Recent advances in palladium-catalyzed sulfonylation via SO2 insertion.

The importance of sulfonyl-group-containing compounds, such as sulfonamides, sulfones, sulfinate esters, and sulfonyl fluorides, in pharmaceuticals, bioactive molecules, and natural products cannot be overstated. The new development of palladium-catalyzed sulfonylation via SO2 insertion represents a crucial advancement in organic synthesis, enabling the direct α,α-difunctionalization of SO2 and providing efficient access to an array of structure-diverse sulfonyl-containing compounds. Although there have been numerous reviews about SO2 insertion, many of them only cover specific aspects of palladium-catalyzed reactions, leading to an oversight of some important works. Besides, these reviews often lack detailed discussions and systematic conclusion on reaction mechanisms, and fail to comprehensively summarize the significant research achievements in palladium-catalyzed reactions over the past few years. Herein, we aim to systematically consolidate the recent advances in palladium-catalyzed sulfonylation via SO2 insertion, elucidate the underlying reaction mechanism, and highlight some unsolved challenges in this segment. This review seeks to serve as a valuable resource for researchers, assisting in the continued development of palladium-catalyzed sulfonylation methodologies.

Primary hepatic neuroendocrine tumors: A case report.

RATIONALE: Primary hepatic neuroendocrine tumors (PHNET) are extremely rare, which makes it difficult for doctors not deeply to be aware of their imaging and pathological characteristics. Therefore, it is challenging to diagnose PHNET accurately without biopsy or surgical excision. The purpose of this study is PATIENT CONCERNS:: A 52-year-old male patient came to our outpatient department with intermittent upper abdominal pain. DIAGNOSES: PHNET. INTERVENTIONS: Biochemical examination and imaging examination were performed prior to operation. Liver tumors were removed by ultrasound scalpel under laparoscopy. Pathology examination of liver tumors was performed after operation. Symptomatic supportive treatment was performed after operation as well, including anti-inflammation and rehydration. OUTCOMES: The results of biochemical examination were generally normal. The results of MRI showed low signal on T1WI, slightly high signal on T2WI/FS and DWI manifestation of high signal. Immunohistochemistry (IHC) showed that synaptophysin (Syn) was positive, CD56 was positive, chromaffin A (CgA) was positive, and Ki-67 was 15%. The patient was generally in good condition and no discomfort or recurrence was reported during 15 months of follow-up. LESSONS: The incidence of PHNET is extremely low. Sometimes the patient has no cirrhosis or hepatitis, and alpha-fetoprotein is not high, but imaging examination shows solid occupation and clear boundaries of the liver tumor, for which doctors should consider the primary liver nerve tumor. The diagnosis of PHNET depends on pathological characteristics. Surgical excision is the main method to treat the disease.

A Combination of Ulinastatin and Xuebijing Amplifies Neuroprotection after Transient Cerebral Ischemia via Attenuating Apoptosis Signal Pathways in Hippocampus.

BACKGROUND: Ulinastatin (UTI) plays the beneficial roles in modifying cerebral ischemic injury evoked by cardiac arrest (CA). XueBiJing (XBJ), comprised of extracts from Chinese herbals, has been used for the treatment of sepsis and ischemic disorders linked to multiple organ dysfunction syndromes. The current study was to find interventions that can enhance effectiveness of these drugs and further to provide a fundamental for their rational application in clinical practice. Thus, we examined how apoptosis signal in the hippocampus is engaged in a facilitating role of UTI and XBJ in improving neural injury and neurological functions after transient cerebral ischemia. METHODS: CA was induced by asphyxia followed by cardiopulmonary resuscitation in rats. Western Blot analysis and ELISA were employed to determine the protein expression of Caspase-3 and Caspase-9 in the hippocampus; and representative apoptosis pathways. The modified neurological severity score (mNSS) and spatial working memory performance were used to assess neurological deficiencies in CA rats. RESULTS: CA increased Caspase-3 and Caspase-9 in the hippocampus CA1 region. A lower dose of UTI did not attenuate upregulation of apoptosis signal pathways evoked by CA. However, a systemic administration of XBJ significantly amplified the inhibitory effects of the lower dose of UTI on apoptosis signal of the hippocampus. In addition, a combination of UTI and XBJ improved mNSS and spatial working memory performance to a greater degree. CONCLUSIONS: Our data indicate that a combination of XBJ and UTI plays a facilitating role in improving neuronal injury and neurological deficits observed in transient cerebral ischemia; and an inhibition of apoptosis signal pathways is involved in neuroprotective effects of united XBJ and UTI.

