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M Shahidullah

Publications and source records attributed to M Shahidullah.

At least 19 recordsLinked to original sources
PubMed2001

Serum zinc and copper levels in the maternal blood and cord blood of neonates.

Estimation of serum zinc and copper in the maternal blood and cord blood of neonates was carried out to correlate the trace metals in the neonates and their mothers in relation to gestational age and birth weight. Sixty-five healthy neonates, both term and preterm and their mothers were selected. This cross sectional study was done at Azimpur Maternity Centre, Dhaka Medical College Hospital and Chemistry Division, Atomic Energy Centre, Dhaka, Bangladesh from July 1997 to June 1998. The estimation of trace metals was carried out by Atomic Absorption Spectrophotometry (AAS). The mean serum zinc levels in the maternal blood and cord blood were 0.47 +/- 0.24 microgram/ml and 0.85 +/- 0.33 microgram/ml respectively and the mean copper levels in the maternal blood and cord blood were 1.37 +/- 0.62 micrograms/ml and 0.31 +/- 0.32 microgram/ml respectively. Cord blood zinc level was significantly higher and cord blood copper level was significantly lower than the corresponding maternal blood levels. There was no significant correlation between gestational age and serum zinc levels in the cord or maternal blood. But significant inverse correlation was found between gestational age and serum levels of copper in the maternal and cord blood.

Bangladesh↗
PubMed2001

Intraocular pressure and vascular effects of sodium azide in bovine perfused eye.

The effects of the nitrovasodilator, sodium azide, on intraocular pressure (IOP) and ciliary vascular tone were compared. IOP was measured in the bovine isolated eye that was perfused via the ciliary artery. Separately, vasodilator effects were assessed after raising the vascular tone using noradrenaline (10 microM). Aqueous humor formation (AHF) rate was estimated by a fluorescein dilution method. Cyclic GMP in the ciliary processes was measured by radioimmunoassay. When compared with controls, sodium azide (10 nmole bolus dose) was found to lower IOP (2.2 +/- 0.3 mm Hg; P < 0.01) via a reduction in AHF (12.19 +/- 0.26 microl/min to 6.36 +/- 0.53 microl/min; P < 0.001). Azide (1 micromole) also reduced ciliary vascular resistance (81.0 +/- 5.5%; P < 0.01). However, the drug was 20x more potent as an ocular hypotensive than as a vasodilator (ED50 0.28 nmole on IOP, 5.55 nmole on vascular effect). Azide (10 nmole) also increased levels of ciliary cyclic GMP (127 +/- 17 fmol/mg protein to 233 +/- 27 fmol/mg protein; P < 0.01). The IOP-lowering effect of azide does not appear to depend on its ability to activate guanylyl cyclase (GC) in vascular smooth muscle, but rather is likely a consequence of direct activation of ciliary epithelial GC.

Animals↗
PubMed2001

Signal transduction from bradykinin, angiotensin, adrenergic and muscarinic receptors to effector enzymes, including ADP-ribosyl cyclase.

Muscarinic acetylcholine receptors in NG108-15 neuroblastoma x glioma cells, and beta-adrenergic or angiotensin II receptors in cortical astrocytes and/or ventricular myocytes, utilize the direct signaling pathway to ADP-ribosyl cyclase within cell membranes to produce cyclic ADP-ribose (cADPR) from beta-NAD+. This signal cascade is analogous to the previously established transduction pathways from bradykinin receptors to phospholipase Cbeta and beta-adrenoceptors to adenylyl cyclase via G proteins. Upon receptor stimulation, the newly-formed cADPR may coordinately function to upregulate the release of Ca2+ from the type II ryanodine receptors as well as to facilitate Ca2+ influx through voltage-dependent Ca2+ channels. cADPR interacts with FK506, an immunosuppressant, at FKBP12.6, FK506-binding-protein, and calcineurin, or ryanodine receptors. cADPR also functions through activating calcineurin released from A-kinase anchoring protein (AKAP79). Thus, some G(q/11)-coupled receptors can control cADPR-dependent modulation in Ca2+ signaling.

ADP-ribosyl Cyclase↗
PubMed2001

Risk factors for acute respiratory infections among the slum infants of Dhaka city.

