Mohammed Hossain | Shahjalal University of Science and Technology (original) (raw)

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Papers by Mohammed Hossain

A management plan is a blueprint for the way your organization is run, both day-to-day and over t... more A management plan is a blueprint for the way your organization is run, both day-to-day and over the long term. It does not have to be a complicated document and there is no standard format for writing one. It may vary from a simple description for a small field or stand to a very detailed multiple resource plan. Forest management is a branch of forestry concerned with the overall administrative, economic, legal and social aspects and with the essentially scientific and technical aspects, especially silviculture protection, and forest regulation. This includes management for aesthetics, fish, recreation, urban values, water, wilderness, wildlife, wood products, forest genetic resources and other forest resource values. Management can be based on conservation, economics, or a mixture of the two. Techniques include timber extraction, planting and replanting of various species, cutting roads and pathways through forests, and preventing fire. Here is given a management plan for Madhupur Sal Forest which is a sustainable forest management plan and its time period is 20 years. The management plan prepared considering three aspect 1. Ecological aspect 2. Economical aspect

The object of this study was to evaluate and improve the guidelines for the Integrated Management... more The object of this study was to evaluate and improve the guidelines for the Integrated Management of Childhood Illness (IMCI) with respect to identifying young infants and children requiring referral to hospital in an area of low malaria prevalence. A total of 234 young infants (aged 1 week to 2 months) and 668 children (aged 2 months to 5 years) were prospectively sampled from patients presenting at a children's hospital in Dhaka, Bangladesh. The study paediatricians obtained a standardized history and carried out a ,physical examination, including items in the IMCI guidelines developed by WHO and UNICEF. The paediatricians made a provisional diagnosis andjudged whether each patient needed hospital admission. Using the paediatrician's assessment of a need for admission as the standard, the sensitivity and specificity of the current and modified IMCI guidelines for correctly referring patients to hospital were examined.

Journal of Cerebral Blood Flow and Metabolism, 2008

In evaluating drugs that enter or are excluded from the brain, novel pharmaceutical strategies ar... more In evaluating drugs that enter or are excluded from the brain, novel pharmaceutical strategies are needed. For this reason, we have developed a humanized Dynamic In vitro Blood-Brain Barrier model (hDIV-BBB) based on a novel human brain vascular endothelial cell line (HCMEC/D3), which closely mimics the BBB in vivo. In this system, HCMEC/D3 was grown in the lumen of hollow microporous fibers and exposed to a physiological pulsatile flow. Comparison with well-established humanized DIV-BBB models (based on human brain and non-brain vascular endothelial cells co-cultured with abluminal astrocytes) demonstrated that HCMEC/D3 cells cultured under flow conditions maintain in vitro physiological permeability barrier properties of the BBB in situ even in the absence of abluminal astrocytes. Measurements of glucose metabolism demonstrated that HCMEC/D3 cells retain an aerobic metabolic pathway. Permeability to sucrose and two relevant central nervous system drugs showed that the HCMEC/D3 cells grown under dynamic conditions closely mimic the physiological permeability properties of the BBB in situ (slope = 0.93). Osmotic disruption of the BBB was also successfully achieved. Peak BBB opening in the DIV-BBB lasted from 20 to 30 mins and was completely reversible. Furthermore, the sequence of flow cessation/ reperfusion in the presence of leukocytes led to BBB failure as demonstrated by a biphasic decrease in transendothelial electrical resistance. Additionally, BBB failure was paralleled by the intraluminal release of proinflammatory factors (interleukin-6 and interleukin-1b) and matrix metalloproteinase-9 (MMP-9). Pretreatment with ibuprofen (0.125 mmol/L) prevented BBB failure by decreasing the inflammatory response after flow cessation/reperfusion.

