No abstract available.
Spina Bifida Occulta*

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection contribute to platelet activation and thrombus formation. Severe coronavirus disease 2019 (COVID-19) is characterized by an increased risk of thromboembolic events that can lead to adverse outcomes in patients with severe disease manifestations. We present the case of a 41-year-old man who died from a pulmonary embolism and review the connection between SARS-CoV-2 infection, increased platelet counts, and the resulting fatal thrombosis. Total knee replacement surgery was performed and the patient was able to ambulate for a few days postoperatively. The platelet count exceeded the upper limit between postoperative days six and nine, reaching 708,000/μL on day 20. SARS-CoV-2 was confirmed 14 days after surgery, and the patient died 23 days after surgery while hospitalized. Autopsy revealed a fatal pulmonary embolism and deep vein thrombosis. If blood clots are caused by increased platelet counts due to COVID-19, it is essential to understand this relationship and prepare for complications that may arise after infection. Several recent studies have shown a link between COVID-19 and coagulation. We propose several considerations for autopsies of unexpected fatal pulmonary embolism during the SARS-CoV-2 endemic period.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection contribute to platelet activation and thrombus formation. Severe coronavirus disease 2019 (COVID-19) is characterized by an increased risk of thromboembolic events that can lead to adverse outcomes in patients with severe disease manifestations. We present the case of a 41-year-old man who died from a pulmonary embolism and review the connection between SARS-CoV-2 infection, increased platelet counts, and the resulting fatal thrombosis. Total knee replacement surgery was performed and the patient was able to ambulate for a few days postoperatively. The platelet count exceeded the upper limit between postoperative days six and nine, reaching 708,000/μL on day 20. SARS-CoV-2 was confirmed 14 days after surgery, and the patient died 23 days after surgery while hospitalized. Autopsy revealed a fatal pulmonary embolism and deep vein thrombosis. If blood clots are caused by increased platelet counts due to COVID-19, it is essential to understand this relationship and prepare for complications that may arise after infection. Several recent studies have shown a link between COVID-19 and coagulation. We propose several considerations for autopsies of unexpected fatal pulmonary embolism during the SARS-CoV-2 endemic period.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection contribute to platelet activation and thrombus formation. Severe coronavirus disease 2019 (COVID-19) is characterized by an increased risk of thromboembolic events that can lead to adverse outcomes in patients with severe disease manifestations. We present the case of a 41-year-old man who died from a pulmonary embolism and review the connection between SARS-CoV-2 infection, increased platelet counts, and the resulting fatal thrombosis. Total knee replacement surgery was performed and the patient was able to ambulate for a few days postoperatively. The platelet count exceeded the upper limit between postoperative days six and nine, reaching 708,000/μL on day 20. SARS-CoV-2 was confirmed 14 days after surgery, and the patient died 23 days after surgery while hospitalized. Autopsy revealed a fatal pulmonary embolism and deep vein thrombosis. If blood clots are caused by increased platelet counts due to COVID-19, it is essential to understand this relationship and prepare for complications that may arise after infection. Several recent studies have shown a link between COVID-19 and coagulation. We propose several considerations for autopsies of unexpected fatal pulmonary embolism during the SARS-CoV-2 endemic period.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection contribute to platelet activation and thrombus formation. Severe coronavirus disease 2019 (COVID-19) is characterized by an increased risk of thromboembolic events that can lead to adverse outcomes in patients with severe disease manifestations. We present the case of a 41-year-old man who died from a pulmonary embolism and review the connection between SARS-CoV-2 infection, increased platelet counts, and the resulting fatal thrombosis. Total knee replacement surgery was performed and the patient was able to ambulate for a few days postoperatively. The platelet count exceeded the upper limit between postoperative days six and nine, reaching 708,000/μL on day 20. SARS-CoV-2 was confirmed 14 days after surgery, and the patient died 23 days after surgery while hospitalized. Autopsy revealed a fatal pulmonary embolism and deep vein thrombosis. If blood clots are caused by increased platelet counts due to COVID-19, it is essential to understand this relationship and prepare for complications that may arise after infection. Several recent studies have shown a link between COVID-19 and coagulation. We propose several considerations for autopsies of unexpected fatal pulmonary embolism during the SARS-CoV-2 endemic period.

