Articles

Broad medleys of research have recognized the microglial activation in perilous psychiatric maladies such as schizophrenia, bipolar disorder, and major depressive disorder. There is a scenario of enlivening of peripheral monocytic cells along with the microglial interactions within the body while considering the Pathogenesis of psychiatric disorders. this review, epitomize and discuss the activation of microglia and monocytic cells in psychiatric disorders, thereby showcasing the potential association between these cell types and the Pathogenisis of the ailment , and proffer perspectives for future research on these processes.

The present article extends the PVSG-WHO criteria into a simplified set of Rotterdam and European Clinical, Molecular and Pathological (RCP/ECMP) criteria to diagnose and classify the myeloproliferative neoplasms (MPNs). The crude WHO criteria still miss the masked and early stages of ET and PV. Bone marrow histology has a near to 100% sensitivity and specificity to distinguish thrombocythemia in BCR/ABL positive CML and ET, and the myelodysplastic syndromes in RARS-T and 5q-minus syndrome from BCR/ABL negative thrombocythemias in myeloproliferative disorders (MPD). The presence of JAK2V617F mutation with increased erythrocytes above 6x1012/L and hematocrit (>0.51 males and >0.48 females) is diagnostic for PV obviating the need of red cell mass measurement. About half of WHO defined ET and PMF and 95% of PV patients are JAK2V617F positive. The combination of molecular marker screening JAK2V617F, JAK2 exon 12, MPL515 and CALR mutations and bone marrow pathology is 100% sensitive and specific for the diagnosis of latent, early and classical ECMP defined MPNs. The translation of WHO defined ET, PV and PMF into ECMP criteria have include the platelet count above 350 x109/l, mutation screening and bone marrow histology as inclusion criteria for thrombocythemia in various MPNs. According to ECMP criteria, ET comprises three distinct phenotypes of true ET, ET with features of early (“forme fruste” PV), and ET with a hypercellular erythrocythemic, megakaryocytic granulocytic myeloproliferation (EMGM or masked PV). The ECMP criteria clearly differentiate early erythrocythemic, prodromal and classical PV from congenital polycythemia and idiopathic or secondary erythrocytosis. The burden of JAK2V617F mutation in heterozygous ET and in homozygous PV is of major clinical and prognostic significance. JAK2 wild type MPL515 mutated normocellular ET and MF lack PV features in blood and bone marrow. JAK2/MPL wild type hypercellular ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) is the third distinct CALR mutated MPN. The translation of WHO into ECMP criteria for the classification of MPNs have a major impact on prognosis assessment and best choice for first line non-leukemogenic approach to postpone potential leukemogenic myelopsuppressive agents as long as possible in ET, PV and PMGM patients.

Starting from observation of pathogenesis of KURU disease we try to investigate the immunologic role played by central nervous systems. A deeply knowledge in the transmission model of this pathology can be an imaging/diagnostic tool to Verify the progression of this prion molecule from gastro intestinal systems to the brain. (After cannibalistic behavior). The prions can be considered a sort of trace ant in KURU to monitoring this process and immune- brain relationship. Interesting information can be obtained useful to produce new pharmacological strategies in some other degenerative brain disease involving innate immune system activation.

