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"Pendahuluan: Hipoksia plasenta pada bayi prematur menyebabkan stres oksidatif yang merusak protein penaut endotel kapiler plasenta. Kerusakan pada kapiler plasenta diharapkan dapat menggambarkan perubahan permeabiltas kapiler otak yang menyebabkan perdarahan intraventrikel.Metode: Penelitian observasional potong lintang terhadap 58 sampel plasenta bayi prematur. Hipoksia dinilai dari saturasi vena umbilikal, respon jaringan terhadap hipoksia dari kadar HIF-1α, stres oksidatif dari kadar malondialdehid (MDA) dan glutation (GSH). Integritas lapisan endotel dinilai dengan histomorfologi, ekspresi protein N-kaderin dan okludin dengan imunohistokimia, Glial fibrillary acidic protein (GFAP) sebagai petanda kerusakan perivaskular astrosit dan perdarahan intraventrikel dinilai dengan ultrasonografi kepala.Hasil: Kadar HIF-1α lebih tinggi tidak bermakna pada kelompok hipoksia dibandingkan kelompok non hipoksia (uji t tidak berpasangan, p = 0,122); Kadar MDA jaringan plasenta lebih tinggi tidak bermakna sedangkan GSH lebih rendah tidak bermakna (Mann Whitney, p = 0,414 dan p = 0,810). Gambaran histomorfologi lebih tidak utuh tidak bermakna (Chi-square, p = 0,066), sedangkan ekspresi N-kaderin dan okludin lebih rendah bermakna (Chi-square, p = 0,001). Kadar GFAP serum lebih tinggi bermakna (Mann Whitney, p = 0,05). Korelasi tidak bermakna antara ekspresi N-kaderin dan okludin dengan perdarahan intraventrikel (Spearman?s rho, p = 0,869 dan p = 0,341).Kesimpulan: Hipoksia pada plasenta menyebabkan perubahan ekspresi protein penaut endotel kapiler plasenta, secara molekuler sudah menyebabkan perubahan permeabilitas lapisan endotel kapiler plasenta tetapi secara struktural belum. Perubahan ekspresi protein penaut endotel kapiler plasenta tidak berhubungan dengan perdarahan intraventrikel.

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Introduction: Plasental hypoxia in premature infants causes oxidative stress which inflicts damage to endothelial protein junction of placental capillary. It is expected that damaged of placental capillary can demonstate permeability changes in brain capillary that can cause intraventricular hemorrage.

Method:.a cross sectional observational study conducted on 58 placenta of premature infants. Hypoxia is determined by umbilical venous saturation. Tissue response to hypoxia determined by the level of HIF-1α, stress oxidative by the level of malondialdehide (MDA) and glutation (GSH). Endothelial layer integtrity by histomorfologi overview, N-cadherine and occludin by immunohistochemistry. Glial fibrillary acidic protein (GFAP) as perivascular astrocyte disruption marker and intraventricular hemorrhage carried by head ultrasound.

Result: The levels of HIF-1α was not significantly higher in hypoxia group compared to non hypoxia group (unpaired t test, p = 0,122); The level of placental MDA was not significantly hingher while GSH was not significantly lower (Mann Whitney, p = 0,414 and p = 0,810). Histomorpological overview was not significantly not intact (Chi-square, p = 0,066), while the expression of N-cadherine and occludin were significantly lower (Chi-square = 0,001). There was not significant correlation between protein junction expression with intravenrticular hemorrhage (Spearman?s rho, p = 0,869 and p = 0,341).

Conclution: Hypoxia causes lower expression of N-cadherin and occludin, moleculary it cause placental endothelial capillary permeability but structurally it does not. Protein expression changes does not correlate with intraventricular hemorrhage."

