Dental and skeletal changes in mild to moderate Class II malocclusions treated by either a Twin-block or Xbow appliance followed by full fixed orthodontic treatment

Objective:To compare the short-term skeletal and dental effects of two-phase orthodontic treatment including either a Twin-block or an XBow appliance.Materials and Methods:This was a retrospective clinical trial of 50 consecutive Class II cases treated in a private practice with either a Twin-block (25) or XBow (25) appliance followed by full fixed orthodontic treatment. To factor out growth, an untreated Class II control group (25) was considered.Results:A MANOVA of treatment/observation changes followed by univariate pairwise comparisons showed that the maxilla moved forward less in the treatment groups than in the control group. As for mandibular changes, the corpus length increase was larger in the Twin-block group by 3.9 mm. Dentally, mesial movement of mandibular molars was greater in both treatment groups. Although no distalization of maxillary molars was found in either treatment group, restriction of mesial movement of these teeth was seen in both treatment groups. Both treatment groups demonstrated increased mandibular incisor proclination with larger increases for the XBow group by 3.3°. The Wits value was decreased by 1.6 mm more in the Twin-block group. No sex-related differences were observed.Conclusions:Class II correction using an XBow or Twin-block followed by fixed appliances occurs through a relatively similar combination of dental and skeletal effects. An increase in mandibular incisor inclination for the XBow group and an increased corpus length for the Twin-block group were notable exceptions. No overall treatment length differences were seen.     

Stillbirths and early neonatal mortality in rural Northern Ghana

Objective To calculate perinatal mortality (stillbirth and early neonatal death: END) rates in the Upper East region of Ghana and characterize community‐based stillbirths and END in terms of timing, cause of death, and maternal and infant risk factors. Methods Birth outcomes were obtained from the Navrongo Health and Demographic Surveillance System over a 7‐year period. Results Twenty thousand four hundred and ninty seven pregnant women were registered in the study. The perinatal mortality rate was 39 deaths/1000 deliveries, stillbirth rate 23/1000 deliveries and END rates 16/1000 live births. Most stillbirths were 31 weeks gestation or less. Prematurity, first‐time delivery and multiple gestation all significantly increased the odds of perinatal death. Approximately 70% of END occurred during the first 3 postnatal days, and the most common causes of death were birth asphyxia and injury, infections and prematurity. Conclusion Stillbirths and END remain a significant problem in Navrongo. The main causes of END occur during the first 3 days and may be modifiable with simple targeted perinatal policies.     

Targeting versus tinkering: Explaining why the clinic is frustrated with molecular mapping of disease mechanisms

We argue that our common diseases should not necessarily be taken as a sign of physiological error. Regulatory networks developed by evolutionary forces to support reproductive fitness happen to include disease as a side-effect. For example, inflammatory and autoimmune diseases are secondary to a strong defence against infections. An evolutionary perspective can help us understand why many drugs targeted to single molecules or linear signaling pathways fail in clinical trials. We present the hypothesis that a tinkering research strategy, as compared with the prevailing reductionist approach, may be more likely to help us find the tools needed to interfere optimally with disease-generating networks. One application of the hypothesis can be to analyze how manipulation with diet and gut microbial flora influences multiple sclerosis patients, rather than to first map in detail the molecular disease mechanism and then develop targeting drugs.     

Obstructive sleep apnea syndrome. Analytical study of 63 cases

Obstructive sleep apnoea (OSA) is a relatively common disorder, in developed country with prevalence estimated to lie between 2 and 4% in adult population. The diagnosis of this syndrome is made on the basis of characteristic clinical features and the results of nocturnal polysomnography. There is no data concerning the OSA in developing country. It is therefore of interest to determine the clinic and polysomnographic profile of this disease and to landmark factors correlated with severity in our country. This was achieved by studying a set of 63 OSA. The mean of age was 53 + 13 years with sex ratio 1. The means of Epworth sleepiness scale score, BMI and Apnoea/Hypopnoea index (AHI) were respectively 16 + 4, 38.8 + 7 kg/m2 and 51.7 + 28.6. 44% of patients have OSA severe with IAH > 50/h. Arousal index and desaturation index were respectively 36.4 + 21.7 and 49 + 26. Trial of continuous positive airway pressure (CPAP) therapy was proposed first to 40 patients, 17 were able to use CPAP.     

