Skin problems after a tsunami

BACKGROUND: On December 26, 2004, the biggest earthquake for 40 years, measuring 9.0 on the Richter scale, triggered a tsunami that pounded the coastal areas of South Asia and East Africa. The effects of the tsunami on skin conditions have not been evaluated. OBJECTIVE: To determine the influence of the tsunami on skin conditions by evaluating the skin problems of patients presenting at hospitals after the tsunami. METHODS: Between 5 and 25 January 2005, two dermatologists evaluated patients who complained of skin problems at an outpatient clinic and emergency room of a general hospital in Banda Aceh, Aceh Province, Indonesia. RESULTS: The total number of patients that presented during the study period was 235 (131 males and 104 females), and they had a total of 265 skin problems. In terms of age distribution, most subjects were in their fourth decade (23.0%), followed by the third (22.6%) and fifth decade (16.6%). The most prevalent skin problems were infections-infestations (32.5%), followed by eczemas (29.8%) and traumatic skin disorders (29.4%). In males, traumatic skin disorders were most common. The great majority of infection-infestation cases involved superficial fungal infections. Contact dermatitis accounted for three-quarters of eczema cases, and mainly involved the arms (40.0%) and legs (27.1%). The majority of traumatic skin disorders were lacerations, punctures and penetrations, and the feet (44.7%) and hands (18.8%) were most frequently affected. CONCLUSIONS: Unhygienic conditions, exposure to a hazardous environment and contact with various objects during and after the tsunami probably increased the prevalence of infections-infestations, traumatic skin disorders and contact dermatitis. To prevent these problems and associated secondary bacterial infections, health-related education and early medical management are required.     

Hypoxic ischemic encephalopathy (asphyxia)

This article concerns itself with the effects of HIE on the brain of the full-term infant. Several treatment options are available, with phenobarbital being the drug of choice, but the course remains observation and careful monitoring of the at-risk infant.     

Identification and localization of muscarinic acetylcholine receptor proteins in brain with subtype-specific antibodies

mRNAs encoding five genetically distinct muscarinic ACh receptors are present in the CNS. Because of their pharmacological similarities, it has not been possible to detect the individual encoded proteins; thus, their physiological functions are not well defined. To characterize the family of proteins, a panel of subtype-selective antibodies was generated against recombinant muscarinic receptor proteins and shown to bind specifically to each of the cloned receptors. Using immunoprecipitation, three receptor proteins (m1, m2, and m4) accounted for the vast majority of the total solubilized muscarinic binding sites in rat brain. These receptor subtypes had marked differences in regional and cellular localization as shown by immunocytochemistry. The m1-protein was present in cortex and striatum and was localized to cell bodies and neurites, consistent with its role as a major postsynaptic muscarinic receptor. The m2-receptor protein was abundant in basal forebrain, scattered striatal neurons, mesopontine tegmentum, and cranial motor nuclei; this distribution is similar to that of cholinergic neurons and suggests that m2 is an autoreceptor. However, m2 was also present in noncholinergic cortical and subcortical structures, providing evidence that this subtype may presynaptically modulate release of other neurotransmitters and/or function postsynaptically. The m4-receptor was enriched in neostriatum, olfactory tubercle, and islands of Calleja, indicating an important role in extrapyramidal function. These results clarify the roles of these genetically defined receptor proteins in cholinergic transmission in brain.(ABSTRACT TRUNCATED AT 250 WORDS)     

CLINICAL FEMINISATION AND SEX HORMONE CONCENTRATIONS IN NIGERIAN MEN WITH CIRRHOSIS WITH AND WITHOUT HEPATOCELLULAR CARCINOMA

SUMMARY The study explored the incidence of clinical feminisation and the sex hormone levels of 18 Nigerian patients with liver cirrhosis (LC) alone and 18 patients with LC and hepatocellular carcinoma (HCC). The incidence (11%) of clinical feminisation in Nigerian patients was lower than values reported from other countries and there was no association between feminising signs and the sex hormone levels of the patients. Plasma oestradiol and sex hormone-binding globulin (SHBG) levels were significantly higher and testosterone lower in patients with liver diseases than in 18 age-matched normal controls. Serum concentrations of oestradiol were also found to be significantly higher in patients with LC alone than in those with LC and HCC. A possible promotive role for oestrogens in the development of HCC from the cirrhotic liver is discussed.     