Journal of Cellular Physiology, 2006

Brain ischemia is associated with an acute release of pro-inflammatory cytokines, notably TNF-α a... more Brain ischemia is associated with an acute release of pro-inflammatory cytokines, notably TNF-α and IL-6 and failure of the blood–brain barrier. Shear stress, hypoxia-hypoglycemia, and blood leukocytes play a significant role in blood–brain barrier failure during transient or permanent ischemia. However, these mechanisms have not been studied as independent variables for in vitro ischemia. The present study, using a dynamic in vitro blood–brain barrier model, showed that flow cessation/reperfusion under normoxia–normoglycemia or hypoxia–hypoglycemia without blood leukocytes in the luminal perfusate had a modest, transient effect on cytokine release and blood–brain barrier permeability. By contrast, exposure to normoxic–normoglycemic flow cessation/reperfusion with blood leukocytes in the luminal perfusate led to a significant increase in TNF-α and IL-6, accompanied by biphasic blood–brain barrier opening. Enhanced permeability was partially prevented with an anti-TNF-α antibody. In leukocyte-free cartridges, the same levels of IL-6 had no effect, while TNF-α caused a moderate increase in blood–brain barrier permeability, suggesting that blood leukocytes are the prerequisite for cytokine release and blood–brain barrier failure during reduction or cessation of flow. These cells induce release of TNF-α early after ischemia/reperfusion; TNF-α triggers release of IL-6, since blockade of TNF-α prevents IL-6 release, whereas blockade of IL-6 induces TNF-α release. Pre-treatment of blood leukocytes with the cyclooxygenase (COX) inhibitor, ibuprofen, inhibited cytokine release and completely preserved blood–brain barrier permeability during the reperfusion period. In conclusion, loss of flow (flow cessation/reperfusion) independent of hypoxia–hypoglycemia plays a significant role in blood–brain barrier failure by stimulating leukocyte-mediated inflammatory mechanisms. © 2005 Wiley-Liss, Inc.

Neuroscience, 2003

Multiple drug resistance occurs when cells fail to respond to chemotherapy. Although it has been ... more Multiple drug resistance occurs when cells fail to respond to chemotherapy. Although it has been established that the drug efflux protein P-glycoprotein protects the brain from xenobiotics, the mechanisms involved in the regulation of expression of multiple drug resistance genes and proteins are not fully understood. Re-entry into the cell cycle and integrity of the p53 signaling pathway have been proposed as triggers of multiple drug resistance expression in tumor cells. Whether this regulation occurs in non-tumor CNS tissue is not known. Since multiple drug resistance overexpression has been reported in glia and blood vessels from epileptic brain, we investigated the level of expression of multidrug resistance protein, multidrug resistance-associated proteins and lung resistance protein in endothelial cells and astrocytes isolated from epileptic patients or studied in situ in surgical tissue samples by double label immunocytochemistry. Reverse transcriptase-polymerase chain reaction and Western blot analyses revealed that multiple drug resistance, multidrug resistance protein, and lung resistance protein are expressed in these cells. Given that lung resistance proteins have been reported to be preferentially expressed by tumors, we investigated expression of tumor suppressor genes in epileptic cortices. The pro-apoptotic proteins p53 and p21 could not be detected in "epileptic" astrocytes, while endothelial cells from the same samples readily expressed these proteins, as did normal brain astroglia and normal endothelial cells. Other apoptotic markers were also absent in epileptic glia.

