The combined therapy of TCM and WM may have great clinical value and a potential for decreasing the relapse or metastasis rate in stage II and III colorectal cancer after conventional WM therapy.

Prolactinoma is the most common type of primary pituitary tumors. It occurs more frequently in women than in men. Dopaminergic agonists are effective in the shrinkage of prolactin-secreting pituitary tumor and are preferred in some patients. However, pituitary radiotherapy may enable the long-term removal of prolactin-secreting tumor cells. Recent evidence suggests that prolactinoma is a heterogeneous disorder with complicated and multifactorial etiology and pathogenesis. Apparently, a thorough understanding of prolactinoma tumorigenesis would be important. To facilitate investigations on tumorigenesis of prolactinoma, animal models for prolactinomas have been developed. These models have expedited our progress in the recent years. Many researchers consider the F₃₄₄ rat to be the most sensitive strain of rats to estrogen (E₂)-induced prolactinoma formation. Nonetheless, E₂ treatment for 60 days also induces the formation of pituitary prolactin-secreting adenoma in male Sprague-Dawley (SD) rats. Evidently, the SD rat is also a good animal for prolactinoma investigations. Following E₂ implantation, prolactinomas developed in the eutopic adenohypophysis in situ and/or ectopic pituitary grafted under the renal capsule in SD rats. These observations favor the hypothesis that prolactinoma growth is the result of pathological changes in the adenohypophysis and/or hypothalamus. In the latter case, abnormal release of hypothalamic dopamine, GABA, or brain-gut peptides (such as cholecystokinin, vasoactive intestinal polypeptide, galanin, angiotensin, opioid peptide, gastrin, gastrin-releasing peptide, pancreatic polypeptide, and adrenocorticotropic hormone) results in some of the pathological changes that may lead to hyperprolactinemia and/or prolactinoma development. Dysregulation of prolactin synthesis and secretion may be the result of prolactin gene modulation. In E₂-induced rat prolactinomas, prolactin mRNA contents and the expression of some proto-oncogenes, e.g. c-myc and c-ras, TGFα and TGFβ1 mRNA were significantly changed. The above findings are consistent with results in human prolactinoma development. In addition, in rats abnormal expression of the prolactin gene was correlated with hypomethylated status of CpG sites in exons 1, 2 and 4 of the prolactin gene, as well as the increase in hypersensitive sites to DNase 1 in the encoding region of the prolactin gene. In E₂-treated rats, a point mutation with a base substitution from cytidine (C) to adenine (A) was found at the –36-bp site of the proximal promoter of the prolactin gene in eutopic pituitary prolactinomas, but no change was observed in the same sequence of the prolactin gene in ectopic prolactinoma. The association of a base substitution with the hyperexpression of the prolactin gene in eutopic prolactinomas suggests that different mechanisms may mediate the formation of eutopic and ectopic prolactin-secreting tumors. Melatonin decreases the expression of the prolactin gene in vitro sug...

Background Benign convulsions with mild gastroenteritis (BCWG) is a common condition in children in Asia and is generally not associated with pH or electrolyte imbalances. When BCWG is diagnosed, a lumbar puncture is usually recommended to rule out potential intracranial infections. This study examined the clinical characteristics of BCWG and evaluated the necessity of lumbar puncture. Methods Medical records of children admitted to the First Hospital of Jilin University with BCWG between January 2018 and May 2019 were reviewed and analyzed. Children were stratified by rotavirus positivity or lumbar puncture status. Clinical characteristics and long-term outcomes were compared between groups. Results A total of 51 children were included in the analyses (55.1% rotavirus [HRV] positive). The average age of convulsion onset was 21.12 ± 7.44 months, the male-to-female ratio was 1.8:1, and convulsions occurred primarily between October 2018 and April 2019. The main clinical presentations of BCWG were convulsions, vomiting, diarrhea, and fever. Convulsions occurred predominantly two days after diagnosis of gastroenteritis, were mainly generalized tonic-clonic with 88.2% of children having ≤ 3 convulsions per episode, and had a mean duration of 2.0 minutes (interquartile range [IQR]: 1.0, 3.0). Children with BCWG had mild metabolic acidosis (HCO3− 17.82 ± 3.63 mmol/L) with an elevated anion gap (AG; 20.98 ± 3.00 mmol/L), mild hyponatremia (134.56 ± 2.85 mmol/L), and slightly increased levels of creatine kinase myocardial band (CKMB). HRV + children had more severe acidosis and higher CKMB levels. Cerebrospinal fluid (CSF) samples collected via lumbar puncture were normal. No developmental abnormalities were noted as assessed by the Social Life Ability Scale. Conclusions BCWG is a situation-related seizure, with clinical presentations of tonic-clonic or focal convulsions and mild gastroenteritis (vomiting, diarrhea). Mild metabolic acidosis and hyponatremia may exist. The prognosis of the disease is favorable; lumbar puncture and long-term antiepileptics are unnecessary and should not be recommended.

