As a result of the increasing use of radiologic contrast medium in patients, especially the elderly in severe or clinical condition with attendant comorbidities, such as diabetes mellitus, renal failure, cardiac failure, and volume depletion. Contrast induced nephropathy(CIN)is now the third most common cause of hospital-aquired renal failure and accounts for approximately 11% of the cases. This article mainly introduces the evaluation of laboratory investigations providing insights into the pathophysiology of this disorder and the examination of the important clinical data of CIN including risk factors and diagnosis. The last section deals with renal protection and preventive strategies.

In late 1998, a novel paramyxovirus named Nipah virus, emerged in Malaysia, causing fatal disease in domestic pigs and humans with substantial economic loss to the local pig industry. Pteropid fruitbats have since been identified as a natural reservoir host. Over the last two decades, the forest habitat of these bats in Southeast Asia has been substantially reduced by deforestation for pulpwood and industrial plantation. In 1997/1998, slash-and-burn deforestation resulted in the formation of a severe haze that blanketed much of Southeast Asia in the months directly preceding the Nipah virus disease outbreak. This was exacerbated by a drought driven by the severe 1997-1998 El Ni?o Southern Oscillation (ENSO) event. We present data suggesting that this series of events led to a reduction in the availability of flowering and fruiting forest trees for foraging by fruitbats and culminated in unprecedented encroachment of fruitbats into cultivated fruit orchards in 1997/1998. These anthropogenic events, coupled with the location of piggeries in orchards and the design of pigsties allowed transmission of a novel paramyxovirus from its reservoir host to the domestic pig and ultimately to the human population.
Swine ; lower case oh ; Virus ; Nickel ; Malaysia

Objective Analyze the incidence of contrast induce nephropathy (CIN) and related risk factors after coro- nary angiography (CAG) and percutaneous coronary intervention (PCI) in 216 patients.Methods From November 2005 to January 2006,216 patients undergoing CAG or PCI were enrolled consecutively,clinical and laboratory data were documented and analyzed.Results of the 216 patients,CIN happened in 32 patients,the incidence is 14.7%, in those who underwent emergency PCI,CIN happened in 9 over 41 patients (22.0%),among emergeny coronary ar- tery bypass grafting (CABG) after CAG,CIN happened in 8 of 20 patients,incidence is 40%;among 155 selective operations,CIN happened in 15 patients,9.7%.In those over 70 years old,incidence of CIN is 26.8%,in those

INTRODUCTION: This study was to assess the effectiveness of new bone formation and regeneration by using a rhBMP-2 and beta-TCP as a carrier in rabbits' mandible. MATERIALS AND METHODS: The mandibles of 36 rabbits were exposed and cortical bone was penetrated for this study. The experimental subjects were divided into 3 groups each 12 rabbits; control group, experimental group 1, and experimental group 2. Control group had the defect itself without any treatment, in the experimental group 1, beta-TCP only was grafted, and in the experimental group 2, rhBMP-2 soaked in beta-TCP was grafted. The rabbits were sacrificed after 1, 2, 3, 4, 6, and 8weeks, and new bone formation area was examined and measured for bone quantitative and qualitative analysis with light, fluorescent and polarized microscopy. RESULTS: In the experimental group 1, new bone formation from the adjacent host bone was made by osteoconduction, and in the experimental group 2, direct new bone formation by osteoinduction of rhBMP-2 as well as new bone formation by osteoconduction of beta-TCP were observed. CONCLUSION: rhBMP-2 of experimental group 2 is very effective in the bone formation in early 2weeks and bone remodelling from 3weeks.
Bone Morphogenetic Proteins ; Bone Regeneration ; Calcium Phosphates ; Light ; Mandible ; Microscopy ; Osteogenesis ; Rabbits ; Regeneration ; Transplants