A cross-sectional study was conducted in five slums of Dhaka city. The study population was all adult women of reproductive age having an infant aged less than one year with a view to assessing the prevalence of Acute Respiratory Infections (ARIs) among the slum infants and also to identify the factors responsible for it. A total of 1,008 mothers were interviewed. Among them, 927 had children aged 0-12 months. Mothers with live infants (927) were asked if their children had any disease during the two weeks prior to the interview. Respiratory infection was the highest among the prevalent diseases (ARI 72%, diarrhoeal diseases 28%, measles 4% and others 4%). So, an emphasis was given in this regard. Out of 228 ARI cases, percentage of mild (78%) and severe ARI (11%) were present in children aged less than 6 months, whereas moderate ARI (23%) was higher in 6 months and above age groups. The variation was statistically significant between the two age groups (p<0.05). But there was no significant difference in ARI by sex (p>0.05). In logistic analysis, maternal age below 20 years, working mothers, low housing and socio-economic index, no household possession, no access to piped water and infant's age above 6 months appeared to be significant predictors of ARIs. The risk of acquiring ARI was 3.33 times higher in low socio-economic index, 3 times in no access to piped water, 2.39 times in low housing index, 1.9 times in mother's age below 20 years, 1.85 times in infant's age above 6 months, 1.69 times in working mothers. On the other hand, household possessions had protective effects on ARIs. The study provides important information for policy makers regarding the prevention of ARI among the children of the slum dwellers.

Acute Disease↗
PubMed2000

General anesthetic action at an internal protein site involving the S4-S5 cytoplasmic loop of a neuronal K(+) channel.

The structural bases of general anesthetic action on a neuronal K(+) channel were investigated using the series of homologous 1-alkanols, electrophysiology, and mutational analysis. Domain swapping between dShaw2 (alkanol-sensitive) and hKv3.4 (alkanol-resistant) and site-directed mutagenesis demonstrated that a 13-amino acid cytoplasmic loop (S4-S5) determines the selective inhibition of native dShaw2 channels by 1-alkanols. The S4-S5 loop may contribute to a receptor for both 1-alkanols and the inactivation particle, because the enhanced 1-alkanol sensitivity of hKv3.4 channels hosting S4-S5 mutations correlates directly with disrupted channel inactivation. Evidence of a discrete protein site was also obtained from the analysis of the relationship between potency and alkyl chain length, which begins to level off after 1-hexanol. Rapid application to the cytoplasmic side of inside-out membrane patches shows that the interaction between dShaw2 channels and 1-alkanols equilibrates in <200 ms. By contrast, the equilibration time is >1000-fold slower when the drug is applied externally to outside-out membrane patches. The data strongly favor a mechanism of inhibition involving a discrete internal site for 1-alkanols in dShaw2 K(+) channels. A new working hypothesis proposes that 1-alkanols lock dShaw2 channels in their closed conformation by a direct interaction at a crevice formed by the S4-S5 loop.

1-Butanol↗
PubMed1999

Atriopeptin, sodium azide and cyclic GMP reduce secretion of aqueous humour and inhibit intracellular calcium release in bovine cultured ciliary epithelium.

This study examined the involvement of cyclic GMP, protein kinase G and intracellular Ca2+ movements in the modulation of aqueous humour formation. Using the bovine arterially-perfused eye preparation, drug effects on intraocular pressure and aqueous humour formation rate were measured by manometry and fluorescein dilution, respectively. Drug effects on intracellular [Ca2+] were determined by fura-2 fluorescence ratio technique in nontransformed, cultured ciliary epithelium. Intra-arterial injection of atriopeptin (50 pmol) or sodium azide (10 nmol) produced significant reduction in aqueous humour formation (>38%). This was blocked by selective inhibition (KT-5823) of protein kinase G, but not by selective inhibition (KT-5720) of protein kinase A. Reductions of intraocular pressure produced by atriopeptin or azide were almost completely blocked by KT-5823. ATP (100 microM) caused rapid, transient increase in intracellular Ca2+ followed by a slow decline and prolonged plateau. This response showed concentration-dependent inhibition by atriopeptin, azide or 8-bromo cyclic GMP, and this inhibition of the rapid (peak) Ca2+ increase was enhanced by zaprinast (100 microM; phosphodiesterase inhibitor). KT-5823 blocked the suppression of the peak Ca2+ response but not suppression of the plateau. Arterial perfusion of ATP (0.1-100 microM) produced a concentration-dependent decrease in aqueous humour formation. Aqueous humour formation in the bovine eye can be manipulated through cyclic GMP, operating via protein kinase G. Close parallels appear when Ca2+ movements are modified by similar manipulations of cyclic GMP, suggesting that Ca2+ transients may play an important role in aqueous humour formation and that interplay occurs between cyclic GMP and Ca2+.