Primary myelofibrosis (PMF) is a distinct clinicopathological myeloproliferatve disease (MPD) not preceded by any other MPD ET, PV, CML,... Combined use of bone marrow histology and increased erythrocyte counts above 5.8x1012/L can replace increased red cell mass at time of presentation as the pathognomonic clue for the correct diagnosis of hetero/homozygous or homozygous mutated PV. Erythrocyte counts are in the normal range below 5.8x1012/L in heterozygous JAK2V617F mutated ET and prodromal PV but above 5.8x1012/L in heterozygous-homozygous or homozygous mutated PV. The bone marrow cellularity and morphology in pre-fibrotic ET, prodromal PV and PV carrying the JAK2V617F mutation are overlapping showing clustered increase of large mature pleomorphic megakaryocytes (M) with no increase of cellularity (<60%) in ET. The bone marrow is hypercellular (60%-80%) due to increased erythropoiesis megakaryopoiesis (EM) in prodromal and classical PV and trilinear hypercellular (80%-100% due increased megakaryopoiesis, erythropoiesis and granulopoiesis (EMG) in advanced PV and masked PV. Bone marrow cellularity ranging from normal (<60%) in ET to increased erythropoiesis (EM) in prodromal PV to hypercellular (80-100%) in advanced PV and masked PV largely depends on increasing JAK2V617F mutation load from low to high on top of other biological MPN variables like constitutional symptoms during long-term follow-up. MPL515 mutated ET is featured by an increase of clustered small and giant megakaryocytes with hyper-lobulated staghorn-like nuclei in a normal cellular bone marrow. The third entity of pronounced JAK2/MPL wild type ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) without PV features proved to be caused by calreticulin (CALR) mutation. CALR mutated thrombocythemia is characterized by dual proliferation of megakaryocytic and granulocytic bone marrow proliferation of dense clustered large to giant immature dysmorphic megakaryocytes with bulky (bulbous) hyperchromatic nuclei, which are not seen in MPL515-mutated Thrombocythemia and JAK2V617F-Thrombocythemia, prodromal PV and classical PV. 

Spinal muscular atrophy (SMA) is a genetic and gravely disease, portrayed by motor neuron (MN) death, thereby leading to progressive and accelerating muscle fragility, respiratory collapse, and, in the most severe cases, it even pave the way to death. At the neuromuscular junction (NMJ), abnormally have been reported in SMA, including neurofilament (NF) aggregation at presynaptic terminals, immature and smaller endplates, lowered transmitter release, and, eventually, muscle denervation. In this review the role of Agrin in SMA is studied. This review highlights the antagonizing role of Agrin in SMA

The broad spectrum of heterozygous versus homozygous JAK2V617F mutated MPN consists ET, ET with early features of PV (prodromal PV), classical PV, masked PV, advanced PV and post-PV myelofibrosis. Combined use of bone marrow histology and increased erythrocyte counts above 5.8x1012/L can replace increased red cell mass at time of presentation as the pathognomonic clue for the correct diagnosis of hetero/homozygous or homozygous mutated PV. Erythrocyte counts are in the normal range below 5.8x1012/L in heterozygous JAK2V617F mutated ET and prodromal PV but above 5.8x1012/L in heterozygous-homozygous or homozygous mutated PV. The bone marrow cellularity and morphology in pre-fibrotic ET, prodromal PV and PV carrying the JAK2V617F mutation are overlapping showing clustered increase of large mature pleomorphic megakaryocytes (M) with no increase of cellularity (<60%) in ET. The bone marrow is hypercellular (60%-80%) due to increased erythropoiesis megakaryopoiesis (EM) in prodromal and classical PV and trilinear hypercellular (80%-100% due increased megakaryopoiesis, erythropoiesis and granulopoiesis (EMG) in advanced PV and masked PV. Bone marrow cellularity ranging from normal (<60%) in ET to increased erythropoiesis (EM) in prodromal PV to hypercellular (80-100%) in advanced PV and masked PV largely depends on increasing JAK2V617F mutation load from low to high on top of other biological MPN variables like constitutional symptoms during long-term follow-up. MPL515 mutated ET is featured by an increase of clustered small and giant megakaryocytes with hyper-lobulated staghorn-like nuclei in a normal cellular bone marrow. The third entity of pronounced JAK2/MPL wild type ET associated with primary megakaryocytic granulocytic myeloproliferation (PMGM) without PV features proved to be caused by calreticulin (CALR) mutation. CALR mutated thrombocythemia is characterized by dual proliferation of megakaryocytic and granulocytic bone marrow proliferation of dense clustered large to giant immature dysmorphic megakaryocytes with bulky (bulbous) hyperchromatic nuclei, which are not seen in MPL515-mutated Thrombocythemia and JAK2V617F-Thrombocythemia, prodromal PV and classical PV. 

