Organic Disease Presenting as a Psychiatric Syndrome

Organic illnesses may be misdiagnosed as psychiatric disorders if emotional symptoms precede medical signs or if the medical symptoms mimic a common psychiatric syndrome. Diseases presenting such diagnostic pitfalls include the endocrine syndromes, certain metabolic abnormalities, some neoplastic conditions, multiple sclerosis, and systemic lupus erythematosus. Thorough initial and periodic medical evaluation, including examination of the patient's mental status, is recommended.     

Nonrenewal spike train statistics: causes and functional consequences on neural coding

Many neurons display significant patterning in their spike trains (e.g. oscillations, bursting), and there is accumulating evidence that information is contained in these patterns. In many cases, this patterning is caused by intrinsic mechanisms rather than external signals. In this review, we focus on spiking activity that displays nonrenewal statistics (i.e. memory that persists from one firing to the next). Such statistics are seen in both peripheral and central neurons and appear to be ubiquitous in the CNS. We review the principal mechanisms that can give rise to nonrenewal spike train statistics. These are separated into intrinsic mechanisms such as relative refractoriness and network mechanisms such as coupling with delayed inhibitory feedback. Next, we focus on the functional roles for nonrenewal spike train statistics. These can either increase or decrease information transmission. We also focus on how such statistics can give rise to an optimal integration timescale at which spike train variability is minimal and how this might be exploited by sensory systems to maximize the detection of weak signals. We finish by pointing out some interesting future directions for research in this area. In particular, we explore the interesting possibility that synaptic dynamics might be matched with the nonrenewal spiking statistics of presynaptic spike trains in order to further improve information transmission.     

Leptospirosis among zebu cattle in farms in Kaduna State,Nigeria

ObjectiveTo assess the occurrence of Leptospira spp serovar Hardjo among Zebu cattle in some livestock producing areas of Kaduna State, Nigeria.MethodsSera samples were obtained from 164 Zebu breed of cattle above one year osf age in seven cattle farms were screened for antibodies to Leptospira spp. serovar Hardjo using Enzyme linked immunosorbent assay (ELISA).ResultsAntibodies to Leptospira spp. serovar Hardjo were detected in eighteen (10.98%) out of the 164 animals sampled. There was no significant difference (P>0.05) in seropositivity between the different age groups or between different Zebu breeds.ConclusionThe presence of Leptospirosis among the Zebu breeds of cattle may poses a threat to livestock production and has public health implication due to its zoonotic potential.     

Two independent pathways of regulated necrosis mediate ischemia–reperfusion injury

Regulated necrosis (RN) may result from cyclophilin (Cyp)D-mediated mitochondrial permeability transition (MPT) and receptor-interacting protein kinase (RIPK)1-mediated necroptosis, but it is currently unclear whether there is one common pathway in which CypD and RIPK1 act in or whether separate RN pathways exist. Here, we demonstrate that necroptosis in ischemia–reperfusion injury (IRI) in mice occurs as primary organ damage, independent of the immune system, and that mice deficient for RIPK3, the essential downstream partner of RIPK1 in necroptosis, are protected from IRI. Protection of RIPK3-knockout mice was significantly stronger than of CypD-deficient mice. Mechanistically, in vivo analysis of cisplatin-induced acute kidney injury and hyperacute TNF-shock models in mice suggested the distinctness of CypD-mediated MPT from RIPK1/RIPK3-mediated necroptosis. We, therefore, generated CypD-RIPK3 double-deficient mice that are viable and fertile without an overt phenotype and that survived prolonged IRI, which was lethal to each single knockout. Combined application of the RIPK1 inhibitor necrostatin-1 and the MPT inhibitor sanglifehrin A confirmed the results with mutant mice. The data demonstrate the pathophysiological coexistence and corelevance of two separate pathways of RN in IRI and suggest that combination therapy targeting distinct RN pathways can be beneficial in the treatment of ischemic injury.