Epilepsia, 2007

Summary: Purpose: A biotechnologic breakthrough for the study of drug permeability across the blo... more Summary: Purpose: A biotechnologic breakthrough for the study of drug permeability across the blood–brain barrier (BBB) would be the use of a reproducible in vitro model that recapitulates the functional, structural, and pathologic properties of the BBB in situ. We developed a humanized dynamic in vitro BBB model (DIV-BBB) based on cocultures of human microvascular endothelial cells (HBMECs) from “normal” and drug-resistant epileptic brain tissue with human brain astrocytes (HAs) from epilepsy patients or controls.Methods: HBMECs and HAs were cocultured for 28 days in polypropylene capillaries. HBMECs were exposed to physiologic levels of shear stress generated by intraluminal flow. Permeability to [3H]sucrose, [14C]phenytoin, and [14C]diazepam was measured in control and drug-resistant DIV-BBB with and without pretreatment with the MDR1 inhibitor XR9576. BBB integrity was monitored by transendothelial electrical resistance measurements (TEERs). Cell growth and viability were assessed by measurement of glucose consumption and lactate production.Results: PSucrose and TEER values did not depend on the origin of the endothelium used (epileptic or normal). PPhenytoin was 10-fold less (1.54 × 10−6 cm/s) in drug-resistant BBB models than in controls (1.74 × 10−5 cm/s). MDR1 blockade with XR9576 was effective (3.5-fold increase) only in drug-resistant cultures. PDiazepam in control and drug-resistant DIV-BBB was not affected by XR9576 and did not depend on the epileptic or control origin of endothelia. The overall contribution of epileptic glia to pharmacoresistance was negligible.Conclusions: These results show that, for the substances used, the humanized DIV-BBB recapitulates the physiologic permeability properties of the BBB in vivo and is also capable of mimicking a drug-resistant BBB phenotype.

Brain Research, 2006

Endothelial cells in vivo are continuously exposed to shear stress, a tangential force generated ... more Endothelial cells in vivo are continuously exposed to shear stress, a tangential force generated by the flow of blood across their apical surfaces that affects endothelial cell structure and function. By contrast, the Transwell apparatus cannot reproduce the presence of intraluminal blood flow that is essential for the formation and differentiation of the BBB.

Neuroscience, 2006

Malformations of cortical development (MCD) result from abnormal neuronal positioning during cort... more Malformations of cortical development (MCD) result from abnormal neuronal positioning during corticogenesis. MCD are believed to be the morphological and perhaps physiological bases of several neurological diseases, spanning from mental retardation to autism and epilepsy. In view of the fact that during development, an appropriate blood supply is necessary to drive organogenesis in other organs, we hypothesized that vasculogenesis plays an important role in brain development and that E15 exposure in rats to the angiogenesis inhibitor thalidomide would cause postnatal MCD. Our results demonstrate that thalidomide inhibits angiogenesis in vitro at concentrations that result in significant morphological alterations in cortical and hippocampal regions of rats prenatally exposed to this vasculotoxin. Abnormal neuronal development was associated with vascular malformations and a leaky blood-brain barrier. Protein extravasation and uptake of fluorescent albumin by neurons, but not glia, was commonly associated with abnormal cortical development. Neuronal hyperexcitability was also a hallmark of these abnormal cortical regions. Our results suggest that prenatal vasculogenesis is required to support normal neuronal migration and maturation. Altering this process leads to failure of normal cerebrovascular development and may have a profound implication for CNS maturation.

Brain Research, 2003

Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet... more Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet unknown mechanisms. Ischemia is associated with anoxia, aglycemia and loss of flow (i.e. shearing forces). We tested the hypothesis that loss of shear stress alone does not acutely affect BBB function due to a protective cascade of mechanisms involving cytokines and nitric oxide (NO). To determine the relative contribution of shear stress on BBB integrity we used a dynamic in vitro BBB model based on co-culture of rat brain microvascular endothelial cells (RBMEC) and astrocytes. Trans-endothelial electrical resistance (TEER), IL-6 release and NO levels were measured from the lumenal and ablumenal compartments throughout the experiment. Flow-exposed RBMEC were challenged with 1 h of normoxic-normoglycemic flow cessation (NNFC) followed by reperfusion for 2 to 24 h. NNFC caused a progressive drop in nitric oxide production during flow cessation followed by a time-dependent increase in ablumenal IL-6 associated with a prolonged NO increase during reperfusion. The nitric oxide synthetase (NOS) inhibitor L-NAME (10 microM) abrogated all effects of NNFC, including changes in NO and cytokine production. BBB permeability did not increase during or after NNFC/reperfusion, but was increased by treatment with L-NAME or when the effects of IL-6 were blocked. Flow adapted RBMEC and astrocytes respond to NNFC/reperfusion by overproduction of IL-6, possibly secondary to increased production of NO during the reperfusion. Maintenance of BBB function during and following NNFC appears to depend on intact NO signaling and IL-6 release.