Background: The occurrence of Graves’ disease and Hashimoto thyroiditis after coronavirus disease 2019 (COVID-19) raised concerns that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger thyroid autoimmunity. We aimed to address the current uncertainties regarding incident thyroid dysfunction and autoimmunity among COVID-19 survivors. Methods: We included consecutive adult COVID-19 patients without known thyroid disorders, who were admitted to Queen Mary Hospital from July 21 to September 21, 2020 and had serum levels of thyroid-stimulating hormone, free thyroxine, free triiodothyronine (fT3), and anti-thyroid antibodies measured both on admission and at 3 months. Results: In total, 122 patients were included. Among 20 patients with abnormal thyroid function tests (TFTs) on admission (mostly low fT3), 15 recovered. Among 102 patients with initial normal TFTs, two had new-onset abnormalities that could represent different phases of thyroiditis. Among 104 patients whose anti-thyroid antibody titers were reassessed, we observed increases in anti-thyroid peroxidase (TPO) (P<0.001) and anti-thyroglobulin (P<0.001), but not anti-thyroid stimulating hormone receptor titers (P=0.486). Of 82 patients with negative anti-TPO findings at baseline, 16 had a significant interval increase in anti-TPO titer by >12 U, and four became anti-TPO-positive. Worse baseline clinical severity (P=0.018), elevated C-reactive protein during hospitalization (P=0.033), and higher baseline anti-TPO titer (P=0.005) were associated with a significant increase in anti-TPO titer. Conclusion Most patients with thyroid dysfunction on admission recovered during convalescence. Abnormal TFTs suggestive of thyroiditis occurred during convalescence, but infrequently. Importantly, our novel observation of an increase in anti-thyroid antibody titers post-COVID-19 warrants further follow-up for incident thyroid dysfunction among COVID-19 survivors.

Background: The occurrence of Graves’ disease and Hashimoto thyroiditis after coronavirus disease 2019 (COVID-19) raised concerns that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may trigger thyroid autoimmunity. We aimed to address the current uncertainties regarding incident thyroid dysfunction and autoimmunity among COVID-19 survivors. Methods: We included consecutive adult COVID-19 patients without known thyroid disorders, who were admitted to Queen Mary Hospital from July 21 to September 21, 2020 and had serum levels of thyroid-stimulating hormone, free thyroxine, free triiodothyronine (fT3), and anti-thyroid antibodies measured both on admission and at 3 months. Results: In total, 122 patients were included. Among 20 patients with abnormal thyroid function tests (TFTs) on admission (mostly low fT3), 15 recovered. Among 102 patients with initial normal TFTs, two had new-onset abnormalities that could represent different phases of thyroiditis. Among 104 patients whose anti-thyroid antibody titers were reassessed, we observed increases in anti-thyroid peroxidase (TPO) (P<0.001) and anti-thyroglobulin (P<0.001), but not anti-thyroid stimulating hormone receptor titers (P=0.486). Of 82 patients with negative anti-TPO findings at baseline, 16 had a significant interval increase in anti-TPO titer by >12 U, and four became anti-TPO-positive. Worse baseline clinical severity (P=0.018), elevated C-reactive protein during hospitalization (P=0.033), and higher baseline anti-TPO titer (P=0.005) were associated with a significant increase in anti-TPO titer. Conclusion Most patients with thyroid dysfunction on admission recovered during convalescence. Abnormal TFTs suggestive of thyroiditis occurred during convalescence, but infrequently. Importantly, our novel observation of an increase in anti-thyroid antibody titers post-COVID-19 warrants further follow-up for incident thyroid dysfunction among COVID-19 survivors.

INTRODUCTIONPatients with functional gastrointestinal disorders (FGIDs) have a decreased quality of life (QoL). Psychological illnesses are strongly associated with FGIDs. This study examined the effect of a comprehensive psychological intervention programme designed for refractory FGID patients.

METHODSRefractory FGID patients at a tertiary gastroenterology unit were encouraged to participate in a psychological intervention programme, which included screening for anxiety and depression in patients, educating patients and physicians on FGIDs, and providing early access to psychiatric consultation for patients with significant psychological illnesses. The duration of follow-up was six months. Outcomes were measured using the Irritable Bowel Syndrome-QoL (IBS-QoL) instrument and the EuroQol five dimensions (EQ-5D) questionnaire.

