Porphyrin fluorescence in plasma of various types of porphyria

Fluorescence spectra of plasma porphyrin were measured in 6 patients with the acute intermittent porphyria (AIP), 30 patients with variegate porphyria (PV), 2 patients with hereditary coproporphyria, 2 patients with porphyria cutanea tarda, and in 6 patients with erythropoietic protoporphyria (EPP). It was found that the excitation and emission wavelengths at which maximum fluorescence is seen may help to diagnose and differentiate PV and EPP. In patients with AIP spectrum characteristic for porphyria of such a type was noted in all patients during the attack of disease and in only 33% of patients in remission. Fluorescence spectrum was normal in asymptomatic family members. In variegate porphyria spectrum with a characteristic maximum of fluorescence was noted in all patients during an attack and remission, and 62% of the asymptomatic family members.     

Ahch, the mouse homologue of DAX1: cloning, characterization and synteny with GyK, the glycerol kinase locus

We cloned the murine full-length cDNA encoding Ahch, the mouse homologue of DAX1 (DSS-AHC Region on Human X Chromosome, Gene1) which is the gene responsible for human X-linked adrenal hypoplasia congenita (AHC) and hypogonadotropic hypogonadism (HH). Sequence analysis revealed that the murine and human cDNAs have 65% aa identity and 75% aa similarity overall. The cysteine residues in the putative DNA binding domain, which may interact with Zn2+ ions to form zinc fingers, are 100% conserved between the two species, indicating that the novel zinc-finger structures in DAX1 may be functional. In addition, mouse interspecific backcrosses show that the Ahch gene is closely linked to the glycerol kinase locus, GyK, on the mouse X chromosome, indicating that the order of the loci is conserved in this syntenic region between mouse and human.     

Potential for non-shivering thermogenesis in perfused chicken (Gallus domesticus) muscle

The state of Oregon decided to cover all potentially eligible Medicaid citizens to 100% of poverty. Previously, Oregon had covered persons up to 67% of poverty. In order to keep overall program costs in check. Oregon decided to limit the number of services that its Medicaid program would cover. Oregon's normative choice was to contain program costs by covering all eligible persons up to 100% of poverty, while at the same time uniformly limiting access to certain services for everyone in the overall group of eligible persons. The state developed a prioritization list of medical services and priced the components on the list. The amount of money ultimately available for the Medicaid program was a political decision informed by data about the cost of different services and influenced by the priorities set through an independent process of priority-setting. Physicians were asked to determine what works medically, how well it works, and what benefits accrue to patients. Recognizing that physician perspectives on efficacy might vary from patients' perspectives on valuation of benefits, Oregon's planners developed a method for valuing medical outcomes that stemmed from particular medical interventions. This blend of medical fact and value to patients allowed for comparing valuations by introducing cost considerations. Condition-treatment (CT) pairs linked a medical condition with one or more courses of treatment. The goal was to determine the likely incremental medical benefit from a given treatment. In addition, Oregon developed a Quality-of-Well-Being scale to determine the net patient benefit from medical intervention and used a telephone survey to value that net benefit. A cost-benefit ratio was derived, and a prioritization of CT pairs was developed. The article analyzes and evaluates Oregon's use of cost-benefit calculations in the allocation of Medicaid funds, noting that Oregon itself backed away from many of the implications of its cost-benefit analysis and that the Americans with Disabilities Act has constrained use of quality-of-life judgments in Medicaid resource allocation decision-making.     

Self-calibration based on invariant view recognition: Dynamic approach to navigation

We extend a dynamic approach of behavior generation to the representation of spatial information. Two levels of dynamics integrate dead-reckoning, dominant far from home bases, and piloting, dominant near home bases. When the view-based piloting system recognizes a home base, visual place information recalibrates the dead-reckoning system, inverting the hierarchical ordering of the two dynamic levels by time scale inversion. Reference views taken at discrete home bases are recognized invariantly under rotation of views. This process yields compass information. Continuous translational information is obtained as a neural place representation built from view correlations with a scattered set of local views. This self-calibrating cognitive map couples into a dynamics of heading direction integrating the behaviors of obstacle avoidance and target acquisition. Targets can be designated in terms of the cognitive map. We demonstrate the dynamical model in simulation.     