A management plan is a blueprint for the way your organization is run, both day-to-day and over t... more A management plan is a blueprint for the way your organization is run, both day-to-day and over the long term. It does not have to be a complicated document and there is no standard format for writing one. It may vary from a simple description for a small field or stand to a very detailed multiple resource plan. Forest management is a branch of forestry concerned with the overall administrative, economic, legal and social aspects and with the essentially scientific and technical aspects, especially silviculture protection, and forest regulation. This includes management for aesthetics, fish, recreation, urban values, water, wilderness, wildlife, wood products, forest genetic resources and other forest resource values. Management can be based on conservation, economics, or a mixture of the two. Techniques include timber extraction, planting and replanting of various species, cutting roads and pathways through forests, and preventing fire. Here is given a management plan for Madhupur Sal Forest which is a sustainable forest management plan and its time period is 20 years. The management plan prepared considering three aspect 1. Ecological aspect 2. Economical aspect

The object of this study was to evaluate and improve the guidelines for the Integrated Management... more The object of this study was to evaluate and improve the guidelines for the Integrated Management of Childhood Illness (IMCI) with respect to identifying young infants and children requiring referral to hospital in an area of low malaria prevalence. A total of 234 young infants (aged 1 week to 2 months) and 668 children (aged 2 months to 5 years) were prospectively sampled from patients presenting at a children's hospital in Dhaka, Bangladesh. The study paediatricians obtained a standardized history and carried out a ,physical examination, including items in the IMCI guidelines developed by WHO and UNICEF. The paediatricians made a provisional diagnosis andjudged whether each patient needed hospital admission. Using the paediatrician's assessment of a need for admission as the standard, the sensitivity and specificity of the current and modified IMCI guidelines for correctly referring patients to hospital were examined.

Journal of Cerebral Blood Flow and Metabolism, 2008

In evaluating drugs that enter or are excluded from the brain, novel pharmaceutical strategies ar... more In evaluating drugs that enter or are excluded from the brain, novel pharmaceutical strategies are needed. For this reason, we have developed a humanized Dynamic In vitro Blood-Brain Barrier model (hDIV-BBB) based on a novel human brain vascular endothelial cell line (HCMEC/D3), which closely mimics the BBB in vivo. In this system, HCMEC/D3 was grown in the lumen of hollow microporous fibers and exposed to a physiological pulsatile flow. Comparison with well-established humanized DIV-BBB models (based on human brain and non-brain vascular endothelial cells co-cultured with abluminal astrocytes) demonstrated that HCMEC/D3 cells cultured under flow conditions maintain in vitro physiological permeability barrier properties of the BBB in situ even in the absence of abluminal astrocytes. Measurements of glucose metabolism demonstrated that HCMEC/D3 cells retain an aerobic metabolic pathway. Permeability to sucrose and two relevant central nervous system drugs showed that the HCMEC/D3 cells grown under dynamic conditions closely mimic the physiological permeability properties of the BBB in situ (slope = 0.93). Osmotic disruption of the BBB was also successfully achieved. Peak BBB opening in the DIV-BBB lasted from 20 to 30 mins and was completely reversible. Furthermore, the sequence of flow cessation/ reperfusion in the presence of leukocytes led to BBB failure as demonstrated by a biphasic decrease in transendothelial electrical resistance. Additionally, BBB failure was paralleled by the intraluminal release of proinflammatory factors (interleukin-6 and interleukin-1b) and matrix metalloproteinase-9 (MMP-9). Pretreatment with ibuprofen (0.125 mmol/L) prevented BBB failure by decreasing the inflammatory response after flow cessation/reperfusion.

