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Tufan Ermiş,1 Nasro Ahmed Adan,2 Abdiqani Nor Gacal,1 Ramlo Ahmed Noh,1 Ebubekir Arslan3 1Department of Medical Biochemistry, Somalia Turkey Recep Tayyip Erdoğan Training and Research Hospital, Mogadishu, Somalia; 2Department of Medical Laboratory Science, Health Science Faculty, Mogadishu University, Mogadishu, Somalia; 3Department of Emergency Service, Somalia Turkey Recep Tayyip Erdoğan Training and Research Hospital, Mogadishu, SomaliaCorrespondence: Tufan Ermiş, Department of Medical Biochemistry, Somalia Turkey Recep Tayyip Erdoğan Training and Research Hospital, Wadada Rajap Tayyip Erdoğan, Hodan, Mogadishu, Somalia, Tel +252-613357841, Email tufanermis38@gmail.comPurpose: Our aim in this study is to reveal the blood group distribution by investigating retrospectively the blood types of around 60 thousand patients and donors who applied to Mogadishu Somalia Turkey Recep Tayyip Erdogan Training and Research Hospital between 2018 and 2021.Patients and Methods: The blood group data of 59,442 people were included in this study. 20,414 (34.35%) of the study’s participants were female, 39,023 (65.65%) were male. The blood groups of participants were determined using the slide method and the gel column technique. The frequencies and percentages of O, A, B, AB and Rh blood groups were calculated.Results: The frequencies of ABO blood group distribution indicated that blood group O and Rh+ were predominant in Mogadishu O group: 60.30%, A group: 26.50%, B group: 11.27%, AB group: 1.93%, Rh+ group: 96.49%, Rh− group: 3.43%.Conclusion: This is the first study about blood group distribution in Mogadishu based on a large number of blood type tests and hospital data. The findings of our study can guide the blood center administrators make decisions concerning blood stocking and supply. This study can give an idea about how much fluctuations may occur in the frequency of blood group types in emigrant populations over many years.Keywords: blood types, ABO, Rh, Mogadishu, Somalia

Prion diseases are a group of neurodegenerative and fatal central nervous system disorders. The pathogenic mechanism involves the conversion of cellular prion protein (PrP C ) to an altered scrapie isoform (PrP Sc ), which accumulates in amyloid deposits in the brain. However, no therapeutic drugs have demonstrated efficacy in clinical trials. We previously reported that BMD42-29, a synthetic compound discovered in silico , is a novel anti-prion compound that inhibits the conversion of PrP C to protease K (PK)-resistant PrP Sc fragments (PrP res ). In the present study, 14 derivatives of BMD42-29 were obtained from BMD42-29 by modifying in the side chain by in silico feedback, with the aim to determine whether they improve anti-prion activity. These derivatives were assessed in a PrP Sc -infected cell model and some derivatives were further tested using real timequaking induced conversion (RT-QuIC). Among them, BMD42-2910 showed high anti-prion activity at low concentrations in vitro and also no toxic effects in a mouse model. Interestingly, abundant PrP res was reduced in brains of mice infected with prion strain when treated with BMD42- 2910, and the mice survived longer than control mice and even that treated with BMD42-29. Finally, high binding affinity was predicted in the virtual binding sites (Asn159, Gln 160, Lys194, and Glu196) when PrP C was combined with BMD-42-2910. Our findings showed that BMD42-2910 sufficiently reduces PrP res generation in vitro and in vivo and may be a promising novel anti-prion compound.

The diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD) can only be confirmed by abnormal protease-resistant prion protein accumulation in post-mortem brain tissue. The relationships between sCJD and cerebrospinal fluid (CSF) proteins such as 14-3-3, tau, and α-synuclein (a-syn) have been investigated for their potential value in pre-mortem diagnosis. Recently, deep-learning (DL) methods have attracted attention in neurodegenerative disease research. We established DL-aided pre-mortem diagnostic methods for CJD using multiple CSF biomarkers to improve their discriminatory sensitivity and specificity. Enzyme-linked immunosorbent assays were performed on phospho-tau (p-tau), total-tau (t-tau), a-syn, and β-amyloid (1-42), and western blot analysis was performed for 14-3-3 protein from CSF samples of 49 sCJD and 256 non-CJD Korean patients, respectively. The deep neural network structure comprised one input, five hidden, and one output layers, with 20, 40, 30, 20 and 12 hidden unit numbers per hidden layer, respectively. The best performing DL model demonstrated 90.38% accuracy, 83.33% sensitivity, and 92.5% specificity for the three-protein combination of t-tau, p-tau, and a-syn, and all other patients in a separate CSF set (n = 15) with other neuronal diseases were correctly predicted to not have CJD. Thus, DL-aided pre-mortem diagnosis may provide a suitable tool for discriminating CJD patients from non-CJD patients.

