Selective accumulation of a photosensitizer and the subsequent response in only the lightirradiated target are advantages of photodynamic diagnosis and therapy. The limited depth of the therapeutic effect is a positive characteristic when treating surface malignancies, such as peritoneal carcinomatosis. For photodynamic diagnosis (PDD), adjunctive use of aminolevulinic acid- protoporphyrin IX-guided fluorescence imaging detects cancer nodules, which would have been missed during assessment using white light visualization only. Furthermore, since few side effects have been reported, this has the potential to become a vital component of diagnostic laparoscopy. A variety of photosensitizers have been examined for photodynamic therapy (PDT), and treatment protocols are heterogeneous in terms of photosensitizer type and dose, photosensitizer-light time interval, and light source wavelength, dose, and dose rate. Although several studies have suggested that PDT has favorable effects in peritoneal carcinomatosis, clinical trials in more homogenous patient groups are required to identify the true benefits. In addition, major complications, such as bowel perforation and capillary leak syndrome, need to be reduced. In the long term, PDD and PDT are likely to be successful therapeutic options for patients with peritoneal carcinomatosis, with several options to optimize the photosensitizer and light delivery parameters to improve safety and efficacy.

Since the first-in-man transcatheter delivery of an aortic valve prosthesis in 2002, the landscape of aortic stenosis therapeutics has shifted dramatically. While initially restricted to non-surgical cases, progressive advances in transcatheter aortic valve replacement and our understanding of its safety and efficacy have expanded its use in intermediate and possibly low surgical risk patients. In this review, we explore the past, present, and future of transcatheter aortic valve replacement.
Aortic Valve ; Aortic Valve Stenosis ; Humans ; Prostheses and Implants ; Transcatheter Aortic Valve Replacement*

This study aimed to estimate the medical cost of cancer in the first five years of diagnosis and in the final six months before death in people who developed cancer after human immunodeficiency virus (HIV) infection in Korea. The study utilized the Korea National Health Insurance Service-National Health Information Database (NHIS-NHID). Among 16,671 patients diagnosed with HIV infection from 2004 to 2020 in Korea, we identified 757 patients newly diagnosed with cancer after HIV diagnosis. The medical costs for 60 months after diagnosis and the last six months before death were calculated from 2006 to 2020. The mean annual medical cost due to cancer in HIV-infected people with cancer was higher for acquired immunodeficiency syndrome (AIDS)-defining cancers (48,242 USD) than for non-AIDS-defining cancers (24,338 USD), particularly non-Hodgkin’s lymphoma (53,007 USD), for the first year of cancer diagnosis. Approximately 25% of the cost for the first year was disbursed during the first month of cancer diagnosis. From the second year, the mean annual medical cost due to cancer was significantly reduced. The total medical cost was higher for non-AIDS-defining cancers, reflecting their higher incidence rates despite lower mean medical costs. The mean monthly total medical cost per HIV-infected person who died after cancer diagnosis increased closer to the time of death. The estimated burden of medical costs in patients with HIV in the present study may be an important index for defining healthcare policies in HIV patients in whom the cancer-related burden is expected to increase.

PURPOSE: Leigh syndrome is a kind of mitochondrial disease with a pathological production of lactate and variable clinical manifestations. Recently biochemical assay of the mitochondrial enzyme activity and MRS are becoming a powerful tool for the definitive antemorterm diagnosis of this disease. The aim of this study was designed to determine the usefulness of biochemical enzyme assay and MRS in Leigh syndrome. METHODS: A clinical study of 8 cases of pediatric patients were diagnosed as Leigh syndrome on the basis of clinical manifestations and MRI features at the department of pediatrics, Ulsan university hospital, from July, 1992 to June, 1997. Biochemical enzyme assay of the cultured skin fibroblasts was consulted to hospital for sick children, Toronto, Canada. Cerebral lactates were detected on MRS were analysed in relation to the MRI findings and lactate levels in the CSF. RESULTS: 1) Age at diagnosis ranged from 7 months to 8.9 years; seven were boys and one was girl. 2) Main clinical symptoms were as follows in the order of frequency; seizure(75%), ophthalmoplegia(50%), hemiplegia(50%), hypotonia(50%), respiratory difficulty(50%), developmental delay(38%), consciousness change(38%), mental retardation( 25%). 3) Anatomical locations of the focal lesions detected on the initial MRI were as follows in the order of frequency; putamen(75%), caudate nuclei(63%), medulla oblongata (18,50%), substantia nigra(38%), thalamus(38%). 4) Biochemical enzyme assay revealed deficiency of NADH cytochrome c reductase (complex I) and deficiency of cytochrome c oxidase(complex N) respectively in 2 patients who had markedly elevated serum and CSF lactate levels and lactate/pyruvate ratio. 5) Cerebral lactates were detected by MRS from 6 lesions of 1 week-4 months old in 6 patients who had normal or mildly elevated serum and CSF lactate levels and lactate/pyruvate ratio. CONCLUSION: MRS detected the brain parenchymal lactate non-invasively from the acute or subacute lesions. Therefore, combined evaluation by MRS and biochemical enzyme assay will provide an important information for the diagnosis and estimation of disease activity in pediatric patients who are suspected to have Leigh syndrome.
Brain ; Canada ; Child ; Consciousness ; Cytochromes c ; Diagnosis ; Enzyme Assays* ; Female ; Fibroblasts ; Humans ; Lactates ; Lactic Acid ; Leigh Disease* ; Magnetic Resonance Imaging ; Medulla Oblongata ; Mitochondrial Diseases ; NADH Dehydrogenase ; Pediatrics ; Skin ; Ulsan