Purpose: To determine whether the cornea remodeling-related genes aldehyde dehydrogenase 3A1 (ALDH3A1), lysyl oxidase (LOX), and secreted protein acidic and rich in cysteine (SPARC) were potential susceptibility candidate genes for keratoconus in Korean patients, we investigated the associations of single nucleotide polymorphisms (SNPs) in these three genes in Korean patients with keratoconus.
Methods: Genomic DNA was extracted from blood samples of unrelated patients with keratoconus and healthy control individuals. For screening of genetic variations, all exons from the entire coding regions of the ALDH3A1, LOX, and SPARC genes were directly sequenced to determine the presence of mutations. Control individuals were selected from the general population without keratoconus.
Results: In this study, we detected nine SNPs in ALDH3A1, four SNPs in LOX, and 18 SNPs in SPARC. rs116992290, IVS3-62c>t, rs116962241, and rs2228100 in ALDH3A1 and rs2956540 and rs1800449 in LOX were significantly different between patient and control groups. In the SPARC gene, the distribution of the *G allele of EX10+225 T>G (p = 0.018; odds ratio, 1.869) was strongly associated with the risk of keratoconus in the Korean population. In haplotype analysis, C-G of rs2956540-rs2288393 in LOX(p = 0.046) and C-C-G and G-G-G of rs60610024-rs2228100-rs57555435 (p = 0.021 and p < 0.001), G-A of IVS3-62 a>g - rs116962241 in ALDH3A1(p = 0.048) predisposed significantly to keratoconus. After cross-validation consistency and permutation tests, two locus model was the best SNP variations interaction pattern.
Conclusions Our results suggested that genetic variations in ALDH3A1, LOX, and SPARC genes were associated with a predisposition for keratoconus in Korean individuals. Moreover, variations in ALDH3A1 and LOX may serve as strong biomarkers for keratoconus.

Purpose: To determine whether the cornea remodeling-related genes aldehyde dehydrogenase 3A1 (ALDH3A1), lysyl oxidase (LOX), and secreted protein acidic and rich in cysteine (SPARC) were potential susceptibility candidate genes for keratoconus in Korean patients, we investigated the associations of single nucleotide polymorphisms (SNPs) in these three genes in Korean patients with keratoconus.
Methods: Genomic DNA was extracted from blood samples of unrelated patients with keratoconus and healthy control individuals. For screening of genetic variations, all exons from the entire coding regions of the ALDH3A1, LOX, and SPARC genes were directly sequenced to determine the presence of mutations. Control individuals were selected from the general population without keratoconus.
Results: In this study, we detected nine SNPs in ALDH3A1, four SNPs in LOX, and 18 SNPs in SPARC. rs116992290, IVS3-62c>t, rs116962241, and rs2228100 in ALDH3A1 and rs2956540 and rs1800449 in LOX were significantly different between patient and control groups. In the SPARC gene, the distribution of the *G allele of EX10+225 T>G (p = 0.018; odds ratio, 1.869) was strongly associated with the risk of keratoconus in the Korean population. In haplotype analysis, C-G of rs2956540-rs2288393 in LOX(p = 0.046) and C-C-G and G-G-G of rs60610024-rs2228100-rs57555435 (p = 0.021 and p < 0.001), G-A of IVS3-62 a>g - rs116962241 in ALDH3A1(p = 0.048) predisposed significantly to keratoconus. After cross-validation consistency and permutation tests, two locus model was the best SNP variations interaction pattern.
Conclusions Our results suggested that genetic variations in ALDH3A1, LOX, and SPARC genes were associated with a predisposition for keratoconus in Korean individuals. Moreover, variations in ALDH3A1 and LOX may serve as strong biomarkers for keratoconus.

BACKGROUND: To investigate the role of alpha-adrenergic receptors in the development of delayed afterdepolarization, the effect of alpha-adrenoceptor stimulation and blockade on ouabain induced delayed afterdepolarization(DDAD) was examined in rabbit heart Purkinje fibers. METHODS: Purkinje fibers, taken from adult rabbit(1.8 - 2.0kg) heart anesthetized with penobarbital, were mounted in a Luicite chamber and superfused with Tyrode's solution. The transmembrane potentials were measured by the conventional microelectrode technique while the fibers were being stimulated with rectangular pulses of 50% above threshold voltage. The delayed afterdepolarizations were induced by overdrive excitation in the presence of ouabain. RESULTS: Delayed afterdepolarizations were not observed during superfusion of the control Tyrode's solution containing propranolol(5x10(-7)M). However, the addition of ouabain in the presence of propranolol elicited DADs which were dose-, time- and drive cycle length- dependent. Phenylephrine(PE ; 10(-7)M), and alpha-adrenoceptor agonist, potentiated the ouabain-induced DAD during the initial superfusion(for 10 or 20 min) of the test Tyrode's solution. However, it was followed by attenuating-effects after a superfusion time of 50 to 60 min. Both effects showed ouabain dose-dependence. Ouabain(2x10(-7)M), in the presence of propranolol, depolarized the maximum diastolic potential and shortened the action potential duration, and the addition of PE(10(-7)M) did not affect the characteristics of action potential except a decrease in velocity of phase 0 depolarization. Prazosin, an alpha1-adrenoceptor antagonist, inhibited the PE's enhancing effects of ouabaininduced DDAD at 20 min superfusion, but did not affect the attenuating-effects of PE at 60 min superfusion. On the other hand, yohimbine, an alpha2-adrenoceptor antagonist, did not affect the PE's DAD potentiating-effects at 20 min superfusion, but inhibited the attenunating-effects of PE at 60 min superfusion. CONCLUSION: It is inferred that alpha-adrenergic stimulation induce delayed afterdepolarization and triggered activity in the rabbits, being responsible for the arrhythmia development, and the effects are mainly due to the action of alpha1-subtpe adrenoceptor stimulation.
Action Potentials ; Adult ; Arrhythmias, Cardiac ; Hand ; Heart ; Humans ; Membrane Potentials ; Microelectrodes ; Ouabain ; Prazosin ; Propranolol ; Purkinje Fibers ; Rabbits ; Receptors, Adrenergic, alpha* ; Yohimbine

