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Vandana Joshi

Publications and source records attributed to Vandana Joshi.

15 recordsLinked to original sources
PubMed2006

Correlates of anxiety and depression among HIV test-seekers at a Voluntary Counseling and Testing facility in Pune, India.

OBJECTIVE: We assessed the extent of anxiety/depression/distress using Hospital Anxiety and Depression Scale (HADS) among a cross-section of HIV test-seekers at a Voluntary Counseling and Testing (VCT) facility in Pune, India. METHODS: HADS has 14 items for uniscale with 7 items each for anxiety and depression rated on a four-point Likert scale. Between September 2002 and March 2003, HADS was administered to 150 consecutive HIV tests-seekers attending NARI-Talera VCT facility. Subsequently, HIV testing was done after obtaining informed consent. RESULTS: HADS showed strong internal consistency (Cronbach-alpha 0.77). The prevalence of risk behavior (73.3%) and HIV (45.5%) were high. Education levels influenced anxiety (p = 0.033; 0.008), more so in women (p = 0.044). Repeat test-seekers exhibited significant depression (AOR: 2.9; 95% CI: 1.4-6.1; p = 0.004) and distress (AOR: 2.5; 95% CI: 1.2-5.3; p = 0.017). Marital status influenced the uniscale scores. The HIV positive repeat test-seekers were more anxious (p = 0.035) and depressed (0.037). CONCLUSIONS: Existence of emotional distress among HIV test-seekers, particularly among repeat test-seekers, possibly 'AIDS-anxious' individuals indicates additional counseling needs specifically by introducing gender and education sensitive interventions. VCT staff can be trained to assess emotional distress among HIV test-seekers to formulate long-term intervention.

Adolescent↗
PubMed2006

Prevalence of Salmonella species in various raw meat samples of a local market in Kathmandu.

A cross-sectional study of raw meat samples from the local meat market of Kathmandu Metropolitan City was carried out during September 2002 to May 2003 with special emphasis on isolation and identification of Salmonella bacteria. A total of 123 raw meat samples (55 chicken, 37 buffalo, and 31 goat) were collected and analyzed relative to season. Salmonella spp was found in 11.4% (14/123) meat samples. Eight samples of chicken, that is, 14.5%, five samples of buffalo (13.5%), and one sample of goat (3.3%) were found to be positive for Salmonella. Salmonella prevalence revealed Salmonella (S.) pullorum in 3.3% samples, S. gallinarum in 0.8%, S. typhi in 1.6%, S. choleraesuis in 0.8%, and Salmonella of subgenus I or II group in 4.9% samples. More than 80% meat samples microbiologically processed indicated coliform contamination. Seasonal prevalence of Salmonella was highest in the months of April/May. Surveys revealed unsatisfactory conditions of sanitation in the local meat markets of Kathmandu.

Animals↗
PubMed2005

Activation of RNA metabolism-related genes in mouse but not human tissues deficient in SMN.

Mutations of the survival of motor neuron gene (SMN1) are responsible for spinal muscular atrophies (SMA), a frequent recessive autosomal motor neuron disease. SMN is involved in various processes including RNA metabolism. However, the molecular pathway linking marked deficiency of SMN to SMA phenotype remains unclear. Homozygous deletion of murine Smn exon 7 directed to neurons or skeletal muscle causes severe motor axonal or myofiber degeneration, respectively. With the use of cDNA microarrays, expression profiles of 8,400 genes were analyzed in skeletal muscle and spinal cord of muscular and neuronal mutants, respectively, and compared with age-matched controls. A high proportion of genes (20 of 429, 5%) was involved in pre-mRNA splicing, ribosomal RNA processing, or RNA decay, and 18 of them were upregulated in mutant tissues. By analyzing other neuromuscular disorders, we showed that most of them (14 of 18) were specific to the SMN defect. Quantitative PCR analysis of these transcripts showed that gene activation was an early adaptive response to the lack but not reduced amount of full-length SMN in mouse mutant tissues. In human SMA tissues, activation of this program was not observed, which could be ascribed to the reduction but not the absence of full-length SMN.

Animals↗
PubMed2005

Childhood sexual abuse patterns, psychosocial correlates, and treatment outcomes among adults in drug abuse treatment.