Synaptic adhesion molecules regulate various aspects of synapse development, function and plasticity. These functions mainly involve trans-synaptic interactions and positive regulations, whereas cis-interactions and negative regulation are less understood. Here we report that SALM4, a member of the SALM/Lrfn family of synaptic adhesion molecules, suppresses excitatory synapse development through cis inhibition of SALM3, another SALM family protein with synaptogenic activity. Salm4-mutant (Salm4(-/-)) mice show increased excitatory synapse numbers in the hippocampus. SALM4 cis-interacts with SALM3, inhibits trans-synaptic SALM3 interaction with presynaptic LAR family receptor tyrosine phosphatases and suppresses SALM3-dependent presynaptic differentiation. Importantly, deletion of Salm3 in Salm4(-/-) mice (Salm3(-/-); Salm4(-/-)) normalizes the increased excitatory synapse number. These results suggest that SALM4 negatively regulates excitatory synapses via cis inhibition of the trans-synaptic SALM3-LAR adhesion.

Aim. This study aimed to assess clinical impact of hepatitis C viral load on the development of hepatocellular carcinoma (HCC) and liver-related mortality in HCV-infected patients. Methods. A total of 111 subjects with chronic HCV infection who were available for serum quantitation of HCV RNA were recruited in this retrospective cohort. Cox-proportional hazards models were used to calculate hazard ratio (HR) of developing HCC and liver-related mortality according to serum HCV RNA titers. Results. HCC was developed in 14 patients during follow-up period. The cumulative risk of HCC development was higher in subjects with high HCV RNA titer (log HCV RNA IU/mL > 6) than subjects with low titer (log HCV RNA IU/mL ≦ 6) (HR = 4.63, P = 0.032), giving an incidence rate of 474.1 and 111.5 per 10,000 person-years, respectively. Old age (HR = 9.71, P = 0.014), accompanying cirrhosis (HR = 19.34, P = 0.004), and low platelet count (HR = 13.97, P = 0.009) were other independent risk factors for the development of HCC. Liver-related death occurred in 7 patients. Accompanying cirrhosis (HR = 6.13, P = 0.012) and low albumin level (HR = 9.17, P = 0.002), but not HCV RNA titer, were significant risk factors related to liver-related mortality. Conclusion. Serum HCV RNA titer may be considered an independent risk factor for the development of HCC but not liver-related mortality.

Background: Sorafenib is an orally administered multikinase inhibitor with antiangiogenic and antiproliferative properties. The results of large clinical trials demonstrate that sorafenib prolongs survival and the time to progression of patients with advanced hepatocellular carcinoma (HCC). The aim of the present study was to determine the outcomes of such patients who were routinely treated with sorafenib at multi-institutions in Korea, in contrast to formal clinical trials., Methods: Between August 2007 and March 2012, patients with advanced HCC in seven referral medical centers in Daejeon-Chungcheong Province of Korea were retrospectively enrolled to evaluate treatment response, survival, and tolerability following administration of sorafenib. The treatment response was assessed in accordance with the Response Evaluation Criteria in Solid Tumor 1.1 guidelines., Results: Among 116 patients, 66 (57%) had undergone treatment for HCC, and 77 (66%) were accompanied with Child-Pugh A cirrhosis. The median duration of sorafenib treatment was 67 days (range 14-452 days). Median overall survival and median time to progression were 141 days and 90 days, respectively. Complete response, partial response, and stable disease were achieved for 0%, 2%, and 29% of patients, respectively. Overall median survival, but not the median time to progression, was significantly shorter for patients with Child-Pugh B cirrhosis compared with those with Child-Pugh A cirrhosis (64 days vs 168 days, P = 0.004). Child-Pugh B cirrhosis (P = 0.024) and a high level of serum alpha-fetoprotein (P = 0.039) were independent risk factors for poor overall survival. Thirty-nine (34%) patients experienced grade 3/4 adverse events such as hand-foot skin reactions and diarrhea that required dose adjustment., Conclusions: The clinical outcomes of sorafenib-treated patients with advanced HCC were comparable to those reported by formal clinical trial conducted in the Asia-Pacific region. Underlying hepatic dysfunction was the most important risk factor for shorter survival.