Asymmetric growth of the lateral cerebral ventricle in infants with posthemorrhagic ventricular dilation

Lateral cerebral ventricular volume in 36 preterm infants with or without an intraventricular hemorrhage, and with or without posthemorrhagic hydrocephalus, was measured longitudinally and compared with the ventricular index measurements of the same ventricles. A poor correlation was found (r2 = 0.67). To determine a reason for this poor relationship, we analyzed the volumes of the regions of the ventricles by a segmental volume analysis. The occipital region of the lateral cerebral ventricle enlarged at a much faster rate (1.904 +/- 0.477 ml/day) than either the anterior region (0.546 +/- 0.253 ml/day; p less than 0.01) or the middle region (-0.209 +/- 0.334 ml/day; p less than 0.01) in infants with posthemorrhagic hydrocephalus. The rate of growth of the middle region of the lateral cerebral ventricles was the same for all infants. Linear indexes, such as the ventricular index and the lateral ventricular ratio, do not allow for accurate serial estimates of ventricular size in posthemorrhagic hydrocephalus because of asymmetric growth of the lateral cerebral ventricle. We conclude that sequential volume measurements are more useful than ventricular index measurements to follow ventricular size sequentially in infants with posthemorrhagic hydrocephalus.     

Inhibition of 2-nitropropane-induced rat liver DNA and RNA damage by benzyl selenocyanate

We observed that pretreatment of male F344 rats with benzyl selenocyanate, a versatile organoselenium chemopreventive agent in several animal model systems, decreases the levels of DNA and RNA modifications produced in the liver by the hepatocarcinogen 2- nitropropane. To clarify the mechanisms involved, we pretreated male F344 rats with either benzyl selenocyanate, its sulfur analog benzyl thiocyanate, phenobarbital or cobalt protoporphyrin IX; the latter is a depletor of P450. We then determined (1) the ability of liver microsomes to denitrify 2-nitropropane, (2) effects on 2-nitropropane- induced liver DNA and RNA modifications and (3) amount of nitrate excreted in rat urine following administration of the carcinogen. Pretreatment with benzyl selenocyanate or phenobarbital increased the denitrification activity of liver microsomes by 217 and 765%, respectively, increased liver P4502B1 by 31- and 435-fold, respectively, decreased the levels of 2-nitropropane-induced modifications in liver DNA (29-70% and 17-30%, respectively) and RNA (67-85% and 30-50%, respectively), and increased the 24-h urinary excretion of nitrate by 157 and 209%, respectively. Pretreatment with benzyl thiocyanate had no significant effect on any of these parameters. Pretreatment with cobalt protoporphyrin IX decreased liver P4502B 1 by 87%, decreased the denitrification activity of liver microsomes by 76%, decreased the 24 h urinary excretion of nitrate by 88.5%, but increased the extent of 2-nitropropane-induced liver nucleic acid modifications by 17-67%. These results indicate that the metabolic sequence from 2-nitropropane to the reactive species causing DNA and RNA modifications does not involve the removal of the nitro group. Moreover, they suggest that benzyl selenocyanate inhibits 2-NP-induced liver nucleic acid modifications in part by increasing its detoxication through induction of denitrification, although it is evident that other mechanisms must also be involved.      

Antagonist binding properties of five cloned muscarinic receptors expressed in CHO-K1 cells

A family of five cholinergic muscarinic receptor genes (m1, m2, m3, m4, and m5) has recently been identified and cloned. In order to investigate the pharmacological properties of the individual muscarinic receptors, we have transfected each of these genes into Chinese hamster ovary cells (CHO-K1) and have established stable cell lines expressing each receptor. In the present study we have examined the antagonist binding properties of each muscarinic receptor. Antagonists were chosen that had previously been proposed to be selective for muscarinic receptor subtypes and included pirenzepine, AF-DX 116, methoctramine, dicyclomine, hexohydrodifenidol, hexahydrosiladifenidol, hexocyclium, and silahexocyclium. m1, m2, and m3 receptors express binding properties similar to those expected of high affinity pirenzepine-type receptors of cerebral cortex ("M1"), low affinity pirenzepine-type receptors of atria ("M2 cardiac type"), and the intermediate affinity pirenzepine-type receptors found in exocrine glands ("M2 glandular type"), respectively. The M1/M2 schema cannot readily accommodate the binding properties of the m4 and m5 receptors. Pirenzepine, methoctramine, and hexahydrosiladifenidol were the most selective agents for the m1, m2, and m3 receptors, respectively. None of the antagonists used in this study were uniquely selective for either the m4 or m5 receptors. The diverse binding profiles of individual cloned receptors and the widespread distribution of m1-m4 mRNAs indicate that radioligand binding studies performed on primary tissues may actually be assessing the composite properties of a heterogeneous mixture of muscarinic receptor subtypes.     

Abortion utilization: does travel distance matter?

The further a woman must travel in order to obtain an abortion, the less likely she is to get one. Distance is especially disadvantageous to blacks, and most so to black teenagers. Distance discourages use among rural as well as urban women. Opening new clinics increases abortion use in nearby communities.