Paradental cyst: case report and review of the literature

The origin of paradental cysts is related to inflammatory processes, especially pericoronaritis involving impacted or semi-impacted teeth. The authors present a case of paradental cyst related to lower second molar that did not show clinical evidence of inflammatory process. The main aspects related to its classification, diagnosis and clinical characteristics are also discussed.     

Experimental sinusitis in a rhinogenic model

OBJECTIVES/HYPOTHESIS: The objectives were to determine the optimal sinusitis induction period and to examine microbiological and histopathological changes of sinusitis recovery stage in a rhinogenic sinusitis model. METHODS: A synthetic sponge was inserted into the right-side nasal cavities of rabbits. The sponge was impregnated with a Streptococcus pneumoniae strain in group 1 and with sterile saline solution in groups 2 and 3. After the fourth day of sponge insertion, sinuses were examined by coronal computed tomography scans at two-day intervals until any radiological evidence of sinusitis was observed. When sinusitis was detected radiologically, five rabbits each from groups 1 and 2 were killed for histological examination. To determine the recovery period of sinusitis, sponges were removed from the rest of the rabbits in groups 1 and 2. Rabbits were selected randomly and killed on the 15th and the 30th days of the recovery period, immediately after radiological examinations. Group 3 was considered a sham group. RESULTS: Sinusitis induction was performed in all rabbits in groups 1 and 2 until the 8th day. After the sponges were removed, inflammation persisted until the 30th day of the study. CONCLUSION: In a rhinogenic sinusitis model, although histological features of sinusitis were demonstrated, further studies are required to standardize this model and to examine whether or not the studied bacterial strain spreads from nasal cavity into sinus.     

Admission Hematocrit: A Simple, Useful and Early Predictor of Severe Pancreatitis

Existing predictor systems of severe pancreatitis are cumbersome and can require up to 48 hr to complete. This study aimed to determine whether useful likelihood ratios exist for the prediction of severe pancreatitis, corresponding to various ranges of admission hematocrit. A retrospective cohort of 200 patients admitted with acute pancreatitis was identified. Likelihood ratios were calculated for a priori defined hematocrit ranges. Using multivariate logistic regression, initial hematocrit was evaluated as a predictor of severe pancreatitis as defined a priori by local and/or systemic complications (Atlanta criteria, 1992). Planned subgroup analysis was performed on those with a hematocrit >50%, stratified by 24-hr hematocrit. Fourteen patients (7%) developed severe pancreatitis. Likelihood ratios were 0.45, 0.70, and 7.5 for hematocrit ranges of < or =45, 45.1-49.9, and > or =50%, respectively. Hematocrit (as increases by 5%) was a significant predictor of severe pancreatitis (odds ratio [OR] = 2.8; P = 0.001), length of stay (P < 0.0001), necrosis (OR = 3.9; P = 0.001), and need for intensive care (OR 4.5; P = 0.002). The negative predictive value of the lowest range and positive predictive value of the highest range were 97% (95% CI: 92-99%) and 37% (16-62%), respectively. Lack of normalization of hematocrit by 24 hr did not predict severe pancreatitis. Initial hematocrit appears to be an early, simple, and useful predictor of severe pancreatitis. A normal 24-hr hematocrit does not appear to alter the prediction made by the initial hematocrit.     

Presurgical intravenous parecoxib sodium and follow-up oral valdecoxib for pain management after laparoscopic cholecystectomy surgery reduces opioid requirements and opioid-related adverse effects

BACKGROUND: Opioids are associated with numerous adverse effects. It is unclear if reduced postoperative opioid consumption lowers the incidence and severity of opioid-related adverse effects. This analysis -- from a multicenter, randomized, double-blind trial -- tested if the reduction of opioid consumption among patients who received intravenous preoperative parecoxib 40 mg, followed by oral valdecoxib 40 mg qd postoperatively, in Days 1-4 after outpatient laparoscopic cholecystectomy surgery, reduced opioid-related symptoms. METHODS: Patients received intravenous fentanyl for pain before discharge, and oral acetaminophen 500 mg hydrocodone 5 mg q 4-6 h prn postdischarge for up to 7 days postsurgery. Patients also received intravenous parecoxib 40 mg administered 30-45 min preoperatively, and valdecoxib 40 mg qd up to Day 4 and prn Days 5-7 postsurgery, or placebo. Patients completed an opioid-related Symptoms Distress Scale (SDS) questionnaire every 24 h for 7 days. Opioid use was converted to morphine-equivalent doses (MEDs). Clinically meaningful events (CMEs) for 12 opioid-related symptoms were assessed by three ordinal measures: frequency, severity, and bothersomeness. Reduction of CMEs on Day 1 and number of patient-days with CMEs on Days 1-4 were examined. RESULTS: Cumulative MEDs on Day 0, Day 1, and Days 1-4 were significantly lower in the parecoxib/valdecoxib group compared with the placebo group (P < 0.001). At the end of Day 1, parecoxib/valdecoxib-treated patients had significantly lower SDS scores (P < 0.02), a significantly reduced incidence of CMEs (P < 0.05), and significantly fewer patient-days with CMEs in Days 1-4 than placebo patients (P < 0.05). Patients in the parecoxib/valdecoxib group were less likely to have CMEs for multiple symptoms than those in the placebo group (P < 0.001). CONCLUSIONS: Treatment with parecoxib and valdecoxib significantly reduced the cumulative MED requirements, the incidence of opioid-related adverse effects, and patient-days with CMEs.     

