The flint-clay facies, originally proposed from widespread stratigraphie evidence, is represented by four of its six members within a single commercial deposit of Cheltenham refractory clay in Missouri. Scan electron micrographs show progressive changes in texture from plastic refractory clay (as in ball-clay “swirl” texture) through semi-plastic, semi-flint, to typical flint clay (recrystallized, well-ordered kaolinite). Micrographic evidence supports the interpretation of the origin of the Cheltenham clay earlier made from field and macroscopic evidence. Source material from nearby residual, weathered clay was transported into paludal basins, “digested,” partly recrystallized to kaolinite, brecciated and reconsolidated, essentially completed before being covered by younger Pennsylvanian-age sediments.

The microstructure and oxidation behavior at high temperatures ranging from 900 °C to 1100 °C of equiatomic CrMoNbTaV high-entropy alloy produced by vacuum arc melting were investigated. The phase component, microstructure, and microhardness of the alloy were examined by using X-ray diffraction, scanning electron microscopy equipped with an energy-dispersive X-ray spectroscope, and Vickers hardness tests, respectively. The as-cast alloy consists of a single body-centered cubic (BCC) refractory metal solid solution due to the high mixing entropy effect and exhibits a dendritic microstructure. The alloy has a very high microhardness value of 923 HV due to the strong solid solution strengthening effect. The average microhardness in interdendrites (950 HV) was higher than that in dendrites (896 HV) because of composition segregation. The oxidation kinetic curves of the alloy after exposure to air at 900 and 1000 °C follow the pseudo-parabolic rate law, while the mass gain increases first and then decreases at 1100 °C. The thickness of the oxide layer increases with the increasing of oxidation time. The long rod-shaped oxidation products are composed of Nb2O5, NbO2, CrTaO4, CrNbO4, Ta9VO25, Nb9VO25, and TaO after oxidation at 900 and 1000 °C for 25 h. The oxides of CrTaO4 and CrNbO4 disappear as the oxidation temperature elevated to 1100 °C.

Objective: Refractory status epilepticus (RSE) can influence the outcome of status epilepticus (SE). In the present study, we report the aetiology and predictors of outcomes of RSE in a developing country. Methods: This is a prospective hospital-based study of SE patients (continuous seizures for five minutes or more). Those who had SE persisting after two antiepileptic drugs were defined as having RSE. We present the demographic information, duration, and type of SE, and we note its severity using the status epilepticus severity score (STESS), its aetiology, comorbidities and imaging findings. The outcome of RSE was defined as cessation of seizures and the condition upon discharge, as assessed by the modified Rankin Scale. Results: A total of 35 (42.5%) of our 81 patients had RSE. The median duration of SE before starting treatment was 2 hours (range=0.008-160 h). The most common causes of RSE were stroke in 5 (14.3%), central nervous system (CNS) infections in 12 (34.3%) and metabolic encephalopathies in 13 (37.1%) patients. Some 21 (60%) patients had comorbidities, and the STESS was favourable in 7 (20%) patients. A total of 14 (20%) patients died, but death was directly related to SE in only one of these. Some 10 patients had super-refractory status epilepticus, which was due to CNS infection in 5 (50%) and metabolic encephalopathy in 3 (30%). On multivariate analysis, an unfavourable STESS (p=0.05) and duration of SE before treatment (p=0.01) predicted RSE. Metabolic aetiology (p=0.05), mechanical ventilation (p<0.001) and age >60 years (p=0.003) were predictors of poor outcomes. Conclusions: RSE was common (42.5%) among patients with SE in a tertiary care center in India. It was associated with high mortality and poor outcomes. Age above 60 years and metabolic aetiology were found to be predictors of poor outcomes.

A considerable amount of patients with panic disorder (25 – 30%) is refractory for the first line of treatment, mostly antidepressants, and for psychotherapy. Augmentation and combination strategies are discussed; and a protocol for the treatment of refractory patients with panic disorder is proposed with consists of five steps.

No patients is considered treatment refractory until they have had a trial with monoamine oxidase inhibitors.

Treatment resistance, along with its sibling partial response, remains a common phenomenon in schizophrenia, complicating the disability burden inherent in the disease. Antipsychotic medications are the mainstay of treatment, and treatment resistance has mainly been defined in terms of poor response to antipsychotic medication. At the same time, clozapine, the most effective antipsychotic, remains underutilized at the expense of exposing patients to polypharmacy. We review known causes of disability in schizophrenia, how they impact various areas of everyday functioning, and discuss potential treatment options including but not limited to pharmacological approaches aimed at maximizing treatment response and reducing treatment resistance.

We present the case of a 23-year-old man with a first episode of severe mania, which was refractory to pharmacotherapy. The case demonstrates a rapid response and full recovery after the use of electroconvulsive therapy (ECT). The ECT was administered involuntarily under Section 59(1) (b) of the Irish Mental Health Act 2001 as the patient was unable to consent to the treatment. The case highlights the benefits of ECT for this serious condition and emphasises the importance of retaining the legislative capacity to provide such an effective treatment for patients unable to consent because of severe psychotic illness.