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Biomedical subjects

Q Shao

Publications and source records attributed to Q Shao.

52 records · Page 3Linked to original sources
PubMed1994

A transmission model for a disease with some fatalities.

A stochastic epidemic model which allows some infected individuals to die from the disease is considered. The model includes the general epidemic and the fatal disease model as particular cases. A set of iterative equations is derived from which the probability distribution of the final size of the epidemic can be computed. It is illustrated that the fatal disease model is distinct in that it results in nearly all or hardly anyone being infected in a large population. An easily computed estimator for a key parameter of the model is derived and it is illustrated that it has good efficiency relative to the maximum likelihood estimator, which is very tedious to compute.

Communicable Diseases↗
PubMed1994

Characterization of the translocation process of vitamin D3 from the skin into the circulation.

The cutaneous synthesis of vitamin D3 and the subsequent translocation of vitamin D3 into the circulation are two key steps in the vitamin D endocrine system. To study the kinetic aspects of cutaneous synthesis and translocation of vitamin D3, both in vitro and in vivo chicken models have been developed. To assess the capacity of chicken skin to generate vitamin D3, the concentrations of 7-dehydrocholesterol (7-DHC) in different skin areas were determined. It was found that the highest concentration of 7-DHC was in the leg skin (3524 +/- 937 ng cm-2), which was about 30 times greater than that in the back (120 +/- 62 ng cm-2). Whole body exposure of chickens to UV-B radiation (0.5 J cm-2) resulted in the production of previtamin D3 (preD3) in the skin of the legs and feet (43 +/- 7 and 54 +/- 17 ng cm-2, respectively), whereas no preD3 was detected in the back skin. In vitro, at 40 C, the forward (k1) and reverse (k2) rate constants of the preD3<-->vitamin D3 reaction in the leg skin were greatly increased compared to those in n-hexane (k1, 0.367 vs. 0.0369 h-1; k2, 0.042 vs. 0.0059 h-1). In vivo, the determined rate constants k1, k2, and k3 for the consecutive reactions preD3<-->vitamin D3-->vitamin D3 were 0.257, 0.034, and 0.114 h-1, respectively. To evaluate the circulating concentration of vitamin D3 in response to UV-B radiation, chicken legs were irradiated. The time course revealed a 4-fold increase in the circulating concentration of vitamin D3, with a peak about 30 h postradiation. No appreciable amount of preD3 could be detected in the circulation in the early hours after UV-B radiation, suggesting the existence of a process responsible for the specific translocation of vitamin D3 from the skin into the circulation.

Animals↗
PubMed1993

Hepatic stimulator substance protects against acute liver failure induced by carbon tetrachloride poisoning in mice.

Hepatic stimulator substance was extracted from the liver of weanling Sprague-Dawley rats according to the method of LaBrecque. Quang-Ming mice were injected with carbon tetrachloride to induce acute liver failure. Hepatic stimulator substance suppressed the elevation of ALT and AST induced by carbon tetrachloride in a dose-dependent manner. Hepatic histological changes indicated that hepatic stimulator substance reduced the severity of hepatic lesion induced by carbon tetrachloride and reversed carbon tetrachloride-induced reduction of hepatic mitochondrial succinic dehydrogenase activity. In attempting to elucidate the mechanism or mechanisms of this protective effect, we found that hepatic stimulator substance significantly restored the carbon tetrachloride-induced decrease of hepatocyte plasmalemma and mitochondrial and microsomal membrane fluidity. Hepatic stimulator substance also decreased the malondialdehyde content of carbon tetrachloride-intoxicated mice; restored the liver-reduced glutathione content, which was lowered by carbon tetrachloride intoxication; stimulated liver regeneration, as shown by enhanced DNA synthesis; and increased the 3H-thymidine incorporation into DNA of hepatocytes. We propose that hepatic stimulator substance protects the liver against acute liver failure induced by carbon tetrachloride poisoning, probably by an antioxidative effect on hepatocyte membrane lipid peroxidation, which was increased by free radicals produced from carbon tetrachloride. In addition, hepatic stimulator substance stimulates hepatocyte proliferation. These protective mechanisms may act in concert to protect against carbon tetrachloride injury.

Alanine Transaminase↗
PubMed1993

Growth of lactobacilli, Staphylococcus aureus and Escherichia coli in normal and mastitic milk and whey.