Influence of mutation of the HFE gene on the progression of chronic viral hepatitis B and C in Moroccan patients

The implication of hemochromatosis (HFE) gene mutations in chronic viral hepatitis remains controversial. The aim of the present study was to measure the frequencies of the common HFE gene mutations in Moroccan subjects with chronic viral hepatitis B and C and to assess their influence on the progression of liver disease. H63D and C282Y mutations were screened by the polymerase chain reaction followed by restriction fragment length polymorphism analysis in 170 chronic hepatitis B patients, 168 chronic hepatitis C patients, and 200 healthy controls. A very small proportion of patients infected with hepatitis B virus (HBV) or hepatitis C virus (HCV; 1.8% and none, respectively) were heterozygous for the C282Y mutation, that is, rates not statistically different from those observed in healthy control (2%, P > 0.05). Similarly, the frequency of the H63D allele was not significantly different between HBV (13.8%) or HCV (14.3%) patients and controls (13.5%, P > 0.05). Multivariate analysis showed that carriers of the H63D mutation infected with HBV are at higher risk to progress towards an advanced liver disease when compared with patients infected with HBV with wild‐type (OR = 2.45, 95% CI = 1.07–5.58). In contrast, no association between HFE mutated HCV‐infected patients and an increased risk of disease progression was found (OR = 1.24, 95% CI = 0.61–2.50, P = 0.547). In conclusion, in Morocco the frequency of the HFE C282Y allele is very low and H63D mutation carriage occurs in almost 14% of the patients, a rate similar in chronic hepatitis patients and healthy controls. In the case of chronic hepatitis B, the carriage of the H63D variant represents a risk factor of evolution towards a more active disease. J. Med. Virol. 83:2096–2102, 2011. © 2011 Wiley Periodicals, Inc.     

Simvastatin protects against cholestasis-induced liver injury

Background:

Bile duct obstruction is associated with hepatic accumulation of leukocytes and liver injury. The aim of this study was to evaluate the effect of simvastatin on cholestasis-induced liver inflammation and tissue damage.

Experimental approach:

C57BL/6 mice were treated with simvastatin (0.02 and 0.2 mg·kg⁻¹) and vehicle before and after undergoing bile duct ligation (BDL) for 12 h. Leukocyte recruitment and microvascular perfusion in the liver were analysed using intravital fluorescence microscopy. CXC chemokines in the liver were determined by enzyme-linked immunosorbent assay. Liver damage was monitored by measuring serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Hepatic levels of myeloperoxidase (MPO) were also determined.

Key results:

Administration of 0.2 mg·kg⁻¹ simvastatin decreased ALT and AST by 87% and 83%, respectively, in BDL mice. This dose of simvastatin reduced hepatic formation of CXC chemokines by 37–82% and restored sinusoidal perfusion in cholestatic animals. Moreover, BDL-induced leukocyte adhesion in sinusoids and postsinusoidal venules, as well as MPO levels in the liver, was significantly reduced by simvastatin. Notably, administration of 0.2 mg·kg⁻¹ simvastatin 2 h after BDL induction also decreased cholestatic liver injury and inflammation.

Conclusions and implications:

These findings show that simvastatin protects against BDL-induced liver injury. The hepatoprotective effect of simvastatin is mediated, at least in part, by reduced formation of CXC chemokines and leukocyte recruitment. Thus, our novel data suggest that the use of statins may be an effective strategy to protect against the hepatic injury associated with obstructive jaundice.