Lophomonas blattarum (L. blattarum) is a protozoan parasite living in intestinal tracts of termites and cockroaches. Chen and Meng from China repoted first case of pulmonary L. blattarum infection in 1993. 137 cases have only been reported in literature between 1993 to 2013. Majority of these infections occur in immunocompromised patients and have been reported from China. We report a case of this rare entity in an immunocompetent young Indian male.

Existence of conserved domains in dystrophin and its associated complexes provide an opportunity to understand the role of dystrophin associated signalling and its association with neuronal metabolism in a variety of model organisms. We critically reviewed the studies till 2013 through established search engines and databases. Thus, we review the role of dystrophin and its isoforms in different animal models at developmental stages in the neuronal metabolism to enhance the therapeutic strategies. Dystrophin interacts with other proteins in such a way that, when affected, it results in co-morbidities including autism and other neuropsychiatric disorders. It is speculated that various signalling molecules may converge to disrupt neuronal metabolism not adequately studied. TGF-β, RhoGAP and CAM mediated signalling molecules are the chief cause of mortalities due to respiratory and cardiac involvement but remain underevaluated targets for cognitive impairment in DMD/BMD. Manipulation of these signalling pathways could be potent intervention in dystrophin induced cognitive impairment while complementary therapeutic approaches may also be helpful in the treatment of cognitive impairment associated with DMD/BMD.

Cytokines are immune signaling molecules that also function as neuromodulators. Cytokines are elevated in the peripheral blood of some individuals with mental disorders, suggesting that inflammation may contribute to their illness. Furthermore, immune therapy trials for systemic inflammatory disorders have reported improvements in anxiety and depression as secondary end points. These findings bolster the salutary potential for anti-inflammatory treatment of primary psychiatric populations. However, immunotherapeutic trials in depression and other psychiatric disorders have largely yielded inconclusive or negative results. One possibility is the reliance of clinical trial designs on cross-sectional measurements of inflammatory markers in blood. Peripheral cytokine profiles may not reflect central inflammatory states and cannot disclose dynamic relationships between compartments. Because central cytokines directly modulate neural activity, mapping their dynamic relationships between the periphery and central nervous system may improve future clinical trial designs. Therefore, we performed a systematic search for studies that measured cytokines at multiple time points in paired blood and cerebrospinal fluid samples from humans and nonhuman primates. Our narrative synthesis of these studies found that peripheral and central cytokine fluctuations are uncorrelated in humans under basal conditions. Moreover, an evoked increase in a cytokine's level peripherally may provoke a dramatic increase in a distinct cytokine centrally without eliciting a meaningful change in its own central level (cross-correlation in the absence of autocorrelation). Furthermore, physical and psychological stressors can induce compartment-specific cytokine changes and correlations. These initial observations highlight the need for a more complete map of cytokine dynamics in humans with and without mental illness.

Duchenne Muscular Dystrophy has emerged as a model to assess cognitive domains. The DMD gene variant location and its association with variable degrees of cognitive impairment necessitate identification of a common denominator. Computer architectures provide a framework to delineate the mechanisms involved in the cognitive functioning of the human brain. Copy number variations in the 79 exons of DMD gene were screened in 84 DMD subjects by Multiplex Ligation-dependent Probe Amplification (MLPA). DMD subjects were categorized based on the presence or absence of DP140 isoform. The cognitive and neuropsychological assessments were carried out as per inclusion criteria using standard scales. Instance-based learning theory (IBLT) based on the partial matching process was developed to mimic Stroop Color and Word Task (SCWT) performance on Adaptive Control of Thought-Rational (ACT-R) cognitive architecture based on IBLT. Genotype–phenotype correlation was conducted based on the mutation location in DMD gene. Assessment of specific cognitive domains in DP140 − ve group corresponded to the involvement of multiple brain lobes including temporal (verbal and visual learning and memory), parietal (visuo-conceptual and visuo-constructive abilities) and frontal (sustained and focused attention, verbal fluency, cognitive control). Working memory axis was found to be the central domain through tasks including RAVLT trial 1, recency effect, digit span backward, working memory index, arithmetic subtests in the Dp140 − ve group. IBLT validated the non-reliance of DMD subjects on recency indicating affected working memory domain. Modeling strategy revealed altered working memory processes in DMD cases with affected Dp140 isoform. DMD brain was observed to rely on primacy than the recency suggesting alterations in working memory capacity. Modeling revealed lowered activation of DMD brain with Dp140 − ve in order to retrieve the instances.

Inborn errors of immunity (IEI) can present with infections, autoimmunity, lymphoproliferation, granulomas, and malignancy. IEIs are due to genetic abnormalities that disrupt normal host-immune response or immune regulation. The microbiome appears essential for maintaining host immunity, especially in patients with a defective immune system. Altered gut microbiota in patients with IEI can lead to clinical symptoms. Microbial dysbiosis is the consequence of an increase in pro-inflammatory bacteria or a reduction in anti-inflammatory bacteria. However, functional and compositional differences in microbiota are also involved. Dysbiosis and a reduced alpha-diversity are well documented, particularly in conditions like common variable immunodeficiency. Deranged microbiota is also seen in Wiskott–Aldrich syndrome, severe combined immunodeficiency, chronic granulomatous disease, selective immunoglobulin-A deficiency, Hyper IgE syndrome (HIGES), X-linked lymphoproliferative disease-2, immunodysregulation, polyendocrinopathy, enteropathy, x-linked syndrome, and defects of IL10 signalling. Distinct gastrointestinal, respiratory, and cutaneous symptoms linked to dysbiosis are seen in several IEIs, emphasizing the importance of microbiome identification. In this study, we discuss the processes that maintain immunological homeostasis between commensals and the host and the disruptions thereof in patients with IEIs. As the connection between microbiota, host immunity, and infectious illnesses is better understood, microbiota manipulation as a treatment strategy or infection prevention method would be more readily employed. Therefore, optimal prebiotics, probiotics, postbiotics, and fecal microbial transplantation can be promising strategies to restore the microbiota and decrease disease pathology in patients with IEIs.