Objective To determine the possible mechanism for chronic pancreatitis causing pancreatic duct stones. Methods A total of 172 patients with chronic pancreatitis (n=67) , pan-creatic duct stones (n=62) , and pancreatic injury (n=43) , admitted to from August 2000 to October 2008, preoperatively diagnosed by endoscopic retrograde cholangiopancreatograpby (ERCP) or computed tomography (CT) , and intraoperatively confirmed by exploration and biopsy, were divid-ed into 3 groups. Pancreatic fluid was drawn to test the concentrations of pancreatic stone protein (PSP), lactoferrin (LF) and Ca2+. Results The chronic pancreatitis (the CP group) presented hard consistency, shrinkage and nodular fibrosis of the pancreas; besides the above symptoms, the pancreatic duct stones (the PS group) presented dilatation of the pancreatic ductal system with vari-ous stones ; pancreatic injury (the PI group) presented broken pancreas of different grades with fluid or blood. Compared with that of the PI group, PSP concentration of both the PS group and the CP group was elevated (P<0.05), and was more apparent in the CP group. Concentrations of LF and Ca2+ were also elevated (P<0.05) , which were more obvious in the PS group. Conclusion De-creased concentrations of PSP and increased concentrations of LF and Ca2+ may play very important roles in chronic pancreatitis causing pancreatic stones.

Objective To investigate the effects of atorvastatin calcium on thyroid function, immune response and C-Jun N-terminal kinase/p38 mitogen-activated protein kinase (JNK/p38 MAPK) signaling pathway in rats with hypothyroidism. Methods A total of 30 healthy adult male SD rats were randomly divided into control group, hypothyroid group (PTU group) and atorvastatin calcium treatment group (ACT group), with 10 rats in each group. Rats in the PTU group and the ACT group were injected with PTU subcutaneously at the dorsum of the neck every day for 28 consecutive days; instead of PTU, rats in the control group were injected subcutaneously with 0.3 mL of saline. After 2 weeks of PTU treatment, rats in the ACT group were gavaged with 3 mL of atorvastatin calcium saline solution (containing 5 mg/kg of atorvastatin calcium), which was administered once daily; the control group was gavaged with an equal amount of saline in the same way. The body weight, food intake and water intake of rats were measured weekly. The histopathological changes of the thyroid gland were observed in histopathological sections of rats in each group. Enzyme-linked immunosorbent assay (ELISA) was performed to determine the levels of triiodothyronine (T3), thyroxine (T4), thyroid stimulating hormone (TSH), interferon γ (IFN-γ) and interleukin-4 (IL-4) in serum; quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was performed to detect the mRNA expression levels of IFN-γ, IL-10, Foxp3 and IL-4; western blot was performed to determine the levels of p-JNK/JNK and p-p38/p38 MAPK. Results Compared with control group, PTU-induced hypothyroidism rats showed a significant decrease in body mass and food and water consumption (P < 0.05). After 2 weeks of treatment with atorvastatin calcium, the body mass loss of PTU rats was inhibited, food and water consumption was improved, and the differences were statistically significant (P < 0.05). Atorvastatin calcium was able to significantly increase the serum T3 and T4 levels and decrease the serum TSH level in hypothyroid rats (P < 0.05). Atorvastatin calcium treatment was able to significantly alleviate histopathological changes such as follicular cell proliferation and related hypertrophy induced by PTU, and increase follicular size (P < 0.05). After treatment with atorvastatin calcium, the spleen mass of PTU rats increased significantly, and the expression of IFN-γ mRNA in hypothyroid rats decreased significantly, but the expression levels of IL-10 mRNA, Foxp3 mRNA and IL-4 mRNA increased significantly (P < 0.05). After treatment with atorvastatin calcium, the levels of p-JNK/JNK and p-p38/p38 MAPK in thyroid tissue of hypothyroid rats decreased significantly (P < 0.05). Conclusion Atorvastatin calcium treatment for hypothyroidism has the function of promoting the normalization of thyroid hormone imbalance, balancing Th1/Th2 cytokines, and inhibiting the activation of JNK/p38 MAPK signaling pathway.