RESULTSA total of 1,189 patients (68% female, 80% Chinese, mean age 48.6 years) participated in the programme. Among these participants, 51% had a significant psychological disorder (Hospital Anxiety and Depression Scale [HADS] anxiety or depression score > 7). These participants had a significantly poorer QoL (IBS-QoL and EQ-5D, both p < 0.0001), and were more likely to be single or English-speaking, as compared to the participants without psychological disorders. Participants who completed ≥ 3 months of follow-up (n = 906) showed significant and durable improvement. High baseline HADS anxiety score predicted improvement (p < 0.001), with participant IBS-QoL and EQ-5D scores decreasing over time.

CONCLUSIONThe intervention programme was associated with a clinically meaningful improvement in the QoL of patients with refractory FGIDs. High baseline anxiety was predictive of improvement.

Adult ; Anxiety ; complications ; diagnosis ; therapy ; Depression ; complications ; diagnosis ; therapy ; Female ; Follow-Up Studies ; Gastrointestinal Diseases ; complications ; psychology ; therapy ; Humans ; Male ; Mental Disorders ; complications ; therapy ; Middle Aged ; Quality of Life ; Severity of Illness Index ; Singapore ; Surveys and Questionnaires ; Treatment Outcome

OBJECTIVETo investigate the potential efficacy of panaxadiol saponins component (PDS-C), a biologically active fraction isolated from total ginsenosides, to reverse chemotherapy-induced myelosuppression and pancytopenia caused by cyclophamide (CTX).

METHODSMice with myelosuppression induced by CTX were treated with PDS-C at a low- (20 mg/kg), moderate- (40 mg/kg), or high-dose (80 mg/kg) for 7 consecutive days. The level of peripheral white blood cell (WBC), neutrophil (NEU) and platelet (PLT) were measured, the histopathology and colony formation were observed, the protein kinase and transcription factors in hematopoietic cells were determined by immunohistochemical staining and Western blot.

RESULTSIn response to PDS-C therapy, the peripheral WBC, NEU and PLT counts of CTX-induced myelosuppressed mice were significantly increased in a dose-dependent manner. Similarly, bone marrow histopathology examination showed reversal of CTX-induced myelosuppression with increase in overall bone marrow cellularity and the number of hematopoietic cells (P<0.01). PDS-C also promoted proliferation of granulocytic and megakaryocyte progenitor cells in CTX-treated mice, as evidenced by significantly increase in colony formation units-granulocytes/monocytes and -megakaryocytes (P<0.01). The enhancement of hematopoiesis by PDS-C appears to be mediated by an intracellular signaling pathway, this was evidenced by the up-regulation of phosphorylated mitogen-activated protein kinase (p-MEK) and extracellular signal-regulated kinases (p-ERK), and receptor tyrosine kinase (C-kit) and globin transcription factor 1 (GATA-1) in hematopoietic cells of CTX-treated mice (P<0.05).

CONCLUSIONSPDS-C possesses hematopoietic growth factor-like activities that promote proliferation and also possibly differentiation of hematopoietic progenitor cells in myelosuppressed mice, probably mediated by a mechanism involving MEK and ERK protein kinases, and C-kit and GATA-1 transcription factors. PDS-C may potentially be a novel treatment of myelosuppression and pancytopenia caused by chemotherapy.

Animals ; Antineoplastic Agents ; adverse effects ; Cell Proliferation ; drug effects ; Cyclophosphamide ; adverse effects ; Extracellular Signal-Regulated MAP Kinases ; metabolism ; GATA1 Transcription Factor ; metabolism ; Ginsenosides ; pharmacology ; therapeutic use ; Hematopoiesis ; drug effects ; Mice ; Mitogen-Activated Protein Kinase Kinases ; metabolism ; Myeloid Cells ; drug effects ; pathology ; Panax ; chemistry ; Pancytopenia ; chemically induced ; drug therapy ; pathology ; Phosphorylation ; drug effects ; Proto-Oncogene Proteins c-kit ; metabolism ; Saponins ; pharmacology ; Up-Regulation ; drug effects