Biological significance of enhanced mitochondrial ketogenesis during the early stages after 70% hepatectomy in rats

Ketogenic capacity of mitochondria from the remnant liver of 70% hepatectomized rats was studied in relation to mitochondrial phosphorylative activity. Ketogenic capacity increased to a maximum of 6.04 +/- 0.39 from 3.84 +/- 0.13 of control, with an enhancement of mitochondrial phosphorylative activity 6 hr after hepatectomy, and then decreased to normal levels within 24 hr. Adenylate energy charge, (ATP + 1/2ADP)/(ATP + ADP + AMP), of the remnant liver decreased to 0.825 +/- 0.006 as compared to 0.849 +/- 0.002 of control 6 hr after operation. At 12 hr, total ketone body concentrations of the arterial blood increased concomitant with a fall in ketone body ratio (acetoacetate/3-hydroxybutyrate) which reflects the decreased liver mitochondrial redox (NAD+/NADH) state. These findings suggest that an enhancement of mitochondrial fatty acid oxidation and ketogenesis occurs concomitant with an enhancement of mitochondrial phosphorylative activity in the remnant liver in response to a decreased energy charge after 70% hepatectomy.     

The effects of prenatal protein-energy malnutrition on ossification of fetal rat bones: a biochemical study

In fetal rats whose dams were fed a low-protein diet, 35S sulfate uptake into the growth plate of the long bone and rib was higher than in the control group. The elution pattern of guanidine-HCl extract in gel chromatography revealed that the malnourished group had more high molecular weight proteoglycans in the dissociative condition and a larger aggregated portion in the associative condition than did the control group; however, the same chondroitin-sulfate chain size existed. Calcium content did not differ in both groups. Aggregated proteoglycan or a high molecular weight proteoglycan that existed in the malnourished group probably played an inhibitory role in calcification. Prenatal protein-energy malnutrition may delay the change of proteoglycan character, which could affect mineralization of fetal bones.     

Availability of 4'galactosyllactose (O-beta-D-galactopyranosyl-(1----4)-O-beta-D-galactopyranosyl-(1----4)- D-glucopyranose) in rat

O-beta-D-Galactopyranosyl-(1----4)-O-beta-D-galactopyranosyl-(1----4)-D- glucopyranose (designated as 4'GL) is produced from lactose by Cryptococcus laurentii. The influence of chronic ingestion of 4'GL on body weight gain, organ weight, serum lipids, and liver lipids was investigated in rats. The body weight gains of the 5% and 10% 4'GL-diet groups were higher than that of the control group. Food intake and fecal dry weight were significantly increased (p less than 0.05) by 4'GL feeding. The 4'GL diet produced a significant increase (p less than 0.01) in the wet weight and contents of both the cecum and the colon. However, no significant increase was observed in the weight of the stomach, small intestine, liver, or other organs. The effects of 4'GL on serum and liver lipid levels were not observed in this experiment. The digestion of 4'GL was measured in vitro using the artificial gastric juice, alpha-amylase of human saliva, alpha-amylase of hog pancreas, and mucosa of rat intestine. 4'GL was not hydrolyzed by these enzymes. Long-term ingestion of 4'GL did not cause any induction of 4'GL hydrolyzing enzyme activity in the rat small intestine.     

Deficiency of insulin receptor substrate-1 impairs skeletal growth through early closure of epiphyseal cartilage.

Morphological analyses in and around the epiphyseal cartilage of mice deficient in insulin receptor substrate-1 (IRS-1) showed IRS-1 signaling to be important for skeletal growth by preventing early closure of the epiphyseal cartilage and maintaining the subsequent bone turnover at the primary spongiosa. Introduction: IRS-1 is an essential molecule for intracellular signaling by IGF-I and insulin, both of which are potent anabolic regulators of cartilage and bone metabolism. To clarify the role of IRS-1 signaling in the skeletal growth, morphological analyses were performed in and around the epiphyseal cartilage of mice deficient in IRS-1 (IRS-1(-/-)), whose limbs and trunk were 20-30% shorter than wildtype (WT) mice. MATERIALS AND METHODS: The epiphyseal cartilage and the primary spongiosa at proximal tibias of homozygous IRS-1(-/-) and WT male littermates were compared using histological, immunohistochemical, enzyme cytohistochemical, ultrastructural, and bone histomorphometrical analyses. RESULTS: In and around the WT epiphyseal cartilage, IRS-1 and insulin-like growth factor (IGF)-1 receptors were widely expressed, whereas IRS-2 was weakly localized in bone cells. Chronological observation revealed that height of the proliferative zone and the size of hypertrophic chondrocytes were decreased in WT mice as a function of age, and these decreases were accelerated in the IRS-1 (-/-) cartilage, whose findings at 12 weeks were similar to those of WT at 24 weeks. In the IRS-1(-/-) cartilage, proliferating chondrocytes with positive proliferating cell nuclear antigen (PCNA) or parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor immunostaining had almost disappeared by 12 weeks. Contrarily, TUNEL+ apoptotic cells were increased in the hypertrophic zone, at the bottom of which most of the chondrocytes were surrounded by the calcified matrix, suggesting the closure of the cartilage. In the primary spongiosa, bone volume, alkaline phosphatase (ALP)+ osteoblasts, TRACP+ osteoclasts, and the osteopontin-positive cement line were markedly decreased. Bone histomorphometrical parameters for both bone formation and resorption were significantly lower in IRS-1(-/-) mice, indicating the suppression of bone turnover. CONCLUSION: The IRS-1(-/-) epiphyseal cartilage exhibited insufficient proliferation of chondrocytes, calcification of hypertrophic chondrocytes, acceleration of apoptosis, and early closure of the growth plate. Thus, the data strongly suggest that IRS-1 signaling is important for the skeletal growth by preventing early closure of the epiphyseal cartilage and by maintaining the subsequent bone turnover at the primary spongiosa.     

Q-Switched Alexandrite Laser Therapy for Pigmentation of the Lips Owing to Laugier-Hunziker Syndrome

BACKGROUND: Laugier-Hunziker (LH) syndrome is a rare benign condition in which hyperpigmentation of the lips and buccal mucosa occurs with no systemic associations. OBJECTIVE: We report the response to treatment with the Q-switched alexandrite laser (QSAL) because there are few reports on therapy for LH syndrome. METHODS: The QSAL was used for pigmentation of the lips in a 63-year-old woman with LH syndrome. Laser irradiation was done at 5.0 J/cm2 with a 3 mm spot size. RESULTS: There was 100% clearance of pigmentation of the lips with a single laser treatment, and recurrence was not observed after 6 months. CONCLUSION: The QSAL is very effective for pigmentation owing to LH syndrome.     

Surgical treatment of methicillin-resistant Staphylococcus aureus infection following infrainguinal arterial reconstruction.

A 64-year-old man was referred to our hospital with Methicillin-resistant Staphylococcus aureus (MRSA) infection following infrainguinal arterial reconstruction. As repeated MRSA sepsis occurred, we decided to remove the infected graft with distal revascularization via circuitous graft tunneling to avoid serious infections and allow limb salvage. An iliofemoro bypass was performed via an extra-anatomical bypass, from just below the iliac crest into the musculus quadriceps femoris using an 8 mm-ringed polyester gelatin polypropylene tube graft, with complete debridement of a groin infection. Postoperative 3-dimentional CT angiography revealed that the prostheses was patent and the patient had an uneventful postoperative course. We concluded that this extra-anatomical bypass was a safe procedure and an excellent option for patients with an infected vascular prosthetic graft in the groin after previous revascularization, like in our case with no available autogeneous vein grafts.