Association of herpes zoster ophthalmicus with acquired immunodeficiency syndrome and acute retinal necrosis

We conducted a review to investigate the prevalence of human immunodeficiency virus (HIV), or acquired immunodeficiency syndrome (AIDS), in patients with herpes zoster ophthalmicus, as well as the incidence of acute retinal necrosis after herpes zoster ophthalmicus. All charts of patients seen at our institution between 1987 and 1992 with a primary diagnosis of herpes zoster ophthalmicus were reviewed. Of 112 patients with herpes zoster ophthalmicus, 29 (26%) had HIV or AIDS. All these patients were younger than 50 years at the time of diagnosis. Five of 29 (17%) immunocompromised patients had acute retinal necrosis after herpes zoster ophthalmicus. No acute retinal necrosis was identified in the nonimmunocompromised patients after herpes zoster ophthalmicus. We recommend that all patients younger than 50 years who have herpes zoster ophthalmicus at initial examination be tested for HIV. Additionally, HIV-infected patients should be monitored closely after herpes zoster ophthalmicus for development of acute retinal necrosis. Long-term oral prophylactic as well as initial high-dose intravenous acyclovir may be appropriate in HIV-infected individuals with herpes zoster.     

Delta opioid peptide [D-Ala2,D-leu5]enkephalin blocks the long-term loss of dopamine transporters induced by multiple administrations of methamphetamine: involvement of opioid receptors and reactive oxygen species

Delta opioid peptide [D-Ala2,D-leu5]enkephalin (DADLE) can prolong organ preservation and increases myocardial tolerance to ischemia. Our study examined the protective property of DADLE against methamphetamine- (METH) induced dopaminergic terminal damage in the central nervous system. Because the neurotoxicity of METH involves reactive oxygen species, we also examined if DADLE might be an antioxidative agent in vitro. DADLE at 2 and 4 mg/kg (i.p.), given 30 min before each METH administration (5 or 10 mg/kg, i.p., four injections in a day at 2-hr intervals), dose-dependently blocked the METH-induced long-term dopamine transporter loss. The opioid antagonist naltrexone blocked this action of DADLE in both aspects of striata but tends not to affect the effects of DADLE in the nucleus accumbens. DADLE did not alter changes in body temperature induced by METH. The reduction of striatal dopaminergic content and tyrosine hydroxylase activity caused by METH, however, were not blocked by DADLE. In vitro, DADLE was approximately equipotent to glutathione in inhibiting both superoxide anion formation induced by xanthine oxidase and hydroxyl radical formation evoked by ferrous/citrate complex. DADLE was only slightly less potent than glutathione in inhibiting the iron/ascorbate-induced brain lipid peroxidation. These results suggest that DADLE can protect the terminal membranes of dopaminergic neurons against METH-induced insult but not the loss of dopaminergic content and tyrosine hydroxylase activity and that this action of DADLE might involve opioid receptors as well as the sequestration of free radical.     

Gelsolin is a downstream effector of rac for fibroblast motility

Rac, a member of the rho family of GTPases, when activated transmits signals leading to actin-based membrane ruffling in fibroblasts. Compared with wild-type fibroblasts, gelsolin null (Gsn-) dermal fibroblasts have a markedly reduced ruffling response to serum or EGF stimulation, which signal through rac. Bradykinin-induced filopodial formation, attributable to activation of cdc42, is similar in both cell types. Wild-type fibroblasts exhibit typical lamellipodial extension during translational locomotion, whereas Gsn- cells move 50% slower using structures resembling filopodia. Multiple Gsn- tissues as well as Gsn- fibroblasts overexpress rac, but not cdc42 or rho, 5-fold. Re-expression of gelsolin in Gsn- fibroblasts by stable transfection or adenovirus reverts the ruffling response, translational motility and rac expression to normal. Rac migrates to the cell membrane following EGF stimulation in both cell types. Gelsolin is an essential effector of rac-mediated actin dynamics, acting downstream of rac recruitment to the membrane.