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Biomedical subjects

G Q Chang

Publications and source records attributed to G Q Chang.

11 recordsLinked to original sources
PubMed2006

Distinct phenotypes of obesity-prone AKR/J, DBA2J and C57BL/6J mice compared to control strains.

OBJECTIVE: To characterize and compare three obesity-prone inbred strains, AKR/J, DBA/2J and C57BL/6J, to three control strains, C3H/HeJ, BALB/cByJ and C57L/J, selected based on their normal eating patterns and moderate weight gain on high-calorie diets. METHODS AND PROCEDURES: These six strains were examined at 5 weeks of age while still of normal body weight, and they were maintained for 1 day or 3 weeks on different feeding paradigms with macronutrient diets. Measurements were taken of macronutrient intake, body weight and body fat accrual, circulating hormones and metabolites, and the hypothalamic peptide, galanin. RESULTS: The three control strains each selected a balanced diet with 50% carbohydrate and 15-25% fat when given a choice of macronutrients, and they had similar, normal range of scores for the measures of body weight, adiposity, the hormones, insulin and leptin, and the metabolites, glucose and triglycerides. When compared to this control baseline, the obesity-prone strains with similar total caloric intake to controls selected a diet with significantly more fat (30-40%) and less carbohydrate (<40%). They also had greater adiposity, with the largest differences detected for the AKR/J and DBA/2J strains. These two obesity-prone strains compared to control strains had elevated levels of insulin and leptin. They also had higher triglyceride levels and increased expression and levels of galanin in the hypothalamic paraventricular nucleus. A very different pattern was detected in the obesity-prone C57BL/6J strain, which exhibited a stronger preference for protein as well as fat, normal levels of insulin, leptin and triglycerides, hyperglycemia relative to all other strains, and a small increase in galanin. CONCLUSION: These comparisons to control strains revealed a distinct phenotype in the two obesity-prone strains, AKR/J and DBA/2J, which is very similar to that described in obesity-prone, outbred rats. They also identified a clearly different phenotype in the obesity-prone C57BL/6J strain.

Adipose Tissue↗
PubMed2001

[Clinical effects of revascularization in lower limb ischemia].

OBJECTIVE: To investigate the clinical effects of revascularization in lower extremity for severe ischemia. METHODS: Fifty-six lower limbs with severe ischemia in 49 patients were evaluated retrospectively, who underwent surgical intervention from January of 1995 to December of 2000. By arteriography, the actual anatomic distributions of occlusive disease included infrarenal aorta-bicommon iliac arteries, abdominal aorta-bicommon iliac arteries, iliac artery, and femoral artery or femoropopliteal artery. The indication for surgery was disabling claudication, rest pain and gangrene. Fourteen limbs in 12 cases received arterialization of femoral venous system by artificial venous-arterial fistula. Artificial vascular grafts were implanted in 33 limbs of 28 cases, endarterectomy and patch profundaplasty were performed in 5 limbs of 5 cases, and primary amputation was carried out in 4 cases. RESULTS: During 38 months follow-up in average, 4 limbs were amputated within 52 revascularizated limbs, and accumulated amputation rate was 14.3%. Patency rate was 68.4% in arterial revascularization limbs (26/38 limbs), and limb survival rate was 94.7%(36/38 limbs) by procedure of artificial vascular grafts, endarterectomy and patch profundaplasty. Limb survival rate in procedure of artificial venous-arterial fistula was 85.7%(12/14 limbs). CONCLUSION: In treatment of severe lower extremity ischemia, the effective revascularization can be achieved by artificial vascular bypass, endarterectomy and patch profundaplasty, or arterialization of femoral venous system. Options in the surgical management should depend on individual. Arteriography is essential for revascularization and properly planning a practicable surgical approach.

Adult↗
PubMed2000

Diacylglycerol kinase zeta in hypothalamus interacts with long form leptin receptor. Relation to dietary fat and body weight regulation.

Leptin and its long form receptor, Ob-Rb, in hypothalamic nuclei play a key role in regulating energy balance. The mutation of Ob-Rb into one of its natural variants, Ob-Ra, results in severe obesity in rodents. We demonstrate here that diacylglycerol kinase zeta (DGKzeta) interacts, via its ankyrin repeats, with the cytoplasmic portion of Ob-Rb in yeast two-hybrid systems, in protein precipitation experiments in vitro and in vivo. It does not interact, however, with the short form, Ob-Ra, which mediates the entry of leptin into the brain. Furthermore, we show by in situ hybridization that DGKzeta is expressed in neurons of hypothalamic nuclei known to synthesize Ob-Rb and to participate in energy homeostasis. The mutant ob-/ob- and db-/db- mice exhibit increased hypothalamic DGKzeta mRNA level compared with their wild-type controls, suggesting a role for the leptin/OB-Rb system in regulating DGKzeta expression. Further experiments show that hypothalamic DGKzeta mRNA level is stimulated by the consumption of a high-fat diet. In addition, DGKzeta mRNA is statistically significantly lower in rats and inbred mice that become obese on a high-fat diet compared with their lean counterparts. In fact, it is strongly, negatively correlated with both body fat and circulating levels of leptin. Taken together, our evidence suggests that DGKzeta constitutes a downstream component of the leptin signaling pathway and that reduced hypothalamic DGKzeta mRNA, and possibly activity, is associated with obesity.

Amino Acid Sequence↗
PubMed1998

Neuronal nicotinic acetylcholine receptors in rat trigeminal ganglia.