The growth of three lactobacilli (Lactobacillus acidophilus, L. bulgaricus and L. casei), Staphylococcus aureus and Escherichia coli was followed in normal and mastitic milk and whey using the standard plate count method. L. acidophilus, L. bulgaricus 6032 and L. casei 6028 grew well in normal milk, but had decreased growth in mastitic milk if not pre-adapted in mastitic whey. S. aureus 26003 and E. coli 44102 showed enhanced growth in mastitic milk as compared with their growth in normal milk. These mastitis pathogens grew faster than the lactobacilli in both the normal milk and the mastitic milk. Among the lactobacilli, L. acidophilus and L. bulgaricus grew faster than L. casei in both types of milk samples. All the bacteria tested grew well in the normal and mastitic whey samples. However, they seemed to have enhanced growth in mastitic whey with the exception of L. casei. Pre-adaptation of the bacteria in mastitic whey in subculture markedly improved the growth of both pathogenic and non-pathogenic bacteria in mastitic milk. All the bacteria showed decreased replication in mastitic milk as compared with mastitic whey.

Animals↗
PubMed1993

Macrophages in the urine in acute bacterial cystitis.

In the previous study in this series of studies concerning the role of macrophages in urinary tract infection, we attempted to detect macrophages in the urine of acute bacterial cystitis patients by nonspecific esterase staining of urinary sediment, however none of the leukocytes stained, probably because of cell damage caused by the urine and by centrifugation. In the present study, detection of macrophages in urine was again attempted, this time by prompt transfer of urinary leukocytes to culture medium after minimum centrifugation, 1 hr culture in a glass bottom chamber and non-specific staining of leukocytes adhering to glass. Macrophages in urine were detected by this method, and they comprised 5.9% of the adherent leukocytes, although macrophage spreading, which implies macrophage activation and is often seen in the early stage of nonbacterial prostatitis, was hardly ever observed. The percentages of adherent leukocytes were not correlated with urine osmolarity, probably because the effect of urine was minimized by prompt transfer of urinary leukocytes to culture medium after the urine samples had been collected. There have been quite few studies involving culture of urinary leukocytes in the past. Our simple techniques, such as prompt transfer of urinary leukocytes to culture medium after centrifuging with minimum gravity and for a minimum period of time, appear to be useful in the study of urinary leukocytes using other cells which appear in urinary tract infection, as well as cytokines and antibiotics, to clarify cellular mechanisms of defenses in urinary tract infection.

Acute Disease↗
PubMed1993

[A study of regenerating liver protects against carbon tetrachloride injury in rat].

In our previous study we had demonstrated that regenerating liver of rats had an ability to resist CCl4 injury. In this paper, the underlying mechanism was further investigated. Hepatic stimulator substance from regenerating liver (rHSS) at different time after partial (68%) hepatectomy was extracted and assayed for its biological activity by using 3H-thymidine. The activity is approximately seven-fold as compared with the control. Then, rHSS was given to rats to observe its effect against CCl4 injury both in vivo and in vitro. The results were as follows: rHSS decreases the mortality of CCl4 intoxicated rats and suppresses the elevation of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) induced by CCl4 in vivo. Also rHSS increases the cell viability and decreases the leakage of intracellular ALT of hepatocytes poisoning by CCl4. The above mentioned results suggest rHSS is an important mechanism for regenerating liver to protect against CCl4 poisoning.

Animals↗
PubMed1993

[Effect of human hepatic stimulator substance on intracellular calcium and potassium homeostasis in CCl4-intoxication dissociated hepatocytes].

The human hepatic stimulator substance (hHSS) was extracted from abortive fetal liver according to the method of LaBrecque. The intracellular free calciumion was measured by fluorescent probes Fura-2/AM. Rat hepatocytes were isolated from liver by the method of Seglen and intoxicated by CCl4 vapour, then the changes of [Ca2+]i, the leakage of intracellular K+, ALT and viability of hepatocytes were observed. The results were as follows: The hHSS does exist in the human fetal liver, hHSS could increase the viability of intoxicated hepatocytes, maintain the intracellular calcium homeostasis, and decrease the leakage of intracellular potassium and ALT into the culture medium. These results indicate that hHSS could protect hepatocytes against CCl4 through maintaining calcium homeostasis, preventing potassium leakage and sustaining stability of hepatocyte polasmalemma.

Alanine Transaminase↗
PubMed1993

Investigation of the clinical value of assessing renal size on computed tomography in autosomal dominant polycystic kidney disease.

