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Biomedical subjects

M Saifuddin

Publications and source records attributed to M Saifuddin.

At least 19 recordsLinked to original sources
PubMed2002

Differences in the fatigue of masticatory and neck muscles between male and female.

The purpose of this study was to investigate the nature of fatigue and recovery of masticatory and neck muscles and the differences between sexes in normal subjects during experimentally induced loading. Subjects consisted of eight males (mean age: 27.6 years) and eight females (mean age: 24.2 years) selected from the volunteers in the Faculty of Dentistry, Hiroshima University. The inclusion criteria for the subjects were as follows: (1) good general health, (2) normal horizontal and vertical skeletal relationships, (3) no severe malocclusions and (4) no complaints of temporomandibular disorders. Each subject was requested to bite an occlusal-force meter with 98, 196 and 294 N forces on the first molar region per side for 45 s. Activities of the masseter and sternocleidomastoid (SCM) muscles were recorded during these performances. Fatigue and recovery ratios were calculated with mean power frequency of power spectrum using a fast Fourier transform algorithm. Significant differences in the fatigue ratios between both sexes were found for the masseter muscle with 98, 196 and 294 N bite forces. Meanwhile, the SCM presented a significant difference between both sexes only at 98 N biting. Significant differences in the recovery ratios between both sexes were more prominent in the masseter muscle than in the SCM. These results suggest that the differences in muscle endurance between sexes may have some association with higher susceptibility of craniomandibular disorders in females than in males.

Adult↗
PubMed2001

Human antibodies to major histocompatibility complex alloantigens mediate lysis and neutralization of HIV-1 primary isolate virions in the presence of complement.

Cellular proteins, including major histocompatibility complex (MHC) class I and class II antigens, are incorporated into the membrane of HIV-1 when virions bud from infected cells. Experiments were performed to determine whether human sera that contained MHC class I and/or class II antibodies would lyse or neutralize a primary isolate of HIV. These results demonstrate that in the presence of complement, sera from some alloimmunized persons mediated significant anti-viral activity against an HIV primary isolate. Both lysis and neutralization of virus were observed. The antiviral effects were complement dependent because heat inactivation eliminated most anti-viral effects. Antiviral activity mediated by sera containing MHC alloantibodies in the presence of complement was > or = activity due to sera from HIV-infected persons as reported in this and a previous study. High levels of antibodies to both MHC class I and class II were present in sera that mediated the highest levels of anti-viral activity. Absorption of serum with platelets (which express class I but not class II antigens) substantially reduced their lytic activity. These studies suggest that MHC antibodies mediate potent anti-viral effects on primary isolates of HIV and support the possibility that deliberately alloimmunizing humans might protect against HIV infection.

Antibodies↗
PubMed2001

A quantitative electromyographic analysis of masticatory muscle activity in usual daily life.

OBJECTIVE: This study was designed to investigate whether a quantitative electromyographic (EMG) analysis with a special reference to the EMG amplitude at 98N bite force could reduce the influence of electrode relocation and to examine the reproducibility of masticatory muscle activity in usual daily life within individuals. SUBJECTS AND METHODS: In the first experiment, two sessions of surface EMG recording for masseter and anterior temporal muscles during tapping, and chewing gum and marshmallow were performed for 10 subjects with an interval of at least 1 week with electrode relocation. In the second experiment, two sessions of EMG recording during daytime (142 min, including mealtime) and sleep (142 min) were carried out for 10 subjects with an interval of at least 1 week. The average rectified EMG values were normalised with a special reference to the EMG amplitude induced by a 98N bite force. RESULTS: In the first experiment, high correlation coefficients and no significant differences in the mean normalised values of muscle activity were found between two sessions. Although the average rectified values showed high correlation coefficients, the mean masseter muscle activity while chewing gum was significantly different between two sessions. In addition, the variation in temporal muscle activity between two sessions while chewing gum was significantly smaller in the normalised values than in the average rectified ones. In the second experiment, less intra-individual variation in the normalised values of masticatory muscle activity between two sessions indicated the reproducibility. Normalised masticatory muscle activity showed less variation during mealtimes than during usual daytime and sleep. CONCLUSIONS: This quantitative EMG analysis could estimate the masticatory muscle activity by reducing the influences of electrode relocation, demonstrating an availability of this analysis for the evaluation of masticatory muscle activity in usual daily life.

Activities of Daily Living↗
PubMed2000

Cutting edge: activation of HIV-1 transcription by the MHC class II transactivator.