Adenosine Triphosphate↗
PubMed1999

Inactivation gating of Kv4 potassium channels: molecular interactions involving the inner vestibule of the pore.

Kv4 channels represent the main class of brain A-type K+ channels that operate in the subthreshold range of membrane potentials (Serodio, P., E. Vega-Saenz de Miera, and B. Rudy. 1996. J. Neurophysiol. 75:2174- 2179), and their function depends critically on inactivation gating. A previous study suggested that the cytoplasmic NH2- and COOH-terminal domains of Kv4.1 channels act in concert to determine the fast phase of the complex time course of macroscopic inactivation (Jerng, H.H., and M. Covarrubias. 1997. Biophys. J. 72:163-174). To investigate the structural basis of slow inactivation gating of these channels, we examined internal residues that may affect the mutually exclusive relationship between inactivation and closed-state blockade by 4-aminopyridine (4-AP) (Campbell, D.L., Y. Qu, R.L. Rasmussen, and H.C. Strauss. 1993. J. Gen. Physiol. 101:603-626; Shieh, C.-C., and G.E. Kirsch. 1994. Biophys. J. 67:2316-2325). A double mutation V[404,406]I in the distal section of the S6 region of the protein drastically slowed channel inactivation and deactivation, and significantly reduced the blockade by 4-AP. In addition, recovery from inactivation was slightly faster, but the pore properties were not significantly affected. Consistent with a more stable open state and disrupted closed state inactivation, V[404,406]I also caused hyperpolarizing and depolarizing shifts of the peak conductance-voltage curve ( approximately 5 mV) and the prepulse inactivation curve (>10 mV), respectively. By contrast, the analogous mutations (V[556,558]I) in a K+ channel that undergoes N- and C-type inactivation (Kv1.4) did not affect macroscopic inactivation but dramatically slowed deactivation and recovery from inactivation, and eliminated open-channel blockade by 4-AP. Mutation of a Kv4-specific residue in the S4-S5 loop (C322S) of Kv4.1 also altered gating and 4-AP sensitivity in a manner that closely resembles the effects of V[404, 406]I. However, this mutant did not exhibit disrupted closed state inactivation. A kinetic model that assumes coupling between channel closing and inactivation at depolarized membrane potentials accounts for the results. We propose that components of the pore's internal vestibule control both closing and inactivation in Kv4 K+ channels.

4-Aminopyridine↗
PubMed1998

Mainuddin ahmed

Explore the source record for details and available documents.

Journal Article↗
PubMed1998

KCR1, a membrane protein that facilitates functional expression of non-inactivating K+ currents associates with rat EAG voltage-dependent K+ channels.

Cerebellar granule neurons possess a non-inactivating K+ current, which controls resting membrane potentials and modulates the firing rate by means of muscarinic agonists. kcr1 was cloned from the cerebellar cDNA library by suppression cloning. KCR1 is a novel protein with 12 putative transmembrane domains and enhances the functional expression of the cerebellar non-inactivating K+ current in Xenopus oocytes. KCR1 also accelerates the activation of rat EAG K+ channels expressed in Xenopus oocytes or in COS-7 cells. Far-Western blotting revealed that KCR1 and EAG proteins interacted with each other by means of their C-terminal regions. These results suggest that KCR1 is the regulatory component of non-inactivating K+ channels.

Amino Acid Sequence↗
PubMed1998

Duration of protective immunity conferred by maternal tetanus toxoid immunization: further evidence from Matlab, Bangladesh.