Partial ablation of the pancreas of Sprague Dawley® rats by focused ultrasound reveals no significant adverse effects on glycometabolism function.

To investigate the safety of focused ultrasound (FUS) partial ablation on the pancreas of Sprague Dawley® (SD) rats by histopathological examination of the outcome and investigation of glycometabolism function changes after local ablation. A total of 135 healthy SD rats were randomly divided into three groups (n=45 of each): FUS ½ group, FUS » group, and control group. Levels of serum amylase was measured using the enzyme dynamics method, fasting blood glucose was measured by the glucose oxidase-peroxidase method, fasting serum insulin was measured by direct chemiluminescence assay, and an ELISA was used to measure fasting serum glucagon immediately after treatment, and at 2h, 3days, 1, 2, 3 and 4weeks, 3 and 6months after FUS ablation. Pancreatic tissue was stained with hematoxylin and eosin and the pathology of the ablation area was examined under an optical microscope; additionally, the expression of insulin and glucagon was investigated by immunohistochemistry. Compared with the control group, serum amylase and fasting blood glucose levels in the ablation groups rose significantly immediately after operation; fasting blood glucose, serum amylase, serum insulin and glucagon levels in the ablation groups were significantly different at 2h after treatment, and serum amylase levels in the ablation groups remained significantly different on day 3. Histological findings showed that the coagulation necrosis area gradually shrank, with formation of new blood vessels observed at week 3, and new ducts observable in the ablation area at the 3rd month after FUS ablation, but no formation of islets was observed. Expression of insulin and glucagon in the ablation groups were significantly higher than in the control group at 2h after FUS ablation. There were no significant adverse effects on the glycometabolic function of SD rats after FUS ablation, and the influence of FUS treatment on pancreatic functions were minimal.

Cerebral mTOR signal and pro-inflammatory cytokines in Alzheimer's disease rats.

As a part of Alzheimer's disease (AD) development the mammalian target of rapamycin (mTOR) has been reported to play a crucial role in regulating cognition and can be used as a neuronal marker. Neuro-inflammation is also a cause of the pathophysiological process in AD. Thus, we examined the protein expression levels of mTOR and its downstream pathways as well as pro-inflammatory cytokines (PICs) in the brain of AD rats. We further examined the effects of blocking mTOR on PICs, namely IL-1ß, IL-6 and TNF-α. Our results showed that the protein expression of p-mTOR, mTOR-mediated phosphorylation of 4E-binding protein 4 (4E-BP1) and p70 ribosomal S6 protein kinase 1 (S6K1) pathways were amplified in the hippocampus of AD rats compared with controls. Blocking mTOR by using rapamycin selectively enhanced activities of IL-6 and TNF-α signaling pathways, which was accompanied with an increase of Caspase-3, indicating cellular apoptosis and worsened learning performance. In conclusion, our data for the first time revealed specific signaling pathways engaged in the development of AD, including a regulatory role by the activation of mTOR in PIC mechanisms. Stimulation of mTOR is likely to play a beneficial role in modulating neurological deficits in AD.Targeting one or more of these signaling molecules may present with new opportunities for treatment and clinical management of AD.

[Corrigendum] Anti-inflammatory effects of Gualou Guizhi decoction in transient focal cerebral ischemic brains.