Both macrophages and activated CD4+ T cells can be productively infected by HIV-1, and both cell types express MHC class II molecules. Expression of MHC class II proteins in these cells is regulated by a specific transcriptional coactivator, the class II transactivator (CIITA). In this study, we report for the first time that CIITA expression profoundly influences HIV-1 replication. Stable expression of CIITA in Jurkat cells markedly increased 1) HIV-1 replication as assessed by the p24 Ag production and 2) luciferase expression after transfection with full-length provirus or long terminal repeat constructs. Similarly, transient expression of CIITA increased provirus expression as well as long terminal repeat promoter activity in 293 and HeLa-T4 cells. In contrast, mutant forms of CIITA did not increase HIV-1 expression. This study shows that expression of CIITA increases HIV-1 replication through a transcriptional mechanism.

Cell Line↗
PubMed2000

Expression of MHC class II in T cells is associated with increased HIV-1 expression.

HIV-1 replicates in activated T cells at significantly higher levels than in resting cells. Thus, certain molecules up-regulated during T cell activation appear to be important for HIV-1 replication. In this study, we present evidence suggesting that expression of MHC class II (class II) molecules on CD4+ T cells facilitate HIV-1 replication. T cells that expressed class II supported greater virus replication than T cells lacking class II. The class II+ cells, when either infected with HIV-1 or transfected with an env-minus HIV-1 provirus plasmid, produced 10-20-fold greater virus expression than class II- cells. Anti-class II antibody markedly inhibited virus expression in class II+ cells (but not class II- cells) and also decreased the nuclear binding activity of AP-1, an inducible transcription factor important in T cell activation and HIV-1 expression. Most importantly, the induction of class II expression by transfection of the MHC class II transactivator (CIITA) stimulated HIV-1 replication in Jurkat T cells. Taken together, these data suggest that expression of MHC class II molecules and/or CIITA in T cells enhances HIV-1 transcription.

CD4-Positive T-Lymphocytes↗
PubMed2000

Masticatory muscle activity in children and adults with different facial types.

The purpose of this study was to examine the relationship between the duration of masticatory muscle activity during daytime and vertical craniofacial morphology in children and adults. Thirty children (12 boys and 18 girls) and 30 adults (20 men and 10 women) with normal anteroposterior skeletal relations, acceptable occlusions, and without any temporomandibular joint disorders, were selected as subjects. Activities of the masseter, temporal, and digastric muscles were recorded for 3 hours during daytime, excluding the periods for meals, sleep, and hard-exercise, using a portable electromyogram recording system. A lateral cephalogram was taken of each subject at the intercuspal position to divide the subjects into 3 different facial types, ie, low, average, and high angle groups. Masseter, temporal, and digastric muscle activities mainly consisted of low-amplitude bursts during daytime. Children exhibited longer duration of temporal muscle activity, whereas the masseter muscle presented longer duration of activity in adults. The activities of masseter and digastric muscles were significantly related with the vertical facial type in both children and adults, although temporal muscle activity presented no significant relationship with the craniofacial morphology. The duration of masticatory muscle activity during daytime showed a significant difference between children and adults, indicating a close association with vertical craniofacial morphology in children and adults.

Adult↗
PubMed2000

Interaction of mannose-binding lectin with primary isolates of human immunodeficiency virus type 1.

Mannose-binding lectin (MBL) is present in human serum and plays an important role in innate immunity by binding to carbohydrate on micro-organisms. Whereas the gp120/gp41 of human immunodeficiency virus type 1 (HIV-1) contains numerous N-linked glycosylation sites and many of these sites contain high-mannose glycans which could interact with MBL, the interaction between MBL and primary isolates (PI) of HIV-1 has not been studied. To determine if PI of HIV bind to MBL, a virus capture assay was developed in which virus was incubated in MBL-coated microtitre wells followed by detection of bound virus with an ELISA for p24 antigen. The X4 HIV-1(MN) T cell line-adapted strain and PI of HIV (R5 and X4) bound to MBL. Binding of virus to MBL was via the carbohydrate-recognition domain of MBL since binding did not occur in the absence of Ca(2+) and was blocked by preincubation of MBL-coated wells with soluble mannan. The interaction of virus with MBL-coated wells was also inhibited by preincubation of virus with soluble MBL, indicating that both immobilized and soluble forms of MBL bound to HIV. Although host cell glycoproteins are incorporated into the membrane of HIV, binding of virus to immobilized MBL required expression of gp120/gp41 on virus particles, suggesting the presence of either an unusually high carbohydrate density and/or a unique carbohydrate structure on gp120/gp41 that is the target of MBL. This study shows that PI of HIV bind to MBL and suggests that MBL can selectively interact with HIV in vivo via carbohydrate structures on gp120/gp41.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Immune complexes containing human immunodeficiency virus type 1 primary isolates bind to lymphoid tissue B lymphocytes and are infectious for T lymphocytes.

