The milk and mammary gland (MG) microbiome can be influenced by several factors, such as mode of delivery, breastfeeding, maternal lifestyle, health status, and diet. An increasing number of studies show a variety of positive effects of consumption of probiotics during pregnancy and breastfeeding on the mother and the newborn. The aim of this study was to investigate the effect of oral administration of probiotics Lactobacillus gasseri K7 (LK7) and Lactobacillus rhamnosus GG (LGG) during pregnancy and lactation on microbiota of the mouse mesenteric lymph nodes (MLN), MG, and milk. Pregnant FVB/N mice were fed skim milk or probiotics LGG or LK7 resuspended in skim milk during gestation and lactation. On d 3 and 8 postpartum, blood, feces, MLN, MG, and milk were analyzed for the presence of LGG or LK7. The effects of probiotics on MLN, MG, and milk microbiota was evaluated by real-time PCR and by 16S ribosomal DNA 454-pyrosequencing. In 5 of 8 fecal samples from the LGG group and in 5 of 8 fecal samples from the LK7 group, more than 1 × 10(3) of live LGG or LK7 bacterial cells were detected, respectively, whereas no viable LGG or LK7 cells were detected in the control group. Live lactic acid bacteria but no LGG or LK7 were detected in blood, MLN, and MG. Both probiotics significantly increased the total bacterial load as assessed by copies of 16S ribosomal DNA in MLN, and a similar trend was observed in MG. Metagenomic sequencing revealed that both probiotics increased the abundance of Firmicutes in MG, especially the abundance of lactic acid bacteria. The Lactobacillus genus appeared exclusively in MG from probiotic groups. Both probiotics influenced MLN microbiota by decreasing diversity (Chao1) and increasing the distribution of species (Shannon index). The LGG probiotic also affected the MG microbiota as it increased diversity and distribution of species and proportions of the genera Lactobacillus and Bifidobacterium. These results provide evidence that probiotics can modulate the bacterial composition of MLN and MG microbiota in ways that could improve the health of the MG and, ultimately, the health of the newborn.
Background: Long-acting local anaesthetics (e.g. bupivacaine hydrochloride) or sustained-release formulations of bupivacaine (e.g. liposomal bupivacaine) may be neurotoxic when applied in the setting of diabetic neuropathy. The aim of the study was to assess neurotoxicity of bupivacaine and liposome bupivacaine in streptozotocin (STZ)induced diabetic mice after sciatic nerve block. We used the reduction in fibre density and decreased myelination assessed by G-ratio (defined as axon diameter divided by large fibre diameter) as indicators of local anaesthetic neurotoxicity. Results: Diabetic mice had higher plasma levels of glucose (P < 0.001) and significant differences in the tail flick and plantar test thermal latencies compared to healthy controls (P < 0.001). In both diabetic and nondiabetic mice, sciatic nerve block with 0.25% bupivacaine HCl resulted in a significantly greater G-ratio and an axon diameter compared to nerves treated with 1.3% liposome bupivacaine or saline (0.9% sodium chloride) (P < 0.01). Moreover, sciatic nerve block with 0.25% bupivacaine HCl resulted in lower fibre density and higher large fibre and axon diameters compared to the control (untreated) sciatic nerves in both STZ-induced diabetic (P < 0.05) and nondiabetic mice (P < 0.01). No evidence of acute or chronic inflammation was observed in any of the treatment groups. Conclusions: In our exploratory study the sciatic nerve block with bupivacaine HCl (7 mg/kg), but not liposome bupivacaine (35 mg/kg) or saline, resulted in histomorphometric indices of neurotoxicity. Histologic findings were similar in diabetic and healthy control mice.
Background
Diabetes mellitus and the associated neuropathic complications have become a steadily increasing global health burden. Diabetic patients are estimated to require surgery at least twice as often as nondiabetic patients. Neuropathy may change the way nerves respond to nerve blocks. There is currently no consensus on whether regional anaesthesia techniques should be adopted in these patients. Long-acting local anaesthetics ( e.g . bupivacaine HCl) or sustained-release formulations of bupivacaine ( e.g . liposomal bupivacaine) could prove neurotoxic in the presence of diabetic neuropathy. The aim of the study was to assess neurotoxicity of liposome bupivacaine in streptozotocin (STZ)-induced diabetic mice after sciatic nerve block using a reduction in fibre density and decreased myelination assessed by G-ratio as an indicator of local anaesthetic neurotoxicity.
Results
Prior to performing sciatic nerve block, higher levels of fasting glucose were recorded in diabetic mice compared to nondiabetic mice ( P < 0.001). Likewise, significant differences were noted in the tail flick and plantar test thermal latencies between the groups ( P < 0.001) which confirmed the presence of peripheral sensory neuropathy in diabetic mice. In both, diabetic and nondiabetic mice, sciatic nerve block with 0.25% bupivacaine HCl resulted in a significantly greater G-ratio (axon diameter/large fibre diameter) and an axon diameter compared to nerves treated with 1.3% liposomal bupivacaine or saline (0.9% sodium chloride) ( P < 0.01 ). Moreover, sciatic nerve block with 0.25% bupivacaine HCl resulted in higher fibre density and large fibre and axon diameters compared to the control (untreated) sciatic nerves in both STZ-induced diabetic ( P < 0.05 ) and nondiabetic mice ( P < 0.01 ). No evidence of acute or chronic inflammation was observed in any of the treatment groups.
Conclusions
Under the conditions of this study, sciatic nerve block with bupivacaine HCl, but not liposome bupivacaine or saline, resulted in histomorphometric indices of neurotoxicity. The presence of diabetes did not appear to affect the severity of the histologic findings.
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