BACKGROUND: Helicobacter pylori increases production of reactive oxygen species (ROS), which activates inflammatory and carcinogenesis-related signaling pathways in gastric epithelial cells. Therefore, reducing ROS, by upregulating antioxidant enzyme, such as superoxide dismutase (SOD), may be a novel strategy to prevent H. pylori-associated gastric diseases. Astaxanthin is an antioxidant carotenoid that prevents oxidative stress-induced cell injury. The present study was aimed to determine whether H. pylori decreases SOD activity by changing the levels of SOD1/SOD2 and whether astaxanthin prevents changes in SOD levels and activity in H. pylori-infected gastric epithelial AGS cells. METHODS: AGS cells were pre-treated with astaxanthin for 3 hours prior to H. pylori infection and cultured for 1 hour in the presence of H. pylori. SOD levels and activity were assessed by Western blot analysis and a commercial assay kit, respectively. Mitochondrial ROS was determined using MitoSOX fluorescence. RESULTS: H. pylori decreased SOD activity and the SOD2 level, but increased mitochondrial ROS in AGS cells. The SOD1 level was not changed by H. pylori infection. Astaxanthin prevented H. pylori-induced decreases in the SOD2 level and SOD activity and reduced mitochondrial ROS in AGS cells. CONCLUSIONS: Consumption of astaxanthin-rich food may prevent the development of H. pylori-associated gastric disorders by suppressing mitochondrial oxidative stress.
Blotting, Western ; Epithelial Cells ; Fluorescence ; Helicobacter pylori ; Helicobacter ; Oxidative Stress ; Reactive Oxygen Species ; Stomach Diseases ; Superoxide Dismutase ; Superoxides

STUDY DESIGN: A randomized, controlled animal study. PURPOSE: To investigate the effectiveness of fusion and new bone formation induced by demineralized bone matrix (DBM) strips with jelly strengths. OVERVIEW OF LITERATURE: The form of the DBM can make a difference to the outcome. The effect of different jelly strengths on the ability of DBM to form new bone is not known. METHODS: Forty-eight rabbits were randomized into a control group and two experimental groups. In the control group (group 1), 1.4 g of autologous iliac crest bone was placed bilaterally. In the experimental groups, a high jelly strength DBM-hyaluronic acid (HA)-gelatin strip (group 2) and a low jelly strength DBM-HA-gelatin strip (group 3) were used. The fusion was assessed with manual manipulation and radiographs. The volume of the fusion mass was determined from computed tomographic images. RESULTS: The fusion rates as determined by manual palpation were 37.5%, 93.8% and 50.0% in group 1, group 2, and group 3, respectively (p<0.05). By radiography, the fusion rate of High jelly strength DBM strip was statistically significantly greater than that of the other alternatives (p<0.05). The mean bone volume of the fusion mass as determined by computed tomography was 2,142.2+/-318.5 mm3, 3,132.9+/-632.1 mm3, and 2,741.5+/-380.4 mm3 in group 1, group 2, and group 3, respectively (p<0.05). CONCLUSIONS: These results indicate that differences in the structural and mechanical properties of gelatin that are associated with jelly strength influenced cellular responses such as cell viability and bony tissue ingrowth, facilitating greater bone fusion around high jelly strength implants.
Animals ; Bone Matrix* ; Cell Survival ; Gelatin ; Osteogenesis ; Palpation ; Rabbits ; Radiography ; Spinal Fusion

Wernicke encephalopathy (WE) is an uncommon but severe neurological disorder caused by thiamine (vitamin B1) deficiency. It is characterized by the sudden onset of altered consciousness, ophthalmoplegia, and ataxia. Apart from chronic alcoholism, a lot of other conditions causing malnutrition and decreasing thiamine absorption must be considered as predisposing factors. Due to its low prevalence and clinical heterogeneity, WE is often misdiagnosed, resulting in persistent dysfunctions or death. Therefore, early diagnosis and prompt treatment with intravenous thiamine supplement might prevent encephalopathy and other neurologic or systemic complications of thiamine depletion. We hereby report of our experience of a WE patient who presented with predominantly vestibular symptoms and signs; the patient was successfully diagnosed and treated with high-dose intravenous thiamine repletion.