Mol Med rep 12: [Related article:] 1321­1327, 2015; DOI: 10.3892/m mr.2015.3511 After the publication of the article, the authors noted that they had made an error regarding the spelling of Gualou Guizhi in their manuscript. In the title and on page 1 line 59, Guolou Guizhi should be replaced with Gualou Guizhi.

Anti-inflammatory effects of Gualou Guizhi decoction in transient focal cerebral ischemic brains. [Corrected].

The aim of the present study was to explore the neuroprotective effects of Gualou Guizhi decoction (GLGZD) in a rat model of middle cerebral artery occlusion (MCAO). Sprague-Dawley rats were divided into three groups: Sham (no MCAO), MCAO (MCAO with no GLGZD treatment) and GLGZD (MCAO with GLGZD treatment). Rats in the MCAO and GLGZD groups were subjected to permanent occlusion of the left middle cerebral artery. Neurological function and infarct volume were measured. Microglial activation and inflammatory cell accumulation were measured using immunohistochemistry. mRNA and protein expression of inflammatory mediators were examined using reverse transcription-quantitative polymerase chain reaction and an enzyme-linked immunosorbent assay. The expression of proteins associated with the nuclear factor κ-B (NF-κB) inflammation signaling pathway was analyzed using western blotting. The results of the present study suggested that infarct size was significantly reduced and neurological behavior function was improved in rats with MCAO treated with GLGZD compared with rats in the MCAO group. Amoeboid microglial expansion and inflammatory cell migration were observed in the infarcted areas of rats in the GLGZD group and were not identified in those of the MCAO group. Target mRNA and protein levels, and inflammatory cell infiltration were significantly reduced in the GLGZD group compared with the MCAO model group. Notably, GLGZD treatment induced neuroprotective effects, reducing inflammation and inhibiting NF-κB signaling compared with the MCAO group. Therefore, GLGZD may exhibit anti-inflammatory effects against ischemia-reperfusion brain injury and may be a therapeutic target for ischemic stroke.

Factors Related to Job Burnout Among Community Nurses in Changchun, China.

BACKGROUND: Community nurses are an important component of the community health service system. Job burnout among community nurses not only leads to a decline in satisfaction and an increased turnover rate but also may seriously affect the service quality and professional development of nurses. PURPOSE: This study aims to elicit the conditions and factors that cause job burnout in community nurses in Changchun, Jilin Province, China. METHODS: A questionnaire survey was administered to 420 registered nurses in Changchun using a convenience sampling method. RESULTS: Job burnout was found in 362 community nurses (86.2%), with a total mean job burnout score of 2.27 ± 0.65 points. Job burnout was related to marital status, educational level, job satisfaction, and interpersonal relationship difficulties. CONCLUSIONS: These results indicate that community nurses have a high rate of job burnout. Experts should be employed to train nurses in interpersonal communication skills. The community working environment should also be improved.

Ethyl acetate extract from Jiedu Xiaozheng Yin inhibits the proliferation of human hepatocellular carcinoma cells by suppressing polycomb gene product Bmi1 and Wnt/ß-catenin signaling.

Jiedu Xiaozheng Yin (JXY) is a Chinese herbal decoction used to treat hepatocellular carcinoma (HCC). Previous studies have demonstrated that JXY can inhibit HCC cell proliferation via induction of G0/G1 phase arrest. In this study, we investigated whether the inhibitory effect of JXY on HCC cells is associated with the inhibition of the Wnt/ß­catenin pathway and the polycomb gene product Bmi1. Ethyl acetate extract from JXY (EE-JXY) was prepared. Methyl thiazolyl tetrazolium (MTT) and colony formation assays were used to measure cell proliferation. Immunofluorescence was used to analyze the expression and location of ß-catenin and Bmi1. Immunohistochemistry was used to examine the expression of proliferating cell nuclear antigen (PCNA), c-myc and cyclin D1. ß-catenin, Bmi1, c-myc, cyclin D1 and p16INK4A mRNA levels were detected by RT-PCR. The results demonstrated that EE-JXY inhibited the expression of PCNA, c-myc, cyclin D1 and Bmi1, and upregulated the expression of p16INK4A. We also found that EE-JXY could facilitate ß-catenin translocation from the cytoplasm and nuclei to the cytomembrane. Finally, suppression of cell proliferation and expression of Bmi1 and Wnt/ß-catenin by EE-JXY was confirmed in a mouse xenograft model of HCC. Thus, EE-JXY can inhibit the proliferation of HCC partially via suppression of the Bmi1 and Wnt/ß-catenin signaling pathways.