This study reports on the effects of having a history of childhood sexual abuse (CSA) on treatment outcomes among substance abusing men and women (N = 2,434) in a national, multisite study of drug treatment outcomes. A history of CSA was reported by 27.2% of the women and 9.2% of the men. Controlling for gender, compared to patients without CSA, patients reporting CSA were younger at entry into the current drug treatment, were more likely to be White, were more likely to have a comorbid mental disorder, be alcohol or cocaine dependent, had higher levels of criminal activities, had a higher level of problem recognition, and had a more negative peer influence. Controlling for these correlates, a history of abuse was related to a lower likelihood of posttreatment abstinence.

Adult↗
PubMed2004

Deletion of murine Smn exon 7 directed to liver leads to severe defect of liver development associated with iron overload.

Spinal muscular atrophy (SMA) is characterized by degeneration of lower motor neurons caused by mutations of the survival motor neuron 1 gene (SMN1). SMN is involved in various processes including the formation of the spliceosome, pre-mRNA splicing and transcription. To know whether SMN has an essential role in all mammalian cell types or an as yet unknown specific function in the neuromuscular system, deletion of murine Smn exon 7, the most frequent mutation found among SMA patients, has been restricted to liver. Homozygous mutation results in severe impairment of liver development associated with iron overload and lack of regeneration leading to dramatic liver atrophy and late embryonic lethality of mutant mice. These data strongly suggest an ubiquitous and essential role of full-length SMN protein in various mammalian cell types. In SMA patients, the residual amount of SMN allows normal function of various organs except motor neurons. However, data from mouse and human suggest that other tissues might be involved in severe form of SMA or during prolonged disease course which reinforce the need of therapeutic approaches targeted to all tissues. In addition, liver function of patients should be carefully investigated and followed up before and during therapeutic trials.

Animals↗
PubMed2003

Therapeutic benefits of cardiotrophin-1 gene transfer in a mouse model of spinal muscular atrophy.

Spinal muscular atrophy (SMA) is a recessive autosomal disorder characterized by degeneration of lower motor neurons caused by mutations of the survival motor neuron gene (SMN1). No curative treatment is known so far. Mutant mice carrying homozygous deletion of Smn exon 7 directed to neurons display skeletal muscle denervation, moderate loss of motor neuron cell bodies and severe axonal degeneration. These features, similar to those found in human SMA, strongly suggest the involvement of a dying back process of motor neurons and led us to test whether neurotrophic factors might have a protective role in SMA. We report here the therapeutic benefits of systemic delivery of cardiotrophin-1 (CT-1), a neurotrophic factor belonging to the IL-6 cytokine family. Intra-muscular injection of adenoviral vector expressing CT-1, even at very low dose, improves median survival, delays motor defect of mutant mice and exerts protective effect against loss of proximal motor axons and aberrant cytoskeletal organization of motor synaptic terminals. In spite of the severity of SMA phenotype in mutant mice, CT-1 is able to slow down disease progression. Neuroprotection could be regarded as valuable therapeutic approach in SMA.

Animals↗
PubMed2003

Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle.

Deletion of murine Smn exon 7, the most frequent mutation found in spinal muscular atrophy, has been directed to either both satellite cells, the muscle progenitor cells and fused myotubes, or fused myotubes only. When satellite cells were mutated, mutant mice develop severe myopathic process, progressive motor paralysis, and early death at 1 mo of age (severe mutant). Impaired muscle regeneration of severe mutants correlated with defect of myogenic precursor cells both in vitro and in vivo. In contrast, when satellite cells remained intact, mutant mice develop similar myopathic process but exhibit mild phenotype with median survival of 8 mo and motor performance similar to that of controls (mild mutant). High proportion of regenerating myofibers expressing SMN was observed in mild mutants compensating for progressive loss of mature myofibers within the first 6 mo of age. Then, in spite of normal contractile properties of myofibers, mild mutants develop reduction of muscle force and mass. Progressive decline of muscle regeneration process was no more able to counterbalance muscle degeneration leading to dramatic loss of myofibers. These data indicate that intact satellite cells remarkably improve the survival and motor performance of mutant mice suffering from chronic myopathy, and suggest a limited potential of satellite cells to regenerate skeletal muscle.

Animals↗
PubMed2003

Mutations of SPG4 are responsible for a loss of function of spastin, an abundant neuronal protein localized in the nucleus.