The application of nicotine to the various epithelia served by the trigeminal nerve produces irritation and/or pain by activating neuronal nicotinic acetylcholine receptors (NnAChRS) in sensory neurons. In this study the NnAChRs were identified in rat trigeminal ganglia (TG) using RT-PCR and immunocytochemistry. With RT-PCR the subunits of NnAChRs in rat TG were determined, and with immunocytochemistry the localization of three prominent subunits (alpha 7, alpha 4 and beta 2) were localized in intact TG neurons. The relative abundance of the alpha and beta subunits were: alpha 7 approximately alpha 3 > alpha 6 > alpha 4 approximately alpha 5 > alpha 9 > or = alpha 2, and beta 2 approximately beta 3 > beta 4. This is the first report of the alpha 9 subunit in TG. Immunohistochemical studies revealed that almost all TG neurons contained alpha 7-LI and alpha 4-LI, and that 85% had beta 2-LI. For these three subunits much of the label was internalized. Immunocytochemical studies using antibodies raised against chick alpha 8 subunits did not specifically label rat TG. These data reveal that rat TG neurons contain the entire spectrum of mammalian NnAChR subunits.

Animals↗
PubMed1997

Correlation of DNA fragmentation and chromatin condensation in apoptotic nuclei of the Ser 6 mouse retina.

The form of cell death known as apoptosis was first described in thymocytes. The hallmarks of apoptosis include chromatin condensation, membrane blebbing, formation of apoptotic bodies, and DNA fragmentation. DNA fragmentation can be visualized morphologically by the TdT-mediated dUTP-biotin nick end labeling (TUNEL) method that labels the cut DNA ends. However, at the light microscopic (LM) level, TUNEL-positive nuclei cannot readily be correlated with the other hallmarks of apoptosis. In the retina, chromatin condensation and DNA fragmentation are the major features of developmental cell death as well as photoreceptor degeneration. We performed TUNEL at the electron microscopic (EM) level, which permitted correlation of DNA fragmentation with chromatin condensation. We studied the retinas of transgenic mice (Ser 6) expressing the Pro347Ser mutant rhodopsin gene during developmental cell death (age 7 days) and photoreceptor degeneration (age 21 days). We found that 90% of the nuclei showing chromatin condensation were TUNEL positive as well. Our results demonstrated DNA fragmentation and chromatin condensation in the same cells as they underwent apoptosis in vivo, confirming the notion that these processes are concomitant events, and by implication, that activation of an endogenous endonuclease is an important step in the death process of retinal neurons.

Animals↗
PubMed1996

Localization of substance P NK-1 receptors in rat tongue.

In rat tongue, neurons containing substance P terminate in connective tissue, in taste buds, and in lingual epithelium surrounding taste buds in fungiform, foliate and circumvallate papillae. Although many functions have been attributed to these neurons, virtually nothing is known about their physiological function. As a step towards this end, immunocytochemical methods were used to identify the NK-1 receptors (SPR) in rat tongue. SPR-IR was found in the basolateral membranes of taste cells in fungiform, circumvallate and foliate papillae. SPR-IR was not found in the dorsal epithelium or in any structure that could be clearly identified as a neuron. SPR-IR was also found in von Ebner's glands in circumvallate and foliate papillae and in blood vessels in connective tissue in all three papillae. These data suggest that substance P may play a role in taste and/or in oral pain.

Amino Acid Sequence↗
PubMed1994

Apoptosis leads to photoreceptor degeneration in inherited retinal dystrophy of RCS rats.

PURPOSE: To determine the pathogenetic mechanism of photoreceptor cell degeneration in the inherited retinal dystrophy in Royal College of Surgeons (RCS) rats. METHODS: The dystrophic retinas of the pink-eyed RCS (RCS-rdy-p) rats were examined for DNA fragmentation by agarose gel electrophoresis of retinal DNA and by TdT-mediated biotin-dUDP nick-end labeling (TUNEL) in paraffin sections. Rats ranging in age from 3 to 60 days were examined. RESULTS: Agarose gel electrophoresis of retinal DNA isolated from animals 25, 30, 35, and 40 days old showed a ladder pattern of degradation with bands corresponding to multiples of 180 to 200 base pair subunits. TUNEL study showed increasing labeling of photoreceptor cells with progression of the retinal dystrophy of the RCS rats. CONCLUSIONS: Apoptosis is the dominant mechanism of photoreceptor degeneration in the RCS rat, which has a genetic defect in the phagocytic activity of retinal pigment epithelium. The onset of the degeneration appeared to vary between rod cells in the different regions of the eye.

Animals↗
PubMed1993

Apoptosis: final common pathway of photoreceptor death in rd, rds, and rhodopsin mutant mice.

Mutations in the retinal degeneration, retinal degeneration slow(/peripherin) and rhodopsin genes cause photoreceptor degeneration in humans and mice. Although the phenotypes arising from these mutations are different, suggesting different mechanisms of pathogenesis, we present evidence that apoptosis may be the final common pathway of the disease process linking genotype to phenotype. We observed internucleosomal cleavage of retinal DNA by gel electrophoresis and fragmented DNA at the single cell level by labeling the nicked DNA ends with biotinylated poly(dU). In retinal degeneration mice, DNA fragmentation occurred during the period of photoreceptor degeneration. In retinal degeneration slow mice and in transgenic mice expressing a mutant (Pro347Ser) rhodopsin gene, DNA fragmentation occurred after normal histogenetic cell death (also apoptosis) had ceased. Since DNA fragmentation by internucleosomal cleavage is a cardinal feature of apoptosis, our data suggest that all three of these genetic mutations lead to apoptosis.

Amino Acid Sequence↗
PubMed1993

Chinese families after the death of a child from cancer.

As part of a major study of the impact of childhood cancer on Chinese families, 17 families agreed to be interviewed after the death of their child from cancer. They convey what happens to the child's body after death and what remembrances the family has kept of their child's belongings. They share how they have adjusted and what they would like other parents who have a child with cancer to know. A picture emerges of what it is like to have a child die from cancer in China.

Adult↗