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Objective To evaluate the effects of electrocautery assisted uvalopalatopharyngoplasty (UPPP) for obstructive sleep apnea and hyponea syndrome(OSAHS) .Methods Patients with OSAHS were randomly divided into two groups ,with 14 cases in each group .Group A was operated on with electrocautery ,while group B was operated on with the traditional method .The operative blood loss ,the operation time ,the tunica albuginea off time ,post operative pain ,surgical outcomes and complications were compared between two groups .Results The operative blood loss and the operation time of group A were much less than in group B (all P0 .05) .Two groups of patients both had no serious complications .Conclusion The advantages of electrocautery assisted UPPP consists of less operative blood loss and less operation time .It deserves to generalize and apply in the future clinical treatments .
ABSTRACT
OBJECTIVE@#To explore the treatment effect of H-UPPP on patients with obstructive sleep apnea hypopnea syndrome (OSAHS).@*METHOD@#Seventy-nine patients were enrolled in our study. Among which 49 patients were done with H-UPPP, and the other 30 patients were done with UPPP. AHI and LSaO2 were monitored by polysomnography and plasma endothelins-1 were tested with enzyme linked immunosorbent assay (ELISA) before and after operation.@*RESULT@#Forty-one patients were improved with reduced snoring and daytime sleepiness one year after operation in H-UPPP group,and the overall efficiency was 83.7%. Twenty-six patients were improved with reduced snoring and daytime sleepiness one year after operation in UPPP group, and the overall efficiency was 86.7%. There were significant differences of AHI, LSaO2 and ET-1 before and after operation between the two groups. Negative correlation was showed between AHI and LSaO2, also between LSaO2 and ET-1.@*CONCLUSION@#Both H-UPPP and UPPP were proved to be effective to patients with OSAHS. The perioperative complications with H-UPPP was less than UPPP.
Subject(s)
Adult , Female , Humans , Male , Middle Aged , Apnea , Blood , General Surgery , Disorders of Excessive Somnolence , Blood , General Surgery , Endothelin-1 , Blood , Palate, Soft , General Surgery , Pharynx , General Surgery , Polysomnography , Sleep Apnea, Obstructive , Blood , General Surgery , Sleep Stages , Snoring , Blood , General Surgery , Uvula , General SurgeryABSTRACT
BACKGROUND: Metoprolol is a selective β1-Blocker commonly used in essential hypertension. It is metabolized by CYP2D6. CYP2D6*10, which was identified to decrease activity of CYP2D6, is the main variance in Chinese population. β1-adrenergic receptor, with Ser49Gly and Gly389Arg polymorphisms, is the target of metoprolol. It was still unknown that whether the CYP2D6 and β1-adrenergic receptor had a synergic effect on metoprolol antihypertension therapy. AIM: To clarify the genetic polymorphism associated with metoprolol pharmacokinetics and pharmacodynamics in antihypertension therapy. METHODS: 125 mild-to-med essential hypertension patients were enrolled in this study. Patients were mono-therapied with metoprolol for 12 weeks. Blood pressure was monitored every 4 weeks. PCR-RFLP method was use to identify CYP2D6*10 and β1-adrenergic receptor Ser49Gly and Gly389Arg polymorphisms. Plasma metoprolol concentration was measured by HPLC- fluorescence detection. RESULTS: Trough blood level (C0) of metoprolol was associated with CYP2D6*10 variance in a gene-dose-effect manner, whereas the extent of blood pressure decrease was not significant different in CYP2D6*1*1, *1*10 and CYP2D6*10*10 patients. After 12 weeks metoprolol therapy, Gly49 carriers had stronger decrease in systolic and diastolic blood pressure than that of Ser49 homozygotes. Similarly, subjects homozygous for Arg389 had stronger decrease in blood pressure than that of Gly389 carriers. CONCLUSION: CYP2D6*10 variance significantly change the pharmacokinetics of metoprolol, and the genetic polymorphisms of β1-adrenergic receptor were associated with the pharmacodynamics of metopolol in antihypertension therapy.
ABSTRACT
BACKGROUND: There is a growing recognition that the adipose tissue is an endocrine organ that secretes signaling molecules such as adiponectin and resistin. The peroxisome proliferator activated receptor γ (PPARγ) is expressed in high levels in the adipose tissue. Thiazolidinediones are selective PPARγ agonists with insulin-sensitizing properties. It has been postulated that thiazolidinediones such as rosiglitazone exert their pharmacodynamic effects in part through modulation of resistin (implicated in insulin resistance) and adiponectin (an insulin-sensitizing molecule) expression subsequent to activation of PPARγ. There are conflicting data, however, on the biological direction in which resistin expression is modulated by PPARγ agonists and whether an increase in adiponectin expression can occur in the face of an upregulation of resistin. METHODS: Using the murine 3T3-L1 adipocytes as a model, we evaluated the changes in resistin and adiponectin gene expression after vehicle, rosiglitazone (10 μmol/L, a PPARγ agonist), GW9662 (5 μmol/L, a selective PPARγ antagonist) or GW662 and rosiglitazone co-treatment.RESULTS: In comparison to vehicle treatment, rosiglitazone increased the average adiponectin and resistin mRNA expression by 1.66- and 1.55-fold, respectively (P＜0.05). Importantly, GW9662 also upregulated adiponectin expression (by 1.57-fold, P＜0.05) but did not influence resistin expression (P＞0.05). Co-treatment with rosiglitazone and GW9662 maintained the adiponectin upregulation (1.87-fold increase from vehicle, P＜0.05) while attenuating resistin upregulation (1.31-fold increase from vehicle, P＜0.05) induced by rosiglitazone alone (1.55-fold increase from vehicle, P＜0.05). CONCLUSION: This study presents new evidence that adiponectin transcript is upregulated with both a PPARγ agonist (rosiglitazone) and antagonist (GW9662), while GW9662 co-treatment does not block rosiglitazone-induced adiponectin upregulation. These data collectively suggest that biological mechanisms independent from PPARγ may underlie thiazolidinedione pharmacodynamics on adiponectin expression. Moreover, increased adiponectin expression by GW9662, in the absence of an upregulation of resistin expression, lends further support on the emerging clinical potential of PPARγ antagonists in treatment of insulin resistance. Decreased resistin expression may not be crucial for the insulin-sensitizing effect of rosiglitazone. These findings may serve as a foundation for future dose-ranging and time-course studies of thiazolidinedione pharmacodynamics on adipocytokine expression in human adipocytes.