Skeletal Muscle Ribonuclease Activities in Chronically Ethanol-Treated Rats

Alcoholic myopathy occurs in up to two thirds of alcohol misusers and is characterized by selective atrophy of type II (anaerobic, fast-twitch) fibers; type I (aerobic, slow twitch) fibers are relatively unaffected. Both clinical and animal studies have indicated that skeletal muscle RNA content is reduced in response to ethanol exposure, and contributes to impaired protein synthesis. We hypothesized that the reduction in muscle RNA may be due to raised ribonuclease (RNase) activities that enhance RNA catabolism. To test this hypothesis, we measured the total tissue and plasma RNase activities as well as the activities of general (RNase A) and specific or “restriction” RNases (T₁L, T₂L) in ethanol-treated rats. Chronically treated rats were fed a nutritionally complete liquid diet with 35% of calories as ethanol. Weight-matched controls were pair-fed with isocaloric glucose. Rats were killed at time-points up to 6 weeks. For comparative purposes, the effect of acute (24 hr) starvation was also analyzed in a second group of rats relative to a group of control rats allowed free access to food and water over 24 hr. Results showed that the type II fiber-predominant plantaris muscle exhibited a significant increase in total RNase, RNase A and RNase T₁L activities (increases ranged from +59% to +196%; P-values between 0.025 and 0.01) concomitant with large falls in RNA and protein content. In contrast, none of the RNase activities measured in the type 1 fiber-predominant soleus muscles were significantly affected; compositional changes were also smaller in the soleus. This effect was independent of reduced nutrition. In conclusion, the raised total RNase, RNase A and RNase T₁L activities may contribute to the type II fiber-specific reduction in total RNA in chronically ethanol-treated rats. In turn, this may contribute to the alterations in cellular protein metabolism seen under these treatments.     

Transmission Rate and Reproductive Number of the H5N1 Highly Pathogenic Avian Influenza Virus During the December 2005–July 2008 Epidemic in Nigeria

We quantified the between‐village transmission rate, β (the rate of transmission of H5N1 HPAI virus per effective contact), and the reproductive number, R_e (the average number of outbreaks caused by one infectious village during its entire infectious period), of H5N1 highly pathogenic avian influenza (HPAI) virus in Nigeria using outbreak data collected between December 2005 and July 2008. We classified the outbreaks into two phases to assess the effectiveness of the control measures implemented. Phase 1 (December 2005–October 2006) represents the period when the Federal Government of Nigeria managed the HPAI surveillance and response measures, while Phase 2 (November 2006–July 2008) represents the time during which the Nigeria Avian Influenza Control and Human Pandemic Preparedness project (NAICP), funded by a World Bank credit of US$ 50 million, had taken over the management of most of the interventions. We used a total of 204 outbreaks from 176 villages that occurred in 78 local government areas of 25 states. The compartmental susceptible‐infectious model was used as the analytical tool. Means and 95% percentile confidence intervals were obtained using bootstrapping techniques. The overall mean β (assuming a duration of infectiousness, T, of 12 days) was 0.07/day (95% percentile confidence interval: 0.06–0.09). The first and second phases of the epidemic had comparable β estimates of 0.06/day (0.04–0.09) and 0.08/day (0.06–0.10), respectively. The R_e of the virus associated with these β and T estimates was 0.9 (0.7–1.1); the first and second phases of the epidemic had R_e of 0.84 (0.5–1.2) and 0.9 (0.6–1.2), respectively. We conclude that the intervention measures implemented in the second phase of the epidemic had comparable effects to those implemented during the first phase and that the R_e of the epidemic was low, indicating that the Nigeria H5N1 HPAI epidemic was unstable.     

Screening for depressive symptoms in patients with chronic spinal pain using the SF-36 Health Survey.

BACKGROUND DATA: Depression is a common co-morbidity for patients with complaints of spinal pain, yet often goes undiagnosed in clinical practice. Depressed patients who are not identified do not receive a referral or recommendation for treatments that may help ease their total illness burden. Relative to the total outcomes of spine care this may increase costs, decrease overall functional outcomes, and limit patient satisfaction. Some spine care settings track functional outcomes using a general health status survey. Although a specific and reliable survey to detect depression could be employed, an additional survey would unnecessarily increase responder and analyst burdens if the general health status survey could be used instead. OBJECTIVE: To identify the Mental Component Summary (MCS) cutoff score from the Short Form 36-item Health Survey (SF-36) that best predicts a positive depression score as measured by the Center for Epidemiological Study-Depression Survey (CES-D). STUDY DESIGN: An analysis of the diagnostic properties of the SF-36 MCS Scale as a predictor of depressive symptoms as measured by the CES-D. OUTCOME MEASURES: The SF-36 is a general health survey that contains a MCS score that represents the psychological well-being and general health perception of the respondent. This composite score is norm-based (mean = 50, SD = 10) with lower scores representing poorer health. The CES-D has been well-studied in patients with chronic pain complaints and was used as the gold standard for determining the MCS cutoff score. A CES-D score of 19 or greater was considered positive for depressive symptoms. PATIENT SAMPLE: All patients entering our facility routinely complete the SF-36. Between February 2002 and October 2002, all patients scoring 30 or less on the MCS (MCS < or = 30) also completed the CES-D. Patients who scored 2 standard deviations below the mean (MCS = 30 or less) were considered most at risk for depression. Patients scoring above 30 on their MCS (MCS > 30) were considered less likely to have depressive symptoms and were randomly chosen to complete the CES-D. There were 420 patients who completed both surveys of which there were 99 MCS < or = 30 patients and 321 MCS > 30 patients. METHODS: Receiver operating characteristic (ROC) curves were used to assess the sensitivity and specificity of the SF-36 as a screening tool for detecting depressive symptoms. RESULTS: An MCS score of 35 has a sensitivity of 80% (76-83; 95% confidence interval), a specificity of 90% (87-93), an ROC area of 0.8517 (0.81-0.89), and correctly identified 87% of the sample. CONCLUSION: The SF-36 provides the benefits of a general functional health status measure and additionally appears to provide a screening tool for depressive symptoms. A cutoff score of 35 or less on the MCS scale has a high degree of sensitivity and specificity and is able to identify depressive symptoms in patients with back pain, which can help identify patients who will benefit from mental health treatments.     

