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Background Adrenocortical carcinoma (ACC) is a rare malignant epithelial tumor originating from adrenocortical cells that carries a very poor prognosis. Metastatic or inoperable diseases are often considered incurable, and treatment remains a challenge. Especially for advanced cases such as ACC complicated with renal venous cancer thrombus, there are few cumulative cases in the literature. Case summary The patient in this case was a 39-year-old middle-aged male who was admitted to the hospital for more than half a month due to dizziness and chest tightness. Computed tomography (CT) findings after admission revealed a left retroperitoneal malignant space-occupying lesion, but the origin of the formation of the left renal vein cancer thrombus remained to be determined. It was speculated that it originated from the left adrenal gland, perhaps a retroperitoneal source, and left adrenal mass + left nephrectomy + left renal vein tumor thrombus removal + angioplasty were performed under general anesthesia. Postoperative pathology results indicated a diagnosis of ACC. Postoperative steroid therapy was administered. At 3 mo after surgery, abdominal CT reexamination revealed multiple enlarged retroperitoneal lymph nodes and multiple low-density shadows in the liver, and palliative radiotherapy and mitotane were administered, considering the possibility of metastasis. The patient is currently being followed up. Conclusion ACC is a highly malignant tumor. Even if the tumor is removed surgically, there is still the possibility of recurrence. Postoperative mitotane and adjuvant chemoradiotherapy have certain benefits for patients, but they cannot fully offset the poor prognosis of this disease.

The aim of this study was to investigate the protective roles of H2S on acute renal damage in urinary-derived sepsis. Totally 40 male rabbits were randomly divided into the Control, Sham, Sepsis, NaHS and the dl-propargylglycine (PAG) groups. White blood cell counts (WBC), C-reactive protein (CRP), creatinine (Cr) and blood urea nitrogen were determined in peripheral blood samples. Hematoxylin and eosin staining was performed to detect the morphological changes. The mRNA and protein expression levels were detected by semi-quantitative reverse transcriptase PCR (sqRT-PCR) and Western blot analysis. The results showed that, 72 h after surgery, the WBC and CRP levels in the Sepsis group were significantly elevated, and the expression levels of inducible nitric oxide synthase (iNOS) and HO-1 were significantly up-regulated, compared with the Control and Sham groups, indicating renal damage induced by urinary-derived sepsis. Compared with the Sepsis group, the expression levels of iNOS in the renal tissues of the PAG group were significantly up-regulated, whereas the expression levels of HO-1 in the renal tissue were significantly down-regulated, indicating aggravated renal damage. On the other hand, compared with the Sepsis group, the expression levels of iNOS in the renal tissue of the NaHS group were declined, whereas the expression levels of HO-1 were elevated, together with the declined WBC and CRP levels, indicating alleviated renal functions. We could conclude that iNOS and HO-1 expression levels are elevated in the renal tissue of urinary-derived sepsis. H2S could exert protective effects on the urinary-derived sepsis-associated renal damages by down-regulating iNOS expression and up-regulating HO-1 expression.

The aim of the present study was to investigate the effects of endogenous H2S on the inflammatory response in kidneys following urine-derived sepsis-induced injury. A rabbit model of urine-derived sepsis was established by injecting Escherichia coli into the ligated ureter. Rabbits were randomly divided into the, control, sham, sepsis and DL-propargylglycine (PAG)-treated sepsis groups. The same surgical procedure except for the bacteria injection was performed for the sham group, while the control group was fed on normal diet without any additional treatments. The monitoring of vital signs, routine blood examinations and kidney function tests were performed prior to surgery and at 12, 24, 36 and 48 h following surgery. The serum H2S concentration and kidney cystathionine-γ-lyase (CSE) activity were determined following surgery. Pathological alterations were assessed by hematoxylin and eosin (H&E) staining, and the expression levels of inflammation-associated cytokines were detected by western blot analysis. The results demonstrated that rabbits in the sepsis and PAG groups exhibited a significant increase in rectal temperature, heart rate and respiratory rate following surgery when compared with the sham group; with the PAG group demonstrating the greatest increase. In addition, white cell counts and creatinine and urea nitrogen levels were significantly elevated following surgery in the sepsis and PAG groups when compared with the sham group. The serum H2S concentration and kidney CSE activity were significantly reduced in the sepsis group compared with the sham group, and a significant decrease in the levels of these factors were observed in the PAG group compared with the sepsis group. H&E staining indicated obvious structural abnormalities in kidney tissues in the sepsis group, which were exacerbated by PAG treatment. In addition, PAG treatment significantly increased the expression levels of nuclear factor-κB and interleukin-6, and decreased transforming growth factor-β1 expression when compared with the sepsis group. In conclusion, PAG significantly exacerbated urine-derived sepsis-induced kidney injury potentially via altering the expression of inflammation-associated cytokines.

The aim of the present study was to determine the efficacy of ulinastatin (UTI) for the treatment of sepsis and to investigate the associated molecular mechanisms. Twenty‑four male rabbits were randomly divided into 4 groups, the normal, sham, sepsis model and UTI groups, each containing 6 rabbits. Serum levels of interleukin (IL)‑10 and tumor necrosis factor‑α (TNF‑α) were measured by enzyme‑linked immunosorbent assay (ELISA). Liver, kidney and lung tissues were stained with hematoxylin and eosin (HE) 36 h after sacrifice and morphological changes were observed under an optical microscope. The expression levels of IL‑10 and TNF‑α proteins in rabbit kidney tissue in each group were determined by immunohistochemical detection and western blot analysis. ELISA results indicated that, compared with the sepsis model, IL‑10 levels were significantly higher in the UTI treatment group (183.91±11.521 pg/ml) at 36 h (P=0.000), while serum TNF‑α concentration decreased significantly in the UTI treatment group (31.637±2.770 pg/ml; P=0.000). Results of western blot analysis were consistent with the immunohistochemistry, indicating that UTI upregulates IL‑10 and downregulates TNF‑α levels. In the current study, UTI was demonstrated to effectively treat urinary sepsis and alleviate the inflammatory response in tissues. These effects were mediated by the upregulation of IL‑10 and downregulation of TNF‑α levels.

β-elemene, a non-cellular antineoplastic agent, may be used to effectively inhibit the growth and proliferation of various types of tumor cells by inhibiting the nucleic acid synthesis or inducing their apoptosis and differentiation. The aim of this study was to investigate the expression, as well as the effects, of Mta-1, survivin and Bcl-xL in T24 bladder cancer cells following β-elemene treatment. The expression of the three proteins in T24 cells following β-elemene treatment was analyzed by immunocytochemistry staining and western blot analysis. The survival rate and apoptosis of T24 cells following β-elemene treatment was detected by MTT assay and TUNEL staining. We analyzed the internal corelations between apoptosis-associated genes, tumor metastasis-associated genes (cancer genes) and cell apoptosis, and investigated the mechanism of action by which β-elemene induces the apoptosis of T24 cells at a molecular level. These results provide scientific evidence for further study on the anticancer effect of β-elemene in carcinoma of the urinary bladder. In this study, it is shown that β-elemene downregulates the expression of survivin, Bcl-xL and Mta-1 in tumor cells. The apoptosis of T24 cells is dependent on the dosage and length of incubation time of β-elemene.