Mutations of spastin are responsible for the most common autosomal dominant form of hereditary spastic paraplegia (AD-HSP), a disease characterized by axonal degeneration of corticospinal tracts and posterior columns. Generation of polyclonal antibodies specific to spastin has revealed two isoforms of 75 and 80 kDa in both human and mouse tissues with a tissue-specific variability of the isoform ratio. Spastin is an abundant protein in neural tissues and immunolabeling experiments have shown that spastin is expressed in neurons but not in glial cells. These data indicate that axonal degeneration linked to spastin mutations is caused by a primary defect of neurons. Protein and transcript analyses of patients carrying either nonsense or frameshift spastin mutations revealed neither truncated protein nor mutated transcripts, providing evidence that these mutations are responsible for a loss of spastin function. Identifying agents able to induce the expression of the non-mutated spastin allele should represent an attractive therapeutic strategy in this disease.

Adenosine Triphosphatases↗
PubMed2003

Riluzole attenuates spinal muscular atrophy disease progression in a mouse model.

Spinal muscular atrophy (SMA) is a motor neuron disease caused by mutations of the survival motor neuron 1 gene (SMN1). No curative treatment is available. Mutant mice carrying homozygous deletion of Smn exon 7 directed to neurons display a degenerative process of motor neurons similar to that found in human SMA. To test whether riluzole, which exhibits neurotrophic properties, might have a protective role in SMA, mutant mice were treated with it after the onset of the degenerative process. Riluzole improved median survival and exerted a protective effect against aberrant cytoskeletal organization of motor synaptic terminals but not against loss of proximal axons. These results demonstrate that the disease course of SMA can be attenuated after the onset of neuromuscular defects and may warrant further investigation in a therapeutic trial in SMA.

Animals↗
PubMed2003

Followup of cocaine-dependent men and women with antisocial personality disorder.

Long-term outcomes following drug treatment were examined for cocaine-dependent men (N = 453) and women (N = 254) with and without antisocial personality disorder (ASP). In-depth assessments were conducted at treatment intake in 1991-93 and at 1 and 5 years following treatment discharge. Overall, 47.2% of the males and 34.3% of females were diagnosed with ASP using DSM-III-R criteria derived from the Diagnostic Interview Schedule. All groups reduced their cocaine, marijuana, and alcohol use; reduced their levels of psychological distress; and improved in functioning (e.g., employment, arrests, residential status). At Year 5 ASP was associated with an increased likelihood of heavy alcohol use and additional substance abuse treatment among men, whereas women with ASP were more likely to report psychological problems and to receive mental health treatment and other services than either women without ASP or men with ASP. The findings suggest the need to address the specific treatment needs of male and female cocaine abusers with ASP.

Activities of Daily Living↗
PubMed2003

Treatment processes and outcomes among adolescents with a history of abuse who are in drug treatment.

This study reports on the effects of having a history of physical and/or sexual abuse on treatment processes and posttreatment abstinence among adolescents (N = 803) in a multisite study of drug treatment outcomes. A history of physical and/or sexual abuse was reported by 59% of the girls and 39% of the boys and was related to being White and having higher levels of comorbidity, exposure to other traumatic events, dependence on alcohol and marijuana, problem recognition, and negative peer or family influence. Abused adolescents had more service needs at treatment admission and there was some variation in treatment processes related to gender and abuse status. Youths with a history of physical abuse had a lower likelihood of posttreatment abstinence, except among those who had better rapport with their counselors. Attention to treatment processes and engagement strategies is crucial for treating youths in drug treatment who have a history of abuse.

Adolescent↗
PubMed2002

Neurofilament accumulation at the motor endplate and lack of axonal sprouting in a spinal muscular atrophy mouse model.

Mutations of survival of the motor neuron gene (SMN1) are responsible for spinal muscular atrophy (SMA), a common genetic cause of death in childhood. The cellular mechanism by which mutations of SMN1 are responsible for the selective neuromuscular defect and motor neuron cell degeneration observed in SMA has not been described. We have previously generated mice carrying a homozygous deletion of Smn exon 7 directed to neurons. We report here that these mutant mice display a dramatic and progressive loss of motor axons involving both proximal and terminal regions, in agreement with the skeletal muscle denervation process and disease progression. Moreover, we found massive accumulation of neurofilaments, including phosphorylated forms, in terminal axons of the remaining neuromuscular junctions. This aberrant cytoskeletal organization of synaptic terminals was associated with reduction of branched structures of the postsynaptic apparatus and defect of axonal sprouting in mutant mice. Together, these findings may be responsible for severe motor neuron dysfunction, and suggest that loss of motor neuron cell bodies results from a 'dying-back' axonopathy in SMA. Smn mutant mice should represent a valuable model for elucidating the pathway linking Smn to cytoskeletal organization.

Animals↗