Background/aims: Metformin use has been associated with decreased colorectal cancer risk and mortality among diabetic patients. Recent research suggests that metformin use may decrease the incidence of colorectal adenomas in diabetic patients with previous colorectal cancer. This study aimed to assess the clinical effect of metformin use on the development of colorectal adenomas in diabetic patients without previous colorectal cancer., Methods: Among 604 consecutive diabetic patients who underwent colonoscopic surveillance after initial colonoscopy between January 2002 and June 2012, 240 patients without previous colorectal cancer were enrolled in this study and were divided in two groups: 151 patients receiving metformin and 89 patients not receiving metformin. Patient demographics and clinical characteristics as well as the colorectal adenoma incidence rate were retrospectively analyzed., Results: The incidence rate of total colorectal adenomas was not different according to metformin use (P=0.349). However, the advanced adenoma incidence rate was significantly lower in the metformin group compared with the non-metformin group (relative risk [RR], 0.09; P=0.011). Metformin use was independently associated with a decreased incidence of advanced colorectal adenomas after adjustment for clinically relevant factors (RR, 0.072; P=0.016). In addition, the cumulative development rate of advanced adenomas during follow-up was significantly lower in the metformin group compared with the non-metformin group (P=0.007)., Conclusions: Metformin use in diabetic patients without previous colorectal cancer is associated with a lower risk of advanced colorectal adenomas.

Rheumatoid arthritis (RA) is a chronic and systemic inflammatory disorder that primarily affects the flexible joints and may also affect a number of tissues and organs. The progression of RA involves an inflammatory response of the capsule around the joint, swelling of synovial cells with excess synovial fluid (SF), and the development of fibrous tissue in the synovium. Since the progressive pathology of the disease often leads to the irreversible destruction of articular cartilage and ankylosis of the joint, early diagnosis of RA is essential. Thus, we undertook a comparative proteomic approach to investigate novel biomarkers for early diagnosis using SFs and serums from RA patients. As a result, we identified 32 differentially expressed spots in SFs and 34 spots in serums. The differential expression of the STEAP4 and ZNF 658 proteins were validated using immunoblotting of the SFs and serums, respectively. These data suggest that differentially expressed proteins in SFs and serums could be used as RA-specific biomarkers for the diagnosis and monitoring of RA. Furthermore, these findings advance our understanding of the molecular etiopathogenesis of RA.

Background: The suburban transmission of malaria in Selangor, Malaysia's most developed and populous state still remains a concern for public health in this region. Despite much successful control efforts directed at its reduction, sporadic cases, mostly brought in by foreigners have continued to occur. In addition, cases of simian malaria caused by Plasmodium knowlesi, some with fatal outcome have caused grave concern to health workers. The aim of this study was to investigate the possibility of local malaria transmission in suburban regions of Selangor, which are adjacent to secondary rainforests., Findings: A malaria survey spanning 7 years (2006 - 2012) was conducted in Selangor. A total of 1623 laboratory confirmed malaria cases were reported from Selangor's nine districts. While 72.6% of these cases (1178/1623) were attributed to imported malaria (cases originating from other countries), 25.5% (414/1623) were local cases and 1.9% (31/1623) were considered as relapse and unclassified cases combined. In this study, the most prevalent infection was P. vivax (1239 cases, prevalence 76.3%) followed by P. falciparum (211, 13.0%), P. knowlesi (75, 4.6%), P. malariae (71, 4.4%) and P. ovale (1, 0.06%). Mixed infections comprising of P. vivax and P. falciparum were confirmed (26, 1.6%). Entomological surveys targeting the residences of malaria patients' showed that the most commonly trapped Anopheles species was An. maculatus. No oocysts or sporozoites were found in the An. maculatus collected. Nevertheless, the possibility of An. maculatus being the malaria vector in the investigated locations was high due to its persistent occurrence in these areas., Conclusions: Malaria cases reported in this study were mostly imported cases. However the co-existence of local cases and potential Plasmodium spp. vectors should be cause for concern. The results of this survey reflect the need of maintaining closely monitored malaria control programs and continuous extensive malaria surveillance in Peninsula Malaysia.