Toxoplasma gondii is an obligate intracellular protozoan parasite, which invades a wide range of hosts including humans. The exact mechanisms involved in its invasion are not fully understood. This study focused on the roles of Ca2+ in host cell invasion and in T. gondii replication. We examined the invasion and replication of T. gondii pretreated with several calcium modulators, the conoid extrusion of tachyzoites. Calmodulin localization in T. gondii were observed using the immunogold method, and Ca2+ levels in tachyzoites by confocal microscopy. In light microscopic observation, tachyzoites co-treated with A23187 and EGTA showed that host cell invasion and intracellular replication were decreased. The invasion of tachyzoites was slightly inhibited by the Ca2+ channel blockers, bepridil and verapamil, and by the calmodulin antagonist, calmidazolium. We observed that calcium saline containing A23187 induced the extrusion of tachyzoite conoid. By immunoelectron microscopy, gold particles bound to anti-calmodulin or anti-actin mAb, were found to be localized on the anterior portion of tachyzoites. Remarkably reduced intracellular Ca2+ was observed in tachyzoites treated with BAPTA/AM by confocal microscopy. These results suggest that host cell invasion and the intracellular replication of T. gondii tachyzoites are inhibited by the calcium ionophore, A23187, and by the extracellular calcium chelator, EGTA.
Animals ; Calcium/*physiology ; Calcium Channel Blockers/pharmacology ; Calmodulin/antagonists & inhibitors ; Chelating Agents/pharmacology ; Hela Cells ; Host-Parasite Relations ; Humans ; Ionophores/pharmacology ; Research Support, Non-U.S. Gov't ; Toxoplasma/drug effects/pathogenicity/*physiology

BACKGROUND: A large number of children with psychosocial dysfunction are not recognized within schools or primary care settings. In several research, an increasing amount of attention has been paid to the importance of low family support as a predictor of psychosocial dysfunction in children. Our study examined the agreement and relationship between the lack of family support as measured by the Family APGAR and child psychosocial dysfunction as screened by the Pediatric Symptom Checklist(PSC). Therefore, We studied the usefulness of Family APGAR as a screening tool of child psychosocial dysfunction. METHODS: We set 643 children that are engaged in elementary school. We gave a questionnaire to their parents and made them record the questionnaire which contained the sociodemographic data, past history of child and parents, the Family APGAR and the translated Pediatric Symptom Checklist(PSC). Finally, we analysed only 506 complete data. We use the SAS/PC 6.12 that is a statistical analysis program. RESULTS: Children with a lack of family support(APGAR) were 5.1 times as likely to receive scores indicating dysfunction on the PSC(PSC). Families with a lack of support were significantly more likely to report low parental educational achievement and low income. Sixty percent of children from families with a lack of support were identified as having a psychosocial dysfunction by the PSC rating; however, only 24% percent of the children identified with psychosocial dysfunction by the PSC had scores indicating poor family functioning on the Family APGAR. Families with a lack of support had significantly higher total scores on PSC(mean=20.2) than families with adequate support(mean=11.9). The strength of the agreement between the Family APGAR and the PSC was k=.29. CONCLUSION: A lack of family support is associated with child psychosocial dysfunction as assessed by the PSC. However, the Family APGAR was not a sensitive measure of child psychosocial dysfunction, and thus it supplements, but does not replace the PSC.
Child* ; Educational Status ; Humans ; Mass Screening ; Parents ; Primary Health Care ; Surveys and Questionnaires