Hypothyroidism affects astrocyte and microglial morphology in type 2 diabetes

In the present study, we investigated the effects of hypothyroidism on the morphology of astrocytes and microglia in the hippocampus of Zucker diabetic fatty rats and Zucker lean control rats. To induce hypothyroidism, Zucker lean control and Zucker diabetic fatty rats at 7 weeks of age orally received the vehicle or methimazole, an anti-thyroid drug, treatment for 5 weeks and were sacrificed at 12 weeks of age in all groups for blood chemistry and immunohistochemical staining. In the me- thimazole-treated Zucker lean control and Zucker diabetic fatty rats, the serum circulating triiodo- thyronine （T3） and thyroxine （＇I＂4） levels were significantly decreased compared to levels observed in the vehicle-treated Zucker lean control or Zucker diabetic fatty rats. This reduction was more prominent in the methimazole-treated Zucker diabetic fatty group. Glial fibrillary acidic protein im- munoreactive astrocytes and ionized calcium-binding adapter molecule 1 （Iba-1）-immunoreactive microglia in the Zucker lean control and Zucker diabetic fatty group were diffusely detected in the hippocampal CA1 region and dentate gyrus. There were no significant differences in the glial fibril- lary acidic protein and Iba-1 immunoreactivity in the CA1 region and dentate gyrus between Zucker lean control and Zucker diabetic fatty groups. However, in the methimazole-treated Zucker lean control and Zucker diabetic fatty groups, the processes of glial fibrillary acidic protein immunoreac- tive astrocytes and Iba-1 immunoreactive microglia, were significantly decreased in both the CA1 region and dentate gyrus compared to that in the vehicle-treated Zucker lean control and Zucker diabetic fatty groups. These results suggest that diabetes has no effect on the morphology of as- trocytes and microglia and that hypothyroidism during the onset of diabetes prominently reduces the processes of astrocytes and microglia.

Entacapone promotes hippocampal neurogenesis in mice

Entacapone,a catechol-O-methyltransferase inhibitor,can strengthen the therapeutic effects of levodopa on the treatment of Parkinson’s disease.However,few studies are reported on whether entacapone can affect hippocampal neurogenesis in mice.To investigate the effects of entacapone,a modulator of dopamine,on proliferating cells and immature neurons in the mouse hippocampal dentate gyrus,60 mice(7 weeks old)were randomly divided into a vehicle-treated group and the groups treated with 10,50,or 200 mg/kg entacapone.The results showed that 50 and 200 mg/kg entacapone increased the exploration time for novel object recognition.Immunohistochemical staining results revealed that after entacapone treatment,the numbers of Ki67-positive proliferating cells,doublecortin-positive immature neurons,and phosphorylated cAMP response element-binding protein(pCREB)-positive cells were significantly increased.Western blot analysis results revealed that treatment with tyrosine kinase receptor B(TrkB)receptor antagonist significantly decreased the exploration time for novel object recognition and inhibited the expression of phosphorylated TrkB and brain-derived neurotrophic factor(BDNF).Entacapone treatment antagonized the effects of TrkB receptor antagonist.These results suggest that entacapone treatment promoted hippocampal neurogenesis and improved memory function through activating the BDNF-TrkB-pCREB pathway.This study was approved by the Institutional Animal Care and Use Committee of Seoul National University(approval No.SNU-130730-1)on February 24,2014.

Newly developed autoimmune cholangitis without relapse of autoimmune pancreatitis after discontinuing prednisolone

A 57-year-old man presented with a 2-wk history of painless jaundice and weight Iossl He had a large ill- defined enhancing mass-like lesion in the uncinate pro- cess of the pancreas with stricture of the distal common bile duct. Aspiration cytology of the pancreatic mass demonstrated inflammatory cells without evidence of malignancy. Total serum immunoglobulin G level was slightly elevated, but IgG4 level was normal. After the 2-wk 40 mg prednisolone trial, the patient＇s symptoms and bilirubin level improved significantly. A follow-up computed tomography （CT） scan showed a dramatic resolution of the pancreatic lesion. A low dose steroid was continued. After six months he self-discontinued prednisolone for 3 wk, and was presented with jaundice again. ACT scan showed newly developed intrahepatic biliary dilatation and marked concentric wall thickening of the common hepatic duct and the proximal common bile duct without pancreatic aggravation. The patient＇ s IgG4 level was elevated to 2.51 g/L. Prednisolone was started again, after which his serum bilirubin level became normal and the thickening of the bile duct was resolved. This case suggests that autoimmune pancre- atitis can progress to other organs that are not involved at the initial diagnosis, even with sustained pancreatic remission.

Neurons in the hippocampal CA1 region,but not the dentate gyrus,are susceptible to oxidative stress in rats with streptozotocin-induced type 1 diabetes

In this study, we investigated the effects of streptozotocin-induced type 1 diabetes on antioxi- dant-like protein-1 immunoreactivity, protein carbonyl levels, and malondialdehyde formation, a marker for lipid peroxidation, in the hippocampus. For this study, streptozotocin （75 mg/kg） was intraperitoneally injected into adult rats to induce type 1 diabetes. The three experimental pa- rameters were determined at 2, 3, 4 weeks after streptozotocin treatment. Fasting blood glucose levels significantly increased by 20.7-21.9 mM after streptozotocin treatment. The number of antioxidant-like protein-1 immunoreactive neurons significantly decreased in the hippocampal CA1 region, but not the dentate gyrus, 3 weeks after streptozotocin treatment compared to the control group. Malondialdehyde and protein carbonyl levels, which are modified by oxidative stress, significantly increased with a peak at 3 weeks after malondialdehyde treatment, and then decreased 4 weeks after malondialdehyde treatment. These results suggest that neurons in the hippocampal CA1 region, but not the dentate gyrus, are susceptible to oxidative stress 3 weeks after malondialdehyde treatment.

Duodenal obstruction following acute pancreatitis caused by a large duodenal diverticular bezoar

Bezoars are concretions of indigestible materials in the gastrointestinal tract. It generally develops in patients with previous gastric surgery or patients with delayed gastric emptying. Cases of periampullary duodenal divericular bezoar are rare. Clinical manifestations by a bezoar vary from no symptom to acute abdominal syndrome depending on the location of the bezoar. Biliary obstruction or acute pancreatitis caused by a bezoar has been rarely reported. Small bowel obstruction by a bezoar is also rare, but it is a complication that requires surgery. This is a case of acute pancreatitis and subsequent duodenal obstruction caused by a large duodenal bezoar migrating from a periampullary diverticulum to the duodenal lumen, which mimicked pancreatic abscess or microperforation on abdominal computerized tomography. The patient underwent surgical removal of the bezoar and recovered completely.