This study investigated the interaction of tonsil B lymphocytes with immune complexes containing human immunodeficiency virus (HIV IC) primary isolates and the infectivity of the B cell-bound HIV IC. Treatment of virus with a source of antibody and complement increased HIV IC binding to B cells by 5.6-fold. Most of the HIV IC that bound to B cells were not internalized but remained on the cell surface and were gradually released over 72 h. Cell-bound HIV IC were highly infectious for T cells while virus released by cultured B cells was only slightly infectious. Removal of HIV IC from the B-cell surface by protease treatment reduced the infection of T cells to near-background levels, indicating that infectious virus remained on the B-cell surface. These studies show that B lymphocytes can carry and transfer infectious HIV IC to T cells and thus suggest a novel mode of infection of T cells in lymphoid tissue that could be important for pathogenesis during HIV infection.

B-Lymphocytes↗
PubMed2000

CD4-Negative cells bind human immunodeficiency virus type 1 and efficiently transfer virus to T cells.

The ability of human immunodeficiency virus strain MN (HIV(MN)), a T-cell line-adapted strain of HIV, and X4 and R5 primary isolates to bind to various cell types was investigated. In general, HIV(MN) bound to cells at higher levels than did the primary isolates. Virus bound to both CD4-positive (CD4(+)) and CD4-negative (CD4(-)) cells, including neutrophils, Raji cells, tonsil mononuclear cells, erythrocytes, platelets, and peripheral blood mononuclear cells (PBMC), although virus bound at significantly higher levels to PBMC. However, there was no difference in the amount of HIV that bound to CD4-enriched or CD4-depleted PBMC. Virus bound to CD4(-) cells was up to 17 times more infectious for T cells in cocultures than was the same amount of cell-free virus. Virus bound to nucleated cells was significantly more infectious than virus bound to erythrocytes or platelets. The enhanced infection of T cells by virus bound to CD4(-) cells was not due to stimulatory signals provided by CD4(-) cells or infection of CD4(-) cells. However, anti-CD18 antibody substantially reduced the enhanced virus replication in T cells, suggesting that virus that bound to the surface of CD4(-) cells is efficiently passed to CD4(+) T cells during cell-cell adhesion. These studies show that HIV binds at relatively high levels to CD4(-) cells and, once bound, is highly infectious for T cells. This suggests that virus binding to the surface of CD4(-) cells is an important route for infection of T cells in vivo.

B-Lymphocytes↗
PubMed1999

B lymphocytes in lymph nodes and peripheral blood are important for binding immune complexes containing HIV-1.

We investigated the interaction of HIV immune complexes (HIV IC) with mononuclear cells from lymph nodes and blood. While antibody alone did not affect binding of HIV IC to mononuclear cells, antibody plus complement increased binding by as much as 10-fold and complement alone also increased binding slightly. Most of the increased binding of HIV IC to mononuclear cells was blocked by heat-inactivation of complement and by OKB7 monoclonal antibody, indicating that virus binding was to CR2 on B cells. A similar pattern of antibody and complement dependence for binding of HIV IC was observed with two model systems; Raji and Arent B-cell lines. Most of the HIV IC that bound to lymph node cells were not internalized, but remained on the cell surface and were gradually released. However, even after 48 hr some HIV IC could be detected bound to cells. Under certain conditions, HIV IC were infectious for T cells if bound to B cells but not infectious if added directly to T cells. Additionally, HIV IC bound to B cells led to higher virus replication. These studies show that B lymphocytes from blood and lymph nodes can transfer infectious HIV IC to T cells.

Antigen-Antibody Complex↗
PubMed1999

Masseter muscle activity during the whole day in children and young adults.

Changes in size and shape of the craniofacial skeleton during growth may be related to the masticatory muscle function in daily life. The purpose of this study was to measure the masseter muscle activity during the whole day in children and to investigate the differences between children and young adults. Fifteen children (7.8-13.0 years of age) and 30 young adults (20.3-34.7 years of age), who had acceptable occlusions without any remarkable skeletal discrepancy or temporomandibular disorder, were used as the subjects. In both children and young adults, most high-amplitude bursts of masseter muscle appeared mainly during mealtime, whereas a substantially larger number of low-amplitude ones were widely distributed throughout the whole day. The number and total duration of bursts of masseter muscle activity during the whole day was greater in children than in young adults, although significant differences were not found between the sexes. During daytime and sleep, both the number and total duration of bursts were greater in children. During mealtime, no significant differences in the number of bursts were found between children and young adults, however, the duration of bursts tended to be longer in children. It is concluded that the masseter muscle activity during the whole day is greater in children than in young adults.