Journal of Cellular Physiology, 2006

Brain ischemia is associated with an acute release of pro-inflammatory cytokines, notably TNF-α a... more Brain ischemia is associated with an acute release of pro-inflammatory cytokines, notably TNF-α and IL-6 and failure of the blood–brain barrier. Shear stress, hypoxia-hypoglycemia, and blood leukocytes play a significant role in blood–brain barrier failure during transient or permanent ischemia. However, these mechanisms have not been studied as independent variables for in vitro ischemia. The present study, using a dynamic in vitro blood–brain barrier model, showed that flow cessation/reperfusion under normoxia–normoglycemia or hypoxia–hypoglycemia without blood leukocytes in the luminal perfusate had a modest, transient effect on cytokine release and blood–brain barrier permeability. By contrast, exposure to normoxic–normoglycemic flow cessation/reperfusion with blood leukocytes in the luminal perfusate led to a significant increase in TNF-α and IL-6, accompanied by biphasic blood–brain barrier opening. Enhanced permeability was partially prevented with an anti-TNF-α antibody. In leukocyte-free cartridges, the same levels of IL-6 had no effect, while TNF-α caused a moderate increase in blood–brain barrier permeability, suggesting that blood leukocytes are the prerequisite for cytokine release and blood–brain barrier failure during reduction or cessation of flow. These cells induce release of TNF-α early after ischemia/reperfusion; TNF-α triggers release of IL-6, since blockade of TNF-α prevents IL-6 release, whereas blockade of IL-6 induces TNF-α release. Pre-treatment of blood leukocytes with the cyclooxygenase (COX) inhibitor, ibuprofen, inhibited cytokine release and completely preserved blood–brain barrier permeability during the reperfusion period. In conclusion, loss of flow (flow cessation/reperfusion) independent of hypoxia–hypoglycemia plays a significant role in blood–brain barrier failure by stimulating leukocyte-mediated inflammatory mechanisms. © 2005 Wiley-Liss, Inc.

Neuroscience, 2003

Multiple drug resistance occurs when cells fail to respond to chemotherapy. Although it has been ... more Multiple drug resistance occurs when cells fail to respond to chemotherapy. Although it has been established that the drug efflux protein P-glycoprotein protects the brain from xenobiotics, the mechanisms involved in the regulation of expression of multiple drug resistance genes and proteins are not fully understood. Re-entry into the cell cycle and integrity of the p53 signaling pathway have been proposed as triggers of multiple drug resistance expression in tumor cells. Whether this regulation occurs in non-tumor CNS tissue is not known. Since multiple drug resistance overexpression has been reported in glia and blood vessels from epileptic brain, we investigated the level of expression of multidrug resistance protein, multidrug resistance-associated proteins and lung resistance protein in endothelial cells and astrocytes isolated from epileptic patients or studied in situ in surgical tissue samples by double label immunocytochemistry. Reverse transcriptase-polymerase chain reaction and Western blot analyses revealed that multiple drug resistance, multidrug resistance protein, and lung resistance protein are expressed in these cells. Given that lung resistance proteins have been reported to be preferentially expressed by tumors, we investigated expression of tumor suppressor genes in epileptic cortices. The pro-apoptotic proteins p53 and p21 could not be detected in "epileptic" astrocytes, while endothelial cells from the same samples readily expressed these proteins, as did normal brain astroglia and normal endothelial cells. Other apoptotic markers were also absent in epileptic glia.

Epilepsia, 2007

Summary: Purpose: A biotechnologic breakthrough for the study of drug permeability across the blo... more Summary: Purpose: A biotechnologic breakthrough for the study of drug permeability across the blood–brain barrier (BBB) would be the use of a reproducible in vitro model that recapitulates the functional, structural, and pathologic properties of the BBB in situ. We developed a humanized dynamic in vitro BBB model (DIV-BBB) based on cocultures of human microvascular endothelial cells (HBMECs) from “normal” and drug-resistant epileptic brain tissue with human brain astrocytes (HAs) from epilepsy patients or controls.Methods: HBMECs and HAs were cocultured for 28 days in polypropylene capillaries. HBMECs were exposed to physiologic levels of shear stress generated by intraluminal flow. Permeability to [3H]sucrose, [14C]phenytoin, and [14C]diazepam was measured in control and drug-resistant DIV-BBB with and without pretreatment with the MDR1 inhibitor XR9576. BBB integrity was monitored by transendothelial electrical resistance measurements (TEERs). Cell growth and viability were assessed by measurement of glucose consumption and lactate production.Results: PSucrose and TEER values did not depend on the origin of the endothelium used (epileptic or normal). PPhenytoin was 10-fold less (1.54 × 10−6 cm/s) in drug-resistant BBB models than in controls (1.74 × 10−5 cm/s). MDR1 blockade with XR9576 was effective (3.5-fold increase) only in drug-resistant cultures. PDiazepam in control and drug-resistant DIV-BBB was not affected by XR9576 and did not depend on the epileptic or control origin of endothelia. The overall contribution of epileptic glia to pharmacoresistance was negligible.Conclusions: These results show that, for the substances used, the humanized DIV-BBB recapitulates the physiologic permeability properties of the BBB in vivo and is also capable of mimicking a drug-resistant BBB phenotype.