"Pertumbuhan mukosa usus manusia belum sempurna saat dilahirkan, karena itu usus bayi sering dikatakan sebagai leaky gut. Probiotik diketahui dapat membantu maturasi saluran cerna. Apakah dalam ASI memang terdapat probiotik ataukah suatu kontaminasi, masih diperdebatkan.Penelitian ini bertujuan untuk mengetahui apakah probotik ada dalam ASI bila diberikan suplementasi probiotik pada ibu hamil sejak trimester III dan menyusui, efek terhadap probiotik lain dan IL-8 dalam ASI, IFABP urin dan alfa-1-antitripsin (AAT) serta kalprotektin tinja, saat bayi lahir dan usia tiga bulan, dalam rangka menilai integritas mukosa usus.Dilakukan penelitian uji klinis, paralel dua kelompok dengan randomisasi, samar ganda yang dilakukan di RS Budi Kemuliaan dan klinik-klinik satelitnya sejak Desember 2014 sampai dengan Desember 2015. Jumlah subjek 35 per kelompok. Digunakan probiotikBifidobacterium animalis lactis HNO19 karena bukan merupakan resident bacteria.Lima subjek positif DR10 dalam kolostrum (V0) dan 7 subjek positif saat bayi usia 3 bulan (V3) pada kelompok probiotik. Hasil negatif didapati pada kelompok plasebo. Apusan kulit sekitar payudara negatif pada kedua kelompok. Nilai median IL-8 kelompok probiotik dibanding kelompok plasebo pada V0 dan V3 berturut-turut 2810,1 pg/mL vs. 1516,4 pg/mL (p = 0,327) dan 173,2 pg/mL vs. 132,7 pg/mL (p = 0,211). IFABP V0 dan V3 211,7 ng/mL vs. 842,5 ng/mL (p = 0,243) dan 25,3 ng/mL vs. 25,1 ng/mL (p = 0,466). AAT 136,2 mg/dL vs. 148,1 mg/dL (p = 0,466) dan 24 mg/mL vs. 29,72 mg/mL (p = 0,545). Kalprotektin 746,8 ng/mL vs. 4645,2 ng/mL (p = 0,233) dan 378,6 ng/mL vs. 391,3 ng/mL (p = 0,888).Probiotik DR10 yang diberikan pada ibu hamil sejak trimester III dapat ditemukan dalam kolostrum dan usia 3 bulan pada kelompok probiotik, dan bukan suatu kontaminasi .Tidak terdapat perbedaan bermakna terhadap probiotik lain, kadar IL-8 dalam ASI, IFABP urin, AAT dan kalprotektin tinja pada kelompok probiotik dibanding dengan kelompok plasebo.

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Newborn infants have intestinal hyperpermeability because their gut mucosa is not fully mature yet. It is known that probiotics helps gut maturity. It remains unclear whether probiotics pass through breast milk or whether the positive cultures are the result of contamination. This study aimed to evaluate the effect of probiotic supplementation in pregnant and lactating mothers, with regards to probiotic presence and IL-8

concentration in breast milk, infant urine intestinal fatty acid binding protein (IFABP), as well as fecal ?-1 anti-trypsin (AAT) and calprotectin at birth (V0) and at infant 3

months of age (V3) .

This randomized, controlled trial was double-blind, two parallel groups, probiotic and placebo with 35 subjects in each group. The sudy was done at Budi Kemuliaan Hospital and it’s satellite clinics from December 2014 until December 2015. We used Bifidobacterium

animalis lactis HNO19 (commonly known as DR10) as the supplemental probiotic, as it is not a member of the normal flora.

Probiotik DR10 were found in colostrum at 5 subjects and 7 subjects in V3 breastmilk probiotics group, but none in placebo group. Skin swab of DR10 were negative in both group. Median breast milk IL-8 in probiotic group compare to placebo group at V0 and V3 respectively were 2810.1 pg/mL vs. 1516.4 pg/mL (p = 0.327) and 173.2 pg/mL vs. 132.7 pg/mL (p = 0.211). Infant urine IFABP 211.7 ng/mL vs. 842.5 ng/mL (p = 0.243) and 25.3 ng/mL vs. 25.1 ng/mL (p = 0.466). Infant stool AAT 136.2 mg/dL vs. 148.1 mg/dL (p = 0.466) and 24 mg/mL vs. 29.72 mg/mL (p = 0.545). Stool calprotectin 746.8 ng/mL vs. 4645.2 ng/mL (p = 0.233) and 378.6 ng/mL vs. 391.3 ng/mL (p = 0.888).

Probiotic DR10 were found in colostrum and 3 month-breast milk of women in the probiotic group, but no DR10 in placebo group. However, breast milk IL-8, the presence of other probiotics, and infant gut mucosal integrity were not significantly different between the two groups."