Enteric fever is a major public health problem in developing countries. Due to the problem of resistance to first-line drugs and fluoroquinolone, cephalosporins are currently used for treatment of enteric fever. Cephalosporin resistance in Salmonella spp. is mainly due to production of extended-spectrum b-lactamases (ESBLs). The majority of ESBLs in Salmonella are derivatives of the TEM and SHV b-lactamase families. The objectives of this study were to detect antibiotic susceptibility patterns, ESBL production and TEM-, SHV-and CTX-M-encoding genes (bla TEM , bla SHV and bla CTX-M ) among clinical isolates of Salmonella spp. A total of 134 Salmonella isolates [Salmonella Typhi (n5101), Salmonella Paratyphi A (n531), Salmonella Paratyphi B (n51) and Salmonella Typhimurium (n51)] were included in this study. Multidrug resistance was seen in 5/ 134 (3.73 %) isolates, all of which belonged to serotype S. Typhi. A better susceptibility profile was observed for first-line drugs (ampicillin, chloramphenicol, co-trimoxazole and tetracycline) and cephalosporins (cefotaxime, ceftazidime, ceftriaxone, cefixime and cefepime). However, 131 (97.76 %) of the 134 isolates were resistant to nalidixic acid and one (0.75 %) was resistant to ciprofloxacin. TEM-1-type b-lactamase (bla TEM-1 ) was detected in six (4.47 %) of the 134 isolates, which belonged to the serotype S. Typhi. All six TEM-positive isolates were negative for the bla SHV gene and none of the isolates was positive for the bla CTX-M gene. The presence of the bla TEM gene encoding TEM-1 b-lactamase is believed to confer resistance only to penicillins and early cephalosporins; however, the resistance spectrum of TEM-1 descendants may extend to second-, third-and fourth-generation cephalosporins. The ESBLs derived from TEM-1 differ from their progenitors by as few as 1 aa, and have the ability to hydrolyse third-generation cephalosporins. Therefore, appropriate selection and rotation of antibiotics as well as continuous monitoring of antibiotic susceptibility profiles could help to control the emergence and spread of resistant strains.
Hippocampal subfield atrophy is a prime structural change in the brain, associated with cognitive aging and neurodegenerative diseases such as Alzheimer’s disease. Recent developments in genome-wide association studies (GWAS) have identified genetic loci that characterize the risk of hippocampal volume loss based on the processes of normal and abnormal aging. Polygenic risk scores are the genetic proxies mimicking the genetic role of the pre-existing vulnerabilities of the underlying mechanisms influencing these changes. Discriminating the genetic predispositions of hippocampal subfield atrophy between cognitive aging and neurodegenerative diseases will be helpful in understanding the disease etiology. In this study, we evaluated the polygenic risk of Alzheimer’s disease (AD PGRS) for hippocampal subfield atrophy in 1,086 individuals (319 cognitively normal (CN), 591 mild cognitively impaired (MCI), and 176 Alzheimer’s disease dementia (ADD)). Our results showed a stronger association of AD PGRS effect on the left hemisphere than on the right hemisphere for all the hippocampal subfield volumes in a mixed clinical population (CN+MCI+ADD). The subfields CA1, CA4, hippocampal tail, subiculum, presubiculum, molecular layer, GC-ML-DG, and HATA showed stronger AD PGRS associations with the MCI+ADD group than with the CN group. The subfields CA3, parasubiculum, and fimbria showed moderately higher AD PGRS associations with the MCI+ADD group than with the CN group. Our findings suggest that the eight subfield regions, which were strongly associated with AD PGRS are likely involved in the early stage ADD and a specific focus on the left hemisphere could enhance the early prediction of ADD.
Objective:
Neurodevelopmental disorders NDD are neurologic processing problems that interfere with learning in children. Primary and preschool teachers who are essential links in public health reach out to such children do not receive any formal training to identify these disorders. Hence, a primary and preschool level intervention addressing the issue is proposed.
Materials and Methods:
Primary and preschool teachers of government and government-aided schools and Anganwadi/preschools in the Model Rural Health Research Unit Tirunelveli field practice area will be assigned into two groups. The training module will be developed and validated using neurodevelopmental screening tool (NDST). Before identifying the students using the NDST, the teachers in Group A will get training using the module. Group B is the control group, in which untrained teachers administer the NDST to the children and then will be trained. Neurologists will assess the same children over 1 year.
Results:
The effectiveness of teacher training for the early detection of children with NDD will be assessed. Thus, the validity of the screening for NDD by the teachers will be estimated.
Conclusion:
If successful, the module can be incorporated into the Rashtriya Bal Swasthya Karyakram program of India for the early identification of children with NDD.
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