Brain Research, 2006

Endothelial cells in vivo are continuously exposed to shear stress, a tangential force generated ... more Endothelial cells in vivo are continuously exposed to shear stress, a tangential force generated by the flow of blood across their apical surfaces that affects endothelial cell structure and function. By contrast, the Transwell apparatus cannot reproduce the presence of intraluminal blood flow that is essential for the formation and differentiation of the BBB.

Neuroscience, 2006

Malformations of cortical development (MCD) result from abnormal neuronal positioning during cort... more Malformations of cortical development (MCD) result from abnormal neuronal positioning during corticogenesis. MCD are believed to be the morphological and perhaps physiological bases of several neurological diseases, spanning from mental retardation to autism and epilepsy. In view of the fact that during development, an appropriate blood supply is necessary to drive organogenesis in other organs, we hypothesized that vasculogenesis plays an important role in brain development and that E15 exposure in rats to the angiogenesis inhibitor thalidomide would cause postnatal MCD. Our results demonstrate that thalidomide inhibits angiogenesis in vitro at concentrations that result in significant morphological alterations in cortical and hippocampal regions of rats prenatally exposed to this vasculotoxin. Abnormal neuronal development was associated with vascular malformations and a leaky blood-brain barrier. Protein extravasation and uptake of fluorescent albumin by neurons, but not glia, was commonly associated with abnormal cortical development. Neuronal hyperexcitability was also a hallmark of these abnormal cortical regions. Our results suggest that prenatal vasculogenesis is required to support normal neuronal migration and maturation. Altering this process leads to failure of normal cerebrovascular development and may have a profound implication for CNS maturation.

Brain Research, 2003

Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet... more Loss of blood-brain barrier (BBB) function may contribute to post-ischemic cerebral injury by yet unknown mechanisms. Ischemia is associated with anoxia, aglycemia and loss of flow (i.e. shearing forces). We tested the hypothesis that loss of shear stress alone does not acutely affect BBB function due to a protective cascade of mechanisms involving cytokines and nitric oxide (NO). To determine the relative contribution of shear stress on BBB integrity we used a dynamic in vitro BBB model based on co-culture of rat brain microvascular endothelial cells (RBMEC) and astrocytes. Trans-endothelial electrical resistance (TEER), IL-6 release and NO levels were measured from the lumenal and ablumenal compartments throughout the experiment. Flow-exposed RBMEC were challenged with 1 h of normoxic-normoglycemic flow cessation (NNFC) followed by reperfusion for 2 to 24 h. NNFC caused a progressive drop in nitric oxide production during flow cessation followed by a time-dependent increase in ablumenal IL-6 associated with a prolonged NO increase during reperfusion. The nitric oxide synthetase (NOS) inhibitor L-NAME (10 microM) abrogated all effects of NNFC, including changes in NO and cytokine production. BBB permeability did not increase during or after NNFC/reperfusion, but was increased by treatment with L-NAME or when the effects of IL-6 were blocked. Flow adapted RBMEC and astrocytes respond to NNFC/reperfusion by overproduction of IL-6, possibly secondary to increased production of NO during the reperfusion. Maintenance of BBB function during and following NNFC appears to depend on intact NO signaling and IL-6 release.