We examined relationship between serum creatinine concentration (Scr) and renal size on CT scans on 32 occasions in 25 patients with autosomal dominant polycystic kidney disease (ADPKD). As a result, a significant correlation was observed when the Scr was less than 5 mg/dl, as shown by the correlation coefficient (r) and P values of 0.803 and 0.0001, respectively. However, these values changed to 0.482 and 0.0093, respectively when 2 cases with Scr 6.2 and 6.4 mg/dl were included, and further changed to 0.005 and 0.9775 when an additional 4 cases with Scr 7.8, 9.9, 11.1 and 20.1 mg/dl were included. Renal size is therefore thought to be a useful parameter of renal function when the Scr is less than 5 mg/dl in ADPKD, but not when the Scr exceeds 6 mg/dl, and is regarded as useless for predicting the time at which dialysis would be required.

Creatinine↗
PubMed1992

Hypervitaminosis D associated with drinking milk.

BACKGROUND: Vitamin D has been added to milk in the United States since the 1930s to prevent rickets. We report the unusual occurrence of eight cases of vitamin D intoxication that appear to have been caused by excessive vitamin D fortification of dairy milk. METHODS: Medical records were reviewed and a dietary questionnaire was sent to eight patients who had unexplained hypervitaminosis D. Vitamin D analyses with high-performance liquid chromatography were performed on samples of the patients' serum, the dairy milk they drank, and the vitamin D concentrate added to the milk. RESULTS: All eight patients drank milk produced by a local dairy in amounts ranging from 1/2 to 3 cups (118 to 710 ml) daily. All had elevated serum 25-hydroxyvitamin D concentrations (mean [+/- SD], 731 +/- 434 nmol per liter [293 +/- 174 ng per milliliter]). Six of the eight patients had elevated serum vitamin D3 concentrations. Of the eight patients, seven had hypercalcemia and one had hypercalciuria but normocalcemia (mean serum calcium, 3.14 +/- 0.51 mmol per liter [12.6 +/- 2.1 mg per deciliter]). Analysis of the dairy's vitamin D-fortified milk revealed concentrations of vitamin D3 (cholecalciferol) that ranged from undetectable to as high as 232,565 IU per quart (245,840 IU per liter). An analysis of the concentrate that was used to fortify the milk, labeled as containing vitamin D2 (ergocalciferol), revealed that it contained vitamin D3. CONCLUSIONS: Hypervitaminosis D may result from drinking milk that is incorrectly and excessively fortified with vitamin D. Milk that is fortified with vitamin D must be carefully monitored.

Adult↗
PubMed1992

The vitamin D content of fortified milk and infant formula.

BACKGROUND: The fortification of milk and infant formula with vitamin D has had an important role in eliminating rickets in children and osteomalacia in adults. A recent outbreak of vitamin D intoxication caused by drinking milk fortified with excess vitamin D has led to questions about the level of vitamin D in milk from other producers. METHODS: We used high-performance liquid chromatography to measure vitamin D in samples of 13 brands of milk with various fat contents and 5 brands of infant formula purchased at random from local supermarkets in five Eastern states. RESULTS: Only 12 (29 percent) of the 42 samples of the 13 brands of milk and none of the 10 samples of the 5 brands of infant formula contained 80 to 120 percent of the amount of vitamin D stated on the label. Twenty-six of the 42 milk samples (62 percent) contained less than 80 percent of the amount claimed on the label. No vitamin D was detected in 3 of the 14 samples of skim milk tested (lower limit of assay, 4.7 IU per quart [5.0 IU per liter]). One milk sample labeled as containing vitamin D2 (ergocalciferol) contained vitamin D3 (cholecalciferol). Seven of the 10 samples of infant formula contained more than 200 percent of the amount stated on the label; the sample with the highest concentration contained 419 percent of the stated amount. None of the samples of infant formula contained less than the amount stated. CONCLUSIONS: Milk and infant-formula preparations rarely contain the amount of vitamin D stated on the label and may be either underfortified or overfortified. Since both underfortification and overfortification are hazardous, better monitoring of the fortification process is needed.

Animals↗
PubMed1991

Regeneration of transgenic Lycium barbarum L.

