Vertebral Artery Stenting for Acute Multiple Cerebral Infarctions Caused by Vertebral Artery Dissection After Massage: A Case Report.

Vertebral artery dissection is a rare pathology that can cause ischemic stroke in young people. Cervical massage, especially improper pulling manipulation, is a cause of vertebral artery dissection. We present a case of 32-year-old woman who developed acute multiple posterior circulation ischemic cerebral infarctions as a result of left vertebral artery V4 segment dissection after receiving neck massage. She underwent emergency vertebral artery stent implantation at the site of the dissection. Symptoms were relieved the day after treatment. The patient recovered without adverse complications or endovascular restenosis in the following year.

Availability Bias Causes Misdiagnoses by Physicians: Direct Evidence from a Randomized Controlled Trial.

Objective Empirical evidence on the availability bias associated with diagnostic errors is still insufficient. We investigated whether or not recent experience with clinical problems can lead physicians to make diagnostic errors due to availability bias and whether or not reflection counteracts this bias. Methods Forty-six internal medicine residents were randomly divided into a control group (CG) and experimental group (EG). Among the eight clinical cases used in this study, three experimental cases were similar to the disease of dengue fever (DF) but exhibited different diagnoses, one was actually DF, and the other four filler cases were not associated with DF. First, only the EG received information on DF, while the CG knew nothing about this study. Then, six hours later, all participants were asked to diagnose eight clinical cases via nonanalytic reasoning. Finally, four cases were diagnosed again via reflective reasoning. Results In stage 2, the average score of the CG in the diagnosis of experimental cases was significantly higher than that of the filler cases (0.80 vs. 0.59, p<0.01), but the EG's average score in the two types of cases was not significantly different (0.66 vs. 0.64, p=0.756). The EG and CG had significantly different scores for each experimental case, while no difference was observed in the filler cases. The proportion of diseases incorrectly diagnosed as DF among experimental cases ranged from 71% to 100% in the EG. There were no significant differences between the mean diagnostic accuracy scores obtained by nonanalytic reasoning and those obtained by the reflective reasoning in any cases. Conclusion Availability bias led to diagnostic errors. Misdiagnoses cannot always be repaired solely by adopting a reflective approach.

Manometric asymmetry of the anal sphincter: anatomic evidence and clinical application.

BACKGROUND: Manometric pressure asymmetry of the anal sphincter exists in the anal canal. There are reports about the anatomy of the anal sphincter, but the relationship between the configuration and the pressure asymmetry of the anal sphincter is not clear. This study is to investigate the anatomic evidence and clinical application of anal sphincter pressure asymmetry. METHODS: PC polygram HR at the state of relaxing and squeezing was used in 27 normal children and 12 abnormal ones with fecal incontinence. RESULTS: In normal children, longitudinal pressure gradients existed at eight channels in the anal canal, and the maximal pressure 1 cm from the anal verge. Longitudinal pressure asymmetry changes of eight channels also existed in the anal canal, from 3 cm to 2 cm to 1 cm from the anal verge. The high pressure distribution changed from the posterior to the anterior anal canal. Anteriorly, 1 cm from the anal verge, the maximal pressure was formed in the anal canal. However, neither longitudinal pressure gradients nor longitudinal pressure asymmetry changes were seen in patients with fecal incontinence. CONCLUSION: The configuration and function of the striated muscle complex possibly contribute to the formation of the pressure asymmetry of the anal sphincter, which is essential to anal control.

[Experience of diagnosis and treatment of carcinoma arising from congenital biliary duct cyst].

OBJECTIVE: To summarize the experience in diagnosis, prevention and treatment of carcinoma arising from congenital biliary duct cyst. METHODS: The clinical and pathological data of 185 patients with congenital biliary duct cyst admitted to Chinese PLA General Hospital were analyzed retrospectively. RESULTS: Among 185 patients, twenty-seven cases had carcinomas arising from congenital biliary duct cyst, and the frequency of malignant transformation was 14.6%, which closely related to the age (P < 0.001). The incidences of malignancy for different age groups were: 0 for 0-9 age group, 5.1% for 0-19, 9.1% for 20-29, 16.2% for 30-39, 26.7% for 40-49, 33.3% for 50-59, and 50% for over 60, respectively. Six patients had the history of cyst-enterostomy. Abdominal pain, fever, jaundice and weight loss were the main clinical manifestations. Abdominal ultrasonography, CT, MRI or magnetic resonance cholangiopancreatography, MRCP and endoscopic retrograde choledochopancreatography (ERCP) were the main diagnostic methods. For twenty patients (74.1%), a definite diagnosis was made preoperatively, but it's hard to make an early diagnosis. Nine patients (33.3%) underwent curative resection. CONCLUSIONS: Congenital biliary duct cyst is a premalignant lesion, and the incidence of carcinogenesis increases remarkably with age. The most effective method for prevention of carcinogenesis in choledochal cyst is complete excision of choledochal cyst during childhood, and the prognosis is poor for patients with biliary malignancy.

Ketamine promotes inflammation through increasing TLR4 expression in RAW264.7 cells.

