2014 Vol. 28, No. 2
2014, 28(2): 75-77. doi: 10.7555/JBR.28.20140031
Mucoadhesion can be defined as a state in which two components, of which one is of biological origin, are held together for extended periods of time by the help of interfacial forces. Among the various transmucosal routes, buccal mucosa has excellent accessibility and relatively immobile mucosa, hence suitable for administration of retentive dosage form. The objective of this paper is to review the works done so far in the field of mucoadhe?sive buccal drug delivery systems (MBDDS), with a clinical perspective. Starting with a brief introduction of the mucoadhesive drug delivery systems, oral mucosa, and the theories of mucoadhesion, this article then proceeds to cover the works done so far in the field of MBDDS, categorizing them on the basis of ailments they are meant to cure. Additionally, we focus on the various patents, recent advancements, and challenges as well as the future prospects for mucoadhesive buccal drug delivery systems.
Cardiac troponin-I (cTnI) and -T (cTnT) are sensitive and specific markers of myocardial injury. However, the role of increased cTnI and cTnT in percutaneous coronary intervention (PCI)-related myocardial injury remains controversial. In this prospective, single-center and double-blind study, we aimed to determine the diagnostic and prognostic value of cTnI as well as cTnT (cTns) in PCI-related myocardial injury in a Chinese population. A total of 1,008 patients with stable angina pectoris and non-ST-segment elevation acute coronary syndrome were recruited. The levels of cTnI and cTnT were examined before and after PCI. All patients were followed up for 26?9 months to observe the incidence of major adverse cardiac events (MACEs). Our results showed that post- PCI cTnI and/or cTnT levels were increased to more than the 99th percentile upper reference limit (URL) in 133 (13.2%) patients, among which 22 (2.2%) were more than 5 6 99th percentile URL. By univariate analysis, an elevation in cTns after PCI was not an independent predictor of increased MACEs, HR 1.35 (P 5 0.33, 95%CI: 0.74-2.46). In conclusion, our data demonstrate that the incidence of PCI-related myocardial injury is not common in a Chinese population and minor elevated cTns levels may not be a sensitive prognostic marker for MACEs.
We sought to assess the incidence of aspirin resistance after off-pump coronary artery bypass (OPCAB) surgery, and investigate whether clopidogrel can improve aspirin response and be safely applied early after OPCAB surgery. Sixty patients who underwent standard OPCAB surgery were randomized into two groups. One group (30 patients) received mono-antiplatelet treatment (MAPT) with aspirin 100 mg daily and the other group received dual antiplatelet treatment (DAPT) with aspirin 100 mg daily plus clopidogrel 75 mg daily. Platelet aggregations in response to arachidonic acid (PLAA) and adenosine diphosphate (ADP) (PLADP) were measured preoperatively and on days 1 to 6, 8 and 10 after the antiplatelet agents were administered. A PLAA level above 20% was defined as aspirin resistance. Postoperative bleeding and other perioperative variables were also recorded. There were no significant differences between the two groups in baseline characteristics, average number of distal anastomosis, operation time, postoperative bleeding, ventilation time and postoperative hospital stay. However, the incidence of aspirin resistance was significantly lower in the DAPT group than that in the MAPT group on the first and second day after antiplatelet agents were given (62.1% vs. 32.1%, 34.5% vs. 10.7%, respectively, both P , 0.05). There was no significant difference in postoperative complication between the two groups. DAPT with aspirin and clopidogrel can be safely applied to OPCAB patients early after the procedure. Moreover, clopidogrel reduces the incidence of OPCAB-related aspirin resistance.
This study was aimed to explore the associations between the combined effects of several polymorphisms in the PPAR-γ and RXR-α gene and environmental factors with the risk of metabolic syndrome by back-error propaga?tion artificial neural network (BPANN). We established the model based on data gathered from metabolic syn-drome patients (n = 1012) and normal controls (n = 1069) by BPANN. Mean impact value (MIV) for each input variable was calculated and the sequence of factors was sorted according to their absolute MIVs. Generalized multifactor dimensionality reduction (GMDR) confirmed a joint effect of PPAR-γ and RXR-α based on the results from BPANN. By BPANN analysis, the sequences according to the importance of metabolic syndrome risk fac?tors were in the order of body mass index (BMI), serum adiponectin, rs4240711, gender, rs4842194, family his?tory of type 2 diabetes, rs2920502, physical activity, alcohol drinking, rs3856806, family history of hypertension, rs1045570, rs6537944, age, rs17817276, family history of hyperlipidemia, smoking, rs1801282 and rs3132291. However, no polymorphism was statistically significant in multiple logistic regression analysis. After controlling for environmental factors, A1, A2, B1 and B2 (rs4240711, rs4842194, rs2920502 and rs3856806) models were the best models (cross-validation consistency 10/10, P = 0.0107) with the GMDR method. In conclusion, the interac?tion of the PPAR-γ and RXR-α gene could play a role in susceptibility to metabolic syndrome. A more realistic model is obtained by using BPANN to screen out determinants of diseases of multiple etiologies like metabolic syndrome.
