibition on the morphology and phenotypic transformation induced by PDGF-BB. Through activation of the PDGFR/STAT3 signaling pathway, PDGF promoted the synthetic phenotype transition; thus, regulation of this pathway might contribute to ED therapy.

Bufalin inhibits pancreatic cancer by inducing cell cycle arrest via the c-Myc/NF-κB pathway.

ETHNOPHARMACOLOGICAL RELEVANCE: Bufalin, a cardiotonic steroid isolated from toad venom (bufo gargarizans Cantor or B. melanotictus Schneider), has widely demonstrated antitumor effects and exhibits potential antitumor activity in various human cancer cells lines. AIMS OF THE STUDY: The main characteristic of cancers including pancreatic cancer is the ability of uncontrolled proliferation. The aim of this study is to clarify the underlying mechanism by which bufalin inhibits pancreatic cancer cell proliferation. MATERIALS AND METHODS: The effect of bufalin on the suppression of tumor growth in vivo was studied in a bioluminescent mouse model generated using the pancreatic cancer cell line BxPC3-luc2 and the cytotoxicity was evaluated in BcPc3 and Sw1990 cells with MTT. Flow cytometry and western blotting analyses were utilized to detect the effect of bufalin on the cell cycle and to detect the cell cycle-related proteins, respectively. Then, a luciferase reporter assay was applied to screen the activity of potent transcription factors following bufalin exposure and their expression was detected by western blotting. RESULTS: Bufalin suppressed tumor growth in a bioluminescence mouse model generated using BxPC3-luc2 cells and inhibited cell proliferation in vitro through inducing cell cycle arrest at S phase. Bufalin treatment inhibited cyclin D1 and cyclin E1 expression and therefore increased expression of p27, a regulatory molecular that controls cell cycle transition from S to G2 phase. Furthermore, luciferase reporter screening studies revealed that bufalin inhibited the expression and activity of the transcription factors c-Myc and NF-κB, which might cause cell cycle arrest at S phase and the inhibition of cell proliferation. CONCLUSIONS: Taken together, our results indicate that bufalin can inhibit pancreatic cancer by targeting c-Myc, thus suggesting that the mechanism of c-Myc regulation by bufalin might be worthy of further study regarding its potential as a therapeutic target for pancreatic cancer treatment.