Background: This study aims to retrospectively investigate the comorbidity of ADHD multiple symptoms (behavioral) with alcohol addiction in a sample of adult alcohol-dependent patients and to test their current attentional skills (behavioral and cognitive). Methods: Thirty-two adult alcohol-dependent patients were examined for ADHD using a semi-structured interview and the Mini Mental State Examination to evaluate attention and inhibition functions. Brown ADD Scales were used to specifically examine ADHD syndrome. Patients were compared with thirty matched control participants selected from healthy population in few measures of attentional control and working memory. Results: 50% of patients showed evidence of primary ADHD symptoms: specifically, 28.12% showed criteria for ADHD highly probable, 12.50% for ADHD probable but not certain and 9.38% for ADHD possible but not likely. Patients also revealed several deficits in the selective visual attention, interference control and verbal working memory compared to the control group. Conclusions: These results revealed that adult alcohol-dependent patients had retrospectively high comorbidity with ADHD and significant current deficits of the executive functions. These findings suggest the importance of early diagnosis and treatment of ADHD in order to prevent the development of alcohol dependence.

Pure Erythroid Leukemia (PEL) is an aggressive and exceedingly rare form of acute leukemia. In the 2008 WHO classification PEL was one of the subtypes of acute erythroid leukemia the other subtype being erythroleukemia (erythroid/ myeloid). In the 2016 WHO classification update, erythroleukemia was merged into myelodysplastic syndrome and PEL now is the only type of acute erythroid leukemia.106 cases of acute myeloid leukemia were diagnosed in 28 months in children’s hospital Lahore and PEL constituted 0.94%. Diagnosis of PEL is made by the bone marrow morphology showing predominant Immature erythroid precursors (proerythroblastic or undifferentiated), Periodic Acid- Schiff staining and immunophenotyping. In PEL no specific genetic mutations have been described but complex karyotypes and TP53 mutations are frequently noted. Future collaborative studies to identify the molecular defects will contribute to the development of targeted therapies that might improve the prognosis.

Naturally, microorganisms decompose the organic material existing in nature, both in the presence or absence of oxygen. The majority of materials such as poisonous chemical compounds, heavy metals, would prevent the treatment process from taking place, lead to the entry of these contaminants into the environment results in the emergence of numerous diseases. In the present study, using the TOXChem4.1 simulation model, attempts were made to simulate a wastewater treatment plant and then assess the dispersions of contaminants including 1,2-Dimethylnaphthalene, 1,3-Dinitropyrene, 1,6-Dimethylnaphthalene, 1,6-Dinitropyrene, and 17a-ethinylestradiol (EE2) in concentrations of a common scenario. The results of computer simulations showed that the EE2 contaminant is of the highest percentage of decomposition among others, due to its wider chemical structure. Consequently, it is clear that such contaminant is of the highest mass in the sludge exiting the treatment plant. In addition, the results of the simulations demonstrated that the highest volumes of gaseous pollutants take place in the modulation and initial sedimentation units.

Due to the urgent need for water in all parts of industrial or developing societies, water supply, and transmission facilities are suitable targets for biological risks. Given that even a short interruption in water supply and water supply operations has a great impact on daily activities in the community, the deliberate contamination of urban water resources has irreparable consequences in the field of public health, and the economy of society will follow. Unfortunately, most officials in the public health control departments in our country have received limited training in detecting accidental or intentional contamination of water resources and dealing with the spread of waterborne diseases both naturally and intentionally. For this reason, there is low preparedness in the responsible agencies to deal with waterborne diseases during biological risks. In the first step of this research, a review study has been conducted on water biological risks and operational strategies to deal with them. In the following, it has studied how Escherichia coli (E. coli) bacteria spread in aqueous media. In this regard, the kinetic model of the studied microorganism was analyzed based on the implementation of (Fick Law) in polar coordinates and the combination of (Dirac Distribution) with (Legendre polynomial) distribution. Finally, after studying the factors affecting the microbial pollutant emission coefficient, the effects of all three factors of linear velocity, linear motion time period, and angle of motion on the pollutant emission flux and biofilm diffusion time in the water supply network environment were investigated. Studies have shown that the linear velocity parameter of Escherichia coli with a nonlinear relationship has the greatest effects on the release of microbial contaminants.