Adolescent↗
PubMed1999

Regulation of HIV-1 transcription.

Human immunodeficiency virus type-1 (HIV-1) is a highly pathogenic lentivirus that requires transcription of its provirus genome for completion of the viral life cycle and the production of progeny virions. Since the first genetic analysis of HIV-1 in 1985, much has been learned about the transcriptional regulation of the HIV-1 genome in infected cells. It has been demonstrated that HIV-1 transcription depends on a varied and complex interaction of host cell transcription factors with the viral long terminal repeat (LTR) promoter. The regulatory elements within the LTR interact with constitutive and inducible transcription factors to direct the assembly of a stable transcription complex that stimulates multiple rounds of transcription by RNA polymerase II (RNAPII). However, the majority of these transcripts terminate prematurely in the absence of the virally encoded trans-activator protein Tat, which stimulates HIV-1 transcription elongation by interacting with a stem-loop RNA element (TAR) formed at the extreme 5' end of all viral transcripts. The Tat-TAR interaction recruits a cellular kinase into the initiation-elongation complex that alters the elongation properties of RNAPII during its transit through TAR. This review summarizes our current knowledge and understanding of the regulation of HIV-1 transcription in infected cells and highlights the important contributions human lentivirus gene regulation has made to our general understanding of the transcription process.

Base Sequence↗
PubMed1998

The cAMP-dependent protein kinase A and protein kinase C-beta pathways synergistically interact to activate HIV-1 transcription in latently infected cells of monocyte/macrophage lineage.

The HIV-1 long terminal repeat (LTR) responds to a variety of cellular signal transduction pathways. We demonstrate that the cAMP-dependent protein kinase A (PKA) and protein kinase C (PKC) signaling pathways synergize to increase HIV-1 LTR-mediated transcription and viral replication in a latently infected promonocytic cell line (U1). The LTR-mediated synergy induced by cholera toxin (Ctx), a potent activator of the cAMP-dependent PKA pathway, and the PKC activator phorbol 12-myristate 13-acetate (PMA) was abrogated by a PKC-beta-specific inhibitor (LY333531). In contrast, the LTR-mediated synergy induced by Ctx and TNF alpha was not affected by LY333531. The synergy induced by Ctx and TNF alpha was also abrogated by mutation of the cAMP-responsive downstream sequence elements (DSE) in the 5' untranslated leader region, whereas the DSE mutations did not affect the synergy induced by Ctx and PMA. These distinctions indicate that Ctx cooperates differently with TNF alpha and PMA to activate the HIV-1 LTR. Ctx and PMA synergistically activated AP-1- and NF-kappa B-dependent transcription, even though no cooperative binding of AP-1 or NF-kappa B was observed in gel shift assays. An extensive mutational analysis of the HIV-1 LTR that included the NF-kappa B and AP-1 binding sites revealed no distinct cis-acting element or region within the HIV-1 LTR that was required for the transcriptional synergy. Ctx and PMA also synergistically interact to activate the HTLV-1 LTR. These results indicate that the transcriptional synergy elicited by Ctx and PMA targets multiple functional elements and promoters, requires a cooperative interaction between the PKA and PKC-beta pathways, and differs mechanistically from the transcriptional synergy induced by Ctx and TNF alpha.

Cell Line↗
PubMed1998

Transfer of host T-cell membrane HLA-DR and CD25 to target cells by human retroviruses.

Many enveloped viruses incorporate host membrane proteins, some of which remain functionally active and significantly affect viral phenotype. We investigated whether human retroviruses can transfer host membrane proteins to target cells. Following incubation with HTLV-I, HLA-DR and CD25 were detected on up to 70% of HPB-ALL cells. Similarly, HLA-DR and CD25 were also detected on cells following incubation with HIV-1. Cyclohexamide or azidothymidine (AZT) had no effect on detection, indicating that binding of virus or infection did not induce expression of these proteins. Detection of host proteins on target cells depended on binding as well as fusion of virus to the cell membrane, indicating that these proteins were inserted into target cell membranes. Virions also transferred host proteins to peripheral blood mononuclear cells (PBMCs). This aberrant transfer of T-cell activation proteins by HIV or HTLV may alter the state of activation or proliferation of target cells and contribute to the immunodeficiencies associated with infection by these viruses.