40-year old female with a sellar mass.

Pituicytoma is a rare, low-grade neoplasm that originates in the neurohypophysis of the pituitary gland. We report the clinicopathologic features of a pituicytoma arising in a 40-year-old female who presented with menstrual disorder for 2 months, clinically suggestive of a pituitary microadenoma. The tumor was marked by a proliferation of elongated cells arranged in bundles and interlacing fascicles. The tumor demonstrated positive staining with S-100 protein and patchy staining for glial fibrillary acid protein and Epithelial Membrane Antigen. The tumor did not stain with antibodies to Progesterone receptor and Neu-n. An MIB-1 labeling was lower than 1%. The tumor was subtotally resected and didn't recur after the initial surgery.

A case of endoscopic ultrasound diagnosis of gastric amyloidosis.

A 37-year-old female presented to our hospital with the complaint of abdominal distension for one month. A gastroscopy examination showed extensive chyme retention and varying erosion and ulceration of the gastric body. The pathology showed moderate chronic inflammation and erosion of the gastric body mucosa, with accompanying Helicobacter pylori infection. She accepted treatment for one month. The patient then accepted to undergo endoscopic ultrasonography, which showed that normal structure of the gastric body intumescence was discernible. The pathology showed chronic mild-moderate inflammation of the gastric body mucosa associated with interstitial amyloidosis, with accompanying Helicobacter pylori infection. She accepted treatment for the eradication of Helicobacter pylori, and the original ulcer healed.

Fuzheng Yiliu Granule inhibits the growth of hepatocellular cancer by regulating immune function and inducing apoptosis in vivo and in vitro.

OBJECTIVE: To study the inhibitory effect of Fuzheng Yiliu Granule (FYG) on hepatocellular cancer (HCC) and investigate the mechanism mediating its bioactivity. METHODS: H22 tumor-bearing ICR mice were treated with FYG [3.6 g/(kg·d)] for 5 days. Tumor volume and tumor weight, percentages of CD3(+), CD4(+), CD8(+), and natural killer (NK) cells in peripheral blood, tumor apoptosis and serum levels of interleukin-2 (IL-2), and tumor necrosis factor-α (TNF-α) were evaluated. FYG-containing serum was prepared from SD rats treated for 7 days [high dose 3.6 g/(kg·d); middle dose 1.8 g/(kg·d); low dose 0.9 g/(kg·d)]. Cell cycle, cell viability, and apoptosis were evaluated after HepG2 cell line was cultured in FYG-containing serum for 48 h. The levels of IL-2 and TNF-α in FYG-containing serum were also determined. RESULTS: FYG produced a potent antitumor effect (P<0.01) and induced marked apoptosis of the tumor tissue (P<0.05). Mice treated with FYG had higher percentages of CD3(+) and CD4(+) (P<0.05), and more NK cells (P<0.01) in the peripheral blood than those in the animals treated with normal saline. Mice receiving FYG had the highest serum levels of IL-2 and TNF-α (P<0.01). High-dose FYG-containing serum significantly decreased HepG2 cell viability, inhibited cell proliferation (P<0.05), and induced apoptosis (P<0.01). In addition, the levels of IL-2 and TNF-α of high-dose-containing serum were higher than the blank serum (P<0.01). CONCLUSION: FYG could inhibit HCC growth by regulating immune function and inducing apoptosis of tumor cells in vivo and in vitro.