Connexin (Cx) 36 is known to be a component of gap junctions, and has been suggested to play an important role in epilepsy. In order to determine dynamic changes of Cx36 protein expression in epilepsy and investigate the role of Cx36 in electroencephalographic activity and pathogenesis, we utilized kainic acid (KA) to induce epileptogenesis. We found that epileptic discharges began 71.8 ± 23.7 s after KA administration. Spike frequency and amplitude of epileptiform activity reached maximal levels at 30 ± 5.2 min. The maximum level of spike frequency and amplitude of epileptiform activity was 13.9 ± 0.3 Hz and 198 ± 14.3mV respectively. Employing Western blotting and immunohistochemistry, we demonstrated that hippocampal Cx36 protein expression was significantly increased 6 h after KA kindling compared to control or sham groups, but decreased in 3 d and 7d groups. Our results suggested that the dynamic change of Cx36 expression may play an important role inepilepsy, and the specific manipulation of Cx36 expression may be a potential target for the treatment of epilepsy.

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Background Bronchopleural fistula is a rare but life-threatening event with limited therapeutic options. We aimed to investigate the efficacy and safety of the modified silicone stent in patients with post-surgical bronchopleural fistula. Methods Between March 2016 and April 2020, we retrospectively reviewed the records of 17 patients with bronchopleural fistula and who underwent bronchoscopic placement of the Y-shaped silicone stent. The rate of initial success, clinical success and clinical cure, and complications were analyzed. Results Stent placement was successful in 16 patients in the first attempt (initial success rate: 94.1%). The median follow-up time was 107 (range, 5–431) days. All patients achieved amelioration of respiratory symptoms. The clinical success rate was 76.5%. Of the 14 patients with empyema, the daily drainage was progressively decreased in 11 patients, and empyema completely disappeared in six patients. Seven stents were removed during follow-up: four (26.7%) for the cure of fistula, two for severe proliferation of granulomatous tissue and one for stent dislocation. No severe adverse events (i.e. massive hemoptysis, suture dehiscence) took place. Seven patients died (due to progression of malignancy, uncontrolled infection, myocardial infarction and left heart failure). Conclusions The modified silicone stent may be an effective and safe option for patients with post-surgical bronchopleural fistula patients in whom conventional therapy is contraindicated.

In this study we investigated the potential anti-epileptogenic effect of neuronal connexin Cx36 gap junction blockage via inhibition of microtubule-associated protein 2 (MAP-2) and synaptophysin (SYP) overexpression. Thirty adult male Wistar rats were divided into five groups (six animals per group): control, sham, carbenoxolone (CBX), quinine (QN), and quinidine (QND). An epilepsy model was produced by injecting kainic acid (KA) into the rat amygdala. Broad-spectrum and selective blockers of the Cx36 channel (CBX, QN, and QND) were administered via intraperitoneal injection. Expression of MAP-2 and SYP was assessed by immunofluorescent and immunohistochemical examination. Expression of MAP-2 and SYP was significantly increased after KA administration in the sham group compared with the control group. Expression of MAP-2 and SYP was significantly decreased in the CBX, QN, and QND groups compared with the sham group. The results provide new evidence regarding the key role of MAP-2 and SYP overexpression in three important mechanisms: the modulation of neuronal plasticity, hyperexcitability of the hippocampal neuronal network, and persistent seizure discharge. Furthermore, the reversal of MAP-2 and SYP overexpression following administration of Cx36 channel blockers indicates a potential role for Cx36 channel blockers in anti-epileptogenic treatment and in doing so, highlights a critical need for further investigation of these compounds.