Antibodies, Monoclonal↗
PubMed1997

U5 region of the human immunodeficiency virus type 1 long terminal repeat contains TRE-like cAMP-responsive elements that bind both AP-1 and CREB/ATF proteins.

Activating protein-1 (AP-1) binding phorbol ester responsive elements (TRE) are located downstream of the transcription initiation site in the U5 region of the human immunodeficiency virus type-1 (HIV-1) long terminal repeat (LTR). These downstream sequence elements, termed DSE, can bind cFos and junD and transmit protein kinase C (PKC) activation signals to the LTR. Further studies suggested the DSE might also bind AP-1-related proteins of the CREB/ATF family. Since enhanced HIV-1 expression is associated with activation of the cAMP-dependent protein kinase A (PKA) signaling pathway, we determined whether binding of CREB/ATF proteins to the DSE mediate cAMP/PKA activation of the HIV-1 LTR. In the present study. DSE binding complexes in nuclear protein extracta from colonic epithelial cells are shown to contain ATF-1, ATF-2, and CREB and transfection of either an ATF-2 or PKA expressing plasmid transactivated the DSE. Cholera toxin (Ctx), a potent activator of the cAMP/PKA pathway. Increased HIV-1 virus production from a latently infected promonocytic cell line, U1. Ctx increased LTR promoter activity and increased the CREB content of DSE binding complexes. Transfection of U1 cells with a series of mutant LTR reporter constructs demonstrated that the Ctx response was in large part mediated by the DSE. The Ctx response was also mediated by a heterologous promoter containing multiple TRE sites. Nuclear protein extracts from a T-cell line infected by HIV-1 contained higher levels of CREB/ATF proteins and manifested increased CREB/ATF binding activity. Collectively, these results indicate the DSE are TRE-like cAMP responsive elements that bind both AP-1 and CREB/ATF permitting induction of the HIV-1 LTR by both PKC and PKA activation signals.

Activating Transcription Factor 1↗
PubMed1997

Human immunodeficiency virus type 1 incorporates both glycosyl phosphatidylinositol-anchored CD55 and CD59 and integral membrane CD46 at levels that protect from complement-mediated destruction.

Human immunodeficiency virus type 1 (HIV-1) can be either resistant or sensitive to complement-mediated destruction depending on the host cells. Incorporation of different levels of host cell CD46, CD55 and CD59 may account for this differential sensitivity to complement. However, it has not been determined whether CD46, CD55 and CD59 can all be incorporated at levels which protect virions. To determine whether each of these proteins can protect HIV-1, virions were derived from CHO cells expressing either human CD46, CD55 or CD59. Virions were shown to incorporate both glycosyl phosphatidylinositol (GPI)-anchored CD55 and CD59 as well as transmembrane CD46. Importantly, all three virus preparations were significantly more resistant to complement lysis than control virus. This study demonstrates that HIV-1 incorporates both transmembrane and GPI-anchored complement control proteins from host cells and that both types of protein increase complement resistance of virus.

Animals↗
PubMed1996

Susceptibility of HIV-1 plasma virus to complement-mediated lysis. Evidence for a role in clearance of virus in vivo.

This study was undertaken to directly assess the susceptibility of HIV-1 plasma virus to C-mediated lysis. Plasma from HIV-infected individuals was collected and ultracentrifuged over 20% sucrose to isolate virions from plasma components including anticoagulants, which inhibit C activity. Treatment with C alone in the absence of exogenously added Ab caused lysis of virus from all patients (n = 18) (range 14 to 86%). This lysis occurred via the classical C pathway and was not due to cross-reactive Abs in the C source. Protein A bound a fraction of isolated plasma virus and this binding was blocked by purified human Ig suggesting that anti-HIV Abs bound to plasma virus could be responsible for inducing C activation. A portion of virus bound to CR2 on cells in the absence of exogenously added C indicating that virus activated C in vivo. C levels from six of six patients were determined to be sufficient to lead to lysis of virus in vivo. Since plasma virus appeared more sensitive to C than primary isolates, isolated virus was evaluated for the presence of C control proteins. While primary isolate virions contained CD46, CD55, and CD59, only CD59 was detected on plasma virus. The results of this study strongly suggest that C is activated by a portion of plasma virus in vivo due to the binding of Ab. The resultant opsonization plus subsequent lysis may be important routes of clearance and destruction of plasma virus in infected persons.

Antigens, CD↗