The type-specific PCR and the sequence analysis of 56 kDa gene of Orientia tsutsugamushi infected in field rodents specimens have shown intratypic genetic heterogeneity in genotype Karp. In sequence comparison, this genetic heterogeneity was mainly due to insertion or deletion of a repeated unit in variable domain I (VDI) region. These results suggested that genetic duplication or deletion of the specific sequence rnight be involved in intratypic genetic heterogeneity of Orientia tsutsugamushi.
Genetic Heterogeneity* ; Genotype* ; Orientia tsutsugamushi* ; Polymerase Chain Reaction ; Rodentia ; Sequence Analysis

No abstract available.
Humans ; Liver Function Tests* ; Liver*

Objective To evaluate the diagnosis and therapy of intestinal lymphangiectasia.Methods In this study 15 patients were admitted in our hospital during recent 7 years.Clinical manifestations included hypoalbuminemia,symmetrical edema,emaciation,diarrhea and lymphopenia.Lymphangiography,lympanscintigraphy and biopsy were performed for diagnosis.Therapy conducted included conservative therapy,low-fat and medium-chain triglycerides(MCT)diet,albumin infusions,diuretics,total parenteral nutrition and octreotide.Surgical therapy ineluded thoracic duct-vein anastomasis and segmental resection.Results In this group 8 patients receiving conservative therapy were followed-up from 1.5 to 7 years(average 2.5 years).Symptoms were alleviated in 6 patients.Seven patients underwent operative therapy,among them,4 patients received thoracic duct-exterior jugular vein anastomasis and followed-up from 1 to 5 years,with symptoms mitigated in 2 patients.3 patients underwent local intestinal resection,follow-up from 1 to 3 years found one patient was cured,one was improved,and 1 patient died 3 months afterthe operation. Conclusion Intestinal lymphangiectasia is rather rare and there was no definite and effective therapy.

BCG Vaccine ; adverse effects ; Humans ; Immunologic Deficiency Syndromes ; complications ; Panniculitis ; etiology ; T-Lymphocytes ; Tuberculosis ; etiology

No abstract available.

OBJECTIVETo study the protective effect of Ligustrazine Injection (LI) against cisplatin-induced ototoxicity and to explore its mechanism.

METHODSThirty healthy adult guinea pigs were randomly divided into three groups, 10 in each group, i.e., the normal control group, the cisplatin group, and the LI group. Guinea pigs in the normal control group were intraperitoneally injected with normal saline at 3 mL/kg for 7 consecutive days. Those in the cisplatin group were intraperitoneally injected with cisplatin at 3 mg/kg for 7 consecutive days. Those in the LI group were intraperitoneally injected with LI at 140 mg/kg for 7 days, but cisplatin (3 mg/kg) was intraperitoneally injected from the opposite side starting from the 4th day. Brainstem auditory evoked potential (BAEP) was performed in all animals before and after injection. All animals were sacrificed after the final testing under anesthesia and their cochleas collected. Half the cochleas of each group were collected for silver nitrate staining of cochlear basilar membrane stretched. The other half the cochleas of each group made into paraffin sections to observe the apoptosis of cochlea cells by TUNEL method and the expression levels of c-Jun detected by immunohistochemistry.

RESULTSThere was no statistical difference in the difference of BAEP threshold among the 3 groups before injection (P > 0.05), but the BAEP threshold increased in the cisplatin group and the LI group (P < 0.05). Besides, it was higher in the cisplatin group (P < 0.05). In the cisplatin group, most hair cells were missing, spiral ganglion cells obviously decreased, more TUNEL positive cells occurred, and the expression of c-Jun was stronger. But the aforesaid impairment in the LI group was obviously lessened (P < 0.05).

CONCLUSIONSLI showed certain antagonist effect on cisplatin-induced ototoxicity. Its mechanism might be associated with scavenging oxygen radicals of the cochlea tissue, improving the microcirculation, and fighting against apoptosis.

Animals ; Apoptosis ; drug effects ; Cisplatin ; toxicity ; Cochlea ; drug effects ; metabolism ; pathology ; Evoked Potentials, Auditory, Brain Stem ; Guinea Pigs ; Pyrazines ; pharmacology ; Reactive Oxygen Species ; metabolism

No abstract available.
Humans ; Infant, Newborn*

No abstract available.
Brain Injuries* ; Brain* ; Disability Evaluation* ; Humans ; Perfusion* ; Technetium Tc 99m Exametazime* ; Tomography, Emission-Computed, Single-Photon*

In order to find a highly efficient compound against Clonorchis infection, the anthelmintic activity of disophenol, Tremerad (SYD-230), dithiazanine iodide, dehydroemetine-late-release tablets(RO 1-9334/20), niridazole (Ambilhar), hexachlorophene (G-11), Hetol(1, 4-bis-trichloromethylbenzol) and Bilevon (niclofolan) was tested against Clonorchis sinensis experimentally infected rabbits. All drugs showed a progressive increase in efficacy as the dose rate. They were highly efficient against Clonorchis infection if sufficiently high, potentially toxic doses were given. The efficacy was evaluated by the number of detected worms with vital condition at autopsy after the treatment with above drugs. The high efficacy was observed at the following dose rates of each drugs, i.e. disophenol at a single dose of 30 mg/kg, Tremerad at the daily dose of 200 mg/kg for 10 consecutive days, dithiazanine iodide at the daily dose of 50 mg/kg for 6 consecutive days, dehydroemetine at the daily dose of 10 mg/kg for 10 consecutive days, hexachlorophene at the daily dose of 20 mg/kg for 10 to 15 consecutive days, Hetol at the daily doses from 50 to 100 mg/kg for 5 to 10 consecutive days, and Bilevon at a single dose of 8 mg/kg. Moderate effectiveness was shown in niridazole at the dose of 25 mg/kg for 10 days medication. The use of these anthelmintics for the clinical treatment of Clonorchis sinensis infection is discussed.
parasitology-helminth-trematoda ; chemotherapy-Clonorchis sinensis ; clonorchiasis-rabbit ; disophenol ; Tremerad (SYD-230) ; dithiazanine iodide ; dehydroemetine-late-release tablets(RO 1-9334/20) ; niridazole (Ambilhar) ; hexachlorophene (G-11) ; Hetol(1, 4-bis-trichloromethylbenxol) ; Bilevon (niclofolan)

Various anatomical defects have been described in the surviving co-twin who had stillborn, macerated monozygotic co-twin with disseminated intravascular coagulation. The suggested mechanism was the transfer of emboli or thromboplastic materials of dead fetus to co-twin through placental vascular anastomoses. Multicystic encephalomalacia is the condition defined anatomically by the presence of multiple cavities in the great part of both cerebral hemispheres. The most common pathogenesis is circulatory disturbance caused by neonatal asphyxia during the perinatal period. We experienced two cases of monozygotic twin with deceased co-twin at 26 weeks, 33 weeks of gestation and confirmed the diffuse multicystic encephalomalacia by cranial ultrasonography and MRI in a surviving co-twin. Only one patient has been followed who showed spastic cerebral palsy and severe mental retardation. We report two cases of multicystic encephalomalacia in a surviring co-twin with a intrauterine fetal death and its related literatures.
Asphyxia ; Cerebral Palsy ; Cerebrum ; Disseminated Intravascular Coagulation ; Encephalomalacia* ; Fetal Death* ; Fetus ; Humans ; Intellectual Disability ; Magnetic Resonance Imaging ; Pregnancy ; Pregnancy, Twin ; Twins, Monozygotic ; Ultrasonography