Postcesarean analgesia with spinal morphine, clonidine, or their combination

In this randomized, double-blind trial in 240 women, we investigated the analgesic efficacy and duration of subarachnoid fentanyl 15 microg with morphine, clonidine, or both morphine and clonidine for cesarean delivery. A dose-finding analysis showed similar postoperative efficacy and side effects for groups receiving morphine 100 microg with clonidine 60, 90, or 150 microg. Data from these groups were combined (MC60-150, n = 113) and compared with groups receiving morphine 100 microg (n = 39), clonidine 150 microg (n = 39), or morphine 100 microg plus clonidine 30 microg (n = 41). The four groups differed in the time to patient-controlled morphine use and cumulative morphine consumption (P < 0.0001 and P < 0.001, respectively), with the longest duration and smallest dose in MC60-150. Pain scores were significantly different among groups. Onset of sensory block, ephedrine requirement and incidence of hypotension, patient satisfaction, and recovery were similar. Groups receiving clonidine had greater sedation, those receiving morphine had more severe pruritus, and group MC60-150 showed a trend to more vomiting intraoperatively. Compared with morphine 100 microg or clonidine 150 microg alone, the combination of subarachnoid morphine 100 microg and at least 60 microg of clonidine was found to increase the duration of postcesarean analgesia, reduce opioid requirement, and increase intraoperative sedation. IMPLICATIONS: A multimodal approach to postcesarean analgesia, using subarachnoid bupivacaine, fentanyl, morphine 100 microg, and clonidine 60 microg, improves pain relief compared with morphine 100 microg or clonidine 150 microg alone, but increases intraoperative sedation and may increase perioperative vomiting.     

胃癌阻断新技术降低癌细胞血行转移的临床研究

目的　评价胃癌阻断技术降低胃癌门静脉血内癌细胞播散的效果。方法　 2 3例胃癌患者 ,8例术中未采用胃癌阻断技术者为常规手术组 ,15例采用胃癌阻断技术者为阻断组 ,术前、术中抽门静脉血及阻断区域胃网膜静脉弓内静脉血 ,应用RT -PCR技术测定静脉血内CK19mRNA表达情况。结果　切除胃癌病灶之前 ,门静脉血内CK19mRNA的总阳性率为 34 7% ( 8/ 2 3) ,常规组和阻断组的阳性率分别为 37 5 % ( 3/ 8)和 33 3% ( 5 / 15 ) ;术中牵拉胃癌病灶时 ,常规组门静脉血CK19mRNA的阳性率为 87 5 % ( 7/ 8) ,而阻断组的阳性率为 6 7% ( 1/ 15 ) ,两组差异有统计学意义 (P <0 0 5 ) ;阻断组 15例患者癌灶阻断区域网膜血管弓内静脉血CK19mRNA均阳性。结论　术中采用胃癌阻断技术能有效的阻断胃癌细胞播散 ,防止手术操作引致的癌细胞远处转移     

Directing stem cell differentiation into the chondrogenic lineage in vitro

A major area in regenerative medicine is the application of stem cells in cartilage tissue engineering and reconstructive surgery. This requires well-defined and efficient protocols for directing the differentiation of stem cells into the chondrogenic lineage, followed by their selective purification and proliferation in vitro. The development of such protocols would reduce the likelihood of spontaneous differentiation of stem cells into divergent lineages upon transplantation, as well as reduce the risk of teratoma formation in the case of embryonic stem cells. Additionally, such protocols could provide useful in vitro models for studying chondrogenesis and cartilaginous tissue biology. The development of pharmacokinetic and cytotoxicity/genotoxicity screening tests for cartilage-related biomaterials and drugs could also utilize protocols developed for the chondrogenic differentiation of stem cells. Hence, this review critically examines the various strategies that could be used to direct the differentiation of stem cells into the chondrogenic lineage in vitro.     

Permanent occlusion of the middle cerebral artery upregulates expression of cytokines and neuronal nitric oxide synthase in the spinal cord and urinary bladder in the adult rat

The expression pattern of proinflammatory cytokines, neuronal nitric oxide synthase (nNOS), substance P (SP) and calcitonin gene related peptide (CGRP) in the spinal cord and the bladder in response to permanent middle cerebral artery occlusion (MCAO) was investigated. In this connection, the gene expression of tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta) and interleukin-6 in the lumbosacral spinal cord and the bladder as determined by real-time polymerase chain reaction was upregulated. In the spinal cord, the immunoreactivity of TNF-alpha and IL-1beta was mainly localized in the ventral horn motoneurons contralateral to MCAO. In the bladder, TNF-alpha was mainly expressed in the inflammatory cells. The expression of nNOS immunoreactivity as well as nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) staining in the spinal cord and bladder was also markedly increased in response to MCAO. Furthermore, the temporal and spatial expression of nNOS paralleled that of TNF-alpha and IL-1beta in the spinal cord. On the other hand, there was no noticeable change in gene expression and immunoreactivity of SP and CGRP. The present results have shown that cytokines and nNOS expression are elevated in areas far removed from the primary site of ischemic infarct, namely, the lumbosacral spinal cord and bladder. This together with some neuronal deaths maybe linked to the dysfunction of the latter in a clinical stroke. On the other hand, the apparent lack of SP and CGRP changes following MCAO suggests that the two neurotransmitters are not directly involved.