SUMMERY: Ketamine (KTM), a N-methyl-D-aspartate (NMDA) receptor antagonist, was found to has an anti-inflammatory effect, but some patients suffered from exacerbated pro-inflammatory reactions after anesthesia with KTM. The present study was aimed to examine the underlying mechanism of pro-inflammatory effects of KTM. In this study, RAW264.7 cells were exposed to KTM and NMDA alone or combined for 30 min before lipopolysaccharide (LPS) stimulation. The expression levels of IL-6 and TNF-α were detected by RT-PCR and ELISA, and those of NMDA receptors by RT-PCR in RAW264.7 cells. Additionally, the TLR4 expression was determined by RT-PCR and flow cytometry, respectively. The results showed that in RAW264.7 cells, KTM alone promoted the TLR4 expression, but did not increase the expression of IL-6 or TNF-α. In the presence of LPS, KTM caused a significantly higher expression of IL-6 and TNF-α than LPS alone. NMDA could neither alter the IL-6 and TNF-α mRNA expression, nor reverse the enhanced expression of IL-6 and TNF-α mRNA by KTM in LPS-challenged cells. After TLR4-siRNA transfection, RAW264.7 cells pretreated with KTM no longer promoted the IL-6 and TNF-α expression in the presence of LPS. In conclusion, KTM accelerated LPS-induced inflammation in RAW264.7 cells by promoting TLR4 expression, independent of NMDA receptor.

Panax notoginseng saponins inhibits atherosclerotic plaque angiogenesis by down-regulating vascular endothelial growth factor and nicotinamide adenine dinucleotide phosphate oxidase subunit 4 expression.

OBJECTIVE: To investigate the mechanism of Panax notoginseng saponins (PNS), an effective component extracted from Panax notoginseng, on atherosclerotic plaque angiogenesis in atherosclerosis-prone apolipoprotein E-knockout (ApoE-KO) mice fed with high-fat, high-cholesterol diet. METHODS: Twenty ApoE-KO mice were divided into two groups, the model group and the PNS group. Ten normal C57BL/6J mice were used as a control group. PNS (60 mg/kg) was orally administered daily for 12 weeks in the PNS group. The ratio of plaque area to vessel area was examined by histological staining. The tissue sample of aortic root was used to detect the CD34 and vascular endothelial growth factor (VEGF) expression areas by immunohistochemistry. The expression of VEGF and nicotinamide adenine dinucleotide phosphate oxidase subunit 4 (NOX4) were measured by reverse transcription polymerase chain reaction and Western blotting respectively. RESULTS: After treatment with PNS, the plaque areas were decreased (P<0.05). CD34 expressing areas and VEGF expression areas in plaques were significantly decreased (P<0.05). Meanwhile, VEGF and NOX4 mRNA expression were decreased after treatment with PNS. VEGF and NOX4 protein expression were also decreased by about 72% and 63%, respectively (P<0.01). CONCLUSION: PNS, which decreases VEGF and NOX4 expression, could alleviate plaque angiogenesis and attenuate atherosclerosis.

Overexpression of ETS2 in human esophageal squamous cell carcinoma.

AIM: To study the expression pattern of ETS2 (erythroblastosis virus oncogene homolog 2) in human esophageal squamous cell carcinoma (ESCC). METHODS: Reverse transcription polymerase chain reaction (RT-PCR) and Northern blot were performed to examine the expression level of ETS2 mRNA in 37 pairs of ESCC tissue samples. Western blot and immunohistochemistry were carried out to check the expression level of ETS2 protein in 30 pairs of ESCC tissue specimens. RESULTS: RT-PCR and Northern blot analysis showed that ETS2 mRNA upregulated in 75.7 % (28/37) examined ESCC tissues relative to matched normal tissues. From those 37 cases, 14 cases were randomly selected to perform Western blot and the results revealed that ETS2 protein overexpressed in 71.4 % (10/14) checked ESCC tissues compared with the corresponding normal tissues. Moreover, the expression patterns of ETS2 protein in those 14 cases were identical to those of ETS2 mRNA displayed by RT-PCR or Northern Blot. Immunohistochemistry analysis showed that the expression level of ETS2 protein rose in 75 % (12/16) tumor epithelial cells contrasted to the normal cells. Altogether the expression level of ETS2 protein increased in 73.3 % (22/30) checked ESCC tissue samples contrary to their normal counterparts. CONCLUSION: The results suggested that ETS2 overexpressed in paired human ESCC tissue samples at both mRNA and protein levels and may be associated with the tumorigenesis of esophagus.

Quercetin inhibits left ventricular hypertrophy in spontaneously hypertensive rats and inhibits angiotensin II-induced H9C2 cells hypertrophy by enhancing PPAR-γ expression and suppressing AP-1 activity.