Aim: To evaluate the treatment outcomes of clevudine compared with entecavir in antiviral-naive patients with chronic hepatitis B (CHB)., Methods: We retrospectively analyzed the clinical data of CHB patients treated with clevudine 30 mg/d and compared their clinical outcomes with patients treated with entecavir 0.5 mg/d. The biochemical response, as assessed by serum alanine aminotransferase (ALT) activity, virologic response, as assessed by serum hepatitis B virus DNA (HBV DNA) titer, serologic response, as assessed by hepatitis B e antigen (HBeAg) status, and virologic breakthrough with genotypic mutations were assessed., Results: Two-hundred and fifty-four patients [clevudine (n = 118) vs entecavir (n = 136)] were enrolled. In clevudine-treated patients, the cumulative rates of serum ALT normalization were 83.9% at week 48 and 91.5% at week 96 (80.9% and 91.2% in the entecavir group, respectively), the mean titer changes in serum HBV DNA were -6.03 and -6.55 log(10) copies/mL (-6.35 and -6.86 log(10) copies/mL, respectively, in the entecavir group), and the cumulative non-detection rates of serum HBV DNA were 72.6% and 83.1% (74.4% and 83.8%, respectively, in the entecavir group). These results were similar to those of entecavir-treated patients. The cumulative rates of HBeAg seroconversion were 21.8% at week 48 and 25.0% at week 96 in patients treated with clevudine, which was similar to patients treated with entecavir (22.8% and 27.7%, respectively). The virologic breakthrough in the clevudine group occurred in 9 (7.6%) patients at weeks 48 and 15 (12.7%) patients at week 96, which primarily corresponded to genotypic mutations of rtM204I and/or rtL180M. There was no virologic breakthrough in the entecavir group., Conclusion: In antiviral-naive CHB patients, long-term treatment outcomes of clevudine were not inferior to those of entecavir, except for virologic breakthrough.

Phlebosclerotic colitis is a rare form of ischemic colitis characterized by the thickening of the wall of the affected colon due to fibrous degeneration of submucosal layer of colon and fibrotic obstruction of the colono-mesenteric vein, resulting in the disturbance of venous return from the colon. The pathogenic mechanism of this entity remains unknown but chronic liver disease with portal hypertension is maybe thought to be one of the speculated mechanisms. Here we first report the case of surgically confirmed phlebosclerotic colitis, that was in the early stage but showed the aggressive nature, in a 61-yr-old cirrhotic patients with portal hypertension in Korea.

Background/aims: We studied the prevalence of chronic hepatitis B, C and abnormality on liver function among the population in northwest area of Chungnam., Methods: We have reviewed 40,112 adults who had received medical examination at health promotion center in Dankook university hospital. We studied them retrospectively about HBsAg, HBsAb, anti-HCV, and liver function test (LFT)., Results: Among the study subjects, 22,936 men and 17,176 women were involved. The overall seroprevalence of HBsAg was 4.2%. The prevalence in men (4.5%) was higher than that of women (3.7%) (p<0.001). The seroprevalence of HBsAg in their age was 5.1% in the 5th decade, 4.2% in the 2nd decade, 4.1% in the 4th decade, and 4.1% in the 6th decade. The overall seroprevalence of HBsAb was 65.1%. The overall seroprevalence of anti-HCV was 0.7%. After we reexamined them with HCV RNA or RIBA (Recombinant Immunoblot Assay), the prevalence of chronic hepatitis C was 0.09%. The LFT abnormality in total subjects was 11.4%. The LFT abnormality of chronic hepatitis B and C subjects was 21.72% and 63.2%., Conclusions: The prevalence of chronic hepatitis B and C was lower than that of previous studies. The prevalence of chronic hepatitis B in the 2nd decade was still high.