Hakan Aydin

Prof. Dr. Hakan Aydin

orcid

Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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1 June 2019 in Journal of Veterinary Research
Verified
Journal Article
Open access
PDF file
MTMehmet Ozkan Timurkan
Mehmet Ozkan Timurkan
HAHakan Aydin
Hakan Aydin
ASAhmet Sait
Ahmet Sait
Introduction: Bovine parainfluenza virus-3 (BPIV3) and bovine respiratory syncytial virus (BRSV) are the cause of respiratory disease in cattle worldwide. With other pathogens, they cause bovine respiratory disease complex (BRDC) in ruminants. The aim of the study was the detection and molecular characterisation of BPIV3 and BRSV from nasal swabs and lung samples of cows in and around the Erzurum region of eastern Turkey. Material and Methods: In total, 155 samples were collected. Of animals used in the study 92 were males and 63 females. The age of the animals was between 9 months and 5 years, mean 1.4 years. Most males were in the fattening period and being raised in open sheds; females were in the lactating period and kept in free stall barns. All samples were tested for the presence of viral genes using RT-PCR. Gene-specific primers in a molecular method (RT-PCR) identified BRSV (fusion gene) and BPIV3 (matrix gene) strains at the genus level. Results: RNA from BRSV and BPIV3 was detected in two (1.29%) and three (1.93%) samples, respectively, one of each of which was sequenced and the sequences were aligned with reference virus strains. Phylogenetic analyses clustered the strains in genotype C/BPIV3 and subgroup III/BRSV. Conclusion: The results indicate that BRSV and BPIV3 contribute to bovine respiratory disease cases in Turkey. This is the first report on their detection and molecular characterisation in ruminants in Turkey.

4 May 2019 in Tropical Animal Health and Production
Verified
Journal Article
Closed access
PDF file
MTMehmet Ozkan Timurkan
Mehmet Ozkan Timurkan
HAHakan Aydin
Hakan Aydin

1 October 2019 in Minerva Pediatrica
Verified
Journal Article
Closed access
OAOsman Aktaş
Osman Aktaş
HAHakan Aydin
Hakan Aydin
MTMehmet O. Timurkan
Mehmet O. Timurkan
Viral gastroenteritides are among the causes of higher morbidity and mortality in the childhood period, especially in infants. Although viral-induced diarrheal diseases are important problems in Erzurum, there have been no studies on the molecular prevalence of viral gastroenteritis agents in this region's children. The aim of the prospective study is to determine the molecular prevalence of the most commonly seen viral etiologic agents and their coinfection rates in children under 5 years of age with gastroenteritis in Erzurum, Turkey. Stool samples from 375 children between 0 and 5 years of age who suffered from acute diarrhea were investigated for the presence of Rotavirus, Norovirus, Astrovirus and Adenovirus by reverse transcriptase polymerase chain reaction, followed by conventional PCR techniques. The presence of Rotavirus, Norovirus, Astrovirus and Adenovirus in the specimens was detected by amplification of the VP6, RdRp, ORF-1b and Hexon regions, respectively. Stool samples were also investigated non-viral enteropathogens by conventional techniques. At least one viral pathogen was detected in 59.2% of the stool samples. Rotavirus was the most frequently observed agent (32.3%), followed by Norovirus (20.3%), Adenovirus (9.6%) and Astrovirus (5.6%). All specimens were negative for bacterial pathogens. Twenty seven (7.2%) specimens were positive for intestinal helminths and protozoan. A total of 39 coinfection (10.4%) including 38 dual and 1 triple were detected. The most frequent coinfections were observed between Norovirus plus Rotavirus and Norovirus plus Adenovirus. Single infections or coinfections of the enteropathogenic viruses occur at a significant rate in Erzurum's children. This study draws attention to the necessity of taking account of multiple viral infections in studies on combined vaccines and the treatment of gastroenteritis.

1 September 2016
Verified
Journal Article
Closed access
MKMurat Karamese
Murat Karamese
HAHakan Aydin
Hakan Aydin
ESEmin Sengul
Emin Sengul
VGVolkan Gelen
Volkan Gelen
CSCigdem Sevim
Cigdem Sevim
EKEmre Karakus
Emre Karakus

1 July 2018 in Veterinarski arhiv
Verified
Journal Article
Closed access
MTMehmet Ozkan Timurkan
Mehmet Ozkan Timurkan
HAHakan Aydin
Hakan Aydin
FAFeray Alkan
Feray Alkan

1 March 2023 in Asian Pacific Journal of Tropical Biomedicine
Verified
Journal Article
Open access
FIFatma Ibaokurgil
Fatma Ibaokurgil
HAHakan Aydin
Hakan Aydin
SYSerkan Yildirim
Serkan Yildirim
ESEmin Sengul
Emin Sengul
Objective: To investigate the effects of melatonin on renal inflammation, oxidative stress, apoptosis, as well as DNA and tissue damage in acrylamide-induced nephrotoxicity in rats. Methods: Fifty male rats were randomly divided into five groups. The control group received distilled water by gastric lavage for 11 days and the acrylamide group was administered acrylamide (50 mg/kg, i.g.) for 11 days. The MEL10+ACR and MEL20+ACR groups received intraperitoneal melatonin 10 and 20 mg/kg, respectively, for 11 days, and acrylamide (50 mg/kg, i.g.) was administered 1 h after melatonin injection. The MEL20 group was injected with melatonin (20 mg/kg) for 11 days. Kidney function tests were performed and biochemical and inflammatory parameters were determined. In addition, histopathological, immunohistochemical, and immunofluorescence examinationswerecarried out. Results: Melatonin significantly abated acrylamide-induced rise in serum urea and creatinine levels. Acrylamide caused oxidative stress, inflammation, apoptosis, as well as DNA and tissue damage in the kidneys. Melatonin treatment alleviated acrylamide-induced renal damage by exhibiting antioxidant, anti-inflammatory, and anti- apoptotic effects. Moreover, melatonin significantly ameliorated acrylamide-caused histopathological changes in kidney tissue. Conclusions: Melatonin attenuates acrylamide-induced renal oxidative stress, inflammation, apoptosis, and DNA damage in rats.