Sustained treatment of sickle cell mice with haptoglobin increases HO‐1 and H‐ferritin expression and decreases iron deposition in the kidney without improvement in kidney function

There is growing evidence that extracellular haemoglobin and haem mediate inflammatory and oxidative damage in sickle cell disease. Haptoglobin (Hp), the scavenger for free haemoglobin, is depleted in most patients with sickle cell disease due to chronic haemolysis. Although single infusions of Hp can ameliorate vaso‐occlusion in mouse models of sickle cell disease, prior studies have not examined the therapeutic benefits of more chronic Hp dosing on sickle cell disease manifestations. In the present study, we explored the effect of Hp treatment over a 3‐month period in sickle mice at two dosing regimens: the first at a moderate dose of 200 mg/kg thrice weekly and the second at a higher dose of 400 mg/kg thrice weekly. We found that only the higher dosing regimen resulted in increased haem‐oxygenase‐1 and heavy chain ferritin (H‐ferritin) expression and decreased iron deposition in the kidney. Despite the decreased kidney iron deposition following Hp treatment, there was no significant improvement in kidney function. However, there was a nearly significant trend towards decreased liver infarction.     

Oxime-type acetylcholinesterase reactivators in pregnancy: an overview

Oxime-type acetylcholinesterase reactivators (oxime-AChER) are used as an adjunct in the treatment for organophosphorus anticholinesterase poisoning. Because of the widespread usage and exposure of organophosphorus compounds (OPCs), its poisoning and fatalities is obvious in pregnant women, embryos and fetuses. OPCs irreversibly inhibit acetylcholinesterase (AChE) at nerve synapses. Furthermore, the role of AChE other than neurotransmission termination has been defined in the literature. The growing evidences show that cholinergic mechanisms are involved during growth and development of other organ systems. In contrary to the fact, the data on the use of oxime-AChER in OPC poisoning in pregnancy are scanty. The present review aimed to comprehend the status of oximes in pregnancy in lieu of the published literature. A thorough literature search was performed in January 2013, using ten popular search engines including Medline/PubMed, Google scholar, etc., using nine standard keywords. The search period was set from 1966 to present. The search did not reveal substantial data. No considerable studies were retrieved which could really demonstrate either the beneficial, harmful or even null effect of oxime-AChER usage in pregnancy. Only eighteen relevant articles were obtained for a period of about 47 years. In the literature, there is no report available to demonstrate the risk of using oxime-AChER in pregnancy for the treatment of OPC poisoning. The study reveals that the use of oxime-AChER in pregnancy is largely un-addressed, inconclusive and based on speculation albeit the incidences of OPC poisoning are quite prevalent. Well-designed studies are warranted for a tangible conclusion.     

Incidence of Highly Pathogenic Avian Influenza H5N1 in Nigeria, 2005–2008

Outbreaks of highly pathogenic avian influenza (HPAI) H5N1 occurred in Nigeria between December 2005 and July 2008. We describe temporal and spatial characteristics of these outbreaks at State and Local Government Area (LGA) levels. A total of 25 of 37 States (67.6%; Exact 95% CI: 50.2–82.0%) and 81 of 774 LGAs (10.5%; Exact 95% CI: 8.4–12.8%) were affected by HPAI outbreaks over the period from 2005 to 2008. The incidence risk of HPAI outbreak occurrence at the State level was 5.6% (0.7–18.7%) for 2005, 50.0% (30.7–69.4%) for 2006, 54.5% (29.9–80.3%) for 2007 and 0% for 2008. Only very few LGAs experienced HPAI outbreaks within the affected States. The incidence risk of HPAI outbreak occurrence on a LGA level was 0.3% (0.0–0.9%) for 2005, 6.6% (4.9–8.6%) for 2006, 4.2% (2.9–6.0%) for 2007 and 0% for 2008. The mean period between farmers noticing HPAI outbreaks and reporting them to veterinary authorities, and between reporting HPAI outbreaks and the depopulation of infected premises, was for both 4.5 days; both periods also had medians of 1 day. We have estimated the spatially smoothed incidence risk for the whole outbreak period and identified the existence of a large corridor in the western part of Nigeria and a smaller corridor in south‐eastern part, where the risk of HPAI occurrence was lower than in the rest of the country. The effect of HPAI control policies on the outbreaks patterns are discussed, as well as possible reasons why HPAI did not become endemic in Nigeria.