A simple and effective system for the transformation and regeneration of Lycium barbarum L. has been developed. Young stem segments from Lycium barbarum L. were infected by Agrobacterium tumefaciens harboring a vector containing neomycin phosphotransferase II (npt-II) gene derived from non-oncogenic Ti plasmid. Calli originating from young stem segments on selective induction medium could differentiate into buds on selective differentiation medium rapidly and finally developed into whole plants. NPT-II enzyme activity assay and DNA hybridization indicated that the foreign gene had been integrated into the genome of Lycium barbarum L. and could be expressed in plants.

Kanamycin↗
PubMed1990

Dynamic study on iliac trabeculae of normal Chinese.

We studied 41 iliac bone blocks taken by biopsies from normal Chinese who were divided into several groups by age. On the schedule of 3-11-3-5 days, double tetracycline labellings were administered before bone biopsies. Ten microns undecalcified sections were made with Reichert-Jung microtome and analyzed with Zeizz MOP-Videoplan by light and fluorescent microscopy. The results showed that bone formation had a peak value at adolescence and the mean wall thickness decreased gradually with age. Bone dynamics fluctuated with age because of endocrinological changes in the intrinsic environment. The data we obtained may be used as a reference for clinical investigation of various metabolic bone disorders.

Adult↗
PubMed1989

A study of the history of the Chinese family structures.

"It is...the purpose of this paper to discuss the [Chinese] family structure by starting from the major characteristics of family structures in traditional times and moving on from there to a brief description of family structures in modern China and the directions of change in family structures in present-day China." Consideration is given to family size and interpersonal relationships.

Asia↗
PubMedDate not supplied

Inhibition of cardiac sarcolemma Na(+)-K+ ATPase by oxyradical generating systems.

The Na(+)-K+ ATPase activity and SH group content were decreased whereas malondialdehyde (MDA) content was increased upon treating the porcine cardiac sarcolemma with xanthine plus xanthine oxidase, which is known to generate superoxide and other oxyradicals. Superoxide dismutase either alone or in combination with catalase and mannitol fully prevented changes in SH group content but the xanthine plus xanthine oxidase-induced depression in Na(+)-K+ ATPase activity as well as increase in MDA content were prevented partially. The Lineweaver-Burk plot analysis of the data for Na(+)-K+ ATPase activity in the presence of different concentrations of MgATP or Na+ revealed that the xanthine plus xanthine oxidase-induced depression in the enzyme activity was associated with a decrease in Vmax and an increase in Km for MgATP; however, Ka value for Na+ was decreased. Treatment of sarcolemma with H2O2 plus Fe2+, an hydroxyl and other radical generating system, increased MDA content but decreased both Na(+)-K+ ATPase activity and SH group content; mannitol alone or in combination with catalase prevented changes in SH group content fully but the depression in Na(+)-K+ ATPase activity and increase in MDA content were prevented partially. The depression in the enzyme activity by H2O2 plus Fe2+ was associated with a decrease in Vmax and an increase in Km for MgATP. These results indicate that the depressant effect of xanthine plus xanthine oxidase on sarcolemmal Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals. Furthermore, the oxyradical-induced depression in Na(+)-K+ ATPase may be due to the formation of superoxide, hydroxyl and other radicals.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

Attenuation of changes in G(i)-proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril.

Cardiac dysfunction in animals with congestive heart failure due to myocardial infarction (MI) is known to be associated with a wide variety of defects in receptor and post-receptor mechanisms. Since the heart function have been shown to be improved by treatment with different angiotensin converting enzyme (ACE) inhibitors, we examined the effects of imidapril, an ACE inhibitor, on changes in post-receptor mechanisms involving adenylyl cyclase (AC) and G proteins in the failing heart. Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated daily with 1 mg/kg (orally) imidapril for 5 weeks. The animals were assessed for their left ventricular function and crude membranes were isolated from the viable left ventricle and examined for AC activities as well as G-protein activities and expression. Animals with heart failure exhibited depressions in ventricular function and AC activities in the absence or presence of forskolin, NaF and Gpp(NH)p. The AC activity in the presence of pertussis toxin was increased whereas that in the presence of cholera toxin was decreased in the failing heart. Protein contents and mRNA levels for G(i)-proteins were increased whereas those for G(s)-proteins were unaltered in the infarcted heart. All these changes due to MI were prevented by imidapril treatment. The results indicate that the depressed cardiac function in the failing heart may partly be due to the direct effects of changes in AC and G(i) proteins.

Adenylyl Cyclases↗