BACKGROUND: Quercetin is the most abundant flavonoid in fruit and vegetables and is believed to attenuate cardiovascular disease. We hypothesized that quercetin inhibits cardiac hypertrophy by blocking AP-1 (c-fos, c-jun) and activating PPAR-γ signaling pathways. METHODOLOGY/PRINCIPAL FINDINGS: The aim of this study was to identify the mechanism underlying quercetin-mediated attenuation of cardiac hypertrophy. Quercetin therapy reduced blood pressure and markedly reduced the ratio of left ventricular to body weight (LVW/BW) (P<0.05, vs. spontaneously hypertensive rats (SHRs)). In vitro, quercetin also significantly attenuated Ang II-induced H9C2 cells hypertrophy, as indicated by its concentration dependent inhibitory effects on [³H]leucine incorporation into H9C2 cells (64% reduction) and by the reduced hypertrophic surface area in H9C2 cells compared with the Ang II group (P<0.01, vs. Ang II group). Concurrently, we found that PPAR-γ activity was significantly increased in the quercetin-treated group both in vivo and in vitro when analyzed using immunofluorescent or immunohistochemical assays (P<0.05, vs. SHRs or P<0.01, vs. the Ang II group). Conversely, in vivo, AP-1 (c-fos, s-jun) activation was suppressed in the quercetin-treated group, as was the downstream hypertrophy gene, including mRNA levels of ANP and BNP (P<0.05, vs. SHRs). Additionally, both western blotting and real time-PCR demonstrated that PPAR-γ protein and mRNA were increased in the myocardium and AP-1 protein and mRNA were significantly decreased in the quercetin-treated group (P<0.05, vs. SHRs). Furthermore, western blotting and real time-PCR analyses also showed that transfection with PPAR-γ siRNA significantly increased AP-1 signaling and reversed the effects of quercetin inhibition on mRNA expression levels of genes such as ANP and BNP in hypertrophic H9C2 cells. CONCLUSIONS: Our data indicate that quercetin may inhibit cardiac hypertrophy by enhancing PPAR-γ expression and by suppressing the AP-1 signaling pathway.

Qindan capsule changes adventitial collagen synthesis in spontaneously hypertensive rats.

OBJECTIVE: To investigate the effect of Qindan capsule (QC) on collagen synthesis and the mechanism underlying the process in spontaneously hypertensive rats (SHRs). METHODS: Twentyfour SHRs were divided into three groups: the hypertension model group, the QC treatment group, and the losartan treatment group. Eight Wistar Kyoto (WKY) rats were used as the normal control group. The systolic blood pressure (SBP) of the rats was monitored, and the thoracic aorta adventitia of the rats was segregated. The expressions of transforming growth factor 1 (TGF-ß1), Smad3, and collagens I and were measured by histological staining and reverse transcription polymerase chain reaction. RESULTS: The SBP was significantly higher in the model group than in the normal control group (P<0.01). However, a significant SBP-lowering effect was observed in QC or losartan treatment groups (P<0.05 or P<0.01) after 3 weeks of treatment. QC-treated rats showed a decrease of approximately 40 mm Hg, and the losartan-treated rats showed a decrease of approximately 50 mm Hg at the end of treatment compared with the beginning of treatment. The protein and gene levels of TGF-ß1, Smad3, and collagens I and in the model group were significantly increased compared with those in the normal control group (P<0.01). However, the levels were significantly decreased in the QC or losartan treatment group compared with the model group (P<0.05 or P<0.01). However, there was no significant difference between the QC and losartan treatment groups (P<0.05). CONCLUSIONS: QC could exert its antihypertensive effect through down-regulating TGF-ß1-stimulated collagen expressions. The TGF-ß1/Smad3 signaling pathway may be involved in this process.

A preliminary study of apparent diffusion coefficient in chemotherapy-induced liver damage.

OBJECTIVES: To investigate changes in the hepatic apparent diffusion coefficient (ADC) in patients undergoing chemotherapy. METHODS: We enrolled 54 patients (25 women; mean age 57.0±13.1 years, range 29-89 years) undergoing chemotherapy for tumor and 10 controls (7 women; mean age 55.1±17.5 years, range 23-81 years). The patients were tested for serum alanine aminotransferase (ALT) activity (abnormal, normal) and fatty liver. Hepatic ADC values were compared among controls, patients and subgroups. Pearson correlation coefficient was used to assess the correlation between ADC and ALT activity. RESULTS: Hepatic ADC0,850 (×10(-3) mm2/s) was lower for patients than controls (1.14±0.18 vs. 1.28±0.12, P=0.02) and was lower for patients with than without fatty liver and controls (1.01±0.06 vs. 1.18±0.18 and 1.28±0.12, respectively, all P<0.01), with no significant difference between patients without fatty liver and controls (P=0.07). ADC0,850 was lower for patients with abnormal ALT than normal ALT activity and controls (0.99±0.06 vs. 1.17±0.18 and 1.28±0.12, respectively, all P<0.05), with a significant difference also being seen between patients with normal ALT activity and controls (P=0.04). Hepatic ADC0,850 was not correlated with ALT activity in patients (r=-0.24, P=0.08). CONCLUSIONS: Although ADC did not correlate with ALT values, it did distinguish patient likely to have chemotherapy-induced liver damage as indicated by abnormal ALT values or fatty liver. These mechanisms need to be disentangled.