2014, 28(2): 123-131. doi: 10.7555/JBR.28.20130076
Inositol requiring enzyme-1 (IRE1) is highly conserved from yeasts to humans. Upon the endoplasmic reticu?lum (ER) stress, IRE1 activates X-box-binding protein 1 (XBP1) by unconventionally splicing XBP1 mRNA, which activates the unfolded protein response (UPR) to restore ER homeostasis. In mice, IRE1α inactivity leads to embryonic death and IRE1α plays an essential role in extraembryonic tissues and the placenta. However, its precise action in the embryo proper is still unknown. In this study, the loss of function analysis was performed to investigate the function of Xenopus IRE1α (xIRE1α) during pancreas development. Firstly, the complete open reading frame of xIRE1α was amplified and the expression pattern was detected. The effects of Xenopus IRE1α and XBP1 during embryo development were detected with whole-mount in situ hybridization. The results dem?onstrated that xIRE1α was much closer to human IRE1α when compared with their sequence alignment. xIRE1α was expressed strongly in developing pancreas and the knockdown of xIRE1α inhibited the differentiation and specification of the pancreas. xIRE1α, which was required for cytoplasmic splicing of XBP1 pre-mRNA and XB?P1MO, also showed inhibitory effects on pancreas development. These results suggest that xIRE1α is essential for pancreas development during embryogenesis and functions via the XBP1 dependent pathway.
The aim of this study was to evaluate the effect of naringin on experimentally induced inflammatory bowel dis?ease in rats. Naringin (20, 40 and 80 mg/kg) was given orally for 7 days to Wistar rats before induction of colitis by intrarectal instillation of 2 mL of 4% (v/v) acetic acid solution. The degree of colonic mucosal damage was analyzed by examining mucosal damage, ulcer area, ulcer index and stool consistency. Intrarectal administration of 4% acetic acid resulted in significant modulation of serum alkaline phosphatase, lactate dehydrogenase, super?oxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA) and myeloperoxidase (MPO) content along with colonic nitric oxide (NO), xanthine oxidase (XO) level and protein carbonyl content in the colonic tissue as well as in blood. Naringin (40 and 80 mg/kg) exerted a dose dependent (P < 0.05) ameliorative effect, as it sig?nificantly increased hematological parameter as well as colonic SOD and GSH. There was a significant (P < 0.05) and dose dependant inhibition of macroscopical score, ulcer area along with colonic MDA, MPO activity by the 7 days of pretreatment of naringin (40 and 80 mg/kg). Biochemical studies revealed a significant (P < 0.05) dose dependant inhibition in serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH) levels by pretreat?ment of naringin. Increased levels of colonic NO, XO, protein carbonyl content and DNA damage were also sig?nificantly decreased by naringin pretreatment. The findings of the present investigation propose that naringin has an anti-inflammatory, anti-oxidant and anti-apoptotic potential effect at colorectal sites as it modulates the pro?duction and expression of oxidative mediators such as MDA, MPO, NO and XO, thus reducing DNA damage.
We report a case of a 49-year-old man who was admitted with a 3-hour history of sudden onset of substernal chest pain. Coronary angiography revealed that the left circumflex artery (LCX) was acutely and totally occluded at the mid-portion. In addition, the proximal and mid-portion of the right coronary artery (RCA) had a 60% occlusion. We inferred that the LCX was the culprit artery and primary PCI was successfully performed. Six weeks later, the patient had an eventful course with recurrence of chest pain. Coronary angiography showed no significant stenosis in the previous LCX lesion, while the proximal and middle potion of the RCA had a 90% occlusion. Our case demonstrates the systemic nature of acute coronary syndromes and highlights the inherent instability of coronary artery disease.