BACKGROUND: Chronic pancreatitis (CP) is an irreversible progressive disease that destroys exocrine parenchyma, which are replaced by fibrous tissue. As pancreatic fibrosis is a key feature of CP, reducing fibrotic protein content in the pancreas is crucial for preventing CP. Studies suggest that NF-κB facilitates the expression of fibrotic mediators in pancreas and protein kinase C-δ (PKC-δ) regulates NF-κB activation in stimulated pancreatic acinar cells. Docosahexaenoic acid (DHA) is an omega-3 fatty acid having anti-inflammatory and anti-fibrotic effects. It has been shown to inhibit NF-κB activity in cerulein-stimulated pancreatic acinar cells which is a cellular model of CP. In the present study, we investigated if DHA inhibits expression of fibrotic mediators by reducing PKC-δ and NF-κB expression in mouse pancreatic tissues with CP.METHODS: For six weeks, mice were weekly induced for acute pancreatitis to develop CP. Furthermore, acute pancreatitis was induced by hourly intraperitoneal injections of cerulein (50 μg/kg × 7). Mice were administered DHA (10 μM) via drinking water before and after CP induction.RESULTS: Cerulein-induced pancreatic damages like decreased pancreatic weight/total body weight, leukocyte infiltration, necrosis of acinar cells, and vacuolization were found to be inhibited by DHA. Additionally, DHA inhibited cerulein-induced fibrotic mediators like alpha-smooth muscle actin and fibronectin in pancreas. DHA reduced expression of PKC-δ and NF-κB p65 in pancreatic tissues of cerulein-treated mice.CONCLUSIONS: DHA may be beneficial in preventing CP by suppressing pancreatic expression of fibrotic mediators.
Acinar Cells ; Actins ; Animals ; Body Weight ; Ceruletide ; Drinking Water ; Fibronectins ; Fibrosis ; Injections, Intraperitoneal ; Leukocytes ; Mice ; Necrosis ; Pancreas ; Pancreatitis ; Pancreatitis, Chronic ; Protein Kinases

Cogan’s syndrome is a rare inflammatory disease characterized by non-syphilitic keratitis and vestibulo-auditory symptoms including hearing loss, tinnitus, and vertigo. Although its precise pathogenesis is not known, Cogan’s syndrome is generally considered an autoimmune disease. This hypothesis is supported by the frequently successful remission of hearing loss after steroid administration and the association with other autoimmune disorders such as rheumatoid arthritis. Medical treatment of Cogan’s syndrome depends on disease severity and on how extensive the disease is. The involvement of inner ear pathology requires systemic corticosteroid therapy. In cases of treatment failure or the need for a corticosteroid-sparing effect, other immunosuppressive drugs can be used. We experienced two patients with typical Cogan’s syndrome, presenting bilateral progressive sensorineural hearing loss and dizziness with ocular involvement, which we have successfully treated with systemic steroid administration and immunosuppressive therapy.

In spite of the developing endovascular era, large (15–25 mm) and giant (>25 mm) wide-neck cerebral aneurysms remained technically challenging. Intracranial flow-diverting stents (FDS) were developed to address these challenges by targeting aneurysm hemodynamics to promote aneurysm occlusion. In 2011, the first FDS approved for use in the United States market. Shortly thereafter, the Pipeline of Uncoilable or Failed Aneurysms (PUFS) study was published demonstrating high efficacy and a similar complication profile to other intracranial stents. The initial FDA instructions for use (IFU) limited its use to patients 22 years old or older with wide-necked large or giant aneurysms of the internal carotid artery (ICA) from the petrous segment to superior hypophyseal artery/ophthalmic segment. Expanded IFU was tested in the Prospective Study on Embolization of Intracranial Aneurysms with PipelineTM Embolization Device (PREMIER) trial. With further post-approval clinical data, the United States FDA expanded the IFU to include patients with small or medium, wide-necked saccular or fusiform aneurysms from the petrous ICA to the ICA terminus. However, IFU is more restrictive in South Korea than in United States. Several systematic reviews and meta-analyses have sought to evaluate the overall efficacy of FDS for the treatment of cerebral aneurysms and consistently identify FDS as an effective technique for the treatment of aneurysms broadly with complication rates similar to other traditional techniques. A growing body of literature has demonstrated high efficacy of FDS for small aneurysms; distal artery aneurysms; non-saccular aneurysms posterior circulation aneurysms and complication rates similar to traditional techniques. In the short interval since the Pipeline Embolization Device was first introduced, FDS has been firmly entrenched as a powerful tool in the endovascular armamentarium. As new FDS are developed, established FDS are refined, and delivery systems are improved the uses for FDS will only expand further. Researchers continue to work to optimize the mechanical characteristics of the FDS themselves, aiming to optimize deploy ability and efficacy. With expanded use for small to medium aneurysms and posterior circulation aneurysms, FDS technology is firmly entrenched as a powerful tool to treat challenging aneurysms, both primarily and as an adjunct to coil embolization. With the aforementioned advances, the ease of FDS deployment will improve and complication rates will be further minimized. This will only further establish FDS deployment as a key strategy in the treatment of cerebral aneurysms.