OBJECTIVES: Although maternal tetanus immunization has been shown to be highly effective in the prevention of neonatal tetanus, unresolved questions remain concerning the required minimum number of doses and the resulting duration of effective immunity. This study examined the duration of effective immunity against neonatal tetanus provided by maternal tetanus immunization. METHODS: A randomized, double-blind cholera vaccine trial of 41,571 children and nonpregnant adult women carried out in 1974 in the Matlab comparison area of rural Bangladesh provided a unique opportunity to address dose and immunity issues. RESULTS: Children of women who received either 1 or 2 injections of tetanus toxoid experienced 4- to 14-day mortality levels consistently lower than those of children of unimmunized mothers. Analysis of neonatal-tetanus-related mortality showed that 2 injections of tetanus toxoid provided significant protection for subsequent durations of up to 12 or 13 years. CONCLUSIONS: The data demonstrate that a limited-dose regimen of maternal tetanus toxoid provides significant and extended protection against the risk of neonatal tetanus death.

Adolescent↗
PubMed1997

Sulfhydryl modification inhibits K+ (M) current with kinetics close to acetylcholine in rodent NG108-15 cells.

The effects of sulfhydryl reagents on M-type voltage-dependent potassium currents (IK(M)) were examined in NG108-15 cells transformed to express ml muscarinic acetylcholine receptors (mAChRs), a NGPM1-27 clone. Focal application of glutathione at millimolar concentrations dissolved in acidic solutions caused a transient inward current in NGPM1-27 cells at holding potentials of -30mV, associated with an inhibition of IK(M). The glutathione-induced response was mimicked by cysteine. These effects were also reproduced by superfusion with micromolar concentrations of HgCl2, AgNO3, N-methylmaleimide and p-chloromercuribenzoic acid (pCMB), agents which target protein thiols. Glutathione, HgCl2, AgNO3 and pCMB inhibited the peak conductance of IK(M) without shifting the half activating voltage (V1/2), which was comparable to the acetylcholine (ACh)-induced response. The voltage dependence of time constants for IK(M) deactivation in sulfhydryl reagent-, ACh- and non-treated cells resembled, but differed from that in Ba(2+)-treated cells. These results reveal that there is an accessible cysteine moiety, but not a disulfide bond, either on the M channel protein itself or on a protein directly involved in agonist-M channel coupling.

Acetylcholine↗
PubMed1997

Mobilisation of intracellular calcium by P2Y2 receptors in cultured, non-transformed bovine ciliary epithelial cells.

PURPOSE: To examine extracellular ATP for its ability to mobilise intracellular calcium in bovine ciliary epithelial cells; to establish and characterise P2Y2 receptor-mediated signal transduction in this tissue. METHODS: Bovine ciliary epithelial cells were isolated and cultured until confluence. The cells were reseeded on sterile coverslips and grown to obtain monolayers, then loaded with fura-2. Fluorescence was measured by a computer-controlled spectrofluorimeter and values calculated for intracellular calcium concentration. ATP, its analogues and other drugs were tested for their ability to mobilise intracellular calcium by adding them to the bathing solution. RESULTS: Basal cytosolic calcium in bovine ciliary epithelium was 138.4 +/- 0.8 nM (n = 274). In the presence of extracellular Ca2+, ATP, UTP or ADP induced a transient dose-dependent increase in intracellular calcium (maximum approx. 400%), which declined rapidly. The agonist potency order was UTP = ATP > ADP > AMP. Adenosine, alpha, beta-methylene-ATP and 2-methylthio-ATP were ineffective in mobilising intracellular calcium, as were adrenaline, noradrenaline, acetylcholine and carbachol. The response to ATP and UTP remained, in the absence of extracellular calcium or the presence of nickel. Desensitisation of the calcium response by repeated exposure to ATP was augmented by phorbol-myristate-acetate and abolished by staurosporine. The ATP response was abolished by preincubation with pertussis toxin. Microfluorimetric measurements on single cells established that both pigmented and non-pigmented epithelia responded to ATP or UTP similarly. CONCLUSIONS: In the bovine ciliary epithelium, ATP stimulates P2Y2 receptors coupled to a pertussis toxin-sensitive G protein. The results also suggest that this receptor activates phospholipase C, leading to mobilisation of calcium from intracellular stores.

Adenosine Diphosphate↗
PubMed1997

Atriopeptin lowers aqueous humor formation and intraocular pressure and elevates ciliary cyclic GMP but lacks uveal vascular effects in the bovine perfused eye.

The effects of atriopeptin (AP) on intraocular pressure (IOP), aqueous humor formation (AHF) and ciliary cyclic GMP in bovine eyes perfused in vitro through a ciliary artery were investigated. AHF was monitored fluorophotometrically by perfusing the anterior chamber with Bárány's mock aqueous humor containing fluorescein. To study the effect of AP on cyclic GMP synthesis, eyes were injected with an intra-arterial bolus of AP prior to dissection of the ciliary processes. For comparison, individual ciliary processes, or isolated ciliary epithelial cells were incubated with AP. Cyclic GMP was extracted by homogenization, aqueous partition and column chromatography, and measured by radioimmunoassay (RIA). Decreases in IOP or AHF were seen approximately 15 min after the injection of AP and persisted throughout a 60-80 min perfusion. Arterial perfusion pressure was not significantly altered by AP, even when vascular tone was raised by adding noradrenaline to the perfusate. In whole eyes, ciliary cyclic GMP increased in response to AP. Cyclic GMP in isolated ciliary processes, or cultured ciliary epithelial cells incubated with AP also increased. We conclude that the decrease in IOP in the bovine eye by AP is due to a reduction in AHF, which is independent of any vascular effect. Ciliary cyclic GMP may be the intracellular mediator involved.

Adrenergic alpha-Agonists↗
PubMed1996

Neurological outcome of severe cystic periventricular leukomalacia.

OBJECTIVE: To determine the neurological outcome of a cohort of premature babies having ultrasound diagnoses of severe cystic periventricular leukomalacia. METHODOLOGY: All neonatal intensive care unit admissions born at less than 35 weeks gestation or weighing less than 1500 g underwent serial cranial ultrasounds. Those developing severe bilateral cystic periventricular leukomalacia (12 patients) were then followed clinically to a mean age of 27.3 months. RESULTS: Ten of the 12 patients fulfilling strict ultrasound criteria survived. All had a major neurological handicap, all having spastic quadriparesis and visual impairments, with most suffering global developmental delay and epilepsy. CONCLUSIONS: Severe bilateral cystic periventricular leukomalacia results in major permanent handicap. It is currently impossible to identify most patients with this condition while they are being ventilated. Non-ultrasound techniques are needed to diagnose the condition earlier, and to give guidance to management.

Developmental Disabilities↗
PubMed1995

Microheterogeneity in heteromultimeric assemblies formed by Shaker (Kv1) and Shaw (Kv3) subfamilies of voltage-gated K+ channels.

Single K+ channels were recorded in Xenopus oocytes injected with a 1:1 mixture of mRNAs coding for NGK1 (Kv1.2) and NGK2 (Kv3.1a) voltage-dependent K+ channels. A new class of channels of 18 pS conductance was observed, and was designated as NGK1,2 channels. According to their properties of activation voltages and open life times, four types of NGK1,2 channels with microheterogeneity were detected. The results suggest that voltage-dependent NGK1 Shaker and NGK2 Shaw K+ channels, from different subfamilies, assemble to form heteromultimeric K+ channels, giving rise to a mosaic of characteristics inherited from two parental channels.

Animals↗
PubMed1995

Slow inactivation conserved in heteromultimeric voltage-dependent K+ channels between Shaker (Kv1) and Shaw (Kv3) subfamilies.

Single K+ channels were recorded under the cell-attached mode in Xenopus oocytes injected with an equal amount of mRNAs coding for NGK1 (Kv1.2) and NGK2 (Kv3.1a) voltage-dependent K+ channels. A new class of channels of 20 pS in conductance with three degrees of inactivation was observed. The results suggest that voltage-dependent NGK1 Shaker and NGK2 Shaw K+ channels, from different subfamilies, assemble to form heteromultimeric K+ channels in Xenopus oocytes and show characteristics inherited from two parental channels.

Animals↗
PubMed1995

An evaluation of population projection errors for census tracts.

"In this article we evaluate the accuracy and bias of projections of total population and population by age group for census tracts in three counties in Florida. We use [U.S. census] data from 1970 and 1980 and several simple extrapolation techniques to produce projections for 1990; we then compare these projections with 1990 census counts and evaluate the differences. For the total sample, we find mean absolute errors of 17%-20% for the three most accurate techniques for projecting total population and find no indication of overall bias. For individual age groups, mean absolute errors range from 20%-29%." This is a revised version of a paper presented at the 1993 Annual Meeting of the Population Association of America.

Age Distribution↗